0% found this document useful (0 votes)
88 views828 pages

Textbook of Oral and Maxillofacial Surgery 2014

The 'Textbook of Oral and Maxillofacial Surgery' edited by Rajiv M Borle provides a comprehensive guide to contemporary practices and procedures in the field, incorporating personal experiences and clinical images. It addresses specific conditions prevalent in the subcontinent, such as temporomandibular ankylosis and oral submucous fibrosis, while also covering essential surgical principles and patient care. This first edition aims to serve as a valuable resource for both undergraduate and postgraduate students, with a focus on practical applications and thorough explanations.

Uploaded by

Trung Phong
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
88 views828 pages

Textbook of Oral and Maxillofacial Surgery 2014

The 'Textbook of Oral and Maxillofacial Surgery' edited by Rajiv M Borle provides a comprehensive guide to contemporary practices and procedures in the field, incorporating personal experiences and clinical images. It addresses specific conditions prevalent in the subcontinent, such as temporomandibular ankylosis and oral submucous fibrosis, while also covering essential surgical principles and patient care. This first edition aims to serve as a valuable resource for both undergraduate and postgraduate students, with a focus on practical applications and thorough explanations.

Uploaded by

Trung Phong
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 828

Textbook of

Oral and Maxillofacial Surgery


Textbook of
Oral and Maxillofacial Surgery

Editor
Rajiv M Borle MDS FAOMSI
Professor
Oral and Maxillofacial Surgery
Sharad Pawar Dental College and Hospital
Director
Smile Train Project, Acharya Vinoba Bhave Rural Hospital
Registrar
Datta Meghe Institute of Medical Sciences (Deemed University)
Wardha, Maharashtra, India

Foreword
GE Ghali

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD


New Delhi • London • Philadelphia • Panama
®

Jaypee Brothers Medical Publishers (P) Ltd

Headquarters
Jaypee Brothers Medical Publishers (P) Ltd
4838/24, Ansari Road, Daryaganj
New Delhi 110 002, India
Phone: +91-11-43574357
Fax: +91-11-43574314
Email: [email protected]

Overseas Offices
J.P. Medical Ltd Jaypee-Highlights medical publishers Inc Jaypee Medical Inc
83, Victoria Street, London City of Knowledge, Bld. 237, Clayton The Bourse
SW1H 0HW (UK) Panama City, Panama 111, South Independence Mall East
Phone: +44-2031708910 Phone: +1 507-301-0496 Suite 835, Philadelphia
Fax: +02-03-0086180 Fax: +1 507-301-0499 PA 19106, USA
Email: [email protected] Email: [email protected] Phone: +1 267-519-9789
Email: [email protected]

Jaypee Brothers Medical Publishers (P) Ltd Jaypee Brothers Medical Publishers (P) Ltd
17/1-B, Babar Road, Block-B Bhotahity, Kathmandu, Nepal
Shaymali, Mohammadpur Phone: +977-9741283608
Dhaka-1207, Bangladesh Email: [email protected]
Mobile: +08801912003485
Email: [email protected]

Website: www.jaypeebrothers.com
Website: www.jaypeedigital.com

© 2014, Jaypee Brothers Medical Publishers

The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent
those of editor(s) of the book.
All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic,
mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers.
All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their
respective owners. The publisher is not associated with any product or vendor mentioned in this book.
Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the
subject matter in question. However, readers are advised to check the most current information available on procedures included and
check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and
duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety
precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property
arising from or related to use of material in this book.
This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or
services are required, the services of a competent medical professional should be sought.
Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any
have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity.

Inquiries for bulk sales may be solicited at: [email protected]

Textbook of Oral and Maxillofacial Surgery

First Edition: 2014

ISBN 978-93-5152-009-2
Printed at
Dedicated to
My Parents
Mrs Malati and Dr Mukund Borle
My Patients
Who volunteered themselves and provided me opportunities to learn.
My Patron
Honorable Shri Datta Meghe
Chancellor, Datta Meghe Institute of Medical Sciences (Deemed University)
Who provided me facilities, opportunities and infrastructure to work.
Contributors

Agni Nishit MDS (Oral and Arora Aakash MDS (Oral and Borle Rajiv M MDS FAOMSI
Maxillofacial Surgery) Maxillofacial Surgery) Professor
Associate Professor Associate Professor Oral and Maxillofacial Surgery
Vaidik Dental College and Department of Oral and Sharad Pawar Dental College
Research Center Maxillofacial Surgery and Hospital
Nani Daman (Union Territory) Subharti Dental College Director
India Swami Vivekanand Subharti University Smile Train Project, Acharya Vinoba Bhave
Meerut, Uttar Pradesh, India Rural Hospital
Registrar
Datta Meghe Institute of Medical Sciences
(Deemed University), Wardha
Maharashtra, India

Agrawal Poonam MDS (Oral and Bhola Nitin MDS (Oral and Gadbail Amol MDS (Oral and
Maxillofacial Surgery) Maxillofacial Surgery) Maxillofacial Pathology)
Associate Professor Associate Professor and Head Associate Professor
Saraswati Dental College Sharad Pawar Dental College Sharad Pawar Dental College
Lucknow, Uttar Pradesh, India and Hospital and Hospital
Datta Meghe Institute of Datta Meghe Institute of
Medical Sciences (Deemed University) Medical Sciences (Deemed University)
Sawangi (M), Wardha, Maharashtra, India Wardha, Maharashtra, India

Angik Richa MDS (Oral and Bhoyar Anjali MDS Gaidhane Abhay MD
Maxillofacial Surgery) (Prosthodontics) (Community Medicine)
Associate Professor Postgraduate Diploma in Professor
Awadh Dental Clinical Research Community Medicine
College and Hospital Hospital and Health Care Associate Dean
Jamshedpur, Jharkhand, India Management Global Health Jawaharlal Nehru
Professor and Vice Dean Medical College
Peoples‘ College of Dental Sciences and Datta Meghe Institute of Medical Sciences
Research Center (Deemed University)
Bhopal, Madhya Pradesh, India Wardha, Maharashtra, India

Anjankar AJ MD (Forensic Bora Smriti MDS (Oral and Garg Ketan MDS (Oral and
Medicine) Maxillofacial Surgery) Maxillofacial Surgery)
Professor and Head Assistant Professor Consultant Maxillofacial
Forensic Medicine Nair Hospital Dental College Surgeon
Jawaharlal Nehru Medical Mumbai, Maharashtra, India Nagpur, Maharashtra, India
College
Datta Meghe Institute of Medical Sciences
(Deemed University)
Wardha, Maharashtra, India
viii Textbook of Oral and Maxillofacial Surgery

Garg Rajat MDS (Oral and Nimonkar Pranali V MDS (Oral Sachdeva Sachin Dev MDS (Oral
Maxillofacial Surgery) and Maxillofacial Surgery) and Maxillofacial Surgery)
Consultant Maxillofacial Associate Professor Associate Professor
Surgeon VSPM Dental College Mithila Minority Dental College
Panipat, Haryana, India and Hospital and Hospital
Nagpur, Maharashtra, India Darbhanga, Bihar, India

Singh Divya BDS (Oral and


Maxillofacial Surgery)
Resident Surgeon
Sharad Pawar Dental College
and Hospital
Quazi Syed Zahiruddin MD
Datta Meghe Institute of
Jajoo Suhas N MS MCh (Plastic
(Community Medicine)
Medical Sciences (Deemed University)
Surgery)
Professor Wardha, Maharashtra, India
Professor
Jawaharlal Nehru Medical Community Medicine
College Associate Dean, Global Health
Datta Meghe Institute of Jawaharlal Nehru Medical Vibhute Pawan J MDS

Medical Sciences (Deemed University) College (Orthodontics and Dentofacial

Wardha, Maharashtra, India Datta Meghe Institute of Medical Sciences Orthopedics)


(Deemed University) Associate Professor
Wardha, Maharashtra, India Sharad Pawar Dental College
and Hospital
Datta Meghe Institute of Medical Sciences
(Deemed University)
Wardha, Maharashtra, India

Magarkar Shashwat D MDS Rai Anshul MDS (Oral and Yadav Abhilasha
(Oral and Maxillofacial Surgery) Maxillofacial Surgery) MDS (Oral and Maxillofacial Surgery)
Assistant Professor Assistant Professor Assistant Professor
Government Dental College Department of Trauma and Sharad Pawar Dental College
and Hospital Emergency Medicine and Hospital
Nagpur, Maharashtra, India All India Institute of Medical Datta Meghe Institute of
Sciences, Bhopal, Madhya Pradesh, India Medical Sciences (Deemed University)
Wardha, Maharashtra, India
Foreword

The depth and scope of this book provides the reader a contemporary guide to the knowledge and
procedures undertaken in any leading-edge oral and maxillofacial training program. This work is
attractive to me for many reasons, not the least of which is its completeness and contemporary nature.
This work by Dr Borle is of such a quality that, if need be, it could even be utilized as a curriculum
guideline for oral and maxillofacial surgery education and development.
Additionally, the value and meticulous organization of this work, embracing the entire scope
of oral and maxillofacial surgery, is remarkable not only for its enormous content but also because it
introduces an entirely new cohort of highly qualified contributors to our specialty. The editor has done
a fabulous job and should be commended for bringing these young talents forward for all to be exposed
to in a scholarly venue. There is even a thorough section devoted to such scholarly, but often over-looked, exercises such
as trainee thesis writing.
Beyond the traditional surgery and conditions that are commonplace in the Western world, there is a valuable and
needed section devoted to the management of submucous fibrosis and another on temporomandibular joint ankylosis
with expert coverage of there inherent management difficulties. There is much to appreciate in this solid address of
conditions that rarely exist in the Western world but remain persistent to many of our colleagues.
My mentor, the late RV Walker, often emphasized: “There was always more to learn in the world of oral and
maxillofacial surgery than any single person has the time to achieve or do.” With this new century comes an ever-
expanding frontier of technology pertinent to our wonderful specialty that is so vast that more than one lifetime would
be needed to barely scratch the body of knowledge or attempt to master the skills at hand. Well, these are but a few of
the reasons why a treatise of the kind compiled by Dr Borle, with the help of his contributors, is so comforting as a go-to
resource of all that is contemporary and germane to oral and maxillofacial surgery.
Once again, I commend Dr Borle for this ambitious and monumental project that will surely appeal to a wide
readership, both nationally and internationally, which will forever be captivated by our specialty.

GE Ghali DDS MD FACS


President, American Board of Oral
and Maxillofacial Surgery (2013–2014)
Gamble Professor and Chairman
Department of Oral and Maxillofacial Surgery/
Head and Neck Surgery
Louisiana State University School of Medicine
Shreveport, Louisiana, USA
Preface

This book is not just a compilation of literature but personal experiences of the authors, especially while working in the
rural circumstances have also been incorporated. Clinical pictures of various clinical conditions and photographic
depictions of the surgical procedures have been added for better understanding. Certain diseases such as
temporomandibular ankylosis and oral submucous fibrosis, which are predominantly seen in our subcontinent, have
been discussed in details. The experiences in the management of oral cancer, where patients often report with advanced
diseases and with varied presentation, are shared. The topics such as management of burns, management of soft tissue
trauma and medico-legal aspects of injury, which are not routinely covered in the textbook, have been introduced for
better readership. While writing the text, care has been taken to give explanations based on basics for better understanding
to the beginners. At the same time, the surgical anatomy relevant to the topic has also been discussed.
Some chapters such as Basic Principles of Surgery and Incisions in Maxillofacial Surgery are the highlights of the
book and it is sincerely hoped that not only the undergraduates but also the postgraduate students will be benefitted.
The aspects of instrumentations, commonly used antiseptics, and aseptic technique have been explained in details.
One chapter is dedicated to suture material and technique and plenty of information has been incorporated. The salient
features in the individual chapters are highlighted by inserting text boxes.
All the incorporations have been authenticated by giving necessary bibliography (references) at the end of each
chapter and the appropriate source of information has been acknowledged.
The overall patient care is needed in surgery; and, hence, to generate understanding in postoperative care, airway
management, care of patient under general anesthesia, emergencies, their identification and management, fluid
and electrolyte balance and derangements of the same with management thereof have been discussed to make the
information comprehensive and elaborate.
This is the first edition of the book and lapses, if any, on my part, will be taken care of in the subsequent edition
based on the feedback received from the peers, experts in the field and all other stakeholders, more important the
readers.

Rajiv M Borle
Acknowledgments

I consider myself to be lucky to get proper opportunities at proper time to work and learn. Staying in small town like
Wardha, Maharashtra, India, and joining a rural institute was considered to be a setback but it was proved fruitful as
I came in contact with great personalities who encouraged me, helped me, admired me, and taught me. I am indebted to
my teachers who not only selflessly taught me but also ensured that I do not loose way. I am grateful to my patients who
trusted a stranger like me and provided me opportunity to learn and sharpen my surgical skills.
My sincere thanks are due to my family members, friends and well-wishers for their support, encouragement and
constructive criticism.
I shall be unreasonable if I do not mention my gratitude to my staff and students for their help and for teaching me
computer applications.
I wish to express my sincere gratitude to the contributors, my departmental colleagues and postgraduate students,
who are more computer savvy, and helped me in writing the book.
I shall be failing in my duty if I do not acknowledge my teachers Late Dr SR Johrapurkar, MS, Former Professor
Emeritus of Surgery, Datta Meghe Institute of Medical Sciences (Deemed University), Sawangi (M), Wardha,
Maharashtra; Dr JN Khanna, MDS, Professor Emeritus of Maxillofacial Surgery, Mahatma Gandhi Mission’s Dental
College, Navi Mumbai, Maharashtra, India, and pioneering maxillofacial surgeon of the international fame; Dr DS
Gupta, MDS, Former Professor of Maxillofacial Surgery, Government Dental College, Nagpur, Maharashtra, India; and
my postgraduate guides, who have been my mentors, teachers and role models.
In my professional career, I have come across many great personalities who not only taught me but also most
importantly constructively criticized me; and because of them, I could learn not only basics but also advances in
maxillofacial surgery. To name some of them Dr SV Golhar, MS; Ex-Professor of ENT, Jawaharlal Nehru Medical College;
Dr SN Jajoo, MS, MCH, Plastic Surgery and Professor, Jawaharlal Nehru Medical College; and Dr R Narang, Professor
Emeritus, Mahatma Gandhi Institute of Medical Science, Sewagram, Wardha, Maharashtra, India. I wish to acknowledge
these great personalities with deep sense of humility and gratitude.
I would like to express my sincere gratitude to Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing
Director), Mr Tarun Duneja (Director-Publishing), Mrs Samina Khan (PA to Director), Mr KK Raman (Production
Manager); Mr Sunil Kumar Dogra (Production Executive), Mr Neelambar Pant (Production Coordinator), Mr Akhilesh
Kumar Dubey (Proofreader), Mr Ashutosh Pathak (Proofreader), Mr Manoj Pahuja (Graphic Designer), Mr Vijay Singh
(Graphic Designer), Mr Dilip Kumar (Typesetter), Dr Shyam Chaudhary (Commissioning Editor, Nagpur office) and
staff of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, for expressing personal interest to bring the
book in the present form.
Last but not least, I am indebted to Datta Meghe Institute of Medical Sciences (Deemed University), its Chancellor
and office bearers, for showing faith in me and providing me suitable environments, facilities, support and encouragement
to progress.
Contents

Section 1: Principles of Surgery

1. Basic Principles of Surgery 3


Borle Rajiv M, Rai Anshul, Yadav Abhilasha
• Asepsis and Sterilization 3
• Aseptic Technique 3
• Sterilization 3
• Antiseptic Solutions 6
• Care of Antiseptic Solution 11
• Aseptic Technique 12

2. Sutures 35
Borle Rajiv M, Bora Smriti, Rai Anshul
• Historical Aspects 35
• Properties of Sutures 35
• Principles of Suture Selection 36
• Types of Suture Material 37
• Absorbable Synthetic Suture 37
• Nonabsorbable Suture Material 41
• Metal Suture and Clips 43
• Armamentarium 44
• Suturing Techniques 48
• Ligatures 51
• Suture Removal 51

3. Incisions in Maxillofacial Surgery 54


Borle Rajiv M, Rai Anshul
• Basic Principles of Incision Making 54
• Incisions used in Oral and Maxillofacial Surgery 55
• Commonly used Intraoral Incisions 55
• Extraoral Incisions 58

4. Fluid, Electrolyte Balance and Acid-base Equilibrium 71


Borle Rajiv M, Agrawal Poonam
• Acid-base Balance 71
• Fluid and Electrolyte Imbalance 73
• Acid-base Homeostasis and Disorders 77
xvi Textbook of Oral and Maxillofacial Surgery

• General Principles of Water and Electrolyte Therapy 79


• Fluid Management in Various Systemic Conditions 81
• Parenteral and Enteral Nutrition 82

5. Shock 85
Borle Rajiv M
• Hypovolemic Shock (Oligemic Shock) 85
• Septic Shock 89
• Hypoglycemic Shock 91
• Anaphylactic Shock 92

6. Medical Emergencies in the Clinical Practice 97


Borle Rajiv M, Angik Richa
• Predisposing Factors 98
• Classification of Emergencies in Clinic 98
• Vasovagal Shock/Syncope/Vasodepressor Syncope 99
• Postural Hypotension 102
• Hypoglycemia 103
• Hyperglycemia 105
• Respiratory Tract Emergencies 106
• Hypothyroidism   108
• Hyperthyroidism—Thyrotoxicosis 109
• Myocardial Infarction   111
• Cardiac Arrest 111
• Drug Related Emergencies 115
• Surgical Emergencies   118
• Aspiration of the Foreign Body 120
• Maintenance of Emergency Kit in the Office 121
• Emergency Drugs 122

7. Management of Airway in Maxillofacial Surgery 131


Borle Rajiv M
• Maintenance of Airway 132

8. Biomedical Waste Management 145


Borle Rajiv M, Sachdeva Sachin Dev
• Components of Biomedical Waste 145
• Infectious Waste 146
• Legal Aspects and Environmental Concerns 148

Section 2: Neurological Disorders of Face and General Anesthesia

9. Neurological Disorders of the Face 153


Borle Rajiv M, Rai Anshul
• Trigeminal Neuralgia (Tic Douloureux, Idiopathic Trigeminal Neuralgia) 153
• Glossopharyngeal Neuralgia 157
• Facial Nerve Paralysis 158
Contents xvii

• Frey’s Syndrome 162


• Peripheral Nerve Injuries 162
• Eagle’s Syndrome 168
• Cluster Headache 169
• Temporal Arteritis 171
• Migraine 172

10. General Anesthesia 176


Borle Rajiv M, Angik Richa
• Historical Aspects 176
• Anesthesia after 1846 176
• Introduction of Intravenous Anesthetic Agents 176
• Commonly Used Anesthetic Agents 176
• Indications for General Anesthesia 180
• Preanesthetic Preparation 180
• Preanesthetic Medication 181
• Phases of General Anesthesia 181
• Stages of General Anesthesia 182
• Preanesthetic Evaluation 182
• Induction, Maintenance and Reversal of GA 183
• Complications of General Anesthesia: Intra-anesthetic Problems 185
• Venous Air Embolism 186
• Postanesthetic Care   189

Section 3: Dentoalveolar Surgeries

11. Exodontia 195


Borle Rajiv M, Arora Aakash, Magarkar Shashwat D
• History 195
• Definition of Exodontia 195
• Applied Surgical Anatomy of Teeth and Jaw Bones 195
• Indications for Extraction of Tooth 197
• Contraindications for Extraction 197
• Presurgical Assessment 199
• Methods of Exodontia 200
• Sequence of Procedures to be Undertaken during Extraction 200
• Complications of Exodontia 212

12. Management of Impacted Teeth 222


Borle Rajiv M, Arora Aakash, Magarkar Shashwat D
• Theories of Impaction 222
• Etiology 222
• Impacted Mandibular Third Molars 222
• Applied Surgical Anatomy 222
• Classification of the Impacted Third Molar Impactions 223
• Sequelae of the Impacted Third Molars 225
• Evaluation of the Patient for the Third Molar Surgery 227
• Surgical Procedure 231
xviii Textbook of Oral and Maxillofacial Surgery

• Odontectomy 233
• Complications of Third Molar Surgery 237
• Maxillary Canine Impactions   237
• Diagnostic aids 238
• Classification 238
• No Treatment 238
• Impacted Maxillary Third Molar 239
• Diagnosis 241
• Treatment 241
• No Treatment 241

13. Preprosthetic Surgeries 245


Borle Rajiv M, Bhoyar Anjali, Garg Ketan
• Scope of Preprosthetic Surgery 245
• Anatomical and Physiological Considerations 245
• Vestibuloplasty Procedures 249
• Corrective Surgical Procedures 254
• Hard Tissue Procedures 259

Section 4: Maxillary Sinus

14. Diseases of Maxillary Sinus 275


Borle Rajiv M, Arora Aakash, Nimonkar Pranali V
• Applied Surgical Anatomy 275
• Age Changes in the Maxillary Sinus 275
• Maxillary Sinusitis 276
• Carcinoma of Maxillary Sinus 279
• Oroantral Fistula 281

Section 5: Salivary Glands Pathologies

15. Diseases of Salivary Glands 291


Borle Rajiv M, Agni Nishit, Arora Aakash
• Embryological Development 291
• Surgical Anatomy of Parotid Gland 292
• Identification of the Facial Nerve 293
• Surgical Anatomy of Submandibular Gland 293
• Surgical Anatomy of Sublingual Gland 294
• Diagnostic Aids 297
• Etiology of Tumors 299
• Common Salivary Gland Neoplasm 299
• Approach to the Management of Salivary Gland Tumors 307
• Radiotherapy and Chemotherapy in the Management of Salivary Gland Tumors 310
• Cystic Conditions 311
• Inflammatory Diseases 312
• Salivary Fistula 316
Contents xix

Section 6: Infections of Maxillofacial Region

16. Management of Periapical Infections 321


Borle Rajiv M, Garg Ketan
• Causes 321
• Fate of the Periapical Infection 321
• Pathogenesis of Periapical Lesions 322
• Apicoectomy/Apisectomy 322
• Anatomical Considerations 323

17. Odontogenic Infections 329


Borle Rajiv M, Angik Richa
• Applied Surgical Anatomy 330
• Local Barriers 330
• Fascial Spaces 332
• Spaces Around the Mandible 334
• Spaces Around Maxilla 341
• General Principles of Infection Management 349
• Medicinal Treatment in Orofacial Infections 350
• Selection of Anesthesia 351
• Complications of Maxillofacial Infections 352
• Fungal Infections of the Maxillofacial Area 357

18. Osteomyelitis of the Facial Bones 362


Borle Rajiv M, Yadav Abhilasha, Arora Aakash
• Applied Surgical Anatomy 362
• Pathophysiology of Osteomyelitis 362
• Predisposing Factors 364
• Etiology 364
• Clinical Features 364
• Radiological Features 366
• Principles of Treatment of Osteomyelitis 367
• Different Types of Osteomyelitis and their Clinical Presentations 373
• Osteoradionecrosis 378

Section 7: Maxillofacial Trauma

19. Management of Soft Tissue Injuries 387


Jajoo Suhas N, Yadav Abhilasha, Garg Rajat
• Definition of Wound 387
• Examination and History 387
• Types of Injury 388
• Management of Soft Tissue Injuries 393
• Wound Debridement 394
• Injuries Require Special Consideration 399
xx Textbook of Oral and Maxillofacial Surgery

20. Fractures of Mandible 402


Borle Rajiv M, Arora Aakash, Yadav Abhilasha
• Applied Surgical Anatomy of Mandible 402
• Classification of Fracture Mandible 402
• Clinical Features of the Fracture 405
• Examination of the Patient 407
• Management of the fracture 408
• General Supportive Treatment 409
• Definitive Treatment 411
• Pediatric Fractures 423
• Geriatric Fractures 423
• Condylar Fractures 424
• Fracture Healing 426

21. Fractures of Middle Third of Facial Skeleton 434


Borle Rajiv M, Arora Aakash, Bhola Nitin, Yadav Abhilasha
• Pathophysiology of Maxillofacial Injuries 434
• Involvement of Various Structures during Middle Third Fractures 435
• Classification of the Fractures of the Middle Third (Rowe and Williams) 438
• Dentoalveolar Fracture 438
• Fractures of Maxilla 439
• Fractures of the Zygomatic Bone 449
• Superior Orbital Fissure Syndrome 457
• Fractures of the Zygomatic Arch 459
• Orbital Fractures 460
• Nasal Bone fractures 463
• Nasoethmoidal fractures 467
• Canthoplasty 471
• Priorities in the Management of a Polytrauma Patient 473

22. Facial Burns 477


Jajoo Suhas N, Yadav Abhilasha, Garg Rajat
• Etiology 477
• Evaluation 477
• Facial Burn 485

23. Medicolegal Aspects of Injury 488


Anjankar AJ, Borle Rajiv M, Garg Rajat
• Types of Injuries 488
• Grievous Injuries 488
• Injuries Caused by Mechanical Violence 488
• Differences between Suicidal Wounds and Homicidal Wounds 492
• Age of Injury 492
• Types of Weapon 492
Contents xxi

Section 8: Facial Deformities

24. Introduction to Cleft Lip and Palate 497


Jajoo Suhas N, Yadav Abhilasha, Garg Rajat
• Introduction 497
• Historical Aspect 497
• Epidemiology 498
• Applied Surgical Anatomy 498
• Formation of Palate   499
• Etiology 501
• Classification 502
• Prenatal Diagnosis and Counseling of Parents 504
• Management Protocols for the Patients with Cleft Lip and Palate   505
• Surgical Procedures for Cleft Lip and Palate 511
• Surgical Procedures for Cleft Lip Repair   511
• Secondary Procedures   517
• Palatal Fistula 521
• Scar Revision of the Cleft Lip 522
• Rhinoplasty   524
• Objectives of Corrective Surgery 525

25. Orthognathic Surgery 531


Borle Rajiv M, Bhola Nitin, Vibhute Pawan J
• Historical Aspects 531
• Classification of Facial Deformities 532
• Patient Evaluation and Planning 532
• Occlusal Evaluation and Model analysis 533
• Profile Assessment 533
• Clinical features 535
• Cephalometric analysis 536
• Dental Relations   537
• Posteroanterior Cephalometric Analysis   538
• Soft Tissue cephalometric analysis 539
• Operative Procedures 542
• Complications of Orthognathic Surgery 559
• Distraction Osteogenesis   562
• Distraction Devices and Options 564
• Extraoral Distractor 566

Section 9: Temporomandibular Joint

26. Temporomandibular Joint Disorders 575


Borle Rajiv M, Arora Aakash, Singh Divya
• Temporomandibular Joint Ankylosis 575
• Other Temporomandibular joint Disorders 585
• Myofacial Pain Dysfunction Syndrome 590
xxii Textbook of Oral and Maxillofacial Surgery

Section 10: Neoplastic Conditions of Head, Neck and Face

27. Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 603


Borle Rajiv M, Gadbail Amol, Singh Divya
• Odontogenic Cysts 603
• Development of a Cyst 603
• Classification of the Cyst of Oral Cavity 603
• Etiopathogenesis   604
• General Clinical Features of Odontogenic Cysts 604
• Theories of Cyst Enlargement   605
• Diagnosis of the Cyst 605
• Treatment Modalities of the Cyst 606
• Developmental Cysts of Odontogenic Origin 609
• Odontogenic Cyst of Inflammatory Origin 617
• Non-odontogenic Cysts   619
• Cyst of Soft Tissue of Head, Neck and Face 621
• Dermoid Cyst 624
• Hydatid Cyst 627

28. Odontogenic Tumors 630


Borle Rajiv M, Singh Divya
• According to Who 630
• Who Classification of Odontogenic Tumors 630
• Ameloblastoma 631
• Calcifying epithelial Odontogenic Tumor 646
• Squamous Odontogenic Tumors 649
• Adenomatoid Odontogenic Tumor 650
• Ameloblastic Fibroma 652
• Odontogenic Fibroma 655
• Benign Cementoblastoma 657
• Myxoma (Odontogenic Myxoma, Fibromyxoma) 658
• Odontoma 659
• Malignant Odontogenic Tumors 663

29. Potentially Malignant Disorders of the Oral Cavity 669


Borle Rajiv M, Gadbail Amol
• Concept of Precancer 669
• Potentially Malignant Disorders 669
• Oral Submucous Fibrosis 681
• Lichen Planus 685

30. Oral Cancer 693


Borle Rajiv M, Arora Aakash, Bhola Nitin
• Etiology 694
• Pathogenesis 695
• Carcinogenesis 695
• Clinical Presentation of Oral Cancer 696
• Primary Intraosseous Carcinoma 699
Contents xxiii

• Management of OSCC 710


• Cachexia in Malignancy 732
• Basal Cell Carcinoma 733

Section 11: Important Tips for Postgraduate Students

31. Thesis Writing 745


Gaidhane Abhay, Quazi Syed Zahiruddin
• Preparing Synopsis 745
• Outline of the Study Protocol 745
• Start with Research Question 746
• A Poorly Framed Research Question   746
• Hypothesis 747
• Objectives   748
• Planning the Research 748
• Selecting the Suitable Study Design 748
• Defining the Sampling Methodology and Calculating Sample Size
(Random Error and Level of Significance and Power of Study) 752
• Data Collection: Tools and Techniques (Methods) 755
• Data Quality 756
• Data Analysis and Basic Biostatistics Principles 756
• Writing the Thesis/Dissertation Report 761

32. Seminar and Journal Club Presentation 768


Borle Rajiv M
• Seminar 769
• Journal Club Presentation   772

Section 12: Appendices

Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 777
Borle Rajiv M
• Appendix-I: Hematology 777
• Appendix-II: Biochemical Investigations 780
• Appendix-III: Coagulation 785
• Appendix-IV: Arterial Gas Analysis 787
• Appendix-V: Urine Examination 789

Index 793
Section 1
Principles of Surgery

n Basic Principles of Surgery


n Sutures
n Incisions in Maxillofacial Surgery
n Fluid, Electrolyte Balance and Acid-base Equilibrium
n Shock
n Medical Emergencies in the Clinical Practice
n Management of Airway in Maxillofacial Surgery
n Biomedical Waste Management
1 Basic Principles of Surgery
Borle Rajiv M, Rai Anshul, Yadav Abhilasha

for aseptic principle. Similarly, tissue certain other inanimate objects (motor,
Introduction
respect is also of immense importance hand piece, etc.) used to perform surgi­
The basic principles of surgery remain in achieving the desirable outcome of cal procedure. These practices are desi­
same to any branch of surgery, inclu­ surgery. gned to achieve total absence of all
ding the oral and maxillofacial surgery. living microorganisms and are referred
A surgeon must have apt knowledge of Asepsis and to as ‘sterile technique’.
anatomy, applied physiology, patho­­logi­
cal conditions and more impor­ tantly,
Sterilization
a very sound technique and skills. The The surgical procedures have been Sterilization
skills are acquired through exten­ sive revolutionized from the antiseptic me­
practice. A correct diagnosis is the key thods of Joseph Lister (1865), to the Sterilization is a procedure by which
to successful treatment. There can be aseptic technique of today. Every effort we make an instrument or surface free
a variety of treatment modalities for a is made to prevent the entry of germs from all vegetative bacteria, spores, fun­
single disease, but the diagnosis has to be into a surgical wound by sterilization gi, including the viruses. This can be
single and accurate. Hence, sincere and of instruments, material used for surge­ achieved by:
thorough approach to history taking and ry and preparation of the environments. • Physical methods: Dry heat, moist
clinical examination is required and there The success of surgery including the heat, UV light, ionizing radiations,
cannot be a short­cut to these procedures. quality of healing of the wound, the etc.
A surgeon must train his eyes, fingers and amount of local and constitutional • Chemical methods: Formaldehyde,
mind and should believe in them rather reaction, morbidity to the patient follow­ phenolics, quaternary ammonium
than relying totally on investigations. The ing the surgery depends upon not only compounds, chlorhexidine, sodium
investigations are of great importance the surgical skill but also upon the care hypochlorite, ethylene dioxide, glu­
in making proper diagnosis, but they exercised by the surgeon and his team taraldehyde, etc.
cannot be a substitute for the clinical during the patient care.
methodology and skills. Even for order­ Dry Heat Sterilization
ing the relevant investigations a clinical Heat is the most reliable method of
diagnosis is required. Every case should Aseptic technique sterilization. The moist heat is more
be considered as a new challenge as the effective than dry heat.
patient’s response to a given pathology The word ‘asepsis’ means absence of
and treatment could be different. sepsis (infection). The aseptic techni­ Open Flaming
A sur­geon must have regard for asepsis, que accurately describes the series of The instruments are held over the
sterilization, tissue respect and for all practices employed to prepare environ­ open spirit flame. This method is
the basic principles of surgery to achieve ment, the personnel and the patient simple, not requiring any special
good results, because, the result of a good before the surgery. It is impossible to equip­ ment. It is particularly useful
surgery can get spoiled due to infection sterilize the air and personnel in the in villages, domiciliary services or in
and sometimes it may prove fatal. The operating room. The term sterilization emer­gency when other methods are
antibiotics are a great help in controlling describes the procedures employed to not available. The large instrument
the infection, but they are not a substitute prepare the instruments, supplies and trays, surgical trolley tops can be
4 Principles of Surgery

Moist Heat Sterilization


The moist heat is more effective means
of sterilization than the dry heat. The
methods of using moist heat as a means
of sterilization are:

Boiling
The temperature of boiling water does
not rise above 100°C (212°F) and thus,
only vegetative microorganisms are
killed and the bacterial spores may sur­
vive this procedure. Before the instru­
ments are put in a boiler, it is desi­rable
A B to clean all the instruments of dried,
Figs 1.1A and B: Open flaming crusted secretions, blood and rust as
they tend to prevent the pene­tration of
the heat and thus, render the process of
sterilization ineffective. It is achieved by
thorough cleansing of the instruments
by washing, scrubbing, use of fat solvents
and ultrasonic cleaning.
The instruments to be sterilized are
dipped in boiling water for a period of
one hour. Sodium carbonate (2%) may
be added to the water for alkalinization
which elevates the boiling point of
water, reduces sterilization time and
A B
prevents corrosion of instruments by
Figs 1.2A and B: Hot air oven and glass bead sterilizer reducing O2 content of water. Earlier
boiling was a method of choice, how­
disinfected with this means. However, Table 1.1: Time, temperature ever, it must be remembered that it is
it is no more practiced in the clini­ cycle in an oven only intermediate level disinfection and
cal pra­ctice due to its unreliability its reliability is doubtful in this era of
Temperature Time
(Figs 1.1A and B). HIV and hepatitis.
121°C 6–12 hours
Hot Air Oven Articles that can be sterilized
140°C 3 hours
This is the means of dry heat sterilization 150°C 2½ hours • Surgical instruments
(Figs 1.2A and B). This method is widely 160°C 2 hours • Catheters
used for the articles like anhydrous oils, 170°C 1 hours • Syringes, needles.
petroleum products, talcum powder,
Advantage
etc. which cannot be penetrated by
steam. The conventional ovens are Articles that can be sterilized It is simple and economical.
electrically heated and a blower forces Metallic instruments, powders, oils, grea­
Disadvantages
the hot air in motion around the items ses, culture media and glass articles.
to hasten up the heating and to ensure • Not reliable
Advantages
uniform temperature in all the corners • Instruments tend to get corroded
of the oven. The early models attained • Does not corrode the instruments. • Time consuming
the temperature of 160° to 170°C for • It is simple. • Sharp instruments tend to get dull.
2 hours. The fast table top models
Disadvantages Autoclaving
attain the temperature of 190° to 204°C
with a total cycle time of 6 minutes for • It is time consuming This is the means of moist heat steri­
unwrapped items and 12 minutes for • Sharp instruments are rendered dull lization. It is a method of choice for
the wrapped items. and brittle sterilization of instruments as it reliably
The temperature cycles for dry heat • Rubber gloves, plastic, PVC rubber eliminates even resistant, spore forming
sterilization are as shown in Table 1.1. articles cannot be sterilized. microorganisms, fungi, viruses, along
Basic Principles of Surgery 5

Table 1.2: Time, temperature and available. The articles to be sterilized since steam penetration starts earlier
pressure cycle in an autoclave are first thoroughly cleaned with tap in the upper part than the lower part.
Pressure Temperature Time water, spirit and solvents like ether. The muffler of the drum is eased and
All the blood stains, rust should be the perforated body of the drum (steam
15 psi 121°C 30 minutes cleaned meticulously. The instruments inlets) is exposed to facilitate the entry of
20 psi 134°C 3–5 minutes should be wrapped in muslin, paper steam into the drum (Figs 1.4A and B).
(Flash method) or linen pouches, commercially avail­ Once the heating source is started, all
able autoclaving pouches, porous cas­ the air in the autoclave should be allo­
settes or gauze before putting them wed to escape by opening the outlet
in surgical drum. The articles should valve as the heated air becomes lighter it
with vegetative microorganisms. It be kept loosely in the chamber/drum escapes through the open valve readily
works on the principle of ‘steam under to facilitate proper circulation of the and the autoclave gets filled with pure,
pres­sure’. It provides moist heat in the steam. The articles/material which saturated steam. The saturated steam
form of saturated steam under pressure. require more time for sterilization must is more lethal to the microorganisms
The pressure increases the boiling point be kept on the upper part of the drum than the mixture of air and steam. The
of water. Roughly for every 5 lbs. pres­ air is a bad conductor of the heat and
sure, the boiling point of water rises by if it surrounds the article/instruments
10°C by increasing the latent heat of in the drum the penetration of the heat
energy for boiling of water. Hence, at will be adversely affected. Once the
15 lbs. pressure the boiling point of water desirable pressure is achieved then the
rises to 121°C.
The temperature pressure and steri­
lization time cycle is as shown in Table 1.2.

Mechanism of action
The steam is the mixture of heat and
water vapor. When it comes in con­
tact with any cool surface, it gets con­
densed and heat is released from
water. This heat is taken up by the
surface it comes in contact with. The
heat goes on penetrating in the deeper
layers of the object. Hence, the steam
A B
must come in contact with the objects
Figs 1.3A and B: (A) Vertical loading autoclaves; (B) Front loading autoclaves
that are to be sterilized and thus, the
objects must not be sealed in plastic
wrappers or in the non-porous metallic
containers. The steam and the air move
in vertical direction and therefore
the movement will be quicker and
thereby the penetration of the steam
into the material will also be better if
the articles are placed vertically in the
autoclave.

Procedure
The clinician must be well acquainted
with the various parts of the autoclave
and their operation. The autoclaves
can be vertically or horizontally load­
ing (Figs 1.3A and B). High speed A B
autoclaves capable of producing more Figs 1.4A and B: (A) Dressing drum with open muffler showing perforations in the body
pressure and the temperature thus, of the drum for entry of the steam; (B) Muffler is closed covering the perforated area of the
completing the cycle in less time are drum to prevent contamination
6 Principles of Surgery

time should be counted and depending Articles that cannot be sterilized Disadvantages
on pressure the autoclaving should Powders, oils, greases, thermolabile mate­ • It is not cost effective
be continued till the prescribed time rial like electrical cords of micro-motors, • It tends to corrode the instruments
is completed. The autoclave lid must fiberoptic cable, etc. • It is time consuming.
be closed tightly and it should not be • The residue of chemicals may be carr­
Advantages
opened until the steam is evacuated ied to the tissues along with the instru­
and the inside pressure is brought • Simple ments during the surgery, which can
down to normal by opening the escape/ • Economical evoke undesirable tissue reac­tions.
release valve, after completion of the • Reliable.
procedure to prevent accidental blow­
Disadvantages Antiseptic Solutions
ing of lid. The muffler of the drum
should be immediately closed after the • Tends to corrode the instruments
autoclaving is over, to prevent the entry • Makes sharp instruments dull. Relative Terms in Disinfection
of microorganisms in the sterile drum. level
During the autoclaving care should be Chemiclaving
Antisepsis
taken to prevent entry of boiling water It is also called chemical vapor steri­
into the drum, as it tends to corrode the lization. A combination of formalde­ It is the process to kill pathogenic orga­
instruments. To achieve full quality of hyde, alcohols, acetone, ketones and nisms in the environment of the patient.
sterilization the temperature, pressure steam at 138 KPa (combination avail­ The process may be either bacte­ricidal
and time must be followed. Nowadays able commercially) is used. or bacteriostatic.
auto­claving indicators (chemical and
Disinfection
biological indicators) are available in
the market, which are placed in the Cold Sterilization It is the process to kill pathogenic orga­
drums during autoclaving, their color Articles to be sterilized are immersed nisms from inanimate objects such as
change is an indicator of complete in the chemicals for achieving steril­ surgical instruments.
sterilization (Fig. 1.5). These indicator ization. The commonly used agents
Antiseptic agent
strips may be preserved and pasted in for chemical sterilization are absolute
the autoclave registers as a record and alcohol, carbolic acid 2 percent, glu­ It is a chemical which either kills patho­
proof of autoclaving for medicolegal traldehyde 2 percent (Cidex), formal­ genic organisms or inhibits their growth
purpose. The autoclaved drums must dehyde, chlorhexidine gluconate, eth­ so long as there is contract between
be handled by aseptic care. Normally, ylene trioxide (ETO), etc. the agent and microbe. In general, the
the contents of sterile drum remain term ‘antiseptic’ is reserved for agents
sterile for about 48 hours, however with Articles that can be sterilized applied to the living body surfaces.
increased handling this time decreases Sharp instruments like scissors, blades
Asepsis
rapidly. and suturing needles.
The following articles can be steril­ It is the process by which environment
Articles that can be sterilized
ized in ETO chamber, as immersion in of the patient is protected from contact
Instruments, gauze, cotton, linen, nee­ liquids may spoil them. with infective organisms.
dles, syringes, catheters, drains, auto­ • Splints
Disinfectant
clavable hand pieces, gloves, etc. • Templates
• Handpieces It is a germicidal chemical substance used
• Fibrooptic cables on inanimate objects (non-living objects)
• Micromotor cords, etc. to kill pathogenic micro-orga­nisms but
not necessarily all others.
Articles that cannot be sterilized
Gauze, cotton, gloves, indwelling cathe­ Various Commercially
ters, syringes, hypodermic needles, etc. Available Products
Advantages Korsolex®
• Simple • Gluteraldehyde–7 g
• Thermolabile articles can be sterili­ • 1,6 dihydroxy 2,5 dioxahexane–8.2 g
zed (chemically bound formaldehyde)
Fig. 1.5: Chemical indicator strips, showing • Does not make sharp instruments • Polymethyl urea derivatives–17.6 g
the color change from green to black dull. • Rust inhibitors (trade secrets).
Basic Principles of Surgery 7

Prepared solution remains effective Weak Iodine Solution • Aseptic management of burns
(viable) for 15 days. • Scrubbing
Composition
For disinfection—5 percent for • Cleaning and disinfection of the
30 minu­tes. Iodine tincture IP 66.2 percent instr­u­ment (Immerse for 30 minu­tes)
For sterilization—10 percent for Alcohol 65 percent to • Prolonged storage of clinical thermo­
5 hours. 48 percent v/v meter.

Use 1:30 (aqueous) solution


Sterillium Preoperative painting (preparation) of 35 mL of Savlon is made up to 1 liter
Alcoholic rub—it is used as a hand the skin. with water.
disinfectant.
Special remarks Uses
Composition
• Iodine should be wiped with spirit • Cleaning and disinfection of physi­
• 2-Propanolol: 45 g after 2 minutes of painting. cally dirty wounds where extra deter­
1-Propanolol: 30 g • Idiosyncrasy may occur in sensitive gent (action) is required
• Ethyl hexa decyl dimethyl ammo­ patient. • Cleaning and disinfection of used
nium ethyl sulphate: 0.2 g • Alcohol increases the permeability catheters and appliances.
• Skin protecting substances. of the iodine.
1:30 in 70 percent alcohol solution
It is available in calibrated dis­pen­ • Savlon decreases iodine’s efficiency
sers. For the hand disinfection 3 mL due to its detergent action. 35 mL of Savlon is mixed with 200 mL
solution to be rubbed for 30 seconds. • Iodine-spirit is the best preparation water and made up to 1 liter with
for painting. 95 percent alcohol.
Dettol® • It kills 90 percent of skin bacteria in
one and a half minutes. Uses
Composition
• Skin disinfection (preoperative and
• Chloroxylenol : 4.8 percent Savlon® ,2 (Hospital Concentrate) other invasive procedures)
• Terpineol : 9 percent • Emergency disinfection of clean ins­
Composition
• Absolute alcohol: 13.1 percent truments and equipment (immerse
It is commonly used as a disinfectant • Chlorhexidine gluconate 7.5% v/v for 2 minutes)
in the clinics and for the household • Strong cetrimide 16% w/v • Disinfection of clinical thermom­
purposes. In a lesser strength it is used • Isopropyl alcohol 6.8% v/v. eters.
as an antiseptic solution.
Color Remarks
Lysol® (Concentrated Cresol
,1
Tartrazine (yellow). • Sodium nitrate (4% or four 1 g tab­
Solution) Properties and effects
lets per liter) should be added to the
solution to prevent rusting.
Color Germicide and detergent. • The solution should be changed
Dark brown. weekly.
Dilution and uses • Syringes and needles that have been
Dilution and use
immersed in the Savlon solution
1:100 (aqueous) solution
1:100 in water. It is used for sterilization should be rinsed very carefully with
of sharp instruments, e.g. suturing nee­ 10 ml of Sav­lon is made up to 1 liter with sterile water before use.
dles, knives, scissors, etc. water. • Instruments containing mirrors or
other cemented glass components
Time Uses
should not be immersed in Savlon
Thirty minutes for 100 percent solution • Cleaning and disinfection of the solution.
(i.e. undiluted) and 1 to 2 hours for 1:100 equipment in the vicinity of the pati­ • Prolonged immersion of rubber
solution. ent appliances in Savlon is not recom­
• Storage of previously sterilized instru­ mended.
Special remarks
ment
Lysol is an irritant chemical and causes • Cleaning and disinfection of the Phenol ®
burns when it comes in contact with the postoperative wounds
Composition
skin. Instruments should be cleansed • Swabbing in obstetrics, gynecology
with sterile water before use. and urology 0.5 percent carbolic acid.
8 Principles of Surgery

Properties and effects whenever there is capillary oozing, the sterilization of thermolabile arti­
It is dark pink in color and a strong e.g. after incision and drainage. cles.
irritant and caustic. Pure form may However, it is also believed that the
cause skin burns. infection passes to deeper tissue Eusol® (Edinburgh University
Uses
planes due to frothing. Solution (BP)
• Used in cleaning wounds, bleaching,
Composition
• Disinfection of sharp instruments. boils and as a throat spray and
In 100 percent solution, the instru­ mouth wash. Very diluted form is 1.25 g of boric acid, 1.25 g of bleaching
ments should be immersed for 2 to used in ear syringing to remove wax powder (chlorinated lime), sterile water
3 hours and in 20 percent solution and foreign body. up to 100 mL.
for 24 hours. • Used to remove blood stains from
Mechanism
• Disinfection during cholera epide­ clothes.
mic for disposal of excreta. It releases nascent chlorine and beco­
• Chemical sympathetic block (phe­ Spirit mes useless after 24 hours.
nol in almond oil is used)
Composition Uses
• Diluted solution is used for disin­
fection of dog bite wounds. Methyl alcohol (optimum concentration • To separate slough from infected
• Carbolization (cauterization) of ap­ of 70 percent alcohol is highly effective). wounds, ulcers, bed-sores and burn
pendicular stump and polyps. wounds.4
Uses
• Phenol has antipruritic potential, so • Acidic in pH, therefore it is very
it is used in certain skin lotions. • Disinfection of skin before intramus­ useful in wounds infected with pseu­
• Phenol in almond oil is used as cular and intravenous injections. do­monas bacteria.
an injection treatment for the first • As a solvent for the removal of iodine
degree of internal piles. in preparation of skin for operation. Cidex®
• Two percent carbolic acid solution • Cleaning the stiched wound.
Composition
is used to carbolize (disinfect) the • Cleaning the skin of the surrounding
objects in the OR and wards like ulcer or open wounds. Glutaraldehyde, 2 percent acidic solu­tion.
trolleys, OR table, Boyle’s machine, • As it dissolves the greasy material,
Properties
etc. 50 percent spirit in water (gutta spi­
rit) is used as ear drops. It kills all pathogens. It is bactericidal,
Hydrogen Peroxide (H2O2 ) • Used along with other disinfectants tuberculocidal, pseudomonacidal, virici­
such as iodine-spirit and Cetavlon- dal and fungicidal.
Composition
spirit, for painting the parts before
Time
Twenty volume hydrogen peroxide (one operation.
volume of 20 volume hydrogen peroxide Complete disinfection in 10 minutes,
solution releases 20 volume of nascent Formalin Solution sporicidal within 4 hours.
oxygen).
Composition Uses
Properties and effects
30 percent aldehyde plus 10 percent • Tray system of sterilization with
It is not an antiseptic but a cleansing methane. cidex for large instruments, fibero­
agent. ptic endoscopes with lenses.
Concentration
• Sterilization of small and sharp in­
Mechanism of action and uses
38 to 40 percent w/v solution. struments, catheters and thermom­
• It destroys anaerobic organisms by eters.
Uses
releasing nascent oxygen and there­ • Sterilization of equipment of anes­
fore used for cleaning the wounds • Ten percent solution in water is used thesia and of inhalation therapy.
infected or contaminated with anae­ as preservative for biopsy specimens.3
robes. • Operation theater sterilization (fum­ Special remarks
• It produces frothing and brings out igation 40% solution). • Best disinfectant with rapid action.
debris from the depth of the wound. • Two to five percent solution is used • Cidex is effective even in the pres­
• It produces heat when it comes in for sterilization of surgical gloves ence of protein material.
contact with the tissues. So it pre­ and instruments. • Recommended time is 10 hours to
vents capillary oozing and hence • Tablets of formalin are available, take care of the deep crevices in the
it is used as hemostatic solution which are used in a chamber for instruments.
Basic Principles of Surgery 9

Glycerine Magsulf Solution • Used as a solvent to remove the Mercurochrome


zinc paste of sticking plaster from
Composition Concentration
the skin.
Saturated solution of magnesium sul­ 0.5 to 2 percent solution is made with
phate (MgSO4) crystals and glycerine Gentian Violet water; it is available in crystal form.
(sterile), the solution is boiled for a few
Concentration Properties and effects
minutes and then cooled.
Dilution of 1:100 and 1:1,000 are gen­ It is an inhibitor of 5-hydroxytryptamine
Properties and uses
erally used. (5-HT). Strong solution kills white blood
Since magnesium sulphate is hygro­ cells (WBCs) and damages the granula­
Properties and effects
scopic, it pulls out the fluid from the tion tissue. It has an astringent action.
edematous tissue across the skin or the It coagulates the serous discharge on
Uses
mucosa, which acts as a semipermeable oozing surface and makes the ulcer dry.
membrane and the mixture is exother­ • Used for bed sore dressing.
Uses
mic producing vasodilatation which • Diluted solution is applied on wounds
facilitates reabsorp­ tion of interstitial To dress eczematous lesion with copious with healthy granulation.
fluid from the edematous in the tissue seropurulent discharge. • Strong solution is applied on wounds
thereby reducing edema. It is used to with hypergranulation.
Undesirable effects
reduce edema in: • Applied on exomphalos awaiting
• Prolapsed It colors the ulcer, so the progress of the sur­gery.
thrombosed piles Local healing becomes difficult to judge. • Not used on non-healing ulcer,
• Cellulitis applications because it stains floor of the ulcer
• Paraphimosis and Acriflavine and hence makes it difficult to judge
• This solution is used to give mag­ the progress of the healing ulcer.
Properties
nesium sulphate enema in order to • Diluted solution is used as eye drops.
reduce intracranial pressure. It is available in crystals. It is yellow in
• Glycerine has soothening action. color. Silver Nitrate (AgNO3 )
Concentration Concentration
Turpentine IP
0.5 to 2 percent solution made with Solutions with dilutions ranging from
Properties
sterile water. 1:100 to 1:10000 are available.
It is a highly irritant mineral oil.
Uses Special remarks
Uses
• It is a mild antiseptic and astringent Impregnated cotton sticks are kept in
• Diluted form is used to bring out and on ulcers with purulent discharge. dark container because, on exposure to
kill the maggots from the wounds • Effective on wounds with gram nega­ light, silver nitrate gets destroyed.
and ears.5 tive bacteria.
Uses
• Used as a solvent to remove the • Acriflavine dressing on raw area is
zinc paste of sticking plaster from left after hemorrhoidectomy. • Chemical cauterization of warts and
the skin. hyper/granulation tissue.
Potassium Permanganate • Used for dressing burns (silver sulfa­
Ether diazine)
(KMnO4 )
• Useful in bladder irrigation in cases
Properties
It has oxidizing effect. It is available in of hematuria, due to its cauterizing
It is evaporable, highly inflammable. It crystal form. 1:5000 to 1:10000 solution effect.
makes the surface cool. is made with water.
Chlorhexidine6 (Hibitane®
Uses Uses
Concentrate)
• As surface and the inhalation anes­ • Used as mouth wash, e.g. after tonsil­
thesia. lectomy and in stomatitis. (Condy’s Composition
• Used to clean the dirty skin as it gargles). Contains chlorhexidine gluconate, 5 per­
removes the greasy substances by • Used for urinary bladder irrigation cent w/v (equivalent to chlorhexidine
dissolving them. and wash. gluconate solution, 25% v/v) (Table 1.3).
10 Principles of Surgery

Table 1.3: Mechanism of action of different antiseptics (Ref–McDonnell and Russell. Antiseptic and disinfectants. Clin microbial
Rev. 1999;12:148-58)

Name of antiseptic Target Mechanism of action

Aldehydes- • Gluteraldehyde Cell wall, outer • Gram +ve bacteria and fungi—cross linking of proteins,
membrane Gram –ve bacteria—removal of Mg2+, release of some phospholipids
Virus—Inhibition of DNA synthesis
• Formaldehyde DNA • Reacts with carboxyl, sulfhydril and hydroxyl group also reacts with nucleic
acids thus inhibit RNA and DNA synthesis by cross linking of proteins
• Chlorhexidine and quaternary Cytoplasmic • Generalized membrane damage involving phospholipid bilayers. Low conc.
ammonium compounds membrane affects membrane integrity and high conc. cause congealing of cytoplasm
(cetrimide),
• Phenols Cytoplasmic • Leakage of K+ and other intracellular constituents, uncoupling of oxidative
membrane phosphorylation causing irreversible cell damage
• Halogen—chlorine releasing DNA Inhibition of DNA synthesis
(hypochlorites, bleaching
powder)
H2O2 DNA Causes DNA strand breakage
Iodines Proteins Exact action unknown, enters the cell and attacks proteins (cysteine and
methionine), nucleotides and fatty acids leading to cell death
Alcohol Cell membrane Rapid denaturation of proteins, interference with cell metabolism, leading to cell
lysis

Uses The other important use is as a scoli­


Color

Preparative skin disinfection. cidal agent in the operation of hydatid
Poceau 4R, red. Emergency disinfection of instru­ cysts7 of liver. After evacuating the cyst,

ments. 0.5 to 1 percent of cetrimide solution is
Dilution and uses
instilled into the residual host cavity and
Technique
1:250 aqueous solution. left for 5 minutes. Then it is sucked out.
Apply the diluted solution liberally Other scolicidal agents used are;
Uses
on the surface to be disinfected with • Ten percent povidone–iodone (pro­
• Disinfection of equipment, furniture a sterile swab. Clean the instruments vi­dex).
and fittings in the vicinity of the under running water. Immerse them • Formalin solution–no longer used.
pati­ent. in the solution for 2 minutes. Rinse in • Hypertonic saline.
• Storage of sterile instruments. sterile water before use.
Povidone–Iodine (Betadine®)
8

Antiseptic Technique Cetavlon® Povidone-iodine (PVP-I) is a stable che­


Apply liberally the diluted solution on mical complex of polyvinylpyrrolidone
Composition
the surface of the article to be disinfected (povidone, PVP) and elemental iodine.
with clean (sterile) swab or cloth. Store Cetrimide 0.5 percent w/v, rectified It contains from 9.0 to 12.0 percent avail­
sterile instruments by immersing in the spirit equivalent to 62 to 68 percent v/v able iodine, calculated on a dry basis.
diluted solution up to 8 hours; rinse with of absolute alcohol.
sterile water before use. Products available
Color
Povidone-iodine (5 and 10%) topical so­
Dilution and uses
Carmoisine + erythrosin (pink). lutions, surgical scrub (7.5% w/v) mou­
1:100 aqueous solution. th­
wash (gargle), povidone-iodine oint­
Precautions
Disinfection of wounds and burns, ment, povidone-iodine vaginal pessaries.
skin swabbing in obstetric patients, It should not come in contact with brain,
Properties and effect
washing of hands and scrubbing. meninges or middle ear.
Iodine is recognized as an effective
Technique Dilution and uses
and useful germicide. It is very effec­
Apply the diluted solution liberally on the As per chlorhexidine—it should not be tive against a variety of microorganisms
surface to be disinfected with a sterile swab. used in open wounds and burns because such as viruses, bacteria, protozoa, yeast
1:10 solution in 70 percent alcohol. it contains spirit which is an irritant. and fungi. However, its frequent use is
Basic Principles of Surgery 11

contraindicated because of its insolu­ Do not’s • Vesicant and burns


bility, instability and its staining and • Never mix up old diluted solutions • EO gas is mucosal irritant
irritating properties. with the freshly prepared ones. • Potential carcinogen and mutagen
Many of these undesirable qualities • Never leave diluted solutions for • Highly flammable and explosive.
of iodine could be eliminated by combin­ more than one working day.
ing it with polyvinylpyrrolidone (Povi­ • Never use corks for sealing the bot­ EO Gas Sterilizer
don). This organic polymer is water-sol­ tles. The EO sterilizer has following compo­
uble. When it is combined with iodine, a • Never leave bottles open. nents:
complex is formed in which iodine’s toxic • Capacity of chamber (12 × 12 ×
properties are lost without its bactericid­ Precautions 24 inches to 28 × 67 × 78 inches).
al activity being affected. This complex, • Instruments with glass or metal • Automatic control.
povidone-iodine (polyvinylpyrrolidone components should not be disin­ • Vacuum pumps.
iodine, abbreviated as PVP-1), has been fected with hibitane. • Steam ejector.
used effectively as a surface disinfectant. • Sodium nitrate (0.1% w/v, i.e. 1 g • Digital printer.
Povidone is an effective germicide. tablet per liter) is added to instru­ • Sterilizer and aerator.
High dilutions are active in destroying ment storage solutions to prevent
organisms within 15 seconds. Color rusting. The solution should be Preparing Items for EO Gas
loss is accompanied by the weakening changed at weekly intervals. • Clean and dry.
germicidal activity. • Instruments, especially syringes and • Disassemble detachable parts.
needles that have been immersed • Remove lubricant.
Advantages
in hibitane, should be thoroughly • Lensed instruments, cameras and
• Broad spectrum of action with fun­ rinsed in sterile water before use. films can also be sterilized.
gistatic action. • Prolonged immersion of rubber ap­ Packaging material used for EO gas
• Non-antibiotic pliances in hibitane is undesirable. sterilizer are:
• Immediate action—nonselective • Hibitane concentrate (chlor­hexi­ • Woven fabric.
• Film forming dine) should not come in contact • Non-woven fabric.
• Extremely safe. with brain, meninges or middle ear. • Peel packs and pouches.

Uses Ethylene Oxide (EO) Gas Hydrogen Peroxide Plasma


• As mouth rinse and gargle for Sterilization9 Sterilization
dryness of mouth and minor irrita­
Composition Advantages of H2O2
tion and infections.
• As a local antiseptic and for wound • CFC-12 (12/88). • Dry and non-toxic
dressing. • HCFC-124 (OXYFUME 2000). • Byproducts safely evacuated
• Used for irrigation of bladder, wound • 100 percent EO (67–134 g). • Aeration not required
(subcutaneous) pyothorax and intra­ • EO/CO2 (10/90). • Low temperature
peritoneal cavity. • Simple design of sterilizer
Temperature (85–145°F)
• Non-corrosive
Care of Antiseptic Humidity (30–80%)
solution Disadvantages of H2O2
Advantages of EO Sterilization • Metal tray block radiofrequency
Do’s • Heat sensitive articles can be waves
• Always use recommended dilutions sterilized • Not compatible with cellulose
before use, as directed. • Moisture sensitive articles can be • Nylon becomes brittle.
• Always prepare dilutions in small sterilized
volumes, preferably not more than 1 • Automatic control Ozone Gas Sterilization
liter. • Leaves no film on the surface
• Always use all diluted solutions with­ • Permeates porous packaging mat­ Advantages of Ozone Gas
in 8 hours and discard the remaining erial. Sterilizer
solution at the end of the working • Simple and inexpensive to operate
day. Disadvantages of EO Sterilization • Heat and moisture sensitive
• Always ensure that the mouth of the • Slow process • Safe with titanium, chromium, sili­
bottle is not touched by hands or • Expensive con and teflon
other materials while pouring. • Hazardous with repeated use • Low temperature
12 Principles of Surgery

• No aeration the lesser the time for which the inside be boiled and then allowed to cool to the
• Leaves no residue-converts to O2. environments of the drum are likely room temperature before the antiseptic
to be sterile. The instruments must be agent is added, to avoid its precipitation.
Disadvantages of Ozone Gas removed using a sterile chital forceps.
Sterilization The chital forceps must be sterilized
Aseptic Technique
daily and must be preserved properly.
• Corrosive A sterilized chital forceps must be kept The word ‘Asepsis’ means lack of sepsis.
• Oxidizes steel, brass, copper and in a sterilized container/bottle, which is It is the series of practices undertaken to
aluminum long enough to cover at least two-third prevent the entry of germs in the wound.
• Destroys natural rubber, latex, natu­ the length of the chital forceps as while This topic will be discussed under
ral fibers and some plastics picking up the sterile instruments from following heads:
• Stearothermophilus biologic indica­ the sterile drum, about 2/3rd the length • Planning and design of operating
tors are required to assess the steriliz­ of the forceps will enter the depth of the room.
ation. drum and only the handle shall stay out • Preparation of environments in the
• Cycle time may be up to 60 minutes (Figs 1.6A and B). The container should operating room.
after which ozone is converted back contain a sterile antiseptic solution • Preparation of personnel.
to oxygen safely released in room (2% gluteraldehide or savlon, 1:100 – Preparation of patient.
air. (aqueous) solution (10 mL of Savlon is – Preparation of surgical team.
made up to 1 liter with water) When the • Disposal of hospital waste.
glass bottles are used to store the sterile
Handling of the Sterilized
chital forceps, cotton wool is often added Planning and Design
Instruments to the bottle containing the disinfectant
The autoclaved instruments kept in solution. The cotton wool will soak the
of Operating Room10,11
the dressing drum need to be handled solution and settle at the bottom of the The location of operating room should
carefully to prevent contamination of bottle. This is done because most of the be such that it is isolated from rest of
the instruments and preserve the sterile times the chital forceps is just dropped the hospital units so that to and fro
environments inside the drum. The in the bottle which hits the base of the movement of the public is minimized.
drum should be in good condition and bottle and may break it. The presence The air circulation and water supply
the lid should be airtight. The drum of cotton wool will prevent this and also must be separate. Separate overhead
should not be opened frequently and the prevent noise. The container should be water tanks and separate pipelines
lid should be closed immediately after sterilized daily and fresh solution should should be laid for the operating room
removing the sterile instruments. The be prepared daily. The water used as to prevent retrograde, cross infection
more the frequency of opening the lid solvent for the antiseptic solution should from toilets and other units of hospital.
The operating room (OR) should be
constructed in such a way that it is
divided into unrestricted (non-critical),
semi-restricted (semi-critical) and res­
tricted (critical) area (Box 1.1). This
division prevents direct access into the
operating room thus brings down the
chances of infection. The unrestricted
area is a barrier between the outside
environments and the semi-restricted
area. This unrestricted area harbors the
preanesthetic room, office, changing
rooms, etc. The outside clothing and
foot wear is changed in this area before
advancing into the semi- restricted area
as the outside wears harbor lot of dust
and germs. The personnel must change
A B to sterile scrub suit and change the
Figs 1.6A and B: The sterile chital forceps are immersed in sterile bottles containing outside foot wear to the OR foot wear
antiseptic solution. Care should be taken to use longer bottles to ensure that 2/3rd length made up of rubber or plastic, which is
of the forceps is submerged easily washable and can be disinfected.
Basic Principles of Surgery 13

Box 1.1: Distribution of various zones in


operating room

Non-restricted area
Pre-anesthetic room
Offices
Store
Toilets
Changing areas
Semi-restricted area
Surgeon rooms
Anesthetist rooms
Nurses room
Recovery rooms
Endoscopy room
Minor OR
Restricted area Fig. 1.7A: Inside of the operating room
Operating room (OR)
Scrub area
Sterile storage room The semi-restricted (semi-critical) paints, which give smooth finish. The
Surgical ICU area contains endoscopy rooms, sterili­ walls and the floor should be washable.
zation rooms and sterile store room, No offsets or projections are permitted
postoperative recovery, etc. and serves in OR. all the electrical fittings and water
as a barrier between the unrestricted pipelines in the OR must be concealed.
The foot wear should also be puncture and restricted area. Ceiling fans are not permitted as the
proof to prevent injuries, skid proof The restricted area is a critical area blades of the fan harbor dust and when
and antistatic and nonconductor of where actual operating rooms are pre­ they are switched on the dust gets
electricity. The leather foot wear is sent. Scrub rooms for scrubbing the splashed in the surgical field. The use
not desirable for use in OR as it is not hands and areas for putting on the sterile of exhaust fans in the OR is prohibited
washable and fungal growth can take go­wns and gloves are located outside the and if they are used they should have
place on it. The disposable, sterile shoe main operating room in the critical area. unidirectional air ducts to prevent entry
covers may be worn over the OR shoes. of dust in the OR. The OR should have
They will protect the wearer from spills Designing of an Operating airconditioning and use of pedestal fans
into or onto shoes during procedures Room should be avoided.
when extensive fluid irrigation and/or The size of the operating room should The OR complex should have only
blood loss is anticipated. Some surgeons be adequate for housing all the equip­ one entry and all the windows should
wear plastic or rubber boots. The legs ment and accessories. It should allow be air tight. This prevents multi­
of scrub pants are tucked into boots. free movement of the surgical team directional air flow and entry of dust
The hair must be covered with a cap members. Ideally the size of the OR in the OR. The doors of the operation
and a mask should be put onto prevent should not be less than 500 sq ft. The theater complex which exist between
shedding of dust and microorganisms in operating room should be designed critical area, semi-critical and non-
the operating room or surgical field. in such a way that the floors and walls critical area must not be in single line
The non-restricted (non-critical) should be absolutely plain and easily to break the air velocity. The opera­
area of the operating room (OR) is where cleanable (Fig. 1.7A). They must not ting room must have unidirectional air
the patients are shifted from the ward harbor dust, dirt and microorganisms. flow (desirably lamellar air flow with
on a stretcher to the preanesthetic room The material selected for making floor micro and HEPA filters) with air flow
for the surgery. The outside stretcher should have smooth finish and should velocity of 2 meters/minute, as greater
should never cross beyond this area to have minimum and neatly made or air velocity facilitates transport of light
enter into the semi-restricted area. In the no joints. The material used for the dust particles. The temperature in the
preanesthetic room, the patient’s feet flooring should be non-porous, scratch OR must be maintained to around 20°C
are covered with foot covers (leggings) proof, antiskid and antistatic (epoxy and relative humidity should be less
and hair are also covered with caps, resin flooring). The walls should also than 40 percent. Higher temperature
before shifting into semi-restricted or be covered with smooth material like and humidity facilitates the growth
restricted area. The patient is essentially granite with minimum joints. The ideal of microorganism and fungi. If the
shifted on another stretcher, which plies OR room walls should be of stainless environments are unpleasant, hot and
between the restricted area and the non- steel without sharp line angles and humid they are tiring to the surgeon and
restricted area and in no case goes out of the corners should be molded round. his team. More importantly, it also tends
the OR complex. The ceilings should be painted with oil to desiccate the exposed tissue during
14 Principles of Surgery

the surgery. It is impossible to sterilize substance as this exothermic reaction precautions are taken to minimize the
the air, however, efforts must be made can precipitate accidents due to fire. contamination due to personnel in the
to prevent entry and restrict the growth After the OR is opened the fumes are OR. As mentioned earlier the outside
of microorganism, both vegetative and allowed to settle by opening the vents clothing and foot wear must be change
spore forming (Box 1.1). of the airconditioning system (aeriation to a scrub suit and OR footwear and the
time) and then swabs are taken from hair and nose, mouth should be covered
Preparation of Operating different sites like floor, walls, operating with the cap and mask respectively
table. Trolleys, etc. of OR (two from each before entering into the critical area of
Room site) and these swabs are subjected to the OR. The specification for the cloth
Before commissioning the operating microbiology lab for aerobic and anaer­ to be used for making the masks, gowns
complex a thorough washing and dusting obic culture to detect dread­ful micro­ and drapes is that it should be made
is required. All the walls and inanimate organism like pseudomonas, Clos­t­ up of cotton having a thread count
objects are carbolized with 2 percent ridium tetani, Clostridium welchii. The of 240/sq inch to 270/sq inch for the
carbolic acid solution. The operating OR can be commis­sioned only after reusable stuff and spunbond oleifin for
room is fumigated with the help of obtaining the negative report from disposables ones. The colors is usually
40 percent formaldehyde (350 ml) microbiology laboratory. If the OR is green for better visibility (Figs 1.8A and
added with KMnO4 (174 g) for a room found to be contaminated with these B). The special scrub suit to be worn as a
measuring 1,000 cu Ft. This mixture dreaded organisms the OR should be part of universal precaution kit consists of
procedures an exothermic reaction and closed and rewashing, fumigation and water resistant material and has double-
should be kept in a stainless steel bowl disinfection of the OR should be done. layered pro­tection (Fig. 1.9). Before per­
in the OR. The fumes rapidly spread in Periodic maintenance of the OR should forming the surgery the surgeon and
the OR and kill the microorganisms. be done by daily dusting swabbing and assistants must scrub their hands and put
The OR should be closed in an air tight weekly washing and fumigation. The on the sterile gown and sterile gloves.
manner during this procedure and swabs used for cleaning the OR should
sealed from outside to prevent leakage be earmarked for the OR and in no Hand Scrubbing
of fumes. When it is done for the first case should be used for swabbing other The surgeon must keep his hand clean
time the OR should be kept closed areas. Similarly the outside swabs to prevent any dermatological infec­
for 48 hours and for repeated weekly should never be permitted in the OR. tions. The nails should be trimmed
fumigation it can be kept closed for The floor of the OR should be washed and rounded off (Figs 1.10A to C). The
24 hours. Mechanical fumigators are also with soap and antiseptic solution like hands are washed under running tap
available in which 500 ml of 40 percent sodium hypo­ chlorite of any other water with antiseptic soap solution
formaldehyde and 500 mL of water is used disinfectant like phenolics (phenyl). (phenolic soaps like Lifebuoy, cetrimide
for a room mea­suring thousand cubic feet soaps like Savlon, povidon iodine
(Fig. 1.7B). The machine is switched on Preparation of Personnel 10 per­cent like beta scrub, chlorhexidine
and kept operating overnight. When the It is impossible to disinfect personnel gluconate scrub 4%, etc.) starting from
formaldehyde and KmNO4 solution is and their entry in the OR. However, the tips of the finger up to 2 cm above the
used, it should not be kept near bottles
of ether, spirit or any other inflammable

A B
Fig. 1.7 B: Mechanical fumigator Figs 1.8A and B: Cap, mask, eye wear and scrub suit
Basic Principles of Surgery 15

elbow (Figs 1.11A to F). Foam is gen­ The scrub area sink should be wide are fitted with doctors’ taps (Fig. 1.12B)
erated by vigorous scrubbing the nail enough to facilitate easy scrubbing with­ rather than ordinary taps, to facilitate its
beds and clean with soft brush kept in a out touching anywhere and it should operation with the help of arms to prevent
sterile container containing antiseptic have depth of about 3 feet, which prevents contamination of scrubbed hands during
solutions. The method followed for the splashing of rebound water onto the closing the tap. The peddle operated taps
hand scrubbing is the “Time-Stroke clean hands (Fig. 1.12B). The scrub sinks are ideal in scrub areas as it permits hand
method”. The time is about 3 minutes
and the strokes applied at different sites of
the palm (Fig. 1.11) range between 20 to
30 strokes at each site. The purpose of this
exercise is to make the hands surgically
clean by removing dirt and colonies of
vegetative microorganisms from the
skin creases, hair and nail beds thus
reducing the count of microor­ ganism
as it is impossible to sterilize the hands
(Fig. 1.12A). During this whole exercise, A B
hands are held at a higher level than the
elbow to prevent the water from con­
taminated arms to roll back on the cleaned
forearms and hands (see Fig. 1.10).

C D

E F

Fig. 1.9: The universal precaution suit Figs 1.11A to F: Strokes during hand scrubbing

A B C
Figs 1.10A to C: (A) Watch the hands, nails trimmed and rounded off; (B) Surgical scrub; (C) Holding the hands up so that the water
trickles down the elbows
16 Principles of Surgery

Fig. 1.12A: Areas of the harboring dirt and


microorganisms

free operations. The cleaned hands are Fig. 1.12B: Design of the washing sink
mopped with sterile towel and disinfected
with antiseptic solution.
Alcoholic hand rubs are increasin­
gly available as alternative products for
hand hygiene forward use. The appli­
cation of alcohol as a gel, foam or as a
liquid to clean hands is highly effective
at destroying microorganisms on skin
surfaces. Ethanol or isopropanol, 60 to
80 percent, are even more effective than
detergents or antiseptic soaps, if applied
to clean hands. These products may be
considered by infection control teams
for specific situations within operating
theater practice.

Application of Sterile Gown


After the hand scrubbing the sterile
gown is applied by no touch technique.
The gowns are folded inside out during Fig. 1.13: Gown folded inside out, surgeon touches the inside of the gown with
autoclaving. The sterile gown is picked scrubbed hands
up by the assistant with the help of ster­
ile chital forceps. The surgeon holds
the gown with clean hands touching the waist is considered to be sterile touching the inside out folded cuff only.
the inside of the gown which is folded and should always face the operating He slides the left glove over the left hand
outside (Fig. 1.13). field and sterile trolley on which sterile without unfolding the cuff. Then with
He opens the gown and slides the surgical equipment are kept. the gloved left hand he picks up the
gown over his hands and the body right glove touching only the outside of
without touching the outside of the Putting on Gloves right glove. He slides it over the right
gown. The straps of the gown are tied The gloves are pre-powdered and folded hand and unfolds the cuff over the
by the assistant at the back and the in such a way that the inside of the cuff cuff of the sterile gown. Then with the
straps of the gown are tightened by faces outside during autoclaving. The gloved right hand he unfolds the cuff
the surgeon himself around his wrists surgeon applies sterile gloves powder of left glove over the cuff of gown of the
(Figs 1.14A and B). The front portion over his scrubbed hands and then picks left hand, touching only out side of left
of the gown between the chest and up the left glove with bare right hand, glove. This is called as ‘open method’ of
Basic Principles of Surgery 17

gloving. The surgeon is now prepared Preparation of Patient 1. Preparation of patient in the ward
to undertake the surgical procedure The preparation of patient is divided and
(Figs 1.15, 1.16, 1.17). into two phases: 2. Preparation of the part on table.

Preparation of Patient
in the Ward
In Indian circumstances the patient are
often poor, illiterate, ignorant about per­
sonnel hygiene. Thus, they require a good
preparation before shifting to the operat­
ing room. The preparation comprises of:
• Hospitalization 2 to 3 days prior to
surgery for acclimatization to the
hospital environment for preoper­
ative and to relieve anxiety.
A B
• Bath: The patients should be asked
Figs 1.14A and B: Gowning without touching the outside of the gown
to take a good bath to clean all the
dirt from the body.
• Clothing: The outside clothing
should be discarded and the patient
should be provided clean hospital
clothing.
• When the patient is unable to do
these things of his own due to ill­
ness good nursing care should be
provided to him to complete this
job.
• Preparation of part: The part to be
operated should be washed thoroug­
hly with soap and water. The hair
should be removed by shaving at
least 12 hours prior to the surgery
as on time shaving can produce
scratches on the skin, which breaks
the barrier and facilitates the entry
of microorganism in the operating
Fig. 1.15: Sterile gloves—cuffs folded inside out
area. The clean and shaved part is
vigorously scrubbed with antiseptic
solution like Savlon, chlor­hexidine
or povidon iodine and mopped
with sterile gauge. The cleaned part
is painted with solution like mer­
cury chrome or 2 percent picric
acid, covered with sterile pad and
sealed with adhesive taps to isolate
it and prevent contamination from
fomites.
• Preparation of oral cavity: In maxil­
A B lofacial surgery preparation of oral
Figs 1.16A and B: Closed gloving technique—note the left glove is slided over the hand
cavity is very important to prevent
with the right hand overed by sterile gown. The right cuff is then adjusted with gloved left wound infection. The oral cavity
hand and the right glove is slided using left gloved hand without touching the outside of should be thoroughly inspected
the gloves with bare hands for any septic foci, calculus, tarter,
18 Principles of Surgery

I II
Fig. 1.17A: Open method of gloving: Left glove is picked up with bare, scrubbed right
hand, touching its inside and slided over left hand without uncuffing it

Fig. 1.18: Preparation of the part starts


fron center to periphery

residue of the antiseptic agent and


I II detergent, which could be irritating
Fig. 1.17B: The right glove is picked up with gloved left hand touching only its outside. or harmful to the exposed deeper
It is uncuffed over the cuff of the gown. Then with the gloved right hand the left glove tissue during surgery. Finally the area
is uncuffed. Note that during the entire procedure the out side of the gloves was not is painted with 5 percent povidon
touched by bare hands iodine solution and this should not be
wiped off because microbial activity is
sustained by release of free iodine as
infected carious teeth, infected vigorously using a sterile swab holding the agent dries and color fades from
perio­dontal pockets, etc. and they forceps with a no touch technique, skin. It should remain on skin for at
should be treated/removed. Anti­ i.e. the surgeon does not touch the least 2 minutes. To hasten drying of
septic mouth washes should be swab or any other area with his gloved skin, alcohol may be painted on the
prescribed (chlorhexidine, povi­­don, hands. The scrubbing is started from area without friction before a self–
iodine, etc.) for periodic mouth rin­ the center and goes to periphery and adhering drape is applied. Isopropyl
sing to reduce the count of micro­ the swab is discarded (Fig. 1.18). In no and ethyl alcohol are broad spectrum
organism. Loose teeth should be case the swab from periphery should agents that denature proteins in cells.
extracted as they may come in the touch the central area. This exercise A 70 percent concentration with con­
way of intubations of patient and is first done with swab soaked in tinuous contact for several minutes is
may get knocked out and aspirated antiseptic soap solution like savlon, satisfactory for skin antisepsis if the
during the intubation. cetrimide or povidon iodine (beta surgeon prefers a colorless solution
scrub) for about 2 minutes. The dete­ that permits observation of true skin
rgent facilitates reduction of sur­ color. Because alcohol coagulates
Preparation of Part face tension of the dirt particles and protein, it is not applied to mucous
on Operation Table their easy removal. The mechanical mem­ branes or used on an open
The part which is preliminary pre­ removal of microbiological colonies wound. Isopropyl alcohol is more
pared in the ward preoperatively is and reducing their count of due effective fat solvent than ethyl alcohol.
finally prepared on the table before to antiseptic action is achieved by Both are volatile and flammable. They
the surgery is started. The part on scrubbing. The area is then mopped must not pool around or under the
which the surgery is to be performed with dry sponge or sponge soaked in patient, especially if an electrosurgical
and its adjoining area is scrubbed sterile normal saline to remove the unit or laser will be used.
Basic Principles of Surgery 19

The oral cavity should be prepared rest of the body area and environments Removing Gown
again with chlorexidine or povidon io­ to prevent cross contamination. Hence, The gown is always removed before
dine 5 percent solution to achieve maxi­ the area is isolated by draping the other the gloves at the end of the surgical
mum antisepsis and prevent wound parts with the help of sterile surgical procedure.
contamination. towels exposing only the surgical field The circulator unfastens the neck
The prepared area is the surgical (Figs 1.19A and B). and back closures of the gown so the
area/field and needs to be isolated from

I II III

IV V VI
Fig. 1.19A: Part preparation set and sequential part preparation and draping

I II III

IV V VI
Fig. 1.19B: Sequential part preparation and draping, note the eyes are well protected by applying chloromycetin eye applicaps to
prevent drying and covered with sterile pads to prevent the antiseptic solution from entering in eyes to cause chemical injuries
20 Principles of Surgery

wearer does not contaminate his or her


scrub suit. If wearing a wrap around
gown, the wearer unfastens the waist
closure in front. The gown is always
removed inside out to protect the arms
and scrub suit from contaminated out­
side of the gown. To remove:
• Grasp the right shoulder of the
loosened gown with the left hand
and pull the gown downward from
the shoulder and of the right arm,
turning the sleeve inside out.
• Turn the outside of the gown away
from the body with flexed elbows.
• Grasp the left shoulder with the right
hand and re­move the gown entirely,
A B
pulling it off inside out (Figs 1.20A
to D).
• Discard in a laundry hamper or in a
trash recep­tacle (if disposable).

Removing Gloves
The cuffs of gloves usually turn down
as the gown is pulled off the arms. Use
glove‑to‑glove, then skin‑to­skin techni­
que to protect the clean hands from
the con­taminated outside of the glo­
ves, which bear cells of the patient
(Figs 1.21A and B).
• Grasp the cuff of the left glove with
gloved fingers of the right hand and
pull it off inside out.
• Slip the ungloved fingers of the left C D
hand under the cuff of the right glove Figs 1.20A to D: De-gowning process, note that the gown is removed first without
and slip it off inside out. removing glove, the inside of the gown is not touched with contaminated gloves. Gown is
• Discard gloves in a trash receptacle. always removed first and then gloves are removed
• Wash the hands thoroughly using
antiseptic soap.

Tissue Handling and Tissue


Respect
“Respect the tissue and it will reward you
by providing uncomplicated healing”.
The gentle handling of the tissue dur­
ing the surgery is of paramount impor­
tance for uneventful wound healing
and achieving desirable results out of
the surgical procedure. The forceful
retraction of the tissue, rough handling,
injudicious dissection, excessive use
of electrocautery, using dull scissors/ A B
knife for incision and allowing the Figs 1.21A and B: De-gloving process, the contaminated gloves are removed without
tissue to desiccate during the surgery touching the outside of the glove with bare hands
Basic Principles of Surgery 21

amount to tissue insult, which is bound


to be reacted with more tissue reaction
(inflammation) delayed healing, tissue
necrosis and thus, chances of infection.
The surgeon should handle the tissue
minimally and exercise sound discip­
line and principles to avoid tissue in­
sult (injudicious handling). The ‘tissue
respect’ can be optimized and the
chances of wound related complica­
A B
tions can be significantly minimized if
Figs 1.22A and B: Different types of Bard-Parker handles and blades
the precautions are taken during each
step of the surgery as mentioned below.

Incision
During the surgery the tissue needs to
be incised for creating an access. The
incision is made with sharp Bard-Parker
knife. In oral and maxillofacial surgery,
the commonly used BP hand­led number
3 to 5 on which 15 blade is mounted. Stab
knife (No. 11 blade) is used for incision
and drainage of abscess, inserting drains
or taking gingival crevicular inci­ si­
ons
(Figs 1.22A and B). The skin incisions A B
are not made with electro cautery knife Figs 1.23A and B: Marking the incision with ink
as there are chances of tissue necrosis
and impaired healing however, the
deeper tissues and the mucosal incis­
ions can be made using it. During taking
the incision following principles must
be followed:
• Always mark the incision with mar­
king ink first to avoid mistakes
(Figs 1.23a and B).
• The incision should be taken in nor­
mal skin folds or along the Langer’s
lines to prevent tension across the A B
incision line, to ensure good quality Figs 1.24A and B: Pen grip
of healing and a cosmetic scar, to
prevent dehiscence of the wound
due to tension and to camouflage and is independent of the length of especially when the skin is likely to
the scar. the incision. be lax following the surgery.
• The incision should be long enough • While taking incision, precautions • The knife is held with a pen grip
to facilitate easy passive access to must be taken to avoid injury to vital and the hand is given proper rest to
the deeper structures. This avoids structures like major blood vessels have a better control over the knife
tissue trauma due to forceful retrac­ and nerves. (Figs 1.24A and B).
tion in case of short incision, which • The cross serrations (cross hatch­ • The knife blade is held perpendicular
subsequently leads to more tissue ing) are marked across the incision to the tissues to be incised unless
reactions and inflammation. It is a with the blunt side of knife blade indicated otherwise.
false notion that short incision heals by scratching superficially, which • Controlled, uniform pressure is
faster however the healing along the serves as guidance for proper appro­ applied during making an incis­ion
incision is a simultaneous process ximation of the skin during closer depending on the consistency of
22 Principles of Surgery

Box 1.2: Guide lines for making incision Box 1.3: Ideal requirements of the flap field. The disadvantage with the cautery
• Mark incision with ink • Base should be wider than apex for dissection is that it inflicts more tissue
• Cross hatching good vascularity necrosis due to heat and compromises
• Avoid damage to vital structures • Wide enough to facilitate proper the quality of healing.
• ­Place it in Langerhan’s lines or skin access and cover the surgical defect
folds • Should be raised Full thickness Tissue Retraction
• Hold the knife with pen grip for better • Include or exclude gingival papilla
control and support • The edges must lay on healthy bone The tissues are required to be retracted
• Blade perpendicular to tissue at the time of closure. during the surgery to facilitate good
• Assistant should stretch the skin visibility and access to the surgical site.
• Incise in one stroke applying mode­rate Soft, friable tissues tend to get lacerated
pressure if retracted forcefully or using traumatic
defects as the flap is unsupported retractors like Allie’s forceps or cat’s paw
the structure to be incised and the from below and tends to collapse to retractor. Instead atraumatic retractors
structure should be incised to its full create dehiscence of the wound. like Langenbeck’s (L) retractor should
thickness is one and single stroke, • The flap should be full thickness. be used. Tough, tenacious tissues
as repeated incis­ions may lacerate • In case of intraoral mucoperiosteal should be retracted with retractors like
the edges of the wound which would flaps which include marginal gin­ Allie’s forceps or cat’s paw retractor (e.g.
subsequently compro­mise the heal­ gival, the inter dental papilla should skin, tendons, periosteum, muscle, etc.)
ing process. While the surgeon be either included or excluded from While applying the Allie’s forceps to the
makes an incision the assistant the flap to give better cosmetic skin it should never be applied on the
should stretch the skin to facilitate results (Box 1.3). outer surface of the skin but, should be
the incision (Box 1.2). applied to the inner surface of the skin
Dissection of Tissue flap to avoid ugly bite marks on skin. The
Flap Designing The tissues are dissected by two ways: slippery, glandular structures are held
Whenever a flap is required to be ref­ 1. By blunt dissection or with the help of Babcock’s gland holding
lected during the surgery for creating 2. By sharp dissection. forceps (lymph nodes, salivary glands).
an access to the surgical site following The sharp dissection is less trau­ During fine plastic surgical work on the
basic principles of flap designing must matic and is preferred for tough and skin the tiny edges of flaps should be
be adhered to: tenacious tissues. It should be avoided retracted using skin hooks. The same can
• The base of the flap must be wider when vital structures are in vicinity be used for stretching the edges of the
than the apex to ensure good afferent and can get traumatized. The blunt incision during the suturing for better
and efferent vascularity (Fig. 1.25). dissection is preferred in the tissues approximation of skin edges. A nerve
• The flap should be wide enough to which are soft, fragile and friable and is retraced with the help of blunt nerve
facilitate free, passive and direct where there is anatomical proximity hooks. During intraoral procedures the
access and should cover the surgical with the vital structures. The sharp mouth is kept open using a mouth prop
defect adequately. dissection is done with the help of knife. or a self-retaining Doyen’s, Hyster’s or
• In case of mucoperiosteal flaps the The sharp dissection is less traumatic Dingman’s mouth gag (Figs 1.26A and B,
edges of the flap must not lie on bony to tissues than the blunt dissection as 1.27, 1.28A and B). During laparo­tomies
there is less tissue handling. Further, or thoracotomy the edges of abdominal
the cutting of the tissue with knife is less incision or the ribs are retracted with
traumatic than the cutting with the help the help of self-retaining retractors.
of scissors, as the latter crushes the tissue Some special retractors are designed
while cutting. The blunt dissection is for different sites and surgeries. Some
done with the help of non-cutting edge commonly used retractors in oral and
of scissors, blades by opening action or maxillofacial surgery are condylar
with the help of opening action of the retractor (for condylectomy), mastoid
hemostat tips. The tips of the dissecting retractor (self-retaining), copper mall­
scissors used for blunt dissection should eable retractor for the retraction of the
be preferably rounded and appropriate eyeball, coronoid retractor (forked L
curvature of scissors should be selected retractor) for coronoidectomy of ramal
to gain proper access. Cautery tips osteotomies, chin retractor for the
can also be used for the dissection, its genioplasty, channel retractor during
advantage is that it incises the tissue and osteotomies and the Austin’s retrac­
Fig. 1.25: Base of the flap wider than the simultaneously coagulates the smaller tor during third molar surgeries, etc.
apex blood vessels to provide dry surgical (Figs 1.29 to 1.41).
Basic Principles of Surgery 23

Bone Removal
In oral and maxillofacial surgery bone
removal is often required for gaining
access, osteotomies or during resections
of jaw. This can be done with the help
of:
• Rotary instruments like motor and
bur.
• Osteotomes.
A B
• Chisel and mallet.
Figs 1.26A and B: Doyen’s mouth gag
• Gigli saw.
• Power saw having reciprocating,
oscillating and sagittal blades.
• Bone cutter, rongeur/nibbler, etc.
The rotary instruments include
motor and burs. While doing bone
cutting with these instruments, care
should be taken to avoid excessive heat
generation by avoiding very high speed
and by doing copious irrigation with
cold normal saline. The ideal speed
of the bur should be 20,000 RPM. The
outline of the bony incision should be
marked by drilling serial holes with a
round bur (post-stamp incision) which
are later joined by using flat fissure
bur (Figs 1.42A to D). The incision
should be started with a round bur as
it gets good purchase on the bone and
does not slip and injure the adjoining
soft tissue. The bur should be sharp,
Fig. 1.27: Dingman’s mouth gag as dull burs produce more frictional
heat. If the temperature rises above
40°C, alkaline phosphatase is released
from the osteoblasts and bone necrosis
takes place. The bur should be made
up of either stainless steel or carbide
as they cut the bone with cutting edges
unlike the diamond bur, which does
abrasive cutting and tends to generate
more heat. The diamond burs may be
used for odontectomy rather than bone
cutting. While doing bone cutting with
a rotary instruments precaution should
be taken not to keep any cotton wool or
gauze piece in the vicinity to prevent
accidental entangling and tissue injury.
The soft tissue should be protected
from accidental injury due to slipping
of the bur by proper retraction and
keeping a guard. The operator must
use protective eye glasses as the saline
A B used during the bone cutting may get
Figs 1.28A and B: Mouth props splashed in the eyes.
24 Principles of Surgery

with the cold normal saline is done to


dissipate the heat. While cutting the
bone with gigli saw care should be taken
to ensure that the saw slides smoothly,
long strokes are applied so that the entire
length of the saw is used for cutting rather
than a limited area, as it can lead to make
A that portion dull and the saw breaks.
While cutting the bone with the gigli
saw the adjoining soft tissue should be
retracted and guarded and copious saline
irrigation should be done to avoid over
heating of the bone. The bone/jaw needs
to be supported during bone cutting.
An osteotome splits the bone and
the chisel cuts the bone in a controlled
manner. Following precautions must be
taken while the bone with a chisel or osteo­
tome.
• It should be sharp.
• Too heavy blows should not be appl­
ied as it may result into a frac­ture.
B • The action of mallet should be with
Figs 1.29A and B: Langenback’s retractor wrist movement.
• A mallet with appropriate weight
sho­uld be selected (200 Oz, 500 Oz)
depen­ding upon the density of bone
to be cut.
• The vertical stop cuts must be
marked before actual bone removal
as the bone tends to get split along
with bone grains.
A • The bone/jaw must be well-sup­por­
ted to prevent fracture or disloca­tion.
• A proper purchase should be created
for engaging the chisel or else it will
slip and injure the soft tissue or vital
structures. The soft tissue should be
adequately retraced and guard should
be kept to prevent its laceration. After
the bone cutting all the sharp bone
ends should be rounded off, using a
B bone rasp/bone file. The bone file is
used in a pull motion only as the serr­
Figs 1.30A and B: Nerve hook
ations facilitate filling in this direc­tion.
To and fro motion leads to clogging of
The power saws have different types The nibbler takes out small bites of the bone and causes necro­sis.
of handpieces and blades like oscil­lating, thin, sharp bone. It is available as single
reciprocating and sagittal which are use­ action and double action and with fine Drains
ful in different indications. They often and heavy beaks. A drain is the material that acts as a
produce more precise and fine cuts. A gigli saw is a wire saw and it is held channel for escape of fluid. It is the
The bone cutting with the help of with the help of gigli saw holders and the material used to drain fluids (exudates,
bone cutter requires a sharp instrument bone cutting is done by a see saw action. transudate, hematoma, pus, blood, etc.)
or else the bone tends to get crushed. During the cutting, constant irrigation from the tissue dead spaces or cavities.
Basic Principles of Surgery 25

Purpose • Therapeutic. Box 1.4: Ideal properties of a drain


• Prophylactic. To promote escape of the fluid • It should be non-toxic.
• To prevent accumulation of fluid already collected, e.g. blood, exud­ates, • It should be non-antigenic.
(bile, lymph, blood, exudates). pus (Box 1.4). • It should resist bio-degradation.
• To encourage the obliteration of The drain is kept in situ (indwelling) • It should not have capillarity and
should facilitate free drainage along it.
the dead space otherwise the accu­ to facilitate free, passive and unin­
• It should be sterilizable.
mulated fluid acts as a separa­ting terrupted drainage of fluids along it.
agent and prevents the collapse of When the abscess is drained, to allow
raw surfaces. the drainage of pus a drain is used.
After removal of tumors, the dead space
existing in the tissue is drained with a
drain, as exudates, blood accumulates
in this dead space and can lead to
hematoma and wound infection. The
vacuum drain exerts negative pressure
A and facilitates very good drainage even
if the drain is placed at a non-gravity
dependent site. The corrugated rubber
dam or PVC (portex), drains are required
to be kept at a gravity dependent site to be
more effective. The corrugations prevent
it from getting clogged and permit free
drainage. The gauze drains are not ideal
as they have capillarity and absorb fluids,
swell in size and obstruct the drainage.
They are suitable only for packing the
cavities for achieving hemostasis (e.g.
abscess cavity, cystic cavity which heals
B by secondary intention). The tube drains
Figs 1.31A and B: Cat’s paw retractor also facilitate irrigation of the cavity.
The time for removal of the drain
is not fixed it should be left in place
till the drainage from the wound stops
completely. It is advisable to displace the
drain first, when the soakage becomes
A negligible, as there could be blockage
of the drain due to the thick exudates or
slough, before it is finally removed. If the
drain is kept unduly long or if the aseptic
precautions are not taken the infection
can travel into the wound along it.

Advantages
• Drainage of the collected fluid remo­
ves the nidus of infection.
• It helps in monitoring the hemorr­
hage or leakage at the suture line,
thus, gives warning of future compli­
cations.
• It obliterates the tissue dead space
and removes the separating fluid
and allows the raw surfaces to
B collapse and come in contact so that
Figs 1.32A and B: Skin hook the healing is faster.
26 Principles of Surgery

Disadvantages
• It forms portal of entry for infection.
• It can delay the healing.
• It can lead to breakdown of the sutu­
re line thus used judiciously.
• It can initiate tissue reaction.
• It can get blocked and become no
functional.

Drain Placement
A • The drain used should be
– Soft, so as not to erode the sur­
rounding tissues,
– Smooth, so as not to permit fib­
rin to cling to it.
– Preferably radio-opaque or hav­
ing radio-opaque line along the
tube.
– Made up of a material that
will not disintegrate and leave
foreign bodies in the wound.
– Be brought out through a sepa­
rate stab wound and fixed prop­
erly and
B – It should be non-irritant.
• The stab wound that gives access to
Figs 1.33A and B: Allie’s tissue holding forceps
the drainage cavity should be large
enough to permit free drainage.
• The drain must be placed in the
dependent position if gravity alone is
to accomplish drainage. Sump tube
must be used to remove drainage
‘uphill’, i.e. against the force of gra­
vity.
• The drain should be brought out
through the shortest route to avoid
kinking.
A • Proper daily dressing of the drainage
site should be done to prevent infec­
tion.
• When prosthesis is present, closed
tube system should be used to lessen
the risk of infection.
• It should not damage the nerve or
blood vessel.
• The inner end should not be placed
near the suture lines.
• The drain should be secured pro­
perly.

Precautions
• Drains act as two-way conduits.
B The benefits of prophylactic use of
Figs 1.34A and B: Babcock’s forcep, atraumatic forcep used to hold glandular tissue a drain must be weighed against
Basic Principles of Surgery 27

possible ensuing infection. Careful


dressing of the wound and drain
should be removed as soon as the
purpose is over. It reduces the
likelihood of significant infection.
• It should never be brought out
through the operative incision, but
through separate stab incision. If
drain is brought out through the
A B
operative wound, it not only permits
bacterial ingress and infection of the
Figs 1.35A and B: Cheek retractor
operative wound but also prevents
its closure.
• Fix the drain properly with skin
stitches. If it is detached from skin
surface, refix it. Otherwise, it may
come out or disappear into the
drainage cavity.
• A drain should not be placed through
an area where fibrosis will cause
impairment of function, e.g. across
the joint or near tendon sheaths,
etc.
• Do not drain bowel/vascular ana­
sto­motic suture line, since this may
A B increase chances of anasto­ motic
Figs 1.36A and B: Chin retractor leak.
• Too hard or stiff drain may cause
pressure necrosis of the surrounding
tissues, especially one near a large
blood vessel, tendon, nerve or solid
organ.

Removal of Drain
• The prophylactically placed drain
should be removed as soon as drain­
age has subsided, usually after 48
hours.
A B • The therapeutically placed drain is
Figs 1.37A and B: Austin’s retractor, traumatic and atraumatic, retractor in use during kept in position until the drainage
third molar surgery subsides. The lack of drainage could
be due to blockade of the pores
due to tissue contact or fibrinous
plug, in such cases before removing
the drain it should be displaced
to observe if any drainage is still
present. If the drainage is not present
then it is removed gradually, a 3 to
4 cm of drain is withdrawn each day
and refixed to allow closure of the
drainage tract from its depth, thus
A B preventing pocketing.
Figs 1.38A and B: Channel retractor has a groove which facilitates use of rotary • Tube drains are removed when drai­
instruments along with retraction, used for ramal osteotomies nage output is minimal or ceased.
28 Principles of Surgery

• Corrugated drains are usually remo­


ved on the third day or when there is
cessation of discharge.

Types of Drains
Cotton gauze
A
Gauze acts as a drain by capillary action
in the fabric, which absorbs the fluid
(Fig. 1.43). Once it becomes saturated,
it acts as a plug rather than as a drain,
hence, it should be changed twice every
24 hours.

Uses
To pack a cavity to prevent its closure
and allow healing from floor or to control
diffused oozing, e.g. after incision and
drainage of:
• Injection abscess in gluteal or del­
toid region.
B • Breast abscess, enucleated and infe­
Figs 1.39A and B: Condylar retractor used during TMJ surgery as a guard cted odontogenic cysts, etc.
The gauze drain can also be inserted
in an abscess cavity as a pack cum
drain if the oozing of blood is present
for achieving hemostasis. However, it
must be remembered that gauze has
an undesirable property of capillarity
which impedes the patent drainage and
thus, it should be replaced by corrugated
rubber dam drain once the purpose
of hemostasis is achieved, to facilitate
proper drainage.
A B Advantage
Figs 1.40A and B: Malleable retractor It acts as a temporary drainage.

Disadvantages
• Gets soaked rapidly.
• Gets sealed within 6 hours by fibrin
network.
• When soaked it acts as a moist cha­
nnel for the penetration of bacteria.
• When a soaked gauze is removed,
it is often followed by a gush of
accumulated fluid from the cavity.
• When a pack is left in contact with
the raw surfaces, it damages the
raw surfaces since it becomes adhe­
rent to it. When gauze is soaked in
liquid paraffin the damage to the
A B raw surface can be avoided, but it
Figs 1.41A and B: Eyeball retractor decreases the absorption capacity.
Basic Principles of Surgery 29

Disadvantages
• It becomes soaked by the fluid.
• When a wick is made of folded
gauze, it swells upon soaking which
will obstruct the tract.
• It can adhere to the surface.
• It requires frequent change because
it becomes ineffective due to the
soaking.

Red rubber corrugated drain


A B
(sheet drain)

It is made up of red rubber which is avai­


lable in the form of unsterile sheets, from
which the strips of required length and
bre­ad­ th are cut and sterilized by auto­cla­
ving. With this drain, fluid reaches the sur­
face by gravity hence it must be cov­ered
with the gauze pad (Figs 1.44A and B).

Advantages
• Drainage of the fluid occurs along
the grooves of the drain, so chances
C D of blockage are less.
Figs 1.42A to D: Poststamp incision for controlled bone removal • Red rubber is an irritant. It forms a
fibrous tract around itself, which is
advantageous.
• This drain is used only when there is
minimal amount of discharge.

Disadvantages
If it is used for a prolonged period and
removed at a time, the track of the
drain will start healing from superficial
and deep aspects while the middle
part remains infected. This leads to
sinus formation or pocket formation.
Prolonged insertion leads to release of
sulfur from red rubber drain evoking
adverse tissue reactions.
Being a tough material, it can injure
intestine and can cause fistula, if kept for
Fig. 1.43: Wick drain a longer period, because when the drain
is in the vicinity of the suture line, it may
Wicks wicks can be packed in the cavity to break up the suture line.
The wick is formed from gauge or threads achieve hemostasis. The wick can be It might be sucked into the wound
of ligatures or suture material twisted to­ replaced by corrugated drain after when it is not fixed properly to the
gether or bound loosely. Where the sou­rce 24 hours. surface or not removed carefully.
of drainage cannot be brought to the sur­ • The wick can be impregnated with Currently portex drain is used
face, then a wick can be passed down to it. antiseptic solution or antibiotics instead of red rubber drain as it is less
to ensure local drug delivery in irritant than the red rubber and it also
Advantages
adequate concentration. has a radio opaque line which helps in
• When the oozing of the blood is pre­ • It is economical and easily available detecting the drain radiographically
sent from the abscess cavity due to and can be made of a required size in case the drain is lost in the cacity
presence of friable granulation tissue, in the OT. (Fig. 1.45).
30 Principles of Surgery

Table 1.4: Site-wise preference of the drain

Site Preferable drain

Subcutaneous Gauze wicks,


corrugated sheet
glove drain, soft tube
drain
A Subfascial Tube drain
Intramuscular Tube drain
Extraperitoneal Tube drain or
corrugated sheet
Intraperitoneal Soft drain
Cysts Closed tube drain
Abscess Corrugated rubber
drain

Advantage

Tube drain forms the closed drainage


system so that raw surface cannot be
B contaminated due to entry of bacteria.

Figs 1.44A and B: (A) Corrugated rubber dam drain; (B) Drains in situ, Disadvantages
fixed with sutures • It drains only in the direction of the
gravity.
• If the tube is too thin, the force of
capillarity tends to retard the free
flow of fluid through it.
• It cannot drain viscous fluid.
• It drains the fluid only when the tube
is larger; so the fluid can be replaced
by the air.
• When continuous negative suction
is applied to a tube drain, the tissue
is drawn into the inner hole.
The types of tube drains are as
follows:
Catheters (Red rubber catheter,
Malecot’s catheter and Foley’s
Fig. 1.45: Corrugated portex drain catheter): Use of catheters is similar
to that of sheet drain, but they are
used particularly when the amount of
Uses • To drain retropubic space after drainage is high.
• Drainage of the peritoneal cavity after surgery on the bladder, e.g. cysto­
Advantage
an operation is done for any of the fol­ lithotomy, suprapubic prostatec­-
lowing: enteric perforation, perforated tomy. Catheters can be directly connected to
appendicitis, biliary surgery and sever • To drain subcutaneous tissue after the apparatus, so that the contamination
peritonitis (Table 1.4). removal of multiple enlarged nodes on wound with the drainage is less.
• Drainage of perirenal areas after in neck, groin, etc.
Disadvantage
pyelolithotomy. • After mastectomy, removal of tumors.
• Drainage of large abscess cavity, e.g. • Tube Drain: When the fluid enters The inner end of a catheter can be
after incision and drainage of the the tube, it can be guided into a blocked, due to the obstruction caused
submandibular space abscess. collecting apparatus. by the draining material.
Basic Principles of Surgery 31

Uses Penrose drain Vacuum drain/suction drain (redivac


• To drain large abscess cavity. It is a hollow tube of latex rubber with drain, romovac drain)
• To drain pyogenic abscess. thin wall, and can be made by cutting Principle: Active suction is applied in a
• To drain the infected hydatid cyst of the finger stall of surgical glove. Its tip is continuous manner. So it does not allow
the liver (drain should be put near cut so that both the ends are open. the secretions to collect inside and also
the incision on liver and not in the maintains patency of the drainage tube;
cavity itself). Uses it does not allow the secretions to dry
• To drain retropubic area after pros­ • As a cigarette drain. and occlude the drain site (Figs 1.46A
tatectomy. This prevents the soiling • As a simple drain. to C).
of the skin, if leakage persists. • For sump drainage of the peripan­
• To drain after thoracocentesis, chole­ creatic retroperitoneal tissue in Purposes
cystostomy, cecostomy, cystostomy. patients with infected pancreatic It serves two purposes:
• To drain pelvic abscess. abscess. For this, special drain is 1. The provision of access for accumu­
• To drain peritoneal abscesses. made as follows: lated pus or intestinal contents.
• To drain bladder after Freyer’s pros­ No. 24 or 22 Foley’s catheter is 2. The prophylactic removal of any flu­
tatectomy to give an alternative taken, bulb and the valve of balloon id within the peritoneal cavity (e.g.
pathway, if clot retention occurs. channel are cut. Multiple side holes bile) before its presence can lead
Portex drainage tube: It is made are made on half the length of the to complications. This prophylactic
up of soft portex material. It is elastic catheter. Two or three layers of drainage may be best accomplished
and has side holes as well as terminal ribbon gauze are placed around it by the use of close wound suction
holes at the tip. It causes least irritation, and then it is put in penrose drain drainage. As, it is more important
therefore can be used for a prolonged after cutting side holes onto it. where small amount of drainage
period. It has a radio-opaque line Cigarette drain: Penrose drain that and non-dependent drainage is re­
along its length. Presterilized tubes arehas a gauze within it is called a cigarette quired.
available. drain in cigarette drain; the ooze exists
along and not through the gauze. The Advantages
Uses rubber acts as conduit. • Less irritating to the tissues.
• To drain pleural cavity in: Advantages and uses are same as for • Less likely to cause infection because
– Empyema penrose drain. it is a closed system.
– Hydropneumothorax • It is particularly effective under large
Disadvantages
– Pneumothorax skin flaps, e.g. after radical neck dis­
– Hemothorax. • Secretions cannot be collected in section, modified radical mastectomy.
• To drain postoperatively after an bags, so they cannot be measured. • Closed suction drainage decrea­
operation on heart or lungs. • Chances of infection are more than ses the incidence of infection that
in penrose but less than those in occurs secondary to contamination
Precaution
corrugated rubber drain. of the drain itself and is mandatory
Portex intercostals drainage tube should • Skin irritation and excoriation may in the presence of a foreign body.
be connected to underwater seal bottle occur due to seepage of irritant • It can be placed at a non-dependent
by extension tubing. effluent. site.

A B C

Figs 1.46A to C: Romo-vac drain®


32 Principles of Surgery

Disadvantage: The continuous negative of 36 to 37°C to optimize the mitotic age to the wound site, which reduces
pressure may induce bleeding. activity. exudation from the wound. The AM
stimulates epi­theliali­zation from the
Dressing Indications ulcer bed and/or the wound edge,
A dressing is an adjunct used by a person • Surgical and traumatic wounds. which is considered to be mediated
for application to a wound to promote • Donor site wound dressing. by growth factors and progenitor
healing and/or prevent further harm. • Fungating growth. cells which are released by it. One of
A dressing is designed to be indirect • On abrasions. the most striking effects is its granu­
contact with the wound, which makes lation stimulating effect. This is due
it different from a bandage, which is Types of Dressing to some angiogenic and growth
primarily used to hold a dressing in • Glycerine magsulf dressing: It is factors which are produced by the
place. Dressings are frequently used in the saturated solution of magne­ membrane. Despite being a human
first aid and nursing. sium sulphate (MgSO4) crystals and derivative, it is not rejec­ted, because
The ideal wound dressing should glycerine, since magnesium sul­ the AM does not express the HLA A,
have the following characteristics: phate is hygroscopic, it is used to re­ B, C and the DR antigens.
• Provide mechanical and bacterial duce edema in the cases of cellulitis, Collagen materials have been
protection. excessive postsurgical edema. utilized in medicine and den­ tistry
• Maintain a moist environment at the • Vaseline gauze dressing: The vase­ because of their proven biocom­
wound/dressing interface. line gauze dressing is used to acce­ patibility and capability of promoting
• Allow gaseous and fluid exchange. lerate wound healing. It is non- wound healing. Biolo­gical dressings
• Remain nonadherent to the wound. adhesive and thus ideal for dressing like collagen are imper­meable to bac­
• Safe in use—nontoxic, non-sensiti­ the healthy, raw, granulating wound teria, and create the most physiologi­
zing, and non-allergic (both to the surfaces. It is also used to cover the cal interface between the wound sur­
patient and the medical personnel). raw areas created following the har­ face and the environ­ment. Collagen
• Well acceptable to the patient (e.g. ves­ting of split thickness skin grafts. dressings have other advantages over
providing pain relief and not influ­ • Dry dressing: Dry dressing is used conven­ tional dressings in terms of
encing movement). in wound without granulation, e.g. ease of application and being natural,
• Highly absorbable (for exuding postoperative sutured, healing inci­ nonimmunogenic, nonpyrogenic,
wounds). sion line. hypoallergenic, and pain-free. Colla­
• Absorb wound odor. • Wet dressing: Wet dressing is used gen is a biomaterial that encourages
• Sterile. when ulcer with granulation tissue, wound healing through deposition
• Easy to use (can be applied by i.e. eusol, betadine, saline. and organi­zation of freshly formed
medical personnel or the patient). • Biological dressings: Such as am­ fibers and granulation tissue in the
• Require infrequent changing (if nec­ niotic membrane dressings, col­ la­ wound bed thus creating a good
essary). gen membrane or a skin graft are environ­ ment for wound healing.
• Available in a suitable range of forms the best dressings as they prevent Collagen sheets, when applied to a
and sizes. wound contamination and promote wound, not only promote angiogen­
• Cost effective and covered by health the healing. The other examples esis, but also enhance body’s repair
insurance systems. of the biological dressings are am­ mechanisms. While acting as a me­

ni­
otic membrane, collagen mem­ chanical supp­ort these reduce ede­
Purpose of Dressing brane, fascia. Amniotic mem­brane ma and loss of fluids from the wound
• Controlling the moisture content, (AM), or amnion, is the inner­most site, along with facilitation of migra­
so that the wound stays moist or layer of the placenta and consists of tion of fibroblasts into the wound and
dry, to maintain the optimal wound a thick basement mem­brane and an enhancing the metabolic activity of
humidity to prevent wound from avascular stromal mat­rix. Its proper­ the granulation tissue. Moreover, it is
becoming dry and forming eschar ties such as lack of immuno­genicity, easy to apply and has the additional
preventing direct cell migration fluid loss contro­lling, pain relieving, advantage of stopping bleeding.
across the wound bed. re-epithelialization and granulation • Occlusive dressing: An occlusive
• Protecting the wound from infection. and its stimulating, anti-inflamma­ dressing is an air and water-tight
• Removing slough, and tory, antifibrotic and antimicrobial trauma dressing used in first aid.
• Maintaining the optimum pH and properties make it an ideal biologi­ These dressings are generally made
temperature to encourage healing. cal dressing. It has the advantage of with a waxy coating so as to provide a
To provide thermal insulation by ready availability at no extra cost to total seal, and as a result do not have
maintaining a constant temperature the patient. It provides secure cover­ the absorbent properties of gauze
Basic Principles of Surgery 33

Table 1.5: Different types of material used for dressing and their examples and Box 1.5: Uses of the bandage
properties
As a first aid for the injured part, especially
Type Properties to arrest bleeding

Passive Traditional dressings that provide cover over the wound, e.g. gauze To provide rest and support to the part.
products and tulle dressings To retain dressing and to splint the part.
To prevent inflammatory edema.
Interactive Polymeric films and forms which are mostly transparent, permeable to
products water vapor and oxygen, non-permeable to bacteria, e.g. hyaluronic
acid, hydrogels, foam dressings
Bioactive Dressings which deliver substances active in wound healing, e.g. Bibliography
products hydrocolloids, alginates, collagens, chitosan
1. Berger SA, Kramer M, Nagar H, Finkles­
tein A, Frimmerman A, Miller HI. Ef­
fect of surgical mask position on bacte­
pads. They are typically used to treat Bandage rial contamination of the operative field.
open, or “sucking,” chest wounds to J Hosp Infect. 1993;23:51-4.
alleviate or prevent a tension pneu­ The bandage is the piece of material 2. Dineen P. An evaluation of the duration
mothorax (a serious complication used to cover, support, immobilize or of the surgical scrub. Surg Obstet. 1969;
of a simple pneumothorax). They exert pressure to the part (Box 1.5). 129:1181-4.
are also used in conjunction with a Bandages commonly used in oral 3. Gupta DS, Borle RM. Operation theater
moist sterile dressing for intestinal and maxillofacial surgery discipline. J Indian Dental Association.
evisceration. • Simple roller bandage—single or 1983;55:437-40.
• Occlusive dressings come in various double headed. 4. Humphreys H, Russell AJ, Marshall RJ.
forms, including Vaseline Gauze, • Barrel bandage to retain the dressing The effect of surgical theatre headgear
which sticks to the skin surrounding and support the lower jaw. on bacterial counts. J Hosp Infect. 1991;
the wound using Vaseline. • Four-tailed bandage to support the 19:175-80.
lower jaw (Figs 1.47A and B). 5. Jordan DM. There is a reason for dress
Classification of Wound Dressings • Mastoid bandage for compression codes. Imprint. 1991;38:46-8.
Synthetic wound dressings would bro­ after TMJ surgeries. 6. Lippert S, Gutschik E. Bacterial sedimen­
adly categorized into the following types: • Compression bandage with simple tation during cardiac surgery reduced by
• Passive products roller bandage, crepe bandage or disposable clothing. Scand J Thorac Car­
• Interactive products with elastoplasts. It helps in achiev­ diovasc Surg. 1992;26:79-82.
• Bioactive products ing hemostasis, obliterates tissue 7. Mitchell NJ, Hunt S. Surgical face masks
The properties and examples of dead space and prevents formation in modern operating rooms—a costly
these products are given in Table 1.5. of the hematoma. and unnecessary ritual? J Hosp Infect.
1991;18:239-42.
8. Moylan JA, Fitzpatrick KT, Davenport
KE. Reducing wound infections.Imp­
roved gown and drape barrier per­for­
mance. Arch Surg. 1987;122:152-7.
9. Nagai I, Kadata M, Takechi M, Kuma­
moto R, Ucoka M, Matsuoka K. Studies
on the mode of bacterial contamination
of the operating theater corridor floor.
J Hosp Infect. 1984;15:50-5.
10. Orr NW. Is a mask necessary in the
operating theatre? Ann R Coll Surg Eng.
1981;63:390-2.
11. O’Hara L. The Operating Theater as a
degradation Ritual: A Student Nurse’s
View, Science as Culture. 1989;6:20-8.
12. Pratt RJ, Pellowe C, Loveday HP. Epic
A B phase 1: The development of National
Figs 1.47A and B: Mastoid bandage and ‘four tailed’ bandage Evidence-based Guidelines for Pre­
34 Principles of Surgery

venting Hospital-acquired infections corneal bacterial ulcers. Isr Med Assoc


References
in England associated with the use of J. 2009;11(11):664-8.
short-term indwelling urethral cath­ 1. Rubino JR. Overview of Lysol scientific 7. Topcu O, Kuzu I, Karayalcin K. Effects of
eters in acute care. Different types of studies. Pediatr Infect Dis J. 2000;19(10 peritoneal lavage with scolicidal agents
material used for dressing and their Suppl):S123-4. Review. on survival and adhesion formation in
examples and properties. Technical 2. Ekizoglu MT, Ozalp M, Sultan N. An rats. World J Surg. 2006;30(1):127-33.
Report. London: Thames Valley Uni­ investigation of the bactericidal effect 8. Hemani ML, Lepor H. Skin preparation
versity; 2000. of certain antiseptics and disinfectants for the prevention of surgical site
13. Rehork B, Ruden H. Investigations into on some hospital isolates of gram- infection: which agent is best? Rev
the efficacy of different procedures for negative bacteria. Infect Control Hosp Urol. 2009 Fall;11(4):190-5.
sur­ gical hand disinfection between Epidemiol. 2003;24(3):225-7. 9. Dias FN, Ishii M, Nogaroto SL, et al.
con­se­cutive operations. J Hosp Infect. 3. Braun A. Survival of skin preserved in Steri­lization of medical devices by ethy­­
1991;19:115-27. weak formalin solutions. Bulletin of lene oxide, determination of the dissi­
14. Tunevall TG. Postoperative wound infe­ Experimental Biology and Medicine. pation of residues, and use of Green
c­tions and surgical face masks in a con­ 1996;62(4)1195-966. Fluorescent Protein as an indicator of
trolled study. World J Surg. 1991;15: 4. Dryburgh N, Smith F, Donaldson J, process control. J Biomed Mater Res B
383-8. et al. Debridement for surgical wounds. Appl Biomater. 2009;91(2): 626-30.
15. Verkkala K, Eklund A, Ojajarvi J, Tiit­ Cochrane Database Syst Rev. 2008; 10. Gupta DS, Borle RM. Operation
tanen L, Hoborn J, Makela P. The 16(3):CD006214. Review. theatre discipline. J Indian Dent Assoc.
conventionally ventilated operating 5. Joshi HN, Kansagra PJ, Dayal PK. Facial 1983;55(11):437-40.
theatre and air contamination control myiasis: report of case. ASDC J Dent 11. R. Tomaszewski. Planning a Better
during cardiac surgery—bacteriological Child. 1986;53(1):70-1. Operating Room Suite: Design and
and particulate matter control garment 6. Geffen N, Norman G, Kheradiya NS. Implementation Strategies for Success.
options for low level contamination. Eur Chlorhexidine gluconate 0.02 percent Perioperative Nursing Clinics, 2008;
J Cardiothorac Surg. 1998;14:206-10. as adjunct to primary treatment for 3(1):43-50.
2 Sutures
Borle Rajiv M, Bora Smriti, Rai Anshul

“A suture is a strand of material used to ligate blood vessels and approximate the tissue together1.”
“To suture is the act of sewing or bringing tissues together and holding them in apposition until healing has taken place.”

John Hunter was of opinion that required to break the knot given
HISTORICAL ASPECTS2
suture were basically undesirable, but by the material. It is more im­
The first description of suture was given if needed they should be interrupted portant than straight pull tensile
by Edwin Smith Papyrus in 16th century suture. He preferred bandage or sticking strength. It is measured in kilo­
BC. Sutures have been used as far back as plaster across the wound. gram during manufacture. The
records go both to hold wounds together In 1867, Hister began to use the tensile strength increases with
and to arrest hemorrhage. The thread and catgut treated with an aqueous solution increase in diameter of the su­
instrument for its application were made of carbolic acid (sterile suture). Many ture material.
from any convenient available method. different materials were tried, viz. linen, • Smoothness: The smoother the su­
There is mention in the literature that cotton, horsehair, tendons, intestinal ture material, the easier the passage
various material were used for suturing tissues of various animals, gold, silver of suture through the tissue with least
such as gold wires, horses hair, threads wires, etc. trauma. For example, monofilament
plant fibers, etc. and the quest for the In recent decades, new synthetic prolene is smooth thus preferred in
ideal material continued. filaments such as nylon, polypropylene vascular surgery.
Primitive men in South America and polyester have become available. • Knot security: Monofilament suture
used large black ants to bite the edges of Synthetic absorbable material have also have smooth surface, hence, the
the wound together. Ancient Egyptian been developed. knot will slip and open (more knots
Papyri prefer to the use of linen strips, With the advancements in suture required). Polyfilament are held more
coated with an adhesive mixture of flour technology, sterilization techniques securely (2 to 3 knots are enough).
and honey for skin closure. also improved. Sterilization with cobalt For ex­ample, for proline suture the
East African tribes ligated blood 60 and ethylene oxide is the new the knot stability is poor as compared to
vessels with tendons and closed wound method of choice. the braided silk suture and hence, it is
with strips of vegetation. said that the number of knots should
Gelen (AD150) comments for the be equal to the number of days you
PROPERTIES OF SUTURES
first time on the use of catgut. Although want the proline suture to stay, i.e. it
its most important fact that it is absorbed • Strength: It must be strong enough requires more knots than the braided
and digested by body enzymes was not to maintain tissue in apposition for a material.
discovered until the 18th century. The specified time. • Infection: There is relation between
ancients used it because it was strong – Straight-pull tensile strength: It is the configuration of the suture
and easily available. the minimum amount of tension (multi­filament or monofilament) and
In 900 AD Rhazes of Arabia first required to break the filaments. its propensity to promote infection.
employed ‘kitgut’ to suture abdominal – Kno-pull tensile strength: It is the – Bacterial adherence to the sur­
wounds. minimum amount of tension face of suture
36 Principles of Surgery

– Ability of the bacteria to gain visibility when seen against the suture material are summarized in
access. bloody surgical field. the Box 2.1.
Braided material can hold bac­ • Handling: The sutures should
teria in its interstices where they run smoothly through the tissue. PRINCIPLES OF SUTURE
may be protected from phagocytes. It should have no memory. Knots
SELECTION4
Similarly, the suture having more should bed down easily and be
capillarity tends to attract bacterial secure with minimum numbers of The surgeon has a choice of selecting
colonies and their passage along the throws. a suture material suitable for different
suture deep into the wound. •Elasticity: The suture should have tissue and the needs of a particular
Advantages of monofilament over degree of elasticity to accommodate site and surgery. Adequate strength of
multifilament are as follows: the changes of bulk in wound. the suture material will prevent suture
– Monofilament provides easy pas­ •Memory: Inherent capability of breakage. Secure knots will prevent
sage through the tissue whereas suture to return or to maintain its knot slippage. But the surgeon must
multifilament tends to provide original gross shape (related to understand the nature of the suture
tissue drag (Fig. 2.1A). elasticity, plasticity and diameter). material, the biologic forces in the
– The smooth surface of monofila­ •Plasticity: Measure of the ability healing wound and the interaction of
ment does not support bacterial to deform without breaking and to the suture and the tissues. The follo­wing
growth whereas multifilament maintain a new form after relief of principles should guide the sur­geon in
provides a nidus for infection the deforming force. suture selection.
(Fig. 2.1B). •Pliability: Ease of handling of suture • When a wound has reached maxi­
• Reactivity: It is the cellular response material, ability to adjust knot ten­ mal strength, sutures are no longer
to foreign body. It is more for the sion and to secure knots (related to needed.
natural material. suture material, filament type, and – Tissues that ordinarily heal slow­
• Visibility: Each suture should ide­ diameter). ly such as skin, fascia and ten­
ally be distinguishable at a glance •Capillarity: Extent to which absor­ dons should usually be closed
from another suture. Similarly the bed fluid is transferred along the with non-absorbable sutures.
suture material should have good suture. The ideal properties of the – Tissues that heal rapidly such
as stomach, colon, oral mucosa
and bladder may be closed with
ab­sorbable sutures.
• Foreign bodies in potentially con­
taminated tissues may convert con­
tamination to infection, therefore
– Avoid multifilament sutures,
which may convert a contaminat­
ed wound into an in­fected one.
– Use monofilament or absorb­
able sutures in potentially con­
A B taminated tissues.
Figs 2.1A and B: (A) Magnified view of monofilament; (B) Magnified view of multifilament • Where cosmetic results are impor­
tant close and prolonged apposition
of wounds and avoidance of irri­tants
Box 2.1: Ideal properties of suturing material3 will produce the best re­sult, therefore
– Use the smallest inert monofila­
• It should have a uniform diameter as it avoids breaking points. ment such as materials such as
• It should maintain its tensile strength until its purpose is over. nylon or polypropylene.
• It should have good handling properties. – Avoid skin sutures and close sub­
• It should evoke nil or minimum tissue reaction. cuticularly whenever possible.
• It should not favor bacterial growth.
• The knot should be stable.
– Under certain circumstances, to
• It should have good tensile strength at a smaller diameter. secure close apposition of skin
• It should not have capillarity, should be non-allergic, non-electrolytic and non-carcinogenic. edges, skin closure tape may be
• It should be sterilizable without alteration of physiochemical properties. used.
• It should have good shelf-life. • Foreign bodies in the presence of
• It should be economical.
fluids containing high concentrations
Sutures 37

of crystalloids may act as nidus for Manufacture Chromic Suture Material


precipitation and stone formation. Prepared from submucosa of sheep’s Chromic suture materials have under­
• Regarding suture size: intestine. Sheep submucosa contains gone various intensities of tanning with
– Use the finest size, commen­ rich elastic tissue, which accounts for the salt of chromic acid to delay the
surate with the natural strength high tensile strength. tissue absorption time. Typical examples
of the tissue. of chromic suture and absorption times
– If the postoperative course of Sterilization are:
the patient may produce sudden Catgut is sterilized with gamma radiations • Type A: Plain—10 days
strains on the suture line, reinforce utilizing 2.5 mega-rads or by ethylene • Type B: Mild chromic—20 days
it with retention sutures. Remove oxide. It is sterilized and preserved in 2.5 • Type C: Medium chromic—30 days
them as soon as the patient’s con­ percent formaldehyde and denatured • Type D: Extra chromic—40 days.
dition is stabilized. absolute alcohol inside spools or foils.
Chromic acid method: Immersed ABSORBABLE SYNTHETIC
in 20 percent chromic acid and five parts
United States Pharmacopeia SUTURE
of 8.5 percent glycerin. It sterilizes and
Classification secures a longer stay in pack.
• Class I: Silk or synthetic fibers of Polyglycolic Acid
monofilament, twisted or braided Duration of Stay in Tissue (Dexon)
construction. Catgut retains tensile strength for Synthetic non-protein suture poly­glycolic
• Class II: Cotton or linen fibers or 10 days and chromic catgut for 20 days. acid and made by excursion of fine
coated natural or synthetic fibers Tensile strength is zero after 30 days and strands are then braided to form uniform
in which the coating contributes completely absorbed in 100 days. size. The filaments are uniform in size.
to suture thickness without adding • Color: Green
strength. Absorption • Size: 8 ‘0’ – 2 ‘0’
• Class III: Metal wire of monofila­ Enzymatic digestion by proteolytic enz­ • Length: Non-needled length of 150 cm
ment or multifilament construction. y­
mes derived from lysosomes from • Needle in length: 45 to 75 mm
inflammatory cells (polymorphs and • Tensile strength: Fourteen days post-
Suture Size macrophages) around catgut. Hence, in implantations about 55 percent of
Suture size is based on strength and diam­ the presence of infection catgut is easily original value and at 21 days 20 percent
eter as decided by the United Sta­tes Phar­ absorbed. of original value
macopeia (USP). This system uses “0” as • Packing: Pre-sterilized form of foil
the baseline, average size suture. As suture Uses over wrapped without preservative
diameter decreases, “0”s are added or • Absorption: By esterase enzyme
numbers followed by a “0” (For example, Plain catgut (Figs 2.2A and B) • Time: Hundred days.
000 and 3-0 are the same size). As suture • Ligation of small blood vessels near
diameter increases more “0”, numbers are the surface of skin. Advantages
assigned to the suture material. • Suture subcutaneous tissue, advi­ • Minimum tissue reaction
sable at urinary tract, biliary tract, • Less tissue edema
TYPES OF SUTURE subcutaneous tissue. • Uniform absorption
• Can be used in presence of infec­tion
MATERIAL (TABLE 2.1) Chromic catgut (Figs 2.3A and B)
(as it is not absorbed by phago­cytosis)
• Size-1-0, 2-0: Ligation of medium • Better knot holding property (brai­
Catgut sized blood vessel, peritoneum ded)
History: The term ‘catgut’ is a misnomer. muscle, rectus sheath, liver and • Less fraying of ends (braided).
It is derived from the word ‘kitgut’ spleen, ligation of pedicle.
which means medieval three stringed • Size 2-0: Ligation of cut vessel in vas­ Uses
violin like instrument (dancing master’s ec­tomy closure of ureteric and bla­d­ • Intestinal anastamosis
fiddle), string of which were used by der wound and pyelotomy incision. • Ligation of pedicle to ligate superior
ancient people as suture material. • Size-2-0, 3-0: Intestinal anastomosis. and inferior thyroid vessel, ligation
Lord Baron Joseph Lister (1827–1912) • Size-3-0, 4-0: Muscle layer in cleft lip of splenic and renal pedicle in sple­
treated it with carbolic acid, hardened this surgery. nectomy and nephrectomy
material and reduced the tissue reaction • Size-5-0, 6-0: Plastic surgery and • In biliary surgery
and later treated it with chromic acid. circumcision. • Cosmetic surgery.
Table 2.1: Types of sutures and their properties

Sutures Classification Raw material Absorption Tensile Tissue Contraindication Precaution Use
rate strength reaction
38 Principles of Surgery

Catgut Natural Collagen Not to be given


Plain Monofilament Derived from 70 days Zero after Moderate when prolonged Subcutaneous
Chromic Absorbable sheep or bovine 90 days 30 days Moderate approximation of Absorbs faster
intestine the tissue under
stress is required
Linen Natural, Staple flax fibers Gradual Moderate Cardiovascular None Ligation of superficial
Multifilament, Jute fibers surgery vessels, mucosal suturing
Nonabsorbable without stress
Surgical silk Natural, Filament spun by Moderate Cardiovascular Stich granuloma General, plastic and
Multifilament, silk worm larva to surgery High infection rate ophthalmic surgery
Non-absorbable. form its cocoon Ligating body tissues
Surgical cotton Natural, Staple Egyptian Low tensile Minimal None Frays easily Most body tissues for
Multifilament, cotton fibers strength ligating and suturing
Nonabsorbable
Surgical steel Natural, Alloy of iron, Non- Indefinite Low Should not be used Cutaneous Abdominal wall and
Multifilament, nickel and absorbable with a prosthesis of dysfunction corrode skin closure, sternal
Non-absorbable chromium another alloy break at points of closure, retention, tendon
bending, twisting repair, orthopedic and
and knotting neurosurgery

Coated vicryl Synthetic, Copolymer of 60–90 days 14 days–55% Mild Being absorbable Safety not proved Ligature suture tissues
(polyglactin Monofilament/ lactide and 21 days–20% should not be used in neural and where an absorbable
410) Multifilament, glycolide coated when prolonged cardiovascular suture is desired
Absorbable with polyglactin approximation of tissues
370 and calcium tissue is required
stearate

Contd...
Contd...

Sutures Classification Raw material Absorption Tensile Tissue Contraindication Precaution Use
rate strength reaction
Polydioxanone Synthetic, Polyester polymer 240 days 20 days–70% Minimal Being absorbable Absorbs slowly Abdominal and thoracic
(PDS) Monofilament, 40 days–40% should not be used closure subcutaneous
Absorbable 60 days–20% when prolonged tissue, rectal and colon
approximation of surgery, orthopedic and
tissue is required plastic surgery can be used
in the presence of sutures

Nylon Synthetic, Polyamide Degrades Extremely low None Knot slippery Skin closure,
Monofilament/ polymer at a rate of infection due to Retention, plastic
Multifilament, 15–20% cervices in braided ophthalmic, repair hernia
Non-absorbable per year nylon microsurgery
Polypropylene Synthetic, Polymer of 2 years Minimal None None General, plastic,
(prolene) Monofilament, propylene transient cardiovascular surgery,
Non-absorbable acute skin closure, ophthal­
inflammatory mology
reaction
Collagen Natural Homogenous 56 days Minimal Cannot be used in Opthalmic surgery
Monofilament dispersion of pure slow healing tissue
Absorbable collagen fibrils
from the flexor
tendons of beef

Polyglycolic Synthetic Nonprotein 100 days 30 days Minimal Intestinal anastomosis


acid Absorbable polymer of Ligation of pedicle
glycolic acid
(Dexon)
Sutures 39
40 Principles of Surgery

Vicryl (Polyglactin 910)


Vicryl (Fig. 2.4) is a synthetic absorbable
suture material. Polyglactin 910 is a
co-polymer of glycoline and lactide. It
is polyfilament braided suture manu­
factured by the process of extrusion.
• Color: Violet
A B • Available size: 7-0 to 1-0
• Length: 70 cm
Figs 2.2A and B: Plain catgut
• Retention of tensile strength after
embedding in the tissue: 55 percent
for 14 days and 20 percent for
21 days
• Absorption: Minimal up to 40 per­
cent is completed by 60 to 90 days
by slow enzymatic hydrolysis in
presence of tissue fluid, then the
pieces of fragments are phagocytosed
A B by polymorphs and macrophages.
Figs 2.3A and B: Chromic catgut Due to this reason there is least
tissue reaction. Its absorption is not
affected by infection.
The properties of different suture
material are summarized in Table 2.2.

Advantages
• Minimal tissue reaction
• No fraying of edges
• Excellent handling characteristics
• Good knot stability
• Distinct violet color is visible in
wound
• The unique molecular structure re­
tains strength during healing period
Fig. 2.4: Vicryl suture
and gets absorbed rapidly after func­
tion is served.

Table 2.2: Classification of suture3 Uses


• Intestinal anastomosis
1. Absorbable
• Ligation of pedicle closure of tho­
   a. Synthetic Monofilament–polydioxanone Multifilament—polyglycolic acid racotomy
suture (PDS), polyglyconate (PGA) (DEXON), polyglactin (vicryl) • Closure of laparotomy
   b. Natural Monofilament—catgut Multifilament—collagen • Closure of the deeper tissue
2. Non-absorbable • Mucosal suturing especially in trans­
   a. Synthetic Monofilament—nylon, polyethylene, Multifilament—nylon, polyester oral surgery
polypropylene, polybutester, • Cleft palate surgery
   b. Natural Monofilament—stainless steel, Tant­ Multifilament—silk, linen, cotton • Suturing in pediatric patients
alum, platinum, silver wire • Deeper layer closure.
Newer Newer non-absorbable synthetic Absorbable synthetic suture material
suture material-Dacron, marlex, are Poliglecaprone 25 (monocryl), Polyglyconate
polyglyconate Polydioxanone (PDS), Polyglactin Monofilament synthetic absorbable su­
910 (vicryl coated), Polyglactin 910 ture prepared from a co-polymer of
(vicryl rapid), Ethibond (polybutylate glycolic acid and trimethylene carbo­nate.
coated braided polyster
• Color: Clear or green
Sutures 41

• Size: 6-0 to 2-0 (green) and 5-0 to


1-0 (clear)
• Absorbed: By nonenzymatic hydr­
o­lysis, breaking down into beta-
hydroxybutyric acid, glycolic acid
and carbonic acid (first two excre­ted
in urine)
• Retention of tensile strength: 70
percent up to 2 weeks and 55 percent
up to 3 weeks
• Absorption: Completed by 6 months
• Advantage: Suppleness, flexibility,
mini­­mal tissue drag, ease of tying Fig. 2.5: Silk suture
and good knot security.
It is used in most of the soft tissue Tensile strength: Progressive degrad­
surgeries. NONABSORBABLE SUTURE ation of fibers may result in gradual
MATERIAL loss of tensile strength over a period of
time. It is not absorbed, but is gradu­
Polydioxanone ally encapsulated by fibrous connective
Polydioxanone is a monofilament syn­
Silk tis­sue.
thetic absorbable suture prepared from Silk suture (Fig. 2.5) is also called black, Color: Black for better visibility.
polydioxanone. braided silk, due to its black color and
• Color: Blue, violet or undyed clear the fact that it is multifilament suture Advantages
form prepared by twisting (braiding) these • Does not soak-up fluids, it does not
• Tensile strength: filaments over each other. The black limp or become brittle
– 70 percent retained up to color is for better visibility against the red • Ties down securely and smoothly
2 weeks surgical field. It is natural and nonab­sor­ and securely
– 50 percent up to 4 weeks bable. Although it is categorized under • Economical.
– 14 percent up to 8 weeks. non­absorbable, it is actually an absor­
• Absorption: Minimal until 90 days bable material being protein in nature. Disadvantages
and completed by 6 months. It is However, its absorption takes very long • Stitch granuloma
relatively inert time and thus commonly con­ sidered • Infection rate is high as compared to
• Used: Where catgut is indicated, but to be nonabsorbable (Fig. 2.5). It is the synthetic material.
not used due to tissue approximation most commonly used suture for the
is under tension. closure of the skin incisions due to its Availability
cost effectiveness. • Sterile foil over wrap pack as eyeless
Sizes: The thickness decreases as needled suture
Poliglecaprone 25 Monocryl the size increases 1-0 to 8-0. • Sutupac—Precut lengths of sterile
(Ethicon) Source: Natural silk filament obtai­ sutures in pack of two or six pieces of
• Type: Monofilament ned from silk cocoon. sutures, without needle
• Raw material: Co-polymer of glyco­ Nature: Consists of protein—70 per­ • Non-sterile on reels.
lide and epsilon-caprolactone cent organic protein fibrin, gum—30 per­
• Retention of tensile strength: 50 cent. Types
to 60 percent (Violet: 60–70%)— The degumming of silk is done to 1. According to preparation
remains at one week. 20 to 30 per­ retain natural body and elasticity; the • Perma-hand silk suture
cent (Violet 30–40%) remains at appropriate number of filaments for • Virgin silk suture material pre­
2 weeks and lost in 3 weeks (Violet each size is tightly braided. The suture is pared from gland of silkworm
4 weeks). chromicised for noncapillarity. before pupae stage.
42 Principles of Surgery

2. According to fibering pattern • Tensile strength: Progressive hydro­ Polyproline Suture (Prolene,
• Braided, twisted, floss lysis may result in gradual loss of Surgiline)
• Size and length. tensile strength over a period of time
Eyeless needled suture • Absorption rate: Gradual encap­ • Type: Monofilament
Available size: 9-0 to 3-0 sulation by fibrous connective tissue • Raw material: Isotactic crystalline
Length: 9-0 to 6-0—36 cm • Tissue reaction: Inert, but can evoke stereoisomer of polypropylene
5-0 to 2-0—76 cm minimal inflammatory reaction • Tensile strength: Not subjected to
Reel • Contraindications: Should not be degradation or weakening by action
Size: 6-0 to 4-0 used where permanent retention of of tissue enzymes
Length: 25 m tensile strength is required. • Absorption rate: Non-absorbable
Method of sterilization—autoclaving • Tissue reaction: Can evoke minimal
• Tissue reaction: Acute inflammatory Frequent Uses inflammatory reaction
reaction • General soft tissue approximation • Sterilization: Available in pre-ster­
• Contraindications: Known sensitiv­ and ligation including neurological, ilized state (Fig. 2.7)
ity or allergies cardiovascular procedures. • Not known.
• Frequent uses: Skin sutures. • Ophthalmic surgery—10-0 and 8-0
• Plastic surgery—6-0 to 3-0. Advantages
Uses • Inert as stainless steel and resist
• General soft tissue approximation Polyester Fiber Suture breakdown in infection.
and ligation including neurological, (Mersilene, Dacron) • High degree of smoothness so used
cardiovascular and ophthalmic pro­ in plastic and vascular surgery
cedures • Type: Braided, monofilament • Its sky blue (azure) color gives high
• Fixing of skin graft • Raw material: Polyethylene tere­ visibility
• To suture nerves and grafts in vas­ phthalate • Easy handling
cular surgery (atraumatic silk). • Tensile strength: Not significant • Knot security—poor
change in vivo • Least thrombogenic
Nylon Suture (Ethilon, • Absorption rate: Gradual encapsu­ • Retains tensile strength for years.
lation by fibrous connective tissue
Dermalon) • Tissue reaction: Minimal inflam­ Frequent Uses
Nylon suture (Fig. 2.6) is a synthetic matory reaction • Plastic and maxillofacial surgery
non-absorbable suture. The thickness • Contraindications: Not known • Vascular surgery
varies from 1-0 to 8-0. • Frequent uses: General soft tissue • Cardiovascular surgery
• Type: Monofilament approximation and/or ligation in­ • Tendon repair
• Raw material: Long chain aliphatic cluding neurological, cardiovascu­ • Hernia repair.
polymers, nylon 6 or nylon 66 lar and ophthalmic procedures.

Surgical Steel
• Type: Monofilament
• Raw material: An alloy of iron-
nickel-chromium
• Tensile strength: Indefinite
• Absorption rate: Non-absorbable,
remain encapsulated in body tiss­­-
ues
• Tissue reaction: Minimal
• Contraindications: Should not be
used when prosthesis of another
alloy is implanted as it can cause
Fig. 2.6: Nylon suture galvanism.
Sutures 43

ii. Side-to-side stapler with or without


knife blade.
iii. End to end staple—causing everting
anastomosis.

Advantages
• Metal clips for skin allow quick clo­
sure
• Decreases the operative time
• All clips are easy to remove.

Surgical Staples
It is faster procedures and reduces
Fig. 2.7: Prolene suture operating time. The trauma to tissue
is reduced because tissue handling is
reduced.

Skin Staples
The surgical staples are used for:
• Routine skin closure.
• To secure skin grafts on burn patients.
• For closing the laceration in emer­
gency (Figs 2.8A and B).

Tissue Glues
• Cyanoacrylate: It is used for skin
closure, but it requires perfect hemo­
A B stasis, if they are to work well. They
are expensive as staple, but quick to
Figs 2.8A and B: Skin staples used for closure of the skin
use and do not delay healing.
• Fibrin tissue glue: Tissue glue involv­
ing fibrin works on the conversion
Frequent Uses • Handling properties are good of fibrinogen by throm­bin to fibrin.
Abdominal wall and skin closure; • Knot stability is good. The network has good adhesive
sternal closure, retention, tendon repair, properties and is used for hemostasis
orthopedic and neurosurgery. Disadvantages in liver and spleen surgeries. It has
• It has capillarity and can cause been used for neurosurgery in dural
Surgical Cotton wound infection tears6, in ear, nose and throat sur­
• Type: Twisted (braided) • Tensile strength is poor and gets gery and ophthalmic surgery to
• Raw material: Natural long staple degraded by autoclaving attach implants. It is also used in
cotton fibers (cellulose) • Not desirable in presence of contami­ general surgery for prevention of
• Tensile strength: 50 percent lost in nation. postoperative adhesion of pericar­
6 mon­ths and 30 to 40 percent lost dium to peritonium.
in 2 years
METAL SUTURE AND CLIPS
• Absorption rate: Nonabsorbable,
Ligating Clips
remains encapsulated in body tis­ Humer Hultl5 in Hungary first used
sues mechanical stapling devise used to close Ligating clips offer the surgeon a rapid
• Tissue reaction: Minimal stomach. It gives a strong predictable and secure method of accomplishing
• Contraindications: None suture line. It allows access to difficult hemostasis or ligating arteries, veins,
• Frequent uses: Most body tissues area. nerves and other small structures. It can
for ligating and suturing. There are three basic type of gastro­ be absorbable or non-absorbable. It is of
intestinal stapling device. advantage in deep and difficult to reach
Advantages i. Linear stapler—linear everting staple areas. They are of use particularly in
• It is economical is used for end closure of viscous. microvascular surgery (Fig. 2.9).
44 Principles of Surgery

Fig. 2.10: Proper placement of needle


holder to hold the needle

Fig. 2.9: Ligaclips used to clamp the vessels


coefficient of friction) and suture-coat­ing
materials selected for wound closure are
important factors that must be consi­dered
by the surgeon [Instruments req­ uired
during suturing (Fig. 2.12)].
Disadvantages ARMAMENTARIUM
• They do not bring deeper tissue to­ Ideal Surgical Needle
gether Needle Holder
• Do not control bleeding from edges • Choice of size and type—determined
Characteristics
• Fine approximation is difficult. by characteristics of needle and • It should be made up of high-quality
wound or anatomic areas. stainless steel.
Clearon • Needle should be grasped at three- • It should be of smallest possible
Clearon are a woven polypropylene fourth distance from tip of needle diameter.
delnet tape coated with hypoallergenic (Fig. 2.10). • It should be stable in the grasp of the
adhesive mass. It is extremely porous, • Always check alignment of jaws of needle holder.
which ensure adequate wound venti­ the needle holder. The tip of jaws • It should be capable of implanting
lation. Being transparent progress of should meet first. suture material through tissue with
wound healing can be checked. • Always close needle holder on first minimal trauma.
or second ratchet. • It should be sharp enough to pene­
Ethistrips • Always hold needle holder so that trate tissue with minimal resistance.
It is a woven rayon acetate tape coated on needle point is directed toward • It should be sterile and corrosion-
one side with a hypoallergenic adhesive surgeons thumb. resistant to prevent introduction of
mass. It can be used by themselves or • The tripod grip is ideal for holding microorganisms or foreign materials
to reinforce skin closure. Steristrips are the needle holder as it provides into the wound.
used to buttress the suture and prevent excellent grip, support and stability
spreading of scar. (Figs 2.11A and B). Needle Performance
• Always use needle and needle hol­
Vacum-assisted Closure der as a unit.
Characteristics and
It is the vacum assisted closure (VAC) Wound closure and healing is affec­ Definitions
by creating negative pressure within ted by the initial tissue injury caused • Strength: Resistance to deformation
wound. The wounds are closed unifor­ by needle penetration and subsequent during repeated passes through
mly by applying controlled localized suture passage. Needle selection, sur­ tissue (Increased needle strength
pressure. face characteristics of the suture (e.g. results in decreased tissue trauma).
Sutures 45

• Ductility: Resistance of a needle to


breakage under a given amount of
deformation/bending.
• Sharpness: Measure of the ability of
the needle to penetrate tissue.
• Clamping movement: Stability of
a needle in a needle holder, deter­
mined by measuring the interaction
of the needle body with the jaws of
the needle holder.
A B
Figs 2.11A and B: Tripod grip of the needle holder Parts of Needle
Point
Point is a portion of the needle extends
from the tip to the maximum cross-
section of the body (Table 2.3).

Body
Body part of the needle incorporates the
majority of the needle length. The body
of the needle is important for interaction
with the needle holder and the ability
to transmit the penetrating force to the
point (Table 2.4).

Swage
The suture attachment end creates a
single, continuous unit of suture and
needle. The swage may be designed to
Fig. 2.12: Suturing set tissue holding forceps without and with teeth, permit easy release of the needle and
needle holder, skin hook
suture material (pop-off ).
Table 2.3: Point types
Types of Swage
Point type Design Indication • Channel swage
• Drill swage
Conventional — 3 cutting edges
cutting — Triangular cross-section that
• Non-swaged.
changes to a flattened body Figure 2.13 shows suture and their parts.
— Third cutting edge is on the
inner, concave curvature Needle Coating
(surface-seeking). The needle may be coated with silicone
Reverse cutting — Third cutting edge is on the Skin, tendon sheaths, oral mucosa, to permit easier tissue passage. The
outer convex curvature of the cosmetic and ophthalmic surgery coating helps reduce the force needed
needle (depth-seeking) to make initial tissue penetration and
— Stronger than conventional
cutting needles the frictional forces as the body of the
— A reduced risk of cutting out needle passes through the tissue.
tissue
Side-cutting Flat on the top and bottom surfaces Ophthalmic procedures
Needle Curvature
(spatula) to reduce tissue injury The suturing needles are available in
Taper-point Sharp tip at the point flattens to an Subcutaneous layers, dura, various curvatures and sizes of the body.
(round needle) oval/rectangular shape taper ratio peritoneum, abdominal viscera The different curvatures facilitate easy
(8–12:1) and tip angle (20–35°) needle manoeuvrability of the needle at
Blunt-point Dissects friable tissue rather than cuts Suturing the liver and kidneys different sites. For example, the straight,
curved and half circle needles are suitable
46 Principles of Surgery

Table 2.4: Body types • Needle length: The distance mea­


sured along the needle from the
Body type Indicated Use
point to the swage is termed needle
Straight Easily assessable tissue that can be Microsurgery for nerve and vessel length. Needle length, not chord
manipulated by hand repair length (bite width), is the measure­
Half-curved-ski Rarely used in skin closure ment supplied on suture packages.
Difficult to handle. • Radius: This is the distance from
Curved Optimal course for sutures through Intraoral sutures the body of the needle to the center
tissue Cleft palate repair of the circle along which the needle
Even distribution of tension curves (bite depth).
Designed for confined spaces • Diameter: The gauge or thickness
Compound The body has a tight 80° curvature Ophthalmic surgery of the needle wire is considered the
curved at the tip, which becomes a 45° Microvascular surgery diameter.
curvature throughout the remain­
der of the body Suture Principles
• The needle holder should grasp
the needle at approximately three-
fourth of the distance from the point
of the needle.
• The needle should enter the tissue
perpendicular to the surface, if the
needle pierces obliquely, tear may
develop.
• The needle should be passed through
the tissue following the curve of
needle. The wrists of the surgeon
must move as per the curvature of
the needle to drive the needle in the
Fig. 2.13: Parts of the suture
tissue smoothly.
• The suture should be placed at equal
distance from incision on both sides
and at equal depth.
• The needle should be passed from
free to fixed end.
• The needle should be passed from
thinner to thicker side.
• The needle should be passed from
deeper to superficial tissue.
• The distance the needle is passed
into the tissue should be greater than
the distance from the tissue edge to
ensure some degree of eversion in
anticipation of some degree of scar
contracture.
• The tissue should not be closed un­
Fig. 2.14: Types of needles according to curvature der tension to avoid tear or necrosis
around the suture, undermining of
for suturing the skin which is on surface and the place available at the site for easy tissue can be done to avoid it.
while the ‘J’ curvature is more useful in manoeuvrability of the needle. • The suture should be tied so that
placing sutures in the depth. The 5/8th the tissues are merely approximated
circle needle is used for suturing the Needle Measurements and not blanched.
palatal mucosa (Fig. 2.14). The size of • Chord length: This is the linear • The knot should not be placed on
the needle is selected depending upon distance from the point of the curved the suture line as it may interfere
the toughness of the tissue to be sutured needle to the swage (bite width). with the healing/epithelialization.
Sutures 47

• Consecutive sutures should be placed as short as possible with a given • Extra throws do not add to the
at least 3 to 4 mm apart. material to minimize foreign body strength of a properly tied knot, they
• Closer sutures are indicated in areas tissue reaction. only contribute to its bulk.
of underlying muscle activity like • A seesaw motion or the sawing of
tongue. one strand down over another, Types of Knot
• Extra tissue on one side of incision while tying the knot, may materially • Square knot: The suture is thrown
can cause ‘Dog Ear’. It can be weaken sutures to the point that they around needle holder once and once
obliterated by undermining of excess may break when the second throw is in the in opposite direction between
tissue. Incision is made approx 30° made. ties. It is always prudent to provide
to parent incision on the side of • The two ends of the suture are pulled at least three ties for surface knots. It
undermining. Extra tissue is pulled in opposite directions with uniform is indicate in nylon, polypropylene,
over incision and the appropriate rate and tension, the knot may be polyglycolic acid and catgut may
amount is excised. Incision is the tied securely with less possibility of require more ties.
closed in normal pattern. breakage. • Surgeon’s knot: Requires two throws
• Excessively large sutures, which are • Clamps and hemostats should ne­ver of suture around needle holder on
tightly closed lead to dead space be placed on any portion of the su­ first tie and then one throw in op­
below and epithelialization of the ture, which will remain in situ. Avoid posite direction on the second tie. It
suture tract. the crushing or crimping applica­ has advantage of reducing the slip­
tion of surgical instruments, such as page, while the second tie is put in
Suture Size needle ­holders and artery forceps, to the position. The third tie is usually
• Use finest permissible size, which the strand except when grasping the for the security of the previous knot
commensurate with natural strength free end of the suture during an in­ (Fig. 2.15).
of tissues. strument tie. • Granny knot: First two ties in the
• If postoperative course of patient • Sutures for approximation rather same direction followed by third
may produce sudden strain on su­ than hemo­ static purposes should tie squared on the first. The knot
ture line, reinforce it with retention not be tied too tightly as this causes involves a tie knot in one direction
suture. Remove them as soon as tissue strangulation. While sitting followed by single tie in the same
patient’s condition is stabilized. on the knot to prevent its loosening direction.
hold the knot firmly but without
Knot Tying crushing the thread with plain tissue
Types of Knot Indicated for
The knot the surgeon prefers to use to forceps.
secure the suture will vary according to • After the first loop is tied, it is neces­ Different Suture Material
the material used and the location, depth sary to maintain traction on one end • Square knot is indicated for surgi­
and purpose of the suture. Knots must of the strand for control to avoid cal gut, collagen, surgical silk, virgin
be tied with a technique appropriate loosening. silk, surgical cotton, stainless steel,
for the tissues to be sutured or ligated
and only tight enough to serve their
purpose without slipping. Postoperative
edema must be anticipated. Gener­ally,
synthetic suture materials have very
smooth surfaces. They may require a
different number of throws to achieve
knot security than the natural fibers.
Either instrument tie or the one hand or
two hand tie is used for tying the knot.
Some general principles govern the
tying of all knots, regardless of the suture
material to be tied.
• The completed knot must be firmly
tied so that slippage will be virtually
impossible. The simplest knot is the
most desirable.
• The knot must be small and the
ends of the suture should be cut Fig. 2.15: Types of knots
48 Principles of Surgery

uncoated synthetics, polyester fibers, grafting. The apposition and eversion of tensions in the suture line as the tissue
polyglactin 910. Place first throw in wound edges is more difficult to achieve swelling occurs. The advantage is that
a precise position, for the final knot, and the inclusion cyst may form. If the it is app­lied rapidly; the apposition of
using double loop. Tie second throw suture breaks entire suture line opens wound edges is more complete than with
square. Additional throws advisable leading to dehiscence of the wound. It conti­nuous over-and-over suture. There
in tension. should not be used in the area of existing is less epithelialization of tracts. The dis­
• For polyster fiber, polyglactin 910, tension (Figs 2.17A to C). ad­vantage being that the apposition of
poly­dioxanone, polypropylene, ny­ edges is not as perfect unless proce­dure
lon—a standard technique of flat and Continuous Locking Sutures is mastered well. If the suture breaks
square ties with additional throws if Continuous locking suture is similar entire suture line opens leading to dehi­
indicated by surgical cir­cumstances to continuous suture, but locking is scence of the wound (Fig. 2.18).
and experience of sur­geon. provided by withdrawing the suture
through its own loop. The suture is Mattress Suture
passed perpendicular the incision line. The main purpose of the mattress is to
SUTURING TECHNIQUES
The locking prevents excessive tighten­ provide more tissue eversion. It can
ing of the suture as the wound pro­gresses. be used in the area where wound con­
Simple Interrupted Care should be taken not to excessively tracture could cause dehiscence or
Simple interrupted is most commonly tighten the individual lock. The locking broad scar formation. Types of mattress
used technique. The suture is passed feature may prevent adjust­ment of the are horizontal or vertical.
through both the ends at equal dis­
tance and depth of incision line and
knot is tied on one side of the incision
line. It is strong and the successive
sutures can be placed in a manner to
fit the individual requirements of the
situation. The loosening of one suture
will not cause loosening of other
suture. A degree of eversion of the
tissue can be produced by ensuring
that the depth of the bite is more
than the distance from the suture to
the wound edge. The advantage of
this technique is that it permits good
eversion of wound edges and can be
rapidly applied. If it gets infected the Fig. 2.16: Simple interrupted suture
removal of few sutures would serve the
purpose. The disadvantage is that it
requires practice to master eversion of
edges. However, the eversion is not as
good in difficult wounds as with other
techniques, such as vertical mattress
suture. It does not relive extrinsic
tension from wound edges (Fig. 2.16).

Continuous Over-and-Over A B
First simple interrupted suture is
placed and the needle is reinserted in
continuous fashion such that the suture
is perpendicular to the incision line.
The suture is ended by passing a knot
over the untightened ends of suture.
The advantage is that it is fast technique
and there is even distribution of tension C
over entire suture line. It provides water
tight closure, which is important in bone Figs 2.17A to C: Continuous over-and-over
Sutures 49

needle is same for each entry point. But


the horizontal distance of the point of
pene­tration on the same side differs. The
advantage is that it produces broad con­
tact of wound margins and reinforces
sub­cu­taneous tissue. It relieves extrinsic
tension from wound edges. It also helps
in hemostasis from the skin edges. It has
dis­advantage that it constrict the blood
supply to the edges of incision casing
stran­gulation and necrosis leading to
wound dehiscence if applied too tightly
(Fig. 2.20).

Continuous Mattress
Fig. 2.18: Continuous locking suture Continuous mattress can be rapidly
placed in order to approximate large
laceration in cosmetically unimportant
areas. The disadvantage is that it does
not provide good apposition of the
wound edge or eversion. If the suture
breaks entire suture line opens leading
to dehiscence of the wound.
A
Subcuticular Suture
The subcuticular layer of tough connec­
tive tissue if sutured will hold the skin
edges in close approximation when
cosmetic result is desire. Continuous
short lateral stitches are taken beneath
the epithelial layer of skin. The ends
of suture come at each end of incision
B C and are knotted. This suture gives an
Figs 2.19A to C: Vertical mattress sutures excellent cosmetic scar. The advantage
is that it is more esthetic and reduces
problem associated with suture marking
Vertical Mattress and irritation. The disadvantage is that
The needle is passed from one edge of it does not produce adequate wound
the incision to other and again from approximation, does not evert wound
the latter edge to the first and a knot is edges and is time consuming (Figs 2.21A
tied. When the needle is brought from and B).
the second flap to the first the depth
of penetration is more superficial. The Figure of ‘8’ Suture
advantages are that it provides good Figure of ‘8’ suture is used over extraction
tissue eversion and there is perfect site where it provides protection of surgi­
apposition. It relieves tension from skin cal site and adaptation of gingival papillae
edges and runs parallel to blood supply around adjacent teeth (Figs 2.22A and B).
to edge of flap. The disadvantage is that
it takes more time to apply and produces Buried Sutures
more cross-mark (Figs 2.19A to C). Sutures placed completely under the
epidermal layer of the skin with their
Horizontal Mattress knot also in the tissue are considered
Similar to vertical mattress, but the ‘buried’ or ‘Inverted’. They are not re­
depth of penetration from the incision moved postoperatively as only absorb­
Fig. 2.20: Horizontal mattress line and the depth of penetration of the able material is used. Buried sutures
50 Principles of Surgery

may be continuous or interrupted. The


buried sutures are ideal for suturing the
lacerations of the tongue or for the clo­
sure of the surgical defects of the tongue,
as the regular projectile suture ends and
knots lead to irritation and salivation
(Figs 2.23A to D).

Purse-string Suture
A continuous suture is placed around a
lumen and tightened, like a drawstring,
to invert the opening. A purse-string
suture may be placed around the stump
of the appendix, in the bowel to secure an
intestinal stapling device or in an organ
prior to insertion of a drainage tube.
A B The purse string suture can be used for
Figs 2.21A and B: Subcuticular sutures suturing the soft tissue from the residual
capsular tissue around the neck of the
artificial condyle (condylar reconstruction
plate) so that a nice cuff of tissue is formed
around the artificial condyle.

Through-and-Through—
Retention Sutures
Some surgeons place retention sutures
from inside the peritoneal cavity through
all layers of the ab­dominal wall, includ­
ing the peritoneum. These “through-and-
through” sutures are inserted before the
peritoneum is closed. A simple interrupt­
A B ed or a figure-of-eight stitch is used. The
Figs 2.22A and B: Figures of ‘8’ suture wound is then closed in layers for a dis­
tance of about three-fourth the length. The
retention sutures in this area are drawn
together and tied. It is important that a fin­
ger be placed within the abdominal cavity
to pre­vent strangulation of the viscera in
the closure. The remainder of the wound
is then closed in a similar manner.

Buried Coaptation—Retention
A B Sutures
Some surgeons prefer to close the peri­
toneum with interrupted sutures alter­
nately with the retention sutures that
are placed to penetrate the other layers
from fascia through skin. The retention
su­tures are placed approximately 2 cen­
timeters apart.
The different methods of suturing,
A A their indications, advantages and disad­
Figs 2.23A to D: Buried sutures vantages are summarized in Table 2.5.
Sutures 51

Table 2.5: Methods of suturing along with their advantages, disadvantages and indications

Suture method Advantages Disadvantages Indications

1. Interrupted 1. Strong Require practice to master eversion 1. Area of tension


2. Successive sutures fit individual 2. Site of strong
requirement closure
3. Individual suture can be removed at
the site tension
2. Continuous 1. Fast technique 1. Apposition and eversion is
2. Even distribution of tension difficult to achieve
3. Provides tight closure 2. Break in one suture causes
dehiscence of entire suture line
3. Not indicated in area of tension
3. Locking continuous 1. Fast technique 1. Require mastering
suture 2. Apposition of wound is complete 2. If one suture breaks entire entire
3. Less epithelialization of tracts suture line breaks
4. Vertical mattress 1. Good tissue eversion 1. Time taking
2. Perfect apposition 2. More cross-marks
3. Relieves tension from skin
4. Blood supply parallel to edge
5. Horizontal mattress 1. Broad contact Constrict blood supply to edges of
2. Reinforces subcutaneous incision
3. Relieves extrinsic tension from wound
6. Continuous Applied over large area 1. Apposition is not good Large laceration
2. Eversion is not good

7. Subcutaneous 1. Cosmetically good 1. Adequate wound approximation Cosmetic area


2. Less suture marking and irritation 2. Evert wound edges
3. Time consuming
8. Figure of ‘8’ 1. Protection of the surgical site Extraction socket
2. Proper adaptation of the gingival
papillae

• Stick tie, also referred to as a suture The suture is then pulled out in such a
LIGATURES ligature or transfixation suture, is a way that the part of the suture, which
A suture tied around a vessel to occlude strand of suture ma­ terial attached was inside the tissue will come out and
the lumen is called a ligature or tie. It to a needle. The needle is used to under no circumstances the part of
may be used to affect homeostasis or to anchor the strand in tissue around the suture, which was on the surface
close off a structure to prevent leakage. the vessel before occluding a deep or will pass through the tissue depth as
• Free tie is a single strand of material large vessel. In other words the vessel it is contaminated and can carry the
handed over to the surgeon or assis­ is ligated along with the adjacent infection in deeper tissue planes.
tant to ligate a vessel. A hemostat is tissue (Figs 2.25A to E). The strand
placed on the end of the structure must be of sufficient length to allow Technique of Suture Removal
and the suture tied around the vessel the surgeon to tighten the first knot. Sutures are removed using aseptic and
under the tip of the hemostat. The sterile technique. A sterile suture remov­
knot is tightened by the surgeon’s al tray is prepared for the procedure.
SUTURE REMOVAL
fingers or with the aid of for­ ceps, • Cleanse the area with an antiseptic.
taking care to avoid instrument The sutures are removed under aseptic Hydrogen peroxide can be used
damage to the suture. As the knot precautions. First the suture site is to remove dried serum encrusted
is tightened the assistant gradually cleaned. The suture is grasped with around the sutures.
releases the clamp to ensure proper an instrument and lifted above the • Pick-up one end of the suture with
seat and tightening if the knot around epithelial surface the suture cutting thumb for­ceps. Cut the suture on one
the open end of the vessel (Figs 2.24A scissor is passed through one loop and side as close to the skin as possible,
to E). transected close to the skin surface. where it dips beneath the skin.
52 Principles of Surgery

A B C

Figs 2.24A to E: Free tie: (A) Thread passed


around the clamped vessel; (B) Thread
being tied around the clamped vessel,
watch the thread is parallel to the tissue
to avoid stretch and avulsion of the vessel;
(C) While the knot is tightened, the he­
mo­stat is slowly released; (D) Final knot
tightening and hemostat remove comple­
D E tely; (E) Ligature in place.

A1 A2 B

C D E
Figs 2.25A to E: Transfixing suture: (A) Clamped vessel along with adjoining tissue and the needle takes bite on one side of the clamped
vessel; (B) The needle takes bite on the other side; (C) As the knot tightened, the hemostat is slowly released; (D) Final knot tightening
after the hemostat is removed; (E) Transfixed vessel with cessation of the blood flow.
Sutures 53

A B C D
Figs 2.26A to D: Removal of sutures technique

• Gently pull the suture out through The sutures may not be removed at a 4. Wound closure manual, ETHICON,
the other side while holding the time, but alternate sutures are removed INC, 15, 37-8, 50.
suture with the forceps. The suture from the suture line is done depending 5. Hultl H. II Kongress der Ungarischen
should be removed without pulling on the healing of the surgical site. Gesell­
schaft fur Chirurgie, Budapest,
any portion that has been outside May 1908. Pester Med Chir Presse
the skin back through the skin 1909; 45:108–10.
(Figs 2.26A to D). REFERENCES 6. Toma AG, Fisher EW, Cheesman AD.
Sutures should be removed “before Autologous fibrin glue in the repair of
the epithelium has migrated into deeper 1. Chih-Chang Chu. Wound closure dural defects in craniofacial resections.
parts of the dermis. To prevent widening biomaterials and devices. 1st edition, J Laryngol Otol. 1992;106(4):356-7.
of the scar, the wound edges may be CRC-Press;. 1997. 7. Krizek TJ, Hoopes JE (Eds). Symposium
taped.”7 2. Clifford Snyder. On the history of the su­ on basic science in plastic surgery,
ture. Plastic and reconstructive surgery: St. Louise: Mosby, 1976;15:87.
Time of Suture Removal 1976; 58(4):401-6.
• Skin about face and neck—3 to 5 days 3. Postlethwait RW. Wound healing in
• Other skin sutures—5 to 8 days surgery, Somerville, NJ: ETHICON,
• Retention suture—10 to 14 days. INC., 1971, pp. 8-9.
3 Incisions in Maxillofacial
Surgery
Borle Rajiv M, Rai Anshul

The word ‘incision’ is closely associated • Incision should be given using con­
Basic Principles of
with surgery. Incisions are placed to tinuous and controlled pressure and
drain abscess, excise growths, mobilize Incision Making1 with a single stroke. Multiple soft
tissue and create access to the deeper • A sharp blade of an appropriate size strokes result in more damage to
viscera. Human tissues have an inherent (number) should be used for making the incised tissues and increase the
property that makes their response to an incision. A sharp blade allows amount of bleeding from the surgi­
injury fairly predictable. Depending on incisions to be made cleanly without cal site. It also delays healing due to
this predictability, principles of surgery unnecessary damage to the tissues the resultant tissue damage. Hence,
have evolved, which help to optimize due to repeated strokes. A number long continuous solitary stroke
wound healing and formation of an 15 blade is most commonly used for is preferable intermittent stro­ kes
acceptable scar. making incisions in oral and maxill­ to avoid ragged margins. As one
While placing the incision, it is ofacial surgery. A number 11 blade is approaches towards the end of the
imperative to know the regional ana­ used as stab knife for abscess drai­nage incision the direction of the knife
tomy, blood supply, nature of tissue and number 12 blade is used for oper­ should change from oblique to right
and its healing characteristics to achi­ culectomy, i.e. excision of peri­coronal angle, so that the skin and deeper
eve the desired results. An incision flaps (Figs 3.1A and B). tissue are incised at the same level.
should not only provide free, passive and • The Bard-Parker blade is mounted • An incision should always be deep­
unimpeded access to the deeper tissue, on the suitable handle (e.g. number ened layer-wise. A full thick­ ness
but should also be placed in the areas, 15 blade and number 3 handle). The incision through multiple layers, in
where the chances of damage to the vital surgeon holds the knife with a pen a single stroke should be avoided
structures is negligible and the tension grip, which provides better support to avoid injury to the deeper vital
free closure can be achieved to ensure to the hand and control over the structures. The reason being the in­
rapid healing and esthetically viable scar. knife (Fig. 3.2). nate variations in the microanatomy
An incision should ideally be placed in an
area, where the ensuing scars are hidden
and at the same time do not cause the
functional morbidity to the part.
To achieve these objectives certain
basic principles of surgery must be
adhered to.
A scalpel is used to make an incision.
The word scalpel is derived from the
Latin word ‘scalpere’ which means
‘to cut’. A scalpel has two components, a
handle and a blade. The blade is usually A B
detachable and is disposable. Figs 3.1A and B: Bard-Parker handles and blades
Incisions in Maxillofacial Surgery 55

far as possible. This leads to a better portion of an inci­sion that crosses such a
healing and esthetically acceptable crease often produces conspicuous and
scar. If the incisions cannot be placed unaesthetic scar.
in the lines of mini­mal tension, they On the face and in the neck these
can be made inconspicuous by lines of minimum tension are known
placement inside an orifice such as as Langer’s lines or tension lines of skin
the mouth, nose, or eyelid; within or cleavage lines (Fig. 3.3). They run
hair-bearing areas or location that transversely in the neck and are seen as
can be covered by hair or at the flexion creases. Incisions taken parallel
junction of two anatomic landmarks to these lines heal without the formation
such as the esthe­tic units of the face. of the unsightly scars produced by
Fig. 3.2: Pen grip for holding knife • Use as long incisions as needed. This incisions across them. When tension
provides better exposure and less lines are cut across, they result in undue
handling of the tissue. The healing of retraction of the lips of the wound.
and tissue consistency of individuals both long and short incisions takes
because of which no two individuals the same time and longer incisions
can be treated as similar. It is desir­ do not have any disadvantages as far Incisions used in Oral
able to incise one layer at a time. as healing is concerned. and Maxillofacial
• Incisions on epithelial surfaces Surgery
should always be made with the Relaxed Skin Tension Lines
blade held perpendicular to the The lines of minimal tension, also called Intraoral as well as extraoral incisions
surface. This creates wound edges, relaxed or resting skin tension lines, are are used in the management of the
which are easier to re-approximate as a result of the skin’s adaptation to various pathologies in the field of Oral
and less susceptible to necrosis. function and are also related to the elastic and Maxillofacial surgery. Each incision
• While placing incisions on the nature of the underlying dermis (Fig. 3.3). used is designed based on the basic
skin, the skin should be stretched The intermittent and chronic contraction principles of surgery and is indicated for
between the thumb and index finger of the muscles of facial expression create management of specific conditions.
of the other hand to allow a clean depressed creases on the skin of the face.
incision. These creases become more conspicuous Commonly used
• Mucosal incisions in the oral cavity with aging. Incisions should be made
should always be made resting on within these lines of minimal tension.
Intraoral Incisions
healthy bony tissue, so as to provide Incision made in or parallel to such a line
a healthy base for support of the or crease will become inconspicuous if Ward I2
sutured margins. Also, incision in careful closure is done. Any incision or It consists of mesial release, crevicular
unhealthy mucosal tissue should be and distal incisions. Mesial release incis­
avoided to prevent complication of ion begins from approximately 5 to
wound dehiscence. Hence, incisions 6 mm below mar­ginal gingiva of lower
should preferably be placed on att­ second molar at the mesial root and runs
ached gingiva. upwards obliquely at an angle of 45° to
• Incisions extending to the margi­ the distobuccal line angle of the second
nal and papillary gingiva should molar and extends post­eri­orly cutting the
be so designed that they do not cut distal papilla and then into the crevice of
through the papilla or the margi­ the third molar, if it is partially erupted
nal gingiva. Incision should always and then distally it extends on the anterior
cross the free margin of the gingiva border of the ramus of the mandible
at the mesiobuccal or distobuccal for a distance of 10 mm. While taking
line angle of the teeth. If the papilla mesial release incision, care should be
is cut, it leads to recession of the taken not to allow the knife to slip in the
papillary gingiva and if marginal gingivobuccal vestibule as it can lead to
gingiva is cut, it leads to clefting of damage to the facial artery. It is therefore
the marginal gingiva. advisable for the beginners to take this
• Extraoral incisions in the head, neck incision from the vestibular depth to
and face region should be given free gingiva (bottom to top) to prevent
along the existing resting skin tension the accidental damage to facial artery
lines and should not cross them as Fig. 3.3: Langerhans lines (Figs 3.4A and B).
56 Principles of Surgery

A B
Figs 3.4A and B: Ward I incision Fig. 3.6: Sulcular incision

Indications
Transalveolar extractions of the lower
third molar, which are partially erupted
with adequate depth of buccal vestibule.

Precautions Fig. 3.7: Bayonet flap


• Mesial release should not extend too
inferiorly to avoid cutting the facial
artery. Indications
Fig. 3.5: Ward II incision
• Distal release should not be lin­ It is used in third molar surgeries when
gually oriented to avoid damaging the molar is more lingually situated.
the lingual nerve or minor bleeding Precautions
encountered due to presence of nu­ Similar precautions are warranted as Second Molar Sulcus Incision
trient vessels. mentioned for the ward I incision.
• Distal release should be 10 mm long
with Vestibular Extension
to avoid cutting through tendinous Sulcular Incision (Bayonet Flap)
insertion of temporalis or the fibers The incision is similar to the second
of the masseter muscle or herniation Second Molar Sulcus Incision molar sulcus incision with the addition
of buccal fat pad in the oral cavity. Incision starts on the ascending ramus of an oblique vestibular extension in
following the center of the third molar the sulcus area which is angled forward.
Ward II shelf to the distobuccal surface of the This gives excellent buccal visibility
It consists of mesial release, crevicular second molar and then extends as a (Fig. 3.7).
and distal release incisions. Mesial sulcular incision to the mesiobuccal
release incision begins from approxi­ corner of the second molar (Fig. 3.6).
Second Molar Paramarginal Flap
mately 5 to 6 mm below marginal
gingiva of lower first molar at the distal Indications with Vestibular Extension (L flap)
root and runs upwards obliquely at an Used for transalveolar extraction of L flap is similar to the bayonet flap
angle of 45° to the mesiobuccal line most mesially inclined and superficial only difference being that the incision
angle of the second molar and extends impactions. is made a couple of millimeters away
distally into the crevice of the second from the marginal gingiva. It optimizes
molar up to its posterior surface and marginal attachment healing next to the
Second and First Molar Sulcus
then distally it extends on the anterior second molar (Figs 3.8A and B).
border of the ramus of the mandible Incision
for a distance of 10 mm (Fig. 3.5). Second and first molar sulcus incision Lingual Flap Incision
is similar to the second molar sulcus Lingual flap incision starts on the
Indications incision only difference being that the ascending ramus up to the distobuccal
Transalveolar extractions of the lower sulcular incision is extended to the surface of the second molar and follows
third molar, which are completely uner­ mesiobuccal suface of the first molar. the distal surface of the second molar as
upted and inadequate depth of buccal Due to extra extension, it gives a better a sulcular incision and then continues
vestibule. exposure. lingually to the first molar region.
Incisions in Maxillofacial Surgery 57

B A B
Figs 3.8A and B: Incision for the L flap Figs 3.10A and B: Submarginal incision

A B
Fig. 3.9: Semilunar incision Figs 3.11A and B: Degloving incision (Source: Edward Ellis III, Zide MF. Surgical
approaches to the facial skeleton. Dallas, Texas)

Indications Submarginal Incision3 nasal spine ensures incision placement


It is used for lingual split technique of Submarginal incision has its horizontal inferior to these structures in the maxil­
transalveolar extraction of mandibular component in the attached gingiva with lary anterior region.
third molars. accompanying vertical release inci­
sions. The horizontal incision can be Indications
Semilunar Incision scalloped to conform to the shape of It is used to access the pyriform aperture
Semilunar incision is a slightly cur­ the marginal gingiva. It requires at least region anteriorly and zygomatic but­tress
ved half-moon shaped incision in the 4 mm of attached gingiva. It also res­ posteriorly. This incision is used for vari­
alveolar mucosa. It prevents inci­ sion ults in bleeding into the surgical site ous surgical procedures perfor­med in the
and reflection of the marginal and (Figs 3.10A and B). maxilla such as infraorbital nerve neurec­
papillary gingiva thus avoiding compli­ tomy, Caldwell-Luc oper­ a­
tion, Le-Fort
cations thereof. However, it causes more Indications osteotomy, low level maxillectomy, fixing
bleeding, delayed healing and scarring It is used most commonly in cosmeti­ of Le-fort I, II fractures, zygomatic bone
of mucosa. So also, access to the cally important areas such as maxillary fractures, etc. While closing the degloving
periradicular tissues is restricted. It also anterior teeth for access to the periapical incision which crosses the midline, there
carries a risk of flap margins lying over areas of the tooth. are chances of alar flaring, which can
a bony defect thus violating the basic be avoided by taking alar cinch suture
principles of surgery at times (Fig. 3.9). Degloving Incision (Figs 3.11A and B). The lip len­gth­ening
The incision is usually placed approxi­ can also be achieved with this incision by
Indications ma­tely 3 to 5 mm superior to the muco­ doing V-Y closure in the midline.
It is used for apicectomy of teeth and gingival junction. Leaving unattached
apical curettage. It can be used for trans­ mucosa on the alveolus facilitating the Curvilinear Incision
al­veolar removal of retained fractured closure. Palpation of the inferior extent Curvilinear incision is used in the man­
apical portion of tooth roots. of the pyriform aperture and/or anterior dibular anterior region in the intermental
58 Principles of Surgery

foramina region. It extends ante­ riorly


out into the lip, leaving 10 to 15 mm of
mucosa attached to the gingiva. Once
through the mucosa, the underlying
mentalis muscles are clearly visible. The
muscle fibers are sharply incised in an
oblique approach to the mandible. When
bone is encountered, an ample amount
of mentalis muscle should remain on its
origin for holding deep sutures at closure.
In the body and posterior portion of the
mandible, the incision is placed 3 to
5 mm inferior to the mucogingival junc­
Fig. 3.12: Curvilinear incision Fig. 3.13: Ginwalla’s incision
tion. Leaving unattached mucosa on the
alveolus facilitates closure (Fig. 3.12).

Indications
For open reduction of mandibular frac­
tures of the symphysis and parasym­
physis. For harvesting corticocancellous
graft from symphysis region.

Precautions
• In the anterior region, adequate
tissue should be left back on the
bone for suturing to avoid gaping.
• In the canine area the incision A B
should not be placed lower than 3 to
5 cm to safeguard the mental neuro­
vascular bundle.

Ginwalla’s Incision4
Ginwalla’s incision is placed on the
anterior border of the ascending ramus
of the mandible and extends both ling­
ually and buccally to end in a ‘Y’. It
provides better exposure of the inferior
C D
alveolar nerve for its avulsion (Fig. 3.13).
Figs 3.14A to D: Uni and bicoronal incisions
Indications
Ginwalla’s incision is used for the rior access required for the procedure. flap. The incision is made through
inferior alveolar nerve neurectomy for The coronal incision can be extended skin, subcutaneous tissue, and galea
mana­gement of trigeminal neuralgia. inferiorly, to the level of the lobule of revealing the subgaleal plane of loose
the ear as a preauricular incision to areolar connective tissue overlying the
allow exposure of the zygomatic bone pericranium (Figs 3.14A to D).
Extraoral Incisions
and arch, frontozygomatic suture,
tem­po­romandibular joint (TMJ). The Indications
Coronal Approach5 hemi­ coronal incision begins in the • Used for exposure of frontozygo­
preauricular area on the desired side matic suture, superior orbital rim,
Uni/Hemicoronal Approach of the incision and curves forward at lateral orbital wall, zygomatic arch,
Two factors are considered, while desi­ the midline, ending just posterior to for management of unilateral mid­
gning the line of coronal incision. The the hairline. Curving the hemicoronal face fractures.
first is the hairline of the patient. The incision anteriorly provides the relax­ • For exposure of TMJ in management
second factor is the amount of infe­ ation necessary for retraction of the of ankylosis, trauma.
Incisions in Maxillofacial Surgery 59

Precautions Transfacial Approaches to the Precautions


• During finger dissection at the Mandible • Incision should be 1.5 to 2 cm below
forehead region, there are chances inferior border to avoid injury to
of tearing the pericranium due to its Standard Submandibular marginal mandibular branch of the
adherence to the frontalis muscle, Approach7 facial nerve.
where sharp dissection is advised. • Facial artery should be palpated
• During placement of preauricular The incision is placed approximately before hand to avoid accidental
incision it is essential to mind the 2 finger breadths or 1.5 to 2 cm below injury.
superficial temporal artery, which the inferior border of the mandible to • Preferably, incision should be plac­
runs in anterior to the tragus. avoid injury to the marginal mandibular ed in the neck crease to avoid ugly
nerve, which lies within the above perceptible scar.
Bicoronal Approach6 mentioned distance from the inferior
Same considerations for location of the border of the mandible. The skin creases Retromandibular Incision10
incision as above. In the males the hair below the mandible do not parallel the The incision for the retromandibular
line recession is not predictable and thus inferior border of the mandible, but run approach begins 0.5 cm below the
incision line on the cranial side is cur­ obliquely, posterosuperiorly to antero­ lobule of the ear and continues inferiorly
ved in a zigzag manner, anticipating the inferiorly. 3 to 3.5 cm. It is placed just behind the
future hair loss. The incision begins at one posterior border of the mandible and
superior temporal line to the other tem­ Risdon’s Submandibular may or may not extend below the level
poral line other temporal line (hair band of the mandibular angle, depending
incision). The incision is made through the
Approach8 on the amount of exposure needed.
skin, subcutaneous tissue, and galea reve­ Like the standard submandibular inc­ A modification11 to this incision was
a­ling the subgaleal plane of loose areolar i­
si­
on placed approximately 2 finger­ given by Hind’s, where in the incision is
conn­ec­tive tissue overlying the peri­cr­an­ breadths or 1.5 to 2 cm below the in­ placed at the posterior ramus, just below
ium. At the temporal line the inci­sion is ferior border of the mandible to avoid the earlobule; the advantage being
carried in the temporalis fascia to maintain injury to the marginal mandibular nerve direct access to the posterior border of
the subgaleal plane and exten­ded in the and it curls around the angle of the man­ the ramus (Figs 3.16A to C).
prea­uricular crease up to the lobule of the dible9 (Figs 3.15A and B).
ear on both sides (see Figs 3.14A to D). Indications
Indications Surgeries of the condylar neck and
Indications • Extraoral approach to mandibular ramus.
• Used for exposure of frontozygo­ angle and ramus region.
matic suture, superior orbital rim, • In management of cysts and tumors Precautions
lateral orbital wall, nasoethmoidal of the mandible not amenable to • Injury to the main trunk of facial
area, zygomatic arch, for manage­ transoral approach. nerve should be avoided.
ment of bilateral midface fractures. • In management of low condylar • Injury to the retro­mandibular vein
• For exposure of TMJ bilaterally, in fractures (provides poor access). should be avoided.
management of ankylosis, trauma.
Transfacial Approach
to Mid-Face
Lateral Rhinotomy12
Lateral rhinotomy was first described by
Michaux in 1848, but was popularized
by Moure in 1902. The classical lateral
rhinotomy described by Moure lies
halfway between the medial canthus
and the nasal dorsum extending from
the inner margin of the eyebrow down
along the nasomaxillary groove curving
around the ala to enter into the nose.
The incision begins from the columella
A B laterally along the vestibule of the nose
Figs 3.15A and B: Risdon’s submandibular incision and then follows the ala of the nostril
60 Principles of Surgery

A B C
Figs 3.16A to C: Retromandibular incision

A B
Fig. 3.17: Lateral rhinotomy incision
Figs 3.18A and B: (A) Standard Weber-Ferguson incision;
(B) Weber-Ferguson incision with subciliary extension

and extends along the lateral aspect of Weber-Ferguson Incision with


the nose to end a centimeter below the Lynch Extension
inner canthus of the eye (Fig. 3.17).
Lynch extension14
Indications It is an extension on the medial side
Access to the nasal cavity, for open rhin­ from the medial canthus to the medial
o­plasties and maxillary antrum. end of the upper eyebrow (Fig. 3.19).

Weber-Ferguson Diffenbach Indications


Incision13 It is used for extended maxillectomy and
The basic advantage of Dieffenbach’s ex­ access to the medial orbital wall.
tension is that it is used for low level sub­
total maxillectomy, wedge maxillecto­
Weber-Ferguson Incision
my. It is similar to the lateral rhinotomy
incision with the difference being that in with Subciliary Extension
this incision the upper lip is split in the It is an extension of the lateral rhino­ Fig. 3.19: Weber-Ferguson incision with
area of philtrum (Figs 3.18A and B). tomy incision, wherein inferiorly it lynch extension
Incisions in Maxillofacial Surgery 61

extends from the columella to divide skin and helix of the ear for the entire Disadvantages
the upper lip in the midline. Superiorly length of the attached portion of the • The access is inadequate.
it is 6 to 8 mm medial to the medial pinna. Modificati­ons were suggested to • The chances of damage to the zygo­
canthus, the inci­sion extends laterally, this standard incision such as Blair and mati­cotemporal branch of the facial
not creating a sharp angle, but forming Ivy’s16 ‘inverted hockey stick incision’ and nerve are very high.
a rounded curve to avoid necrosis of the Thoma’s17 ‘vertical angulated incision’ • The horizontal extension of the
tip of the flap and causing a button like (Figs 3.21A and B). hockey stick incision lies on the
dehiscence. The infraorbital extension zygomatic arch, producing unsightly
runs in the crease below the inferior Indications scar.
palpebra upto the lateral canthus. For exposure of the condyle and con­
A modification for esthetic reasons is dylar neck of the TM joint. Al-Kayat Bramley’s Incision18
that the incision extends into the floor Al-Kayat Bramley’s incision is an inverted
of the nasal cavity from the columella Precautions question mark incision. It is an extension
leaving a 60o notch in the nasal floor, • Care should be taken to avoid of the standard preauricular incision,
where the triangular portion of the upper damage to the auriculotemporal wherein the preauricular incision is
lip is inserted during closure (Figs 3.20A nerve. extended superiorly and posteriorly
to C). • Care should be taken to avoid around the attachment of the temporalis
damage to the superficial temporal muscle in an inverted question mark
Indications artery. fashion. It provides increased exposure
Used for access to the maxilla for partial,
subtotal or total maxillectomy.

Precautions
The angle at the junction of the infra­
orbital and lateral nasal incision should
be obtuse to avoid necrosis of the trian­
gular portion of the flap.

Approaches to the
Temporomandibular Joint
Preauricular Incision15 A B
Preauricular incision is given in the pre­ Figs 3.21A and B: Thoma’s angulated vertical incision and hockey stick incision
auricular crease at the junction of facial

A B C
Figs 3.20A to C: (A) Weber-Ferguson incision with subciliary extension; (B) Infraorbital extension; (C) Infraorbital and Borle’s temporal
extension, used when temporalis muscle flap is planned for the reconstruction (Anshul Rai, et al. modified Weber-Ferguson incision with
Borle’s extension (Br J Oral and Maxfac Surg. 2010;45(5):e23-4.)
62 Principles of Surgery

of the TMJ (Figs 3.22A to G). It is the


most popular and commonly practiced
incision for the TMJ ankylosis surgery.
It is the approach to the malar arch
and joint, which gives excellent visibility
with safety, but at the price of longer
incision and wider exposure than is
conventional. It differs from Rowe’s
description in the positioning of the skin
incision and that through the temporal
fascia. Fig. 3.22A: Al-Kayat Bramley’s incision Fig. 3.22B: temporal fascia
The skin incision is question mark marking
shaped and begins about a pinna’s length
away from the ear, anterosuperiorly just
within the hair line and curves backwards
and downwards well posterior of the
main branches of the temporal vessels,
till it meets the upper attachment of
the ear. The incision then follows the
attachment of the ear and just endaurally
as described by Rowe (1972).
The temporal incision must be
carried through the skin and superficial
fascia to the level of temporal fascia. The
nerve filaments run in the superficial
fascia and it is very important that the
full depth of this fascia is reflected along Fig. 3.22C: Point C is the most anterior Fig. 3.22D: Point B is the lowest concavity
with the skin flap. Blunt dissection in concavity of the bony external auditory of the bony external auditory canal. Point F
this plane is carried downward to a point canal. Point Z is the point of the lateral is the bifurcation of the main trunk of the
about 2 cm above the malar arch, where surface of the malar arch midway between facial nerve. Point PG is the lowest point of
the temporal fascia splits. The pocket the upper and lower border, where the most the postglenoid tubercle
formed by the division contains fatty posterior significant twig of the temporal
tissue, which is easily visible through ramus of the facial nerve crosses the arch
the thin lateral layer. Beyond this point,
there should be no attempt at further
dissection of the superficial fascia from
the temporal fascia.
Starting at the root of the malar arch,
an incision running at 45° upwards and
forwards is made through the superficial
layer of the temporal fascia. Once inside
this pocket, the periosteum of the malar
arch can be safely incised and turned
forward as one flap with the outer layer
of temporal fascia, superficial fascia
containing the nerves and skin. The
pocket can be developed anteriorly as
far as the posterior border of the frontal
process of the malar bone and post­eriorly
joined to the preauri­ cular diss­ ection,
which follows closely the cartilaginous
external auditory canal beneath the
glenoid lobe of the parotid gland and Fig. 3.22E: Skin incision in relation to the underlying structures
Incisions in Maxillofacial Surgery 63

Fig. 3.22F: Incision running at 45° upwards


Fig. 3.24: Postauricular approach
and forwards in made through the super­
ficial layer of the temporal fascia, pro­tecting Fig. 3.23: Modified Al-Kayat Bramley’s
the vessels and branches of facial nerve, incision. Note that the incision is not curling
downwards anteriorly, as it is the area of • Might also provide exposure of the
at the same time giving excellent exposure
of the joint future hair loss and the scar may become coronoid process.
visible • Allows harvesting of the temporalis
flap in gap arthroplasty.
without tension. This is in marked • Provides exposure to the zygomatic
contrast to the near impossibility of arch.
approximating the temporal fascia, if it
is incised at a higher level, where it is a Postauricular approach19,20
single layer of tissue. The incision is placed posterior to the
Advantages of Al-Kayat Bramley’s pinna in the retroauricular crease. It is
incision are: cosmetically viable incision (Fig. 3.24).
• There is minimal bleeding and less
sensory loss. The posterior place­ Indications
ment of the skin incision and its Exposure of the condyle for surgeries of
Fig. 3.22G: Closure of Al-Kayat wide backwards and upwards sweep the TMJ.
Bramley’s incision spares the major branches of the
vessels and nerves. Disadvantages
• Facial plane can be easily identi­ • Poor exposure
superficial temporal vessels. A small fied. • Risk of external auditory canal infec­
torturous branch, the auricular artery, • There is excellent visibility. This is tion.
runs backwards from the superficial partly due to large flap and partly • Risk of external auditory canal steno­
temporal artery to the ear. The middle because the unyielding temporal sis.
temporal artery which comes off the fascia is not reflected with the skin as • Temporary or permanent paresthe­
superficial temporal artery perforates in the approach described by Rowe sia of the pinna.
the temporal fascia to supply the tempo­ and Killey (1968).
ralis muscle. This should be divided and • The potential complications of mus­ Endaural Approach21
ligated (Fig. 3.23). cle herniation and fibrosis are avoid­ The incision begins above the level of the
Proceeding downwards from the ed. The muscle is never exposed and zygomatic arch and extends downward
lower border of the arch and articular the superficial layer of the temporal and backward into the intercartilagenous
fossa, the tissues lateral to the joint fascia can be closed without tension. cleft between the tragus and the helix and
capsule are dissected and retracted. The • There is remarkably little post­opera­ then extends inwards along the roof of
base of the neck of the condyle can be tive discomfort or swelling. the auditory meatus for approximately
exposed. The bifurcation of the facial • A good cosmetic result is achieved 1 cm (Fig. 3.25).
nerve is not nearer than 2.4 cm in an except in patients with receding hair
anterior-posterior direction from the line. Indications
postglenoid tubercle. Care is needed • The technique is easily teachable Used for exposure of the condyle for
not to extend deep dissection below the and speedily executed. surgeries of the TMJ.
lower attachment of the ear.
Repair of the layers presents no Indications Disadvantages
problem. The incised outer layer of the • Exposure of the condyle for surgeries • Poor exposure.
temporal fascia can be repaired entirely of the TMJ. • Chances of chondritis.
64 Principles of Surgery

Fig. 3.25: Endaural approach A B


Figs 3.26A and B: Hind’s postramal approach (Source: Edward Ellis III, Zide MF.
Surgical approaches to the facial skeleton. Dallas, Texas)
Postramal (Hind’s)22 Approach
The Hind’s Postramal approach is
indicated for the surgeries involving Indications
the condylar neck and ramal area, e.g. Exposure of infraorbital ridge during
management of the subcondylar or fixing the zygomatic bone and Le-Fort II
ramal fractures of the mandible. It not fractures. Exposure of the orbital floor.
only gives excellent exposure but also
has very good and acceptable cosmetic Precautions
results. The incision runs 1 cm behind It should not cross the lateral canthus
the posterior border of the ramus, to avoid cutting the lymphatic channels
starting a centimeter below the lobule that will lead to excess postoperative
of the ear and extends to the angle of edema.
the mandible. After the skin incision the
parotidomasseteric fascia is carefully Subtarsal Incision25,26
Fig. 3.27: Infraorbital, subtarsal and subciliary
dissected, avoiding damage to the facial Subtarsal incision is placed between the
incisions (Source: Peterson’s Principle of oral
nerve and the retromandibular vein (can subciliary and infraorbital incision. It is
and maxillofacial surgery. Elsevier)
be identified and ligated if necessary). placed in the lower palpebra along the
After exposing the posterior border of tarsal plate (Figs 3.29A to D).
the ramus the pterygomasseteric sling
is incised and the masseter and the Indications
overlying superficial lobe of the parotid Exposure of the infraorbital rim and the
gland are reflected superiorly and orbital floor.
laterally to expose the condylar neck.
After the surgery the pterygomasseteric Precautions
sling should be repositioned by suturing. It should not cross the lateral canthus
Undue force while retracting the parotid to avoid cutting the lymphatic channels
and unnecessary dissection through that will lead to excess postoperative
the parenchyma should be avoided to edema.
prevent damage to the branches of the
facial nerve (Figs 3.26A and B). Subciliary Incision27,28
The incision is made approximately
Incisions Around the Orbit23 2 mm inferior to the eyelashes, along the
(Periorbital Approaches) entire length of the lid. The incision may
be extended laterally approximately 1 to
Infraorbital Incision24 Fig. 3.28: Infraorbital incision 1.5 cm in a natural crease, if more
Infraorbital incision is placed on the exposure is necessary. If no natural
skin. In the skin crease along the infra­ skin crease extends laterally from the
orbital ridge from the medial canthus along the line of minimal skin tension lateral palpebral fissure, the extension
to the lateral canthus. If an extension is along the zygomatic bone (Figs 3.27 and can usually be made straight laterally or
required in the lateral side it should be 3.28). slightly inferolaterally. The depth of the
Incisions in Maxillofacial Surgery 65

The subciliary incision may sometimes


cause ectropion due to contracture dur­
ing healing.

Transconjunctival Incision29,30
The lower eyelid is everted with fine for­
ceps and two or three traction sutures
are placed through the eyelid approxi­
A B mately 4 to 5 mm below the lid margin
to include the tarsal plate in the suture.
A lateral cantho­tomy might be perfor­
med if needed (Figs 3.31A and B). Inci­
sion is placed on the lower palpebral
conjunctiva midway between the inferi­
or margin of the tarsal plate and inferior
conjunctival fornix. Medi­ ally, incision
should not extend beyond the lacrimal
punctum (Figs 3.32A and B, 3.33).

Indications

C D
For exposure of the infraorbital rim for
fixation of fracture passing through the
Figs 3.29A to D: Subtarsal incision (Source: Edward Ellis III, Zide MF. Surgical approaches infraorbital rim.
to the facial skeleton. Dallas, Texas)

A B
Fig. 3.30: Subciliary incision Figs 3.31A and B: Incision of the conjunctiva below the tarsal plate

initial incision is through the skin only


such that the underlying muscle is seen
when the skin in incised completely
(Fig. 3.30).

Indications
For exposure of the infraorbital rim for
fixation of fracture passing through the
infraorbital rim.

Precautions
Care should be taken not to extend the A B
incision laterally in a superior direction to Figs 3.32A and B: Transconjunctival incision (Source: Edward Ellis III, Zide MF. Surgical
avoid crossing the minimal tension lines. approaches to the facial skeleton. Dallas, Texas)
66 Principles of Surgery

A B
Fig. 3.33: Transconjunctival incision with Figs 3.34A and B: Lateral brow incision
lateral canthotomy31

Precautions Upper Lid Blepharoplasty however, may be extended farther later­


Care should be taken to protect the globe Incision32 ally as necessary for surgical access.
of the eye from any trauma. Corneal
shield can be used for this purpose. The incision is placed in a skin wrinkle Approaches to the Parotid
Damage to the lacrimal punctum should in the superior eyelid at least 10 mm Gland
be avoided by restricting the medial superior to the upper lid margin and
extension of the incision. 6 mm above the lateral canthus as it Blair Incision33
extends laterally (Fig. 3.35). If a lid crease Incision begins in the preauricular crease
is not readily detectable, a curvi­linear extending superiorly up to the level of
Lateral Brow Incision
incision along the area of the supratarsal the root of the helix. Inferiorly it turns
The eyebrow is not shaved. The skin is fold that tails off laterally over the lateral laterally around the ear lobule extending
stretched over the orbital rim using two orbital rim works well. The incision, around it up to the mastoid process from
fingers and a 2 cm incision is made. The where it curves down to extend on to the
incision should be parallel to the hair sternocleidomastoid muscle and then
follicles of the eyebrow to avoid cut­ into one of the neck creases. If the neck
ting hair follicles or shafts, which might dissection is planned simultaneously,
retard growth of the eyebrow hair. The the Blair’s incision can be modified and
incision may be made to the depth of extended in the neck to accomplish the
the periosteum in one stroke. Extend­ neck dissection (Figs 3.36A and B).
ing the incision inferiorly along the
orbital rim should be avoided, because Indications
the incision crosses the lines of resting For surgeries of the parotid gland.
skin tension, making the scar very con­
spicuous (Figs 3.34A and B). Precautions
Care should be taken to avoid damage
Indications Fig. 3.35: Upperlid blepharoplasty incision to the superficial temporal artery, the
a. Exposure of the Frontozygomatic
sut­ure and lateral part of the supraor­
bital rim.
b. Exposure of the lateral orbital rim.

Crow’s Feet Incision


Crow’s feet incision is an extension of
the lateral brow incision given if more
inferior exposure is required. The incis­
ion is extended laterally into a crow’s
foot wrinkle at least 6 mm above the A B
level of the lateral canthus. Figs 3.36A and B: (A) Blair incision; (B) Modified Blair incision
Incisions in Maxillofacial Surgery 67

Fig. 3.37: Gutierrez incision Fig. 3.38: Redon and Vaillant incision Fig. 3.39: Adson and Ott incision

auri­culotemporal nerve, the marginal


man­­di­bular nerve while placement of
inci­sion in the neck.

Gutierrez Incision34
The incision has a temporal extension,
a preauricular component and a limb
extending on to the neck in one of the
skin creases. This was described by
Gutierrez in 1903 (Fig. 3.37).

Redon and Vaillant Incision


Their incision was similar to that pro­
posed by Adson. It has a preauricular
sector, which curls around the ear
lobule and then curls again downwards
Fig. 3.40: Samengo incision Fig. 3.41: Appiani’s incision
to extend in one of the neck crease
(Fig. 3.38).
Appiani’s Incision, 198437 need to provide safe skin cover for vital
Adson and Ott Incision 35
The incision lies within the lower portion structures left in the neck after the dissec­
Adson and Ott incision is a ‘Y’ shaped of the scalp and is hidden by the hair tion. For the purpose of radical neck dis­
incision with a preauricular sector, instead of the vertical incision line. The section, three major incision types were
a postauricular sector and a cervical temporal extension of the incision being popularized. However, with chan­­ ging
incision line, that splits off from the site short restricts access. To overcome this trends in management of neck in various
of union of the first two branches. The pitfall, Ferreira JL38 extended the tem­ cancers of the oropharyngeal area and
advantage of this incision is improved poral limb of the incision, but kept it mana­gement of levels 1 to 3 of the neck
esthetics because it lacks a temporal within the hairline (Fig. 3.41). nodes, various other incisions have been
incision line (Fig. 3.39). intro­duced.
Approaches for Neck
Samengo Incision36
Dissection Crile’s ‘Y’ Incision or Triradiate
The incision is similar to the one
described above having a preauricular, Each of the incision advocated for neck Incision
39

a postauricular and a neck extension in dissection represents a compromise be­ The submandibular part of the incision
the incision line (Fig. 3.40). tween free accesses to the surgical site and begins anteriorly a little beyond the
68 Principles of Surgery

and other in the supraclavicular region.


A bipedicled flap is present in between the
two incisions (Figs 3.44B to C and 3.45A).
As there are no vertical incisions the
triangular edges are nonexistent and thus
the chances of necrosis and dehiscence
are minimal. As the incisions fall in the
natural skin creases, the tension is not
present and thus the healing is excellent.
The esthetic results are very satisfactory.
However, the neck dissection through
this incision is technically more deman­
ding and needs lot of practice and thus it
is not suitable for the beginners.

Schobinger Incision42
Schobinger incision is a modification of
Fig. 3.42: Crile’s ‘Y’ incision or triradiate Fig. 3.43: Hayes Martin incision the triradiate incision. In this incision
incision the vertical limb of the incision is curved
posteriorly instead of running straight.
midline near the lower border of the incision. However, it extends into the neck This modification avoids placement of
mandible and extends up to the mastoid as an inverted ‘Y’ in the supraclavicular the vertical component of the incision on
process. The two incisions can meet in the region thus creating four triangular flaps the carotid artery (Figs 3.44A and 3.45B).
submandibular area at an angle of 120o (Fig. 3.43). Which is the main drawback The formation of a sharp triangular area
or can be curved in that area. The vertical as there are chances of compromised still remains the basic disadvantage of
component of the incision lies behind the vas­cul­arity and the necrosis at these sites this incision.
line of the carotid artery and continues and danger of exposing the carotid artery. Apron like incision of Freund and
below the clavicle for 3 to 4 cm (Fig. 3.42). Although the exposure of the structures of Latyshevsky43: Apron incision is used in
the neck is liberal and the neck dissection management of level 1 to 3 cervical lymph
Precautions is easy. nodes in the neck. It begins at the mastoid
The incision should not lie over the process and curves below the lower border
carotid artery to avoid possibility of Precautions of mandible approximately crossing the
complications such as carotid blow out Same as above. SCM, where it is crossed by the omoh­
if at all there is dehiscence of the neck yoid muscle and extends up to the chin
incision line. MacFee Incision41 (Figs 3.46A to C). This is very effective
MacFee incision differs from the above incision for the supraomohyoid neck
Hayes Martin Incision40 two incisions in that it does not have a dissections. The main advantage being
Hayes martin incision has a similar subm­ vertical limb. It consists of two horizontal that there are no triangular areas or sharp
a­ndi­bular component like the triradiate incisions, one in the submandibular area angles and thus the healing is excellent.

A B C
Figs 3.44A to C: (A) Schobinger incision; (B and C) MacFee’s ladder incision
Incisions in Maxillofacial Surgery 69

Apron Like Incision of Freund44 dissections for the midline malignancies


Apron incision of Freund is used in ma­ of the oral cavity.
na­­gement of malignancies of the larynx.
It extends from one mastoid pro­cess to Conley Incision45
the other after crossing the deep neck Conley incision is a modification of the
fold (Figs 3.47A and B). This incision triradiate incision wherein the anterior
with suitable minor modifi­cations can be limb of the submandibular incision and
used for bilateral supraomohyoid neck the posteriorly curved vertical incision
are modified to run as a single incision,
which begins in the submental region
and curves posteriorly at the anterior
border of the trapezius muscle up to
the clavicle. The posterior part of the
submandibular incision is given at a
right angle approximately below the ear
lobule.
The Conley incision was modified by
Lasaridis et al.46 (1994), which is shown Fig. 3.48: Conley incision
in the figure as dotted line (Fig. 3.48).

B A B
Figs 3.45A and B: (A) MacFee’s incision; Figs 3.47A and B: Apron like incision of Freund
(B) Shobinger’s incision

A B C

Figs 3.46A to C: Apron like incision of Freund and Latyshevsky


70 Principles of Surgery

16. Blair VP, Ivy RH. Brown JBs Essentials 31. Zide BM, McCarthy JG. The medial
References
of Oral Surgery, 2nd edition. St Louis: cant­hus revised. An anatomical
1. Edward Ellis III, Zide MF. Surgical CV Mosby; 1937. basis for can­tho­pexy. Ann Plast Surg.
approaches to the facial skeleton. 17. Thoma KH. Tumors of the condyle and 1983;11:1-9.
Dallas, Texas. temporomandibular joint. Oral Surg. 32. Pospisil et al. Review of the lower
2. Ward TG. The split bone technique for 1954;7:1091. blepharoplasty incision as a surgical
removal of lower third molars. Br Dent 18. Al-Kayat A, Bramley P. A modified approach to zygomatic-orbital frac­
J. 1956;101:297-304. preauricular approach to the tempo­ tures. Br J Oral Maxillofac Surg. 1984;
3. Luebke RG. Surgical endodontics. Dent romandibular joint and malar arch. Br 22:261-8.
Clin North Am. 1974;18:379-91. J Oral Maxillofac Surg. 1979;17:91. 33. Blair VP. Surgery and Diseases of the
4. Ginwalla MSN. Surgical treatment of 19. Posnick JC, Goldstein J, Clokie C. Mouth and Jaws, 3rd edition, St Louis;
tri­ge­minal neuralgia of the third divi­ Advantages of the postauricular coro­ CV Mosby; 1920.pp.492-523.
sion. Oral Surg Oral Med Oral Pahol. nal incision. Ann Plast Surg. 1992; 34. Gutierrez-Perez JL. Parotid sialolithiasis
1961;14:1300-04. 29:114. in Stensen’s duct. Med Oral Patol Oral
5. Munro IR, Fearon JA. The coronal 20. Alexander RW, James RB, Postauri­cular Cir Bucal. 2006;11(1):E80-4.
incision revisited. Plast Reconstr Surg. approach for surgery of the temporo­ 35. Alfred W Adson, William O Ott. Preser­
1994;93:185. mandibular articulation. J Oral Surg. vation of the facial nerve in the radical
6. Shepherd DE, Ward-Booth RP, Moos 1975;33:346. treatment of parotid tumors. Arch
KF. The morbidity of bicoronal flaps 21. Davidson AS. Endaural condylectomy. Surg. 1923;6(3):739-46.
in maxillofacial surgery. Br J Oral Br J Plast Surg. 1956;8:64-7. 36. Samengo LA. Consideraciones sobre
Maxillofac Surg. 1985;23:1-8. 22. Hinds EC. Correction of prognathism la cirugia conserva dora de la glan­
7. Ellis E, Zide MF. Transfacial approa­ by subcondylar osteotomy. J Oral dula parotida. Pren Med Argent 1961;
ches to the mandible. In: Ellis E, Zide Maxillofac Surg. 1958;16:209. 48:1586.
MF III (Eds). Surgical Approaches 23. Zide BM, Jelks Gw. Surgical Anatomy of 37. Appiani E, Delfino MC. Plastic incisions
to the Facial Skeleton, 2nd edition. the Orbit. New York, Raven Press, 1985. for facial and neck tumors. Ann Plast
Philadelphia: Lippincott Williams and 24. Werther JR. Cutaneous approaches to Surg. 1984;13(4):335-52.
Wilkins; 2005. Section 5. pp.151-89. the lower lid and orbit. J Oral Maxillofac 38. Ferreira JL, Maurino N, Michael E, et al.
8. Risdon F. Ankylosis of the tempo­ Surg. 1998;56:60. Surgery of the parotid region. J Oral
romandi­bular joint. J Am Dent Assoc. 25. Converse JM, Smith B, Wood-Smith D. Maxillofac Surgery. 1990;48:803-7.
1934; 21:1933. Orbital and naso-orbital fractures. In: 39. Crile GW. Excision of cancer of the
9. Dingman RO, Grabb WC. Surgical Converse John Marquis (Ed). Recon­ head and neck. JAMA. 1906;47:1780-
anatomy of the mandibular ramus of structive Plastic Surgery 2nd edition, 86.
the facial nerve based on the dissection 1972. 40. Martin H, del Valle B, Ehrlich J, et al.
of 100 facial halves. Plast Reconstr Surg 26. Bagain ZH, Malkawi Z, Hadidi A, Neck dissection. Cancer 1951;4:441-99.
Transplant Bull. 1962;29:266-72. et al. Subtarsal approach for orbital 41. MacFee WF. Transverse incisions for
10. Hind EC. Correction of prognathism floor repair. J Oral Maxillofac Surg. neck dissection. Annals of Surgery.
by subcondylar osteotomy. J Oral Surg 2008;66:45-50. 1960;151:279-84.
(Chic). 1958;16(3):209-14. 27. Wray RC, Holtmann B, Ribaudo JM, 42. Schobinger R. The use of a long anterior
11. Hinds EC, Girotti WJ. Vertical sub­ et al. A comparison of conjunctival skin flap in radical neck resection. Ann
condylar osteotomy: a reappraisal. and subciliary incisions for orbital Surg. 1957;146:221.
Oral Surg Oral Med Oral Pathol. 1967; fractures. Br J Plast Surg. 1977;30:142. 43. Latyshevsky A, Freund HR. Long upper
24(2):164-70. 28. Patel PC, Sobota BT, Patel NM, et al. flap skin incision for radical neck
12. Maran AGD, Gaze M, Wilson JA. Stell Comparison of transconjunctival ver­ dissection. Surgery. 1960;47:206-9.
and Maran’s Head and Neck Surgery. sus subciliary approaches for orbital 44. Freund HR. Principles of Head and
Oxford: Butterworth-Heinemann; 1994. fractures: A review of 60 cases. J Cra­ Neck Surgery, 2nd edition. New York:
pp.176-92. niomaxillofac Trauma. 1998;4:17. Appleton Century Croft.1979.
13. Dieffenbach JF. Die Operative Chir­urgie, 29. Bourguet J. Notre traitement chirurgical 45. Babcock WW, Conley J. Neck incision
Vol I. FA Brockhaus, Leipzig. 1845. de poches sous les yeux sans cicatrice. in block dissection. Arch Otolaryngol.
14. Bennett JE, Lynch JB, Lewis SR, Blocker Arch Fr Bell; Chir. 1928;31:133. 1966;84:554-7.
TG Jr. The operative treatment of cancer 30. Suga H, Sugawara Y, Uda H, et al. The 46. Lasaridis N, Dalabiras S , Karakassis D.
of the lip. Am Surgeon. 1962;28: 537. transconjunctival approach for orbital Modification of the Conley incision for
15. Rowe WC. Surgery of temporomandibu­ bony surgery: In which cases should it neck dissection. J Oral Maxillofac Surg.
lar joint. Proc R Soc Med. 1972;65:383. be used? J Craniofac Surg. 2004;15:454. 1994;52:1046-9.
4 Fluid, Electrolyte Balance
and Acid-base Equilibrium
Borle Rajiv M, Agrawal Poonam

um and plasma proteins. Sodium is the


Introduction Acid-Base balance
primary determinant of osmolality and
About a billion years ago, life began tonicity. It distributes predominantly The pH of body fluids is maintained
in the sea. The sea possessed unique in the extracellular fluid compartment within a narrow range despite the ability
properties for the maintenance of life. with nearly equal concentrations in of the kidneys to generate large amounts
The water that surrounds the cells of the interstitial fluid and plasma. Intra­ of bicarbonate and the normal large
verte­brates and of humans, i.e. the cellular fluid contains only trace amo­ acid load produced as byproducts of
extracellular water has an electrolyte unts of sodium. This is maintained by metabolism.
composition similar to what the sea an active sodium pump in the cells. Compensation for acid-base deran­
had in prerecorded times, inspite of all Any change in sodium concentration in ge­­ments is either respiratory (for meta­
the countless changes in evolution that any of the fluid compartments causes a bolic derangements) or metabolic (for
have occurred.1 compensatory shift in free water. respiratory derangements). Normal acid-
The total body water (TBW) is usually The normal adult takes in 2 to 3 liters base homeo­ stasis prevents metabolic
divided into two main compartments: of water per day in various forms. When acidosis and alkalosis. Under normal cir­
1. The extracellular compartment (ECC) normal oral intake (enteral) is impossible cumstances blood PCO2 is tightly main­
and or impractical, intravenous fluid replace­ tained by alveolar ventilation, con­trolled
2. The intracellular compartment (ICC). ment (parenteral) is indicated. Among by the respiratory centers in the pons and
The average water content of men is the electrolytes, sodium and pota­ssium medulla oblongata. If it gets disturbed it
approximately 60 percent of total body are the electrolytes of main concern will result in respiratory acidosis or alka­
weight and of women is 50 percent of and their disturbances will lead to losis.3,4
total body weight, as the men have more varied clinical signs and symptoms. A A safe and effective parenteral nut­
muscle mass, which has higher water wide variety of intravenous fluids are rition became feasible in the 1960s as
content, while females have more fat and available for the replacement of fluid a consequence of the development of
less water content. The total body water loss and electrolytes. It can be delivered inert materials for intravascular feeding
(TBW) is about 80 percent of total body by crystalloid or colloid solutions. catheter, together with pharmaceutical
weight in new­born, which is gradually Colloid solutions have the advantage of advances in the formulation of feeding
lost. The young indi­viduals have TBW expanding intravascular vol­ ume with solutions. It is the intravenous provision
of about 70 per­cent which is gradually minimum fluid loss. of all nutritional requirements without
reduced at old age to 60 percent due to The adequacy of fluid and electrolyte the use of the gastrointestinal tract (GIT).
loss of lean muscle mass due to muscle replacement must be monitored. key The primary indication of total parenteral
wasting.2,3 para­meters are weight loss or gain, urine nutrition is for those patients whose gut is
The water is freely diffusible from output and electrolyte analysis. Peri­ not functioning to allow for the delivery
one compartment to ano­ther, but ele­ operative fluid management is of utmost of enteral nutrition such as patients with
ctrolytes do not as they req­uire an acti­ve importance in maintaining home­ostasis severe inflammatory bowel disease,
mechanism. This is of utmost importance in the sur­ gical patient. Perioperative entero­cutaneous fistulae, pancreatitis or
in deciding, which intravenous fluids be hydration improves the recovery process short bowel syndrome. Peri­pheral par­
used during surgery. The volumes of fluid and results in fewer postoperative com­ enteral nutrition is admi­nistered through
compartments depend highly on sodi­ plications.2-4 a peripheral intra­ venous line with an
72 Principles of Surgery

osmolarity below 900 milliosmoles/L, for about two-thirds (80%) of TBW and solutes in intracellular (IC) water. The
to prevent venous phlebitis. Nutritional 40 percent of total body weight. Extra­ principal EC electrolytes are cationic
support plays an integral role in the cellular water (20% of total body weight) sodium and anionic chloride. Total body
healing and recovery of the trauma can further be divided into interstitial sodium includes 30 percent in structural
patient. It has been shown clearly that (three-fourths of extracellular or about tissue like bone.
the enteral route of feeding is preferable 15% of total body weight) and intravas­ The principal electrolytes in the IC
if possible to maintain gut mucosal cular (one-fourth of extracellular, or 5% compartment are cationic potassium
integrity, enhance immunocompetence of total body weight). Water movement and organic phosphates (Table 4.2). The
and decrease the incidence of septic between the spaces is regulated by ionic three electrolytes sodium, potassium
complications.5 and colloid osmotic pressure gradients and chloride are tightly regulated by re­
across semipermeable membranes. The nal function. A major mechanism of ele­
In Homeostasis normal adult takes in 2 to 3 liters of wa­ ctrolyte control is regulation of glo­mer­
Water is the most important constituent ter per day in various forms. The body ular filtration rate (GFR). The tubular
of the body present in all the tissues easily adjusts to the variations, primarily cells reabsorb more than 95 percent of
(Table 4.1). It accounts for about 55 per­ through renal regulation, conservation the water and electrolytes filtered and
cent of our weight (range 45%–60%, up or excretion. About 200 mL water is gen­ are subjected to paracrine and hormonal
to 75% in newborns). erated as metabolic end product. influences. Control over the electrolyte
Water is distributed between intra­ Fluid loss has been categorized as com­position of EC compartment is affe­
cellular and extracellular compartments sensible and insensible. The sensible loss cted through selec­ tive reabsorption of
(Box 4.1). Intracellular water accounts includes urine, blood loss, gastroin­testinal ele­ctrolytes from plasma filtrate generated
suction and massive diarrhea. Insensible at the glom­erulus.1-3,6
water is lost through vapori­zation (lungs
Table 4.1: Fluid distribution in various and skin) and ranges between 500 and
compartments 1,000 mL per day, depending on the factors
Regulation of Osmolality
like environmental conditions, presence Sodium in EC compartment and pota­s­
For a 70 kg man
of fever, etc. This is through the lungs sium in IC compartment largely deter­
Plasma 3,500 cc (200–400 mL) and skin (300–600 mL). mine osmolality and the adjust­ ments
Interstitial fluid 10,500 cc Nor­­mal sensible loss is through the urine
in the active transport of these solutes
Intracellular fluid 28,000 cc (800–1,500) and stool (150–250 mL). Theseacross the cell membrane influence
losses depend directly on water intake and
the regulation of body fluid osmolality.
diet consistency. The goal of fluid therapy
However, fluctu­ations in the volume of
is to balance intake with loss, creating TBW principally influence tonicity.
Box 4.1: Percentage wise fluid distribution neither deprivation nor extreme excess.1-3,6 The principal mechanisms for con­
in various compartments
trol of tonicity are regulation of anti­
Total extracellular diuretic hormone released into the
Composition of Solutes in
Volume—20% of body weight blood by the hypothalamus. Osmolality
Plasma—5% of body weight
Extracellular and Intracellular of body water is tightly maintained in
Interstitial fluid—15% of body weight Water the range of 285 to 295 mOsm per liter
Total intracellular The composition of solutes in extra­ despite wide variations in salt and water
Volume—40% of body weight
cellular (EC) water differs from that of intakes.1-3,6

Table 4.2: Ionic concentration of different fluid compartments

Plasma (mEq/L) Interstitial fluid (mEq/L) Intracellular (mEq/L)


Cations (154) Anions (154) Cations (153) Anions (153) Cations (200) Anions (200)
Na 142
+
Cl 103

Na 144
+
Cl 114

K+ 150 SO4––  
150
K+ 4 HCO3– 27 K+ 4 HCO3– 30 Mg++ 40 HPO4–––
Ca++ 5 SO4–– Ca++ 3 SO4–– Na+ 10 HCO3– 10
3 3
Mg 3
++
PO4 –––
Mg 2
++
PO4 –––
Proteins 40
Organic acids 5 Organic acids 5
Proteins 16 Proteins 1
Fluid, Electrolyte Balance and Acid-base Equilibrium 73

Colloid Osmotic Pressure Disturbances of as longitudinal tongue furrows, dry mu­


Colloid is a term used to collectively • Volume, cous membrane, dry axillae and sunken
describe the large molecular weight • Concentration, and eyes.6,11-13
(nomi­nally MW > 30,000) particles pre­ • Composition.3,7-9
sent in a solution. In normal plasma, the Treatment
plasma proteins are the major colloids Disorders of Fluid Volume • Estimate magnitude of hypovolemia.
present. As the colloids are solutes they • Determine rate of correction of hy­
Hypovolemia
contribute to the total osmotic pressure po­­
volemia without increasing the
of the solution. This component due The term ‘hypovolemia’ refers to decre­ pre­load on the heart.
to the colloids is typically quite a small ased intravascular volume and not dec­ • Determine appropriate type of fluid to
percentage of the total osmotic pressure. reased EC volume and this disorder be used.
It is referred to as colloid osmotic res­ults from insufficient function of the The replacement fluid should predo­
pressure (or sometimes as the oncotic normal mechanisms of intravascular minantly fill and remain in intravascular
pressure). volume maintenance. space because hypovolemia is depletion
Oncotic pressure or colloid osmotic of the volume of the intravascular space.
Pathophysiology
pressure is a form of osmotic pressure Replacement fluids given intravenously
exerted by proteins in blood plasma Decreased effective intravascular vol­ume consist of crystalloid solution, made of
that usually tends to pull water into the
can occur in the presence of decreased, water and small solutes and crystalloid
circulatory system from the EC compart­ normal or increased EC volume. Decr­ solutions, consisting of water, electro­
ment. eased EC volume leads to depletion of lytes and higher-molecular-weight pro­
Throughout the body, dissolved co­intravascular volume, which is most teins or polymers.1,3,7,8,14,15
m­­­
pounds have an osmotic pressure. common and can arise from increased
Because large plasma proteins cannot loss of EC fluid, failure to replete normal Fluid Excess/Hypervolemia
easily cross through the capillary walls,
losses or a combination of both. Bleeding, The term ‘hypervolemia’ denotes incre­
their effect on the osmotic pressure of diarrhea, vomiting and excessive skin ased EC volume with or without incre­ased
the capillary interiors will, to some ex­
loss of fluid (swea­ting, burns) can quickly intravascular volume. Hypervolemia is an
tent, balance out the tendency for fluiddeplete EC and intravascular volumes.10 increase of EC volume with peri­pheral
to leak out of the capillaries. In otherHypo­ volemia with normal EC volume edema, ascitis or other fluid col­lection.
words, the oncotic pressure tends to pull
occ­urs as a result of any disorder that The intravascular volume may be low,
fluid into the capillaries. In conditions
alters the balance between intravascular normal or high.
where plasma proteins are reduced, e.g. and extra­ vascular fluid compartments. • Hypervolemia with decreased in­
from being lost in the urine (proteinuria)
Sepsis (peritonitis, septicemia), acute travascular volume: Sodium along
or from malnutrition, the result of low res­­pi­ratory distress syndrome (ARDS), with anions is the predominant
oncotic pressure can be excess fluid sho­ ck and other critical illnesses alter solute in the EC space; increased
buildup in the tissues (edema). Plas­ this balance by increasing permeability EC volume indicates an abnormally
ma colloid osmotic pressure (COP) is an of vasculature. The result is an increase increased quantity of sodium and
important determinant in the appear­ancein the nonintravascular fluid volume water. Excessive sodium retention
of edema especially pulmon­ary edema. (inter­ stitial compartment, pleural effu­ or hypervolemia may occur ap­
The normal human plasma COP av­er­sions, ascites) at the acute expense of the propriately in states of inadequate
ages 25.4 mm Hg. The COP is 15 percent intra­vascular volume. effective circulation, such as heart
less in patients on bed rest than in the am­ Volume depletion causing inade­ failure or suboptimal filling of vas­
bul­atory patients (increase in am­bulatory
quate systemic perfusion can lead to alt­ cular space resulting from loss of
patients is secondary to re­ duction in
e­red mental status, confusion, lethargy fluids in other compartments, as oc­
plasma volume associated with exercise).and coma; cold skin and extre­mities from curs with hypoalbuminemia, portal
There is gradual, but progressive and sig­
vaso­con­striction; cardiac ischemia and hypertension or increased vascular
ni­ficant decrease in COP with age. COP is
dysfun­ction; liver and kidney failure. Re­ permeability to solute and water.
also less in females as compared to males.
duced skin turgor has been claimed to The evidence of inadequate circula­
be the most characteristic finding in the tion may be found, including tachy­
Fluid and Electrolyte physical examination of dehydrated pa­ cardia, peripheral cyanosis and
tient.10 Cellular dehydration, interstitial altered mental status. If EC volume
Imbalance space dehydration and poor perfusion are is high, rales and wheezes consis­
The disorders in fluid balance are cla­ presumably responsible for many of the tent with pulmonary edema may be
ssified into three general categories: other classic signs of hypovolemia such present.
74 Principles of Surgery

Patients with hypervolemia due signify that the intravascular volume • Treatment with 5% dextrose in water
to endocrine disorders or renal fail­ is increased. and/or enteral water will reduce hy­
ure may have findings specific to   Hypervolemic hypernatremia (i.e. perosmolality.
under­­lying cause. hy­per­tonic sodium gain) results from • Loop diuretics like furosemide can be
an increase in total body sodium and used to induce natriuresis and cou­n­
Diagnosis water, where the net increase in total teract volume expansion so long as
It is diagnosed as follows: body sodium is greater than that of kidney function is preserved.
• Edema, ascites or any other evid­ water (i.e. sodium gain > water gain) • Patients with severe renal insuffi­ci­
ence of increased EC volume. and is associated with intravascular ency and volume overload may req­
• Intravascular volume may be judged and extracellular fluid volume uire hemodialysis.
to be normal, low (hypovolemia) or expan­sion. There is increase in total • Hypervolemia with increased in­
high. exchangeable Na+ and K+ in excess t­r­a­vascular volume: In these pa­
• Potential causes of increased EC of the increment in total body water tients, severely increased intravas­
volume such as renal insufficiency, (TBW), resulting in a relative free cular volume will be manifested by
congestive heart failure, liver disease water deficit. pulmonary edema, hypoxemia and
or some other mechanism of sodium   The causes for hypervolemia with respiratory distress. If intravenous
retention, or excessive sodium ad­ primary increased sodium retention fluids are being administered, these
mi­­ni­stration, may be present. (hypernatremia) are: should be discontinued unless bl­
Treatment: The need for treatment • Excessive intravenous sodium admi­ ood transfusions are necessary for
and the treatment approach depends ni­stration severe anemia. Intravenous furose­
on the mechanism of hypervolemia. – Hypertonic saline administr­ at­ mide (Lasix, 10–80 mg) is given, with
Hypervolemia associated with sever­ ion (3% saline) repeated doses every 30 minutes
ely decreased or markedly increased – Increased sodium bicarbonate dep­ending on the diuretic respo­nse.
intravascular volume requires rapid admi­nistration during manage­ Supportive care includes oxygen,
and aggressive treatment. ment of lactic acidosis changes in the patient’s position and
• Hypervolemia with primary incre­ – Replacing hypotonic insensible mechanical ventilation if necessary.
ased sodium retention: The other loss with 0.9% saline The patient need to be monitored
major mechanism of hypervolemia • Mineralocorticoid excess critically for the detection of conges­
is primary excessive function of the – Hyperaldosteronism tive cardiac failure due to increased
normal mechanisms that ensure so­ – Congenital adrenal hyperplasia. preload and also signs of pulmonary
dium and water balance. Normal EC • Excessive salt intake: drinking sea edema, which require appropriate
volume is maintained by a com­plex water. interventions like oxygen therapy
interactive system that includes renin, • Chronic orthostatic hypotension and monitoring of electrolytes espe­
angiotensin, aldosterone, glomerular   The clinical features of hypern­ cially when potassium wasting di­
filteration, renal tubular handling of atremia resulting from CNS dys­fun­ uretics (loop diuretics) are prescribed
sodium and water, atrial natriuretic ction due to brain cell shrinkage are in high doses for the longer duration.
factor and anti­diuretic hormone along • Confusion • Increased extracellular volume
with the intake of sodium and water • Neuromuscular excitability without change in intravascular
in the diet. Hyperfunction of some of • Hyper-reflexia volume (Table 4.3): These are usu­
these mechanisms, such as hyper­ • Seizures ally chr­onic conditions. Edema and
aldosteronism or excessive intake of • Coma ascites do not by themselves cause
sodium or dysfunction of others, such • Cerebro-vascular damage with sub- imm­ ediate problems, but edema
as renal dysfunction or decreased cortical or subarachnoid hemorrhage may impair skin care and lead to im­
glomerular filteration, cause net posi­ • Venous thrombosis mobility, while ascites may become
tive sodium balance with inevitable • Urine sodium is typically greater uncomfortable, may cause respira­
expansion of the EC volume. Edema than 20 mEq/L and urine osmolarity tory distress and hypoxemia and may
is often a major feature of increased is greater than 300 mOsm/L. become infected (spontaneous bac­
EC volume. Edema always indicates Treatment of these patients should terial peritonitis).3,7-9
increased EC volume except when be targeted at both the correction of
there is localized mechanism of fluid the hypernatremia and the attain­ Electrolyte Imbalance
transudation or exudation, e.g. local ment of a negative H2O balance.
venous insufficiency, cellulites, lym­ • Discontinue any sodium sources or Hyponatremia
phatic obstruction or trauma. The offending agents, then induce natri­ Hyponatremia denotes decrease in
presence of edema may or may not uresis to remove excess sodium. so­di­um ion concentration.
Fluid, Electrolyte Balance and Acid-base Equilibrium 75

Table 4.3: Extracellular fluid volume imbalance

Deficit Excess
Type of sign
Moderate Severe Moderate Severe

Central nervous Sleepiness, apathy, Decreased tendon None None


system slow responses, anorexia, reflexes.
cessation of visual activity Anesthesia distal
extremities, stupor, coma.

Gastrointestinal Progressive Nausea, vomiting, refusal At surgery : Edema of stomach,


decrease in to eat, silent ileus colon, lesser and greater omenta
food consumption and distension and small bowel mesentery
Cardiovascular Orthostatic hypotension, Cutaneous lividity, Elevated venous pressure,
tachycardia, collapsed veins, hypotension, distant distension of peripheral veins,
collapsing pulse heart sounds, cold increased cardiac output, loud
extremities, absent heart sounds, functional murmur
peripheral pulses Bounding pulse, high pulse
pressure, increased pulmonary,
2d sound, gallop
Tissue Soft, small tongue with Atonic muscles, sunken Subcutaneous pitting edema, Anasarca, moist rales,
longitudinal wrinkling, eyes basilar rales vomiting, diarrhea
decreased skin turgor
Metabolic Mild decrease temperature Marked decrease None None
97°F–99°F (per rectal). temperature, 95°F–98°F
(per rectal)

Essentials of diagnosis is seen in congestive heart failure, ne­ or hyperpro­ teinemia (> 10 g/dL)
Sodium less than 135 mEq/L. p­hrotic syndrome, cirrhosis, pro­tein- when serum sodium was measured
• Altered mental status or new onset losing enteropathy and preg­ nancy. by flame photometry. This is no lon­
of seizure disorder. These disorders have in com­ mon ger a problem with the use of ion-
• Most cases discovered by review of edema, ascites, pulmonary e­de­ ­ma or spe­cific sodium electrodes.
routinely obtained serum electro­ other evidence of increased EC vol­ 5. Hyponatremia with hyperglycemia
lytes. ume. However, these patients app­ ­ (Hypertonic hyponatremia): Hyp­
1. Hyponatremia with decreased ext­ ear to have inability to maintain nor­ er­­g­lycemia with hyponatremia is ass­
racellular volume: Decreased EC mal effective intravascular vol­ ume o­ciated with decreased TBW rather
volume leads to vigorous water con­ because of forces generating exc­essive than with increased TBW relative
servation, primarily mediated by venous and extravascular volume. to total solute. Hyponatremia in
inc­reased ADH release stimulated Hypo­ natremia is a conse­ quence of the presence of hyperglycemia can
by atrial receptors and increased ADH release in response to decreased be addressed in several ways. First,
thirst leading to increased water in­ intravascular volume, even though laboratory measurement of ser­ um
take. Hyponatremia is facilitated in total EC volume is increased and total osmolality will give a correct ass­
adrenal insufficiency because lack body water is high. essment of water balance; serum
of cortisol causes collecting ducts 3. Hyponatremia with normal extra­ osmolality will be higher than estim­
to be excessively permeable to wa­ cellular volume: Hyponatremia in ated from serum sodium. Another
ter movement, leading to impaired association with normal EC volume way is to correct the serum sodium
maximum water excretion. Further­ is seen with psychogenic water ing­ for the degree of hyperglycemia.One
more, ADH levels in adrenal insuffi­ es­tion, decreased solute intake, and empiric correction is to add to the
ciency may remain elevated despite most commonly, the syndrome of measured serum sodium 1 mEq/L
hyponatremia, suggesting that there inappro­ priate secretion of ADH for every 60 mg/dl the ser­um glu­
is an abnormal ADH response to de­ (SIADH). cose is increased above 100 mg/dL.
creased serum osmolality. 4. Hyponatremia without hypotoni­ Hy­ po­natremia associated with de­
2. Hyponatremia with increased ex­tr­ city: Hyponatremia without hypo­ c­reased osmolality is often asy­­­m­p­t­
a­cellular volume: Hyponatremia in tonicity was commonly seen in pati­ omatic until serum sodium falls below
the presence of increased EC volume ents with severe hyper­trigly­ceridemia 125 mEq/L, but the rate of cha­nge is
76 Principles of Surgery

clearly important. Sev­ere sy­m­ptoms- b. Serum osmolality greater than of inorganic ions; this restores cell
including altered men­tal status, sei­ 300 mOsm/kg. volume to near-normal, but at the
zures, nausea, vo­mi­­ting, stupor and c. Evidence of increased solute admi­ expense of dis­ru­pted cellular function.
coma occur when ser­ um sod­ ium nistration. With persi­ stence of hypertonicity,
is less than 115 mEq/L when hy­po­ d. Polyuria with dilute urine (diabetes brain cells generate and take up
natremia develops acut­ely or when it insipidus). idiogenic osmoles, sometimes called
is less than 105 to 110 mEq/L during e. Inadequate water intake. ‘organic osmolytes’. As cell volume is
chronic hypo­natr­emia. f. Altered mental status. determined from the amount of solute
contained within the cell, organic
Laboratory findings Clinical features osmolytes resist the movement of
Serum electrolytes, glucose, creatinine Hypernatremia and hyperosmolality water out of the cells and maintain
and urea nitrogen, serum osmolality, should be suspected in patients with brain volume close to normal.
urine osmolality, urine Na+, and urine dec­re­
ased access to water, especially Many of the organic osmolytes are
cre­atinine (to calculate fractional exc­ with altered mental status or those taken up from the EC space by the
retion of Na+) should be measured. with a history of polyuria. The elderly for­mation of specific membrane
Low serum osmolality 280 mOsm/kg patients living in a chronic care facility cha­ nnels. These channels do not
confirms hyponatremia due to increased are especially susceptible. However, qui­ckly disappear or reverse funct­
water relative to solute. many patients are identified through ion when hypernatremia is correc­
An association has been found bet­ routine electrolyte determinations. The ted. Therefore, rapid restoration of
ween hyponatremia with hypo­kalemia severity of water deficit is estimated water to the body may theoretically
and severe body potassium depletion. from the serum electrolytes and body cause overexpansion of these cells,
Hypokalemia may also predispose pati­ weight. resulting in cerebral edema. The
ents with hyponatremia to osmotic following formula is very helpful in
demyelination syndromes and ence­ Signs and symptoms calculating the anticipated changes
pha­lopathy. As with hyponatremia, hypernatremia and in serum [Na+] in the hypernatremic
hypertonicity affect primarily the brain. patient given intravenous fluids. The
Treatment Acute decrease in the size of brain cells rate of correction of serum [Na+] can
Severity of hyponatremia ([Na+]< can lead to altered mental status, impaired be estimated. This formula estimates
120 mEq/L), acuteness of onset and the thinking and loss of consciousness is an the amount of change in serum [Na+]
pre­sence of neurologic symptoms (con­ association of cerebral hemorrhage and when 1 L of any fluid is administered:
fusion, stupor, coma or seizures) deter­ hypertonicity and hypernatremia, thought Serum Na+ = Fluid [Na+]
mine how quickly treatment should be to be due to tearing of blood vessels due to Serum[Na+] /TBW+ 1
instituted. brain shrinkage. This formula demonstrates how
Of the underlying problems lead­ little the serum [Na+] changes when
ing to hyponatremia, the most straight Treatment normal saline ([Na+]= 154 meq/L) is
forward and easily corrected is hypo­ 1. Calculation of water deficit: All given to a hypernatremic patient.3, 7-9
volemia. Administration of normal sa­ patients with hypernatremia have
line repletes the intravascular volume increased serum osmolality and the Potassium Abnormalities
and inhibits ADH release by reducing amount of water needed to correct The normal dietary intake of potassium
the hypovolemic stimulus. Water excre­ this state can be calculated from the is approximately 50 to 100 mEq daily
tion is enhanced by the increased GFR, following equation: and in the absence of hypokalemia, the
and urine should become quickly and TBW(L) = Normal TBW(L) × (140/ majority of this is excreted in the urine.
near maximally dilute, facilitating water [Na+]). Ninety-eight percent of the potassium
excretion. 2. Rate of correction of hyperna­ tr­ in the body is located within the IC
Hypokalemia should be corrected, emia: Just as with hyponatremia, too compartment at a concentration of
as this has been associated with com­ rapid correction of hypern­ atremia approximately 150 mEq/L and it is the
plications of hyponatremia and its treat­ may be harmful. Cerebral edema major cation of IC water. Although the
ment. with neurologic complications may total EC potassium in a 70 kg male would
occur during correction as a result amount approximately to only 63 mEq
Hypernatremia of a compensatory mechanism inte­ (4.5 mEq/L × 14 L), this small amount
nded to maintain normal brain is critical to cardiac and neuromuscular
Essentials of diagnosis
cell volume. In response to deve­ l­ function. In addition, the turnover rate
a. Serum sodium greater than opment of hypertonicity, brain cells in the EC fluid compartment, may be
145 mEq/L. fairly rapidly increase the amount extremely rapid.
Fluid, Electrolyte Balance and Acid-base Equilibrium 77

Hyperkalemia should be added to a liter of intravenous Hypercalcemia


The signs of a significant hyperkale­mia fluid and the rate of administration sho­ The symptoms of hypercalcemia are
are limited to the cardiovascular and gas­ uld not exceed 40 mEq/h unless the ECG va­ gue and of gastrointestinal, renal,
trointestinal systems. The gastrointesti­ is being monitored. In the absence of mus­ cu­
loskeletal and central nervous
nal symptoms include nausea, vomiting, specific indications, potassium should system origin. The early manifestations
intermittent intestinal colic and diarrhea. not be given to the oliguric patient or to of hyp­er­calcemia include easy fatigue,
The cardiovascular signs are apparent on patients during the first 24 hours after las­s­­itude, weakness of varying degree,
the electrocardiogram (ECG) initially, severe surgical stress or trauma.3, 7-9 ano­rexia, nausea, vomiting and weight
with high, peaked T waves, widened QRS loss. With higher serum calcium levels,
complex and depressed ST segments. Calcium Abnormalities lassi­tude gives way to somnambulism,
Disappearance of T waves, heart block The majority of the 1,000 to 1,200 g stupor, and finally, coma. Other sym­
and diastolic cardiac arrest may devel­ of body calcium in the average-sized ptoms include severe headaches, pain
op with increasing levels of potassium. adult is found in the bone in the form of in the back and extremities, thirst, poly­
Treatment of hyperkalemia consists of phosphate and carbonate. Normal daily dipsia and polyuria. The critical level for
immediate measures to reduce the se­ intake of calcium is 1 to 3 g. Most of this serum calcium is 15 mg/dL or higher and
rum potassium level, withholding of ex­ is excreted via the GIT and 200 mg or less un­less treatment is instituted promptly,
ogenous potassium and correction of the is excreted in the urine daily. The normal the sym­ptoms may rapidly progress to
underlying cause if possible. Temporary serum level is 8.5 to 10.5 mg/dL, about death. The two major causes of hyper­
suppression of the myocardial effects of a half of which is non-ionized and bound calcemia are hyperparathyroidism and
sudden rapid rise of potassium level can to plasma protein. An additional non- cancer with bony metastasis.
be accomplished by the intravenous ad­ ionized fraction (5%) is bound to other A serum calcium concentration of
ministration of 1 g of 10 percent calcium substances in the plasma and interstitial 15 mg/dL or higher requires emergency
gluconate under ECG monitoring. Serum fluid and the remaining 45 per­cent is the treatment. Oral or intravenous inorganic
potassium levels may be transiently de­ ionized portion that is responsible for phosphates effectively lower serum cal­
creased by administration of bicarbon­ neuromuscular stability. Determination cium by inhibiting bone resorption and
ate and glucose with insulin (45 mEq of the plasma protein level, therefore, is forming calcium-phosphate com­ plexes
NaHCO3 in 1,000 ml/D10% with 20 units essential for proper analysis of the serum that are deposited in soft tissues and
regular insulin), which promote cellular calcium level. bone. If intravenous phosphorus is used,
uptake of potassium. However, the defin­ it should be given slowly over a period
itive treatment of hyperkalemia requires Hypocalcemia of approximately 12 hours, once daily
the enteral administration of cation ex­ The symptoms of hypocalcemia, which for no more than 2 or 3 days. Inorganic
change resins (Kayexalate) or dialysis. may be seen when serum levels are phosphates are contraindicated in pati­
below 8 mg/dL, include numbness and ents with hyper­­phosphatemia or renal
Hypokalemia tingling of the circumoral region and failure. Intravenous sodium sulfate also
The more common problem in the sur­ the tips of the fingers and toes. The signs lowers serum calcium by increasing uri­
gical patient is hypokalemia, which may are of neuromuscular origin and include nary excretion of calcium. It is less effe­
occur as a result of: hyperactive tendon reflexes, positive c­tive than phosphate salts, however and
• Excessive renal excretion. Chv­ostek’s sign, muscle and abdominal probably is no more effective than nor­
• Movement of potassium into cells. cramps, tetany with carpopedal spasm, mal saline.3, 7-9
• Prolonged administration of potas­ convulsions (with severe deficit) and pro­
sium-free parenteral fluids with con­ longation of the Q-T interval on the ECG.
Acid-Base Homeostasis
tinued obligatory renal loss of pota­ The common causes include acute pan­
ssium (20 mEq/day or more). creatitis, mas­ sive soft-tissue infections
and Disorders1,3,7,8
• Total parenteral hyperalimentation (necrotizing fasciitis), acute and chronic
with inadequate potassium replace­ renal failure, pancreatic and small-bowel Pathophysiology
ment. fistulas. The treatment is directed toward Arterial pH is largely determined by the
• Loss in gastrointestinal secretions correction of the underlying cause and relative concentrations of bicarbonate
(persistent vomiting, diarrhea). repletion of the deficit. Acute symptoms HCO3 and carbon dioxide (CO2) in the
Hypokalemia is best dealt by pre­ may be relieved, by the intravenous blood. The former is controlled prin­
ven­tion. In the replacement of gastro­ administration of calcium gluconate or cipally by renal conservation or excre­
intestinal fluids, it is safe to replace the calcium chloride. Calcium lactate may tion of bicarbonate and hydrogen ion,
upper limits of loss, because an excess is be given orally, with or without supple­ the latter largely by pulmonary ven­til­
readily handled by the patient with normal mental vitamin D, in the patient requir­ ation. Decreased arterial pH is called
renal function. Not more than 40 mEq ing prolonged replacement. ‘acidemia’ and increased arterial pH
78 Principles of Surgery

alka­lemia’. The disturbances respon­si­ of hydrogen ion, e.g. is countered by It results from an increased intake of
ble for these changes are acidosis and corresponding opposite effects of the acids, an increased generation of acids or
alkalosis, respectively and these chan­ buffer components. This minimizes pH an increased loss of HCO3. The body resp­
ges are described as ‘metabolic’ (not change at the expense of consumption of onds by producing buffers, increasing
due to an increase or decrease in CO2) some of the buffer components, limiting ventilation (Kussmaul respirations),
or ‘respiratory’ (due to primary increase the maximum buffering capacity. For the incr­e­a­sing renal reabsorption and
or decrease in CO2). HCO3-CO2 system, however, physiologic generation of bicarbonate. The kidney
mechanisms greatly increase the buffer will also increase secretion of hydrogen
Acid-base Buffering Systems capacity. For example, metabolic acid­ and thus increase urinary excretion
The major acid-base buffering system in osis can be countered by decreased of ammonium ions. One of the most
the blood involves CO2 and HCO3 anion. arterial PaCO2 whereas a respiratory common causes of severe metabolic
CO2, HCO3 and carbonic acid (H2CO3) acidosis is countered by increased serum acidosis in surgical patients is lactic
are interconverted according to the HCO3. Because the lungs can eliminate a acidosis. With shock, lactate is produced
following reaction: vast amount of CO2 per day, this serves as a byproduct of inadequate tissue
as a very powerful buffering system. perfusion. The treatment is to restore
H+ + HCo3– ↔ H2CO3 ↔ CO2 + H2O
Similarly, the kidneys can eliminate perfusion with volume resuscitation
The relationship between the spe­ HCO3 if necessary or can regenerate rather than to attempt to correct the
cies that define pH is known as the Hen­ HCO3. abnormality with exogenous HCO3.
derson-Hasselbalch equation:
HCo3–
Classification of Acid-base Metabolic Alkalosis
pH = 6.1+ log
0.0301×PaCO2
Disorders
Essentials of diagnosis—as follows:
Acid-base disorders are classified ac­
Under normal conditions, the cording to whether there is a primary Alkalemia with increased serum (HCO3).
balance between these components is ab­normality in plasma HCO3 concentra­ • Lethargy and confusion progressing
tightly controlled. Within 95 percent of tion, plasma PaCO2 or both (Table 4.4). to seizures in severe cases.
confidence limits, the pH of the arterial Abnormal pH due to altered HCO3 • Ventricular and supraventricular
blood is between 7.35 and 7.43. For concentration with PaCO2 changes in arrhy­thmias.
PaCO2, the limits are 37 mm Hg and response to the primary disorder is re­ • Altered oxyhemoglobin binding inc­
45 mm Hg. Bicarbonate concentration ferred to as either metabolic acidosis re­ases PaCO2 and decreases PaO2.
normally varies between 22 mEq/L or metabolic alkalosis. When the defect Metabolic alkalosis consists of the
and 26 mEq/L. If hydrogen ions are in pH is due primarily to altered PaCO2 triad of increased [HCo3–], increased
added to the blood, the reaction shifts the condition is referred to as either pH and decreased serum chloride
rightward, with production of CO2 and respiratory acidosis or respiratory alka­ concentration. Because the decline in
water. Normally, the CO2 so produced losis. A change in HCo3– brings about chloride does not equal the rise in HCO3,
is rapidly eliminated by the lungs. The a compensatory change in PaCO2 and the anion gap always increases.
HCO3 – CO2 buffering system is the a primary change in PaCO2 stimulates The principal causes of metabolic
major EC buffer. Other minor EC buffer a compensatory adjustment in serum alkalosis include:
systems also contribute to stabilization HCo3–. The compensatory changes may • Addition of HCO3 to the plasma
of the pH. After EC buffering occurs, a take minutes (PaCO2) or hours to days • Loss of hydrogen ion
second IC phase takes place over the (HCo3–) to reach a steady state. • Volume depletion
next several hours. The main IC buffer • Chronic use of chloruretic diuretics
systems include hemoglobin, protein, Metabolic Acidosis • Potassium depletion.
dibasic phosphate and carbonate in Treatment includes replacement of
Essentials of diagnosis—as follows:
bone. The ratio of EC to IC buffering is the volume deficit with isotonic saline
approximately 1:1 unless the acid load is • Decreased serum HCo3– with appro­ and potassium once adequate urine
very large or continues over a long period xi­mately decreased PaCO2 (simple output is ensured.
of time. Contribution by both the EC and metabolic acidosis).
IC buffers means that an exogenous • Evidence that low serum HCo3– is Respiratory Acidosis
acid load (or deficit) has a volume of primary problem (and not due to Respiratory acidosis is asso­ ciated
distribution approximately equal to that compensation for hypocapnia). with the retention of CO2 secon­dary
of the total body water (50%–60% of ideal • May present with peripheral vaso­di­ to decreased alveolar ven­ti­­l­ation. The
body weight). Finally, both HCO3 and CO2 l­ation; depressed cardiac contr­acti­ principal causes are nar­­ cotics, CNS
act as a ‘dynamic’ buffering system. For lity in severe acidosis; fatigue, weak­ injury, pleural effus­ ion, pneumonia,
usual buffers, the addition or removal ness, stupor, coma. mucus plug, pain from abdominal or
Fluid, Electrolyte Balance and Acid-base Equilibrium 79

Table 4.4: Acidosis – alkalosis

Type of acid- Defect Common causes BHCO3/H2CO3 = 20/1 Compensation


base disorder

Respiratory Retention of CO2 (decreased Depression of respiratory Increase denominator.


acidosis alveolar ventilation) center morphine, CNS injury. Ratio less than 20 : 1
Pulmonary diseases
emphysema, pneumonia
Respiratory Excessive loss of CO2 Hyperventilation: Emotional Decreased denominator. Renal; excretion of
alkalosis (Increased alveolar severe pain, assisted Ratio greater than 20 : 1. bicarbonate, retention
ventilation) ventilation, encephalitis of acid salts, decreased
ammonia formation
Metabolic Retention of fixed acids or Diabetes, azotemia, Decreased numerator. Pulmonary (rapid); increase
acidosis loss of base bicarbonate lactic acid accumulation, Ratio less than 20 : 1 rate and depth of breathing;
starvation. renal (slow); as in respiratory
Diarrhea, small bowel acidosis
fistulae.
Metabolic Loss of fixed acids; Gain of Vomiting or gastric suction Increased numerator. Pulmonary (rapid); Decrease
alkalosis base bicarbonate; Potassium with pyloric obstruction; Ratio greater than 20 : 1 rate and depth of breathing;
depletion Excessive intake of Rena (slow) as in respiratory
bicarbonate; Diuretics alkalosis

thoracic injuries, abdominal distention • To treat shock. Drops per minute × drop factor = mL
and ascites. As compensation is pri­ • To replace electrolyte and water per hour
marily renal, it is a delayed response. deficits. The drop factor is obtained by
Treatment is directed at the correction of • To provide water, electrolytes and dividing 60 by the number of drops that
the underlying cause and at measures to nutrients for maintaining the daily are needed to deliver 1 mL. For example,
ensure adequate ventilation. needs of the patient. if 15 drops from an infusion set deliver
• To avoid creating new disturbances 1 mL, the drop factor is 60/15 = 4.1
Respiratory Alkalosis as a result of the therapy.1
Most cases are acute in nature and sec­
ondary to alveolar hyperventilation. Eti­ Route of Administration Fluid and Electrolyte Therapy16
ologies include pain or anxiety, neurol­ Food and fluids should be given by Four general categories of fluid are
gic disorders, drugs such as salicylates, the oral route (either by mouth or by available for parenteral administration
fever or gram-negative bacteremia, nasogastric tube). The enteral feeding (Table 4.5):
thy­r­o­­toxicosis or hypoxemia. Acute hy­ is the best for the patient and should be • Red blood cells (RBCs).
pocapnia can cause an uptake of potas­ started as early as possible. The enteral • Coagulation replacement products.
sium and phosphate into cells and in­ feeding activates the physiological • Colloid solutions.
creased binding of calcium to albumin, systems, it facilitates selective absor­ • Crystalloid solutions.
leading to symptomatic hypokalemia, ption of fluid and electrolytes thus the RBCs and coagulation products have
hypophosphatemia and hypocalcemia, chances of imbalance are less, the fluid excellent volume-expanding capa­­city.
with subsequent arrhythmias, paresthe­ is absorbed slowly and excreted and
sias, muscle cramps and seizures. Treat­ thus the chances of acute increase in Colloid Solutions
ment is directed at the underlying cause, preload on the heart and chances of CCF
Colloid solutions are generally adminis­
but may also require direct treatment of are reduced. The last advantage is more
tered in a volume equivalent to the
hyperventilation. relevant in patients with compromised
volume of blood lost. They are also called
renal and cardiac function. If this is not
plasma expanders as they increase the
possible, intravenous therapy, rather
colloidal osmotic pressure, pull water
General Principles of
than subcutaneous therapy (hypod­
from interstitial compartment into the
Water and Electrolyte ermoclysis), should be used.1 intravascular compartment.
Therapy Clinically, there are two types of
Rate of Administration fluids that are used for intravenous drips;
Objectives of Therapy The rate of administration of fluids crystalloids and colloids. Crystalloids
The aims of water and electrolyte ther­ intra­venously can be determined from are aqueous solutions of mineral salts or
apy are: the follow­ing rule. other water-soluble molecules. Colloids
80 Principles of Surgery

Table 4.5: Solutions used for fluid therapy

Solution Composition (per 100 mL) Indications

Lactated ringer’s Lactic acid 0.24 ml - To replace body fluids


(hartman’s solution) Sodium hydroxide 0.115 g - To buffer acidosis
Dilute hydrochloric acid a - Shock and other hypoperfusion states
sufficient quantity
Sodium chloride 0.6 g
Potassium chloride 0.04 g
Calcium chloride 0.027 g
Water for injection qs
Dextrose and normal Dextrose anhydrous 5% w/v - To raise total fluid volume
saline (dns) Sodium chloride 0.9% w/v - To correct hypoglycemia
Water for injection qs - Used as a vehicle for administration of drugs
Isotonic saline Sodium chloride 0.9 g - 
to raise plasma volume, when rbc mass is adequate
(normal saline) Water for injection qs - To replace body fluid
Isolyte M Dextrose anhydrous 5.0 g - For iv maintenance therapy
(maintenance solution Sodium chloride 91.00 mg
with 5% dextrose injection) Potassium chloride 0.15 g
Sodium acetate 0.28 g
Sodium metabisulfite 21.0 mg
Dibasic potassium phosphate 0.13 g
Water for injection qs.
Isolyte G Dextrose anhydrous 5.0 g - Gastrointestinal/osses (hyperemesis, diarrhea resulting
(gastric replacement Sodium chloride 0.37 g in hypovolemic shock).
solution with 5% Potassium chloride 0.13 g
dextrose injection) Ammonium chloride 0.37 g
Sodium sulfite 15 mg
Water for injection qs
Isolyte E Dextrose amhydrous 5.0 g - Burns
(extracellular replacement solution Sodium a Getate 0.64 g - Fasciitis
with 5% dextrose injection) Sodium chloride 0.50 g - Peritonitis
Potassium chloride 0.075 g
Calcium chloride 0.052 g
Sodium metabisulfite 0.020 g
Magnesium chloride 0.031 g
Water for injection qs
Dextrose 5% Dextrose anhydrous 5% w/v - To raise total volume
Water for injection qs - To reverse dehydration
- To prevent hyperosmolar state
- To maintain adequate renal tubular flow (to facilitate
water secretion)
Dextrose 10% Dextrose anhydrous 10% w/v - Prevention and correction of hypoglycemia
Water for injection qs
Dextrose 25% Dextrose anhydrous 25% w/v - Prevention and correction of hypoglycemia
Water for injection qs
Dextrose 50% Dextrose anhydrous 50% w/v
Water for injection qs
Mannitol Mannitol (inert form of - To raise intravascular volume
(solution of mannitol in water or sugar mannose) 20% - To reduce interstitial and intracellular edema
normal saline) - To promote osmotic diuresis.
Haemaccel Polymer of gelatin derived - To expand plasma volume (1.5 L blood loss can be
(3.5% infusion solution) Polypeptides 3.5 g replaced with haemaccel)
Water for injection
Fluid, Electrolyte Balance and Acid-base Equilibrium 81

contain larger insoluble molecules, such excess of chloride. It is preferred over fluids in pediatric patients. The safe use
as gelatin. The blood itself is a colloid. lactated Ringer’s solution (which of IV fluid therapy in children requires
Colloids preserve a high colloid os­ contains a hypotonic concentration. accurate prescribing of fluid and careful
motic pressure in the blood, while, on the Normal saline, 0.9 percent NaCl monitoring.
other hand, this parameter is decreased is isotonic and is used when brain A calculated dose of desired IV fluid
by crystalloids due to hemodilution. injury, hypochloremic metabolic should be administered using pediatric
How­ ever, there is still controversy to alkalosis or hyponatremia is present. fluid infusion pump to avoid complica­
the actual difference in efficacy by this • Balanced salt solutions: Balanced tions.
difference. Another difference is that salt solutions (Lactated Ringer’s The fluid requirement for the dehy­
crystalloids generally are much cheaper sol­u­tion/Hartman’s solution) are drated pediatric patients is calculated
than colloids. intended to mimic the composition by Holiday and Segar’s formula given as
In plasma, the oncotic pressure of ECFV. However, the amount under:
is only about 0.5 percent of the total of other electrolytes is far less Total fluid replacement per day =
osmotic pressure. This may be a small than normal req­ uire­ ments, hence Maintenance + Deficit fluids
percent but because colloids cannot should not be used as a metabolic Deficit is calculated as follows:
cross the capillary membrane easily, maintenance fluid. • No dehydration = 50 ml/kg
oncotic pressure is extremely important • Hypertonic saline: The rationale for • Some dehydration = 100 ml/kg
in transcapillary fluid dynamics. their use is that small volumes will • Severe dehydration = 150 ml/kg
• Albumin (5%): These solutions expand plasma volume by osmotic
are chosen when crystalloids fail translocation of extracellular and Presume the value for the replacement
to sustain plasma volume for more intracellular water. This could mini­ of fluid deficit is ‘X’
than few minutes due to a low mize storage space requirements The Maintenance dose of fluids per day
colloidal osmotic pressure. This will at remote sites. However, the very as per the Holiday and Segar’s Formula
be most appropriate when there is high osmolality (some are more is as under:
an abnormal loss of protein from than 900 mOsm/kg H2O) causes he­ • For the first 10 kg of weight of the
vascular space, e.g. peritonitis, molysis at the point of injection. patient = 100 mL/kg
extensive burns. • Dextrose (5%): Five percent dex­ • Plus the quantity for additional wei­
• Albumin (25%): A colloid solution trose functions as free water, because ght from 11 to 20 kg of the patient =
of 25 percent or ‘salt-poor’ albumin the dextrose is metabolized. It is iso- 50 mL/kg
contains purified albumin at five osmotic and thus, does not cause • Plus the quantity for additional
times the normal concentration. hemolysis, which would occur if pure weight of the patient above 20 kg =
When admi­ni­stered it has the poten­ water was injected intravenously, 20 mL/kg
tial to expand the plasma volume by because of rapid movement of water For example the maintenance fluids for
up to 5 times the volume provided. It into the RBC interior. a patient weighing 24 kg,
is selected when the current plasma • For first 10 kg 100 mL/kg - 1000 mL
volume is diminished, but blood pres­ • For next 10 kg 50 mL/kg - 500 mL
sure is acceptable and the total extra Fluid Management • For next 4 kg 20 mL/kg - 80 mL
cellular fluid volume is expanded. in Various Systemic Thus, a patient who weighs 24 kg
• Dextran 70 (6%): A colloid solution Condition16-18 shall require 1580 ml/24 hours as main­
of 6 percent dextran 70 in normal tenance fluids, to which the deficit fluids
saline is administered for the same are added to get the whole day’s fluid
indications as 5 percent albumin. Pediatric Patients requirement.
• Hetastarch: Hetastarch (6 G/dL of There are a few special considerations Presume the value for the maintenance
normal saline) is an alternative to relevant to pediatric fluid management fluid is ‘Y’
5 percent albumin for intravascular in addition to those for the adult. The Then X + Y = Z becomes the total fluid
vol­ume support. neonate has limited ability to dilute requirement, per day, for the patient.
or concentrate urine and has a high
Crystalloid Solutions fluid requirement. Thus, neonates Patient with Compromised
Crystalloid solutions are used both to should not be without fluid for more Cardiac Status
provide maintenance water and electro­ than 3 to 4 hours; otherwise, significant Fluid management of the heart failure
lytes and for intravascular volume dehydration may result. patient is directed to maintain the optimal
expan­sion. The pediatric patients are very sus­ cardiac preload, avoid over admi­ni­stration
• Normal saline (Isotonic saline): ceptible to fluid discrepancies and elec­ of sodium, diminish ede­ma and correct
Osmotic to plasma water sodium trolytic imbalance. Whenever possible common electrolyte abnormalities. Pati­
concentration, but contains an the enteral route should be used for ents with a history of cardiac failure
82 Principles of Surgery

scheduled for major or prolonged surgery should be made to prevent precipitating intravascular hypovolemia. The Par­
should have moni­toring instituted preo­ conditions that would require dialysis k­land formula prescribes fluids based
peratively and an intravascular fluid during the immediate postoperative pe­ on the percentage of the body surface
challenge (i.e. 500–1000 mL of cry­ riod (hyperkalemia, pulmonary edema, area burned [% body surface area (BSA)
stalloid/70 kg) performed to iden­tify the metabolic acidosis). Hemodynamics burned] (2 mL/kg)/(% BSA-burned)
optimal preload. Avoid exacerbating sho­uld be closely monitored. If hypovo­ during the first 8 hours and (2 mL/kg)/
tissue edema by frequent monitoring lemia develops, colloid should be used (% BSA-burned) during the next
of preload and arterial blood pressure early, one that should avoid producing 16 hours. The formula prescribes ([0.25
coupled with support of contractility and vascular overexpansion. Likewise, one mL/kg]/[% BSA-burned])/h for 8 hours,
control of vascular resistance. must avoid interstitial fluid overload, then ([0.125 mL/kg]/[% BSA-burned])/h
These patients have impaired ability which would require acute postopera­ for 16 hours, then 5 percent dextrose in
to excrete fluids during the fluid mobi­ tive dialysis. Crystalloid replacement of water, ([0.8 mL/kg]/[% BSA-burned])/h,
lization, which occurs postoperatively. third-space losses should be limited to plus 5 percent albumin, ([0.015 mL/kg]/
The objective in managing fluid post­ 1 to 2 mL/kg/h, while blood loss should [% BSA-burned])/h for 24 hours.
operatively should be to give as little be replaced with colloid or RBCs. Cor­
crystalloid as is consistent with main­ rection of sodium, potassium and aci­ Pregnant Pre-eclamptic Patient
taining adequate overall cardiovascu­ dosis can be achieved by the use of Goals of fluid management of the pre­
lar performance. Thus, fluid should be isotonic fluid without potassium and gnant pre-eclamptic patient are:
maintained at a low maintenance rate with reduced amounts of chloride and • To restore the contracted intra­vas­
and should include flushing fluid and increased amount of buffer. Initially, cular volume.
sodium in that consideration. an infusion of 30 percent of calculated • To avoid excessive intravascular fluid
maintenance fluid rate is important be­ administration because of normal
Patient with Cerebral Edema cause approximately 70 percent of nor­ postpartum fluid mobilization.
Fluid management of patients with cere­ mal fluid requirements are used in ex­ • To replace increased sensible (sweat)
bral edema is directed at main­taining creting solute via the kidney, a route no and insensible (respiratory) losses
cerebral perfusion pres­ sure, avoiding longer available. Na, K, pH, HNo3–, and due to labor.
elevations of cerebral venous pressure glucose should be monitored at regular • To be prepared to replace rapid
and hypertension, pre­­venting large cha­ intervals. blood loss.
n­ges in plasma osmolality (par­ti­cularly • To avoid hypotension due to anes­
depression of plasma osmolality) and thetic induced vasodilation in order
avoiding hyper­glycemia. Patient with Adult Respiratory to preserve uteroplacental flow.
Cerebral edema formation is rela­ted Distress Syndrome • To maintain normoglycemia.
to capillary pressure, COP, and permea­ Fluid management of the patient with • To avoid decreasing the COP further.
bility. ad­ult respiratory distress syndrome • To prevent pulmonary and cerebral
The capillary pressure is between (ARDS) emphasizes keeping the CVP edema.
the arterial and venous pressures. Thus, and pulmonary wedge pressure (PWP) Plasma volume is decreased in pre-
systemic arterial or venous hypertension or pulmonary artery occlusion pressure eclamptic patients due to elevated lower
needs to be prevented. The normal brain (PAOP) as low as possible, consistent body venous pressure due to uterine
capillary bed is essentially imper­meable to with good ventricular function and main­ compression, the pressure induced
sodium, mannitol and pro­tein, although taining co­l­l­oid osmotic pressure. natriuresis seen in hypertension, severe
water freely crosses. The damaged capi­ vasoconstriction and hypoproteinemia
llary bed becomes excessively permeable Acute Burn Patient secondary to proteinuria. After parturi­
with greatest conductivity to the smallest Fluid management of an acutely burnt tion, fluid retained during pregnancy is
molecules, thus favoring use of colloid. patient focuses on restoration of plasma quickly mobilized and excreted in the
volume and a shift of the ECFV into the normal patient.
Anuric Renal Failure Patient burnt but viable tissue, accompanied by
increased losses caused by loss of the Parenteral and enteral
Undergoing Nontransplant
normal barrier function of the skin. Fluid
Surgery is mobilized from uninjured tissues by
nutrition
Fluid management of the anuric renal reduced filtration due to compensatory The majority of patients are previously
failure patient for nontransplant surgery arteriolar vasoconstriction and reduced healthy and may be returned to an oral,
should avoid excessive intravascular flu­ venous pressure, which diminish capi­ liquid, blenderized, soft or normal diet
id administration, ECFV expansion and llary pressure and by lymphatic return. in a very short period of time. Although
correct (at least not worsen) electro­ The net result is a transfer of fluid from amino acid and lipid solutions are
lyte and acid base problems. Attempts normal tissue into the injured tissue and readily available, the condition of an
Fluid, Electrolyte Balance and Acid-base Equilibrium 83

oral and maxillofacial surgery patient intake of nitrogen is less than 5 g/d, may also be used by mouth as a
rarely warrants the expenses and body protein is catabolized. A number complete diet or supplement. Although
potential complications. For short-term of amino acid solutions are available. a blender is all that is needed to
nutrition, feeding tubes can be easily These are supplied in 3 percent, prepare tube feedings, the commercial
placed. For long-term nutrition, feeding 5 percent, 7 percent, 8.5 percent and preparations ensure nutritional balance
gastrostomies are less risky than total 10 percent solutions. The 3 percent and as well as convenience. Liquid diets
par­enteral nutrition. Total parenteral nu­ 5 percent solutions are generally used for for tube feeding use casein, soybeans
tr­ition is reserved for patients with inef­ peripheral intravenous administration. or egg albumin for the protein source
fective gastrointestinal function and not All solutions are expensive. In view of the Additionally, some use lactose as a
for compromised oral function. difficulties, expense and questionable carbohydrate and a few are even ‘high’
Calories come from three sources usefulness when administered peri­ in fiber. These compositions may be
car­ bo­ hydrate, protein and lipid. The pherally, their use in oral and maxillo­ important in certain patients. For
yields are 4 Kcal/g and 9 Kcal/g, res­ facial surgery patients. example, lactose intolerance is not
pec­ tively. Carbohydrate is the most Lipids are the greatest source of uncommon. All of these solutions are
effi­cient source of calories. In normal calories per gram. Additionally, lipids hypertonic when used in recommended
circumstances, it is metabolized through add palatability to our diets. Lipids concentration. It is important to start
the citric acid cycle to CO2 and water. yield 9 Kcal/g by beta oxidation to two tube feedings diluted at least 50 percent
In anaerobic metabolism (shock), lac­ carbon fragments, which are then with water and to gradually increase
tic acid accumulates. Small amounts of metabolized through the citric acid both the concentration and rate of
carbohydrates (100–150 g/dl) amelio­ cycle if carbohydrate is present. In the administration, if no, vomiting and
rate protein catabolism in starvation by absence of carbohydrate, the frag­ments diarrhea may result. Most of the
about one-third, termed protein sparing. are condensed to acetoacetate and beta- preparations yield between 0.5 and
For peripheral parenteral use, carbohy­ hydroxybutyrate, resulting in ketonuria. 1 cal/mL when used at recommended
drate is supplied as dextrose, fructose Fatty acid emulsions prevent or correct strength. Lastly, some of the products are
and invert sugar in 2.5 percent, 5 percent essential fatty acid deficiencies when high in sodium content, consideration
and 10 percent solutions with water or linoleic acid is provided at 3 percent to should be given to patients who are on a
electrolytes. Fructose and invert sugar 5 percent of total calories. When used, sodium restricted diet.2
solutions are significantly more expen­ no more than 60 percent of the calories
sive than dextrose and offer no apparent should come from lipid. These solutions REFERENCES
advantage. From, the preceding, it ap­ are quite expensive and their use in
pears that 1 L of 5 percent or 10 percent oral and maxillofacial surgery patients 1. Brensilver JM, Goldberger E. Metabolic
solution should yield 200 and 400 Kcal seems limited. acidosis syndromes Hyperkalemia.
respectively. The manufacturers prepare A variety of vitamin solutions are In: A Primer of Water, Electrolyte and
their solutions using hydrated sugars available for intravenous administration Acid-Base Syndromes. 8th edition
and consequently the yield is 170 and in both supplemental and therapeutic New Delhi: Jaypee Brothers Medical
340 calories, respectively. Five percent preparations with or without trace Publishers. 1996. pp. 239-49.
alcohol solutions with 5 percent dextrose minerals. Most of these do not contain 2. Davis LF. Fluids, electrolytes, and
are also a calorie source. Alcohol yields vitamin K. Casual use of vitamin supple­ nutrition in the oral and maxillofacial
7 Kcal/g, or 5.6 Kcal/mL as prepared. For ments is not without potential risks, surgery patient. Oral and Maxillofac
a variety of social reasons, alcohol solu­ as toxic effects of all the fat-soluble Surg Clin of NA. 1992;4(3):720-3.
tions are not popular for supplying calo­ vitamins and some of the water-soluble 3. Rosemary A Kozar, Friedrick A Moore.
ries, but some clinicians do use them for vitamins occurs. Unless signs of vitamin Fluid and electrolyte management of
short-term management of alcohol with­ deficiency are present there is no real the surgical patient, 6th edition. New
drawal. indication for vitamin supplementation York: McGraw-Hill Inc;1994. pp. 61-95.
Protein represents the building for oral and maxillofacial surgery 4. Mengoli LR. Excerpts from the
blocks of all tissue. However, the body patients who receive peripheral intra­ history of postoperative fluid therapy
does not store protein; it is present only venous therapy for only a short time. The American Journal of Surgery.
as functional tissue. Excess protein Feeding tubes are easily placed and 1971;121:311-21.
not needed for tissue anabolism is are preferred to intravenous therapy 5. Giannakopoulas Helen, Carrasco
metabolized as carbohydrate after in almost all situations. They should Lee, Jason Alabakoff, et al. Fluid and
deamination. The amino group ends up be placed as soon as it is determined electrolyte management and blood
as urea. Protein metabolism is measured that oral intake will be compromised product and usage. Oral and Maxillofac
as nitrogen, in which 6.25 g of protein or contraindicated for longer than 24 Surg Clin N Am. 2006;18:7-17.
equals 1 g nitrogen. In starvation, 12 to to 36 hours. The goal is to provide 30 6. Abou-Khalil B, Scalea TM, Trooskin
15 g of nitrogen is lost per day. When to 35 Kcal/kg/d. The flavored products SZ, et al. Hemodynamic responses to
84 Principles of Surgery

shock in young trauma patients: need fluid and electrolyte requirements. Br J hae­morrhage: observations from 20
for invasive monitoring. Crit Care Med. Anesth. 1975;47(143):141-50. con­secutive hypotensive patients. Br
1994;22:633-9. 10. Dorrington KL. Skin turgor: do we Med J (Clin Res Ed). 1986;292: 364-6.
7. Bongard FS, Sue DY. Fluids, electrolytes understand the clinical sign? Lancet. 15. Grocott MPW, Mythen MG. Fluid ther­
and acid-base. Current critical care, 1981. pp. 264-5. apy. Baillere’s Clinical anaes­the­siol­ogy.
diagnosis and treatment, 2nd edition. 11. McGee S, Abernethy WB, Simel DL. Is 1991;13:363-81.
Lange Medical Books: McGraw-Hill; the patient hypovolemic? JAMA. 1999 16. Tonnesen AS. Anesthesia, 3rd edition.
2002. pp. 14-77. 17;281(11):1023-9. New York: Churchill Livingstone Inc;
8. Richard M Langford, Monty C Mythen. 12. Sinert R, Spektor M. Clinical assess­ 1990.pp.1595-616.
Acute life support and critical care: ment of hypovolemia. Ann Emerg Med. 17. Salmon JB, Mythen MG. Pharmacology
fluid, electrolyte, and acid-base balance 2005;45(3):327-9. and physiology of colloids, Blood
and blood transfusion. In: Bailey H, 13. Davis JW, Parks SN, Kaups KL, et al. Review. 1993;7:114-20.
Love McN (Eds). Short practice of Admision base deficit predicts trans­ 18. Vincent JL, Sun Q, Dubois MJ. Cli­nical
surgery. 24th edition. London: Arnold fusion requirements and risk of com­ trials of immunomodulatory the­ ra­-
Publishers. 2004. pp. 55-77. pli­cations. J Trauma. 1996;41:769-74. ­pies in severe sepsis and septic shock.
9. Jenkins MT, Giesecke AH, Johnson 14. Sander-Jensen K, Secher NH, Bie p, Clinical Infectious Diseases. 2002;34:
ER. The postoperative patient and his et al. Vagal slowing of the heart during 1084-93.
5 Shock
Borle Rajiv M

Although shock is an identified clinical iomyopathy, conduction disorders, Hemorrhagic shock is a type of hypo­
entity for more than hundred years its valvular pathologies, congestive car­ volemic shock, but all the hypovolemic
precise definition has emerged slowly. diac failure (CCF), cardiac tampon­ shocks are not necessarily hemorrhagic
Elder Gross1 defined shock as “a rude ade, etc. shocks.
unhinging of the machinery of the • Loss of fluid (vehicle) hypovolemic
body.” It is clear from this definition shock: Causes—acute blood loss, Causes
that it is inaccurate and far from loss of fluids due to burns, septice­ Traumatic injuries, fractures of the long
precise. The proper definition is “shock mia, peritonitis, vomiting, diarrhea, bones, rupture of viscera, chest injuries,
is a clinical condition characterized by crush injuries, etc. polytrauma, rupture of aneurysm, open­
a state of hypoperfusion of the tissues • Failure of reservoir (loss of peri­ ing of varices, acute blood loss from
secondary to discrepancy between the pheral vascular resistance/vaso­di­ peptic ulcer, hemorrhoids, postpartum
volume of blood available in vascular latation): Causes—vasogenic shock, hemo­rrhage.
reservoir and effective circulating neurogenic shock, endotoxin shock.
blood volume”. The shock may also In this condition due to vasodi­ Hemorrhagic Shock
be defined as “inadequate delivery of latation the capacity of vascular bed Hemorrhage is defined as an accidental
oxygen and the nutrients to maintain increases, peripheral vascular resistance extravasation of blood due to injury
normal tissue and cellular function”. drops, although the blood volume is or disease of the blood vessel. The
The initial cellular injury due to hypo­ normal. The neurogenic shock is a type blood loss can lead to a stage of
perfusion is usually reversible, but if the of vasogenic shock in which the spinal hypovolemia and if untreated can lead
hypoperfusion is severe and prolonged cord injury or spinal anesthesia causes to a hypovolemic shock secondary to
enough it becomes irreversible. The vasodilatation due to loss of sympathetic the hemorrhage. Thus, hemorrhagic
clinical manifestations of the shock vascular tone. shock is a type of hypo­volemic shock,
are as a result of the sympathetic and but all the hypovolemic shock need
neuroadrenergic stress responses, in­ HYPOVOLEMIC SHOCK not be secondary to the hemorrhage.
ade­quate oxygen delivery and end organ The common cause of severe blood loss
(OLIGEMIC SHOCK)
dysfunction. Cannon’s observations2 are accidental injuries, polytrauma,
on the battle field during the World Hypovolemic shock is the most common postpartum hemorrhage, fractures of
War I led to many contributions to type of shock, which results from the loss the long bones, intraperitoneal bleeds
the understanding of the shock. He of circulating blood volume. This may secondary to the blunt trauma to the
was first to describe the ‘fight or flight result due to depletion of body fluids due abdomen leading to the visceral injuries
response’, secondary to elevated levels to loss of plasma, (burns, crush injuries), such as laceration of liver or spleen,
of the catacholamines in the blood, as a fluids and electrolytes (vomiting, diar­ severe, gastrointestinal (GI) bleeding
compensatory mech­anism. rhea, peritonitis, septicemia) or whole secondary to peptic ulcers, through the
The state of hypoperfusion can be blood (acute hemorrhage). It results in verices in cases of cirrhosis of liver, etc.
created by either of the following: a state of hypovolemia. When the whole The intraperitoneal bleed is occult in
• Failure of the pump (Heart)—Car­ blood is lost it is called hemo­rrhagic nature and about 2 liters of blood can
diogenic shock: Causes—tachy­arrhy­ shock, which is of prime importance to be lost intraperitoneally. The shaft of
thmias, bradyarrhythmias, car­ d­ the surgeon. femur fracture can lead to sequestration
86 Principles of Surgery

of about 750 mL of blood in the muscle flow decreases and the venous return and cyanosed due to tissue hypoxia. The
compartment in the vicinity. The also decreases, the skin appears pale consciousness is lost, the BP falls further
scalp lacerations may appear small, and the peripheral veins collapse. The and the peripheral pulse becomes ex­
but bleed sizably as the scalp vessels extremities become cold. As a result of tremely rapid and thready and may not
do not contract due to presence of hypotension the perfusion pressure falls be palpable in the peripheral arteries.
dense aponeurosis, which prevents and the renal perfusion decreases which The metabolism turns anaerobic due to
their collapse. Normally in a healthy leads to oligouria (urine output < 20 mL/ severe hypoxia and results in metabolic
individual the total blood volume is hour). The body tries to compensate acidosis. The body temperature is sub
about 5 to 5.5 liters. When the blood this phenomenon by drawing the normal and the core temperature falls.
is lost acutely following the trauma extracellular fluid into the intravascular The patient become severely pale and
the clinical signs of the hypovolemia compartment in an attempt to maintain when this pallor is super added with
become evident. the blood volume. This results into cyanosis this is called ‘ashen gray pal­
hem­o­dilution, which compromises lor’. The respiration is rapid, shallow
Pathophysiology of Hemorrhagic oxy­gen carrying capacity of the blood. due to air hunger and the patient may
Shock This phenomenon is facilitated by the show Cheyne-stokes breathing. This is
Immediately following the trauma fact that the vasoconstriction in the a picture of hemorrhagic shock. If the
due to the sight of blood and pain, the peripheral vessels leads to severe drop blood loss is compensated by fluid re­
anxiety level is optimum, which leads in the hydrostatic pressure within the suscitation and blood transfusion and
to secretion of catecholamine in the vessels and the drop is so severe that further bleeding is arrested the clinical
body and causes vasoconstriction, the extracellular fluid migrates into the signs are reversible, this is called revers­
tachycardia, sweating, breathlessness. empty vessels. This complex picture of ible hemorrhagic shock. However, the
Normally, with the blood loss of less clinical signs and symptoms is called patient can slip into irreversible hemor­
than 10 percent there are no gross effects peripheral circulatory failure3 (PCF) rhagic shock, if the blood loss continues
on vital signs (Box 5.1). (Box 5.2). uninterrupted and is more than 40 per­
However, when the blood loss If the bleeding continues further in cent of TBV, which results into death
exceeds 10 percent of total blood volume excess of 30 percent, the patients be­ (Table 5.1).
(TBV) more conspicuous clinical signs come drowsy due to cerebral hypoxia
and symptoms are apparent. There is Compensatory Mechanism
restlessness, pallor and perspiration. As Box 5.2: Clinical features of the mild The compensatory mechanism, which
the blood volume is depleted tachycardia hemorrhagic shock occurs after the hemorrhage includes:
ensues to maintain adequate blood Mild shock— loss up to 20% • Adrenergic response: The loss of
supply to all the organs. Fall in blood • Adrenergic constriction circulating intravascular volume
pressure within large vessels results in – Pallor and cool extremities results in increased vascular tone,
increase adrenosympathetic activity – Sweat in hand and feet which increa­ses peripheral vascular
of autonomic nervous system (ANS) – Patient feels cold and thirsty resistance, resulting in a redistribu­
- Tachycardia/hypotension
and inhibition of vagal tone. Thus, tion of blood flow amongst the or­
- Tachypnea
tachycardia increases further, this - Collapsed peripheral veins gans of the body. The blood flow to
is called Marey’s reflex. The pulse oliguria those organs that are ‘auto regu­l­ated’
becomes rapid, low volume and the - Altered sensorium is maintained at the expense of cuta­
respiratory rate increases. The selective - Peripheral circulatory failure neous, splanchnic and renal bed,
peripheral vasoconstriction is brought
about to maintain adequate blood Table 5.1: Clinical features of moderate and severe hemorrhagic shock
flow to vital organs like brain, heart
and kidneys. Due to the cutaneous Moderate shock (reversible) Severe shock (irreversible)
vasoconstriction the peripheral blood • 20–40% blood loss Loss more than 40%
• Adrenergic constriction—pallor and cool • Coma/hypoxic encephalopathy
extremities • Severe hypotension
Box 5.1: Clinical features of the mild blood – Sweat in hand and feet • Pulse nonpalpable
loss (up to 10%) – Patient feels cold and thirsty • Cheyne-Stokes respiration
• Severe tachycardia/hypotension, • Deep cyanosis
Blood loss up to 10%, no gross clinical
peripheral pulse may not be palpable • Metabolic acidosis
manifestations apart from
• Tachypnea • Anuria
• Tachycardia
• Mild pallor • Collapsed peripheral veins • Hypothermia
• Mild hypotension – Severe oliguria • Death
• Anxiety, tremors • Altered sensorium
Shock 87

which depend upon sympathetic inhibited, promoting glucose mobi­ produce leukotrienes which are
tone for blood flow. lization, protein catabolism and potent vasoconstrictor and cardiac
• The increased sympathetic activity negative nitrogen balance. It also depressants.
increases myocardial contractility, results into retention of sodium • During profound acute hemorrhagic
enhances venous return, improves and water in proximal tubules of shock the transcellular membrane
stroke volume and induces tachy­ nephron. potential difference in skeletal mus­
cardia. The cardiac output increases, • Adrenocorticotrophin (ACTH) rele­ cle falls from –90 to –60 mV. This pro­
the pulmonary circulation improves ase is stimulated in hemorrhagic duces increased intracellular water
and so does the myocardial oxygen shock by decreased blood volume, and influx of extracellular sodium
consumption. The blood pressure is decreased arterial pressure, pain, and chloride and efflux of intracellu­
maintained by increase in total pe­ hypoxia and hypothermia. Cortisol lar potassium, which produces cel­
ripheral resistance and cardiac out­ released by adrenal cortex does lular swelling. The decreased pro­
put. not produce feed back inhibition of duction of adenosine triphosphate
• Loss of the circulating intravascular ACTH release in acute hemorrhagic (ATP) with anaerobic metabolism
volume decreases capillary hydro­ shock. But the feed back is restored results in diminish ability to control
static pressure. This leads to trans­ once the blood volume is re- sodium pump and produces cellu­
capillary influx of exracellular fluid expanded. Cortisol potentiates the lar dysfunction. The inflammatory
into the blood vessel as a result of action of epinephrine and glucagon mediators generated in response to
the alteration in sterling forces. This on glucose metabolism. Increased injury and hemorrhage like tumor
causes expansion of intravascular cortisol secretion also results in renal necrosis factor (TNF-alpha), inter­
values and diminished blood vis­ sodium and water retention. leukins, platelet activating factor,
cosity. • Antidiuretic hormone (ADH) is leukotrienes, thromboxane A2, and
• The hemodilution decreases oxygen secreted in response to hypovolemia, complement activation system have
carrying capacity of the blood. This which facilitates reabsorption of been implicated in cellular and he­
decreases delivery of oxygen to the water in the distal tubule of nephron. modynamic dysfunction.
tissue, which leads to increased an­ ADH is potent vasoconstrictor.
aerobic metabolism and accumula­ • Activation of renin–angiotensin sys­­ Therapy of Hemorrhagic Shock
tion of lactic acid. The resultant tis­ tem occurs in shock in response to
Fluid resuscitation
sue acidosis produces a rightward increased sympathetic stimulation
shift of oxyhemoglobin dissociation of juxtaglomerular cells via a beta- The Ringer lactate solution (balanced
curve, decreasing the affinity of he­ adrenergic mechanism, decrease salt solution) is the most preferred
moglobin for oxygen, thereby mak­ renal perfusion pressure and com­ crystalloid fluid used in shock. It rapidly
ing more oxygen available to tissue. posi­tional changes in tubular fluid. restores the lost volume and it is safe
Hypoxia also stimulates respiratory Renin liberates angiotesin I from the and economical. When the patient is
centers leading to hyperventilation renal tubules, which is converted admitted in emergency room a wide bore
and respiratory alkalosis. to angiotensin II in lungs, which is needle is inserted into an appropriate
• Arteriolar constrictions and loss potent selective vasoconstrictor. It vein by venipuncture. If the veins are
of circulating volume diminishes selectively constricts the vasculature collapsed, immediate venesection (cut
renal blood flow. The urinary output of splan­ chnic organs, kidney and down) is done and a cannula is inserted
decreases as water and sodium are skin. It also stimulates prostaglandin, into the vein, preferably of arm or leg.
retained. The clearance of urea and production and release of aldosteron A catheter is inserted in subclavian
acid, as well as buffering capacity are and ACTH. The aldosteron increases vein or jugular vein to measure central
diminished leading to loss of control sodium reabsorption in distal neph­ veinous pressure (CVP). The Ringer
of acid base balance. eron in exchange of potassium and lactate solution is non-sugar, nonco­
• The change in blood volume leads hydrogen ion and represents the lloidal, crystalloid solution with similar
to marked release of epinephrine principal mechanism by which the concentration of sodium to that of plasma
and norepinephrine from the kidney may excrete the accumulated and is suitable in initial stage of fluid
adrenal glands early in the course by products of anaerobic meta­ replacement. Simultaneously, efforts are
of hemorrhagic shocks. It induces bolism and prevent the cellular made to arrest the bleeding. The infusion
vasoconstriction and tachycardia, damage. Prostaglandin particularly is given at a rapid speed so that in
resulting in increased cardiac output PGE2 and kallikreins produced in 45 minutes about 1,000 to 2,000 mL fluid
and blood pressure. Glycogenolysis, kidneys increase renal blood flow. is given. It is generally observed that BP
lipolysis and skeletal muscles are The macrophages produce platelet will return to normal and become steady
stimulated and insulin release is activating factor and the mast cells after infusion of 1 to 2 liters of such fluid.
88 Principles of Surgery

But it is a transient elevation of BP in as albumin but shorter half life, is used low position to improve venous drainage
view of continued blood loss, hence a as plasma expander. When the whole and to maintain cerebral perfusion.
blood sample should be sent for blood blood is not available, blood substitutes However, this position is good in some
grouping and cross matching. During like plasma or dextran should be used.6 types of shocks, particularly in neuro­
massive amount of transfusion, lactate When whole blood is available these genic shock. Its utility in true hypo­
acidosis is feared by some surgeons, substances should not be used, before volemic shock is not established. The
however, it is unwarranted as it is rapidly blood transfusion as they may cause patients with multiple trauma often
converted into bicarbonate in the liver. difficulty in cross matching and may have chest and abdominal injuries
The resuscitation should always be inhibit clotting system and exacerbate and use of Trendelenburg or head low
started with crystalloid solution even if bleeding. These fluids resuscitate the position may interfere with respiratory
the blood is available. If the resuscitation intravascular and interstitial fluid exchange than those left in supine
is started with cold, banked blood which volume rapidly but only quantitatively. position. The beneficial effect can be
has more potassium concentration, For qualitative replacement transfusion obtained easily by elevating both the
ensuing hyperkalemia will adversely of fresh whole blood is indicated. It legs, while maintaining the head, trunk
jeopardize the myocardial contr­ is better to withhold the transfusion and arms in supine position.
actibility. Some clinicians fear the of whole blood until surgical arrest of
post-resuscitation fluid overload with hemorrhage or at least until just before Mast garment
use of crystalloid solution as it mig­ induction of anesthesia. In case of severe The on field anti-shock garment (tight
rates rapidly in the interstitial space to hemorrhage the blood transfusion is trousers) is called MAST garment.7 With
maintain the equilibrium, leading to started immediately. mild pressure applied to extremities,
pulmonary edema; however, effective To know how much fluid is to be the garment helps in controlling some
lymphatic system takes care of it. The given, blood pressure, pulse rate, urine veinous bleeding. When applied at
use of colloidal substances that remain output, CVP, hematocrit values [hemo­ high pressure, the resultant increase in
in the intravascular compartment is globin, packed cell volume (PCV)] should total peripheral resistance may elevate
advocated by some in place of crystalloid be monitored. the systemic pressure, while reducing
for resuscitation. Administration of fluid cardiac output and peripheral perfusion.
preparation which contains colloidal Adjuvant Therapy
sub­stances like albumin expands intra­ Pulmonary support
Drugs
vascular space volume and reduces the In hypovolemic shock, the oxygen satur­
resuscitation fluid need to prevent post- Sedatives and analgesics are commonly ation is usually found to be normal in
resuscitation fluid over load. However, used in patients with shock to alleviate pain blood. However, due to hypovolemia the
the colloids are costly, may bind to and anxiety. Morphine is used commonly circulatory efficiency is compromised.
decrease ionized calcium, decrease and should be given intravenously as The oxygen therapy is indicated, if other
circulating levels of immunoglobulin, subcutaneous admini­stration in presence complicating factors like pneumothorax,
decrease immune response to tetanus of shock will not produce desired results pulmonary contusion, aspiration, airway
toxoid and decrease the levels of serum owing to peripheral vasoconstriction. obstru­ction is present, which may fur­
albumin.4 More importantly they com­ It should be avoided in patients with ther compound the existing defect in
promise the extracellular com­part­ment, head injury and in children. In children, oxy­genation due to shock. The patency
further which is already com­promised barbiturates are preferred. Relief of pain of airway must be ensured and where
in hemorrhagic shock, rather than is not mandatory in shock, but if the ever indicated ventilatory support must
restoring it. Hydroxyl starch (Hetastarch) patient is in severe pain due to fracture, be given.
and artificial colloid derived from amylo­ peritonitis, etc. pain control is necessary.
pectin, with colloid properties similar to Pethidine can be used intramuscularly, Steroids
that of albumin, is less expensive than but has slight vasodilator effect. In hypovolemic shock adrenocorti­
albumin and has longer half life. It is also cal depletion was observed, which was
used in resuscitation. Vasopressors supposed to be contributory factor for
Hypertonic saline can be effective The use of vasopressors during the shock shock.8 But subsequent studies have
initial resuscitation solution as it results may increase blood pressure, but at the shown that adrenocortical production
in lower water load than equivalent cost of further increased peripheral resis­ is stimulated in hypovolemic shock. The
resuscitation with balanced salt sol­ tance and diminished tissue perfusion. use of steroids is indicated in elderly
ution.5 However, it requires critical Hence, they are seldom used in shock. patients, Addison’s disease, patients on
moni­ toring of electrolytes to prevent corticosteroid therapy and postadre­
hypernatremia and hyperosmolar coma. Positioning nalectomy patients. In trauma patients
Dextran in 40 kD and 70 kD solutions, is Most first aid courses teach that the with hypovolemic shock administration
also a colloid which has similar activity patient in shock should be kept in head of steroids is not indicated.
Shock 89

Chronotropic agents • Immunosuppression


SEPTIC SHOCK
These drugs are selectively used in – Neutropenia, immunosuppres­
patients with bradycardia. Atropine is Sepsis, septic syndrome and septic shock sive the­rapy, corticosteroid ther­
most commonly used drug in this group define the condition of human response apy, compliment deficiencies.
followed by isoproterenol. The latter to infection. Although any agent capable – Major surgery, trauma, burns.
has an advantage that it increases heart of producing infection, including viruses, – Invasive procedures.
rate and is also vasodilator for systemic bacteria, parasites, fungi may generate – Catheters, intravascular devices,
arterial and capillary sphincters. The septic shock, the most common causative Prosthetic devices, hemodialysis
advantages of administering these drugs organism in this era of antibiotics are and peritoneal dialysis catheters,
must be carefully weighed against its gram-negative bacteria and occasionally endotracheal tubes.
disadvantages. gram-positive bacteria. The initial – Prior antibiotic treatment.
infectious process appears to be only – Prolonged hospitalization.
Inotropic drugs stimulus for a series events that may – Other factors—Childbirth, septic
The patients in severe septic, traumatic culminate in death, even in absence of abortion, and malnutrition.
and cardiogenic shock may require infection at the time of death. The gram-
these drugs. The most commonly used negative organisms supplanted gram- Clinical Manifestations
drugs in this group are dopamine and positive organisms as the predominant Gram-negative infections usually start
dobutamine. These drugs in low dose cause of septic shock after the widespread with onset of chills and temperature
increase myocardial contractibility and application of antibiotics for gram- elevation above 38°C (101°F). Two pha­
increase renal blood flow by inducing positive infections. Despite increasingly ses are often described:
renal vasodilation. They also increase powerful gram-negative antibiotics, 1. Early warm shock (Box 5.3).
peripheral vascular resistance and the incidence of gram-negative sepsis 2. Late cold shock (Box 5.4).
should be used carefully in low doses. remains very high. Proposed cause
for this increasing incidence include a Early Warm Shock
Monitoring developing reservoir of resistant and Early warm shock is characterized by
Continuous bed side monitoring of virulent organisms, concentration of the cutaneous vasodilatation. The bact­
circulatory efficacy, including assess­ patients in critical care settings, more erial endotoxins increase the body
ment of heart rate, arterial blood extensive operation in elderly and poor temperature. To bring the temperature
pressure, urinary output and peripheral risk patients, initial salvage of severely down cutaneous vasodilatation occurs,
perfusion remains the corner stone of injured and a growing population of which decreases peripheral vascular
resuscitation. Adequate resuscitation is patients immunosuppressed by organ resistance and BP falls, but the cardiac
indicated when adequate cerebral fun­ transplant protocols, radiotherapy and output increases as the left ventricle
ction and renal output is restored. The chemotherapy. The most common has less resistance to pump against.
mea­­surement of CVP is done by passing source of gram-negative sepsis is genito­ Adrenergic response further increases
a catheter in right internal jugular vein. uri­
nary tract infections secondary to
The catheter end is gradually pushed in instrumentation of urinary tract. Second Box 5.3: Stages of warm shock
superior vena cava and the catheter is most common cause is res­piratory tract
connected to saline monometer. By the infections followed by alimentary tract, Gram-negative sepsis
level of saline one can assess the CVP. including biliary sys­ tem. Prolonged ↓
If the CVP is low, infusion is indicated indwelling catheters are major source of Stage of red shock (warm shock)
and if it is more infusion may not be infection. ↓
required. A balloon tipped Shwan- The common organisms, which are Hypermetabolic state
Ganz catheter is rarely required in the concerned with gram-negative shock are ↓
initial emergency department treatment Escherichia coli, Klebsiella, Aerobacter, Heat production
for hemorrhagic shock. It measures Proteus, Pseudomonas and Bacteroides. ↓
pulmonary artery and pulmonary wedge Occasionally the septic shock can be Peripheral vasodilatation for heat loss
pressure, thermodilutional cardiac seen secondary to the fulminating gram- ↓
output and allows sampling of blood positive infections. Skin appears red, well purfused, veins
from pulmonary artery for accurate distended
measure­ment of blood gases in mixed Predisposing Factors ↓vascular resistance
venous blood. Extremes of age ↑cardiac output
Electrocardiogram (ECG) in severe • Primary diseases: Liver cirrhosis, Adrenergic response-further ↑cardiac out­
hypovolemic shock: ECG will show signs alco­ho­lism, diabetes mellitus, car­ put
of myocardial ischemia with depression dio­pul­monary diseases, solid mali­ Rapid pulse
of ST-T segment. gnancy, hematologic malignancy. BP ↓
90 Principles of Surgery

Box 5.4: Stages of white shock or cold Box 5.5: Stages to septic shock surgical drainage and debridement is
shock a definitive treatment. USG/CT guided
First stage
drainage for deep seated infection is
Vasogenic component:
Circulating toxins cause an intravascular indicated. The use of antibiotics based
• Pooling of large volume of blood
inflammatory response on specific culture and sensitivity
in skin due to dilated A-V shunts,

reducing the circulating blood tests is desirable.10 Antibiotic must be
Damage to capillaries
volume. selected on basis of suspected organism

Second stage prior to the sensitivity test and often a
Exit of fluid from intravascular to
Hypovolemic component:
extravascular space combination of antibiotics is used in
• Generalized leakage of intravascular
↓ the beginning, before the sensitivity
fluid into the interstitial tissue
Hypovolemia test. Antibiotics like cephalothin (6 to
through the capillary walls, which
• Diminished venous return
suffer widespread damage due to 8 g/day IV), Gentamycin (5 mg/kg/day),
• Diminished pulmonary circulation
bacterial toxins. Clindamycin or Chloromycetin, when
• Shock lung syndrome
– Subsequently
• Diminished filling of left heart infection with Bacteroides is suspected
Deranged cardiac function due to toxins.
• Diminished output are the antibiotics to start with.
• Hypotension Correction of pre-existing fluid defi­
• Hypoperfusion
show leukocytosis, but leukopenia in cit is essential in septic patients and
• Hypoxia.
immunesuppressed and debilitated
Peripheral vasoconstriction and skin becomes should proceed rapidly, though care­
cold, pale. patients. Thrombocytopenia may be fully, using pulmonary wedge pressure
early indicator of gram-negative sepsis. and cardiac output as a guide to tar­
Mild hypoxia, compensatory hyper­ get appropriate replacement volumes,
the cardiac output. At this stage the ventilation, respiratory alkalosis and so that the detri­mental effects of fluid
skin appears pink, warm, dry and altered sensorium are seen early in this overload can be avoided. Monitoring is
well perfused. The cutaneous veins shock (Box 5.5). essential because fluid replacement is
remain full. The pulse rate is high and massive in these patients. Resuscitation
blood pressure is low. The patient may Pathophysiology requirement in excess of 10 L of lactated
rapidly progress to evidence of altered Septic shock is the result of numerous Ringers solution are common. The use
organ function, most often renal and complex interactions between exog­ of corticosteroids in the treatment of
pulmonary. Unlike most other shocks, enous and endogenous mediators and septic shock was controversial, but after
the patient who is normovolemic has host response to these stimuli. As a well controlled prospective clinical trials
hypotension in spite an increased response to sepsis and bacterial endo­ it has been noticed that the use of high
cardiac output and reasonable filling toxins many mediators are released in doses of corticosteroids did not confer
pressure. The high cardiac output is often body like interleukin (IL-1 alpha, beta, a survival advantage over nonsteroid
associated with a decrease in oxygen IL-6, IL-8, IL-11), Cachectin-TNF alpha, treated controls. The only indications of
utilization and a narrowed arteriovenous TNF beta (tumor necrosis factor), cyto­ steroid treatment are hypoadrenalism
oxygen difference. kines from macrophages; neutrophils, and patients taking steroids for immu­
endothelial cells, prostaglandins, kinins nosuppression and anti-inflammatory
Late Cold Shock through arachidonic acid and cyclo- action.
In the late cold shock there is increased oxygenase pathways particularly PGE2,
vascular permeability due to release of kallikreins, throboxane–A2, nitric oxide, Vasoactive Drugs
toxic products into the circu­lation. This hormones, etc. This produces a wide­ The vasoactive drugs with only alpha-
leads to hypovolemic state, dec­reased spread systemic inflammatory response adrenergic action are of limited value in
venous return, decreased right heart often referred as systemic inflammatory the treatment of this type of shock. Use
filling, reduced blood flow in pulmo­ response syn­drome (SIRS).9 It precipi­ of vasoactive drug with mixed alpha and
nary bed, decreased left heart filling tates a series of complex reactions in the beta-adrenergic receptors may be indi­
and so is the cardiac output and the body, which results in cellular dysfunc­ cated. Dopamine is initial inotropic drug
shock results. Early volume replace­ tion, organ failure, multiple organ fail­ used. Dopamine has some vasopres­
ment frequently increases cardiac ure and death. sor effect at higher doses and that may
output and produces a hyperdynamic be required in volume loaded patients
circulation, while the patient later Management with persistent profound hypotension.
in shock is unresponsive to volume The only effective way of reducing Augmentation of impaired myocardial
replacement and has low cardiac out­ mortality in septic shock is prompt performance in septic shock is a reason­
put with increasing metabolic acidosis. diagnosis and treatment. The control able goal. Dobutamine often increases
Concomitant laboratory investigations of infection by antibiotics and early cardiac output with less tachycardia and
Shock 91

arrythmias than dopamine. The beta- brain requires about 70 mL of blood flow • Sweating.
adrenergic vasodilatation from dobuta­ per minute/100 g of brain matter and • Fainting, unconsciousness.
mine infusion may not be tolerated by about 3 to 5 mL of oxygen/min/100 g of • Due to the release of catacolamines,
these hypotensive patients. Vasodila­ brain matter.14 The glucose requirement corticosteroids, glucagon the patient
tor drugs have been shown to improve is about 5 to 7 mg/min/100 g of brain will have tachycardia, marginal rise
cardiac output and oxygen delivery in matter. Any discrepancy in this will lead in blood pressure.
normotensive septic patients. Their use to its malfunctioning and if it persists • This condition is very dangerous
in septic shock is limited due to low for a long, it may lead to irreversible when the patient is in sleep and
systemic pressure or decreased cardiac damage or in very severe conditions alteration in level of consciousness
filling pressure. More potent vasopres­ may lead to death. The normal blood may go unnoticed. This can lead to
sors despite their obvious detrimen­ glucose level in the blood is 80 to unconciousness, tongue fall and
tal effect on peripheral perfusion, may 120 mg/dL while fasting, and 120 to respiratory obstruction.
be transiently unavoidable in patients 140 mg/dL, postprandially. When the
who have persistent life-threatening blood sugar level drops to less than Prevention
hypotension, despite optimal fluid and 50 mg/dL, hypoglycemia results. The A clinician must evaluate the patient
dopamine infusion. Noradrenaline is a children withstand the hypoglycemia a thoroughly. The patients who are
potent alpha receptor and is effective in little better and can sustain the falling diabetic should have adequate control
raising pressure in patients in whom the blood sugar level up to 40 mg/dL. The of blood sugar level. They should be
measures described above have failed. hypoglycemia is more serious clinical given morning appointments so that
Its use is sometimes preferred over high problem than the hyper glycemia, as it they had good rest at night and are fresh.
dose dopamine because the cardiac may be fatal if not corrected timely. Long waiting in crowded, warm waiting
effects are less. Epinephrine, a potent rooms adds to anxiety and tends to
alpha and beta adrenergic activity, may exhaust the patient. It is important to
support the blood pressure, who fail to Causes know whether the patient has taken
respond to noradrenaline. The hypoglycemia can occur not only break­fast or not than the morning
Treatment with steroids,11 fibro­ in the patients of diabetes taking oral dose of insulin or oral hypoglycemic as
nectines and naloxone have been dis­ hypoglycemic or insulin, but it can skipping of breakfast can lead to hypo­
appointing. Specific immunotherapy also happen in nondiabetics, who are glycemia. The patient should always be
with monoclonal IgM antibodies of core starving and are exposed to stress. The categorized into:
lipopolysaccharides12 have shown to chances of the hypoglycemia are more • IDD-insulin dependent diabetics.
be effective in small group of patients. common in the former group. • Patients on oral hypoglycemics.
Monoclonal antibodies13 to TNF are also • Diabetic patient who has taken dose • Patients controlled by diet and exer­
available and appear promising in pa­ of insulin or oral hypoglycemics, but cise.
tients with septic shock. has missed breakfast or meal. Such The first two varieties suggest severe
patients may land in hypoglycemia, and moderate disease and patients with
if exposed to stress. such disease require more attention.
HYPOGLYCEMIC SHOCK
• Strenuous, long procedures in The patients who have been starv­
The body tissues require continuous warm, humid environments can ing or have skipped their meals should
supply of glucose and oxygen to fulfill pre­ci­­pitate hypoglycemia. be supplemented with oral glucose,
their metabolic needs. When there is • Starvation—the oral surgical pati­ before the clinical procedure. Long sit­
inad­equate supply of either of these the ents, having inflammatory path­ tings should be avoided. The environ­
metabolism shifts to anaerobic side, ologies of jaws (like fracture, peri­ ments should be cool and pleasant and
there is catabolism and gluconeogenesis coronitis, acute infections) are often stress should be managed properly.
to meet the energy needs of the body and unable to take adequate diet and are
metabolic end products of anaerobic vulnerable to land in hypoglycemia Management
metabolism like lactic acid, accumulate when exposed to stress.
in the body, leading to metabolic acidosis. • Postoperative patients who are not
Management of Hypoglycemia
This alternative metabolic pathway supplemented adequately with par­ in a Conscious Patient
is absent in the brain, which depends enteral therapy taking into account As soon as the early signs of the hypogly­
only on the oxidative phosphorylation, their energy requirements. cemia are detected the procedure
for its metabolic needs. Hence, the should be discontinued and patient
brain is very susceptible to hypoxia and Clinical Features should be kept in supine position in
hypoglycemia. The deficiency of either • Mental confusion, giddiness, lack of well aerated environments. The patient
of these results in its dysfunction and fine coordination, feeling of weak­ness. should be given oral glucose powder in
the patient looses consciousness. The • Slurred speech, blurring of vision. the form of hypertonic solution. It must
92 Principles of Surgery

be ensured that the patient is conscious breathing). Anaphylactic shock can lead • Aeroallergens: Domestic/labor­atory
failing to which chances of aspiration to death in a matter of minutes, if left animals, pollen
are high. An ampule of 25 or 50 percent untreated. • Food additives: Monosodium glu­
dextrose may be broken and the patient Anaphylaxis can be typically divided tamate, metabisulfite, preservatives,
be administered the solution orally. The between ‘true anaphylaxis’ and ‘pseu­ colors, natural food chemicals
diabetics who are susceptible to develop do-anaphylaxis’ or an ‘anaphylactoid • Topical medications (e.g. antisep­
hypoglycemia may be asked to keep reaction’. The symptoms, treatment tics).
glucose biscuits with them and eat 2 to and risk of death are identical, but the Allergic reactions to β-lactam an­
3 biscuits whenever they get feeling of anaphylaxis is always caused directly tibiotics represent the most frequent
drowsiness. by degranulation of mast cells or baso­ cause of drug reactions mediated by im­
phils, i.e. mediated by immunoglobulin munological mechanisms.16 The safety
Management of Hypoglycemia E, (IgE) and pseudoanaphylaxis occurs profile of cephalosporins is generally
in an Unconscious Patient due to all other causes.15 The distinc­ good although a wide range of allergic
In an unconscious patient admini­ tion is primarily made by those studying reactions have been caused by β-lactam
stration of oral glucose is dangerous as mechanisms of allergic reactions. antibiotics (Fig. 5.1). It is possible to
the patient may aspirate. Such patients classify these reactions by the Levines
are given IV dextrose in the form of 25 or Causes classification system, which is based on
50 percent solution. It may be repeated Anaphylaxis is a severe, generalized alle­ the time of the onset of the reactions.17
after some time, if needed. The patients rgi­c reaction. After an initial exposure Some reactions to penicillin and cepha­
usually recover fast, however, during ‘sensitizing dose’ to a substance like bee losporin antibiotics are known to be me­
the period of unconsciousness critical sting toxin, the person’s immune system diated by IgE antibodies. These include
evaluation and monitoring is necessary. becomes sensitized to that allergen. anaphylactic and urticarial reactions,
Efforts should be made to prevent On a subsequent exposure to ‘shocking while other reactions to β-lactam anti­
tongue fall and basic life support (BLS) dose’, an allergic reaction occurs. This biotics such as serum sickness, hemo­
should be given wherever necessary. reaction is sudden, severe and involves lytic anemia, maculopapular rashes and
Even after the patient has recovered the whole body. Stevens-Johnson syndrome are not IgE
he should be observed for some time Hives and angioedema (swelling mediated.18 IgE-mediated (immediate
to identify and treat any subsequent of the lips, eyelids, throat, or tongue) onset) reactions are estimated to occur
episode of hypoglycemia. often occur. Angioedema may be severe in less than one in 100,000 patients. The
enough to block the airway. Prolonged frequency of hypersensitivity reactions
anaphylaxis can cause heart arrhythmia. to cephalosporins is less than to the
ANAPHYLACTIC SHOCK
penicillins. It has been estimated that
Anaphylaxis is an acute systemic (multi- Common nearly 75 percent of fatal anaphylactic
system) and severe type I hypersensiti­ • Insect stings: Most commonly hon­ reactions result from the administra­
vity (allergic) reaction in humans and ey­bee, Australian native ants, wasps tion of penicillin. Of all the injectable
other mammals. The term comes from • Foods: Most commonly peanuts, cephalosporins, ceftriaxone, cefuroxime
the Greek words ‘ανα’, i.e. ana (against) tree nuts, egg, seafood, cows milk, and oral cefaclor are the most frequently
and ‘φúλαξις’, i.e. phylaxis (protection). dairy products, seeds reported ones in allergic reactions.19 The
Minute amounts of allergens may cause • Medications: Most commonly an­ major antigenic determinant of benzyl­
a life-threatening anaphylactic reaction. tibiotics, non-steroidal anti-inflam­ penicillin is benzylpenicilloyl, which is
Anaphylaxis may occur after ingestion, matory drugs formed by the nucleophilic attack on the
skin contact, injection of an allergen • Unidentified (no cause found). penicillin molecule by the amino group
(ana­ phylactogen) or in some cases, of proteins found in the plasma or cell
inhal­ation. Less Common membrane.20
Anaphylactic shock, the most severe • Physical triggers (e.g. exercise, cold) In penicillin, because of the fusion of
type of anaphylaxis, occurs when an aller­ • Biological fluids (e.g. transfusions, im­ a five-member sulfur ring (the thiazoli­
gic response triggers a quick release of m­­unoglobulin, antivenoms, semen) dine ring) to the β-lactam ring, the high
large quantities of immunological med­ • Latex tension within the β-lactam ring results
i­­ators (histamines, prosta­gl­andins and • Tick bites in an increased chemical reactivity,
leuko­trienes) from mast cells, leading to • Hormonal changes: Breastfeeding, while in cephalosporins a six-member
sys­temic vaso­dil­­ation (associated with menstrual factors sulfur ring (the dihydrothiazine ring)
a sudden drop in blood pressure) and • Dialysis membranes (hemodialysis- fuses to the β-lactam ring and there is
edema of bronchial mucosa (resulting associated anaphylaxis) a lower tension in the β-lactam ring for
in bronchoconstriction and difficulty • Hydatid cyst rupture conjugation to carrier protein (Fig. 5.2).
Shock 93

with a receptor on the surface of mast


cells. If the antibody binds to its specific
antigen, then the antibody triggers
degranulation of the mast cell.
Mast cells become the major effec­
tor cells for immediate hypersensitivity
and chronic allergic reactions.23 Mast
Fig. 5.1: Chemical structure of penicillin and cephalosporin cells are large cells found in particularly
high concentrations in vascularized
connective tissues just beneath epithe­
lial surfaces, including the submucosal
tissues of the gastrointestinal (GI) and
respiratory tracts and the dermis that
lies just below the surface of the skin.
They contain large granules that store a
variety of mediator molecules including
the vasoactive amine, histamine. Hista­
mine causes dilation of local blood ves­
sels and smooth-muscle contraction.
Fig. 5.2: Penicillin conjugation to the carrier protein Other molecules in the mast cell gran­
ules include lipid inflammatory media­
Therefore, haptenization of protein tors such as PG D2 and leukotriene
Pathophysiology
by penicillin is quicker and more effi­ C4 as well as tumor necrosis factor-α
cient than by cephalosporin and the Classified as a type I hypersensitivity, (TNF-α), a cytokine. The importance
conjugate formed by penicillin is more anaphylaxis is triggered when an antigen of TNF-α is most noted in the activa­
stable.21 binds to IgE antibodies on mast cells tion of the endothelium. TNF-α, the
Some drugs like polymyxin mor­ based in connective tissue throughout prototype of the TNF family cytokines,
phine, radiocontrast X-ray dye and others the body, which leads to degranulation can induce endothelial cells to present
may cause an ‘anaphylactoid’ reaction of the mast cells (the release of inflamm­ E-selectin and ICAM-1, both of which
(anaphylactic-like reaction). This is atory mediators).22 are cell adhesion molecules (CAM) that
usually due to a toxic reaction, rather These immune mediators cause mediate the ‘roll and stick’ mechanism
than the immune system mechanism many symptoms, including common of leukocyte extravasation, termed dia­
that occurs with ‘true’ anaphylaxis. The sym­ptoms of allergic reactions, such as pedesis. While, this process is essen­
symptoms, risk for complications without itching, hives and swelling. Anaphylactic tial for the recruit of leukocytes to a
treatment and treatment are the same, shock is an allergic reaction to an localized area during an inflammatory
however, for both types of react­ions. Some antigen that causes circulatory collapse response, it can be catastrophic in cases
vaccinations are also known to cause and suffocation due to bronchial and of systemic infection. Point in case, the
‘anaphylactoid’ reac­tions. Ant­i­­toxins and tracheal swelling. presence of said infection in the blood­
antivenins may cause similar reactions. Different classes of antibodies are stream or sepsis, is accompanied by the
In certain indivi­duals, strenuous physical produced by B cells to bind and destroy release of TNF-α by macrophages in
activity can induce anaphylaxis. substances that the immune system liver, spleen and other systemic sites.
Anaphylaxis can occur in response to has identified as potentially dangerous The systemic release of TNF-α causes
any allergen (anaphylactogen). Common pathogens. Each B cell produces thou­ vasodilatation, which leads to a loss of
causes include insect bites or stings, food sands of identical antibodies that blood pressure and increased vascular
allergies (peanuts and tree nuts are the can attack a single, small part of a permeability, leading to a loss of plasma
most common, (though not the only) and pathogen. In susceptible individuals, volume and eventually to shock.
drug allergies. Pollens and other inhaled antibodies may be produced against TNF-α, along with the other mast
allergens rarely cause anaphylaxis. In innocuous antigens or allergens, such cell granule contents become exocy­
ophthalmology, the dye fluorescein used as components of common foods or tosed upon activation of the mast cell.
in some eye exams is a well known trigger. plants. One class, the IgE antibodies, Activation is achieved only when IgE,
Some people have an anaphylactic can trigger anaphylaxis. Production of bound to the high-affinity Fcε receptors
reaction with no identifiable cause, in IgE antibodies may persist for months, (FcεR1), are cross-linked by multiva­
which case the anaphylactic reaction is even in the complete absence of the lent antigen. The FcεR1 is a tetrameric
said to be idiopathic. allergen. These IgE antibodies associate receptor composed of a single α chain,
94 Principles of Surgery

responsible for binding the IgE, associ­ substances. This causes constriction Box 5.6: Clinical features to anaphylaxis
ated with a single β chain and a disul­ of the airways, resulting in wheezing,
fide linked homodimer of γ chains that difficulty breathing. Anaphylaxis
initiate the cell signal pathway.24 Cyto­ • Gastrointestinal symptoms such as • Severe respiratory distress, wheeze, stri­
dor
solic Ca2+ and Phosphokinase C signal abdominal pain, cramps, vomiting
• Cyanosis, hypoxia
the degranulation of the mast cell. Mast and diarrhea.
• Hypotension tachycardia, ST changes,
cells with bound highly cytokinergic • Histamine causes the blood vessels
arrhy­thmias, myocardial insufficiency,
IgE attract other mast cells even in the to dilate (which lowers blood arrest
absence of antigen crosslinking, which pressure) and fluid to leak from the • Hypoperfusion
explains for the persistence of the allergy bloodstream into the tissues (which • Unconsciousness
to particular allergen. lowers the blood volume). These • Urticaria (hives), pruritis, flushing, tears
effects result in shock. Fluid can • Angioedema (swelling of the lips, face,
Pathophysiology leak into the alveoli (air sacs) of the neck and throat): laryngeal edema can
of Pseudoanaphylaxis lungs, causing pulmonary edema. be life-threatening
Pseudoanaphylaxis presents with the • Abdominal cramps, vomiting
same clinical signs and symptoms Clinical Features of Anaphylaxis
as true anaphylaxis, but it does not • Mucocutaneous: Rhinitis, conjunc­
involve IgE antibodies. Instead, mast tival erythema and tearing, flushing, Treatment
cell degranu­ lation is triggered either itch, urticaria, angioedema.
Box 5.7: Treatment of anaphylactic shock
by the activation of the complement • Abdominal/pelvic: Nausea, vom­
system or by a pharma­cological reaction iting, abdominal pain, pelvic pain
a. Early identification
on the mast cell’s surface.25 Histamine, (described as being ‘like uterine con­
b. Basic life support
which is released in both true IgE- tractions’), delayed vaginal disch­
based allergic reactions and in these arge. c. Nasal O2 8–10 lit/min
anaphylactoid reactions, is responsible • Neurological: Vascular headache d. Inj adrenaline 0.5 to 1 mg (1:10000)
SC/IM/IV depending severity
for the resulting signs and symptoms, (typically described as ‘throbbing’),
e. Inj hydrocortisone hemisuccinate
which are consequently identical. dizziness, collapse (with or with­ 100–200 mg IV
The complement system contains out unconsciousness), confusion,
f. Inj Soda bicarbonate 1 millimol/kg/min
three proteins (C3a, C4a, and C5a) that incontinence. of hypoxia (not to over load)
are called anaphylatoxins because of • Respiratory/chest: Dysphagia and g. Antihistaminics
their role in triggering pseudoana­ph­ylaxis. stridor due to upper airway angio­ Once the patient is reviewed
The most common trigger for this mech­ edema (laryngeal), throat and/or h. Critical monitoring
anism is an intravenous infusion of an chest tightness, dyspnea, cough, i. Maintenance on steroids
iodine-containing radiological contrast whe­eze, cyanosis. (dexamethasone)
medium. The mechanism by which other • Cardiovascular: Palpitations, tach­ j. Antihistaminics
substances, commonly called histamine y­cardia, bradycardia (relative or k. Nasal O2 as directed by ABG analysis
liberators, trigger mast cell degranulation, ab­solute), ECG changes (T and ST and clinical condition
is poorly understood. Some substances chan­ges), hypotension, cardiac arrest
are known to be effective liberators in (Box 5.6).
susceptible people, including egg white, Management
strawberries and a variety of medications. Diagnosis
• Diagnosis is based on fulfilling five
Acute Management
Symptoms main clinical criteria Anaphylaxis is a medical emergency
Symptoms of anaphylaxis are related to • Sudden onset and rapid progression. that requires immediate treatment.
the action of IgE and other anaphyla­ • Life-threatening problem with air­ Parenteral epinephrine is the drug of
toxins, which act to release histamine way, breathing and circulation. choice, though it is preferred intramu­
and other mediator substances from • Sever-hypoxia and cyanosis. scular or subcutaneous. Intravenous
mast cells (degranulation). Histamine • Severe hypotension. epin­ephrine (1:10,000 dilution) should
induces vaso­dilation of arterioles and • Skin or mucosal changes, for exam­ple be administered only in severe hypoten­
constriction of bronchioles in the lungs, widespread urticaria/angioedema. sive shock because of its potential for
also known as bronchospasm (constric­ Apart from its clinical features, tachyarrhythmias.
tion of the airways). blood tests for tryptase (released from • Place the patient in the supine posi­
• Tissues in different parts of the mast cells) might be useful in diagnosing tion (or left lateral position when
body release histamine and other anaphylaxis.26 vomiting is present)
Shock 95

• Resuscitate with intravenous saline Box 5.8: Priorities in the management of as dopamine or high-dilution epineph­
(20 mL/kg body weight, repeated up anaphylactic shock rine (1:10,000). Individuals who use
to a total of 50 mL/kg over the first Emergency management of anaphylaxis
b-blockers (and possibly angiotensin-
half hour) • Stop administration of causative agent converting-enzyme inhibitors, although
• Support the airway and ventilation (if relevant), assess reaction severity and the evidence is incomplete) may not
• Give supplementary oxygen (8– treat accordingly respond completely to epinephrine,
10 L/min) • Call for assistance in which case glucagon should be ad­
• Give adrenaline IM (lateral thigh)
• Intramuscular 1:1000 (1 mg/mL) ministered at a dose of 5 to 15 µg/min
0.01 mg/kg (maximum dose 0.5 mg)
adre­na­line at a dose of 0.01 mg/kg • Set-up IV access intravenously. Glucagon has inotropic,
(0.01 mL/kg) body weight up to a • Lay patient flat (elevate legs if tolerated) chronotropic and vasoactive effects that
maximum dose of 0.5 mg (0.5 mL) • Give high flow oxygen + airway/ are independent of b-receptors and it
injected into the lateral thigh (vastus ventilation support if needed also causes endogenous catecholamine
lateralis) has the advantage that it can If hypotensive, also: release.
• Set-up additional wide-bore IV access
be given without delay, is absorbed
(i.e. 14G or 16G in adults) for normal
more reliably than injections into saline infusion
Critical Care Monitoring
other locations or subcutaneously, • Give IV normal saline bolus 20 mL/kg The time course of anaphylaxis can be
is anecdotally effective in most cases over 1–2 mm under pressure classified as ‘uniphasic’, ‘protracted’ or
when given early and avoids the • If there is inadequate response, an ‘biphasic’.29 Although most reactions
potentially lethal effects of large intra­ immediate life-threatening situation, respond rapidly to treatment and do
or deterioration:
venous bolus injections (Boxes 5.7 • Start an IV adrenaline infusion, as per
not recur (uniphasic reactions), an
and 5.8). hospital guidelines/protocol observation period is recommended.
OR This is because, in some patients,
Management of Persistent • Repeat IM adrenaline injection every symptoms may fail to improve or may
Airway Tract Obstruction 3–5 mm, as needed worsen as the effect of adrenaline
and or Hypotension Abbreviations: IM: Intramuscular, IV: Intra­ wears off (protracted anaphylaxis)
If the patient is still unresponsive after venous. Brown SGA. Anaphylaxis: clinical or may return after early resolution
the treatments outlined above, there are concepts and research priorities. Emerg (biphasic reaction). No clinical feature
several further options: Med Australias. 2006;18:155-169. consistently identifies patients at risk of
• Persistent bronchospasm may re­ a biphasic reaction. Expert consensus is
spond to treatment with additional that a reasonable length of observation
bronchodilators. If intubation is re­ Supportive Therapy after symptom resolution is 4 to 6 hours
quired, continuous puffs of salbuta­ Other supplementary therapy for ana­ in most patients, with more prolonged
mol through an aerosol port directly phylaxis includes the use of H1 and H2 observation in those with severe or
into the ventilation circuit may help antihistamines. For example, diphen­ refractory symptoms and those with
to ‘break’ severe bronchospasm. hydramine, 25 to 50 mg intravenously reactive airway disease, as most fatalities
• Persistent stridor may respond to and ranitidine, 50 mg intravenously or associated with anaphylaxis occur in
continuous nebulized adrenaline 150 mg orally. Current recommenda­ these patients.30
(5 mg in 5 mL (i.e. five 1 mg ampo­ tions are to administer these agents in
ules) in addition to parenteral combination, because H1 and H2 block­
REFERENCES
adrena­ line. Surgical airway inter­ ade is more effective than H1 blockade
ven­tion (crico­ thyrotomy) may be alone in preventing symptomatology of 1. Gross SG. A System of Surgery: Patho­
required though not advisable. It anaphylaxis. Inhaled b2-agonists (e.g. logical, Diagnostic, Therapeutic and
serves only purpose of overcoming salbutamol) are useful when broncho­ Operative. Philadelphia, Pa.: Lea and
upper airway obstruction but in view spasm is present. Corticosteroids (e.g. Febiger, 1872..
of brochospasm it is not useful. hydrocortisone in acute emergency 2. Walter Bradford Cannon. Bodily Chan­
• Persistent hypotension may be due and once the patient is stable, methyl­ ges in Pain, Hunger, Fear and Rage:
to either profound vasodilation or prednisolone, 125 mg intravenously or An Account of Recent Researches into
cardiac failure. Anecdotally, vaso­ prednisone, 50 mg orally; the intrave­ the Function of Emotional Excitement,
dilation may respond to vasopres­ nous route of administration is often Appleton, New York, 1915..
sors such as metaraminol or va­ used for more severe reactions) may 3. Dornhorst C. The pathogenesis and
sopressin.27 In patients who have help prevent or minimize second phase mana­gement of peripheral circulatory
pre-existing heart failure or are tak­ reactions. Hypotensive patients should failure. Ann R Coll Surg Engl. 1970;
ing β-blockers, a phosphodiesterase receive intravenous fluid support with 46(3):172-5..
inhibitor such as glucagon may be crystalloid or colloid and severe cases 4. Poole GV, Meredith JW, Pennell T,
tried.28 may require vasopressor agents such et al. Comparison of colloids and
96 Principles of Surgery

crysta­lloids in resuscitation from hem­ 14. Rengachary SS, Ellenbogen RG, Prin­ 23. Kitaura J, Kinoshita T, Matsumoto M, et
o­­rrhagic shock. Surg Gynecol Obs­tet. ciples of Neurosurgery, (Eds) Edin­ al. “IgE- and IgE+Ag-mediated mast cell
1982;154(4):577-86.. burgh: Elsevier Mosby, 2005. migration in an autocrine/paracrine
5. Chiara O, Segala M. Hypertonic saline 15. Limmer D, Mistovich JJ, Krost WS (No­ fashion”. Blood. 2005;105(8):3222–9.
solutions in resuscitation in hemo­ vember 17, 2005). “Anaphylactic and 24. Paolini R, Jouvin MH, Kinet JP (Octo­
rrhagic shock. An experimental study. Anaphylactoid Reactions – Prehos­pital ber 1991). “Phosphorylation and de­
Minerva Chir. 1997;52(6):753-62.. Pathophysiology”. EMSRes­­pon­der.com. phosphorylation of the high-affinity
6. Gruber UF. Volume expansion and 16. Gomez MB, Torres MJ, Mayorga C receptor for immunoglobulin E im­
flow promotion in shock. Postgrad et al. Immediate allergic reactions to mediately after receptor engagement
Med J. 1969;45(526):534-38. b-lactams: facts and controversies. and disengagement”. Nature. October
7. Gaffney FA, Thal ER. Hemodynamic Curr Opin Allergy Clin Immunol. 1991;353(6347): 855–8.
effects of medical anti-shock trou­ 2004;4:261-6. 25. Joris, Isabelle; Majno, Guido. Cells,
sers (MAST garment). J Trauma. 17. Weiss ME, Adkinson NF. β-lactam tissues, and disease: principles of
1981;21(11): 931-7. alle­
rgy. In: Mandel GL, Bennett JE, general pathology. Oxford [Oxford­
8. Gregory D, Rushing. Effects of Hemorr­ Dolin R (Eds) Principles and Practice shire]: Oxford University Press. 2004.
hagic shock on adrenal response in a rat of Infectious Diseases. 6th edition pp. 538-9.
model. Ann Surg. 2006;243(5):652-6. Edinburgh:Churchill Livingstone; 2005. 26. Schwartz LB. “Diagnostic value of
9. Alberti C, Brun-Buisson C. Systemic pp.318-26. tryptase in anaphylaxis and mastocyto­
inflammatory response and progre­ 18. Hoffman DR, Hudson P, Carlyle SJ, sis”. Immunology and allergy clinics of
ssion to severe sepsis in critically ill et al. Three cases of fatal anaphylaxis North America. 2006;26 (3):451–63.
infected patients. Am J Respir Crit Care to antibiotics in patients with prior 27. Schummer W, Schummer C, Wipper­
Med. 2005;171(5):461-8. histories of allergy to the drug. Ann mann J, et al. Anaphylactic shock: is
10. David Simon. Antibiotic selection for Allergy. 1989;62:91-3. vasopressin the drug of choice? Anes­
patients with septic shock. Critical 19. Romano A, Mayorga C, Torres MJ, the­siology. 2004;101:1025-7.
Care Clinics-Volume 16, Issue 2 (April et al. Immediate allergic reactions to 28. Zaloga GP, DeLacey W, Holmboe E,
2000), Copyright © 2000 WB Saunders cephalosporins: cross-reactivity and et al. Glucagon reversal of hypotension
Company. selective responses. J Allergy Clin in a case of anaphylactoid shock. Ann
11. Bone RC, Fisher CJ Jr, Clemmer TP, Immunol. 2000;106:1177-83. Intern Med. 1986;105:65-6.
et al. A controlled clinical trial of 20. Madaan A, Li JT. Cephalosporin 29. Stark BJ, Sullivan TJ. Biphasic and
high-dose methylprednisolone in the allergy. Immunol Allergy Clin North protracted anaphylaxis. J Allergy Clin
treatment of severe sepsis and septic Am. 2004;24:463-76. Immunol 1986;78(1 Pt 1):76-83.
shock. N Engl J Med. 1987;317:653-8. 21. Perez-Inestrosa E, Suau R, Montanez 30. Sampson HA, Munoz-Furlong A, Cam­
12. Fink MP. Adoptive immunotherapy of MI, et al. Cephalosporin chemical pbell RL, et al. Second symposium
gram-negative sepsis: use of mono­ reactivity and its immunological on the definition and management
clonal antibodies to lipopolysaccharide. implications. Curr Opin Allergy Clin of anaphylaxis: summary report—
Crit Care Med. 1993;21(2 Suppl):S32-9. Immunol. 2005;5:323–30. second National Institute of Allergy
13. Hinds CJ. Monoclonal antibodies in 22. Murphy, Kenneth (November 27, and Infectious Disease/Food Allergy
sepsis and septic shock. BMJ. 1992; 2007). Janeway’s Immunobiology (7th and Anaphylaxis Network symposium.
304(6820):132–3. edition). New York: Garland Science. J Allergy Clin Immunol. 2006;117:391-7.
6 Medical Emergencies
in the Clinical Practice
Borle Rajiv M, Angik Richa

A variety of patients are treated in the patients are often ignorant and in the Obtaining history and detecting
clinic for varied ailments and with wide Indian circumstances illiterate also. early clinical signs of underlying medical
spectrum of procedures with variable They do not understand the impor­ condition is an art and needs conti­
degree of invasiveness. All the patients tance of disclosing the history of nuous practice. No clinician is immune
that are treated may not be healthy and medical conditions they suffer from to these mandatory and important
may have associated medical conditions to the surgeon, as they often feel it clinical steps at any stage of the carrier
which make them prone to develop is irrelevant and unnecessary. Some and they are required to be carried
complications when subjected to stress. patients purposefully tend to hide out religiously as a ritual. The medical
No person or no clinic is immune to the information about their medical history, direct and indirect questions to
complications and emergency situ­ illness for the fear of being advised obtain relevant information, physical
ations, similarly no clinician can rest to undergo some investigations or examination to know the medical condi­
assured that an accident will not occur opinion from the relevant specialist tions the given patient is having, so
in his clinic or an emergent situation which they feel unnecessary for under that suitable alteration in the surgical/
will never crop up with his patient going treatment for the present illness. dental treatment plan can be made to
in his carrier. If a clinician says that Similarly, some clinicians also tend to minimize the medical complications. In
he/she has never met with compli­ be casual towards the history taking the other words, the famous quotation
cations then there are only two possi­ and physical examination under the ‘to be forewarned is to be forearmed’ is
bilities that either this statement is pretex of paucity of time. It has been apt and practical.
false or the clinician never treats the observed very often in the clinical The average life expectancy has
patient. The medical emergencies do practice that a patient is asymptomatic increased due to advancements in the
not occur in the clinic alone, but can and when a blood pressure is recorded medical science and so has the aware-
occur at any place including home or or random blood sugar is assessed they ness for health care. Thus, more number
at any other public place. The patients turn out to be hypertensive or diabetic. of patients from the geriatric age group
may have predisposing medical illness On recollection of the events, they seek dental treatment. Such patients
or may have a hidden medical disorder come out with the history of headache, may have associated illnesses like
which the patient may not be aware of. blackouts, giddiness, feeling tired­ hypertension, IHD, diabetes as they are
Such patients have reduced capacity ness after moderate work or feel­ ing more prevalent in the elderly popu­lation
to withstand the increased physical of breathlessness, which they kept on and as fall out of the modern life­style
and psychological stress induced by ignoring for a long time. They never and food habits. The fast lifestyle has
exposure to the surgical procedure. consult the clinician and remain created paucity of time and the patient
It is therefore imperative to obtain undiagnosed and untreated for years as well as the clinician wants more and
detailed, relevant medical history of unless the symptoms are severe or more procedures to be done in lesser
the patient to get a forewarning and some complication precipitates. Such sittings thus, prolonging the duration
also perform relevant physical exami­ patients may not have any perceptible of the treatment and increasing the
nation to detect the clinical signs of the pro­blems otherwise, but when an addi­ stress associated with long duration of
hidden/unknown medical condition tional stress of surgery is imposed on treatment. Certain dental procedures
which may predispose the precipit­ them the decompensation takes place are time consuming and need to be
ation of the emergent situation. The and complications ensue. completed in a single sitting. All these
98 Principles of Surgery

factors contribute to increased stress do not occur. The stressful conditions opportunity to take suitable measures
and greater chances of vasovagal epi­ such as physical stress, pain, sleepless or alteration in the treatment plan to
sodes and other complications in the nights, poor dietary intake and anxiety prevent the complications. The medical
dental clinics. may impose additional stress and the conditions which can predispose such
The dental surgeon does not treat a physiological compensatory mechan­ complications are given in Box 6.1.
tooth, but he essentially treats a diseased isms may not be able to compen­sate for
tooth of a living individual. The tooth this additional stress imposed on the Classification of
never walks in the dental clinic, but body and get exhausted to precipitate
the person with a diseased tooth seeks a stage of decompensation to produce
Emergencies in Clinic
the dental treatment. It is therefore complications and emergencies which The emergencies occurring in the clinic
imperative to know the individual warrant urgent life saving inter­vention. If could be mild to severe and life- threat­
seeking treatment, thus, ‘never treat a not identified in time and left untreated ening. They could be further class­ified
stanger’. they may lead to life-threatening com­ as medical emergencies, surgical emer­
plications. An average dental clinic may gencies and the non-medical emer­
not be well equipped to combat these gencies, which could hamper the medi­
Predisposing Factors
emergencies nor may the requisite cal or surgical procedure or complicate
The medical emergencies can occur expertise be made available in time. the same if no backup mechanism is
more frequently in the patients, who Hence, it is of paramount importance in place (Box 6.2). The example being
have medical disorders. Usually during to identify those medical conditions power failure and no generator backup
the sedentary lifestyle the compensa­ or know the predisposing factors that in between the surgical procedure. The
tory mechanisms come into play and can lead to catastrophic complications. failure of hand piece or micromotor
due to the physiological compensa­ The preoperative identification of the during the removal of impacted tooth,
tory mechanisms the complications pre­disposing condition provides an failure of power saw during the oste­
otomy could be quiet disturbing if the
backup is not available. Explosions due
to presence of volatile liquids or gases
Box 6.1: Predisposing factors for medical emergencies
in the operating room could be of signif­
Physiologic conditions icant concern. The entire medical and
1. Extreme geriatric patients dental field has become mechanized
2. Pregnancy and technology dependent and the so­
Pathological conditions phisticated equipment have become a
1. CVS disorders reality in practice thus the aspect of fail­
a. Hypertension ure of equipment and keeping backup
b. Ischemic heart diseases (angina pectoris, old myocardial infarction) mechanisms has become more signifi­
c. Patients with previous coronary angioplasty or bypass surgeries
cant and relevant.
d. Cardiomyopathies
e. Disorders of rhythm (sinus bradycardia, ectopic beats, other arrhythmias) The common medical emergencies
f. Patients with valvular pathologies and prosthesis are fainting, bronchospasm, ischemic
2. Respiratory disorders attack, hypoglycemia to cardiac arrest,
a. Bronchial asthma etc. which can be fatal if not treated
b. Hyper-reactive airway promptly and the surgical emergencies
3. Endocrine disorders
a. Diabetes
are those which require active surgical
b. Addison’s disease intervention failing to which life can be
c. Thyrotoxicosis and hypothyroidoism endangered. The example being acute
4. Liver disorders respiratory obstruction secondary to
a. Cirrhosis aspiration of foreign body in the larynx
b. Hepatitis
or acute laryngeal edema in anaphylac­
5. Renal disorders—neprotic syndrome, glomerulonephritis, chronic renal failure,
azotemia, uremia tic shock or Ludwig’s angina warranting
6. CNS disorders—epilepsy, cerebrovascular accident immediate cricothyroidotomy or tra­
7. Drugs—long-term corticosteroid therapy, antihypertensive, barbiturates, aspirin, cheostomy to maintain patency of air­
oral hypoglycemic, insulin, prolonged therapy with diuretics leading to electrolyte way. Another example being acute hem­
imbalance particularly hypokalemia. orrhage requ­iring surgical intervention
8. Immunosuppressed conditions—HIV, TB, malnourishment, debilitating disorders,
to arrest the source of bleeding.
cachexia.
9. Psychological disorders—anxiety disorders The emergencies can be classified as
shown in box 6.2.
Medical Emergencies in the Clinical Practice 99

Box 6.2: Classification of medical emergencies gets reversed fast. The hallmark of
this condition is the vagal stimulation
• Medical emergencies
– Unconciousness
leading to vasodilatation, bradycardia
Causes—vasodepressor syncope, orthostatic hypotension, Addison’s crisis and pooling of the blood in the peri­
– Respiratory distress pheral veins. Diminished venous return,
Causes—bronchospasm, laryngospasm, hyperventilation, anaphylactic shock, diminished cardiac output and fur­
Acute pulmonary edema, LVF ther loss of perfusion pressure lead to
– Altered level of consciousness
diminished blood supply to the brain,
Causes—hypoglycemic shock, hyperglycemic shock, hypothyroidism, hyper­
thyroidism, CVA cerebral hypoxia and fainting.
– Convulsive disorders The brain is the vital organ which
Causes—status epilepticus, lidocaine overdose works through out the life even when the
– Adverse drug reactions person is sleeping the brain functions.
Causes- toxicity, allergic reactions, anaphylactic shock Thus, it requires the uninterrupted
– Chest discomfort/pain
supply of energy. The brain has only one
• Surgical emergencies
– Acute bleeding, e.g. rupture of viscera, PPH metabolic pathway, i.e. oxidative pho­
– Aspiration of foreign body in the stomach, larynx, trachea, bronchus sphorylation.
– Ludwigs angina (laryngeal edema) It means that the brain requires
– Acute appendicitis, perforation peritonitis, acute, fulminating cellulitis of limbs) uninterrupted supply of oxygen and
• Non-medical emergencies glucose for its metabolic activity and
– Electricity failure
– Failure of equipment
without it the functioning of the brain is
– Explosions due to volitile liquids and gases hampered. If the blood perfusion to the
brain is hampered, the brain malfunc­
tions and unconsciousness is pre­
Table 6.1: Stages of suncope, pathophysiology and clinical signs of syncope cipitated. The brain requires about 70 mL
of blood flow per minute/100 g of brain
Stage Causes Pathophysiological Clinical signs matter and about 3 to 5 mL of oxygen/
events min/100 g of brain matter. The glucose
requirement is about 5 to 7 mg/min/
Presyncopal Psychogenic stress— Release of • Tachycardia,
stage or fear, anxiety, emotional catecholamines and • Palpitations 100 g of brain matter. Any discrepancy
prodroma out break, extreme cortisol from adrenal • Tremors in this will lead to its malfunc­tioning
pain. cortex and sympathetic • Flushing and if it persists for a long may lead to
Physical stress—long nerves as a result • Raised BP, sweating irreversible damage or in very severe
upright posture, warm, of compensatory • Palmar sweating conditions procedure may lead to death.
humid environments mechanism for stress • Increased rate of
The patients seeking dental treat­ment
(Fright or flight respiration
phenomenon) are often apprehensive and ner­ vous.
There is a rampant belief in the population
Syncope Stimulation of • S ympathetic • Giddiness
mechanoreceptors withdrawl • Feeling of not well that the dental treat­ment, especially the
(c type afferent vagal • Vagal stimulation • Nausea, vomiting extraction of the tooth is very painful.
fibers in the heart) • Release of acetyl • Rolling of eyeballs Some people are very apprehensive and
choline • Fainting some have a phobia of surgical lights,
• Slowing of heart • Unconciousness environments of the hospital, sight of
• Peripheral • Bradycardia
blood, needles or sur­gical equipment and
vasodilatation • Hypotension
• Pooling of blood in • Feeble, low volume even the smell of the medicaments. On
veins of extremities pulse expo­sure to these things, stress is built up
and the splanchnic • Cold clammy skin and sub­sequently vasovagal attack pre­
area • Cold sweating cipi­tates. Such persons are nervous and to
• Cerebral hypoxia hide their fear, they are often extra talkative
or curi­ously look at the procedures carried
Vasovagal Shock/ this benign clinical condition (Table 6.1). out on other patients. Their palms are wet
It is defined as ‘the reversible loss of due to palmar sweating when handshake
Syncope/Vasodepressor consciousness secondary to transient is done with them, such patients need
Syncope cerebral ischemia’. to be identified and counseled before
Syncope or fainting are the terms which This is the commonly encountered the procedure is started to reduce their
are interchangeably used to designate clinical entity and usually benign and anxiety.
100 Principles of Surgery

Anxiety reduction protocols and pre­ Due to the vagal stimulation there is Clinical Presenation
me­di­cation with tranquilizers and atro­ a discharge of acetyl choline in the body
pine sulfate (vagolytic) is often bene­ which leads to bradycardia, reduced force Presyncopal Stage (Aura)3
ficial in averting the syncopal episode. of contraction, diminished cardiac output It is characterized restlessness, anxiety,
It is usually observed that the chil­ and peripheral vasodilatation. Thus, there tremors, palpitations, tachycardia, mar­
dren are least prone to have a vasovagal is expansion in the size of vascular bed and ginal rise in BP, feeling of warmth due to
attack as they cry and give way to their the blood is pooled in dilated peripheral the release of catecholamines in response
emotions. The females also give way to veins, especially that of the leg and to stress (fight or flight phe­n­o­menon).
their emotions readily by screaming and splanchnic area. This reduces the venous This is called aura or presyncopal stage.
thus they have relatively less incidence return, reduces filling of heart chambers
of the vasovagal attack as compared to during diastole and subsequently the Syncopal Phase
the young adult males. The latter group cardiac output also diminishes. The stimulation of vagus takes place
tries to hide their emotions and do The BP falls due to vasodilatation and the clinical sequence changes. The
not want to express their anxiety and (loss of peripheral vascular resistance), patient complains of not being well,
fear due to dominant ego. It builds an reduced cardiac output and reduced nausea, and sometimes actually vomits.
emotional stress within them which in force of contraction. All these events There is cold sweating, rolling of eyeballs,
turn precipitates a ‘fight or flight phe­ lead to a discrepancy between effective clenching, jerking and fainting.4
nomenon’ (release of adrenaline and circulating blood volume and blood There is severe bradycardia, and the
cortisol) to combat the stress and the available in the vascular reservoir. pulse volume is very low, that sometimes
reflex vagal stimulation takes place to There is hypotension, fall in perfusion it is not palpable in peripheral arteries.
precipitate the vasovagal attack.1 The pressure, leading to inadequate tissue There is hypotension and the patient
elderly males are matured and have perfusion and hypoxia. looses consciousness due to cerebral
had the experience thus they do not The brain is very susceptible to hypoxia. The extremities are cold clammy
succumb to the stress commonly. hypoxia and thus patient faints and falls. and the patient appears pale. The patient
The flat posture brings the feet and head falls down and the pulse improves and
Etiology to same level which improves venous gradual recovery takes place.5
Etiology can be divided in two varieties. return and improves cerebral blood
1. Psycogenic: Fear, anxiety, sight of flow. This brings about improvement Management6
surgical light, smell of medicaments, in cerebral perfusion, filling of heart The vasovagal shock is relatively be­
sight of blood, sight of surgical instru­ chambers and the cardiac output. At nign clinical condition. However, may
ments, emotional outbreak due to the same time the baroreceptors are sometimes lead to life-threatening
unpleasant news/event, pain, etc. also stimulated due to hypotension, complications like asystole and cardiac
2. Non-psycogenic: Long upright post­ which leads to abolition of vagal tone, arrest. Generally the proper positioning
ure, stress, starvation, secondary to sympathetic stimulation and gradual of the patient leads to recovery and no
acute adrenal insufficiency, etc. recovery takes place. The blood pressure active management may be required.
improves, bradycardia gets corrected, The treatment will ensure a speedy,
Pathophysiology2 the perfusion pressure improves and uneventful recovery. Management of
Due to any kind of stress on the body tissue perfusion is restored. vasovagal syn­cope is given in Box 6.3.
there is release of catecholamines and
corticosteroids in the body which is
Box 6.3: Management of vasovagal syncope
manifested clinically as tachycardia,
inc­reased myocardial contractibiliy, a. Stop the procedure
increased cardiac output, palpitations, b. Remove instruments—rubber dam, gauze, cotton from oral cavity
flushing, stimulation of sweat glands c. Position in head-low, feet-up position
resulting in sweating, rise in BP, as a d. Lossen tight clothing
e. Aromatic fumes inhalation, mist stimulant or sprinkle cold water on face for reflex
compensatory mechanism to combat
stimulation
the stress. This is called ‘fight or flight’
phenomenon or presyncopal stage. As If no recovery
a result of this stimulation, the vagal f. Injection Atropine 0.6 mgIM/IV
afferent C type fibers (mehanoreceptors) If no recovery
situated in the heart are stimulated, g. Look of other causes like hypoglycemia, Addison’s crisis (hydrocortisone, dextrose 25%)
which brings about the vagal stimulation h. Start BLS
i. Summon medical help
(see Table 6.1).
Medical Emergencies in the Clinical Practice 101

(see Box 6.3). If the patient does not


recover with his treatment early then
BLS should be started and possibility of
other causes should be evaluated.

Vasodepressor Syncope
Due to Acute Adrenal
Insufficiency7
The acute adrenal deficiency or adrenal
crisis is a potentially dangerous life-
threatening condition. The adrenal
glands are the paired glands with two
distinctly identifiable structures, a cortex
Fig. 6.1: Head low (Trendelenburg) position and the medulla. The adrenal cortex
secretes about 30 steroid harmones out
of which the cortisol, a glucocorticoid is
of great importance as it helps the body
to adapt to the stressful situations and
thus vital for the survival.
Addison8 (1855) described the
clinical signs of adrenal cortical defi­
ci­ency and it was named after him as
Addison’s disease, which is an inci­
dious and progressive condition. The
incidence of this condition is very low
(0.3 to 1, in 100,000) and occurs in both
the sexes and at all the sexes including
the infants. The clinical features are late
to occur and appear only after about
A B 60 to 70 percent of gland is destroyed.
Figs 6.2A and B: Compression of the inferior vena cava in During normal life the patient may be
supine position: (A) Supine; (B) Lateral asymptomatic, but under the stressful
conditions like exposure to the surgery
The patient is kept in a head low Thus, the pregnant females who the additional demand of cortisol can­
posi­tion, to facilitate venous return to land into a vasovagal shock are kept not be met with and the signs and
the heart and to ensure gravity assisted in left lateral position with elevation of
symptoms of acute adrenal deficiency
blood flow to the brain to correct the feet. The reflex medullary stimulation are precipitated. The adrenal gland of
cerebral hypoxia. The disadvantage is induced by inhalation of aromatic a normal adult secretes about 20 mg
with the head low (Trendelenbrg) posi­ fumes, asking the patient to swallow of cortisol, however in the stressful
tion (Fig. 6.1) is that the abdominal vis­ liquor of ammonia (mist stimulant), conditions additional quantities can
cera presses upon the diaphragm and which irritate the nasal and pharyngeal be secreted. The secretions of the
hampers the respiration by restricting free nerve endings, respectively and cortex are governed by the hypo­
the chest expansion. Hence, rather than induce reflex meduallary stimulation. thalamic-pitutary-adrenocortical axis.9
putting the patient in a head low position Sprinkling of cold water on face In the stressful conditions, this axis
it is desirable to give semirecumbent stimulates the cutaneous free nerve is stimulated and the levels of the
position (head, chest and abdomen are endings and lead to reflex medullary glucocorticoids are rapidly elevated in
in one plane as the patient lies in supine stimulation. Usually this will help the the blood.10
position, while the feet are raised to 30° to patient to recover however; if the brady­
facilitate the veinous return). cardia is intense then vagolytic drugs Predisposing Factors
The supine position is not desirable like atropine sulphate (0.6 mg IM or The patients who can land in an adrenal
in a pregnant female patient as the IV) may be injected. Corticosteroids crisis are:
gravid uterus will compress the inferior are usually not required but, they are • Patients with Addison’s disease—des­­
vena cava and obstruct the venous life saving if the vasodepressor syncope tru­ction of the gland due to tumors,
return (Figs 6.2A and B). is secondary to adrenal insufficiency infections, hemorrhage, thro­m­­bosis
102 Principles of Surgery

Box 6.4: Rule of TWO Table 6.2: Clinical features and management of adrenal insufficiency

• Patients on 20 mg/day of cortisol Predisposing Clinical features Management


therapy factor
• For two weeks or longer
• Within two years of dental/surgical • Addison’s disease • Weakness Conscious
treat­menta • On exogenous • Tiredness • Terminate the
steroid therapy • Fatigue treatment
Stressful condition • Nausea • Position with leg
• Traumatic injuries • Vomiting elevated
• Extensive dental • Constipating • ABC
Box 6.5: Clinical events in adrenal
procedure • Abdominal aim • O2 administration
deficiency
• Temperature • Diarrhea • Administer
change • Salt craving 100 mg of
• Weakness, fatigue
• Exercise • Postural dizziness hydrocortisone
• Orthostatic hypotension
• Muscle or joint pain and repeat every
• Severe hypotension
Sign 6–8 hourly
• Bradycardia
• Weight loss • Additional
• Loss of conciousness
• Hyperpigmentation supportive
• Hyperkalemia leading to skeletal
• Hypotension therapy
muscle paralysis
• Vitiligo Unconscious
• Hypoglycemia
• Articular calcification • Supine with leg
• Death occurs due to hypotension and
elevated
hypoglycemia
• BLS
• 100 g
hydrocortisone IV
or IM
• IV access
autoimmune disorders, adrenalec­
tomy for removal of tumors.
• Patients who are on long-term
steroid therapy (Rule of TWO— which are usually fatal, if not addressed Postural Hypotension12
patients on 20 mg/day of cortisol in time (Box 6.5).
therapy for 2 weeks or longer and Postural hypotension is also known as
within 2 years of dental/surgical Management orthostatic hypotension (Table 6.3).
treatment) (Box 6.4). The treatment comprises of (Table 6.2): Postural hypotension is defined as a
• Sudden withdrawal of the steroid • Supine position with feet elevation. disorder of autonomic nervous system
therapy. • Basic life support comprising of in which syncope occurs when patient
The stressful conditions that can maintenance of airway, ventilator assumes an upright position. It may also
precipitate the adrenal crisis in the support, nasal O2 at the rate of be defined as a drop in systolic pressure
com­promised patients are: 5 liters/min, establish IV line, cir­ by 30 mm Hg or greater and 10 mm
• Surgery cul­ a­tory support comprising of Hg fall in the diastolic blood pressure.
• Anesthesia inotropic support with dopamine Postural hypotension increases with
• Psychological stress drip (4 mg diluted in 5% dextrose). the age and is relatively uncommon in
• Alcohol intoxication • The drug of choice is sodium hydro­ infants and children. The systolic blood
• Hypothermia cortisone hemisuccinate in a dose pressure decreases by 2 mm Hg with
• MI of 100 to 200 mg IV as it is short each inch rise in the level of patients
• Acute infarctions acting and the action is prompt. The head above heart level and vice versa.
• Hypoglycemia dose may be repeated if required. There is an immediate drop in 5 to
• Fever Hydrocortisone is a glucocorticoid 40 mm Hg of blood pressure when an
• Asthma without any mineralocorticoid action. individual tilts from supine position into
Dexamethasone in a dose of 8 to upright position. The cardiovascular
Clinical Features of Adrenal Crisis 12 mg IV can also be given. It is a system brings the pressure to normal in
The clinical features of the adrenal crisis long-acting drug and initiation of 30 seconds to 1 minute.
are similar to that of vasodepressor action is late. Hence, it should not be
syncope. The patient becomes dizzy, given in the acute condition, but it
lethargic, hypotensive and looses con­ can be used for subsequent therapy Reflex Mechanisms
sciousness fast. The complications asso­ once the patient has recovered. It has Various reflex mechanisms are activated
ciated with this condition are severe a mineralocorticoid action and thus to maintain oxygen and glucose supply
hypotension and severe hypoglycemia, it is superior in subsequent therapy.11 to brain (Table 6.3).
Medical Emergencies in the Clinical Practice 103

Table 6.3: Pathophysiology, clinical events and management of postural hypotension

Predisposing factors Pathophysiology Clinical manifestation Management


•  dministration or ingestion
A Failure of the baroreceptor Prodromal • Assessment of consciousness
of drugs reflex mediated increase in the • Pallor • Activation of office
• Prolonged convalescence or peripheral vascular resistance in • Dizziness emergency system
recumbency response to postural changes • Blurred vision • Supine position
• Enadequate postural reflex • Nausea • ABC
• Late stage pregnancy • Diaphoresis • Administer O2
• Advanced stage • Postural hypotension • Monitor vitals
• Venous defects in legs Syncopal • Definitive management if
• Recovery from • BP low delayed recovery
sympathectomy for essential • Heart rate is normal or • Discharge
hypertension slightly raised
• Addison’s disease • May exhibit minor
• Physical exhaustion or convulsions
starvation Consiousness return once patient
• Chronic postural hypotension is supine
(Shy-Drager syndrome)

Table 6.4: Clinical features and management of hypoglycemia

Predisposing factors Clinical features Management


•  iabetics on oral hypoglycemia or insulin
D • Feeling of tiredness, fatigue, lethargy Conscious patient
who skipping meal or exposed to stress • Blurring of vision Terminate procedure
• Bizarre behavior Hypertonic glucose solution orally
• Starvation • Sleepiness Monitor vitals
• Slurring of speech Unconscious patient
• Hot humid stressful conditions • Lack of muscle coordination Supine position with elevation of feet
• Sweating—warm, moist skin Patent airway
• Mild tachycardia Nasal O2 @ 5 lit/min
• Headache IV dextrose 25% or 50%
• Altered level of consciousness/ Monitor vitals
unconsciousness Hydrocortisone 100–200 mg IV
• If untreated, coma and death occurs Injection glucagon 1 mg/kg of body weight

• There is reflex arteriolar contraction increase in the peripheral vascular resis­ During the homeostasis the excess of
mediated by baroreceptors located tance in response to positional change. glucose is converted in glycogen which
at carotid sinus and aortic arch Rapid decrease in blood pressure and is stored in the liver (Table 6.4).
increasing the heart rate. no change in the heart rate is pathogno­ During the stages of starvation this
• The arteriolar tone increases and monic for it. The patient does not exhibit glycogen is mobilized with the help of
the intrinsic and the sympathetic any prodromal signs. The patient looses glucagon and the cortisol. The insulin
stimulation causes venous constri­c­ consciousness, when the cerebral blood plays a major role in glucose absorption,
tion increasing the venous return. flow drops below the critical level. Syn­ its uptake and utilization by the tissue
• The reflex increase in respiratory cope is short lived, once the patient is and the conversion into the glycogen. In
rate and the venous return to right placed into supine position the blood the conditions of stress and starvation,
heart via change in intra-abdominal flow is returned and the conscious re­ glucose deficiency is precipitated and
and intrathoracic pressure. gained. the body meets its energy requirements
• Release of various neurohormonal by breakdown of glycogen into glucose
substance. (glycogenolysis) or by breakdown of
Hypoglycemia
If the cardiovascular system fails to proteins and fats (neoglucogenesis).
respond to the depressed blood pres­ Glucose is required for the metabolic The process of protein breakdown is
sure the patient goes into hypotension. needs of the body. The energy is derived referred to as catabolism.13
Postural hypotension is a result of a fail­ by oxidation of the glucose in presence of The normal blood glucose level is
ure of the baroreceptor reflex mediated oxygen to meet the metabolic demands. 80 to 120 mg/dl during fasting and 120
104 Principles of Surgery

to 140 mg/dL, postprandially. When on the body and are likely to land in properly and identify the subjects who
the blood glucose level falls below hypoglycemia. The inflammatory condi­ are likely to land in hypoglycemia and
70 mg/dL it is termed as a state of hypo­ tions of the jaws like pericoronitis, frac­ take proper precautions to avoid it.
glycemia. The brain is the most sus­ ture, painful ulcers hamper the dietary The detailed medical history, drug
ceptible organ to the hypoglycemia as intake. The patient is also stressed out due history, dietary habits and status, recent
it entirely depends on glucose for its to pain and sleepless nights and if such episodes of jaw pain which could affect
energy requirements for its metabolic patients are taken for performing dental/ dietary intake, sleepless night, and hot
functions.14 The alternative mechanism surgical procedures without proper eva­ humid environments must be taken into
of energy deriving is not present and luation and treatment are most likely to account. In presence of the positive his­
thus it gets affected fast and starts land in hypoglycemic attack. Hence, it tory, suitable alteration in the treatment
malfunctioning. If the blood sugar falls is important to understand that not only plan should be done to prevent hypogly­
further, the patient faints and becomes the diabetics, but also the non-diabetics cemia.18
unconscious due to the derangement of who are starving are liable to land in • Before taking up a patient for dental
the functions of the brain. The children hypoglycemia if due care is not taken.16 treatment one must ensure that
tolerate the hypoglycemia better than the patient has had his meal or
the adults and the lowered blood sugar Clinical Features breakfast. If the patient has missed
levels up to 50 mg/dL are tolerated and Hypoglycemia is a more dangerous morning dose of oral hypoglycemic,
hypoglycemia precipitates when the complication than the hyperglycemia it would not matter a marginal
blood sugar level falls below 40 mg/dL.15 as in the latter case plenty of time is hyper­glycemia is always acceptable
available to treat it and does not result in than the hypoglycemia.
Predisposing Factors for the mortality instantly. Hypoglycemia could • If the patient is to be operated under
be fatal if not treated promptly.17 GA and is kept fasting for 5 to 6 hours
Hypoglycemia As the patient becomes comatose prior to the surgery, intravenous dex­
apart from the damage to the brain the trose should be infused to pre­vent
Diabetics on Insulin or Oral
other complications secondary to un­ hypoglycemia.
Hypoglycemic Drug Therapy consciousness’ such as tongue fall, as­ • The diabetic patients should be given
If the patient is taking insulin or the drugs piration may occur which could be fatal preferably morning appointments
like biguanides or sulfonylurea deri­ (see Box 6.5). The hypoglycemia during so that they had a good sleep in the
vatives, it is necessary to keep nice balance the sleep is often considered more dan­ night and have properly rested and
between glucose intake and the drugs. gerous the patient is sleeping as when its not stressed.
As the drugs are important the glucose detection could be very difficult. Thus, • The long waiting in the waiting room
intake in the controlled manner is equally while treating the diabetic patients with should be avoided.
important. If such patient takes the drugs insulin or oral hypoglycemic the night • The environments should not be hot
and misses the breakfast or a meal the dose is often less and the patient is coun­ and humid.
chances of precipitating hypoglycemia seled for proper dietary regime (Box 6.6).
are high. Similarly during a non-stressful As the hypoglycemia is more serious Treatment of Hypoglycemia
condition the balance between the complication its timely identification and Once the hypoglycemic episode is identi­
action of the drug and dietary intake is treatment are of paramount importance. fied it requires a prompt treatment.
maintained and the hypo­glycemia does As the prevention is the best treatment
not precipitate. But, if such a patient is the clinician must evaluate the patient Treatment in a Conscious Patient
exposed to the stress and the glucose • Stop the procedure.
requirement increases for deriving more • Put the patient in a supine position.
Box 6.6: Clinical features of hypoglycemia
energy owing to increased metabolic • The environments should not be
needs, the increased needs may not be 1. Feeling of tiredness, fatigue, lethargy crowded and poorly ventilated.
met with and the hypoglycemia pre­ 2. Blurring of vision • Administer hypertonic glucose solu­
cipitates. Secondly, the glucose uptake 3. Bizarre behavior tion orally (70–100 g in 50–100 mL
and the utilization is also defective in the 4. Sleepiness water).
5. Slurring of speech
diabetics and thus they are the potent • Monitor the level of consciousness
6. Lack of muscle coordination
candidates for hypoglycemia in stressful 7. Sweating—warm, moist skin and the vital signs.
conditions. 8. Mild tachycardia The patient usually recovers fast.
9. Headache Additional therapy with IV dextrose
Starvation 10. Altered level of consciousness/ (25%) infusion or steroid administration
Even the non-diabetics who are starving unconsciousness is not required in a conscious patient if
11. If untreated, coma and death occurs.
fail to comply with the increased stress the hypoglycemia is diagnosed early.19
Medical Emergencies in the Clinical Practice 105

Treatment in an Unconscious lack of insulin (type I diabetes) or due in the liver (gluconeogenesis) takes
to improper uptake of the glucose by the place. The triglycerides are converted
Patient
tissue like muscles and adepose tissue into free fatty acids in the liver which are
• Place in supine position with feet (type II diabetes). taken up by the muscle to derive energy
slightly elevated. The glucose is also produced by and ketone bodies are generated as
• Maintain patency of airway. glucogenolysis in the liver. The appea­ metabolic end products which provide
• Establish IV line. rance level of the glucose in the urine is the breath a typical fruity and sweet odor.
• IV infusion of 1 to 2 ampules of called glycosuria. The glyco­suria occurs This stage is called diabetic ketosis.20
25 percent dextrose. The first ampule when the blood glucose goes above If the insulin deficiency is severe the
is administered fast. In very severe the renal threshold of 180 mg/dL. The the gluconeogenesis and ketogenosis
cases, 50 percent dextrose infusion is glycosuria could be due to increase in conti­nue to occur regardless of the blood
administered, which can be repeated blood sugar level after high carbohydrate glucose levels. The utilization of the
depending of recovery of the patient. meals (alimentary glycosuria), due to renal ketones may not keep pace with its pro­
• Glucagon: it can be given in a dose pathology (renal glycosuria) or sometimes du­ction and the ketones (acetoacetate
of 1 mg/kg of body weight, via im during pregnancy (pregnancy glycosuria). and beta hydroxybutirate) accumulate in
or iv route. The glucagon raises the The blood glucose in the diabetics is high the blood, decreasing its pH and this con­
blood sugar level by breakdown of and is the cause of persistent glycosuria. dition is called diabetic ketoacidosis. The
glycogen in the liver. The response The excretion of the glucose in the urine ketones decrease the myocardial contra­
to the glucagon is variable and the increases osmotic pressure of urine due to ctibility and the response of the arterioles
onset of action takes place in 10 to its large molecular size and draws water to the catecholamines. The excess of
20 minutes with peak action occur­ resulting in increased quantity of the urine ketone is excreted in the urine (ketonuria).
ring in 45 to 60 minutes. (polyurea). The ketoacidosis affects the respir­
• Epinephrine can also be given if The sodium and potassium are ation and the respiratory rate increases.
glucagon or 50 percent dextrose also drawn and excreted along with the The hyperventilation is an attempt by the
is not available. The epinephrine water. The presence of the ketone bodies body to counter the metabolic acid­osis
is given in a dose of 0.5 mg or promote secretion of the sodium and with respiratory alkalosis. The typical deep
1 ampule of 1:1,000 strength and is potassium in urine in the distal tubules and gasping type of respi­ration which has
administered by subcutaneous or to cause further wasting of electrolytes variable rate is called kussmaul breathing
IM route. The epinephrine raises resulting in electrolyte imbalance. respi­ration. The loss of respiratory effici­
the blood glucose levels, but it is The state of dehydration is produced ency leads to loss of consciousness and
not recommended to be used in which results in excessive thirst (polydi­ diabetic coma is precipitated. The very
hypertensive and patients with CVS psia). The inability of the body tissue high blood sugar level tend to dehydrate
disorders (see Table 6.4). to uptake the glucose, mobilization of the tissue including the brain.
• Monitor vital parameters. glycogen and triglycerides, depilation
• Basic life support. of the muscle mass as the aminoacids Etiology of Diabetic Coma
• Prevention of the tongue fall and are broken down to produce glucose The most common causes for diabetic
aspiration. and ketone bodies along with the loss coma21 are:
• IV injection of dexamethasone 4 to of water contribute to weight loss and • Severe insulin deficiency.
8 mg. increased appetite leading to polyphagia • Moderate insulin deficiency (hyper­
The blood sugar monitoring is done (Box 6.7). glycemic non-ketotic hyperosmolar
periodically to prevent the recurrence In absence of insulin, the breakdown coma).
of the condition and the patient is of glycogen into glucose (glycogeno­ • Poor patient adherence to treatment
monitored periodically. lysis), conversion of proteins into glucose regimen, diet control.
• Alcoholism.
• Severe infections.
Hyperglycemia Box 6.7: Clinical features of hyperglycemia
The blood glucose gets elevated after Clinical Feature
• H yperglycemia (bl glucose > 250 mg/dL)
a meal. It remains elevated for 2 to The Clinical features of hyperglycemia is
• Dehydration dry, warm skin, loss of tur­
3 hours later and is slowly reduced by gor, wrinkling of the tongue listed in Box 6.7.
renal excretion or by conversion into the • Fruity, sweet odor to breath
glycogen and uptake by the tissue due to • Kussumaul’s respiration Management
the action of insulin. The blood glucose • Tachycardia–thready, weak pulse The patient with the presence of clinical
level remains elevated in the diabetic • Normal or low blood pressure signs and symptoms is considered as
• Altered level of consciousness.
patients for a longer period either due ASA IV category risk for dental/surgical
106 Principles of Surgery

treatment. Hence, the consultation of stimulation (release of acetylcholine) • Supraclavicular, intercostal retr­action
the physician is necessary. However, if brings about the contraction and the and nasal flaring.
a patient is detected with hyperglycemia adrenergic (release of catecholamines) • Apprehensive and anxious.
and ketosis in the dental clinic the stimulation produces dilatation. In non- • Rapid shallow respiration (40/min).
following treatment may be started: asthamatic patients, the constriction of • Raised BP.
• Terminate the procedure and remove the smooth muscle protects the lungs by • Tachycardia.
dental material, instruments from contracting and preventing the aspira­ • Diaphoresis.
the mouth. tion when stimulated by foreign body. • Agitation.
• Put the patient in a supine position However, in an asthamatic patient the • Confusion.
with the legs slightly raised. response is exaggerated producing the • Cyanosis.
• BLS to be started. clinical signs of respiratory distress.
• Summon medical help. The bronchoconstriction is more pro­ Prevention
• Establish IV line and start IV infusion nounced in small bronchi and bron­ • History of asthma, hyper-reactive
with isotonic saline to keep the IV chioles 0.4 to 0.1 µm in diameter. The airway disorders.
line patent. inflammation of the airway and edema • History of allergic tendencies.
• Administer nasal oxygen through a and the secretions in an asthamatic pa­ • History of drug therapy.
face mask at the rate of 5 lit/min. tient also contribute to narrowing of the • Avoid local anesthesia solution
• Shift the patient to medicine emer­ bronchial lumen and airway obstruc­ containing epinephrine (as sulfites
gency. tion. are added to prevent oxidation of
• Insulin needs to be administered, The bronchoconstriction (spasm) epinephrine) in susceptible patients.
but has to be administered carefully can be induced by drugs like aspirin • Avoid drugs like aspirin, diclofenac
and only by the competent person through the activation of cyclo-oxygenase sodium, ibuprofen, valdecoxib, me­
where proper monitoring facilities pathway by release of vasoactive amines. fen­amic acid, piroxicam, keto­ pro­
are available. Normally crystalline Severe allergic reactions to the drugs can fen, rofecoxib, etc. (NSAIDS) in the
insulin is administered for rapid also lead to bronchospasm. asthematic patients and patients
action in place of depot insulin. The The other causes which precipitate hav­ing allergic tendencies.
dose of insulin varies depending on the asthamatic (bronchospasm) attack • Avoid physical and psychological
the blood sugar levels. Care must are: stress.
be taken to prevent hypoglycemia • Allergy to inhaled pollen, fungal • Perform cutaneous sensitivity test
as the latter is more dangerous. The spores, drugs like penicillin, vaccines, before injecting drugs in susceptible
hydration of the patients is main­ aspirin, sulfites used as preservative patients.
tained towards the higher side in local anesthetic solution. It is usu­
to flush out the ketone bodies by ally a type I hypersensitivity reac­tion Management
administrating high quantity of IV mediated through the IgE anti­bodies. • Terminate dental procedure and
fluids taking into account the renal • Lower respiratory tract infections. remove all materials and instru­
efficiency so as to prevent cardiac • Physical exertion. ments from the mouth.
overloading and congestive failure. • Psychological stress. • Keep the patent in the upright posi­
The IV fluids with dextrose are • Climatic conditions (cold). tion in a well-ventilated environ­
avoided.22 ment and loosen all tight clothing.
• The treatment in a comatose patient Clinical Features • Calm down the patient as anxiety
is similar except that it should be • Feeling of tightness in the chest/ can further complicate the things.
provided promptly and the life suffocation. • Basic life support
saving support as indicated be pro­ • Cough: Dry or productive. • Administration of O2 through face
vided timely and promptly. • Dyspnea. mask, nasal hood or nasal catheter
• Audible wheezing on inspiration at the rate of 5 to 7 L/min. The
Respiratory Tract and expiration. presence of hypoxia, hypercarbia
• Auscultatory rhonchi both inspir­ and cyan­ osis are indications for
Emergencies atory and expiratory (prolonged). oxygen admini­stration. In view of
• Patient prefers to sit or stand up as broncho­spasm little air enters the
Bronchospasm the breathlessness gets worse in zone of pulmonary ventilation, but
The entire tracheobroncheal tree con­ lying position. it must be ensured that whatever
tains smooth muscles which are con­ • Use of accessory muscle of respir­ation small quantity of air is reaching
trolled by the autonomous nervous like intercostals, sternom­astoid, abdo­ the lungs should be saturated with
system. The parasympathetic (vagal) minal, neck and truncle muscles. oxygen.
Medical Emergencies in the Clinical Practice 107

• Administration of bronchodilator Due monitoring of BP, heart rate Clinical Features


(in case of mild bronchospasm) and rhythm is warranted. • It is usually precipitated by anxiety
– Through the aerosol inhaler or – Other drugs like hydrocortisone and fear at the site of injection,
nebulizers the bronchodilator sodium succinate can be given in instruments (Table 6.5).
drugs like b-2 adrenergic agon­ a dose of 100 to 200 mg IV. It helps • The patient complains of tightness
ists (epinephrine, albuterol, iso­ in reducing the airway edema, of chest and suffocation and is
pro­terenol drugs) these drugs suppress antigen anti­ body rea­ unaware that he is overbreathing.
also have alfa agonistic action ction and also protects the tissue • Palpitations, tachycardia, chest pain.
and hence should be used judi­ against the adverse effects of The later could be difficult to differ­
ciously in patients with HT, dia­ hypoxia to certain extent. entiate from the angina attack and
betes, IHD, thyrotoxicosis. – Sedatives which can depress the thus, ECG may be useful.
– In severe bronchospasm apart respiration should not be given. • Dizziness, light headedness, visual
from the aerosol bronchodilators – The patients should be kept un­ abrasions, numbness or tingling
the drugs are required to be der follow-up to detect and treat of the finger tips and rarely tetany
administered intravenously for any recurrent episode of bro­ (carpopedal spasm). These signs
prompt relief as this is more chospasm. The follow up the­ are due to the fact that the PCO2
serious condition. rapy with aerosol sprays, oral or decreases from normal level of 35
The drugs like deriphyllin parenteral broncodilators like to 40 torr to less than 35 torr and the
(theo­­phylline and etofylline) can deriphyllin and steroids are pre­ pH of the blood increases to 7.55
be given by intravenous or intra­ scribed. from normal of 7.3 to 7.4, as a result
mus­cular routes. It can be given of hyperventilation. The changes
in mild to moderate cases of Status Asthmaticus are referred to as hypocapnia or
broncho­spasm or as a follow up The staus asthmaticus is the most severe hypocarbia and respiratory alka­
therapy after the acute phase is clinical form of the asthma and if not losis. These changes bring about
mana­ged. treated promptly may be fatal. The patient the cerebral vasoconstriction which
Injection of aminophylline experiences wheezing, dyspnea, hypoxia could explain the light headedness,
in a dose of 250 mg, diluted in and other signs and symptoms which do dizziness, giddiness and blurring of
20 to 50 ml of 5 percent dextrose not respond to the routine 2 to 3 doses of vision.
by slow intravenous route can the beta adrenergic drugs. It represents • Globus hystericus (feeling of foreign
be given. Aminophylline has true and severe medical emergency which body in the throat), epigastric dis­
beta agonist action which is could be fatal due to severe respiratory com­fort.
not selective and thus it also distress, hypo­tension, severe hypoxia, • Muscle pain/cramps, tremor, stiff­
stimulates the beta receptors in hypercapnea and acidosis. ness, rarely carpopedal tetany. As the
the heart and can produce arrhy­ The management is similar to that of pH of the blood increases to 7.5, the
thmias. To prevent the same, the acute, severe bronchospasm, but needs ionic calcium in the blood decreases
drug is always given in a diluted to be given promptly and aggressively. although the total calcium remains
form and slowly. Due monitoring normal. The decrease in the ionic
of the pulse and heart rhythm is Hyperventilation calcium results in the neuromuscular
necessary during administration The hyperventilation is defined as the irritability and excitability resulting
of amino­phylline. It can be given ventilation in excess of that is required into tingling, spasm, cramps, num­
as a slow infusion, diluted in one to maintain normal PaO2 (arterial O2 bness of hands and perioral region,
pint of 5 percent dextrose as a tension) and PCO2 (arterial CO2 tension). carpopedal spasm.
follow-up therapy after the acute It is produced either by increase in fre­
stage is over to prevent relapse of qu­ency or depth of respiration or both. Management
bronchospasm. Majority of the cases of hyperventil­ • Prevention by identifying the anxi­ous
Epinephrine is the most po­ ation are due to extreme anxiety however patients and alleviating the anxiety
tent bronchodilator and is the organic conditions like pain, metabolic by counseling and premedi­cation.
drug of choice in very severe and acidosis, cirrhosis, hypercapnia, drug • Terminate dental procedure and re­
life threatening bronchospasm. intoxication and central nervous disor­ move all the material from the mouth.
Epinephrine 1:1,000 is adminis­ ders can also cause it. • BLS
tered (0.5 mg), subcutaneously The hyperventilation secondary to • Calm down the patient by reassur­
or 1:10,000 (0.5 mg) is admin­ the anxiety is usually seen in the patients ance or drugs like diazepam 5 to
istered IV. Epinephrine 1:1,000 who do not give way to their emotions 10 mg or midazolam 3 to 5 mg by IM
should not be administered IV. and attempt to tough it out. or IV route.
108 Principles of Surgery

Table 6.5: Clinical features, precipitating factors and management of hyperventilation

Etiology Clinical features Pathophysiology Management

• Extreme anxiety Cvs • Increased rate and depth • Terminate procedure


• Pain • Palpitation. Tachycardia of respiration decreases • Position—comfortable in sitting posi­
• Metabolic acidosis • Precordial pain the co2 level leading tion
• Drug intoxication Neurologic to respiratory alkalosis • Abc
• Hypercapnea • Dizziness causing vasoconstriction • Remove foreign body and tight
of the cerebral vessels bindings
• Cirrhosis • Light headedness
and thus ischemia • Calm the patient
• Central nervous system • Disturbance of consciousness
• Catecholamine release • Correct alkalosis
disorder • Disturbance of alteration due to stress
• Numbness and tingling of Gaseous mixture of 7% co2 and 93% o2.
• Alkalosis resulting in
extremeties Patient asked to breathe in full face
decreased ionic calcium
• Tetany (rare) mask to breathe in and out co2 enriched
ions
Respiratory exhaled reservoir
• Shortness of breath • Drug management if necessary
• Dryness of mouth Diazepam (10–15 mg orally), mida­
Git zolam
• Globus hystericus • Subsequent dental treatment
• Epigastric pain • Discharge
Musculoskeletal pain
• Muscle pain
• Cramps
• Tremor
• Stiffness
• Carpopedal tetany
Psychological
• Tension
• Anxiety
• Nightmare

• Ask the patient to hold hands in front in either form may be subclinical to an Box 6.8: Clinical features of myxedema
of nose and mouth like a mask and acute life-threatening situation. • Large thick tongue
breathe the exhaled CO2 rich exhaled The clinical features of hypo­thyro­ • Intolerance to the cold
air in and out. The face mask or hood idism vary as per the age of its precipita­ • Muscle weakness
can be used to cover the nose and tion and vary in duration and the severity • Dry edematous skin with puffy hands
mouth to recirculate the exhaled air as per the degree of deficiency (Box 6.8). and face
• Lack of sweating
in and out during breathing. If it precipitates at early fetal life it re­ • Bradycardia, BP near normal
• The patient usually recovers with sults in Cretinism and if it precipitates at • Loss of hair from the brows, alopecia
time, calming down and rest. the adulthood it is called as Myxedema. • Lethargy, slow to speak and react
The hypothyroidism could be primary, • Hoarseness of voice
(thyroid gland dysfunction), secondary • Altered menstrual pattern in females
Hypothyroidism • Goiter
(pituitary dysfunction) or tertiary (due
The thyroid gland secretes the h­o­r­­­­ to dysfunction of hypothalamus) the
m­ones, thyroxine (T4), triiodo­thy­ro­­ myxedema is 3 to 10 times more com­
nine (T3) and calcitonin, which are mon in females. The basal metabolic sedatives and opioids which are com­
vital for the regulation of most of the rate is severly retarded in these patients monly used in dentistry and oral surgery
biochemical activities in the body. and their capacity to withstand stress for controlling anxiety and pain. The
The thyroid dysfunction could be due is severely compromised. The patients healing potential is also compromised
to overproduction (thyrotoxicosis) or who are not adequately treated for thy­ in such patients.
under production (hypothyroidism) roid deficiency are unusually sensitive The patient when exposed to stress
of these hormones. The dysfunction to CNS depressant drugs including the or drugs can land into a myxedema coma
Medical Emergencies in the Clinical Practice 109

characterized by severe hypothermia, • Definitive treatment comprises of Box 6.9: Clinical features of
hypotension, hypoventilation, hypoxia administration of massive doses hyperthyroidism
and hypocapnia. of T3 and T4, which need to be
• Anxious, nervous patients
continued for a long period even • Warm, wet, sweaty palms
Prevention of Complications after the recovery. • Tremors
The mortality rate after myx­ • Elevated BP
During Dental Procedures edema coma is very high, i.e. 40 • Tachycardia with raised sleeping pulse
to 50 percent and thus it needs to • Hyperdynamic circulation and functional
Proper identification of the patients
cardiac murmurs
having hypothyroidism is necessary be identified to prevent it and pre­ • Exophthalmos
by obtaining detailed medical his­tory, cautionary measures to be taken • Raised body and core temperature due to
drug history and the clinical mani­ rather than facing such severe com­ increased BMR
festations present, if any, before taking pli­cations. • Thyroid nodules.
such patients for the surgery, medical
con­sultation and proper treatment of Hyperthyroidism— Box 6.10: Clinical features of
hypo­thyroidism is mandatory.
The patients might be sensitive to
Thyrotoxicosis thyroid storm

seda­tives, opioids, antihistaminics, The thyrotoxicosis begins insidiously • Hyperpyrexia (105°C)


which may be avoided, as even with to produce a more severe crisis the • Cardiac arrhythmias
the normal dose the moderate to se­ thyroid storm. Although this is a rare • Acute pulmonary edema
• Profound delirium
vere over­dose reactions may be pre­ emergency it can be seen in the pati­ents
• Vomiting
cipitated. with untreated or inadequately treated • Diarrhea
patients of hyperthyroidism. The patients • Dehydration
who have thyrotoxicosis are unusually • Electrolyte imbalance
Management of Complications sensitive to epinephrine and it can • May be fatal if untreated.
The patient may loose consciousness in precipitate shooting of blood pressure
the dental office because of two possi­ to the dangerous pro­ portions, severe
bilities tachycardia and tachy­ arrhythmias.sensitized (Box 6.9). Similarly drugs like
1. Due to fear—in this case the con­ Such patients should be sedated before atropine, which is vagolytic should also
sciou­s­ness is regained after the rou­ the dental therapy, but the sedation be avoided. The use of atropine which
tine steps are undertaken. could be ineffective if the anxiety is increases the heart rate by suppressing
2. An undiagnosed, untreated patient not psychological and is hormonally vagus can initiate the thyroid storm.
having hypothyroidism looses the mediated. The thyro­toxicosis is usually The ‘thyroid storm’ differs from the
consciousness and fails to respond associated with cardiovascular disorders.severe thyrotoxicosis by the presence
to the resuscitative measures. The patients who are under treatment of hyperpyrexia (105°F) and may reach
In both the situations: and are euthy­ roid (normal levels of lethal level within 24 hours (Box 6.10).
• Stop the dental procedure. thyroid hormone) do not pose increased This is a severe stage of hypermetabolism
• Supine position with elevation of risk during the dental treatment. Hence, and the increased body demand of
feet. it is necessary to evaluate the patients energy puts additional load on the CVS
• Prevent tongue fall. with positive thyroid dysfunction historyproducing clinical signs and symptoms
• Periodic monitoring of vital signs. and take corrective steps to avoid the of cardiac dysrhythmias, cardiac failure
• BLS. serious complications (Box 6.9). and acute pulmonary edema. Thyroid
• Establish IV line. storm also produces profound delirium,
• Nasal O2 through hood or mask. Clinical Features vomiting, diarrhea and vomiting leading
• Warming blankets to protect The patients should be ideally euthyroid to a stage of dehydration and electrolyte
against hypothermia. before starting the dental therapy. imbalance.
• Summon medical help. Marginal cases can be treated with
• Pharmacological support symp­ due care, with slightly increased risk. Management
to­­matically, sodium hydrocorti­ The use of vasoconstrictors in local The untreated and undiagnosed patient
sone succinate 100 to 2000 mg, anesthetic solution should be avoided. of thyrotoxicosis is likely to become
inotropic support raises BP, at­ The epinephrine induces dysrhythmias, uncon­scious due to vasodepressor syn­
ropine to correct bradycardia, angina attacks and precipitate the cope and needs to be treated on lines
IV dextrose 25 percent to correct thyroid storm in hyperthyroid patients of treating any unconscious patient and
hypoglycemia. whose cardiovascular system is already basic life support needs to be provided.
110 Principles of Surgery

• Terminate the dental procedure Box 6.11: Precipitating factors agent. The aspirin therapy should be
• Supine position with elevation of the for angina attack discontinued 48 to 72 hours prior to
feet • Physical activity the dental extraction to facilitate new
• Start BLS • Hot, humid environment crop of platelets in the circulation
• Summon medical help • Cold weather and to prevent postsurgical bleeding
• Heavy meals
• Establish IV line episode. The decision to stop the
• Emotional stress (argument, anxiety,
• Nasal O2 sexual excitement) antiplatelet therapy should be taken
• Transfer the patient to medical • Caffine in consultation with the physician.
emergency department • Cigarette smoking • Reducing the length of the appoint­
• Definitive treatment with antithyroid • High altitude ment—the appointments should be
drugs (propylthiouracil) preferably in the morning. It is de­
• Additional measures comprise of sirable to prescribe sedatives a night
admi­­­nistration of propranolol to ssary to prevent life-threatening compli­ before to ensure the patient had a
block the adrenergic mediated ef­ cations. good sleep and rest and is fresh and
fects of thyroid hormone, high doses The steps in identification of the relaxed. The environments should
of gluco­corticoid to prevent acute high-risk individuals are: be cool and comfortable. The ap­
adrenal insufficiency, O2 admini­ • History of chest pain, tightness, pointments should be shorter so that
stration, cold packs to reduce body suffocation (dyspnea) on exertion the patient is not over stressed. If the
temperature, IV fluids to maintain • Any previous medical treatment the patient shows the signs of fatigue,
proper electrolyte balance and the patient is undergoing (sorbitrate, anxiety or lethargy, the vital signs
hydr­ation. antihypertensive, aspirin) should be monitored. The BP and
• Known cases, cardiac arrhythmias pulse may be elevated. The patient
Anginal Attack in the Dental or hypertension should be allowed to rest and then
Office • Thyroid disorders discharged.
The chest pain secondary to coronary • Diabetics. • The angina patients are the best
insufficiency is a common manifestation If the patient has a positive history candidates to be given O2 supple­
of ischemic heart disesase. The precise of angina pectoris, a consultation from ments through the nasal catheter or
description of this condition is “a chara­ the physician should be sought to know hood during the dental procedure at
cteristic thoracic pain, which is usually his coronary status and the severity of a flow rate of 3 to 5 liters, to minimize
substernal and usually preci­pitated by the condition. Suitable alterations in the chances of myocardial ischemia.
stress, exercise, emotions, heavy meal the treat­­ment plan and necessary pre­ • Pain control during the procedure—
and is characteristically reduced by cautions should be taken. The pati­ents the acute pain is extremely stressful
vasodilator drugs and rest”. with stable angina represent ASA-III risk and efforts must be made to avoid the
The pain is often described as tight­ while as the patients with an unstable pain in the angina patients. The pain
ness, stiffness, squeezing, suffo­ cating, angina (daily epi­sodes of angina pain) of a dental procedure is prevented
strangling rather than a sharp pain and represent ASA- IV risk. by appropriate local anesthesia.
is often radiates to the left arm, lower The use of vasoconstrictor should
jaw. Management of Anginal Attack be avoided. Instead of using vaso­
in Dental Office constrictor in local anesthetic solu­
Predisposing Factors • Stress reduction protocol with pro­ tion the long acting agents like bupi­
The patients who have coronary insuffi­ per counselling use of sedatives. vacaine should be used.
ciency may not have clinical symptoms The known cases of angina are often • Premedication with nitroglycerine—
at rest or during the sedentary life; how­ prescribed anti-platelet drugs like the nitroglycerine tablets (0.3–0.6 mg)
ever the coronary insufficiency mani­ aspirin. The aspirin therapy prolongs can be administered 5 minu­tes prior
fests as an angina attack due to the the bleeding due to loss of platelet to the treatment by sublingual route
precipitating factors (Box 6.11). aggregation. Aspirin irreversibly ace­ or 30 minutes prior to the treatment
The dental therapy is often stressful tylates platelet cyclo-oxygenase for by the oral route to prevent angina
and the patient is apprehensive and their life span of 8 to 10 days. Aspirin attack. The nitro­ glycerine tablets
anxious. Thus, prevention of angina therefore inhibits the production should be available chairside in case
episodes in the dental office, its early of proaggregatory thromboxane A2 the patient develops attack during
detection and management are nece­ and is also an indirect antithrombic the treatment.
Medical Emergencies in the Clinical Practice 111

Ischemic Attack in Dental Office ers have an additional advantage in potenti­ally more dangerous than
its antiarrhythmic action. 0.01 mg/mL of exogenous vasoconstric­
Management of the Ischemic
The opioids help only in reducing tor administered in the tissue, the use
Attack in the Dental Office the angina pain, but are not useful as of vasoconstrictors are a relative con­
• Terminate the dental procedure. they do not treat the cause, but are train­dication in patients on beta blo­
• The patient does not prefer to be only symptomatic in nature. ckers. Elective dental procedure is per­
in supine position and wants to sit. • Summon medical assistance and formed in patients with international
Place the patient in the comfortable shift the patient to medical emer­ normalized ratio (INR) 2 to 3 without
position. gency for the further management. the development of bleeding problems.
• BLS. The 80 percent of the patients presents
• Nasal O2 therapy. with angina like pain (Table 6.6). The
Myocardial Infarction
• Administration of vasodilators— pain is described like ‘there is heavy
the nitroglycerine can be given as Myocardial infarction23 (MI) is a clini­ rock or someone sitting on the chest’.
sublingual tablets (0.3–0.6 mg) and cal syndrome caused by a deficient A Levine sign (clench at the chest
can be repeated after 5 minutes if coronary arterial blood supply to a with fist) is present. MI is suspected
needed not to exceed 3 tablets in region of myocardium that results in when the first episode of chest pain is
15 minutes. The nitroglycerine eli­ cellular death and necrosis (Table 6.6). experienced on rest or during dental
mi­nates the angina pain in 2 to treatment. The patient may present
4 minutes dramatically. The action Predisposing Factors with previous stable pattern of angina
of the the nitroglycerine is to relax The predisposing factor for MI is the with either increased intensity or
the vascular smooth muscles and decreased blood supply to the coronary frequency.
produce vasodilatation of the coro­ arteries as occurs with the coronary
nary arteries, diminishing the vas­ thrombosis or increased in the level of
Cardiac Arrest
cular resistance and improving the cardiac workload without increase in the
coronary blood flow. It also causes oxygen supply as occurs in the stressed Cardiac arrest is the most serious compli­
decrease in peripheral vascular resis­ condition. The situation of decreased cation faced by a medical personnel. A
tance through arterial and more spe­ perfusion is called myocardial ischemia. prompt diagnosis and immediate CPR
cifically venous dilatation. It leads to The anterior descending artery is the can prevent many deaths.24
diminished venous return, decrease most common site for clinically signifi­ Definition: Cardiac arrest is defined
cardiac output and decrease in car­ cant atherosclerosis with the occlusion as the abrupt cessation of cardiac pump
diac workload leading to less O2 of the vessel and due to the lack of function that results in death, which
requirement by the myocardium. collateral circulation, infarction occurs may be averted if prompt intervention is
The side effects of nitroglycerine with myocardial necrosis through the instituted.
therapy include fullness and thro­ distribution of the occluded artery.
bbing headache, flushing, tachy­car­ The patient with myocardial infarction Etiology
dia and hypotension. The nitrogly­ should be identified and thorough • Hypovolemia
cerine therapy is contraindi­cated in medical history should be taken along • Hypoxia
the patients who are in hypotension. with the prescribed medication for the • Acidosis
The patients with coronary artery patient. • Hypokalemia/Hyperkalemia
spasm are known to respond to cal­ • Hypoglycemia/hyperglycemia
cium channel blockers, nife­de­pine Management • Hypothermia
(10–20 mg), when given sublingually. Post MI patients are on anticoagulants, • Drugs—tricyclic antidepressants,
The other examples of calcium chan­ beta blockers, ACE inhibitors, nitrates phe­­n­o­thiazines, beta blockers, As­
nel blockers are veripa­mil and diltia­ or calcium channel blocker. Elective pirin, acetaminophen
zem. The veri­pamil blocks the influx procedures should be avoided at least 6 • Cardiac temponade
of calcium ions and its supply to the months after MI. Acute problems should • Tension pneumothorax
myocardial contractile mechanism be managed pharmacologically first by • Thrombosis
and depresses the inotropic state and antibiotic and analgesics. The extraction • Thromboembolism
reduce the myocardial O2 consump­ should be done under more controlled • Trauma
tion. It also induces the coronary and environment. Stress reduction pro­
peripheral vasodilatation and helps tocol should be followed and sedation Clinical Features
in reducing the systemic vascular re­ is reco­mmended. Although the endo­ Clinical features of cardiac arrest is
sistance. The calcium channel block­ genous catecholamine released is given in Box 6.12.
112 Principles of Surgery

Table 6.6: Precipitating factors, clinical features and management of angina attack

Predisposing factors Precaution Clinical manifestation Pathophysiology Management


A 90%—Coronary • Stress reduction Symptoms Sudden occlusion of • Terminate procedure
artery disease • Oxygen flow at 3–4 • Pain—severe intolerable the major coronary • Diagnose—differentiate
B Obesity–Male in 5th L/min prolonged, 30 min artery due to acute anginal pain with non-
and 6th decade • Sedation n2O + O2 chocking, crushing, thrombosis, subintimal anginal pain.
C Stress • Pain control retrosternal pain, hemorrhage, or rupture • Position—usually upri­ght
• Less duration of radiating to left arm, atheromatous plaque is comfortable to the
treat­ment hand, epigastrium, leading to myocardial patient
• 6 months after mi shoulder, neck, jaw. ischemia, hypoxia, • Abc
• Nausea acidosis and eventually • Summon medical
• Vomiting infarction. Infarction assistance
• Dizziness causes alteration in the • Administer nitroglycerine
• Palpitations contractility of the heart (contraindicated in
• Cold leading to loss of function hypotensive patients)
• Perspiration to the extent to left • Antiplatelet therapy—
• Sense of impending ventricular damage aspirin—325 mg orally
doom • Manage pain—parenteral
Signs opioid, n2o + o2
• Restlessness • Monitor vitals
• Acute distress • Prepare and manage
• Skin pale and moist complication (cardiac
• Heart rate—bradycardia arrest)
to tachycardia • Transfer to hospital
emergency

Box 6.12: Identification of cardiac arrest results. More the time lapse in giving • Maintain patency of airway-neck
the CPR, more severe is likely to be extension, chin lift, oropharynegeal
• S udden and abrupt loss of conscious- the ischemic encephalopathy. The airway, intubation, suction
ness. brain does not stand hypoxia for more • If no breathing give 2 breaths mouth
• Absence of respiration (if preceded or
than 3 minutes and if the patient is not by mouth, mouth to endotracheal
intervened by respiratory arrest).
• Loss of central and peripheral pulses. resuscitated immediately, irreversible tube, ambu bag, etc.
• Heart sound not audible (blank cerebral damage can occur. • Look for signs of a pulse in peripheral
precardium). as well as major arteries (carotid,
Management femoral)
Management of cardiac arrest is divided
Presentations of Cardiac Chest compressions
into two protocols.
Arrest 1. Basic life support (BLS). The chest compressinons are done by
• Asystole 2. Advanced cardiac life support keeping the patient on a hard surface.
• Pulseless electrical activity (including (ACLS). The operator kneels down by the side
electromechanical dissociation) of the patient if the patient is kept on
• Ventricular fibrillation Basic Life Support the floor or stands by the side of the
• Pulseless ventricular tachycardia. bed. The heels of the hand are kept
Cardiopulmonary resuscitation25
The cardiac arrest can also be secon­ over each other and on the xiphoid
dary to: Cardiopulmonary resuscitation consists sternum without flexing at elbows, and
• Ventricular fibrillation. of three main parts, the ABC: not on the ribs as ribs can fracture with
• Ventricular asystole. 1. A—Airway compression. The sternum is depressed
The time elapsed from the event of 2. B—Breathing by generating force through the muscles
arrest is not known in the unwitnessed 3. C—Circulation of the trunk and compress 1 ½ to 2 inch.
cardiac arrest. Time available at disposal Steps: – Give 15 compressions
is very important. As the cardiac arrest • Establish unresponsiveness – Continue with 4 cycles of 2 breaths
takes place profound cerebral hypoxia • Check for breathing to 15 compressions.
Medical Emergencies in the Clinical Practice 113

Chest compression techniques • A smart blow on the chest can also • When a victim is unresponsive, the
• Position yourself at victim’s side stimulate the heart, but the chances tongue can block the upper airway,
• Make sure the victim is lying on his of fibrillations are high. the head tilt-chin lift maneuver
back on a firm, flat surface if the • Deliver compression in smooth lifts the tongue, reliving the airway
victim is laying facedown; carefully fashion at a rate of 100 compressions obstruction.
roll him into his back. per minute (Fig. 6.3). Things to avoid with head tilt chin
• Loosen or remove all cloth covering lift:
Opening the airway and giving the
the victim’s chest. You need to be • Do not press deeply into the soft
Breaths
able to see the skin. tissue under the chin because this
• Put the heel of one hand on the • Perform the head tilt-chin lift or jaw- might obstruct the airway.
center of the victim’s bare chest thrust maneuver in case of cervical • Do not use the thumb to lift the chin.
between the nipples. spine injuries. • Do not close the victim’s mouth
• Straighten your arms and position • Give mouth-to-mouth breaths to the completely (unless mouth to nose
your shoulder directly over your victim. breathing is the technique of choice
hands. • Give mouth to mask breath to the for the victim).
• Push hard and fast. Press down 1½ victim.
Mouth-to-mouth breathing
to 2 inch with each compression. Performing the head-tilt chin lift:
For each chest compression, make • Place one hand on victim’s forehead Mouth-to-mouth breathing is a quick,
sure you push straight down on the and push with your palm to tilt the effective way to provide oxygen to the
victim’s breastbone. head back. victim. The rescuer’s exhaled air contains
• At the end of each compression, • Place the fingers of the other hand approximately 17 percent oxygen and
make sure you allow the chest to under the bony part of the lower jaw 4 percent carbon dioxide. This is enough
recoil or re-expand completely. Full near the chin. oxygen to supply the victim’s need.
chest recoil allows more blood to • Lift the jaw to bring the chin forward. • Hold the victim’s airway open with a
refill the heart between chest com­ • The head tilt-chin lift relieves airway head tilt-chin lift.
pressions. Incomplete chest recoil obstruction in the unresponsive • Pinch the nose closed with your
will reduce the blood flow created by victim. thumb and index finger.
chest compressions.

Fig. 6.3: Steps in basic life support


114 Principles of Surgery

• Take a regular (not deep) breath and lift the jaw. Perform a head tilt- • Draw an imaginary line between
and seal your lip around the victim’s chin lift to open the airway. the nipples. Place two fingers on the
mouth creating an airtight seal. • While you lift the jaw, press firmly breastbone just below this line. This
• Give 1 breath (blow for 1 second) and completely around the outside will allow you to compress on the
watch for the chest to rise as you give margin of the mask to seal the mask lower half of the breastbone. Do not
the breath. against the face. press on the xiphoid process.
• If the chest does not rise, repeat • Deliver air over 1 second to make the • To give chest compressions, press
the head tilt-chin lift give a second victim’s chest rise. the infant’s breastbone down, but
breath (blow for 1 second). Watch 1/3 to 1/2 the depth of the chest.
Cardiopulmonary resuscitation for
for the chest to rise. • After each compression completely
children (1 year of age to puberty)
26
release the pressure on the breast­
Prevention of risk of gastric inflation
Infants and children who develop bone to allow the chest to recoil or
• Giving breaths too quickly or with cardiac arrest often do not have enough re-expand completely.
too much force, air is likely to enter oxygen delivery to the brain and heart • Deliver compressions in a smooth
the stomach rather than the lungs. and other vital organs even before the fashion at a rate of 100 compressions
This can cause gastric inflation. heart stops pumping blood. It is very per minute (see Fig. 6.3).
• Gastric inflation frequently develops important to give effective breaths
(breaths that make the chest rise) for Advanced Cardiac Life Support
27
during mouth-to-mouth, mouth to
mask or band to mask ventilation. infants and children during CPR. Advanced cardiac life support (ACLS)
Gastric inflation can result in serious is intended to achieve adequate venti­
Difference in depth of chest
complications, such as vomiting, aspi­­ lation, control cardiac arrythmias, stabi­
compressions
ration or pneumonia. Reduce the risk lize blood pressure and cardiac output
of gastric inflation by avoiding giving • Child age 1 to puberty: Press down and restores organ perfusion. The acti­
breaths too rapidly or too force­fully. 1/3 to ½ the depth of the chest with vities carried out to achieve these goals
To prevent gastric inflation: each compression. include:
• Taken 1 second to deliver each • Adult: Press down 1½ to 2 inches • Intubation with endotracheal tube.
breath. with each compression. • Defibrillation/cardioversion and/or
• Deliver enough air to make the For very small children you may use pacing.
victim’s chest rise. either one or two hands for chest • Insertion of an intravenous line.
compressions. Make sure you compress Ventilation with O2 (room air, if is not
Mouth to mask technique
the chest 1/3 to 1/2 the depth of the imm­ edi­ately available) may promptly
To use a mask, the lone rescuer is at the chest with each compression. reverse hypoxemia and acidosis. The
victim’s side. This position is ideal when speed with which defibrillation/cardio­
CPR for infants
performing 1-rescuer CPR because you version28 is carried out is an important
can give breaths and perform chest The infants BLS sequence is: element for successful resuscitation.
compressions when positioned at the • Airway When possible, immediate defibrillation
victim’s side. The lone rescuer will hold • Breathing should precede intubation and inser­
the mask against the victims face and • Circulation. tion of an intravenous line; CPR should
open the airway with a head tilt-chin lift. Steps: be carried out while the defibrillator is
Steps to use a mask to give breaths to • Check for response by tapping being charged. As soon as diagnosis of
the victim: infant’s feet. ventricular tachycardia (VT) and ventri­
• Position yourself at the victim’s side. • Head tilt chin lift maneuver. cular fibrillations (VF) is obtained, a 200
• Place the mask on the victim’s face, • Relief of airway obstruction by posi­ J shock is delivered. Additional shocks
using the bridge of the nose as a tioning. at higher energies, up to maximum of
guide for correct position. • Mouth-to-mouth and nose breath­ 360 J are tried if initial shock does not
• Seal the mask against the face— ing for an infant. successfully abolish VT or VF.
using your hand that is closer to the • Palpation of central pulse in an in­ Epinephrine 1 mg intravenously,
top of the victim’s head, place the fant finding the brachial artery. is given after failed defibrillation and
index finger and thumb along the attempts to defibrillate are repeated. The
Chest compression techniques in infant
border of the mask. Place the thumb dose of epinephrine may be repeated
of your other hand along the lower Two finger chest compression technique after intervals of 3 to 5 minute.
margin of the mask. in infant: If the patient is less than fully con­
• Place the remaining fingers of your • Place the infant on a firm, flat surface scious upon revision, prompt intu­
hand closer to the victim’s neck • Move or remove clothing from the bation, ventilation and arterial blood
along the bony margin of the jaw infant’s chest gas analysis should be carried out.
Medical Emergencies in the Clinical Practice 115

Intra­venous NaHCO3, is no longer con­ Drug Related anesthetic into biologically inactive
sidered routinely necessary and may be substance.
dangerous in large quantities, as it abol­
Emergencies29 • Body weight: The greater the lean
ishes the hypoxic drive of respiration. Local anesthetics are an integral part of weight, the larger the dose of the drug
The patient who is persistently acidotic the dental treatment plan. Whenever the individual can tolerate before an
after successful defibrillation and intu­ potentially painful procedures are overdose develops. This relationship
bation should be given 1 mEq/kg NaH­ considered, analgesics are prescribed for does not apply to obese person since
CO3 initially and additional 50 percent of relief of pre-existing pain or alleviation blood flow to adipose tissue is sparse as
dose repeated every 10 to 15 minutes. of potential postoperative pain, anti­ compared with that supplying muscle.
After initial unsuccessful defibrill­ biotics are used in management of The usual blood level of lidocaine in
ation attempts, with persistent electrical infection and central nervous system the brain required to induce seizure
inst­ability, bolus of 1 mg/kg lidocaine depressant are prescribed for all phases activity is 7.5 µgm/mL of blood. Hypo­
is given intravaneously and dose is of dental treatment for prevention and responsive patients may not exhibit
repeated in 2 minutes in those patients management of dentistry related fears. seizure until the brains blood level
who have persis­tent ventricular arrhy­ These four drug categories constitute attains a significantly higher level of
thmias or remain in VF. This is followed the overwhelming majority of all drugs lidocaine whereas hyperresponsive
by a continuous infusion at a rate of 1 used in the practice of dentistry. patients may exhibit seizures at brains
to 4 mg/min if lidocaine fails to pro­ Classifying adverse drug reactions— blood level below 7.5 µgm/mL of
vide control, other antiarrhythmic Pallasch30 proposed the following classi­ blood.
therapies should be tried. For persistent fication: • Pathological process:31 The pre­
hemodynamically unstable ventricular • Overdose—direct extension of the sence of pre-existing disease may
arrhythmia as, intra­­venous amiodarone, pharmacological action of the drugs. alter the bloods ability to transform
has emerged as the treatment of choice • Deleterious effects on chemically, ge­ a drug into a biologically inactive
(150 mg over 10 min, followed by 1 mg/ netically, metabolically or morpho­ substance. Most amide local anes­
min for up to 6 hours and 0.5 mg/min logically altered recipient. thetics undergo biotrans­for­mation
thereafter) intravenous procainamide • Initiation of immune or allergic in the liver, with a small percentage
(loading dose of 100 mg/5 min to a reaction. of drug unchanged in the kidney.
total dose of 500 to 800 mg, followed by Any disease state that reduces or
continous infusion at 2 to 5 mg/min) may Overdose increases hepatic blood flow is likely
be tried for persisting, hemodynamically A toxic reaction is a condition that to alter various pharmacokinetic pa­
stable arrythmias; or bretylium tosylate results from exposure to toxic amounts ra­­­­meters of amide local anes­thetic.
(loading dose 5 to 10 mg/kg in 5 min; of a substance that does not cause Patients with cardiovascular disease
maintenance dose 0.5 to 2 mg/min) may adverse effects when administration especially CCF demonstrate blood
be tried as an alternative for unstable in smaller amount. It refers to those level of local anesthetics almost
arrythmias. Intravenous calcium gluco­ clinical signs and symptoms resulting twice of those found in healthy indi­
nate is no longer considered safe for absolute or relative over administration vidual receiving the same doses.
routine administration. It is only used of its target organs or tissues. Clinical This difference results from several
in patients in whom acute hyperkalemia signs and symptoms of overdose are factors including a red­ u­
ced blood
is known to be triggering event for related to direct extension of the normal volume from drug distri­bution and
resistant VF, in the presence of known pharmacological actions of the drug. diminished hepatic blood flow
hypocalcemia or in patients who have Local anesthetic overdose reaction. secondary to low cardiac output.
received toxic doses of calcium channel • Genetics: It has been reported that
antagonists. Predisposing Factors with increasing frequency that
Cardiac arrest secondary to brady­ certain individual possess genetic
Patient factors
arrythmias or asystole is managed differ­ deficiency in the enzyme serum
ently, patient is promptly intubated, • Age: Drug absorption, metabolism cholinesterases reduced in the liver
CPR is continued, attempt is made and excretion may be imperfectly circulates in the blood and is respon­
to control hypoxemia and acidosis. developed in young age group or sible for biotransformation of two
Epinephrine and/or atropine are given diminished in older age groups. important drugs, i.e. succiny­lcholine
intravenously or by intracardiac route. Underdeveloped or decreased liver and ester type of local anesthetic.
The prognosis is generally very poor function may result in higher blood • Attitude and environment: The
in this form of cardiac arrest even with level of the drugs because the indi­ psychological attitude of the patient
successful electrical pacing. vidual cannot transform the local greatly influences the ultimate effect
116 Principles of Surgery

of the drug. This is considerably Table 6.7: Clinical features of local anesthetic toxicity
important with sedative hypnotics
and opioid analgesics. Signs Symptoms
• Sex: The only instance of sexual Low to moderate overdose levels • Headache
difference in the human occurs in • Confusion • Lightheadedness
females during pregnancy at which • Talkativeness • Dizziness
time renal function may be altered • Apprehension • Blurred vision, inability to focus
leading to impaired excretion of • Excitedness • Ringing in ears
• Slurred speech • Numbness of tongue feeling
certain drugs and their accumulation • Generalized stutter • Drowsiness
in the blood, potentially increasing • Muscular twitching and tremor of the • Disorientation
the risk of overdose. facer and extremities
• Drug factors: The drugs vasoactivity, • Nystagmus
dose and root of administration, • Elevated blood pressure
• Elevated heart rate
speed of administration, vascularity
• Generalized tonic clonic seizure followed
of the injection site and the presence by CNS depression, depressed blood
of vasoconstrictor influences the risk pressure, heart rate and respiration
of overdose.
• Prevention: Careful evaluation of the
patient before the start of treatment twitching and tremor, commonly noted teristically of a degree of severity related
along with careful drug administra­ in the muscles of the face and the distal to the degree of stimulation preceding it.
tion can minimize the risk of over­ parts of the extremities. The patient may Therefore, if the patient suffers intensive
dose in almost all situations. also exhibit nystagmus (involuntary eye tonic clonic seizures, postseizure dep­
movement). The blood pressure, heart ression is more profound, probably
Clinical Manifestation rate and respiratory rate increase. characterized by unconsciousness and
Onset, intensity and duration—rapid IV Headache may also be a symptom of respiratory depression or respiratory
injection produces signs and symptoms overdose (sec­ondary to local anesthetic arrest. If the stimulatory phase was
of overdose rapidly, with seizure or induced dilatation of cerebral blood mild (e.g. talkativeness or agitations),
unconsciousness may develop within vessels). In addition, many patients ini­ the depressant phase will also be mild,
seconds. These signs and symptoms tially re­port of having a generalized feel­ perhaps consisting of only a period
develop approximately 5 to 10 minutes ing of lightheadedness and dizzi­ ness, of disorientation and lethargy. Blood
after drug administration if plain anes­ i.e. different from that associated with pressure, heart rate and respiratory rate
thetic solution is administered and alcohol. These symptoms then prog­ress are usually depressed during this phase,
30 minutes if vasopressor is included. The to visual and auditory disturbances (e.g. again to a degree proportionate to the
severity of reaction is great, the reaction difficulty in focusing, blurred vision and degree of previous stimulation.
is self-limiting because of continued ringing in the ears [tinnitus]). Numbness Although the sequence just desc­ribed
redistribution and bio­trans­formation. of the tongue and perioral tissues represents the usual clinical ex­pression of
Signs and symptoms of local anes­ commonly develop, as does a feeling of local anesthetic overdose, the excitatory
thetic toxicity are given in Table 6.7. being either flushed or chilled. As the phase of the reaction may be extremely
Local anesthetics depress excitable reaction progresses and if the anesthetic brief or even absent. This is especially
membranes. The cardiovascular system blood level rises, the patient experiences true with lidocaine and mepivacaine, in
and CNS are especially sensitive and drowsiness and disorientation and may which overdose may appear.
are considered target organs for local eventually cause unconsciousness. Signs
anesthetic drugs. The usual clinical and symptoms of mild local anesthetic Pathophysiology
expression of local anesthetic overdose overdose may resemble psychomotor or
is one of apparent stimulation followed temporal epilepsy. CVS effect
by a period of depression. On intraoral injection the drug slowly
Minimal to moderate blood levels— Moderate to High Blood Levels enters the circulation. As the blood level
the initial clinical signs of overdose As the local anesthetic blood level rises, the systemic actions are noted
in the CNS are usually excita­ tory. At continues to rise, clinical manifesta­ depending on the blood level.
low over dose blood levels, the patient tions of overdose progress to a gene­ Zero to 1.8 µg/mL—normal blood
usually becomes confused, talkative, ralized convulsive state with tonic- level after intraoral injection.
apprehensive and excited; speech may clonic seizures. After this “stimulatory” No cardiovascular effect 1.8 µg/ml is
be slurred. A generalized stuttering or “excitatory” phase, a period of gene­ the minimal effective dose of lignocaine
follows, which may progress to muscular ralized CNS depression ensues; charac­ for antidysrhythmic action.
Medical Emergencies in the Clinical Practice 117

1.8 to 6 μg/mL—antidysrhythmic activity and an electroencephalographic functioning. To a degree, the body’s own
action. Can be used in the management pattern con­sistent with generalized CNS mechanisms can compensate for this;
of ventricular dysarthymia, especially in depression. Respiratory depression and however, respiratory and circulatory
ventri­­cular extrasystole and ventricular arrest are also noted. support can enhance the chances of
tachycardia. The fact that local anesthetics are survival significantly. If blood levels of
5 to 10 µg/mL—ECG alteration. CNS depressants on the one hand, but the local anesthetic rise even further,
There is increase in the P-R interval that CNS stimulation is the first clinical cardiovascular depression is produced
QRS duration and sinus bradycardia, manifestation of this depression may and respiration is increasingly impaired
myocardial depression and peripheral seem con­ tradictory. The stimulation by uncoordinated muscle spasm during
vasodialation. and subsequent depression produced the seizure. Brain function is affected
10 µg/mL and above—it leads to by high blood levels of local anesthetics even more through reduced cerebral
accentuation of the electrophysiological result solely from depression of neuronal blood flow and hypoxia.
and hemodynamic effects resulting in activity. The cerebral cortex receives Phentolamine mesylate32 accelerates
massive peripheral vasodilation and inhibitory and facilitatory (stimulatory) recovery from oral soft tissue anesthesia
intensive myocardial depression. The impulses. If it is considered that these in patients who have received local
heart rate decreases ultimately cardiac two groups of neurons are depressed anesthetic injections containing a vaso­
arrest may result. selectively by different blood levels of local constrictor. The proposed mechan­ism is
anesthetics, this seeming con­ tradiction that phentolamine, an alpha-adrenergic
Central nervous system effect
is explained. At anesthetic blood levels antagonist, blocks the vasocon­striction
Central nervous system (CNS) is extre­ capable of pro­ducing seiz­ures, the inhi­ associated with the epinephrine used
mely sensitive to the level of local bitory pathways in the cerebral cor­ in dental anesthetic formul­ations, thus
anesthetic. LA readily crosses the tex are depressed, not title stimulatory enhancing the systemic absorption of
blood brain barrier (BBB) progressively pathways. This depression of inhibitory the local ane­sthetic from the injection
depresses the CNS function. Till the pathways allows facilitatory neurons to site.
level of less than 5 µg there is no adverse function unopposed, lead­ing to increased
reaction. At cerebral blood levels excitation of the CNS and ultimately to Allergy
between 0.5 and 4.0 jig/mL, lidocaine seizures. As the local anesthetic blood Allergy is defined as a hypersensitive
can terminate various forms of seizure. level increases still further, stimulatory response to an allergen to which the
Most clinically useful local anes­thetics neurons are depressed along with individual has been previously exposed
possess this anticonvulsant property inhibi­tory neurons, producing a state of and to which that individual has develo­
(both pro­ caine and lidocaine having generalized CNS depression. ped antibodies. It manifests itself as
been used to terminate or decrease The duration of the seizure, although drug fever, angioedema, urticaria and
the duration of grand mal or petit mal primarily dependent on the local anes­ dermatitis, depression of blood for­ming
seizures). This anticonvulsant action thetic blood level, can be further modi­ organs, photosensitivity and anaphy­
may be related to a depression of fied by the acid-base status of the pati­ laxis. In marked contrast to overdose
hyperexcitable cortical neurons present ent. The higher the PaCO2, the lower the in which clinical manifestation related
in epileptic patients. local anesthetic blood level required to directly to the normal pharmacology of
As the blood level of lidocaine precipitate generalized seizures. In con­ the drug, the observed clinical picture in
rises above 4.5 jig/mL, early signs and trast, the lower the PaCO2 the greater the allergy is always a result of an exaggerated
symptoms of CNS alteration appear. drug blood level required for producing response by immune system.
These are usually related to increased seizures. Lowering a patient’s PaCO2 It is desirable that the patient who
cortical irritability (e.g. agitation, talk­ through hyperventilation raises the cor­ has history of drug allergies the cuta­
ativeness, and tremor). Numbness of the tical seizure threshold to local anesthet­ neous sensitivity must be checked by
tongue and perioral tissues may result ics and lessens the chance that a drug giving intradermal test dose. If the pati­
from the rich blood supply to these may cause seizures. ent is allergic to penicillin all the drugs
tissues, allowing the drugs to produce a Drug-induced seizures, in and of falling in the catagory of beta-lactam
blockade of the nerve endings. themselves, are not necessarily fatal. antibiotics should be avoided. Although
With further increase in cerebral However, the mortality rate in untreated the local anesthetics seldom evoke
blood level to 7.5 jig/mL or greater animals is more than 60 percent. allergic reactions it must be remem­
(lidocaine), generalized tonic-­ clonic The duration of the seizure appears bered that the preservatives used in the
seizures develop. Following this period to be a critical factor in determining local anesthetic solution are capable of
of CNS stimulation, a further increase the degree of morbidity. The convul­ producing allergic reaction.
in cerebral blood level of the local ane­ sing brain requires greatly elevated The milder allergic reactions can
sthetic results in termination of seizure oxygen and glucose levels to continue be treated with withdrawal of the
118 Principles of Surgery

drug evoking the allergy reaction and also adverse drug reaction. Psychogenic
Surgical Emergencies
admini­stration of antihistaminics and responses rarely occurs. Allergic reac­
steroids. The major or immediate type tion such as erythema or angioedema of The surgical emergencies encountered
of reactions such as bronchospasm to the mucous membrane and lips, are not in the dental office are hemorrhage,
frank anaphylaxis warrant aggressive uncomman after topical application of aspiration of the foreign body in the
and prompt treatment to prevent life- these drugs. The reason of high level of larynx, bronchus or the stomach.
threatening episodes. The details of toxicity is that it is absorbed rapidly and
the management of the anaphylactic the blood level rises rapidly. Safer use Hemorrhage
reaction is discussed in the Chapter 5, of topical anesthetics may be achieved Hemorrhage is defined as extravasation
on Shock. through either amide type topical an­ of the blood from the blood vessels. The
esthetics or benzocaine combined with commonly encountered hemorrhage is
Idiosyncrasy their judicious application. the postdental extraction hemorrhage,
Idiosyncrasy may be defined as an however, other causes like accidental
indivi­dual’s unique hypersensitivity to a Antibiotics injuries to larger blood vessels due to
particular drug, food or other sub­stance. Are given either prophylatically to slipping of knife or high speed rotary
CNS stimulation after the insertion of prevent infection or in special circum­ instruments can also lead to hemorr­
known CNS depressant drugs such as stances such as to prevent infective hage.
barbiturates or hista­mine blockers. Id­ endocarditis. To avoid development of
iosyncratic reaction covers an extrem­ resistance to bacterial strains and allergy Etiology
ely wide range of clinical expression any antibiotic should be used only when The common causes of postdental
type of expres­sion including depression therapeutic indication exists. The dose extraction hemorrhage are:
following adminis­tration of a stimulant, and the sequence of antibiotic admi­ • Local causes:
stimula­tion following administration of nistration should be monitored. The – Inflammation/granulation tis­sue.
depres­­sant. Hyperpyrexia following ad­ major advan­tage of oral administration – Damage to neurovascular bun­
ministration of muscle relaxant, such as of the drug is the decreased likelihood dle.
succinylcholine. of adverse drug reaction. If parenteral – Excessive soft tissue laceration.
administration of antibiotic, parti­ cu­ – Malignant growth.
Management
larly penicillin, is required the drug – Vascular lesions.
Because of the unpredictable nature of should be given only after the sensiti­- • Systemic causes:
idiosyncratic reaction their management vity test and in controlled circumstances – Coagulopathies—hemophilia
is of necessity symptomatic. The essen­ where the facilities for managing se­ A, B, deficiency of other clotting
tials of basic life support—P- A- B- C (po­ vere all­ergic reactions and emergency factors, afibrogenemia
sition, airway, breathing and circulation) management are in place. And the – Bleeding disorders—(ITP), thr­o­
are vital. If idiosyncracy represents as sei­ patient should be observed for about m­­bo­cytopenia, thrombasthenia,
zure the treatment protocol for seizure is 1 hour. von Willibrand’s disease
followed. – Hypertension
Analgesics – Liver disorders
Dentistry Drug-related The two major categories of analgesics – Renal disorders—uremia
are considered nonopoids and opoids. – Drugs—aspirin, anticoagulants.
Emergencies The NSAIDs such as ibuprofen and
The various drugs used in the dentistry naproxen are extremely popular and Management
are local anesthetics antibiotics and safe. Most adverse reactions are gastritis, The management of the hemorrhage
analgesics. nausea and constipation. Other effects should be undertaken promptly. One
are like headache, dizziness and pruritis. should not just rely on the local mea­
Local Anesthetics Major side with aspirin and other sures to arrest the hemorrhage as
The ester group of local anesthetics NSAIDs, includes mild urticaria, renal they may not be effective alone if the
carry a risk of allergic reaction, which tubular necrosis to bronchospasm and patient has systemic pathology like a
being the potential reason for the de­ fatal anaphylaxis. While prescribing the coagulopathy. Similarly, one should
velopment of the amide group of LA. NSAIDs care should be taken to avoid not delay the local measures for the
Although allergic reaction is rare, the prescribing them to the patients with want of investigations as by the time
common reactions to amide group of APD and asthma. Similarly, the patients the report of the investigations are
LA are psychogenic response (vasode­ should be instructed to take the drugs available, by that time sizable blood
pressor syncope and hyperventilation). after meals and H2 blockers or antacids loss can occur. Thus, the local measures
Topically applied local anesthetic may may be prescribed. should be started and simultaneously
Medical Emergencies in the Clinical Practice 119

Table 6.8: Investigations for the unknown bleeder and their interpretation • Investigations
BT Platelet APTT APTT Hemostatic Causes
– Screening investigations like BT,
Normal- 3–5 count defect CT.
minute by Duke’s – INR.
or Ivy methods – Platelet count.
I N N N Platelet von Willebrand’s disease – PT.
function, (vWD), aspirin therapy, – PPT.
Vascular uremia, storage pool defect – Individual factor assay (Table
disorder
6.8).
I D N N Thrombocy­ Secondary
topenia causes, Idiopathic
Thrombocytopenic Purpura
Investigations
N N I N Extrinsic Oral anticoagulants, • Bleeding time: Normal—3 to 5 min­
pathway Vitamin K deficiency, utes by Duke’s or Ivy methods
deficiency of Factor VII • The clotting time (Normal Lee-
(shortest half life) White 9–14 min)—prolongation of
N N N I Intrinsic Heparin, hemophilia A/B, CT is suggestive of coagulopathy,
pathway von Willebrand’s disease liver disorders, renal disorder
(vWD)
(uremia), anticoagulant therapy. It is
N N I I Common Heparin therapy,
usually prolonged in Factor VIII, IX,
pathways liver disease, vitamin
K deficiency, Oral XI, XII and rarely factor X deficiency.
anticoagulant therapy, However, it is just a gross screening
Factor V, X, II, I deficiency investigation and may not localize
I D I I Multiple DIC, Liver disease the defect accurately. The bleeding
pathways time may also be prolonged.
N N N N Mild von Willebrand’s • Torniquet test—positive test is
disease (vWD), vascular sugges­tive of capillary fragility and
disorder, platelet function
vitamin C deficiency.
defect, Factor XIII
deficiency • Platelet count (normal 250,000–
400,000/cumm) less than 70,000/
Abbreviations: I : Increased; N : Normal; D: Decreased cumm.
• Prothrombin time (normal 15 sec­
history should be obtained and if • Thermal onds by Quick’s method)—the pro­
necessary samples should be drawn for – Hot packs. longation of the prothrombin time is
appropriate investigations to diagnose – Cold compressions. suggestive of deficiency of Factor IV,
the systemic pathology. – Electrocautery. V, VII, X and fibrinogen deficiency.
• Chemical It is also prolonged in heparinized
Local measures
– Local application of thrombin. patients.
The local site of bleeding should be – Adrenaline packs. • Partial thromboplastin time—the nor­
properly cleaned of blood clots to facilitate Systemic measures mal time is to be standardized by each
proper inspection of the bleeding site to • History laboratory as it depends on the tissue
identify the source of bleeding, type of – History of bleeding disorders/ procoagulant used for this test. If it is
bleeding (arterial, veinous, capillary), episodes. Family history for coa­ prolonged it is suggestive of Factor VIII,
presence of granulation tissue, etc. to gulo­pathy or bleeding disorders. IX, XI, XII, II, V, VII and X deficiency.
facilitate selection of proper modality to – History of drug therapy like aspi­ • Combined evaluation of PT and PTT-
arrest the bleeding. rin, anticoagulants. Sometimes the – If PT is Prolonged and PTT is
• Mechanical: patient may not be aware of names nor­mal.
– Curettage of the granulation of the drug in such cases history of – If PT is normal and PTT is prol­
tissue. IHD, HT, coronary bypass surgery, onged.
– Pressure packs. angioplasty may be suggestive as • Thromboplastin generation test.
– Suturing. such patients are commonly pre­ • Individual factor assay—on the basis
– Ligation of the damaged blood scribed the drugs like antiplatelet of the above investigations if the de­
vessels. (Aspirin) or anticoagulants (Cou­ ficiency of a particular factor is deter­
– Application of the gel foam, marin derivatives). mined or suspected then the assay of
oxidized cellulose. – History of liver and renal disor­ that factor is to be done for diagnos­
– Application of bone wax. ders. tic and therapeutic purposes.
120 Principles of Surgery

Systemic Treatment If the foreign body is aspirated d. Increased BP


The systemic treatment comprises of: in the respiratory passage and if it is e. Tachycardia
• Establish IV line large it will get lodged in the larynx to f. Inability to speak
• Crystalloid infusion to replace the produce acute laryngeal obstruction g. Inability to cough
volume due to mechanical obstruction due h. Cyanosis.
• Injection of vitamin K to the foreign body and/or acute – Second phase (2–5 minutes)
• Injection ethambutol laryngospasm secondary to it. If the a. Loss of consciousness,
• Transfusion of the whole blood aspirated foreign body is small it will b. Decreased respiration
• Platelet rich plasma pass through the larynx into the tra­ c. Decreased BP
• Fresh frozen plasma cheas and subse­quently into the main d. Bradycardia.
• Platelet concentrates bronchus or small bronchioles, if the – Third phase (>4–5 minutes)
• Factor VIII concentrate. aspiration is assisted by the gravity. a. Coma
The foreign body is usually aspirated b. Absent vital signs
Aspiration of the in the right bronchus as it is vertical c. Fixed, dilated pupils not res­
and the left bronchus is oblique due ponding to the light
Foreign Body to presence of the heart on the left d. Death.
The aspiration of the foreign body side. The diameter of the trachea
(FB) during the dental procedure can and bronchus is small in children the Management
occur if proper care is not taken during chances of total obstruction are high in Although not routinely required every
the procedure. It can occur in the them even with the smaller objects. dental/oral surgical clinic must have a
anesthetized patients or in conscious The aspirated foreign body in the laryngoscope (working condition) and a
patients as well. In the latter case, therespiratory passage will not produce an Magill’s forceps. The identification and
immediate life-threatening emergency
foreign body is most likely to be aspirated prompt action are of vital importance as
in the esophagus than the trachea due to immediately unless it is lodged in the the airway obstruction is the major cause
the protective reflexes. However, it can larynx or the trachea and is of large of sudden cardiac arrest, especially in
be aspirated in the trachea as well. The enough size to cause complete obstruc­ the children.
common types of foreign bodies that tion. The partial obstruction warrants • As soon as the condition is recog­
can be aspirated are tooth, endodontic certain important steps to be undertaken nized, place the patient in the lateral
instruments, post and core or the rubber to prevent sub­ sequent problems like decubitus position.
dam clamps. infection. • Encourage the patient to cough
If the foreign body is swallowed vigorously.
accidentally in the esophagus it will Clinical Signs • If the foreign body is retrieved con­
not cause any respiratory distress, but • Partial obstruction sult the medical specialist before
does cause discomfort due to abb­ – Discomfort and feeling of foreign discharging the patient.
ression of injuries to the lining and body. • Back blow application and Heimlich
gives a persistent feeling of foreign body – Persistent and vigorous bouts maneuver,33 abdominal thrust, chest
sensation even after it is removed or of cough if the FB is in larynx or thrust.
has passed in the stomach. The foreign tracheobroncheal tree. • Laryngoscope to visualize the FB
bodies swallowed in the esophagus – Labored/paradoxical respi­ration. and if retrievable pick up with a
generally come out on coughing or pass – Wheeze. Magill’s forceps.
in the stomach and due to peristalsis are – Tachycardia. • X-rays to determine the site of FB.
passed in the stools. They seldom cause – Altered voice. This is possible only when the patient
any significant problems, however, – Cyanosis may be present. has partial obstruction and time is
sharp foreign bodies may injure the lin­ – Lethargy, disorientation due to available to do these exercises.
ing of the GI tract and produce clinical hypoxia. • Bronchoscopy to remove the FB.
manifestations. Periodic radiological • Total respiratory obstruction In more severe cases where the
examination to know the location of the – First phase (1–3 minutes) obstruction is severe and time is more
foreign body and examination of stool a. The patient is conscious precious efforts are made to establish
is necessary to confirm its safe passage b. Universal chocking signs, airway, if the FB is in the larynx then
in the stool. If the clinical symptoms inability to breath the cricothyroidectomy or tracheostomy
develop then the appropriate surgical c. Struggling paradoxical res­ should be performed immediately. Once
intervention is required depending piration and sounds without the air-way is established the rest of the
upon the site and type of pathology. air movements treatment for removal of the FB can
Medical Emergencies in the Clinical Practice 121

be undertaken. In the patients who are been given local anesthesia, where
cyanosed, hypoxic, unconscious appro­ the protective reflexes may be
priate life-saving therapy with oxygen compromised. This cannot be done
inhalation, pharmacological support in the patients who have exaggerated
to combat hypoxia, acidosis should be gag reflex. The pharyngeal packing is
started. the most effective way in the patients
The back slaps or blows are applied who are intubated, to prevent the
to remove the foreign body from the aspiration in the airway.
airway of the child or the infant. The • Chair position: trendelenburg posi­
child is saddled over the rescuer’s tion (head low) to prevent gravity
arm with head lower then the trunk, assi­sted aspiration of the FB in the
in a prone position (Fig 6.4). The back Fig. 6.4: Heimlich maneuver for infants airway.
blows or slaps are applied between the • Suctioning the oral cavity.
scapulae.34 • Ligating the dental floss to the
The manual thrusts are series of endodontic instruments to facilitate
exercises applied to the upper abdo­ easy retrieval.
men (abdominal or supradiaphramatic
thrust) or the lower chest (chest thrust). Maintenance of
They increase the intrathoracic pressure
suddenly, producing an artificial cough
Emergency Kit in the
to expel the FB. The abdominal thrust is office36 (Table 6.9 and
a soft tissue thrust and does not include Box 6.13)
pressure on the rib cage or sternum. It
can be given in a standing position when As it has been discussed earlier in
the patient is conscious and able to stand. this chapter it is quite clear that the
It can also be given in an unconscious dental or minor surgical procedures
A
patient when the patient kept in a supine are not immune to complications. The
position (Figs 6.5A and B). While doing complications may not be procedure
the abdominal thrust, the operator must specific and can be related to vital
apply pressure with the heels of the hand systems of the body because we treat
just below the rib cage. It is done in such the patient and not the tooth. The
a way that the damage to the rib cage and patient may have medical compro­
the intra-abdominal visceral organs like mise or underlying conditions that
liver and spleen is avoided. can precipitate a serious complication.
The chest thrust should be given as It is necessary that every clinician
an alternative to abdominal thrust in should have an adequate knowledge
special conditions like children below of clinical examination; he should be
age of 1 year (see Fig. 6.4), pregnant able to asses and identify the clinical
females and extremely obese victims, signs, interpret the investigations and
but it is strictly contraindicated in old should be able to at least suspect an
patients as the ribs are likely to fracture B abnormality so that proper evaluation
due to osteoporosis. Figs 6.5A and B Abdominal thrust, and consultation is done prior to the
Heimlich maneuver dental therapy and complications are
Prevention averted. The history taking is an art
In spite of conscious efforts of preventing Such accidents can be avoided by: and needs practice and patience to get
the aspiration of the foreign body, the • Application of the rubber dam relevant information from the patient.
small objects such as burs, endodontic • Oral packing: a pharyngeal curtain This skill can be sharpened by practice
instruments, inlays, debris fall into the can be created by placing 4 by 4 inch only. In the Indian circumstances due
oropharynx which can be subsequently gauze pad in the posterior portion to poverty and ignorance, the patients
swallowed or aspirated by the patient. of the oral cavity which effectively are undiagnosed and untreated for their
The concept of sitting dentistry where prevents the small particles or liquids medical disorders for years together and
the patient is kept in a supine or into the airway. The pharyngeal sometimes they are diagnosed only after
semisupine position in the dental chair curtain is especially useful in the a complication is precipitated. Many
enhances the chances of aspiration.35 patients who are sedated or have a times the patients feel that giving
122 Principles of Surgery

Table 6.9: Composition of the emergency kit37 or 1 mL ampoules, containing 1:1,000


adrenaline in water. It is the life-saving
Sl No Equipment Drugs drug in dire emergencies like cardiac
1. BP apparatus Adrenaline IP 1:1000 arrest, severe bronchospasm.
2. Stethoscope Atropine sulfate
3. Percussion hammer Sodium hydrocortisone succinate Dose
4. Torch (battery) Dextrose 25 and 50 percent • 0.2 to 0.5 ml subcutaneously or intr­
5. Larynoscope Aminophylline a­muscularly.
6. Magills intubating forcep Dopamine
• 0.25 ml diluted in saline, slow intra­
7. Water’s oropharyngeal airway Diazepam, midazaolam
8. Nasopharyngeal airway Fortwin venously.
9. Assorted endotracheal tubes Sodium bicarbonate • 0.5 ml intracardiac.
10. Sterile gloves Tab nitroglycerin
11. Artery forceps Injection nitroglycerin Indications
12. Needle holder Phenergan/avil • Allergic reactions, e.g. analphylactic
13. Scissors Promethazine (perinorm)
shock, angioneurotic edema of larynx
14. BP handle and blade Water for injection
15. Retractors Furosemide (lasix) (Injection is given intra­mus­cularly)
16. Nebulizer Aerosol spray epinephrine, salbutamol • Acute attack of bronchial asthma
17. O2 cylinder with flow meter IV fluids dextrose 5 percent Ringer lactate, normal (injection is given subcutaneously)
and humidifier saline • Cardiac arrest due to drowning,
18. Pulse oxymeter IV set electrocution, during stokes-Adams
19. AMBU bag Scalp vein set
syndrome and hypersensitive carotid
20. Face mask, hood IV cannula
21. Tourniquet suction catheters Disposable syringes with needles 2 mL, 5 mL, and 10 mL
sinus. The drug is more effective
in ventricular standstill. It can be
given as an intracardiac injection.
Box 6.13: Norms for maintenance of the kit 0.2 to 0.3 mL of 1:1,000 adrenaline
solution should be injected through
• It should be freely accessible
• The place for keeping the emergency kit should be constant and should not be changed.
a cardiac puncture, most commonly
The location should be high lighted by a placard or sign board. in the 4th or 5th intercostals space,
• All the staff working must be oriented towards it. 5 to 7 cm lateral to sternum. Before
• It should be periodically checked for the working condition of the equipment, shortfall injecting, make sure that the tip of
in the drugs, expiry date of the drugs and prompt rectification should be made. The the needle is in the cardiac chamber
list of contents should be pasted a chart on the cover of the kit for the convenience of
by withdrawing the blood, because
periodic inspection. When ever the drugs are used they should be immediately replaced
to maintain proper inventory. injection of adrenaline into cardiac
muscle precipitates ventricular fibril­
lation which offers resistance to
the history of medical disorders to a medical emergency department for the correction.
dental surgeon is unnecessary and if definitive treatment. It cannot be done • Hemostasis: Adrenaline in a concen­
one discloses the history the concerned unless the dental office is equipped with tration of 1:10,000 to 1:20,000 is used
doctor will advice investigations and necessary life-saving equipment and the topically to control bleeding from
medical consultation which as per the drugs. Thus every clinic must have an arterioles and capillaries, e.g. packs
patients point of view is unnecessary emergency kit and a place to resuscitate soaked in adrenaline solution are
and will only delay their dental treat­ the patient (Box 6.13). used to control epistaxis, bleeding
ment. Hence, it is more important on after tooth extraction, capillary oozing
part of a treating dental surgeon to be from large raw surface after excision
Emergency Drugs38
meticulous in history taking and in of a tumor, hemorrhage after hemorr­
clinical examination. The injectable (Inj.) drugs are stored in hoidectomy, etc.
In spite of due precautions, some­ ampules, vials or bulbs. The ampules • Along with local anesthetic: To pro­
times the complications occur and it is are single dose, while as the vials or l­
ong the action of local anesthetic
needless to say that it is the moral duty bulbs are multidose (Table 6.10). agent because of its vasoconstric­
of the treating doctor to be able to give tor ef­fect, adrenaline 1:100,000 or
necessary first aid treatment and BLS Injection Adrenaline IP 1:200,000 concentration is given along
to the patient to keep the patient safe Adrenaline tartrate is manufactured with local anesthetics. Adrena­ line
until the competent medical help is under the trademark of adrenaline. should not be used for finger block or
available or the patient is shifted to the Injection of adrenaline is available in 0.5 ear lobule or for local ane­sth­esia on
Medical Emergencies in the Clinical Practice 123

Table 6.10: Emergency drugs

Name of the drugs Dose Indications/uses

1. Atropine sulfate (anticholinergic) 0.6 mg IM/IV 1. Vasovagal shock


2. Prevention of bradycardia
3. Preanesthetic medication
4. To reduce salivary secretions.
2. Adrenaline tartarate 1:1000 0.5–1.0 mg IV/SC or intracardiac, to be 1. Cardiac arrest
repeated every 5 minute 2. Anaphylactic shock
3. Severe laryngobrancheal spasm.
3. Dexamethasone 4–20 mg of base im or IV 05–50 mg per 1. Cereberal edema
day orally 2. Allergic conditions
3. Anti-inflammatory
4. Shock
5. Immunosuppression
4. Sodium hydrocortisone sodium 100 mg IM/IV Stat; may be repeated once 1. Shock
succinate/hemisuccinate (short-acting or twice 2. Status asthmaticus
glucocorticoid). TN-lycortin S. 3. Acute adrenal insufficiency
4. Anaphylactic reaction
5. Allergic reaction.
5. Pheniramine maleate. TN- avil Orally—25­­–50 mg tabs 1. Allergic reactions
25 mg 1 tid 2. Rigors
50 mg 1 bid 3. Sedative
ampule—1–2 mL IM 12 hrly 4. Anaphylactic shock
Vial 1–2 mL IM 12 hrly 5. Angioneurotic edema.
6. Promethazine hydrochloride. TN- Orally, 10 mg, 2 mg tabs 1. Allergy
Phenargan Injection 2 mL 2. Nausea.
7. Diazepam (benzodiazepine derivative. Orally 5–40 mg 1. Antianxiety
Note: It should not be mixed with other Injection 10 mg, 3–4 times IV 2. In acute muscle spasm
drugs for IV infusion. 3. Spastic neurological disease
4. Tetanus
5. Electroconsulsive therapy
6. Orthopedic manipulation.
8. Deriphyllin (bronchodialator). 2–4 mL. Up to 2–3 time daily IV. (2 mL in 1. Bronchial asthma
Ethophylline 169.4 mg, 1 minute IM and sc also; as a combined 2. Cardiac insufficiency
   Theophylline 50.6 mg, per 2 mL injection with dextrose). 3. Central respiratory disorder
injection. 4. Renal and cardiac edema.
9. Aminophylline (methylxanthine) 250–500 mg diluted in 20–50 mL of 5% 1. Status asthmaticus.
dextrose; infuse IV over 20–30 minute
repeat as required
10. Mephentermine (adrenergic drug). Orally 10–20 mg tabs or IM or IV (to 1. Shock in myocardial infarction
TN-mephentine prepare iv drip 2 vials of 30 mg. Each are 2. Hypotension due to spinal anesthesia
added to 500 mL of 5% dextrose sol) 3. Other hypotensive states.
11. Dopamine( adrenergic alfa and beta 0.2–1.0 mg per minute 1. Shock cardiogenic
agonist) 2. Severe congestive heart failure.
12. Frusemide. TN- lasix Orally, 40 mg tabs. In edema 20–80 mg. 1. Edema in congestive heart failure
Single dose daily 2. Hepatic or renal disease
3. Toxemia of pregnancy
4. Mild and moderate hypertension
5. Cereberal edema.
13. Isosorbide dinitrate. TN-sorbitrate Sublingual 5–10 mg for immediate action, 1. Angina pectoris.
orally 5–10 mg 6 hourly.
14. Pentazocin. TN-fortwin Orally 50–100 mg tabs 1. Moderate to severe pain after surgery
30–60 mg im/sc 2. Trauma, colic, burns
3. Preanesthetic medications.

Contd...
124 Principles of Surgery

Contd...

Name of the drugs Dose Indications/uses

15. Metoclopramide. TN- perinorm. (more 25–50 mg IM orally, 5–10 mg thrice daily 1. Premedication
effective if combined with H2 blocker) 2. Migraine
3. Antiemetic.
16. Ringer lactate 1 pint 2 pint IV 1. Dehydration
2. Burns.
17. Dextrose ampule 25–50% 1–2 amp Hypoglycemia/Hypoglycemic shock
18. Hemaccel(plasma expander) 1 pint Hypovolemic shock.
19. Sodium bi carbonate 1 mL mole/kg body weight 50% of dose Metabolic acidosis.
repeated every 10–15 min IV
20. Spirit of ammonia 1 drop in nose Reflex stimulation in fainting or hysteria.
21. Normal saline 1 pint 2 pint 1. Hypo-osmolality
2. Vehicle for intravenous drug administration.
22. Oxygen 3–5 lit/min 1. Hypoxia
2. Shock
3. Cardiorespiratory failure.
23. Pethidine 50 mg IM 1. Severe pain
2. Preanesthetic medication.

the penis because there are chances (acidic) resulting in a concentration of solution is given by intravenous drip,
of gangrene of these struc­tures are 4 mcg/mL. After judging the response commencing at the rate of 2 mcg/kg/
supplied by end arteries. with a test done of 2 to 3 mL, solution is min (one drop of this solution contains
• To have bloodless field: 1:100,000 to administered at the rate of 0.5 ml per 26.66 mcg or 400 mcg in 15 drops, i.e.
1:200,000 solution is injected subcu­ 1 minute, according to the blood pres­ 1 mL) to a maximum dose of 50 mcg/
taneously before thyroi­dec­tomy and sure response. If noradrenaline is to kg/min or till central venous pressure
palatal surgery. be used and infused in normal saline, (CVP) is 10 to 15 cm of water.
vitamin C (500–1000 mg) should be Dopamine drip should not be conti­
Adverse Reactions added to make the solution acidic. nued for more than 72 hours otherwise
• Palpitation, tremors, pallor, head­ it will lead to tachyphylaxis.
ache. Indications
• If injected rapidly and intravenous­ • Treatment of hypotension of circul­ Indications
ly, adrenaline may cause sudden atory failure. • Hypotension with inadequate card­
marked increase in blood pressure, • Hypotension following removal of iac output, to increase peri­ pheral
precipitating subarachnoid hemorr­ chromaffin cell tumors. circulation.
hage and hamiplegia. • Open heart surgery.
• Ventricular arrhythmias. Side Effects • Renal failure (renal vasodilator dose
• Acute pulmonary edema in patients • Same as for adrenaline. is 1–2.5 mcg/kg/min).
with cardiac decompensation. • Extravasation in subcutaneous tissue • Cardiac failure.
• Anginal pain. causes necrosis of the skin. • Shock.

Injection Noradrenaline Injection Dopamine Precautions


Injection noradrenaline is available as It is available in 5 ml ampoule, con­tai­ • With the rate of 50 mcg/kg/min,
0.2 percent solution in 2 ml (2 mg/mL) ning 40 mg/ml solution. It is a vasopre­ ensure adequate urinary output.
ampules. It is inactive in neutral pH. It is ssor given in cases of hypo­ten­sion. • It should be administered via a central
a vasopressor. vein. Extravasation may cause local
Dose ischemia. If any extravasation is
Dose A 5 mL ampoule, containing a total of noted, the area should be infiltrated
2 mL of noradrenaline is added to 200 mg solution, is added to 500 mL of immediately with 10 to 15 mL of
1000 mL of 5 percent dextrose solution normal saline or 5 percent dextrose. The normal saline containing 5 to 10 mg
Medical Emergencies in the Clinical Practice 125

of phentolamine as soon as possible • Acute myocardial infarction (effu­ • Blurring of vision and precipitation
to prevent sloughing and necrosis in sion bradycardia). of glaucoma in elderly patients.
ischemic areas. • Antihypertensive. • Skin rash and local dermatitis.
• Over dosage not responding to
withdrawal of drip should be treated Side Effects Precautions
with phentolamine or other alpha- • Congestive heart failure (CHF), bra­ • In the elderly, the drug precipitates
adrenergic blocking agents. d­y­cardia, aggravation of A-V condu­ glaucoma and causes retention of
• Smaller dosage and special care ction defects. urine
are neces­ sary in patients recently • Bronchospasm. • In chronic lung diseases it dries up
treated with monoamine oxidase • Hypoglycemia unresponsiveness. secretions.
(MAO) inhib­itors. • Nausea and vomiting.
• Dopamine should not be added to • Uterine hypomotility and prolonged Injection Hydrocortisone
sodium bicarbonate or other alka­ labor. Hydrocortisone hemisuccinate powder
line intravenous agents. • Thrombocytopenia and leukopenia. is available in a bulb containing 100 mg
• Dopamine should not be with­drawn hydrocortisone, reconstituted with 2 mL
spontaneously as due to the devel­ Injection Atropine Sulphate of water for injection. It is a short-acting
opment of dopamine depen­dence, • 0.65 mg/mL (1 mL) ampules: glucocorticoid usually preferred for
sudden withdrawl leads to severe – As a preanesthetic medication, immediate action in emergencies. It lacks
hypotension. intramuscularly, 30 minutes be­ mine­ralocorticoid action.
fore surgery to prevent vaso­vagal
Contraindications shock and also to dry out the se­ Indications
• Pheochromocytoma. cretions if general anesthesia is to • Life-threatening emergencies, e.g.
• Uncorrected cardiac tachyarrhythy­ be given. anaphylactic shock, status asth­
mias. – Before pleural taping, ascetic tap­ maticus, hypoglycemia, thyrotoxic
• Ventricular fibrillation. ing, intercostals tube insertion, etc. crisis, Addision’s crisis, hypercalce­
Stop or decrease the dosage, if – In treatment of colics and dys­ mia, etc.
– urine output is diminishing. menorrhea, along with mor­ • Intra-articularly in osteoarthritis,
– There is increase in tachycardia. phine painful fascial nodules, etc.
– There is development of new arrhy­ – Bradyarrhythmias. • Topically injected in the treatment
thmias. – Parkinsonism—to relieve trem­ of keloids.
ors and rigidity. • As retention enema, 100 mg hydro­
Injection Propranolol • 6 mg/mL (1 mL) ampules: In the cortisone dissolved in 120 mL of
It is available in 1 mg/mL ampules. It is treat­ment of organophosphorus normal saline is given each night in
nonselective beta blocker. poisoning, 2 to 4 mg atropine sul­ the treatment of ulcerative colitis.
phate is injected by slow intra­ • Delays wound healing.
Indications
venous injection. More atropine is
• Thyrotoxic crisis: Along with other given depending upon the severity Injection Aminophylline
measures, e.g. hydrocortisone, cool­ of intoxication and response to first This drug is available in a 10 mL ampule
ing measures, intravenous fluids, dose to maintain full atropinization. (250 mg/10 ml). It is potent bronchodi­
etc. Propranolol (intravenous) injec­ In severe cases the dose is repeated at lator.
tion 2 to 10 mg is given slowly with 5 to 10 minute intervals. The patient’s
cardiac ECG (electrocardiogram) respiration, blood pressure, pulse Dose
monitoring and is repeated every and salivation should be observed 250 mg diluted in 20 mL of 10 per­
4 hours. to prevent over-atropinization. The cent glucose is injected intravenously
• Pheochromocytoma: Alpha–adren­ pulse rate should not be allowed to and very slowly or given in 5 percent
ergic blocking agents to reduce exceed 120/min. dextrose drip. It is not given undiluted
blood pressure in pheochromocyto­ • As a preanesthetic medication to pre­ and fast as it can produce severe
ma may lead to severe tachycardia, vent bradycardia and reduce secre­ cardiac arrhythmias. The monitoring of
giving propranolol 1 to 5 mg intra­ tions. pulse during the administration is very
venously controls this complication. important.
However, beta-blockade may lead Side Effects
to severe hypertension in pheochro­ • Reduction in salivation, leading to Indications
mocytoma. dry mouth and dysphagia. • Bronchial asthma.
• Cardiac arrhythmias. • Retention of urine. • Cardiac asthma.
126 Principles of Surgery

• Cheyne-Stokes respiration. Injec­tion Dose • Focal seizures in head injury.


may be followed by an intravenous 50 to 100 mg intramuscularly or intra­ • Cardiac arrhythmias, espically digi­
infusion at the rate of 1 mg/kg/h venously, but slowly. talis induced cardiac arrhyth­mias.
to maintain therapeutic level or • Chorea.
injection can be repeated after every Indications • Trigeminal neuralgia.
4 hours. Same as morphine except acute left
ventri­cular failure (IVF). Side Effects
Side Effects • Intolerance.
• Nausea, vomiting. Side Effects • Cerebellar ataxia.
• Epileptiform fits, preceded by twit­ Same as morphine. • Nausea, vomiting.
ch­ing of mouth or severe hyperven­ • Gum hypertrophy on prolonged use.
tilation. Injection Diazepam • Megaloblastic anemia, lymphadeno­
• Can precipitate cardiac arrhythmias Injection diazepam is available in a pathy, osteoporosis.
by virtue of its beta agonist action. 1 mL ampule containing 5 mg/mL
• Collapse and death. solution; also available as 10 mL bulp Injecton Avil (Pheniramine
(5 mg/mL). it is anxiolytic, sedative and Maleate)
Injection Morphine muscle relaxant. It is an antihistaminic. It is available in
It is available in a 1 mL ampule, contain­ 1 mL ampoule containing 22.75 mg/mL
ing the solution with a concentration of Dose solution.
15 mg/mL. it is natural, potent opioid 5 to 10 mg intravenously or intramus­cul­
analgesic. arly. Action
It inhibits the action of histamine release
Dose Action on gastrointestinal tract, uterus and blood
5 to 20 mg subcutaneously or intramus­ • As muscle relaxant in tetanus. vessels, but no effect on bronchospasm,
cularly. It raises pain threshold and also • As preanesthetic medication. hypotension and gastric secretion.
causes peripheral vasodilation, causing • In the treatment of convulsions:
shifting of blood from pulmonary to Psych­ motor epilepsy and status Indications

peripheral vasculature reducing cardiac epil­epticus. • Allergic reaction, e.g. drip rigor,
work and pulmonary pressure. • As tranquilizers. blood transfusion rigors, drug reacti­
ons like urticaria, etc.
Indications Injection Diphenylhydantoin • Pruritus.
• As an analgesic, e.g. in colic (given The 2 mL ampule containing 5 mg/mL • Hypnotic.
along with atropine) and myocardial solution available for intravenous use
infarction. only. Side Effects
• As a preanesthetic medications • Sedation, lassitude, fatigue.
• In acute left ventricular failure. Dose • Dryness of mouth, blurring of vision.
Intravenous dose should not exceed 50 • Nausea, vomiting, epigastric distress.
Side Effects mg/min. It should not be given intra­ • Blood dyscrasias.
• Hypotension. muscularly and should not be given in 5
• Respiratory depression. percent dextrose (acidic solution). Drug
• Drug dependence. precipitates in acidic pH.
Injection Promethazine
• Urinary retention. Hydrochloride (Phenergan)
• Tolerance. Action It is an antihistaminic and tranquilizer.
• It causes miosis and bradycardia and It inhibits spread of seizure discharge Ampules of 2.5 percent solution contain­
thus not indicated in head injury. in brain by decreasing intraneuronal ing 30 mg/mL.
sodium. It restores the balance between
exci­tatory glutamate pathway and inhi­ Indications
Injection Pethidine bitory gamma aminobutyric acid (GABA) • Same as for avil.
(Meperidine) pathway. It does not sedate the patient. • As hypnotic.
It is available in a 2 mL ampule contain­ • As a preanesthetic medication.
ing the solution with concentration of Indications • Lytic cocktail to produce hypo­ther­
50 mg/mL. it is synthetic opioid anal­ • Convulsions of grand mal epilepsy mia. The cocktail is prepared from
gesic. and status epilepticus. the following drugs and mix­ture is
Medical Emergencies in the Clinical Practice 127

injected intravenously in fractional Sodium bicarbonate dose in mEq/L • Orthostatic hypotension.


doses: = 0.5 × wt in kg × (Desired HCO3 – • Rapid diuresis in elderly patients may
Promethazine 50 mg Actual HCO3) precipitate into retention of urine.
Chlorpromazine 50 mg Arbitrarily it can be given in a dose • It can cause hepatic coma in the
Pethidine (meperidine) 100 mg of 1 mEq/kg of body weight/min of presence of liver disease.
hypoxia. Over correction of the acidosis • Cardiac arrest can occur after intra­
Injection Insulin is not recommended as it suppresses the venous injection.
Plain insulin is available in a concen­ hypoxic drive of respiration. • Hearing loss, if large doses of furo­
tration of 40 units per mL in 10 mL bulb. This drug is used in the treatment of somide are used in a patient with
metabolic acidosis. severe renal failure.
Dose • Lactic acidosis following D-C shock
For diabetic ketoacidotic coma, 10 to during cardioversion Injection Mannitol
15 units intravenous bolus, followed by • Respiratory acidosis (severe) Injection mannitol is a sugar (polyhy­
5 to 6 units/h or add 100 to 120 units of • Hyperkalemia. droxyaliphatic alcohol) and is available
insulin to 1000 mL of isotionic saline. as 20 percent solution in a 350 ml glass
The solution is given at the rate of Side Effects bottle. It is an osmotic diuretic.
10 drops/min (40–50 mL/h). Reduce the • Metabolic alkalosis.
rate by 50 percent once blood glucose • Edema due to sodium retention. Dose
comes down to 250 mg percent. 10 to 20 percent solution should be infused
Injection Lasix (Furosemide) rapidly in 15 to 20 minutes in a dose of 0.5
Indications This drug is prepared from furosemide to 1 g/kg body weight, but infusion rate
• Diabetic ketoacidotic coma. which is also called furosemide or fur­ should not be more than 3 g/min.
• Glucose insulin drip in hyperkalemia semide. Its concentration is 10 mg/mL
• Positive Hollander’s test–following and 2 ml ampules are available con­ Action
vagotomy, to test for achlorhydria taining 20 mg solution. It acts on the When injected intravenously, mannitol
(completeness of vagotomy). Insulin loop of Henley and prolonged use may is not metabolized, but rapidly filtered
should be given in a dose of 0.2 unit/ result in potassium deplition and hypo­ by the glomeruli. Being nonabsorbable,
kg body weight. kalemia. it exerts considerable activity which
• Other Indications interferes with the back diffusion of
– Treatment of diabetes, IDDM, Dose water and reabsorption of sodium in the
NIDDM with secondary failure, 20 to 40 mg intravenously or intramuscu­ tubules, causing osmotic diuresis. To be
pregnancy with diabetes, surgery larly. effective, mannitol has to be admi­nistered
of diabetes and complication of rapidly in sufficiently large doses.
diabetes mellitus. Indications
– Insulin shock for the treatment • In the treatment of pulmonary edema Indications
of schizophrenia. (given intravenously). • To induce diuresis in case of barbi­
• To induce forced diuresis in the turate poisoning, to increase the
Side Effect treat­ment of barbiturate poisoning. urinary elimination of barbi­turate.
Hypoglycemia. • In the treatment of mannitol-resis­ • Any condition of threatened acute
tant acute oliguria. oliguric renal failure from prerenal
Injection Sodium Bicarbonate • Advanced renal failure. causes (severe gastroenteritis). In such
Injection sodium bicarbonate is available • In prostatectomy, while closing the cases, prior correction of hypo­volemia
in 10 ml ampule containing 7.5 percent urinary bladder and postoperatively, with adequate amount of fluids is
solution (1 mL contains 1 mmol of so­ after 4 hours to induce diuresis and necessary. If urine flow rate increases
dium bicarbonate). It is buffering agent thus to prevent clot retention. to 100 mL/h more mannitol is given
given in cases of metabolic acidosis. to maintain the high urine flow rate.
Side Effects If no diuresis occurs after the initial
Dose • When used unintelligently, Lasix can mannitol infusion. Patient should be
To calculate the amount of bicarbonate precipitate serious water and elec­ treated for acute renal failure and no
to correct a base deficit/acidosis; it is trolyte disturbances due to exces­ more mannitol should be given.
assumed that the normal bicarbonate sive loss of sodium (Na), pota­ssium • Preoperatively at the time of certain
concentration in blood is 26 mmol/l (K), Chloride (Cl) and water, leading operations (e.g. aortic surgery,
and that the extracellular fluid volume is to weakness, fatigue, dizziness and surgery in deeply jaundiced patient)
20 percent of mean body weight. cramps. to prevent acute renal failure.
128 Principles of Surgery

• After severe traumatic injuries and Injection Mephentine Side Effect


in hemolytic transfusion reactions It is prepared from mephentermine sul­ Cardic arrest, if excessive dose is given
to prevent renal failure. fate, 1 mL ampule contains 15 mg/mL sol­ rapidly. Cardiac rhythm monitoring is
• To reduce intracranial tension and ution and 10 mL vial contains 30 mg/mL indicated during the administration.
to treat cerebral edema, e.g. after solution. It is a vasopressor.
cerebrovascular accident (CVA), head Injection Lignocaine
injury, hepatic encephalopathy. Indications Injection lignocaine is prepared under
• Hypotension secondary to spinal the trademark of Xylocard 2 percent. The
Precautions anesthesia (SA), e.g. in a patient 2 percent lignocaine HCl, 5 mL vial for
• Mannitol should be used with caution undergoing cesarean section. dilution in drip infusion. Each milliliter of
in a patient with decompensated Dose: 15 to 45 mg intravenously solution contains lignocaine anhydrous
heart. in a single injection. The dose is 20 mg.
• It should not be used in a patient repeated if necessary; or intravenous
with head injury before confirming infusion of 0.1 percent mephentine Dose
or ruling out the subdural or intra­c­ in 5 percent dextrose. Rate and • In cardiac arrhythmia, 50 to 100 mg
erebral hematoma by CAT (Compu­ duration of drip should be regulated administered as 2.5 to 5 mL of
terized axial tomography) scan, etc. by the patient’s response. 20 per­­cent lignocaine over a per­iod of
but can be used in rapidly deterio­r­ • Prevention of hypotension attendant 2 minutes, followed by intravenous
ating patient, to buy time for trans­- to SA or surgical procedures and infusion at the rate of 1 to 2 mg/min,
fer of the patient to neurosurgical hypotension that occurs or occurring according to the need to the patient
hospi­tal or for special investigations in recovery room. (add one 50 mL vial of 2% lignocaine
even when diagnosis is not confir­ Dose: 30 to 45 mg, intramus­ to 500 mL of infusion solution).
med. cularly or intravenous infusion of • In congestive cardiac failure, shock
• Potassium chloride, 10 to 20 mEq 0.1 percent mephentine in 5 percent. or renal insufficiency, dose should
and sodium bicarbonate may be be reduced to 0.5 to 1 mg/min.
added to mannitol depending upon Precautions • Intravenous drip should be given for
blood chemistry report. • Should be used cautiously in pati­ 2 or 3 days or at least for 24 hours.
• There should not be extravascular ents taking MAO inhibitors or hyper­ • If overdose occurs (as shown by
leakage. tensive patients. prolongation of PQ or widening of
• Intravenous (IV) set should either • When shock is primarily due to loss QRS and QT complex), the drip rate
be flushed with isotonic saline or of blood or fluid, circulating blood should be reduced.
changed when mannitol is followed volume replacement is done first.
by blood. Indications
• Mannitol infusion should be moni­ Contraindication Ventricular arrhythmia (not supraven­
tored with serum osmolality and Hypotension caused by phenothiazines. tricular arrhythmia), multiple extrasys­
it should not be given if serum toles and tachycardia in connection with:
osmol­ality is more than or equal to • Myocardial infarction
320 mosmol/L.
Injection Potassium chloride • During cardiac surgery
Available in 10 ml ampule containing • Diagnostic procedures, e.g. cardiac
Adverse Reactions 150 mg/mL of KCl. cat­heterization and angiocardiogra­
• Precipitates CHF in a patient with phy.
decompensated heart. Dose
• When used repeatedly fluid overload Simplest method is to add 1 g of KCl Contraindications
occurs in a patient with established to 500 ml of fluid being infused. Each • Atrioventricular (AV) block of all
acute renal failure. Maximum dose gram of KCl is equivalent to 13.4 mmol degrees.
should not exceed 20 g/h. Infusion of K+; 4 g of KCl per day is sufficient • Bradycardia
can be repeated after 6 hours, to prevent depletion. Not more than • Patient with a known history of
provided pro­per fluid and electrolyte 20 mmol should usually be given in hyper­sensitivity to local anesthetic
balance is maintained. 2 hours and each 500 mL fluid infused or amide group of drugs.
should never have more than 1.5 g of
Contraindication KCl (40 mmol/liters added to it). Precautions
Mannitol should not be used in a • Lower doses are used in cases of
patient with shock, cardiac failure and Indication severe liver damage and effect is
established renal impairment. Hypokalemia. watched carefully.
Medical Emergencies in the Clinical Practice 129

• Care must be taken in cases of 15. Barkin RM, Rosen P. Hypoglycemia.


References
pronounced renal insufficiency. Editors: Emergency Paediatrics: A
• Treatment with lignocaine should not 1. Glick G, Y U PN. Haemodynamic Guide to ambulatory care, 4th edition.
be performed without ECG control. changes during spontaneous Vasovagal St Louis: Mosby; 1994.
• Too rapid infusion may be lethal. reactions. Am J Med. 1963;34:42. 16. Owen OE, et al. Pathogenesis and
2. Leonard M. An approach to some diagnosis of Diabetes mellitus. In: Rose
Injection Calcium Gluconate dilemmas and complications of office LF, Kaye D (Eds). Internal medicine for
Available in 10 mL ampules containing oral surgery. Aust Dent J. 1995;40(3). dentistry, 2nd edition, St Louis, 1992.
10 percent w/v calcium gluconate (1 g). 3. Martin GJ, et al. Prospective evaluation 17. Patel JC, Despande PS. Diabetes
of syncope Ann Emerg Med. 1984;13: mellitus. The cause of death: its
Dose 499. ranking. Indian J Med Sci. 1977;31:150.
• In tetany, 2 g intravenous injection 4. Cutino SR. Vasovagal Syncope asso­ 18. Skyler JS. Complications of Diabetes
is given slowly and repeated if ciated with seizure activity Gen Dent. mell­ itus: Relationship to metabolic
necessary. 1994;42(4). dys­ functions, Diabetes care. 1979;2:
• After each 1000 ml of blood trans­ 5. Fried berg CK. Syncope: Pathological 499.
fusion, 1 g is injected intravenously. physiology, differential diagnosis and 19. Little JW, Fallace DA. Diabetes. In:
• In epididymo-orchitis, 1 g is given treatment. Mod concepts Cardiovasc Little JW, Fallace DA (Eds). Dental
intravenously and slowly at 8 hours Dis. 1971;40:55. manage­ ment of medically compro­
intervals. The role is yet controver­ 6. Leonard M. Syncope: treating fainting mised patients, 4th edn. St Louis: Mos­
sial. Cardiac arrhythmias can be in the dental office. Dent Today. by; 1994.
precipitated during the administra­ 1996;15(1). 20. Kitabchi AE, Wall BM. Diabetic ketoac­
tion of this drug and thus critical 7. Webb WR et al. Cardiovascular idosis, Med Clin North Am. 1995;79:9.
monitoring is warren­ted. responses in acute adrenal insuffi­ ci­ 21. Nabarro JD. Diabetes in UNITED
ency Surgery. 1965;58:273. KINGDOM: A personal series, Diabetic
Indications 8. Addison T. On the constitution and med. 1991;8(1).
• Tetany. the local effects of diseases of the 22. Raskin P. Treatment of Insulin
• After 1000 mL of blood transfusion. suprarenal capsules. London: Samuel dependent Diabetes mellitus with
• As an inotropic drug in cardiac arrest. Highly, 1855. portable insulin infusion devices, Med
• Hypoparathyroidism. 9. Zaloga GP, Marik P. Hypothalamic- Clin North Am. 1982;66:1269.
• As a coagulant (factor V). pituitary-adrenal insufficiency. Crit 23. American heart association: Coronary
Care Clin. 2001;17:25-41. heart disease and Angina pectoris, Dal­
Bupivacaine (Sensorcaine) 10. Guyton AC. The adrenocortical las, 1998, American heart association.
It is a new local analgesic drug. It is hormones. In human physiology and 24. AHA Scientific position: Sudden
4 times more potent than lignocaine. It mechanism of disease, 5th edition. cardiac death, Dallas, 1998, American
has longer duration of action of about 5 Philadelphia, WB Saunders, 1992. heart association.
to 6 hours. 11. Streeten DHP. Corticosteroid therapy. 25. Cummins RO, Eisenberg MS:Prehos­
II. Complications and therapeautic pital cardiopulmonary resuscitation: is
Dose indications. JAMA. 1975;232:1046. it effective? JAMA. 1985;253:2408.
2 mg/kg. 12. Hickler RB. Ortostatic hypotension and 26. Orlowski JP. Optimal position for
syncope, N Engl J Med. 1977;296:336. external cardiac massage in infants and
Preparations—Inj bupivacaine 0.5 per­ 13. Olefsky JM. Diabetes mellitus. In: children, Crit Care Med. 1984;12:224.
cent. Bennett JC, Plum F (Eds). Cecil 27. Eisenberg MS, Hallstrom A, Bergner
Textbook of medicine, 4th edition. L. The ACLS score predicting survival
Calculation of dose of Drug Philadelphia: WB Sanders; 1996. from out of hospital cardiac arrest,
for children 14. University group diabetes programe. JAMA. 1981;246:50.
Child dose = Age/(age + 12) × Adult dose Effects of hypoglycaemic agents on 28. Eisenberg MS and others. Defibrillation
(Young’s formula). vascular complications in patients by emergency medical technicians,
Child dose = Age/20 × Adult dose with adult onset diabetes II. Mortality Crit Care Med. 1985;13:921.
(Dilling’s formula). results Diabetes. 1970;19:785.
130 Principles of Surgery

29. Caranasos GJ. Drug reactions in Schwartz 32. Paul A Moore. Pharmacokinetics of 35. American heart association and
GR and others, Editors: Principles and Lidocaine With Epinephrine Follow­ national academy of sciences, National
practice of emergency medicines Phila­ ing Local Anesthesia Reversal With research council: standards and
delphia, WB Saun­ders;1978. Phentolamine Mesylate. Anesth Prog. guidelines for CPR and emergency
30. Pallasch TJ. Principles of pharmaco­ 2008;55(2):40–48. cardiac care. JAMA. 1992;268(16).
therapy. V. Toxicology and adverse 33. Heimlich HJ. A Life saving maneuver to 36. Malamed SF. Managing medical emer­
drug reactions. Anesth Prog. 1989; prevent food choking. JAMA. 1975;234: gencies. J Am Dent Assoc. 1993;1240.
36(2):41–45. 398. 37. American Dental association: ADA
31. Arthur GR. Pharmacokinetics of local 34. American heart association and guide to dental therapeutics, Chicago.
anaesthetics. In Stri chartz GR, (Ed): national academy of sciences, National The association, 1998.
Lpcal anaesthetics, Handbook of research council: standards and 38. Goodman, Gillman’s the pharmacolo­
experimental pharmacology, Vol 81, guidelines for CPR and emergency gical basis of therapeutics, 9th edition.
Berlin, 1987, Springer - Verlag 1987;81. cardiac care. JAMA. 1980;244:453. New York. Mcgraw Hill; 1996.
7 Management of Airway
in Maxillofacial Surgery
Borle Rajiv M

The oral cavity constitutes the upper part common in an unconscious patient, who complication secondary to these condi­
of the aerodigestive tract. The path­o­lo­ has bilateral parasymphysis fracture of tions. Similarly the conditions like cer­
gies and the surgeries performed in this the mandible or who has undergone vical necrotizing fasciitis can also cause
area have direct bearing on the airway. mandibular resection across the midline. airway edema. When the cervicofacial
A specialized care of the patient is requi­ During severe trauma to the facial infections extend to the mediastinum
red, while managing the patho­logies of skeleton, the fracture segments get by either the anterior or posterior fac­ial
the orofacial region to maintain patency displaced posteriorly and cause imp­ planes, can cause severe respiratory com­
of the airway and to prevent airway inge­ment and narrowing of the airway. plications due to sepsis.
complications. The chances of aspiration Severe bleeding from the fracture sites, The conditions like temporo­
of secretions or blood or foreign bodies presence of clots in the nasal cavity, mandi­bular joint (TMJ) ankylosis, oral
in the airway are enhanced during the oral cavity and pharynx and the foreign sub­ mucous fibrosis, etc. are chara­
transoral procedures or the procedures bodies like avulsed teeth are likely to be cteri­zed by severe trismus. While per­
carried out in the nasal or pharyngeal aspirated in the tracheobronchial tree, if forming surgeries on such a pati­ent it
areas. Similarly the handling of this area the airway is not properly guarded. As the is a challenging task to intubate these
can enhance the chances of airway obstru­ inflammatory edema sets in, the airway patients for administration of the
ction due to edema secondary to surgical is further compromised leading to airway general anesthesia and for guarding the
handling. There are certain conditions obstruction. The facial fractures are airway, as laryngoscopy is also not pos­
in which there is pronounced trismus usually associated with head injury and sible. In such patients either blind nasal
and the laryngoscopy is not possible and the patients are often semiconscious/ intubation, retrograde intubation or
an alternative access is required to be unconscious and the relative risk of fiber­optic bronchoscope guided endo­
created to the airway for maintaining its aspiration, acute respiratory obstruction, tracheal intubation is required. If such
patency, like an endotracheal intubation bronchospasm or pneumonitis are facilities are not available or fail then
for administration of the anesthesia and enh­ an­ced. The trau­matized brain has alternative procedures like tracheostomy
for subsequent airway care. A sound reduced tolerance to hypoxia and thus are required for securing the airway.
knowledge of the respiratory passage, any hypo­xic environment secondary to After ablative surgical procedures
its anatomy and physiology and the airway obstruction can worsen the head like major head and neck cancer resec­
thor­ough understanding of causes and injury by inducing irreversible hypoxic tion the patient requires prolonged ane­
mana­ge­ment of respiratory obstructive brain injury. s­­thesia and prolonged intubation post­
con­ditions are of paramount importance The routine endotracheal intubation operatively. Such patients might also
to a maxillofacial surgeon. is not possible in cases of cervical spine require ventilatory assistance for some
The most common cause of respir­ fractures. So, to maintain the patency of time. As the patients are nonam­bulatory
atory obstruction in an uncon­ scious airway, sometimes an alternative acc­ the lower airway care is also imperative,
patient, irrespective of the cause of ess to the airway is created (crico­thy­roi­ hence to facilitate the maintenance of
unconsciousness, is the tongue fall. dectomy or tracheostomy). patency of respiratory passage, to alle­
Hence, even after minor surgical pro­ The airway complications are also viate the respiratory dead space and to
cedures of short duration under general known to happen in the patients with facilitate the trach­eo­bronchial suctions
anesthesia the patency of airway is severe maxillofacial infections like Lud­ to clear the secre­tions, tracheostomy is
required to be maintained by preventing wig’s angina or sublingual space infec­ preferred over the conventional endotr­
the tongue fall. The tongue fall is more tion. The laryngeal edema is the common acheal intubation.
132 Principles of Surgery

In short the knowledge of airway away from the posterior pharyngeal and does not extend to the other open
anatomy, physiology and modalities to wall. The head may be turned on one end (pharyngeal end) of the airway. It is
maintain its patency is of great impor­ side, so that the secretions accumulate basically meant for administering oxygen
tance to the clinician in general and on the dependent area and the airway to the patient by attaching a catheter to
a maxillofacial surgeon, in particular. is patent (Figs 7.1 and 7.2). To pre­vent it. As it is short, the stellate cannot be
Airway management happens to be the aspiration of the secretions, vomitus or used for sucking out the secretions in
first and the foremost life saving priority blood into the lower airway, patient may the airway. If the airway is blocked due
in the management of any emergency. be put into head low position. to secretions, a thin rubber catheter is
passed through the main opening in the
Insertion of Airway body of the airway to carry out suction.
MAINTENANCE OF AIRWAY1
Insertion of oropharyngeal or naso­ The nasopharyngeal airway is
phary­ngeal airway prevents tongue fall smal­ler in diameter than the orophar­
Jaw Thrust Chin Lift Maneuver (Figs 7.3A to C). The Water’s oropharyn­ yngeal airway and it is much smaller in
Jaw thrust chin lift maneuver is an geal airway is inserted transorally. The length than the endotracheal tube, as
impor­ tant procedure to prevent the airway occupies the space between the it reaches only up to the hypopharynx.
airway obstruction due to tongue fall tongue and the posterior pharyngeal It serves the same purpose as the oro­
in an unconscious patient or a patient wall and through the lumen of the airway pharyngeal airway. It is more suitable, if
reco­vering from general anesthesia. the patient can breathe. The airway has the airway is required to be maintained
First the upper airway is cleared of saliva, multiple holes. This is to ensure that, if in place for longer time and can be
mucous, blood, foreign bodies like some holes are blocked due to contact secured with adhesive tapes. It is better
fragments, teeth, denture, etc. The neck with the mucosa or due to mucoid tolerated by the patients than the
is then extended, mandibular angles secretions, the patient can still breathe oropharyngeal airway. The only disad­
pushed anteriorly and the chin lifted through the remaining patent holes. vantage is that being smaller in diameter
up. This procedure shifts the posterior There is a stellate in the airway which it can get blocked due to secretions and
one-third of the tongue and soft palate ends short of the length of the airway needs periodic suctioning to prevent

A B
Figs 7.1A and B: Jaw thrust chin lift head tilt maneuver Fig. 7.2: Nasopharyngeal airway

A B C
Figs 7.3A to C: (A) Metallic oropharyngeal airway; (B) PVC oropharyngeal airway; (C) Oropharyngeal airway in place
Management of Airway in Maxillofacial Surgery 133

its blockade. Sometimes after the thyroidectomy is the procedure, which Contraindications
procedure under general anesthesia can be done rapidly and takes lesser • Inability to identify landmarks (cri­
the endotracheal tube can be partially time than the tracheostomy. It does co­­thyroid membrane).
withdrawn, so that its tip is out of larynx not require neck extension (which • Underlying anatomical abnormality
in the hypo­pharynx and the same can be is contraindicated in case of cervical (tumor).
left in place as a nasopharyngeal airway spine fractures) and can be done with • Tracheal transection.
till the patients recovers completely only a stab knife and the handle of • Acute laryngeal disease due to infec­
from the anesthesia. the knife can be introduced in the slit tion or trauma.
incision and rotated to 90° to dilate the • Small children under 10 years of
Application of the Tongue incision. A small diameter endotracheal age (a 12–14 gauge catheter over the
Stitch tube is inserted to maintain the airway needle may be safer).
Application of tongue stitch horizontally temporarily. The cricothyroid mem­
through the tongue substance and brane being superficial is less prone for Anatomy
draw­ing the tongue out also prevents complications. The cricothyroid membrane lies between
tongue fall (Fig. 7.4). The tongue stitch The procedure was first described in the thyroid cartilage superiorly and the
should be given using a large round 1805 by Vicq d’Azyr, a French surgeon cricoid cartilage inferiorly. It can be felt by
body needle and a silk thread of 1–0 and anatomist. A cricothyrotomy (also palpating the neck anteriorly and finding
size should be used. The tongue stitch called thyrocricotomy, cricothy­roid­­o­ first the thyroid cartilage that is the most
is never placed vertically in the tongue tomy, inferior laryngotomy, inter­crico­ prominent cartilage in the neck. After that
as during the drawing out of tongue, thyrotomy, coniotomy or emer­­gency air­ you need scroll down your index finger
the tongue may get split in midline due way puncture) is an emergency incision until you can fell the space between the
to tear. Both the ends of the thread are through the skin and cricothyroid mem­ thyroid and cricoid cartilages. This space
held with an artery forceps and clamped brane to secure a patient’s airway during is the place of the cricothyroid membrane
to the shirt of the patient, so that the certain emergency situations such as an (Fig. 7.5).
tongue is retained in the protruding airway obstructed by a foreign object
state. or laryngeal edema, a patient who is Material
not able to breathe adequately on their • Material required for sterile technique
Cricothyroidectomy2 own or in cases of major facial trauma, (gloves, mask, cap and gown).
It is the easiest and the fastest emergency which prevent the insertion of an endo­ • Povidone-iodine solution for steril­
procedure for maintaining the airway tracheal tube through the mouth. A izing the skin.
patency temporarily. Cricothyroid mem­ cricothyrotomy is usually performed • Sponges.
b­rane is punctured with a 16 to 18 gauge as a last resort, when control of the air­ • Drapes and rolled bath towel.
hypodermic needle and maintained way by usual means (an endotracheal • Number 11 scalpel blade mounted
in position till definitive measures like intubation) has failed or is not feasible. on number 3 or 5 handle.
tracheostomy is performed. The crico­ This technique is considered easier and • 1 percent lidocaine without epi­
faster than a tracheostomy and hence nephrine in a 10-cc syringe with a
preferred over the tracheostomy in dire 25-gauge needle.
emergency. This procedure does not • Two mosquito artery forceps or two
require manipulation of the cervical Kelly clamps.
spine. Cricothyrotomy is only a tempo­- • Low pressure cuffed tracheostomy tube.
rary airway for life-saving situations. It is not • A 10-cc syringe to inflate the balloon
suitable for prolon­ged ventilation due to on the tracheostomy tube.
its small size. A definitive airway (tracheo­ • Bag-valve-mask (Ambu bag-airway
stomy or endotracheal intu­bation) must maintenance breathing unit) con­
be performed later in hospital. nected to a oxygen source.
• Adhesive tape.
Indications
• Severe facial or nasal injuries (that do Technique
not allow oral or nasal intubation). • Arrange all the necessary equip­ment/
• Massive midfacial trauma. instruments and test the trache­
• Possible cervical spine trauma pre­ ostomy tube by inflating the tube
venting adequate neck extension. with air from 10-cc syringe. Place the
• Anaphylaxis. material on a sterile towel placed on a
Fig. 7.4: Tongue stitch • Chemical inhalation injuries. Mayo stand or bedside table.
134 Principles of Surgery

(no 16) needle through the crico­


thyroid membrane in the trachea as
an interim measure.
• With the mosquito or Kellys clamp in
the left hand, insert the clamp into the
incision and spread it. This is sufficient
to provide an airway for a patient with
supraglottic airway obstruction.
• With the right hand insert the small
diameter tracheostomy tube or the
orotracheal tube through the incision
into the trachea, directing it caudally.
• Connect the bag-valve unit to the
tube and ventilate the patient with
100 percent oxygen.
• Observe respiratory movements of
the chest and auscultate for breathe
Fig. 7.5: Anatomy of laryngotracheal area sounds, which should be bilaterally
equal.
• One of the most important aspect is to • Anesthetize the skin over the mem­ • Inflate the tube balloon if cuffed
position the patient. He or she should brane using a syringe with 25-gauge tube is used to prevent aspiration
be supine, ideally a rolled towel or needle with the 2 percent lidocaine. of blood or secretions in the lower
sand bag under the shoulders and • Make a transverse incision of the skin respiratory passage.
with the neck in hyperextension. The over the cricothyroid membrane • Cut a sponge halfway down the
extension of the neck is strictly contra­ using the number 11 blade (Figs 7.6A middle and wrap it around the tube
indicated in presence of cervical and B). if an orotracheal tube is being used
spine fractures. However, in such • Identify the membrane and then and then fashion a necklace to place
situation, it can be performed safely continue the incision through it app­ the tube in place. If the tracheostomy
without giving the neck extension or roximately 1 cm on each side of the tube is used, secure the wings of the
mobilization of the neck. midline. In dire emergency, the skin tube by tying the tapes around the
• Disinfect the skin from the sternal and the cricothyroid membrane are patient’s neck. In both cases do not
notch to chin and laterally to the incised together with a stab incis­ use the tape to tie tightly because it
base of the neck. ion and the incision is dilated by can cause erosion of the skin.
• Observe sterile technique. inserting the handle of the BP knife • Do the suction of the secretions/
• Identify the cricothyroid membrane and rotating it by 90 degrees. Or blood in the trachea.
as described above. by simply introducing a wide bore • The chest X-ray may be ordered to
check the position of the tube.
• It is only an emergency procedure
and if the tube is required to be
maintained in situ for longer period
tracheostomy should be performed
and the cricothyroid membrane
opening should be decanulated. The
tracheostomy is more practical and
logical option for better airway man­
agement for longer duration.

Tracheostomy3
Negus4 1938 coined the term tracheo­
stomy. Tracheotomy is an incision or
cutting into the trachea while tracheo­
stomy refers to a window made in the
A B anterior wall of trachea just below the
Figs 7.6A and B: Cricothyroidectomy procedure larynx. It provides an alternative airway,
Management of Airway in Maxillofacial Surgery 135

bypas­sing the upper passages. It is a life-


be retracted laterally, during the tra­ Relations
saving procedure and every clinician cheostomy to prevent damage to its The anterior surface of the trachea is
must be competent enough to perform contents. The strap muscles of the neck convex and covered, in the neck, from
it in emergency. such as sternothyroid run parallel to the above downward, by the isthmus of
trachea and if vertical incision is taken the thyroid gland, the inferior thyroid
Surgical Anatomy for tracheostomy they are easy to retract veins, the arteria thyroidea ima (when
The trachea is membranous posteriorly laterally. that vessel exists), the sternothyroideus
and is formed of semicircular cartilag­ and sternohyoideus muscles, the cervical
inous rings anteriorly and laterally. The Applied Surgical Anatomy of fascia and more superficially, by the
spaces between the rings are mem­ Trachea anastomosing branches between the
branous. The cricoid cartilage is present The trachea is a cartilaginous and mem­ anterior jugular veins. In the thorax,
below the thyroid cartilage and is the b­ranous tube, extending from the lower it is covered from before backward
only complete ring. The trachea has 16 part of the larynx, on a level with the sixth by the manubrium sterni, the remains
to 20 rings. The upper tracheal rings are cervical vertebra, to the upper border of the thymus, the left innominate vein,
covered by the isthmus of the thyroid of the fifth thoracic vertebra, where it the aortic arch, the innominate and left
gland. The trachea extends inferiorly divides into the two bronchi, one for each common carotid arteries and the deep
and posteriorly below the manubrium of lung. The trachea is nearly but not quite cardiac plexus. Posteriorly it is in contact
the sternum and divides into two main cylindrical, being flattened posteriorly; with the esophagus. Laterally, in the neck,
bronchi. The point of the bifurcation is it measures about 11 cm in length; its it is in relation with the common carotid
called carina. The trachea runs inferiorly diameter from side-to-side is from arteries, the right and left lobes of the
and posteriorly. To make it prominent 2 to 2.5 cm, being always greater in thyroid gland, the inferior thyroid arteries,
and to draw out the portion of the the males than the females. In a child and the recurrent laryngeal nerves. In the
trachea which goes behind the sternum, the trachea is smaller, more deeply thorax, it lies in the super­ior mediastinum
the neck is needed to be extended during placed, and more movable than in the and is in relation on the right side with
the tracheostomy. The esophagus is adults. The adult trachea measures 10 the pleura and right vagus and near the
present deep to the trachea. On either to 13 cm from cricoid cartilage to the root of the neck with the innominate
side, lateral to the trachea, the carotid carina (bifurcation of trachea). If the artery. On its left side is the left recurrent
sheaths are present which contain the neck is extended roughly about half, laryngeal nerve, the aortic arch and the
internal carotid artery, internal jugular this length is within the confines of left common carotid and subclavian
vein and the vagus nerve. The tributaries the neck making surgery easy. Hence, arteries (Figs 7.7A to C). On either side,
of the internal jugular vein may cross tracheostomy is performed with the lateral to the trachea, the carotid sheaths
the anterior wall of the trachea and need neck hyperextended. This is achieved are present which contain the internal
to be ligated during the tracheostomy. by placing a sandbag or towel roll under carotid artery, internal jugular vein and
The carotid sheath is also required to the shoulder blade of the patient. the vagus nerve (Fig. 7.8).

A B C
Figs 7.7A to C: Anatomy and relations of trachea
136 Principles of Surgery

curves downward and backward between nerves and from the sympathetic; they
the two bronchi. It ends on each side in are distributed to the trachealis muscles
an imperfect ring, which encloses the and between the epithelial cells.
commencement of the bronchus. The At the level of thoracic inlet the
cartilage above the last is somewhat trachea dives anteroposteriorly behind
broader than the others at its center. thymus, innominate vein and inno­
minate artery thus complicating tra­
The Fibrous Membrane cheo­stomy procedure in elderly.
The cartilages are enclosed in an elastic
fibrous membrane, which consists of Indications for Tracheostomy
two layers; one, the thicker, passing over • Emergency:
the outer surface of the ring, the other – Severe laryngeal trauma.
over the inner surface: at the upper – Foreign body in larynx.
and lower margins of the cartilages – Head injury with unconsciou­
Fig. 7.8: Anatomical structures in relation
to trachea
the two layers blend together to form a sness is one of the most common
single membrane, which connects the indi­cation.
rings with one another. They are thus • Elective:
The cartilages of the trachea vary invested by the membrane. In the space – Elimination of upper respiratory
from 16 to 20 in number: each forms behind, between the ends of the rings, dead space.
an imperfect ring, which occupies the the membrane forms a single layer. – Inflammation of larynx.
anterior two-thirds or so of the circum­ The muscular tissue consists of two – Laryngeal malignancy or laryn­
ference of the trachea, being deficient layers of nonstriated muscle, longitudinal gopharyngeal growth.
behind, where the tube is completed and transverse. The longitudinal fibers – Laryngeal edema due to allergy,
by fibrous tissue and unstriped mus­ are external and consist of a few scattered infection, trauma.
cle fibers. The cartilages are placed bundles. The transverse fibers (Trachealis – Laryngeal stenosis secondary to
horizontally above each other, separa­ muscle) are internal and form a thin layer trauma or infection.
ted by narrow intervals. They measure which extends transversely between the – Sleep apnea.
about 4 mm in depth and 1 mm in ends of the cartilages. – Orofacial injuries.
thickness. Their outer surfaces are – Comatose patient who is put on
flattened in a vertical direction, but the Mucous Membrane ventilator.
inner surfaces are convex, the cartilages The mucous membrane is continuous – Respiratory failure in adult and
being thicker in the middle than at the above with that of the larynx and below children.
margins. Two or more of the cartilages with that of the bronchi. It consists of • Others:
often unite, partially or completely and areolar and lymphoid tissue and presents – Congenital airway anomalies.
they are sometimes bifurcated at their a well-marked basement membrane,
extremities. They are highly elastic, but supporting a stratified epithelium, the Uses of Tracheostomy
may become calcified in advanced life. surface layer of which is columnar and • Relieves upper airway obstruction.
In the right bronchus the cartilages vary ciliated, while the deeper layers are • Reduces airflow resistance.
in number from 6 to 8; in the left, from composed of oval or rounded cells. • Protects against aspiration.
9 to 12. They are shorter and narrower Beneath the basement membrane there • Provides access for toilet of tracheo­
than those of the trachea, but have the is a distinct layer of longitudinal elastic bronchial tree.
same shape and arrangement. The fibers with a small amount of intervening • Allows positive pressure ventilation.
peculiar tracheal cartilages are the first areolar tissue. The submucous layer is • Allows administration of general an­
and the last. composed of a loose meshwork of con­ esthesia.
The first cartilage is broader than the nective tissue, containing large blood • Relieves alveolar hypoventilation in
rest and often divided at one end; it is vessels, nerves and mucous glands; the pulmonary disease.
connected by the cricotracheal lig­a­ment ducts of the latter pierce the overlying • Pathway to deliver medication or
with the lower border of the cric­ oid layers and open on the surface. humidification.
cartilage with which or with the succe­
eding cartilage, it is sometimes blended. Vessels and Nerves Types of Tracheostomy
The last cartilage is thick and broad The trachea is supplied by the inferior
in the middle, in consequence of its thyroid arteries. The veins end in the According to the indication
lower border being prolonged into a thyroid venous plexus. The nerves are • Emergency tracheostomy.
triangular hook-shaped process, which derived from the vagus, the recurrent • Elective tracheostomy.
Management of Airway in Maxillofacial Surgery 137

According to the level Types of Tracheostomy Tubes tracheostomy is to be maintained for a


• High level tracheostomy: It is per­The tracheostomy tubes are available long period of time (for months).
formed above the isthmus of thyroidas, PVC tubes and metallic tubes The metallic tracheostomy tube has
gland. (1st and 2nd rings). (Figs 7.9 and 7.10). The PVC tubes are an inner and outer tube and a stellate.
• Mid level tracheostomy: At the level
with or without cuff. The plain tube is It is used, when the tracheostomy is
of isthmus (2nd and 3rd). used to maintain the patency of airway. intended to be kept patent for longer
• Low level tracheostomy: Performed Apart from the maintenance of airway, period in patients of laryngectomy,
below the isthmus (4th to 6th). the cuffed PVC tube serves variety of head injury; comatose patients or if
other purposes like the cuff makes the per­ma­nent tracheostomy is planned.
Sizes of Tracheostomy Tube tube self-retaining, seals the trachea The basic advantage is that as there are
• Neonates to 3 months: 4.5 to 5 mm. when inflated and prevents aspiration two tubes, the inner and the outer, the
• 3 to 12 months: 5 to 5.5 mm. in lower respiratory passage and general inner tube can be removed and cleaned
• 1 to 3 years: 5.5 to 6 mm. anesthesia can be administered through intermittently, during such periods the
• Adults: 8 mm. it. However, the basic disadvantage with outer tube is left indwelling to main­
It is being said that the size of the the PVC tube is that it can get blocked tain the patency of airway and thus
tracheostomy tube needed for the parti­ due to thick secretions, if proper care the chances of blockade are less. The
cular patient is roughly equal to the size is not taken during the postoperative patients can be educated and can do the
of the patient’s little finger. phase. It is not ideal to be used if the cleaning themselves at home.

Technique
Keep ready the sterilized standard tra­
cheostomy tray/set, which should be
present in every ward (Fig. 7.11). The
neck should be extended by placing the
sandbags below the shoulder to make the
trachea prominent (Figs 7.12A and B).
In emergency tracheostomy, a vertical
incision is placed in the midl­ine below
the thyroid cartilage (Fig. 7.13). As all
strap muscles of the neck are placed
vertically, it is easy to retract them if
A B
vertical incision is taken. In the emergency
Figs 7.9A and B: PVC tracheostomy tubes: (A) Noncuffed; (B) Cuffed situations, as the tracheostomy is to be
performed in the shortest possible time
it is not desirable to do layer-by-layer
dissection, but with one or two strokes
of the knife the trachea is exposed. In
dire emergency cricothyroidectomy is a
faster and safer alternative to open the
airway and after the airway is secured,
the tracheostomy be done.
In the elective tracheostomy the
incision is taken horizontally to hide the
scar in neck creases for cosmetic reasons
(Figs 7.14A and B). After infiltrating
the area with 2 percent lidocaine with
adrenaline, skin incision is made. The
deeper dissection is done by incising
the deeper layers one-by-one and retrac­
ting them using atraumatic Langenbeck
retractors. Care must be taken to avoid
A B damage to the common carotid artery or
Figs 7.10A and B: (A) Metallic tracheostomy tube; (B) Outer and inner tubes with stellate internal jugular veins, the vagus and the
138 Principles of Surgery

recurrent laryngeal nerve which is the


branch of the vagus. The upper rings of
the trachea lie deep to the isthmus of the
thyroid and by retracting the isthmus
the rings are made visible (Fig. 7.15). If
the isthmus is bulky and comes in the
way of surgery it can be clamped and
divided. The trachea can be felt by finger
as a cartilaginous, ringed (hoist pipe-
like) structure. To confirm the presence
of trachea, a syringe filled with normal
sterile saline is taken and the needle is
inserted in the structure and aspiration
is done. Aspiration of air in the syringe
confirms that it is the trachea. A cricoid
hook (Fig. 7.16) is inserted around the
trachea to stabilize it and a vertical
incision is taken in the anterior wall
Fig. 7.11: Tracheostomy set of trachea over the 3rd, 4th, and 5th
tracheal rings. Handling of tracheal
lining will result into a bout of cough
and after it has subsided the incision
is dilated with the tracheal dilator
(Fig. 7.17) and tracheostomy tube is
inserted into the trachea (Fig. 7.18). In
place of the vertical incision a Bjork flap
can also be taken to create the opening
in the trachea (Figs 7.19A to C). The
Bjork flap can be inferiorly or superiorly
pedicled. The basic disadvantage with
A B the inferiorly pedicled Bjork flap is that
Figs 7.12A and B: Position of the patient for tracheostomy, the neck is extended by if the flap is not stitched outside, it may
placing sandbag below the shoulder and head is supported with a ring pillow fall in the tracheal lumen and block it.

A B
Fig. 7.13: Anatomical landmarks Figs 7.14A and B: Incision for the elective tracheostomy
Management of Airway in Maxillofacial Surgery 139

Fig. 7.15: Exposure of trachea Fig. 7.16: Cricoid hook

The tube is secured in place by either


suturing to the skin or by tying the straps
around the neck to prevent accidental
decanulation (Figs 7.20A and B).

Subsequent Care of Tracheostomy


Tube
• Handle the tracheostomy tube with
sterile gloved hands.
• Maintain proper hygiene and asep­
Fig. 7.17: Tracheal dilator sis around the tracheostomy site.
• Watch for the signs of surgical emphy­
sema in immediate post-tracheos­
tomy period to detect false passage,
if any. Similarly observe for the signs
of respiratory distress, intermittently.
The air blast should be checked to
detect the blockade of the tube due to
thick secretions. The air blast is chec­
ked by holding the cotton wool fibers
over the tube opening and observing
its deflection during the expiration.
• Cover the tracheostomy tube with
a single layer of moist gauge to
humidify the inhaled air.
Fig 7.18: Final tube placement

A B C
Figs 7.19A to C: Inferiorly and superiorly pedicled Bjork flaps
140 Principles of Surgery

is kept as stand by and the edges of the


wound are kept retracted with retractors,
so that, in case of any respiratory distress
after decanulation of the tube, a metallic
tube can be reinserted. The tube must be
decanulated under aseptic care. It is a
safe practice to observe the patient for a
period of at least 1 hour after decanulation
of the tracheostomy tube to detect any
signs of respiratory distress. The wound
can be closed by loose primary sutures
or can just be covered with sterile gauze
piece soaked in povidone iodine and
A B taped with adhesive tape, and allowed to
Figs 7.20A and B: Securing the tube with tape straps around the neck heal by secondary intention.

Complications
• Perform suctions intermittently to • Give steam nebulization to the pati­ Perioperative complications
prevent blockage of the tube due to ents every 6 hourly to liquify the of tracheostomy
secretion. However, deep tracheal secretions (Mucolytic action) and • Hemorrhage: Due to damage to
suction should be done judiciously reduce con­ gestion of the tracheal inter­nal jugular vein or its tributaries
and when needed as it stimulates and lower airway lining which can be or as a result of damage to the thyroid
the vigorous coughing. induced due to the tracheal handling, isth­mus
• Handle the suction catheters asepti­ irritation due to nonhumidified air • False passage
cally and do not use open ended inhalation and subclinical infection. • Surgical emphysema
catheters at tip, as they may suck the • Chest physiotherapy comprising of • Pneumothorax
fragile tracheal lining and induce frequent change in the position of • Air embolism
bleeding. Dip the suction catheter the patient, chest exercises, tapping • Cricoid cartilage damage
in a bottle containing sterile normal etc. is given to the patient. • Recurrent laryngeal nerve damage.
saline to flush out the thick secretions
present in it to prevent its clogging and Decanulation of the Tracheostomy Late postoperative complications
after switching off the suction keep the Once the purpose is over the tracheo­ • Complications due to difficult decan­
catheter submerged in a dilute, sterile stomy tube should be decanulated nu­lation
antiseptic solution in a bottle. (removed) as early as possible. More • Tracheocutaneous fistula
• Keep the environment humid by the time it is kept indwelling more are • Tracheoesophageal fistula
keep­ing a kettle of boiling water in the chances of the chest infection. If • Tracheal stenosis
the room, as dry air tends to irritate the metallic tube is placed, then prior • Tracheoinnominate artery fistula.
the tracheal lining and tends to dry out to the removal the tube lumen should
the secretions, thus blocking the tube. be plugged with a gauze piece and the Endotracheal Intubation
• If a cuffed tube is used, inflate and patient should be observed for breathing. A ‘definitive airway’ is defined as a
deflate the cuff every half hourly to The patient should be able to breath cuffed tube passed below the vocal cord
prevent ischemic necrosis of the comfortably through the gap between (folds), either through the nasal or oral
tracheal lining. Before the cuff is the inner tracheal wall and the sides of cavity. Orotracheal intubation is the
deflated suck the secretions present the tube. This suggests that there is no most reliable and time-proven method
in the upper airway using separate obstruction above the tracheostomy of securing a definitive airway, including
catheter, so that when the cuff is site. The same is not possible in cuffed emergency situations.
deflated the secretions are not aspi­ PVC tube as the outer diameter of the
rated in lower respiratory passage. PVC tube is larger and the deflated cuff Indications for Tracheal
• If the metallic tracheostomy tube is also occupies lot of space and does Intubation
used, remove the inner tube and clean not facilitate the free air circulation
Need for airway protection
it periodically to prevent its blockade. by its sides and thus the patient will
• Put 2 to 3 drops of sodium bicar­ experience respiratory distress, if it is • Comatose or intoxicated patients who
bonate (soda bicarb) or normal saline blocked by plugging with gauze piece are unable to protect their airways.
through the tracheostomy tube to unlike the metallic tube. When the PVC In such patients, the throat muscles
liquify the secretions. tube is decanulated the metallic tube may lose their tone so that the upper
Management of Airway in Maxillofacial Surgery 141

airway obstructs or collapses and air Endotracheal Tubes airway, often provides an adequate seal
cannot easily enter into the lungs. Fur­ The endotracheal tubes may be flexible for mechanical ventilation. An excessive
ther­more, protective airway reflexes or preformed and relatively stiff. They leak can sometimes be corrected through
such as coughing and swall­ owing, are usually made of red rubber, flexible the placement of a larger (0.5 mm larger
which serve to protect the airway plastic or silicone, though they may be in internal diameter) endo­ tracheal
against aspiration of secre­­tions and armored with metallic rings to prevent tube, although in difficult-to-ventilate
foreign bodies, may be absent. With kinking (Figs 7.21A and B). Adult tubes patients even children may need to use
tracheal intubation, airway patency is have an inflatable cuff to seal the lower cuffed tubes to allow for high pressure
restored and the lower airways can be airways against air leakage and gross ventilation, if the leak is too great to
protected from aspiration. aspiration and the cuff also makes the overcome with the ventilator.
• Risk for aspiration. tube self-retaining (Figs 7.22A and B). The south pole tubes are directed
• Upper airway bleeding—to prevent The cuff must be maintained diligently towards the leg end of the patients and
aspiration. in order to avoid complications from are especially suitable for the maxillary
• Vomiting—to prevent aspiration. over­inflation, which can include rupture surgeries and the cleft lip and palate
• Risk for obstruction. of the trachea, tracheomalacia or trach­ surgeries (Fig. 7.23). The north pole
• Severe maxillofacial fractures. eo­eso­phageal fistula. Many of the com­ tubes are directed towards the head and
• Neck hematoma. plications of overinflated cuffs can be are useful for the surgeries in the lower
• Stridor—due to laryngospasm. traced to cuff pressure against the tra­ jaw and face (Fig. 7.24).
• Laryngeal, tracheal injury/fractures. cheal wall causing ischemia of the
mucosa underneath. Route for Intubation
Where the need for assisted Smaller pediatric tubes generally For infants and young children, oral
ventilation is felt are uncuffed, as the cricoid cartilage, intub­ation is easier than nasal. Nasal
• Apnea. the narrowest portion of the pediatric route carries risk of dislodgement
• Inadequate respiratory effort:
– Hypoxia.
– Cyanosis.
– Tachyapnea.
– Hypercarbia.
• Diagnostic manipulations of the air­
way such as bronchoscopy.
• Endoscopic operative procedures to
the airway such as laser therapy or A B
stenting of the bronchi.
Figs 7.21A and B: (A) Armoured ETT; (B) No kinking in the armoured tube even after
• Patients, who require respiratory acute bending
support including cardiopulmonary
resuscitation.

Contraindications for Tracheal


Intubation
Absolute
• The possibility to adequately secure
and maintain airway by less invasive A B
means.
Figs 7.22A and B: (A) ETT with cuff; (B) ETT without cuff
• Cervical spine fractures.

Relative
• Severe midface fractures.
• Severe laryngeal trauma with tra­
cheal separation.
• Blind techniques are contraindicated
in the setting of major upper airway
or neck injuries.
(Evaluation of the airway before intu­
bation is discussed in this chapter). Fig. 7.23: South pole tube Fig. 7.24: North pole tube
142 Principles of Surgery

of adenoid tissue and epistaxis, but pediatrics but generally in children the upper incisors to the larynx. Loose,
advan­­­­tages include good fixation of less than 10 years old cuffed tubes filled or capped teeth, especially up­
tube. Because of good fixation, nasal are avoided to minimize subglottic per incisors, may be protected from
route is preferable to oral route in child­ swelling and ulceration. Inflation of the laryngoscope blade by a guard.
ren undergoing intensive care and the cuff with air makes the tube self- • General anesthesia (GA) is induced
requir­ ing prolonged intubation. The retaining and prevents aspiration by an intravenous or inhalational
nasal intu­bation is of great help during of the secretions and blood in the agent along with muscle relaxant.
the transoral surgeries as the oral tube tracheobronchial tree. The intravenous agents like thiopen­
comes in the way of the surgical field. • North pole tube—used for lower tal sodium or propofol are commonly
The nasal route is indicated in most face surgeries. used. These agents are pushed slowly
of the maxillofacial procedures. Nasal • South pole tube—used for maxillary and during the same the pulse and
tubes can be left in situ after major head surgeries such as cleft palate. respiration are monitored. The short-
neck procedures, where the tube is • Armoured or flexomettalic tubes—It acting muscle relaxants like succinyl­
required to be left in situ postoperatively is flexible and at the same time rein­ choline is injected quickly, after the
for maintaining the patency of the forced with metallic rings and does patient is administered intravenous
airway. In the cases of the multiple not kink. It is suitable for head and anesthesia. The succinylcholine is
facial fractures, where nasal intubation neck surgeries which require ma­ never mixed with thiopental sodium
is contraindicated and the oral tube is nipulation of the neck (see Fig. 7.22). as they are inpalatable and can lead
likely to interfere with surgical field and to precipitation. Similarly, while in­
prevent intermaxillary fixation (IMF) Size of Tube jecting the thiopental sodium, care
during the fracture reduction, the oral Because the airway of a child is narrow, must be taken to ensure that the in­
intubation is done and the outer end a small amount of edema can produce travenous cannula is indwelling and
of the tube is drawn out through the severe obstruction. Edema can easily be patent as the extravasation of this
floor of the mouth, below the chin. It caused by forcing in a tracheal tube that drug can produce severe tissue reac­
is called submental or transmylohyoid is too tight. tion and necrosis.
intubation (discussed under trauma). The correct diameter of the tube is • Absence of reflexes (pharyngeal,
that, which results in a small leak at a laryngeal and corneal reflex) and
Position of Tube pressure of about 25 cm of water (the tip adequate muscular relaxation are
The tip of tube should be at midtrachea should be at midtrachea, between the necessary for laryngoscopy.
(between the clavicles on an AP chest clavicles on an AP chest X-ray). • Relaxation must be good and can
X-ray). The position of the tube is For normally nourished children be monitored by stimulation on the
checked by auscultation (equal air entry more than about 2 years old, the follow­ facial nerve.
on each side and by chest X-ray). If the ing formula to calculate the internal di­ • The laryngoscope blade is inserted
tube is passed too deep it will cross the ameter of the tube is likely to be of the from the right side of the patient’s
carina and enter the right bronchus as correct size: mouth to prevent the tongue block­
it has a straight course unlike the left Internal diameter of tube (mm) = ing the view of the larynx, while
bronchus, which is oblique. In such (age in years ÷ 4) + 4 watching the blade tip as it is ad­
cases the left lung remains unperfused Roughly correct tube size can be vanced alongside the tongue to­
and air entry will be diminished or indicated by: wards the midline.
absent on the left side. In this case the Inner diameter: It can be estimated • When the epiglottis is seen, the tip is
tube should be withdrawn, so that its tip by the size of the child’s little finger. inserted firmly, but not forcibly into
is above the carina and finally the tube (For neonates, 3 mm internal diameter the vallecula and is used to lift the
is secured after verification of equal air is accepted while for premature infants base of epiglottis forward to reveal
entry on both the sides. 2.5 mm internal diameter may be neces­ the cords.
sary). • Backward pressure on the thyroid
Type of Tubes Length: It can be estimated by cartilage by an assistant may help to
• Noncuffed tubes (plain tubes) are doubling the distance from the corner of bring the cords into view.
commonly used in prepubescent the child’s mouth to the ear canal. • A gum-elastic bougie may be very
children. In cross section the airway helpful for intubations with its tip
in children is circular, which makes Technique curved anteriorly, passed into the
plain tracheal tube fits better than • A small ring pillow should usually be trachea and used as an introducer.
cuffed tube (see Fig. 7.23). placed under the occiput to flex the • The tube, passed over the bougie may
• Cuffed tubes less than 6.0 mm and neck and extend the atlanto-occipital be helped by keeping the laryngos
not inflated are accepted for use in joint. This straightens the path from cope in the mouth and by rotating the
Management of Airway in Maxillofacial Surgery 143

tube 90 degrees anticlockwise as the • Equal bilateral chest movements of the patients, one those who were not
bevel reaches the larynx (Fig. 7.25). with ventilation. given any medication and only regional
• Tube is introduced to the final posi­ • Fogging of the tube due to passage of (local) anesthesia was given. The other
tion using Magill’s forceps (Fig. 7.26) humid air coming from lungs. class had those treated under GA. The
and secured using a suture or an • An absence of stomach contents in clinicians felt it necessary to find other
elastic tape (Fig. 7.27). the tube. modalities, where the patients could be
The other modalities for intubation treated in the dental office only without
are retrograde intubation, blind nasal Concious Sedation5 the necessity of GA. The patients
intubation, fiberoptic laryngoscope or The field of dentistry requires many compliance, mood, pain perception,
bronchoscope assisted intubation or clinical procedures to be performed pain threshold may be altered in such a
laryngeal mask ventilation (Fig. 7.28). in the clinics in the dental chairs. The way that his/her level of apprehension
patients are often apprehensive and goes down, pain threshold increases
Observational Methods to anxious. The patient needs to be pro­ without loosing patient compli­ance.
Confirm Correct Tube Placement perly prepared psychologically for effec­ In between the stage, where the
• Direct visualization of the tube pass­ tive management. The dental chair is patient is given only regional anesthesia
ing through the vocal cords. not a place, where general anesthesia and the extreme end of the spectrum,
• Clear and equal bilateral breath can be administered and the patients are where the patient is fully anesthetized
sounds on auscultation of the chest. set-ups for doing the minor procedures, by giving GA there is a lot of gray area,
• Absent sounds on auscultation of which was time consuming and costly. In which can be used to treat the patients
the epigastrium. the past there were only two categories effectively on the OPD basis. If we
understand the pain physiology it is
seen that the spectrum of pain control is
as follows:
• Patient given only regional anesth­
esia and no medication.
• Regional anesthesia with sedation.
• N2O + sedation.
• Neuroleptanalgesia.
• Neuroleptanesthesia.
• Dissociative anesthesia.
• General anesthesia.
The width of this spectrum is utilized
for the management of the patients.
Fig. 7.25: Laryngoscope with blades of Fig. 7.26: Magill’s forceps
different sizes The conscious sedation does not
mean the stage of analgesia of the GA.
To understand the conscious seda­
tion the definition of the consciousness
should be understood.
It means the patient favorably res­
ponds to command, the patient is able

Fig. 7.27: Laryngoscopy and insertion of ETT Fig. 7.28: Laryngeal mask airway
144 Principles of Surgery

to clear his airway as all the protective nitrous oxide is commonly practiced form of outdoor anesthetics is dissocia­
reflexes are well preserved (Box 7.1). modality for minor oral surgical proce­ tive anesthesia with ketamine.
These goals can be achieved by dures. The most commonly practiced The conscious sedation is mostly
giving many medications, like benzo­ indi­cated for minor pediatric proce­
diazepines, barbiturates, nitrous oxide, dures (Box 7.2).
opioids, ketamine and GA. The route of Box 7.1: Aims of conscious sedation The procedures that are performed
administration could be oral, parenteral are dental extraction of pediatric pa­
or inhalation. There is a thin dividing 1. To alter the mood of the patient, so tients, removal of sutures of pediatric
line between the sedation and anesthesia that the acceptability of the procedure patients especially after cleft lip surgery,
increases the anxiety is alleviated.
while using certain drugs like nitrous I and D, debridement of facial wounds,
2. To alter the pain perception and pain
oxide, thiopental sodium, secobarbital, threshold. burn dressing, reduction of fractures or
hexobarbital, etc. as this phenomenon 3. To alter the physiological parameters dislocations, etc. (Box 7.2).
is dose related. If more does are used it minimally.
can have anesthetic effect and in lower 4. To preserve all the protective reflexes
to that the patient is able to clear his REFERENCES
doses analgesic, sedative or tranquilizing
own airway.
effect. The past literature mentions 5. To have patient under command 1. Adams AP, Hevitt PV, Grand CN
the use of lytic cocktails comprising during the procedure. (Eds): Emergency Anesthesia 2nd edn.
of pentazocine lactate, diazepam and Oxford University Press, 1998.
phenergan to be given preoperatively 2. Walls RM. Cricothyroidotomy, Emerge
along with the regional anesthesia. Med Clin North Am. 1988;6:725.
Box 7.2: Indications for conscious sedation
The more refined version is conscious 3. Benett JD. High Tracheostomy and
sedation. other errors – Revisited. J Laryngol Otol
1. Pediatric patients where compliance is
In precise, the commonly practiced not present. 1996;110(11):1003-7.
modalities of conscious sedation are 2. Apprehensive patients. 4. Negus VE. Explanation of Respiratory
premedication to the patient with pen­ a. The procedures where adequate Failure Sometimes Occurring After
tazocine lactate and or diazepam in a anesthesia/analgesia cannot be Successful. Tracheotomy Ann OtoL
dose 15 to 30 mg and 2.5 to 5 mg, respec­ obtained by regional anesthesia Bhin and Laryng (Sept). 1938;47:608.
and GA is not necessary.
tively. In children, instead of diazepam, 5. Benett CR. Conscious Sedation as an
b. Where profound analgesic effect is
Phenergan (promethazine) is used. required. alternative to General anesthesia. NY
Regional anesthesia combined with State dent J. 1976;42:351.
8 Biomedical Waste
Management
Borle Rajiv M, Sachdeva Sachin Dev

In accordance with the rules framed by Keeping in view inappropriate bio- different, necessitating different meth­
the Ministry of Environment and Forests medical waste management, the Minis- ods/options for their treatment/dis­posal.
and notified as the Biomedical Waste try of Environment and Forests notified In Schedule I of the Biomedical Waste
(management and handling) Rules, July the ‘Biomedical Waste (management and (management and handling) Rules, 1998,
1998: every hospital generating biomed- handling) Rules, 1998’ in July 1998. In ac- therefore, the waste origin­ ating from
ical waste (BMW) needs to set-up requi- cordance with these Rules (Rule 4), it is the different kinds of such esta­ blishments,
site BMW treatment facilities on site or duty of every ‘occupier’, i.e. a person who have been categorized into 10 different
ensure requisite treatment of waste at has the control over the institution and, or categories (Table 8.1) and their treat­ment
common treatment facility. No untreat- its premises, to take all steps to ensure that and disposal options have been indica-
ed BMW can be stored beyond a period waste generated is handled without any ted.
of 48 hours. adverse effect to human health and envi-
The cost of construction, operation ronment. The hospitals, nursing homes,
and maintenance of system for managing clinics, dispensaries, animal house, path- Components of
BMW represents a significant part of ological laboratories, blood banks, etc. Biomedical Waste
overall budget of a hospital, if the BMW are therefore required to set in place the (Box 8.1)
rules have to be implemented in their biological waste treatment facilities. It is
true spirit. Two types of costs are required however not mandatory that every institu- • Human anatomical waste (tissues,
to be incurred by hospitals for BMW tion has to have its own waste treatment organs, body parts, etc.).
management, internal and external. facility. The rules also envisage that com- • Animal waste (as above, generated
Internal cost is the cost for segregation, mon facility or any other facilities can be during research/experimentation,
mutilation, disinfection, internal storage used for waste treatment by entering into from veterinary hospitals, etc.)
and transportation including hidden cost a memorandum of understanding with • Microbiology and biotechnology
of protective equipment. External costs the service provider. However, it is obliga- waste such as, laboratory cultures,
are offsite transportation, treatment and tory on part of the occupier to ensure that microorganisms, human and ani-
final disposal. the waste is treated within a period of mal cell cultures, toxins, etc.
Hospital is one of the complex 48 hours.1 • Waste sharps, such as hypodermic
institutions, which are frequented by needles, syringes, scalpels, broken
people from every walk of life in the glass, etc.
Definition2
society without any distinction between • Discarded medicines and cytotoxic
age, sex, race and religion. This is over ‘Biomedical waste’ means any solid drugs.
and above the normal inhabitants of and/or liquid waste, including its con­ • Soiled waste, such as dressing, band­
hospital, i.e. patients and staff. All of tainer and any intermediate pro­ duct, ages, plaster casts, material contami-
them produce waste, which is increasing which is generated during the diag­nosis, nated with blood, etc.
in its amount and type due to advances treatment or immunization of human • Solid waste (disposable items like tu­
in scientific knowledge and is creating its beings or animals or in research per­ bes, catheters, etc. excluding sharps).
impact. The hospital waste, in addition taining there to or in the production or • Liquid waste generated from any of
to the risk for patients and personnel tes­t­ing there of. The physi­cochemical and the infected areas.
who handle these wastes pose a threat biological nature of these components, • Incineration ash.
to public health and environment. their toxicity and potential hazard are • Chemical waste.
146 Principles of Surgery

Table 8.1: Color coding for different waste containers • Hospital acquired infection (HAI)
(Nosocomial) to the patients due to
Option Waste category Color coding spread of infection.
• Risk of infection outside the hospital
Category No. 1 Human anatomical Yellow
for waste handlers/scavengers and
Category No. 2 Animal waste Yellow
eventually general public.
Category No. 3 Microbiology and biotechnology Yellow, Red
• Occupational risk associated with
Category No. 4 Waste sharps Blue/White translucent puncture
hazardous chemicals, drugs, etc.
proof
• Unauthorized repackaging and sale
Category No. 5 Discarded medicines and cytotoxic Black
of disposable items and unused/
Category No. 6 Solid Yellow, Red
date expired drugs.
Category No. 7 Solid Red, Blue/White translucent
Category No. 8 Liquid waste Drained after treatment Environmental Concerns
Category No. 9 Incineration ash Black
The following are the main environ­
Category No. 10 Chemical waste Black mental concerns with respect to impro­
per disposal of biomedical waste mana­
Box 8.1: WHO classification of biomedical gement:
waste3 • Spread of infection and disease
through vectors (fly, mosquito, insects,
Infectious: Waste from surgery and auto­ etc.), which affect the in-house as well
psies on patients with infectious diseases.
as surrounding population.
Sharp: disposable needles, syringes, saws,
blades, broken glasses, nails or any other • Spread of infection through contact/
item that could cause a cut. injury among medical/non-medical
Pathological: tissues, organs, body parts, personnel and sweepers/rag pickers,
human flesh, fetuses, blood and body fluids. especially from the sharps (needles,
Pharmaceutical: drugs and chemicals blades, etc.).
that are returned from wards, spilled,
outd­ated, contaminated, or are no longer
• Spread of infection through unautho­
required. rized recycling of disposable items
Radioactive: waste contaminated with such as hypodermic needles, tubes,
radioactive substances. blades, bottles, etc.
Fig. 8.1: Universal symbol of hazardous
biomedical waste • Reaction due to use of discarded
Universal symbol of hazardous bio­ medicines.
medical waste is shown in Figure 8.1. • Toxic emissions from defective/inef­
• Pathological wastes: tissues, organs, fi­­cient incinerators.
body parts and body fluids. • Indiscriminate disposal of incin­er­
Infectious Waste
• Contaminated sharps: needles sy- ator ash/residues.
The infectious waste is the material con­ ringes, pasteur pipettes, broken glass
taining pathogens in sufficient concen­ and scalpel blades. Infectious Waste Management
tration or quantity that, if exposed can • Contaminated carcasses: Body parts Plan6
cause diseases. For example, waste from and bedding. The vital steps for safe and scientific
surgery, autopsy, patients with infectious • Miscellaneous contaminated was­ management of biomedical waste in any
diseases. tes: include those from surgery and establishment are:
autopsies, contaminated labora- • Handling
Types of Infectious Waste4 tory wastes, dialysis unit wastes and • Segregation
• Isolation waste: generated by pati­ conta­minated equipment. • Mutilation
ents who are isolated. Color coding of waste disposal con- • Disinfection7
• Cultures and stocks of infectious tainers are given in Table 8.1. • Storage
agents and associated biologicals, e.g. • Transportation
wastes from the production of biologi- Health Hazards Associated • Final disposal
cals, discarded live and attenu­ated vac- with Poor Management The key to minimization and effec­­
cines and culture dishes and devices. of Biomedical Waste5 tive management of biomedical was­te
• Biological wastes: blood as well • Injury from sharps to staff and waste is segregation (separation) and iden­
as serum, plasma and other blood handlers associated with the health tification of the waste. The most appro­
products. care establishment. priate way of identifying the categories of
Biomedical Waste Management 147

biomedical waste is by sorting the waste bustible containers and steam steril- • Chemical disinfection
into universally color coded plastic bags ization requires packaging materials • Irradiation
or containers. Biomedical waste should such as low-density plastics that al- After treatment, the wastes or their
be segregated into containers/bags at low steam penetration and evacua- ashes can be disposed off by discharge
the point of generation in accordance tion of air. into sanitary sewer systems (for liquid or
with Schedule II of Biomedical Waste • Carts and recyclable containers that ground-up waste) or buried in sanitary
(management and handling) Rules 1998 are used repeatedly for transport and land­fills.
as given in Table 8.1. The BMW should be treatment of bagged waste should
segregated at the point of its generation be disinfected after each use. Single- Steam/Autoclaving Treatment
as it is not possible to segregate it later use containers should be destroyed • Containers that can be used effecti­
without undue risk. Only 15 to 20 per­ as part of the treatment process. vely in steam sterilization are plastic
cent of BMW is hazardous, but if it is • Infectious waste should not be com­ bags, metal pans, bottles and flasks.
not segregated then it is 100 percent pacted before treatment. This process High-density polyethylene and poly­­
hazardous. The contaminated sharps could damage the packaging and dis- propylene plastic should not be used
are the most dangerous. perse the contents or it could interfere in this process, because they do not
• Designation: The waste needs to be with the effectiveness of treat­ment. facilitate steam penetration to the
designated as per the WHO classifi­ • Outside the hospital, infectious waste waste load. Heat-labile plastic bags
cation. should be transported in closed, allow steam penetration of the waste,
• Segregation: The waste generated leak-proof dumpsters or trucks. but they may crumble and melt. If
in a hospital needs to be segregated • The waste should be placed in rigid heat-labile plastic bags are used,
and stored in the different containers or semirigid, leak-proof containers they should be placed in another
as per the color coding mentioned in before being loaded onto trucks. heat-stable container that allows
the Table 8.1. steam penetration such as a strong
• Packaging: The packaging of the Storage paper bag or they should be treated
waste needs to be done properly to The BMW must not be stored in the with gas/vapor sterilization.
avoid accidental spillage, handling hospital premises for more than • Waste that contains antineoplastic
by the children or lay men as it is 48 hours. It is ideal to do the BMW on drugs, toxic chemicals or chemi­
highly contagious and can lead to daily basis. However, if it is to be stored cals that would be volatilized by
hazardous spread of the infection. for its final disposal it must be stored steam should not be steam-sterili­
securely ensuring that: zed.
Packaging of Infectious • The area of the storage is in the
Waste8 secluded, remote corner. Gas/Vapor Treatment
• Liquid infectious wastes can be • The area is well cordoned by proper Gas/vapor sterilization uses gaseous or
placed in capped or tightly stoppe­ fencing and locked. vaporized chemicals as the sterilizing
red bottles or flasks. Large quantities • The BMW must be stored in rigid agents. Ethylene oxide is the most
may be placed in containment tanks. or semi-rigid, leak proof containers comm­­­only used agent, but should be
• Solid or semisolid wastes may be to prevent spillage and spread of used with caution since it is a suspected
placed in plastic bags. infection through the vectors (flies). human carcinogen. Because ethylene
• Select tear-resistant bags. Plastic • The universal symbol of hazardous oxide may be adsorbed on the surface of
bags are judged by their thickness or BMW must be prominently displa­ treated materials, the potential exists for
durability as evaluated by the ASTM yed and warning notice in the worker exposure when sterilized mat­
dart test (ASTM 1975). vern­acular language must be pro­ erials are handled.
• Do not place sharp items or items minently dis­played.
with sharp corners in the bags Standards for Incinerators
(Place sharps in impervious rigid, Treatment and Disposal Incineration is a high-temperature dry
puncture-resistant containers made oxi­dation process that reduces organic
Methods9
of glass, metal, rigid plastic or wood). and combustible waste to inorganic, in-
• Do not load a bag beyond its weight The following methods are practiced to combustible matter and safe manage-
or volume capacity. render the biomedical waste inert and ment of wastes from health care activities
• Keep bags away from coming into safe for its final disposal so that the risk (Box 8.2).
contact with sharp external objects. of infection transmission is minimized
• Consider double bagging. to the community as a whole. Waste types not to be incinerated
• Some treatment techniques required • Steam sterilization • Pressurized gas containers.
special packaging characteristics. For • Incineration • Large amounts of reactive chemical
example, incineration required com- • Thermal inactivation waste.
148 Principles of Surgery

Box 8.2: Standards for incinerators unit. Biological indicators for the BMW need to wear heavy duty gloves
microwave shall be Bacillus subtilis to prevent accidental needle pricks or
• Combustion efficiency (CE) shall be at spores using vials or spore strips with injuries due to sharps. The personnel
least 99 percent
at least 1 × 10 to the power of four need to be immunized actively against
• The temperature of the primary cham­
spores per milliliter. tetanus and hepatitis B.
ber shall be 800 ± 50°C
• Shall not be used for cytotoxic, haza­
• Height of the chimney 80 feet as
per environment pollution prevention rdous or radioactive wastes, conta­
nor­ms. minated animal carcasses, body Legal Aspects and
• Suitably designed pollution control parts and large metal items. Environmental
devices should be installed/retrofitted
Concerns10
with the incinerator to achieve the Standards for Deep Burial
above emission limits, if necessary • A pit or trench should be dug about Indiscriminate disposal of infected and
• Wastes to be incinerated shall not be
2 meters deep. It should be half-filled hazardous waste from hospitals, nursing
chemically treated with any chlorinated
disinfectants with waste then covered with lime homes and pathological laboratories
• Chlorinated plastics shall not be incin­ within 50 cm of the surface, before has led to significant degradation of
er­ated filling the rest of the pit with soil. the environment, leading to spread
• It must be ensured that animals do of diseases and putting the people to
not have any access to burial sites. great risk from certain highly contagious
Covers of galvanized iron/wire mes­ and transmission prone disease vec­tors.
• Silver salts and photographic or rad­ hes may be used. The site should This has given rise to considerable envir­
io­­graphic wastes. be well cordoned off by fencing and on­mental concerns. The first stan­dard on
• Halogenated plastics such as poly­ the signal of hazardous biomedical the subject to be brought out in India was
vinyl chloride (PVC). waste should be displayed promi­ by the Bureau of Indian Standards (BIS),
• Waste with high mercury or cadm­ nently. IS 12625:1989, entitled ‘Solid Wastes-
ium content, such as broken ther­mo­ • The deep burial site should be rela­ Hospitals-Guidelines for Management’,
meters, used batteries, and lead-lined tively impermeable and no shallow but it was unable to bring any improve­
wooden panels. well should be close to the site. ment in the situation. In this scena­
• Sealed ampoules or ampoules con­ • The site should be in an area, which rio, the notification of the ‘Biomedical
taining heavy metals. is not flood prone. waste’ (Management and Handling)
Rules, 1998 assumes great significance.
Standards for Liquid Waste Contingency Measures The Central Govt. has notified these
The liquid waste generated in the hos­ Contingency measures should be deve­ rules on 20th July, 1998 in exercise of
pital should never be passed in the mu- loped to deal with emergencies that oc- section 6, 8 and 25 of the Environment
nicipal sewerage lines without proper cur during the handling, transportation (Protection) Act, 1986. Prior to that,
treatment. The liquid waste should be or disposal of infectious waste. Emer­ the draft rules were gazetted on 16th
collected in a reservoir, disinfected and gencies include spills of liquid infectious October, 1997 and Public suggestion/
treated before releasing it into the sew- waste, ruptures of plastic bags or other comments were invited within 60 days.
erage lines. The treated liquid waste containers holding infectious waste and These suggestions were considered be­
must meet the following criteria before equipment failures. fore finalizing the rules.
it is released in the sewerage:
• pH 6.5 to 9.0. Staff Training Scope and Application
• Suspended solids 100 mg/L To practice the healthy methods of the of the Rules
• Oil and grease 10 mg/L biomedical waste management it is These rules apply to all those who
• Bioassay test 90 percent survival of empirical that all the personnel including generate, collect, receive, store, trans­
fish after 96 hours in 100 percent doctors, nurses, paramedics, lab assis­ port, treat, dispose or handle biomedical
effluent. tants need to be oriented and trained in waste in any form. According to these
the practices of biomedical management. rules, it shall be the duty of every occ­u­pier
Standards for Microwaving All the practices are ineffective unless of an institution generating bio­medical
• The microwave should completely every member is oriented and under­ waste, which includes hos­pitals, nursing
and consistently kill the bacteria stands the impor­tance of these methods homes, clinics, disp­en­saries, veterinary
and other pathogenic organisms and his/her role in the team. institution, animal houses, pathology
that are ensured by approved biolo­ The personnel protection measures laboratories, blood banks, etc. to take
gical indicator at the maximum include cap, masks, gloves, gumboots all steps to ensure that such wastes are
design capacity of each microwave and aprons. Those who handle the handled without any adverse effect to
Biomedical Waste Management 149

human health and the environment. They with respect to imple­ mentation of preventing hospital acquired infec­
have to either set-up their own facility these rules. The occupier or operator tions in England associated with the
within the time frame or ensure requisite can also appeal against any order of the use of short-term indwelling urethral
treatment at a common waste treatment authority, if they feel aggrieved to such catheters in acute care: Technical
facility or any other waste treatment other authority as the Government of the report. London: Thames valley univer­
facility. Every occupier of an institution, State/UT may think fit to constitute. sity; 2000.
which is gene­rating, collecting, receiving, 6. Rutala WA, May Hall cg. The society
storing, trans­porting, treating, disposing of hospital epidemiology of America.
References
and/or handling biomedical waste in Position paper: medical waste. Infec­
any other manner, except such occupier 1. Garner JS. Hospital Infection control tion control Hosp Epidemiol. 1992;13:
of clinics, dispensaries, pathology lab­ practices advisory committee. Guide­line 38-48.
o­r­atories, blood banks, etc. which pro­ for isolation precautions in hospitals. 7. Johan, et al. Role of disinfectants in
vide treatment/service to less than Infect control Hosp Epi-demio. 1996;17: infection control. Dent Clin North Am.
1,000 patients per month shall make an 54-80. 1991;35(2).
application in prescribed form to the 2. Reinhardt PA, Gordon JG. Infectious 8. Recommended practice: Selection and
prescribed authority for grant of autho­ and medical waste management. Chel­ use of packaging systems. AORN J.
rization to carry on the work. Whenever sea, MI: Lewis Publishers. 1991. 1992;56(6):1096-100.
an accident occurs concerning biome­ 3. Tikhomirov E. WHO Programme for 9. AAMI: Good hospital practice: Flash
dical waste, it has to be reported to control of hospital infections. Chemio- sterilization–steam sterilization of
this authority. Each State and Union therapia. 1987;3:148-51. pati­ent care items for immediate use,
Territory (UT) Government shall be req­ 4. Ayliffe GAJ, Fraise AP, Geddes AM, Mit­ Arling­ton Va, 1992, American national
uired to establish a prescribed autho­rity chell. Control of Hospital Infection, 4th standards institute.
for this purpose. The respec­tive govern­ edition. London, Arnold. 2000. p. 101. 10. Statutory instrument no 3246. The con­
ments would also con­ stitute advisory 5. Pratt, et al. The development of nati­ trol of substances hazardous to health
committees to advise the Governments onal evidence–based guidelines for regulations. London. HMSO, 1994.
Section 2
Neurological Disorders of Face
and General Anesthesia

n Neurological Disorders of the Face


n General Anesthesia
9 Neurological Disorders
of the Face
Borle Rajiv M, Rai Anshul

Apart from the motor and sensory inn­ involve any division of trigeminal nerve, of the 5th cranial nerve, accompanied by
er­­
vation, the face has autonomic inn­ but it commonly involves the mandi­­bu- spasmodic contractions of facial muscles,
ervation from the sympathetic chain lar, maxillary divisions than the ophth­al- often initiated by a ‘trigger zone’.
and the parasympathetic innervation mic division. First complete description
from the mid-brain outflow. The major of TN was given by John Locke in 1677. Etiology
sensory nerve of the face is the trigeminal Nicolas Andre2 in 1756 coined the term Although the etiology is not always
nerve (Vth cranial nerve). The muscles ‘Tic Douloureux’. In 1773, John Fothergill established, certain etiological factors
of mastication are supplied by the motor gave full and acc­ urate description, are proposed. When the etiology is not
division of the trigeminal nerve while henceforth known as Fothergill disease.3 established it is termed idiopathic.
muscles of facial expression are supplied The proposed etiological factors are
by the facial nerve (VIIth cranial nerve). Various Other Descriptions of divided into the following:
The parasympathetic supply to the Trigeminal Neuralgia • Peripheral causes:
orbit comes from the Edinger-Westphal Trigeminal neuralgia is a sudden, – Nerve compression.
nucleus and is relayed through the usually unilateral, severe, brief, stabbing, – Nerve trauma.
occulomotor (IIIrd cranial) nerve. The recurrent pain in the distribution of one – Nerve back talk.
secretomotor fibers to the parotid and or more branches of Vth cranial nerve.4 – Aneurysm around the nerve.
submandibular salivary gland are derived Peterson5 defined it as “It usually – Demyelination of the nerve.
through the inferior and superior salivary presents with sharp, electric shock-like – Herpes zoster infection.
nucleus, respectively.1 pain in the face or mouth. Pain is intense, • Central causes:
The face is commonly involved in lasting for brief period of seconds to – Microaneurysm around the nerve
the neurological disorders such as, facial 1 min. After which there is refractory root.
nerve paralysis, trigeminal neuralgia, period during which pain cannot be – Cerebro-Pontine (CP) angle tum­
glossopharyngeal neuralgia, vascular re-initiated for a period of time”. ors.
headaches, migraine, Frey’s syndrome, IHS definition (International Head­­ – Multiple sclerosis.
neuroparalytic occular conditions such ache Society): Painful unilateral affec­tion – Demyelination of the nerve.
as diplopia, etc. Some of the common of the face, characterized by brief electric – Nerve back talk.
neurological disorders involving the shock-like pain limited to the distribution – Pulsations of basilar artery (Fig.
face have been discussed in this chapter. of one or more divisions of trigeminal 9.1).
nerve. Pain is commonly evoked by trivial – High petrous ridge.
stimuli including washing, shaving,
TRIGEMINAL NEURALGIA smoking, talking and brushing the teeth,
(TIC DOULOUREUX, but may also occur spontaneously. The Clinical Features
IDIOPATHIC TRIGEMINAL pain is abrupt in onset; terminations may • The incidence of trigeminal neuralgia
NEURALGIA) remit for varying periods. is 4 in 1,00,000 and thus, it is relatively
British Journal of Anesthesia6 (2001): rare.
The trigeminal neuralgia (TN) is defined Paroxysmal episodes of sudden, usually • The patients are usually in the 5th –
as “An intermittent, paroxysmal, sharp unilateral, severe recurrent pain of 6th decade of life.
shooting, stabbing, lancinating pain in the shearing, stabbing or lancinating type, in • It has a female predilection (Sex:
distribution of trigeminal nerve”. It can the distribution of one or more branches F > M).
154 Neurological Disorders of Face and General Anesthesia

tions during the day, origin and referred


areas, any previous treatment and its
results, etc. It must be remembered that
pain is a symptom and not a sign and the
fact that it is experienced by the patient
only, hence he/she only can describe it in
a best way. The other common causes
like caries, periapical infection pulpitis,
etc. must be ruled out. Investigations are
required to rule out other causes for pain
and in some cases may help in locating
the cause of trigeminal neuralgia but
the diagnosis of TN is often made on
basis of history and clinical examination.
The radiographs, computed tomography
(CT) scan, magnetic resonance imaging
(MRI) and angiography may be able to
Fig. 9.1: Relation of basilar artery with the sensory root of TN
locate the cause in some cases, but it is
invariably inconclusive and thus most of
the cases are labeled as idiopathic.
• It is more commonly seen on the right from the pain. This induces hyper­
side (side predilection: right side). keratosis of the skin of the face on Role of Diagnostic Nerve
• The mandibular division is most the involved side. Block
comm­only involved followed by the • During the attack the patient’s The diagnostic nerve block is often given
maxillary and the ophthalmic divisi­ facial expressions are peculiar and to confirm the diagnosis of neuralgia.
ons (Division predilection: V3 > V2 > give a significant clue towards the The local anesthetic solution is injected
V1). diagnosis. As the pain is precipitated around the peripheral branch, where the
• The pain is often described as sharp, on facial movements the patient trigger zones are located and not around
shooting, stabbing and lancinating. tends to guard the facial movements the main nerve trunk in the distribution
• It comes in paroxysms, lasts for a producing a ‘mask face’ appearance. of which the actual pain occurs. Because,
few seconds and disappears only to • The pain is present when the patient if the main nerve trunk is blocked, all
reappear after some time. is awake, it may prevent him from the sensations are lost and pain due to
• The pain is precipitated by touching going to sleep but will seldom dis­ even an inflammatory pathology will
certain cutaneous areas in the distri­ turb the sleep. also get abolished and the result will be
bution of the nerve. These areas are • The pain responds to the treatment inconclusive. If the trigger zones are not
described as ‘trigger zones’. with anticonvulsants. well circumscribed then a local infil­
• The pain is invariably unilateral • The patient may have undergone teration in the region of the trigger zone
in distribution. It can cross over to multiple dental extractions on the should be given. Effort must be made to
other side after the pain on the side involved side due to improper di­ block the most peripheral part of the nerve
has ceased. agnosis of this condition and mis­ and not the main trunk of the nerve.
• Between the two attacks of pain there taking it as an odontogenic pain. The diagnostic block will block the
is a short period during which the trigger areas and the neuralgic pain
nerve cannot be excited and pain Diagnosis is abolished. If the pain is due to the
does not occur, this period is called There are no definitive diagnostic organic pathology such as odontogenic
‘refractory period’. During this period tests. The diagnosis is based purely on path­ology will not get eliminated. Secon­
the nerve is hyposthetic. This can be the history and clinical findings and dly the diagnostic block will not only help
explained due to depolari­zation of the hence the clinician must give a ‘patient in differentiating the neur­algic pain from
nerve and the fatigue of the sodium listening’ and should not jump to con­ the other pains due to other inflammatory
pump, due to repeated stimulation. clusions or work with a prejudiced pathologies, but the patient can be
• The patient refrains from shaving, mind. After listening to the complaints exp­lained how the part would remain
cleaning the teeth due to the fear of of the patient leading questions may be anesthetic, if any destructive surgical
precipitation of attack of pain. asked to get full information about the procedure like peripheral neurectomy
• During the pain the patient vigoro­ pain, its nature, duration, precipitating, or alcohol injection is carried out, to get
usly rubs the cheek to get the relief aggravating and relieving factors, varia­ relief of the pain.
Neurological Disorders of the Face 155

Sweet’s Diagnostic Criteria for TN7 a day. The side effects are drowsiness • Destructive
(White and Sweet) and gingival hypertrophy. – Peripheral neurectomy
• The pain is paroxysmal. The patient who is prescribed – Inferior alveolor nerve neurec­
• The pain may be provoked by light these drugs must always be instru­cted tomy
touch to the face (trigger zone). to refrain from driving, swimming, – Supraorbital nerve neurec­to­my
• The pain is confined to trigeminal working in industries near machinery – Infraorbital nerve neurectomy
distribution. to avoid mishaps. The side effects – Supratrochlear nerve neurec­
• The pain is unilateral. associated with pheny­ toin sodium tomy.
• The clinical sensory examination is therapy are: – Peripheral nerve blocks with alco­­
normal. – Slurred speech hol, phenol, glycerol, hot water,
If the patients’ pain fails to meet any – Abnormal movements etc. (Fig. 9.2).
of the 5 forgoing criteria, the diagnosis – Gingival hypertrophy The inferior alveolar nerve neurec­
of idiopathic TN is uncertain and the – Folate deficiency. tomy is done intraorally through a
treatment required may be substantially • The drug like phenobarbitone, dia­ Ginwalla’s incision (inverted ‘Y’ incision,
different. ze­­
pam may be prescribed as an Fig. 9.3), taken in the retromolar area.
adju­­vant therapy. The mandibular foramen is located
Treatment • Gabapentin is also prescribed in a on the medial side of the ramus of
The treatment modalities for trigeminal dose of 100 to 200 mg 2 to 3 times a the mandible. Using a nerve hook,
neuralgia are divided into the following: day. the inferior alveolar nerve and artery
• Medicinal treatment (conservative) • Clonazepam 1.5 mg/day. The side are drawn forward, ligated and the
• Surgical treatment—which can be effects associated with this therapy distal end is avulsed by performing the
further divided into: are drowsiness, fatigue, lethargy.
– Peripheral: • Tab oxcarbazepine, 1200 mg/day,
- Destructive. the side effects are hyponatremia,
- Nondestructive. double vision.
– Central: • The role of B1, B6, B12 preparations is
- Destructive. not established, but they are often
- Nondestructive. prescribed as ‘nerve tonic’.
The medicinal treatment is usually
Medicinal Treatment the first line of treatment. Apart from
The medicinal treatment comprises of the routine complications associated
drug therapy. The prescription of anti­ with the medicinal treatment another
con­vulsants is commonly practiced. complication is the drug tolerance.
• Carbamazepine, (Tegretol®, Maze­ As the treatment is given over a long
tol®) in a dose of 100 to 200 mg three period the pain does not respond to the Fig. 9.2: Peripheral branches of the TN
times a day, is usually adequate in doses of the drugs, which were effective where the neurectomies or nerve blocks can
con­trolling the pain effectively. The earlier to produce adequate pain relief be done
dose of carba­mazepine should not and the doses of the drugs need to be
exc­eed 2 g/day. The usual immediate increased or combination of the drugs
side effects with carbamazepine are are required to be prescribed to certain
dizziness, loss of fine neuromuscular patients for effective pain relief. The
coordination, dro­wsiness, tremors, patient sometimes does not respond
gas­trointestinal (GI) disturbances. to the medicinal treatment or may not
The side effects of long-term therapy be able to afford the cost of the therapy
are bone marrow depression leading where the surgical line of treatment
to agranulocytosis, tolerance to the comes into consideration.
drug which leads to increased dose
requirement and ineffectiveness of Surgical Treatment
the therapy. The surgical treatment can be described
Dilantin sodium/Phenytoin sodi­ under following heads:
um is also used to control the pain; it
may be used alone or in combination Peripheral Procedures
with carbamazepine. Dilantin is given These procedures are further divided
in a dose of 50 to 100 mg 2 to 3 times into the following: Fig. 9.3: Ginwalla’s inverted ‘Y’ incision
156 Neurological Disorders of Face and General Anesthesia

corticotomy in the buccal cortical bone artery forceps. Finally the infraorbital Central Procedures
right up to the mental foramen. foramen is decorticated, using a bur to
The mental nerve neurectomy is prevent the regeneration of the nerve Nondestructive
done through an intraoral incision as the decorticated foramen heals com­ These procedures are sensory root dec­
taken in the labial vestibule in the lower pletely by bone formation. o­­­
m­ pression (Figs 9.4A to D), when
anterior to premolar area. The mental Injection of alcohol, phenol, boiling aneurysms are present around it. The
nerve and its branches are identified water is given in the vicinity of the nerve, resection of CP angle tumors or other SOL
and clamped with an artery forcep. which causes destruction of the nerve is the non-destructive procedures. The
The peripheral branches are dissected by inducing the xanthenes degener­ pulsations of the inferior cerebellar artery
and avulsed. The proximal end is then ation of the nerve. Proper care must are suppose to cause demyelination of
avulsed. The mental foramen is decor­ be taken, while giving the injection as nerve and provocation leading to pain.
ticated to prevent the nerve reg­ ener­ these agents can cause sloughing of the Inter­positioning of inert material between
ation. soft tissue. the artery and the sensory root causes
The infraorbital nerve neurectomy decompression of the sensory root and
is also performed intraorally through a Nondestructive Procedures relieves the pain.
deglo­ving incision taken in the upper The surgical procedures that do not da­
labial vestibule from the incisor to the mage the nerve are called nonde­structive Destructive Procedures
second premolar area. A full thickness procedures. These procedures comprise • Injection of alcohol or glycerol (Gly­
flap is raised and the infraorbital fora­ of nerve decompression pro­cedures in cerol rhizotomy) in the Gass­erian
men is located. The infraorbital nerve cases where the nerve is compressed ganglion (Fig. 9.5).
is grasped with an artery forceps near by bony fragments, impac­ ted tooth, The alcohol or glycerol injection
the foramen; its peripheral branches aneurysms, sclerosed and narrowed in the Gasserian ganglion results
are dissected and avulsed. Finally the foramina. Nerve blocks with long-acting in the destruction of neurons and
proximal end of the nerve is also avulsed local anesthetics (bupivacaine) may be thus, prevents the conduction of
from the foramen by twisting it over the given for temporary pain relief. pain and other sensory impulses. It
was a popular treatment modality
in the past but it lacked specificity.
The alcohol diffuses in the adjoining
areas and destroys it, resulting into
the neurological deficit in the other
normal regions of trigeminal nerve.
The most catastrophic result was the
involvement of ophthalmic division,
which resulted in neuroparalytic
keratitis, corneal ulcers and in some
patients blindness, secondary to it.
The other complication was anes­
thesia dolorosa (phantom pain).

A B

C D
Figs 9.4A to D: Decompression of the sensory root by inserting barrier between the
inferior cerebellar artey and the sensory root Fig. 9.5: Glycerol injections
Neurological Disorders of the Face 157

Causes
• Etiology of vagoglossopharyngeal
neu­r­a­lgia is unknown. It has been
propo­sed to be due to posterior root
dem­ yelination possibly secondary
to pressure from intracranial aneur­
ysm or a preceding periton­ sillar
infection.
• Neuralgia in these areas has been
associated with calcified stylohyoid
ligament in which chronic pressures
A B on 9th and 10th cranial nerve com­
plex have existed in the region of
Figs 9.6A and B: Thermocoagulation of the ganglion foramen spinosum.
• Glossopharyngeal neuralgia is beli­
eved to be caused by irritation of the
9th and 10th cranial nerve.
• In most cases, the source of irritation
is never found. Some possible causes
for this type of nerve pain (neuralgia)
are:
– Blood vessels pressing down on
the glossopharyngeal nerve.
– Growths (lesions) at the base of
the skull.
– Tumors or infections of the
Fig. 9.7: Sectioning to the sensory root throat and mouth.
(Rhizotomy)
Clinical Features
• Percutaneous high frequency radio Fig. 9.8: Balloon rhizotomy Symptoms usually begin in people
gangliolysis (Thermocoagulation) over 40 years of age and there is no
(Figs 9.6A and B). predilection for the sex. The left side
In this procedure an electrode • Tractectomy—division of spinotha­ is involved more than the right side.
is introduced, percutaneously in the lamic tract is the ultimate treatment Symptoms include severe pain in areas
Gasserian ganglion, through the fo­ modality for relief from severe neu­ connected to the 9th cranial nerve:
ramen ovale. The patient is not given ralgic pain or pain associated with • Back of the nose and throat (naso­
any anesthesia as per locating the terminal malignancy. ph­arynx)
area in which the electrode is present, For these intracranial procedures • Back of the tongue
pain is elicited by applying low-volt­ two common surgical approaches are • Ear
age current. The patient gets pain in taken, Dandy’s temporal approach • Throat
the corresponding area of trigeminal and Frazier’s posterior fossa approach. • Tonsil area
nerve and that is how the electrode • Larynx.
is located in proper area of ganglion. The pain occurs in episodes and may
Then a high frequency current is ap­ GLOSSOPHARYNGEAL be severe. It can sometimes be triggered
plied, which brings about selective NEURALGIA by:
destruction of ganglion, spar­ing the • Chewing
other uninvolved divisi­ons. The gan­ Vagoglossopharyngeal neuralgia or glos­ • Coughing
gliolysis produced by this method sopharyngeal neuralgia (cranial mon­o­ • Laughing
results in stereotactic lesions in the neuropathy IX) is a condition in which • Speaking
gas­serion ganglion (see Figs 9.6A and there are repeated episodes of severe • Swallowing.
B). pain in the tongue, throat, ear and The pain is less intense than tic dou­
• Rhizotomy—division of the sensory tonsils, which can last from a few seconds loureux, but the systemic side effects that
root is called rhizotomy (Fig. 9.7). to a few minutes. It involves the IX and X accompany an attack are wide- spread and
• Balloon compression rhizotomy cranial nerve in their sensory, motor and include excessive salivation, lacri­mation,
(Fig. 9.8). autonomic fibers. vertigo and involuntary movements of
158 Neurological Disorders of Face and General Anesthesia

the pharynx and larynx. Syncope may infranu­clear lesions or nuclear lesions,
occur, with progressive hypo­ten­sion and which result in different set of clinical
bradycardia. In rare cases, asystole and features. For understanding these clini­
cardiac arrest has been noted. cal features, adequate knowledge of
The attack is usually triggered by intra- and extracranial anatomy of the
swallowing or surface stimulation of the facial nerve is required.
tongue or pharynx or when tasting bitter
or spicy foods. Etiology
Clinical manifestations are attributed (Rainer Schmelzeisen 1999)
to indiscriminated artificial synpase lesi­ • Congenital
ons of the mixed 9th and 10th cranial • Neurological
ner­ves, of the autonomic areas served by • Neoplastic
the sensory component of the 9th cranial • Infection
ner­ve, the greater petrosal nerve and of • Other causes (idiopathic)
the pharngeal plexus of both 9th and • Iatrogenic Fig. 9.9: The corticonuclear fibersdotted
10th cranial nerve and the sinus nerve of • Traumatic. lines depict fibers supplying upper face
Hering. (Bilateral) while thick line() depicts the
Classification fibers supplying lower face
Investigations The facial nerve paralysis can be classified
• Computed tomography (CT) scan according to the site of the pathology:
Nuclear Lesions
and MRI of the head to identify • Supranuclear lesions
tumor or inflammation of the glosso­ • Nuclear lesions When the facial nerve nucleus in the
pharyngeal nerve. • Infranuclear lesions. pons is involved the neighboring struc­
• Angiography to find out whether a tures are invariably involved. The neigh­
blood vessel is pressing on the nerve. Supranuclear Lesions boring structures are:
Involving upper motor neuron path­ • Principal sensory nucleus of trige­
Treatment ways, is usually a part of hemiplagia. minal nerve
The goal of treatment is to control pain. The movements of the contralateral • Spinal nucleus of trigeminal nerve
Over-the-counter pain killers such as lower part of face are more severely • Nucleus of abducens nerve
aspirin and acetaminophen are not very affec­­ted than those of upper face and • Motor nucleus of trigeminal nerve
effective for the relief of neuralgia. vol­
un­ tary movements are weak or • Extrapyramidal tracts
The most effective drugs are anti­ absent, while the emotional movements • Vestibulocochlear nerve
convulsant medications, such as carba­ are unaffected. This is due to the fact The involvement of abducent nerve
mazepine, gabapentin and phenytoin. that the corticonuclear fibers going to nucleus results in the paralysis of lateral
Some antidepressants, such as amitrip­ the upper face are bilateral, while as rectus muscle. Paralysis of muscles of
tyline, may help certain patients. those going to lower face are unilateral mastication results due to involvement
In severe cases, when pain is difficult in distribution (Fig. 9.9). The etiological of motor nucleus of trigeminal nerve and
to treat, surgery to take pressure off the factors for the supranuclear palsy are: sensory loss of face may result due to
glossopharyngeal nerve may be needed. • Infarcts involvement of principal sen­sory nucleus
This surgery is generally considered effec­ • Cerebrovascular accident or spinal nucleus or spinoth­alamic tract.
tive. If a cause of the neuralgia is found, • Tumors
treatment should control the underlying • Head injury To summarize the clinical features of the
problem. Intracranial rhizotomy of the • Congenital abnormalities and agen­ nuclear lesions:
posterior root of the 9th and 10th cranial esis • Sensory deficit in distribution of tri­
nerves, as well as tractotomies can be • Secondaries. geminal nerve.
attempted for relief. • Paralysis of muscles of mastication.
Clinical Features of Supranuclear • Diplopia due to lateral rectus par­
FACIAL NERVE PARALYSIS Lesions alysis.
• Upper motor neuron pool paralysis • Hearing impairment.
The facial nerve is the 7th cranial nerve. • Lower face involved – Lesions at petrous temporal reg­
Its paralysis results in paralysis of the • Upper face unaffected ion.
muscles of facial expression and certain • Emotional movements spared • Lesions in facial canal-chorda tym­
ocular complications. The paralysis • Voluntary movements affected pani involvement—Taste sensation
may result from supranuclear lesions, • Often associated with hemiplegia. impaired
Neurological Disorders of the Face 159

A B
Fig. 9.10: Loss of wrinkling over the fore- Figs 9.11A and B: Facial nerve paralysis on right side—obliteration of nasolabial fold,
head (Left) due to paresis of facial nerve drooping of corner of mouth, lagophthalmos, loss of wrinkling on forehead

• Nerve to stepedius damaged—hy­ • Flattening of nasolabial fold (Figs


peracusis. 9.11A and B).
• Inability to blow, whistle.
Infranuclear Lesions • The lips remain in contact on the
The lesions that occur at the level of stylo­ paralyzed side, but cannot be
mastoid foramen. The eti­ology is uncer­ pursed for whistling. When the smile
tain but results from edema of the nerve is attempted, the angle of the mouth
and compression of the fibers in the sty­ is drawn up on the normal side but
lomastoid foramen or in the facial canal. on the affected side the lips remain
The etiological factors are: closed, giving a characteristic ‘trian­
• Exposure to cold. gular appearance’.
• Herpes zoster infection. • During the mastication the food
• Damage or division of the nerve accumulates in the cheek, due to the
Fig. 9.12: Bell’s sign
during surgery (parotid surgery, paralysis of buccinator and dribb­
mastoi­dectomy, middle ear surgery). les or is pushed out through the of central origin involving superior
• Involvement of the nerve in mali­ paralyzed lips. rectus and inferior oblique muscles. It
gnant tumors of the parotid gland. • The tongue appears to deviate to is very conspicuous in a patient with
• Fractures of the base of the skull. the paralyzed side on protrusion, Bell’s palsy.
but if it is seen taking the incisors as • The lagophthalmos (widening of the
Bell’s Palsy guidance it is not so. palpebral fissure) loss of blink­ing and
Bell’s palsy is defined as an idiopathic • The platysma and the muscle of inability to close the eye results in
par­esis or paralysis of facial nerve of sud­ aurical are paralyzed. exposure keratitis, corneal ulceration
den onset. The condition was descri­ • The ala nasi does not move properly and may result in blind­ness.
bed by Sir Charles Bell (1821), who with respiration. • The reaction of muscle on electrical
dem­ on­strated separation of motor and • There is a widening of the palpebral stimulation are altered (suggestive
sensory innervation of face. It has female fis­s­ure (lagophthalmos) due to the un­ of degeneration).
predilection especially pre­gnant females. o­­pposed action of levator palpe­brae. • The involvement of nerve to stape­
It has usually unilateral involve­ment and • Tears fall down (epiphora) as the dius results in hyperacusis.
can happen at any age. lacrimal puncta are not in contact
with the conjunctiva and result in Management
Clinical Features the dryness of the conjunctiva. The management is divided into the
The peripheral lesions lead to complete • Blinking is absent. following:
involvement of the face and the vol­un­ • There is loss of corneal reflex and if • Conservative.
tary emotional and associated move­ the patient tries to close the eye, the • Surgical.
ments are equally involved. eyeball rolls up, this is called Bell’s sign – Definitive.
• There is asymmetry of the face. (Fig. 9.12). Bell’s phenomenon or sign – Rehabilitative.
• Dropping of the corner of mouth. is reflex upward, and slightly outward,
• Dropping of eyebrow. deviation of the eyes in response to Medicinal Treatment
• Loss of wrinkling over the forehead forced closure, or attempted closure, • It comprises of prescription of
(Fig. 9.10). of the eyelids. This is a synkinesis cor­
ti­
co­
steroids as they have anti-
160 Neurological Disorders of Face and General Anesthesia

infla­mmatory properties. Predni­sol­ These procedures are as follows: Rehabilitating Surgeries


one, in a dose of 1 mg/kg/day for • Decompression of the nerve trunk The rehabilitating surgeries are perfor­
10 days in divided doses, to start • Anastomosis of the severed nerve med to correct the facial deformities for
with, which is gradually tapered ends when it occurs secondary to pe­n­ cosmetic rehabilitation of the patient
and withdrawn over a period of 2 to etrating injuries, surgical trauma, etc. using static fascia lata slings, innervated
3 weeks. It helps in reducing the nerve • Cross nerve innervations using a or denervated muscle slings, which are
edema and inflammation. If the facial cer­vical plexus C3 and C4 (3–12 cm), purely nonfunctional. These surgeries
nerve paralysis is secondary to the gre­ater auricular nerve, sural nerve can be described as follows.
herpes zoster infection, antiviral drugs (35 cm) grafts and anastomosing
like acyclovir may be useful. The facial the distal and proximal ends of the Fascia Lata Slings
nerve paralysis due to peripheral severed nerve or to the opposite facial The fascia lata slings are harvested from
inflammatory lesions (Bell’s palsy) nerve, (Figs 9.13A to D) spinal acce­ the lateral thigh. The slings are nothing
responds well to this treatment and ssory nerve or hypoglossal nerve, but the tendinous insertion of the lateral
almost complete recovery takes place. using the microvascular surgical fascia lata muscle. These slings are used
However, the lesions causing nerve technique. The disadvantage of this to correct the drooping of the corner of
damage, central lesions may not procedure is that the facial muscles the mouth by suturing the upper end of
respond to the treatment. Empirical will contract in unwanted manner the sling to zygomatic arch, the lower
therapy in form of vitamin B1, B6 and with the movements of the part end of the sling is divided into three and
B12 preparations (Neurontin, Sion­ supplied by the nerve anastomosed. they are sutured to the orbicularis oris,
euron® and neurobione, macraberine) Thus, cross innervation from the levator labii superioris alaeque nasi and
are also given. contralateral facial nerve is most the depressor anguli oris, respectively.
• Physiotherapy in the form of trans­ desired. These procedures are useful These slings lift the corner of the mouth,
cutaneous electrical nerve stimula­ only when attempted early, before but it fails to match the movements of the
tion (TENS), with galvanic current the facial muscles have become normal side of the face while the patient
stimulation is given, which produces flaccid. Even after achieving the ana­­ smiles, as they are passive and the facial
satisfactory results. Exercises, mas­ to­mical continuity of the nerve by deformity becomes obvious. Instead
sage and hot fomentations are also anastomosis the physiological con­ of the fascia lata slings nonabsorbable
prescribed. tinuity of the nerve is not assured. suture material like prolene can also be
• Protection of the eye is necessary • Rehabilitating surgeries like passive used (Figs 9.14A to F). The fascia lata
as the patient has lagophthalmos, fascia lata slings, regional muscle slings can also be used to correct the
lack of blinking, exposure kera­- transfers for cosmetic and functional lagophthalmos by tunneling them in a
titis. Wearing of protective glasses, rehabilitation of the patient. supratarsal plane below the skin of the
lub­ri­­­cating eye drops (hydroxy pro­ eyelids and suturing them on one side to
pyl methyl cellulose eye drops, arti­ the deep temoral fascia and on the other
ficial tears) are prescribed, especially Protocol for Nerve Repair side to the medial canthal ligament.
when the lacrimal punct­um is gro­ssly • The procedures like nerve anasto­
displaced and the tears do not spread mosis, grafting or cross nerve anasto­ Regional Muscle Transfer
over the eye and fall apart (epiphora). mosis are useful if they are done timely, Temporal muscle or masseteric muscle
Lubricating eye drops (methylcellu­ as the facial nerve paralysis becomes slings are used to rehabilitate the
lose drops) are pre­scri­bed to prevent chronic the muscles undergo wasting patient (Figs 9.15A to D). When these
dryness of the eyes and keratitis. the muscle atrophy occurs and there is muscles are used they are innervated,
loss of contractile tissue in the muscle during the act of mastication the facial
Surgical Treatment and its replacement with collagenous movement takes place, to avoid this
The surgical treatment can be divided and fatty tissue (Figs 9.13A to D). undesirable movement the muscle
into corrective and rehabilitative. The cor­ • The protocol that needs to be follo­ should be denervated. The limitation
rective treatment is done with the inten­ wed for nerve repair or grafting is as of this procedure is that it provides only
tion of restoring the nerve fun­ction, before follows: cosmetic correction, when the face is
the facial muscles have become flaccid. – Immediate (0–3 weeks)—nerve static, but during the movements the
The essential elements for the successful ana­­s­t­o­mosis deformity is conspicuous and thus, they
outcome for surgical treat­ment are: – Delayed (3 weeks–2 years)— provide only passive correction.
• Intact facial nerve grafting or nerve cross over
• Healthy muscles – Late (over 2 years)—regional Correction of lagophthalmos
(preservation of neuromuscular coor­ muscle transfer or distant micro­ The complication of lagophthalmos
di­n­ation). vascular muscle transfer. and lack of blinking reflex is expo­sure
Neurological Disorders of the Face 161

A B

C D
Figs 9.13A to D: Cross nerve innervation

A B C

D E F
Figs 9.14A to F: Harvesting fascia lata graft, anastomosing with deep temporal fascia and suturing to the corner of mouth and inner
canthal ligament after tunneling through the subcutaneous tunnels
162 Neurological Disorders of Face and General Anesthesia

abnormal sweating and salivation. It can


also include discharge from the nose,
when smelling certain food.

Treatments
• Injection of botulinum toxin type A
• Surgical transection of the nerve
fibers
• Application of an ointment contain­
ing an anticholinergic drug such as
A B
scopolamine.

PERIPHERAL NERVE
INJURIES

Introduction
The neuron or nerve cell is the structural
unit of the nervous system. It is able to
transmit impulses between the central
C D nervous system (CNS) and all the parts
Figs 9.15A to D: Harvesting temporalis muscle flap, splitting into three slings and suturing of the body. There are two basic types
to orbicularis oris, levator and depressor anguli oris and correction of lagophthalmos by of neurons, viz. sensory and motor,
tarsorrhaphy which differ significantly in their basic
struc­
ture and impulse transmission
keratitis, corneal ulceration and blind­ and parasympathetic fibers to the paro­ (Table 9.1).
ness. To prevent these compli­ cations tid gland. As a result of severance and However, the basic composition of the
the lagophthalmos is corrected by either inappropriate regeneration, the fib­ axon, dendrite and cell body remain the
a tarsorrhaphy (Figs 9.15A to D) or by ers may switch courses, resulting in same, so does the impulse propa­gation.
narrowing the wide palpebral fissure us­ ‘gustatory sweating’ or sweating in the Cell body contains nucleus, cyto­
ing fascia lata slings (see Figs 9.14A to F). anticipation of eating, instead of the plasm and various organelles found in
normal salivatory response. It is often other cells. It is located at a distance from
seen with patients who have undergone the axon or main pathway of impulse
FREY’S SYNDROME
endoscopic thoracic sympathectomy, transmission in the sensory nerve.
Frey’s syndrome (also known as Bail­ wherein part of the sympathetic trunk Hence, it has no active involvement in
larger syndrome, Dupuy syndrome, is cut or clamped to treat sweating of nerve conduction and only provides
auriculotemporal syndrome or Frey- the hands or blushing. The subsequent metabolic support for the neuron. The
Baillarger syndrome) is a food related regeneration or nerve sprouting leads to cell body of motor nerve differs from
syndrome, which can be congenital or
acquired and can persist for life.
The symptoms of Frey’s syndrome Table 9.1: Differences between the sensory and motor neurons
are redness and sweating on the cheek
area adjacent to the ear. They can Sensory neuron Motor neuron
appear when the affected person eats, Transmit impulses from peripheral organs to Transmit impulses from brain to peripheral
sees, thinks about or talks about certain the brain organs
kinds of food which produce strong Consists of: 1. Cell body of the motor neuron is inter­
saliv­
ation. Observing sweating in the 1. Peripheral processes—dendrites, groups posed between the axon and dendrites.
region after eating a lemon wedge may of free nerve endings which respond to 2. Cell body provides vital metabolic supp­
be diagnostic. stimuli ort to the neuron in addition to active
2. Axon which transmits the impulses from impulse transmission
Frey’s syndrome often results as
the dendrites centrally 3. Axon synapses with muscle cells.
a side effect of parotid gland surgery. 3. Centrally located cell body or soma, pri­
The auriculotemporal branch of the marily concerned with vital metabolic
trigeminal nerve carries sympathetic func­tions. Not involved in impulse trans­
fibers to the sweat glands of the scalp mission
Neurological Disorders of the Face 163

Fig. 9.17: Structure of the myelinated nerve

Myelinated Nerve
collagenous endoneurium, but when
It has a central core of axon filled with traction forces exceed the nerve’s
viscous intracellular fluid—axoplasm, capacity to stretch, injury occurs. If
which is surrounded by myelin (lipid the force applied is great enough, a
sheath) which is specialized secretion complete loss of continuity may oc­
form of Schwann cell. The nodes of cur. More often, however, continuity
Ranvier are present at regular intervals is retained.
of 0.5 to 3 mm (Fig. 9.17). • Lacerations such as those created by
Fig. 9.16: Cell body/soma/perikaryon a knife blade are another common
Nonmyelinated Nerve peripheral nerve injury type. Whereas
sensory nerve cell body, as it is placed It is also surrounded by Schwann cell these can be complete transections,
between the axon and dendrites. Hence, sheath, but it does not secrete myelin. more often some nerve element of
it has an active role in nerve conduction It has slower rate of conduction as continuity remains.
as well as nutritional support of the compared to myelinated nerve. • Compression is a third common type
nerve (Fig. 9.16). of peripheral nerve injury. These in­
Etiology of Peripheral Nerve juries include the ‘Saturday night pal­
Axon Injuries sy’ due to radial nerve compression
It is a single process extending from • Local anesthetic injections as well as entrapment neuropathies
the cell body and varies in length and • Impacted third molar removal and do not involve a severance or
diameter. The maximum and minimum • Preprosthetic surgery—mandibular tearing of the neural elements. Total
length ranges from 1 meter to few milli­ vesti­buloplasty loss of both motor and sensory func­
meters. The dia­meter of the axon ranges • Endosseous dental implant place­ment tion may occur, but the pathophysi­
from maximum 20 microns to mini­ • Orthognathic surgery—bilateral sagi­ ology responsible for these deficits is
mum 1 micron. The dia­meter is directly t­­tal split osteotomy unclear because complete nerve con­
proportional to velocity of conduction. • Facial trauma—fractures tinuity is maintained. Two pathologi­
The axons conduct impulse away from • Gunshot injuries or lacerations cal mechanisms are believed to be
cell body. Axons terminate in many • Endodontic and periradicular sur­gery involved in these injuries, mechani­
branched filaments called telodendria • Salivary gland surgery—parotidecto­ cal compression and ischemia.
and they contain numerous vesicles and my
mitochondria. • Treatment of benign and malignant Classification of Nerve Injuries
lesions of the head and neck. Seddon divided nerve injuries by seve­
Dendrites rity into three broad categories:
Dendrite means ‘tree’ in Greek. They are Basic Injury Types 1. Neuropraxia.
the terminal branches of the multipolar It is important to know the basic 2. Axonotmesis.
neurons. The distal ends of sensory neu­ types of injuries that the neuron is 3. Neurotmesis.
rons also called receptors, which are the likely to encounter to understand the
most distal segment of neuron that car­ pathophysiology of nerve injury. Neuropraxia
ries impulses towards the cell body and • Stretch related injuries are the most The mildest injury type, does not involve
is composed of arborization of free nerve common. Peripheral nerves are loss of nerve continuity and causes
endings. inherently elastic because of their functional loss, which is transient. This
164 Neurological Disorders of Face and General Anesthesia

three injury types described by Seddon’s


into five categories according to severity
(Table 9.2).
• A first-degree injury is equivalent to
Seddon’s neuropraxia
• A second-degree is equivalent to
axonotmesis
• Third-degree nerve injuries occur
when there is disruption of the
axon (axonotmesis) and also partial
injury to the endoneurium. This
Fig. 9.18: The train is stopped because of local damage to the rail (demyelinating block), categorization places a third-degree
more distal parts of the rail as well as energy supply system still being intact. Repair of between Seddon’s axonotmesis and
the local damage might take a considerable time. Courtesy: From Lundborg G (Ed): Nerve neurotmesis. Dependent on the ex­
injury and repair. New York, Churchill Livingstone; 1988. pp. 78-79 tent of the endoneurial damage, fun­
ctional recovery may be possible.
• Sunderland divides Seddon’s neu­ro­
t­mesis into fourth- and fifth-degree
injuries. In a fourth-degree injury, all
portions of the nerve are disrupted
except the epineurium. Recovery is
not possible without surgical inter­
ven­tion.
• A fifth-degree injury involves com­
plete severance of the nerve.
• A sixth injury pattern was added by
Mackinnon and Dellon to describe
mixed combination of Sunderland’s
five degrees of injury. In this some
nerve fascicles may exhibit normal
function and others have varying
degrees of injury.

Physiologic Conduction Block


Type ‘A’ Conduction Block
Fig. 9.19: The rail is damaged and has disappeared distal to the level of injury. The track
is still intact and new rails can easily be laid down in correct position. Courtesy: From
Results due to intraneural circulatory
Lundborg G (Ed): Nerve injury and repair. New York, Churchill Livingstone; 1988. pp. 78-79
arrest/metabolic (ionic) block with no
nerve fiber pathology. It is immediately
symptom transience is thought to be such injuries because of the remaining reversible (Fig. 9.21).
due to a local ion-induced conduction uninjured mesenchymal latticework that
Type ‘B’ Conduction Block
block at the injury site, although subtle provides a path for subsequent sprouting
alterations in myelin structure have also axons to reinnervate their target organ It results from intraneural edema or meta­
been found (Fig. 9.18). (Fig. 9.19). bolic block with little or no nerve fiber
pathology. It is associated with incre­ased
Axonotmesis Neurotmesis endoneural fluid pressure. It is reversible
Axonotmesis occurs when there is com­ Neurotmesis involves disconnection of within days or weeks (Fig. 9.22).
plete interruption of the nerve axon a nerve. Functional loss is complete and
and surrounding myelin, whereas the recovery without surgical interven­tion Symptomatic Classification
surrounding mesenchymal structures does not usually occur, because of scar
including the perineurium and epineu­ formation and the loss of the mesen­ Anesthesia
rium, are preserved. Axon and myelin chymal guide that properly directs It is complete absence of any stimulus
degeneration occur distal to the point of axonal re-growth (Fig. 9.20). dete­ction and stimulus perception, inclu­­
injury, causing complete denervation. Sunderland’s8 classification system d­­ing mechanoreceptive and noci­ce­ptive
The prospect of recovery is excellent in of nerve injuries further stratifies the stimuli. It is usually associated with a
Neurological Disorders of the Face 165

sation. It may be fur­ther divided as


follows:
• Hypoesthesia: Decreased touch and
pressure stimuli detection.
• Hyperesthesia: Increased touch and
pressure stimuli detection.
• Hypoalgesia: Decreased nociceptive
stimulus detection.
• Hyperalgesia: Increased nociceptive
stimulus detection.
• Synesthesia: Difficulty in quickly
and accurately localizing the point of
sti­mulus application.

Dysesthesia
It is an alteration in sensibility in which
there is abnormal stimulus detection
and stimulus perception that may be
Fig. 9.20: The rails as well as the tracks are destroyed. The result is a great deal of perceived as unpleasant and painful. It
misdirection. Courtesy: From Lundborg G (Ed): Nerve injury and repair. New York, Churchill may be further divided into the follow­ing:
Livingstone; 1988. pp. 78-79 • Allodynia—characterized by sharp,
first pain perception on light touch.
Table 9.2: Comparison between Seddon’s and Sunderland’s classification
• Hyperpathia—characterized by dull,
Seddon’s classification Sunderland’s classification second pain on pressure stimulus.
They are associated with neuromas,
Neuropraxia: Stretch injury First degree entrapment, compression and sympa­
Axonotmesis: Few axons are injured Second degree theti­cally maintained pain.
temporary damage, recovery may not Third degree
be complete Fourth degree Neural Response to Trauma
Neurotmesis: Complete severance of Fifth degree Before regeneration of nerve fibers can
nerve—recovery incomplete occur, a series of degenerative proce­
sses occur, some of which directly affect
regeneration. The success of regen­era­
tion depends largely on the severity of
the initial injury and resultant degen­er­
ative changes.
Pathological changes are mild or
absent in first-degree injuries in which
the mechanism is conduction block
alone and no true degeneration or reg­
en­eration occurs.
In second-degree injuries (axono­
tmesis) there is little histological change at
Fig. 9.21: If the local energy supply is interrupted, the train cannot move in spite of intact the injury site or proximal to it; however,
nerve fiber. The moment the energy supply is restored (electric wire repair) the train can distal to the injury site, a calcium-medi­
start again. Courtesy: From Lundborg G (Ed): Nerve injury and repair. New York, Churchill ated process known as Wallerian (or
Livingstone; 1988. pp. 78-79) anterograde) degeneration is known to
occur.
severe injury interrupting the inte­grity and stimulus perception that may In third-degree injuries, a more
of the axons. Sensory recovery is unpre­ be perceived as unpleasant, but is not signi­ficant trauma-induced local reac­t­
dictable and slow. pain­ ful. Stimulus detection may be ion occurs. These intrafascicular injuries
decreased or increased and may affect involve retraction of the severed nerve
Paresthesia noci­cep­tion or mechanoreception. fiber ends due to the elastic endon­
It is an alteration in sensibility in which Pat­i­­­­ents may com­­plain of numbness, eurium. Local vascular trauma leads to
there is abnormal stimulus detection tingling or itch­ ing or swollen sen­ hemorrhage and edema, which results
166 Neurological Disorders of Face and General Anesthesia

in Wallerian degeneration. They initially


become active within 24 hours of injury,
exhibiting nuclear and cytoplasmic
enlarge­ ment as well as an increased
mitotic rate. These cells divide rapidly
to form undifferentiated daughter cells
that upregulate gene expression for a
multitude of molecules to assist in the
degeneration and repair process. An
initial Schwann cell role is to help remove
the degenerated axonal and myelin debris
Fig. 9.22: If the electric wire system is more severely damaged (type b), e.g. by a falling and then pass it on to macrophages. The
tree, the repair takes longer. Still the rail (nerve fiber) is intact. Courtesy: From Lundborg macrophages have migrated into the
G (Ed): Nerve injury and repair. New York, Churchill Livingstone; 1988. pp. 78-79 traumatized region, primarily through a
hemopoietic route, passing through the
walls of capillaries, which have become
in a vigorous inflammatory response. nied by proliferating Schwann cells and permeable in the injury zone. Schwann
Fibroblasts proli­ferate and a dense fib­ peri- and endoneurial fibroblasts. Vigor­ cells and macrophages work together to
rous scar causes a fusiform swelling of ous cellular proliferation peaks within the phagocytose and clear the site of injury in
the injured segment. Interfascicular 1st week and continues for a prolonged a process that requires 1 week to several
scar tissue also develops so that the period. The nerve ends become a swol­ months.
entire nerve trunk, which is left in conti­ len mass of disorganized Schwann cells, Endoneural mast cells also play a
nuity, is permanently enlarged. Often, capillaries, fibroblasts, macrophages and pivotal role in this process, proliferat­
it is adherent to perineural scar tissue collagen fibers. Regenerating axons reach ing markedly within the first 2 weeks
as well. Distal to the injured segment, the swollen bulb of the proximal stump post- injury. They release histamine and
Wall­erian degeneration follows a sequ­ and encounter formidable barriers to seroto­nin, which enhance capillary per­
ence very similar to that observed in further growth. Many axons form whorls me­ a­
bility and facilitate macrophage
second-degree injuries. One important within the scar tissue or are turned back migra­tion. During the initial stages, the
differ­ence is that the intrafascicular along the proximal segment or out into endoneural tubes swell in response to
injury impairs axonal regeneration and the surrounding tissue. Some of the regen­ the trauma, but after the first 2 weeks
there­ fore, the endoneurial tubes re­ erating axons may reach the distal stump, they become smaller in diameter. By 5 to
main dener­vated for prolonged periods. an accomplishment that is dependent on 8 weeks, the degenerative process is usu­
While denervated, the endoneurial multiple factors, including the severity of ally complete and nerve fiber remnants
tubes begin to shrink in a process that the original injury, the extent of the scar composed of Schwann cells within an en­
rea­ches a maximum at approximately 3 formation and the delay before the axons doneural sheath are all that remain.
to 4 months postinjury. The endoneurial reach the injury site. Endoneurial tubes
sheath progressively thi­ckens secondary left unoccupied for prolonged periods un­ Nerve Regeneration
to collagen deposition along the outer dergo progressive shrinkage and fibrosis, Neuroregeneration refers to the regro­
surface of the Schwann cell basement ultimately becoming completely obliter­ wth or repair of nervous tissues, cells or
membrane. If the endoneurial tube does ated by collagen fibers. cell products. Such mechanisms may
not receive a regenerating axon, pro­ include remyelination, generation of new
gressive fibrosis ultimately obliterates it. Wallerian Degeneration neurons, glia, axons, myelin or synapses.
Stacks of Schwann cell processes repre­ The primary histological change in Neuroregeneration differs between the
senting collapsed endoneurial tubes, this involves physical fragmentation of peripheral nervous system (PNS) and
known as the bands of Büngner, become axons and myelin, a process that begins the central nervous system (CNS) by the
important guides for sprouting axons within hours of injury. Ultrastructurally, functional mechanisms and especially,
du­ring reinnervation. both neurotubules and neurofilaments the extent and speed. While the peripheral
In fourth and fifth degree injuries, lo­ become disarrayed and axonal contour nervous system has an intrinsic ability for
cal reaction to the severe trauma is pro­ becomes irregular, due to varicose swell­ repair and regeneration, the CNS is, for
nounced. Endoneurial tubes, as well as ings. By 48 to 96 hours postinjury, axonal the most part, incapable of self-repair and
fasciculi, are disrupted and Schwann cells continuity is lost and conduction of regeneration. For example the olfactory
and axons are no longer confined. The impulses is no longer possible. Myelin and the optic nerves are considered as
epineurium is also damaged and reactive disintegration lags slightly behind that direct extension of the brain matter and
epineurial fibroblasts are present at the of axons, but is well advanced by 36 to once damaged by trauma or inflamm­
severed ends within 24 hours accompa­ 48 hours. Schwann cells play a key role ation, they fail to regenerate permanently.
Neurological Disorders of the Face 167

There is currently no treatment for reco­ inside of the basal lamina. The key stimulus for growth as well as a guide for
vering human nerve function after injury histologic structures during axonal the advancing axon.
to the CNS.9 regeneration appear to be Schwann
Neuroregeneration in the PNS occ­ cell and its basal lamina. Schwann Tinel’s Sign
urs to a significant degree.10 Axonal cells multiply in the distal nerve Tinel’s sign is a way to detect irritated
spro­uts form at the proximal stump and segment and when contacted by an nerves. It is performed by lightly tapping
grow until they enter the distal stump. axon sprout undergo a cascade of (percussing) over the nerve to elicit
The growth of the sprouts is governed changes that triggers the production a sensation of tingling or “pins and
by chemotactic factors secreted from of myelin. Remyelination is a slow needles” in the distribution of the nerve.
Schwann cells. process and hence, nonmyelinated It is a sign of regeneration of the nerve.
Injury to the peripheral nervous sys­ axons are likely to regenerate initially.
tem immediately elicits the migration • Cellular recovery: Chromatologic Central nervous system regeneration
of phagocytic cells, Schwann cells and chan­ges are most pronounced bet­ Unlike peripheral nervous system, in­
macrophages to the lesion site in order to ween 1 and 3 weeks after axotomy jury to the central nervous system is not
clear away debris such as damaged tissue. and cells recover from chromatolysis followed by extensive regeneration. It is
When a nerve axon is severed, the end over seve­ral weeks to months. The limited by the inhibitory influences of
still attached to the cell body is labeled cells are hyperchromatic with pre­ the glial and extracellular environment.
the proximal segment, while the other dominant Nissl bodies in the mean The hostile, nonpermissible growth en­
end is called distal segment. After injury, time. Nissl bodies are stacked endo­ vironment is in part created by the mi­
the proximal end swells and experiences plasmic reti­­­­culum with attached ri­ gration of myelin-associated inhibitors,
some retrograde deg­e­­ner­ation, but once bosomes indi­­cating massive cellular astrocytes, oligodendrocytes, oligoden­
the debris is cleared, it begins to sprout anabolic response to injury. drocyte precursors and microglia.
axons and the presence of growth cones • Receptor recovery: If regeneration The environment within the CNS,
can be detected. The proximal axons are is complete by 6 months following especially following trauma, counteracts
able to regrow, as long as the cell body is injury, tactile dome receptors are the repair of myelin and neurons. The
intact and they have made contact with indis­t­inguishable from normal, unin­ growth factors are not expressed or re-
the neurolemmocytes in the endoneurial jured receptors. expressed, for instance the extracellular
channel. Human axon growth rates can matrix is lacking laminins. Glial scars rap­
reach 2 mm/day in small nerves and Neurotrophic Factors idly form and the glia actually produce
5 mm/day in large nerves. The distal seg­ Neurotrophic factors such as nerve factors that inhibit remyelination and
ment, however, experiences Wallerian growth factor, brain-deri­ved neuro­tro­ axon repair. Slower degeneration of the
degeneration within hours of the injury; phic factor, ciliary neuro­trophic factor distal segment than that which occurs in
the axons and myelin degenerate, but and many others have been identified the peripheral nervous system also con­
the endoneurium remains. In the later and are thought to be important in the tributes to the inhibitory environ­ment,
stages of regeneration the remaining nerve repair process. Schwann cells also because inhibitory myelin and axonal
endoneurial tube directs axon growth produce neurotrophic factors, including debris are not cleared away as quickly.
back to the correct targets. During Wal­ nerve growth factor (NGF), at the site of All these factors contribute to the forma­
lerian degeneration, Schwann cells grow injury. tion of what is known as ‘glial scar’, which
in ordered columns along the endo­ Nerve growth factor is involved in axons cannot grow across. The proximal
neurial tube, creating a band of Büngner nerve cell survival and maintenance segment attempts to regenerate after
(boB) that protects and preserves the in the normal state and appears to be injury, but its growth is hindered by the
endoneurial channel. Also, macrophages an important component of the nerve environment. It is important to note that
and Schwann cells release neurotrophic repair process as well. It is released central nervous system axons have been
factors that enhance regrowth. Healing from peripheral nerve target organs proven to regrow in permissible environ­
of nerve injuries is unique among tissues, and transferred to the nerve cell body ments; therefore, the primary problem to
because the pro­cess is greatly dependent via retrograde axonal transport. Nerve CNS axonal regeneration is crossing or
upon cellular repair rather than tissue growth factor receptor concentration eliminating the inhibitory lesion site.
repair. on the Schwann cells forming the bands
• Axonal recovery: Within hours of of Büngner increases after injury. The Management of Peripheral
axotomy, small axoplasmic outgro­ NGF that binds to these receptors on Nerve Injuries
wths or sprouts protrude from the the Schwann cells is presented to the
severed tips. An exaggerated second regrowing axon sprouts. This NGF up­ Nonsurgical/Medicinal
sprouting occurs after 2 to 3 days. taken by the axon is then transferred • Steroids—reduce the edema aro­und
These sprouts advance distally retrograde from the growth cone to the nerve and is useful in neuro­
along the Schwann cell tubes on the the cell body, providing a continued praxia (Prednisolone 5–10 mg TID).
168 Neurological Disorders of Face and General Anesthesia

• Nerve tonics—vitamin B1, B6, B12— Lentini (1975) formulated the hy­
EAGLE’S SYNDROME
they are supposed to facilitate nerve pothesis that persistence of the mes­
fiber regeneration and are useful in Eagle’s syndrome is a rare condition, enchymal elements (Reichert cartilage
cases of neuropraxia and axono­tmesis. where an elongated styloid process residues) could undergo osseous meta­
• In the cases with acute neuralgic (> 30 mm) is in conflict with the adjacent plasia as a consequence of trauma or
pain, drugs like carbamezapine of anatomical structures. Eagle syndrome mechanical stress during the develop­
gabapentine can be prescribed. It is was first described by Watt W Eagle in ment of the styloid process.12
pu­rely symptomatic treatment. 1937 and is characterized by recurrent The ossification of muscular tendons
• Physiotherapy—in the form of electri­ pain in the oropharynx and face. leading to irritation of the structures
cal nerve stimulation (TENS) and in The styloid process is a slender nearby.13
cases of motor nerves exercises and out­­growth at the base of the temporal The abnormal length associated
massage therapy can be given. bone, immediately posterior to the mas­ with abnormal angulation of the styloid
toid apex. It lies caudally, medially and process.14
Surgical anteriorly toward the maxillo-ver­tebro-
• Decompression: It is used if nerve phar­yngeal recess (which contains caro­ Clinical Features
com­­ pression occurs resulting into tid arteries, internal jugular vein, facial In 1937, Eagle described 2 possible clini­
neu­­r­o­praxia. It is usually done when nerve, glossopharyngeal nerve, vagal cal expressions attributable to elongated
due to bone deposition in the nerve nerve, and hypoglossal nerve). styloid process, as follows:
canal; there is pressure on the nerve With the stylohyoid ligament and the The ‘classic Eagle syndrome’ is typi­
leading to neuropraxia. Here, enlar­ small horn of the hyoid bone, the styloid cally seen in patients after phary­
gement of the canal boundaries is process forms the stylohyoid apparatus, ngeal trauma or tonsillectomy and it
done to relieve the pressure on the which arises embryonically from the is characterized by ipsilateral dull and
nerve. Reichert cartilage of the second branchial persistent pharyngeal pain, centered in
• Anastomosis: It is microsurgical repair arch. Eagle defined the length of a normal the ipsilateral tonsillar fossa, that can
of the severed ends of the nerve. It is styloid process at 2.5 to 3.0 cm. be referred to the ear and exacerbated
useful, when there is no loss of nerve This syndrome was characterized by rotation of the head. A mass or
tissue as in accidental clean surgical by symptoms typically occurring after bulge may be palpated in the ipsilateral
transection of the nerve. phar­yngeal trauma or tonsillectomy. It tonsillar fossa, exacerbating the patient’s
• Cross innervation: It is useful when manifests as a nagging dull, long-term symptoms. Other symptoms include
there is motor nerve deficit due to a ache in the throat, sometimes radi­ating dysphagia, sensation of foreign body in
lesion in the course of the nerve. In to the ipsilateral ear and the sensation the throat, tinnitus or cervicofacial pain.
this repair, a nerve is grafted to con­ of a foreign body in the throat. Occa­ The ‘second form’ of the syndrome
nect the affected nerve to the normal sionally, it manifests as odyn­o­phagia, (‘stylocarotid syndrome’) is characterized
functional nerve on the other side of dysphonia, increased sali­ vation, and by the compression of the internal or
the body using micro­surgical repair. headache. external carotid artery (with their perivas­
• Nerve grafts: It is use of a nerve cular sympathetic fibers) by a laterally or
Frequency
segment from one part of the body medially deviated styloid process. It is
to reconstruct and repair an affected
An elongated styloid process occurs in related to a pain along the distribution
nerve in some other part using micr­
about 4 percent of the general popul­ of the artery (carotodinia), which is
o­surgical technique. ation, while only a small percentage provoked and exacerbated by rotation
(between 4 and 10.3%) of these patients and compression of the neck. It is not
are symptomatic.11 So the true incidence correlated with tonsillectomy. In case
Other Painful Conditions is about 0.16 percent, with a female-to- of impingement of the internal carotid
Other painful conditions involving the male predominance of 3:1. artery, patients often refer supraorbital
head, neck and face area such as: pain and parietal headache. In case of
– Myofacial pain dysfunction syn­ Etiology external carotid artery irritation, the pain
d­rome Eagle (1937–1948) considered sur­ gical radiates to the infraorbital region.
– Eagle’s syndrome trauma (tonsillectomy) or local chronic
– Temporal arteritis irritation could cause osteitis, periosteitis Differential Diagnosis
– Migraine or tendonitis of the stylo­hyoid complex Temporomandibular disorders, laryn­
– Cluster neuralgias are discussed with consequent reac­tive, ossifying hyper­ gopharyngeal dysesthesia, hyoid bursi­
in brief. plasia.12 tis, sluder syndrome, glossopharyngeal
Neurological Disorders of the Face 169

neuralgia, esophageal diverticula, trige­ Pathophysiology may explain the occurrence after aerobic
minal neuralgia, migraine-type head­ Cluster headaches have been classified exercise. Napping causes a headache for
aches, sphenopalatine neuralgia, cervical as vascular headaches. The intense some sufferers, while for others lack of
arthritis, temporal arteritis, unerupted or pain is caused by the dilation of blood sleep triggers them. The role of diet and
impacted molar teeth, faulty dental pros­ vessels, which creates pressure on the specific foods in triggering cluster head­a­
theses, otitis, salivary gland disease, pos­ trigeminal nerve. While this process is ches is controversial and not well under­
sible tumors. the immediate cause of the pain, the stood.
etiology (underlying cause or causes) is
Treatment not fully understood. Smoking
Primary line of management is analg­e­ Nicotine may trigger cluster headaches
sics and anti-inflammatory medications. Hypothalamus and the affliction is often found in people
Sev­ere cases, which do not respond to Among the most widely accepted theor­ with a heavy addiction to cigarette smo­
analgesics and anti-inflammatory medi­ ies is that cluster headaches are due to king.
cations, may require partial styloidec­ an abnormality in the hypothalamus;
tomy. Dr Goadsby, an Australian specialist in Signs and Symptoms
the disease has developed this theory. This Cluster headaches are excruciating unil­
can explain, why cluster headaches frequ­ ateral headaches of extreme intensity.
CLUSTER HEADACHE
ently strike around the same time each The duration of the common attack
Cluster headache, nicknamed ‘suicide day and during a particular season, since ranges from, as short as 15 minutes to
headache’, is a neurological disease that one of the functions the hypothalamus 3 hours or more. The onset of an attack
involves, as its most prominent feature, performs is regulation of the biological is rapid and most often without the
an immense degree of pain. ‘Cluster’ clock. Metabolic abnor­malities have also preliminary signs that are characteristic
refers to the tendency of these headaches been reported in patients. of a migraine. However, some sufferers
to occur periodically, with active periods The hypothalamus is responsive report preliminary sensations of pain
interrupted by spontaneous remissions. to light—day length and photoperiod; in the general area of attack, often
The cause of the disease is currently olfactory stimuli, including pheromo­ referred to as ‘shadows’, that may warn
unknown. It affects approximately 0.1 nes; steroids, including sex steroids and them an attack is imminent. Though
percent of the population and men are corticosteroids; neurally transmitted in­ the headaches are almost exclusively
more commonly affected than women. formation arising in particular from the unilateral, there are many documented
The condition was originally named heart, the stomach and the repro­ductive cases of ‘side-shifting’ between cluster
Horton’s neuralgia after Dr BT Horton, system; autonomic inputs; blood-borne periods or even rarer simultaneous
who postulated the first theory as to stimuli, including leptin, ghrelin, angio­ (within the same cluster period) bilateral
their pathogenesis. tensin, insulin, pitui­tary hormones, cy­ headache. Trigeminal neuralgia can
tokines, blood plas­ ma concentrations also bring on headaches with similar
History of glucose and osmol­arity, etc. and the qualities. However, with trigeminal neu­
The first complete description of cluster stress. These particular sensitivities may ralgia the pain is mostly located around
headache was given by the London underlay the causes, triggers and meth­ the ‘cheek’ area and is described as
neurologist Wilfred Harris in 1926. He ods of treatment of cluster headache. being more lance-like in quality.
named the disease migrainous neur­algia.
Cluster headaches have been called Triggers Pain
by several other names in the past includ­ Nitroglycerin (glyceryl trinitrate) can The pain of cluster headaches is mark­
ing erythroprosopalgia of Bing, ciliary some­times induce cluster headaches in edly greater than in other headache con­
neuralgia, erythromelagia of the head, suff­
erers in a manner similar to spon­ ditions, including severe migraines and
Horton’s headache (named after Bayard taneous attacks. Ingestion of alcohol or experts believe that it may be the most
T Horton, an American Neurologist), his­ chocolate is recognized as a common severe pain known to medical science. It
taminic cephalalgia, petrosal neuralgia, trigger of cluster headaches, when a per­ has been described by female patients as
sphenopalatine neuralgia, vidian neu­ son is in cycle or susceptible. Expo­sure to being more severe than childbirth.
ralgia, Sluder’s neuralgia and hemicra­ hydrocarbons (petroleum solvents, per­ The pain is lancinating or boring in
nia angioparalyticia. Sluder’s neuralgia fume) is also recognized as a trigger for quality and is located behind the eye
(syndrome) and cluster pain can often be cluster headaches. Some patients have a (periorbital) or in the temple, sometimes
temporarily stopped with nasal lidocaine decreased tolerance to heat and becom­ radiating to the neck or shoulder.
drops. ing overheated may act as a trigger, which Analogies frequently used to describe
170 Neurological Disorders of Face and General Anesthesia

the pain are a red-hot poker inserted Cluster headaches occurring in two long as 10 minutes. Once an attack is
into the eye or a spike penetrating from or more cluster periods lasting from 7 to at its peak, oxygen therapy appears to
the top of the head, behind one eye, 365 days with a pain-free remission of have little effect, so most people have an
radiating down to the neck or sometimes 1 month or longer between the clusters oxygen provider close. Alternative first-
having a leg amputated without any are considered episodic. If the attacks line treatment is subcutaneous admini­
anesthetic. occur for more than a year without a stration of triptan drugs, like sumatriptan
pain-free remission of at least 1 month, and zolmitriptan. Because of the rapid
Other Symptoms the condition is considered chronic. onset of an attack, the triptan drugs are
The cardinal symptoms of the cluster Chronic clusters run continuously with­ usually taken by subcutaneous injection
headache attack are ptosis, lacrimation, out any ‘remission’ periods between rather than by mouth. But these drugs
rhinorrhea and less commonly, facial cycles. The condition may change from are expensive.
blushing, swelling or sweating. These chronic to episodic and from episodic Nonnarcotic treatment botox inje­
features are known as the autonomic to chronic. Remission periods lasting c­­tions along the occipital nerve, as well
symptoms. The attack is also associated for decades before the resumption of as sarapin (pitcher plant extract) injec-
with restlessness, the sufferer often clusters have been known to occur. tions.
pacing the room or rocking back and Lidocaine and other topical anes­
forth. Less frequently, he or she will Treatment thetics sprayed into the nasal cavity may
have an aversion to bright lights and Cluster headaches often go undiagnosed relieve or stop the pain, normally in a
loud noise during the attack. Nausea for many years, being confused with few minutes, but long-term use is not
rarely accompanies a cluster headache. migraine or other causes of headache. suggested due to the side effects and
The neck is often stiff or tender in the Cluster headaches are considered benign, possible damage to the nasal cavities.
aftermath of a headache, with jaw or but because of the extreme and often Other abortive remedies that work
tooth pain sometimes present. Some debilitating pain associated with them, a for some include ice, hot showers, cool
sufferers report feeling as though their severe attack is nevertheless treated as a or lukewarm water sprayed on the
nose is stopped up and that they are medical emergency by doctors, who are face around the sinus, temple and ear
unable to breathe out of one of their familiar with the condition. areas, breathing cold air, application of
nostrils. Over-the-counter pain medications White Flower analgesic balm beneath
(such as aspirin, paracetamol and ibu­ the nostrils, caffeine and drinking large
Cyclical Recurrence and Regular profen) typically have no effect on the amounts of water in the early stages of
Timing pain from a cluster headache. Unlike an attack. Vigorous exercise has been
Cluster headaches are occasionally other headaches such as migraines and shown in some cases to be very effective
referred to as ‘alarm clock headaches’, tension headaches, cluster headaches in relieving and aborting an acute attack
because of its ability to wake a person do not respond to biofeedback. by increasing the levels of oxygen within
from sleep and because of the regularity Medications to treat cluster head­ the body. This could also be due to an
of its timing in that both the individual aches are classified as either abor­tives increase in adrenaline and changes in
attacks and the clusters themselves can or prophylactics. In addition, short- blood pressure.
have a metronomic regularity; attacks term transitional medications (such as Hyperbaric oxygen therapy has been
striking at a precise time of day each steroids) may be used, while prophylac­ used successfully in treating cluster
morning or night is typical, even precisely tic treatment is instituted and adjusted. headaches though it was not shown to
at the same time a week later. This has With abortive treatments often only be more successful than surface oxy­-
prompted researchers to speculate an decrea­sing the duration of the headache gen.
involvement of the brain’s ‘biological and preventing it from reaching its peak
clock’ or circadian rhythm. rather than eliminating it entirely, pre­ Prophylactic Treatment
ventive treat­ment is always indicated for A wide variety of prophylactic medicines
Episodic or chronic cluster headaches, to be started at the are in use like calcium channel blocker
In episodic cluster headache, these first sign of a new cluster cycle. verapa­mil at a dose of at least 240 mg
attacks occur once or more daily, often at daily. Steroids, such as prednisolone, are
the same times each day, for a period of Abortive Treatment also effective, with a high dose given for
several weeks, followed by a headache- During the onset of a cluster headache, the first 5 days or longer before tapering
free period lasting weeks, months or some patients respond to rapid inhal­ down. Methysergide, lithium and the
years. Approximately 10 to 15 percent of ation of pure oxygen (12–15 liters per anticonvulsant topiramate are recomm­
cluster headache sufferers are chronic; minute in a nonrebreathing mask). ended as alternative treatments. Muscle
they can experience multiple headaches When used at the onset this can abort relaxants and atypical anti-psychotics
everyday for years. the attack in as little as 1 minute or as have also been used.
Neurological Disorders of the Face 171

Magnesium supplements, melato­ verse facial and supraorbital arteries, • Loss of appetite
nin, tricyclic antidepressants including which are torturous, nodular, and often • Weight loss (> 5% of total body wei­
amitriptyline and nortriptyline are some pulseless. ght)
of the other drugs used. The temporal artery also supplies the • Muscle aches
optic nerve and one of the most serious • Excessive sweating.
Differential Diagnosis and gratefully rare, complications of Additional symptoms that may be
• Chronic paroxysmal hemicrania tem­poral arteritis is blindness. The treat­ associated with this disease are:
(CPH) is a condition similar to clus­ ment of choice for temporal arteritis is • Mouth sores
ter head­ache, but CPH responds well prednisone, which is very effective. • Joint stiffness
to treatment with the anti-inflamma­ The major concern with temporal • Joint pain
tory drug indomethacin and the at­ arteritis is vision loss, although if allowed • Hearing loss
tacks are much shorter, often lasting to progress, it may affect arteries in other • Bleeding gums
only seconds. areas of the body. This condition is • Facial pain.
• Some people with extreme head­ potentially vision threatening, however,
aches of this nature (especially if they if treated promptly, permanent vision Signs and Tests
are not unilateral) may actually have loss can be prevented. Vision is Palpation of the head shows scalp sen­
an ictal headache. Anticonvulsant threatened, when the inflamed arteries si­ti­vity and often shows a tender, thick,
medications can significantly improve obstruct blood flow to the eyes and optic pal­pable artery on one side of the head.
this condition. nerves. If untreated, permanent vision The affected artery may have a weak­
• It is also possible to have two or more loss can occur from oxygen deprivation ened pulse or no pulse. About 40 per­­
different types of headaches, com­ to the retina and optic nerve. cent of people will have other non-
plicating diagnosis and treatment. The cause of temporal arteritis is specific symptoms such as respiratory
unknown, but is assumed to be, at least complaints (most frequently dry cough)
in part, an effect of the immune response. or mononeuritis multiplex (weakness
TEMPORAL ARTERITIS
The disorder has been associated with and/or pain of multiple individual nerve
Temporal arteritis or giant cell arteritis is a polymyalgia rheumatica. It has also been groups). Rarely, ocular palsies (paralysis
systemic inflammatory illness that affects associated with severe infections, high of eye muscles) may occur. Fever may be
people over the age of 50 and is more doses of antibiotics and chronic disorders the only symptom (the person presents
common in females. It is a primary arterial such as rheumatoid arteritis and systemic with a persistent fever of unknown origin).
disorder that manifests as an arteritis lupus erythematosus. The symptoms
with giant cell and chronic inflammatory occur because of inflammation. The Investigations
infiltrate, intimal thickening and throm­ disorder may exist independently or Blood tests are nonspecific.
bosis. It generally starts slowly with the may coexist with or follow polymyalgia • A sedimentation rate (ESR) is almost
development of fatigue and malaise over rheumatica (a disorder characterized by always very high.
several weeks. It may also cause low- abrupt development of pain and stiffness • A hemoglobin or hematocrit may be
grade fevers and weight loss. Patients will in the pelvis and shoulder muscles). normal or low.
also experience muscle and joint aches in About 25 percent of people with giant • Liver function tests may be abnormal
their hips and shoulders, but only rarely cell arteritis also experience polymyalgia if the disorder is systemic.
true joint swelling. rheumatica. • Alkaline phosphatase may be elev­a­
As part of the inflammatory process, ted.
major large arteries are inflamed in Symptoms A biopsy and analysis of tissue from
particular the temporal artery (artery at • Fever the affected artery is also done.
the side of head near the temples). Since • Headache
the temporal artery supplies blood to – On one side of the head or the Treatment
the jaw and top of the head, symptoms back of the head. The goal of treatment is to minimize irre­
include headache, scalp tenderness – Throbbing. versible tissue damage that may occur,
and soreness of the jaw after chewing or • Scalp sensitivity, tenderness when because of lack of blood flow (isch­e­mia).
talking. Patient often complains of deep touching the scalp Corticosteroids such as prednisone
throbbing, unilateral headache over the • Jaw pain, intermittent or when chew­ are commonly prescribed to reduce in­
maxillary, zygomatic, preauricular, tem­ ing flammation. If symptoms suggest cere­
po­ral and occipital region. The pain is • Vision difficulties bral vasculitis, corticosteroid treatment
aggravated by lying down or stooping, but • Blurred vision, double vision may be started even before a biopsy
can be relieved by carotid compression. • Reduced vision, blindness in one or con­firms the diagnosis (to reduce the
There is exquisite tenderness over the both eyes risk of complications). Aspirin may be rec­
course of the superficial temporal, trans­ • Weakness, excessive tiredness ommended in addition to corticosteroids.
172 Neurological Disorders of Face and General Anesthesia

Medications that suppress the immune migraine affects approximately equal usually of unformed flashes of white
system (such as cyclophosphamide) are numbers of prepubescent boys and and/or black or rarely of multicolored
occasionally prescribed. girls; propensity to migraine headache is lights (photopsia) or formations of
known to disappear during preg­nancy, dazz­ling zigzag lines (scin­tillating scot­
although in some women migraines oma). Scintillating sco­ toma is the
MIGRAINE
may become more frequent during pre­ most common visual aura preceding
Migraine is a neurological syndrome g­nancy. migr­ aine and was first described by
characterized by altered bodily percep­ 19th century physician Hubert Airy,
tions, severe headaches and nausea. Signs and Symptoms scin­till­
ating scotoma usually begins
Physio­logically, the migraine headache The signs and symptoms of migraine as a spot of flickering light near or in
is a neurological condition more common vary among patients. Therefore, what a the center of the visual fields, which
to women than to men. patient experiences before, during and prevents vision within the scotoma.
The pain associated with migraine is after an attack cannot be defined exactly. The scotoma area flickers, but is not
proposed to be vascular in origin. Extra The four common phases of a migraine dark. The scotoma then expands into
and intracranial vessels like superficial attack: one or more shimmering arcs of white
temporal, supraorbital, frontal, internal, 1. The prodrome, which occurs hours or colored flashing lights. An arc of
external and common carotid, internal or days before the headache. light may gradually enlarge, become
maxillary and middle meningeal (extra­ 2. The aura, which immediately pre­ more obvious and may take the form
cranial portion) arteries are commonly cedes the headache. of a definite zigzag pattern, sometimes
identified sources. 3. The pain phase, also known as called fortification spectrum, because
The onset of this condition is before headache phase. of its resemblance to the fortifications
16 years of age and disorder affects 4. The postdrome. of a castle or fort seen from above; often
females twice as often as males. arranged like the battlements of a castle,
The typical migraine headache is Prodromal Phase hence, the alternative terms ‘fortification
unilateral and pulsating, lasting from 4 Prodromal symptoms occur in 40 to spectra’ or ‘teichopsia’ (the sensation
to 72 hours,15 symptoms include nausea, 60 percent of migraine sufferers. This of a luminous appearance before the
vomiting, photophobia and phono­ phase may consist of altered mood, irri­ eyes, with a zigzag, wall-like outline).
phobia (increased sensitivity to sound).16 tability, depression or euphoria, fatigue, Some patients complain of blurred or
Approxi­mately one-third of people who yawning, excessive sleepiness, craving for shimmering or cloudy vision, as though
suffer migraine headache perceive an certain food (e.g. chocolate), stiff muscles they were looking through thick or
aura—unusual visual, olfactory or other (es­pe­cially in the neck), constipation or smoked glass or, in some cases, tunnel
sensory experiences that are a sign that diarrhea, increased urin­ation and other vision and hemianopsia (Hemianopsia:
the migraine will soon occur.17 visceral symptoms.20 These symptoms the loss of half of a field of vision).
Initial treatment is with analgesics usually precede the headache phase of The somatosensory aura of migraine
for the headache, an antiemetic for the the migraine attack by several hours or consists of digitolingual or cheiro-oral
nausea and the avoidance of triggering days. paresthesias, a feeling of pins-and-
condi­tions. The cause of migraine head­ needles experienced in the hand and
ache is idiopathic; the accepted theory Aura Phase arm as well as in the nose-mouth area
is a disorder of the serotonergic control For the 20 to 30 percent21 of individuals on the same side. Paresthesia migrates
system, as PET scan has demonstrated the who suffer migraine with aura. This aura up the arm and then extends to involve
aura coincides with diffusion of cortical comprises focal neurological pheno­ the face, lips and tongue.
depression consequent to increased mena that precede or accompany the Other symptoms of the aura phase
blood flow (up to 300% > base­line). attack. They appear gradually over 5 to can include auditory or olfactory halluc­
There are migraine headache vari­ 20 minutes and generally last fewer than in­ations, temporary dysphasia, vertigo,
ants, some originate in the brainstem 60 minutes. The headache phase of the tingling or numbness of the face and
(featuring intercellular transport dys­ migraine attack usually begins within extremities and hypersensitivity to
function of calcium and potassium ions) 60 minutes of the end of the aura phase, touch.
and some are genetically disposed.18 but it is sometimes delayed up to several
Studies of twins indicate a 60 to 65 per­ hours and it can be missing entirely. Pain Phase
cent genetic influence upon their pro­ Symptoms of migraine aura can be The typical migraine headache is unil­­
pensity to develop migraine headache.19 visual, sensory or motor in nature.22 ateral, throbbing and moderate to
Moreover, fluctuating hormone levels Visual aura is the most common severe and can be aggravated by phy­
indicate a migraine relation: 75 percent of the neurological events. There is sical activity. Not all these features are
of adult patients are women, although a disturbance of vision consisting necessary. The pain may be bilateral
Neurological Disorders of the Face 173

at the onset or start on one side and Diagnosis was and some report impaired thinking
become generalized and usually it Migraines are underdiagnosed and mis­ for a few days after the headache has
alternates sides from one attack to diagnosed. The diagnosis of migraine passed.
the next. The onset is usually gradual. without aura, according to the Interna­ Migraine headaches can be a symp­
The pain peaks and then subsides and tional Headache Society, can be made tom of hypothyroidism.
usually lasts 4 to 72 hours in adults and 1according to the following criteria, the
to 48 hours in children. The frequency of ‘5, 4, 3, 2, 1 criteria’: Depolarization Theory
attacks is extremely variable, from a few • 5 or more attacks. A phenomenon known as cortical spread­
in a lifetime to several a week and the • 4 hours to 3 days in duration. ing depression can cause migraines.27 In
average migraineur experiences one to • 2 or more of—unilateral location, cortical spreading depression, neurologi­
three headaches a month. The headache pulsating quality, moderate to severe cal activity is depressed over an area of the
varies greatly in intensity. pain, aggravation by or avoidance of cortex of the brain. This situation results
The pain of migraine is invariably routine physical activity. in the release of inflammatory mediators
accompanied by other features. Nausea • 1 or more accompanying symp­ leading to irritation of cranial nerve roots,
occurs in almost 90 percent of patients toms—nausea and/or vomiting, most particularly the trigeminal nerve,
and vomiting occurs in about one-third pho­to­phobia, phonophobia. which conveys the sensory information
of patients. Many patients experience For migraine with aura, only two for the face and much of the head.
sensory hyperexcitability manifested by attacks are required to justify the diag­
photophobia, phonophobia and osmo­ nosis. Vascular Theory
phobia (Osmophobia or olfactophobia The pnemonic ‘POUNDing’ (Pulsa­ Migraines can begin when blood ves­
refers to a fear, aversion, or psychological
ting, duration of 4–72 hours, unilateral, sels in the brain contract and expand
hypersensitivity to smells or odors) and nausea, Disabling) can help diagnose inappropriately. This may start in the
seek a dark and quiet room. Blurred vi­ migraine. If 4 of the 5 criteria are met, occipital lobe, as arteries spasm. The
sion, nasal stuffiness, diarrhea, polyuria,then the positive is the likelihood ratio for reduced flow of blood from the occipital
pallor or sweating may be noted during diagnosing migraine.24 lobe triggers the aura that some indi­
the headache phase. There may be lo­ Migraine should be differentiated viduals who have migraines experience
calized edema of the scalp or face, scalp from other causes of headaches such as because the visual cortex is in the oc­
tenderness, prominence of a vein or ar­ cluster headaches. These are extremely cipital area.25
tery in the temple or stiffness and ten­ painful, unilateral headaches of a When the constriction stops and the
derness of the neck. Impairment of con­ piercing quality. The duration of the blood vessels dilate, they become too
centration and mood are common. The common attack is 15 minutes to 3 hours. wide. The once solid walls of the blood
extremities tend to feel cold and moist. Onset of an attack is rapid and most vessels become permeable and some
Vertigo may be experienced. Lighthead­ often without the preliminary signs that fluid leaks out. This leakage is recognized
edness, rather than true vertigo and a are characteristic of a migraine. by pain receptors in the blood vessels
feeling of faintness may occur. Diagnosis can also be substantiated of surrounding tissue. In response, the
by exerting digital pressure over the body supplies the area with chemicals
Postdromal Phase common carotid artery and/or noting which cause inflammation. With each
The patient may feel tired or ‘hungover’ the relief of the pain by giving ergo­ heart beat, blood passes through this
and have head pain, cognitive difficulties tamine tartarate. sensitive area causing a throb of pain.25
(learning difficulties), gastrointestinal The vascular theory of migraines is
sym­ ptoms, mood changes and weak­ Pathophysiology now seen as secondary to brain dysfun­
ness.23 Some people feel unusually refre­ Migraines were once thought to be ction.
shed or euphoric after an attack, whereas initiated exclusively by problems with
others note depression and malaise. blood vessels. The vascular theory of Serotonin Theory
Often, some of the minor headache migraines is now considered secondary Serotonin is a type of neurotransmitter, or
phase symptoms may continue such as to brain dysfunction25 and claimed to “communication chemical” which passes
loss of appetite, photophobia and light­ have been discredited by others.26 Trig­ger messages between nerve cells. It helps
headedness. For some patients, a 5 to points can be at least part of the cause, to control mood, pain sensation, sexual
6 hours nap may reduce the pain, but and perpetuate most kinds of headaches. behavior, sleep, as well as dilation and
slight headaches may still occur when the The effects of migraine may persist constriction of the blood vessels among
patient stands or sits quickly. Normally for some days after the main headache other things. Low serotonin levels in the
these symptoms go away after a good has ended. Many sufferers report a sore brain may lead to a process of constriction
night’s rest. feeling in the area, where the migraine and dilation of the blood vessels which
174 Neurological Disorders of Face and General Anesthesia

trigger a migraine.25 Triptans activate sero­ citrus, onions, dairy products and may also be beneficial in the prophylaxis
tonin receptors to stop a migraine attack. fermented or pickled foods. of migraines due to its antagonistic
effects on the 5-HT2A and 5-HT2C re­­
Neural Theory Management ce­ptors.
When certain nerves or an area in the Conventional treatment focuses on three
brainstem become irritated, a migraine areas: Ergot Alkaloids
begins. In response to the irritation, the 1. Trigger avoidance. Ergot drugs can be used either as a pre­
body releases chemicals which cause 2. Symptomatic control. ventive or abortive therapy. It is a vaso­
inflammation of the blood vessels. These 3. Prophylactic pharmocological drugs. constrictor, which controls the painful
chemicals cause further irritation of the vasodilation thought to be neurhormon­
nerves and blood vessels and results in Paracetamol or Nonsteroidal ally induced. However, ergotamine
pain. Substance P is one of the substances Anti-inflammatory Drugs (NSAIDs) tart­rate tablets (usually with caffeine),
released with first irritation.28 Pain then The first line of treatment is over-the- though highly effective and long lasting
increases because substance P aids in counter abortive medication. (unlike triptans), have fallen out of favor
sending pain signals to the brain. Simple analgesics combined with due to the problem of ergotism.
caffeine may help. During a migraine att­
Unifying Theory ack, emptying of the stomach is slowed, Steroids
Both vascular and neural influences resulting in nausea and a delay in absor­ Single dose of IV dexamethasone, when
cause migraines. bing medication. Caffeine has been shown added to standard treatment, is argued
• Stress triggers changes in the brain. to partially reverse this effect. to decrease headache recurrence.
• These changes cause serotonin to be Excedrin migraine: It is a combi­
released. nation of aspirin, acetaminophen and Other Agents
• Blood vessels constrict and dilate. caff­eine. If over-the-counter medications do not
• Chemicals including substance P Analgesics combined with antie­ work or if triptans are unaffordable,
irritate nerves and blood vessels metics: Antiemetics by mouth may help the next step for many doctors is to
causing pain. relieve symptoms of nausea and help prescribe Fioricet or Fiorinal, which is
prevent vomiting, which can diminish a combination of butalbital (a barbi­
Triggers the effec­tiveness of orally taken analge­ turate), paracetamol (in Fioricet) or acet­
A migraine trigger or ‘precipitant’ is any sia. In addition some antiemetics such yl­salicylic acid (more commonly known
factor that, on exposure or with­drawal, as met­o­­clopramide are prokinetics and as aspirin and present in Fiorinal and
leads to the development of an acute help gastric emptying, which is often caffeine. While the risk of addiction is
migraine headache. Triggers may be impa­ i­
red during episodes of migraine. low, butalbital can be habit-forming if
categorized as behavioral, environmental, Combi­nations available are aspirin with used daily and it can also lead to rebound
infectious, dietary, chemical or hormonal. metoclopramide; paracetamol/cod­eine headaches.
Migraine attacks may be triggered by: for analgesia, with buclizine as the antie­ Amidrine®, Duradrin® and Midrin®
• Allergic reactions. metic and paracetamol/meto­clopramide. is a combination of acetaminophen,
• Bright lights, loud noises and certain The earlier these drugs are taken in the dich­loralphenazone and isometheptene
odors or perfumes. attack, the better their effect. often prescribed for migraine head­
• Physical or emotional stress. Some patients find relief from taking aches.
• Changes in sleep patterns. other sedative antihistamines, which Antiemetics may need to be given by
• Smoking or exposure to smoke. have antinausea properties, such as suppository or injection where vomiting
• Skipping meals. Benadryl (diphenhydramine). dominates the symptoms.
• Alcohol.
• Menstrual cycle fluctuations, birth Serotonin Agonists Status Migrainosus
control pills, hormone fluctuations Sumatriptan and related selective Status migrainosus is characterized by
during the menopause transition. serotonin receptor agonists are excellent
migraine lasting more than 72 hours,
• Tension headaches. for severe migraines or those that do not
with not more than four hours of relief
• Foods containing tyramine (red wine, respond to NSAIDs or other over-the- during that period. It is generally under­
aged cheese, smoked fish, chic­ ken counter drugs. stood that status migrainosus has been
livers, figs and some beans), mono­ refractory to usual outpatient manage­
sodium glutamate (MSG) or nitrates Antidepressants ment upon presentation.
(like bacon, hot dogs and salami). Tricyclic antidepressants have been Treatment of status migrainosus
• Other foods such as chocolate, nuts, long established as highly efficacious con­­
sists of managing comorbidities
peanut butter, avocado, banana, prophylactic treatments. Nefazodone (i.e. correcting fluid and electrolyte
Neurological Disorders of the Face 175

abnor­ malities resulting from anorexia 6. Trigeminal neuralgia–pathophysio­logy, 18. Ogilvie AD, Russell MB, Dhall P, et
and nausea/vomiting often accom­ diagnosis, and current treatment. Bri­tish al. ‘Altered allelic distributions of the
panying status migrainosus) and usually Journal of Anesthesia. 2001;87: 117–32. serotonin transporter gene in migraine
admini­ stering parenteral medication 7. White JC, Sweet WH. Pain: Its mech­ without aura and migraine with aura’.
to ‘break’ (abort) the headache. First anisms and neurosurgical control. Cephalalgia. 1998;18(1):23-6.
line therapy consists of IV fluids, meto­ Spr­i­ngfield, IL, Charles C Thomas, 1955. 19. Gervil M, Ulrich V, Kaprio J, Olesen J,
clopramide and triptans or DHE. 8. Sunderland S (Ed). Nerve injuries and Russell MB (September 1999). ‘The rela­
their repair: A critical appraisal. New tive role of genetic and environmental
Noninvasive Medical York, Churchill livingstone; 1991. p. 221. factors in migraine without aura’. Neu­r­
Treatments 9. Recknor JB, Mallapragada SK. Nerve o­logy. 1999;53(5):995–9. PMID 10496258.
Transcranial magnetic stimulation, bio­ Regeneration: Tissue Engineering Stra­ 20. Silberstein, Stephen D. Atlas of Migra­
feed­­
back, hyperbaric oxygen therapy te­gies, in The Biomedical Engineer­ing ine And Other Headaches. Lon­ don:
are some of the noninvasive techniques Handbook: Tissue Engineering and Ar­ Taylor and Francis Group, 2005.
employed. tificial Organs, Bronzino JD, (Ed). 2006, 21. Mathew NT, Evans RW. Handbook of
Bruxism, clenching or grinding of Taylor and Francis: New York. headache. Hagerstown, MD; Lippincott
teeth, especially at night, is a trigger for 10. Yiu G, Zhigang H. Glial inhibition of Williams and Wilkins, 2005.
many migraineurs. A device called noci­ CNS axon regeneration. Nature Reviews 22. Silberstein SD. Headache in Clinical
ceptive trigeminal inhibitor (NTI) takes Neuroscience. 2006;7:617-27. Practice, 2nd edn. London: Taylor and
advantage of a reflex limiting the force of 11. Eagle W. Elongated styloid process: Fur­ Francis Group, 2002.
clenching. It can be fitted over the front ther observation and a new synd­rome. 23. Kelman L. ‘The postdrome of the
teeth at night, preventing contact be­ Arch Otolaryngol. 1948;47: 630-40. acute migraine attack’. Cephalalgia.
tween the back teeth. Massage therapy of 12. Lentini A. Gli aspetti clinici e radiologici 2006;26(2): 214–20.
the jaw area can also reduce such pain. delle anomalie dell’apparato stilo- 24. Detsky ME, McDonald DR, Baerlocher
joideo. Radiol Med. 1975;61:337-3640. MO, et al. ‘Does this patient with hea­
13. Kaufman SM, Elzay RP, Irish EF. Sty­ dache have a migraine or need neur­
REFERENCES
loid process variation. Radiologic and oim­aging?’ JAMA. 2006;296(10): 1274–
1. Gray’s Anatomy: The Anatomical Basis clini­cal study. Arch Otolaryngol. 1970; 83.
of Clinical Practice, 40th edn (2008), 91(5):460-3. 25. Alexander Mauskop; Fox, Barry. What
Churchill-Livingstone, Elsevier. 14. Baddour HM, McAnear JT, Tilson HB. Your Doctor May Not Tell You About
2. Bagheri SC, Farhidvash F, Perciaccante Eagle’s syndrome. Report of a case. (TM): Migraines: The Breakthrough
VJ. Diagnosis and treatment of patients Oral Surg Oral Med Oral Pathol. 1978; Pro­gram That Can Help End Your
with trigeminal neuralgia. J Am Dent 46(4):486–94. Pain (What Your Doctor May Not Tell
Assoc. 2004;135:1713. 15. The International Classification of You About...(Paperback). New York:
3. Wilkins RH. Historical perspectives. Head­ache Disorders, 2nd edn. Ceph­a­ Warner Books; 2001.
In: Rovit RL, Murali R, Jannetta PJ lalgia. 2004;24(suppl 1):1–160. 26. Cohen AS, Goadsby PJ. “Functional
(eds). Trigeminal neuralgia. Baltimore: 16. Gallagher RM, Cutrer FM. “Migraine: neuroimaging of primary headache
Williams and Wilkins. 1990;pp. 1–25. diagnosis, management, and new disorders”. Curr Pain Headache Rep.
4. International association for study of treatment options”. Am J Manag Care. 2005;9(2):141–6.
pain; Clinical Journal of Pain 2002. 2002;8 (3 Suppl): S58–73. 27. Lauritzen M. “Pathophysiology of the
5. Peterson AM, Williams RL, Fukui MB, 17. ‘Guidelines for all healthcare professi­ migraine aura. The spreading depres­
et al. Venous angioma adjacent to onals in the diagnosis and management sion theory”. Brain. 1994;117 (Pt1):199–
the root entry zone of the trigeminal of migraine, tension-type, cluster and 210.
nerve: implications for management medication-overuse headache, January 28. Sheena K Aurora. Pathophysiology of
of trigeminal neuralgia. Received: 30 2007, British Association for the Study of migraine headache. Current Pain and
March 2001. Headache. Headache Reports. 2001;5(2):179-82.
10 General Anesthesia
Borle Rajiv M, Angik Richa

volume percent can produce anes­thesia relaxation that previously could be ob­
HISTORICAL ASPECTS without dilut­ing the oxygen in room air tained only with deep levels of general
Surgical procedures were uncommon to hypoxic levels. It was used to support anesthe­sia.
before 1846. The understanding of the both respiration and circulation, crucial
pathophysiology of disease and of the properties at the time when human phy­ INTRODUCTION OF
rationale for its treatment by surgery siology was not understood well enough INTRAVENOUS ANESTHETIC
was rudimentary due to lack of sat­ for assisted respi­r­ation and circulation
isfactory anesthesia. Limited means of to be made possible. Ether is not toxic to
AGENTS
attempting to relieve surgical pain were vital organs. In 1935, Lundy9 demonstrated the clinical
available such as drugs like al­ cohol, In 1847, a Scottish obstetri­cian James use­fulness of thiopental, a rapidly act­ing
hashish and opium derivatives taken Simpson introduced chloroform.5 It be­ thiobarbiturate. It was originally consid­
orally. Unconsciousness induced by a came quite popu­lar because of its more ered useful as a sole anesthetic agent, but
blow to the head or by strangulation did pleasant odor. The drug is a hepa­totoxic the doses re­quired resulted in serious de­
provide relief from pain, although at a and a severe cardiovascular depressant. pression of the circula­tory, respiratory and
high cost. The most common method Despite the relatively high incidence of nervous systems. Thiopental has been
used to achieve a relatively quiet surgery intra­operative and postoperative deaths accepted as an agent for the rapid induc­
was simple restraint of the patient by associated with the use of chloroform, tion of general anesthesia. Various com­
force. Nitrous oxide was synthesized it was used for 100 years, espe­cially in binations of intravenous (IV) drugs from
by Priestley in 1776.1 Diethyl ether and Great Britain. Nitrous oxide was disused several classes have been used recently
nitrous oxide were first used by Den­tists. after the apparent failure in Boston in as anes­ thetic agents, usually together
In 1845, Horace Wells2 first attempted to 1845 and was reintroduced in 1863 into with nitrous oxide.10 The commonly used
demonstrate the use of nitrous oxide for American dental and surgical practice, general anesthetic agents are either in­
dental extraction at the Massachusetts by physician, Gardner Q Colton.6 halational agents or the drugs that can be
General Hospital in Boston, but it failed. In 1868, the admin­istration of nit­ adminis­tered intra­venously (Table 10.1).
William TG Morton3 invented and rous oxide with oxygen was de­s­cribed by
revealed of the anesthetic inhalation Edmond Andrews,7 a Chicago surgeon COMMONLY USED
by using ether on the patient, before and thereafter the two gases became
ANESTHETIC AGENTS
whom, in all time, surgery was agony.4 available in steel cylinders, greatly
increasing their practical­ity.
In 1929, the anesthetic properties Propofol11
ANESTHESIA AFTER 1846
of cyclopropane were accidentally dis­ • It is an alkylphenol sedative-hyp­notic.
Although rarely used today, ether was covered by chemists.8 Cyclopropane was • Ideal induction agent in many situ­
the first ‘ideal’ anesthetic agent. Chemi­ perhaps the most widely used general ations except in cases of:
cally, it is readily made in pure form. It anesthetic for the next 30 years. – Suspected hypotension
is relatively easy to administer, since it The skeletal muscle relaxants (neu­ – Patients with preoperative hypo­
is a liquid at room temperature, but is ro­­mus­cular blocking agents) were also volemia especially in emergency
readily vaporized. Ether is more potent, discovered. In 1940s, anesthesiologists care. It is contraindicated in chil­
unlike nitrous oxide and thus, a few used curare to provide the muscular dren < 3 years of age.
General Anesthesia 177

Table 10.1: Classification of general anesthetic agents is dec­ reased and the bronchospasm
Inhalational may be abolished as it has a bron­
Gas Volatile liquids codilator action. Unlike the routine
Nitrous oxide Ether intravenous anesthetics (thiopen­ tal
Halothane sodium), ketamine does not act upon
Isoflurane the reticular activating system of the
Sevoflurane midbrain, but acts upon the cortex and
Desflurane the limbic system. Thus hallucinations,
Enflurane disagreeable dreams, delirium and
Intravenous
excite­ment are precipitated during the
Inducing agents Slower acting drugs
reco­very. The unpleasant dreams may
Thiopentone sodium Benzodiazepines—Diazepam, Lorazepam, Midazolam
persist for several days in adults. It
Methohexitone sodium Dissociative anesthesia—Ketamine
Propofol Opioid analgesia—Fentanyl
produces postemergence hallucinations
Etomidate
and dysphoria, more commonly in
adults, but occasionally in children.
Ketamine in an IV dose of 1 to 2 mg/kg
• Duration of action: 5 to 10 minutes— Ketamine13,14 of body weight and IM dose of 4 to
extremely short and desirable. 5 mg/kg of body weight, has been used
• It has a very valuable property in Ketamine is a phencyclidine deriva­tive. as an intra­ muscular or intravenous
examination of the patients with Greenfield15 described the use of keta­ injec­tion to sedate combative children
head injury where serial neu­ mine hydrochloride, a drug that al­ters in emer­gency departments at doses of
rological examinations can be per­ the patient’s awareness for his surroun­ 2 to 5 mg/kg. A revised weight dosage
formed simply by turning-off the dings, but does not produce the typical relationship has been established by
drip and waiting for 10 minutes and state of unconsciousness. Ketamine Greenfield15 and is based on intra­mus­
assessing neurologic function. induces a ‘dissociative anes­thesia’ cular adminis­tration.
• Dosage: Induction dose is 1 to chara­­
cterized by stage of sed­ ation, • Up to 50 Lbs—0.5 to 1.0 mg/Lb,
2.5 mg/kg IV bolus for children and immo­ bility, amnesia and marked • 50 to 100 Lbs—1.0 to 1.5 mg/Lb,
adults. For maintenance the dose is analgesia. Since ketamine acts pri­ • Above 100 Lbs—1.5 mg/Lbs plus
50 to 200 microgram/kg/min. and marily on thalamus and cortex and N2O:O2 (50:50).
for sedation the dose is 25 to 100 not on the reticular activating system, At these dosage levels, conscious­
micro­­gram/kg/mg.12 the patient does not appear to be ness is generally maintained together
• Associated desirable side effects— asleep, but rather dissociated from the with protective reflexes and stable vital
– Antiemetic effect environment. After the administration signs. The duration of effect varies from
– Causes amnesia the dissociation occurs in 15 seconds 20 to 40 minutes and can be prolonged
– Lowers intra cranial pressure and unconsciousness becomes appa­ by the addition of N2O:O2 in a 50:50
– Antiepileptic effect rent in another 30 seconds. Intense mixture. At higher doses, ketamine is
• Used commonly in oral surgery analgesia and amnesia are established known to produce psychotomimetic
pra­ c­ tice as a day-care anesthetic rapidly. The state of unconsciousness effects, including hallu­cinations, during
agent. The patient can be taken lasts for about 10 to 15 minutes and the recovery period and occasionally
under gen­­eral anesthesia for short the analgesia persists for about 40 to there are delayed bizarre disturbances.
pro­­­­ced­ures, induced on propofol 45 minutes following a single dose Preci­pitation of delirium or violent and
and be discharged on the same day administration. Respiration is usually irrational response to stimuli is the
of surgery after regaining cons­cio­u­ not depressed with proper dosages. undesired property during the recovery
s­­ness in view of minimal posto­pera­ The hypoxic and hypercarbic stim­ from ketamine anesthesia.
tive side effects and hence minimal ulation of the respiration is not seriously Ketamine is contraindicated in
care is required. affected following usual doses of keta­ pati­ents with hypertension, psy­ chi­
• Undesirable effects: It causes signi­ mine. It is associated with increased atric dis­orders and glaucoma. Main­
ficant hypotension especially in oral secretions, therefore necessitating tenance of an unobstructed airway
cases of hypovolemia. premedi­cation with an anticholinergic is an important property of ketamine
• Undesirable side effects after hy­ drug such as an antisialagogue. The anesthesia. Keta­mine is found to be
po­volemia: The undesirable side impor­tant pro­perty of ketamine is the a safe anesthetic for minor oral surgi­
effect of long-term infusion is Pro­ pre­servation of the pharyngeal and the cal procedures especially in the chil­
pofol infusion syndrome. laryngeal reflexes. The airway resistance dren.
178 Neurological Disorders of Face and General Anesthesia

Isoflurane—2-chloro-2- bonding to glutamate receptors mimics Muscle relaxation is often adequate


(difluoromethoxy)-1,1,1- the effects of NMDA (N-methyl-D-asp­ for maxillofacial operations at normal
trifluoro-ethane artate). It activates cal­cium ATPase levels of anesthesia. Complete muscle
through an increase in membrane paralysis can be attained with small doses
Isoflurane—2-chloro-2-(difluorome­ fluidity and binds to the D subunit of of muscle relaxants. All commonly used
thoxy)-1,1,1-trifluoro-ethane is a halo­ ATP (Adenosine triphosphate) syn­­thase muscle relaxants are markedly poten­
genated ether used for maintenance of and NADH (Nicotinamide_aden­ ine_tiated with Isoflurane, the effect being
anesthesia. Together with enflurane and dinu­cleotide dehydrogenase) dehydro­ most profound with the nondepolarizing
halothane, it replaced the flammable genase. In addition, a number of generalones. Neostigmine reverses the effect of
ethers used in the pioneer days of sur­ anesthetics attenuate gap junction com­ non-depolarizing muscle relaxants in
gery. Its use in human medicine is now m­unication, which could contribute to the presence of Isoflurane. All commonly
starting to decline, being replaced by anesthetic action. used muscle relaxants are compatible
sevoflurane, desflurane and the intrave­ with Isoflurane. Isoflurane can produce
nous anesthetic propofol. Properties coronary vasodilation at the arteriolar
Isoflurane is always administered Induction of and recovery from isoflu­ level.
in conjunction with air and/or pure rane anesthesia are rapid. Isoflurane
oxygen. Often nitrous oxide is also has a mild pungency, which limits the Side Effects
used. Although its physical properties rate of induction, although excessive In susceptible individuals, isoflurane
mean that anesthesia can be induced salivation or tracheobronchial secre­ anes­thesia may trigger a skeletal mus­cle
more rapidly than with halothane, its tions do not appear to be stimu­lated. hypermetabolic state leading to high ox­
pungency can irritate the respiratory Pharyngeal and laryngeal reflexes ygen demand and the clinical syndrome
system, negating this theoretical advan­ are readily obtunded. The level of known as malignant hyper­thermia. The
tage conferred by its physical properties. anesthesia may be changed rapidly syndrome includes nonspecific fea­
It is usually used to maintain a state of with isoflurane. Isoflurane is a pro­ tures such as muscle rigidity, tachycar­
general anesthesia that has been induced found respiratory depressant. Res­ dia, tachypnea, cya­ nosis, arrhy­
thmias
with another drug, such as thiopentone piration must be monitored closely and and unstable blood pressure (It should
or propofol. It vaporizes readily, but supported when necessary. As anes­ also be noted that many of these non-
is a liquid at room temperature. It is thetic dose is increased, tidal volume specific signs may appear with light
completely non-flammable. Isoflurane, decreases and respiratory rate is un­ anesthesia, acute hypoxia, etc.). An in­
USP, is supplied in 100 mL and 250 mL changed. This depression is partially crease in overall metabolism may be
amber-colored bottles. reversed by surgical stimulation, even reflected in an elevated temperature
at deeper levels of anesthesia. Blood (which may rise rapidly early or late in
pressure decreases with induction of the case, but usually is not the first sign
anesthesia, but returns towards normal of augmented metabolism) and an in­
with surgical stimulation. Progressive creased usage of the CO2 absorption
increase in depth of anesthesia pro­ system (hot canister). PaO2 and pH may
duces corresponding decrease in blood decrease and hyperkalemia and a base
pres­sure. Nitrous oxide diminishes the deficit may appear. Treatment includes
Structure of isoflurane inspiratory concentration of isoflurane discontinuance of triggering agents (e.g.
required to reach a desired level of Isoflurane), administration of intrave­
anesthesia and may reduce the arterial nous dantrolene sodium and applica­
Mechanism of Action hypotension seen with isoflurane alone. tion of supportive therapy. Such therapy
Isoflurane reduces pain sensitivity (anal­ Heart rhythm is remarkably stable. inclu­des vigorous efforts to restore body
g­esia) and relaxes muscles. The mech­ With controlled ventilation and normal temperature to normal, respiratory and
anism by which general anes­ thetics PaCO2, cardiac output is maintained circulatory support as indicated and
produce the anesthetic state is not despite increasing depth of anesthesia, management of electrolyte-fluid-acid-
clearly understood, but likely involves primarily through an increase in heart base derange­ments.
interactions with multiple receptor sites rate which compensates for a reduc­
to interfere with synaptic trans­mission. tion in stroke volume. The hypercapnia Nitrous Oxide
Isoflurane binds to gamma-amino but­ which attends spontaneous ventilation Nitrous oxide, commonly known as
yric acid (GABA) receptors, gluta­ mate during isoflurane anesthesia further happy gas, laughing gas and NOX, is a
receptors and glycine receptors and increases heart rate and raises cardiac chemical compound with the chemical
also inhibits conduction in activated output above awake levels. Isoflurane formula N2O. At room temperature, it is
potassium channels. Glycine inhibition does not sensitize the myocardium to a colorless, nonflammable gas, with a
helps to inhibit motor function, while exo­genously administered epinephrine. pleasant, slightly sweet odor and taste.
General Anesthesia 179

It is used in surgery and dentistry for cited) potential. Unlike many anesthet­ acceptability in pediatric patients is
its anesthetic and analgesic effects. It ics, however, N2O does not seem to affect good.
is known as ‘laughing gas’ due to the calcium channels. Unlike most general • Sevoflurane differs from halothane,
euphoric effects of inhaling it. The gas anesthetics, N2O appears to affect the enflurane, isoflurane and desflu­
was first synthesized by English che­mist GABA receptor. rane, as all these drugs (except sevo­
and natural philosopher Joseph Pries­ flurane) are metabolized to reactive
tley1 in 1775. Sevoflurane acyl halide intermediates with the
Nitrous oxide has been used for Sevoflurane is a fluorinated methyl iso­ potential to produce hepatotoxicity
anesthesia in dentistry since the 1840s. propyl ether having properties inter­ as well as cross sensitivity between
The most common use is as a 50:50 mediate between isoflurane and des­ drugs.
mix with oxygen, commonly known as flurane. • Sevoflurane and desflurane because
Entonox or Nitronox delivered through a of their lower blood and tissue solu­
de­mand valve. Nitrous oxide is typically bilities permit more precise control
administered by dentists through a over the induction of anes­thesia and
demand valve inhaler over the nose more rapid recovery when the drug
that only releases gas when the patient is discontinued.
inhales through the nose. • Sevoflurane and desflurane, like
Because nitrous oxide is minimally Mechanism of Action isoflurane, do not produce evidence
metabolized, it retains its potency Sevoflurane induces a reduction in jun­ of convulsive activity on the EEG
when exhaled into the room by the ctional conductance by decreasing gap either at deep levels of anesthesia
pati­ent and can pose an intoxicating junction channel opening times and or in the presence of hypocapnia or
and prolonged-exposure hazard to the increasing gap junction channel closing audi­­tory stimulation. Sevoflurane
opera­ ting staff if the room is poorly times. Sevoflurane also activates calcium can suppress convulsive activity
ventilated. Where nitrous oxide is dependent ATPase in the sarcoplasmic indu­­ced with lidocaine.
administered, a continuous-flow fresh- reticulum by increasing the fluidity of • Induction and emergence from
air ventilation system or nitrous-scaven­ the lipid membrane. It also appears the anesthesia are fast and rapid
ging system is used to prevent waste gas to bind the D subunit of ATP synthase changes in depth can be achieved. It
buildup. and NADH dehydogenase and also is desirable for use in inpatient and
Nitrous oxide is a weak general anes­ binds to the GABA receptor, the large outpatient surgery but its high cost
thetic and so is generally not used alone conductance Ca2+ activated potassium and high open flow system makes it
in general anesthesia. It is mainly used channel, the glutamate receptor, and the expensive to use.
as analgesics and not as anesthetic. In glycine receptor. It is rapidly absorbed • It can be used both for induction
general anesthesia it is used as a carrier into circulation via the lungs, however and maintenance.
gas in a 2:1 ratio with oxygen for more solubility in the blood is low. The half-
powerful general anesthetic agents such life is 15 to 23 hours. Ether
as sevo­flurane or desflurane. Diethyl ether, also known as ether and
Nitrous oxide (N2O) is a dissociative ethoxyethane, is a clear, colorless and
drug that can cause analgesia, deperso­
Properties highly flammable liquid with a low
nalization, derealization, dizziness, euph­ • The vapor pressure of sevoflurane boiling point and a characteristic odor.
oria and some sound distortion. resembles that of halothane and It is used as a common solvent and
iso­flurane, permitting delivery of has been used as a general anesthetic.
Mechanism of Action this anesthetic via a conventional Although, it is not commonly used
It acts as an NMDA receptor antagonist at unhea­ted vaporizer. nowadays and sevoflurane is widely
partial pressures similar to those used in • Compared with isoflurane, recovery used. Alchemist Raymundus Lullus
general anesthesia. The evidence on the from sevoflurane anesthesia is 3 to is credited with discovering the com­
effect of N2O on gamma aminobutyric 4 minutes faster and the difference pound in 1275 AD, although there is no
acid (GABA) receptor currently is mixed, is magnified in longer duration contemporary evidence of this. It was
but tends to show a lower potency po­ surgical procedures (> 3 hours). first synthesized in 1540 by Valerius
tentiation by acting as a positive alloste­ • Sevoflurane is non pungent, has Cordus, who called it ‘oil of sweet vitriol’
ric modulator of the receptor. N2O, like minimal odor, produces broncho­ (oleum dulcis vitrioli), the name given
other volatile anesthetics, activates twin- dilation similar in degree to isoflu­ because it was originally discovered by
pore potas­sium channels, albeit weakly. rane and causes the least degree of distilling a mixture of ethanol and sulfu­
These channels are largely responsible airway irritation among the currently ric acid. William TG Morton participated
for keep­ing neurons at the resting (unex­ available volatile anesthetics. The the first public demonstration of ether
180 Neurological Disorders of Face and General Anesthesia

anesthesia on October 16, 1846 at the result from the metabolism of halothane any asso­ ciated systemic disease.
Ether Dome in Boston, Massachusetts.16 to trifluoroacetic acid via oxidative To evaluate the conditions of the
Ether was sometimes used in place of reactions in the liver. About 20 percent pulmonary parenchyma X-ray chest
chloroform because it had a higher thera­ of inhaled halothane is metabolized by is done. The renal and hepatic status
peutic index, a larger difference between the liver and these products are excreted is evaluated by performing the RFT
the recommended dosage and a toxic in the urine. The hepatitis syndrome and LFT respectively. The RFT (also
overdose. Ether is still the preferred an­ had a mortality rate of 30 to 70 percent. called KFT) comprises of assessment
esthetic in some develop­ing nations due Concern for hepatitis resulted in a of serum Na+, K+, creatinine and
to its high therapeutic index (~1.5–2.2).17 dramatic reduction in the use of halo­ urea concentration. The LFT is done
Today, ether is rarely used. The use of thane for adults. It was replaced in the by assessing the serum bilirubin
flammable ether waned as non-flamma­ 1980s by enflurane and isoflurane. SGOT, SGPT levels. The last two
ble anesthetic agents such as halothane Halothane is clinically the most investigations (RFT, LFT) are done
became available. Additionally, ether potent trigger as compared to isoflurane prior to the administration of GA
had many undesirable side effects, such for malignant hyperthermia, due to diff­ only when specifically indicated
as post­anesthetic nausea and vomiting. erence in the calcium releasing potency as all the anesthetic agents are
of individual anesthetics at cellular level, metabolized in lever and execrated
Halothane which leads to increased intracellular by the kindeys. Other investigations
Halothane vapor (or Fluothane) is an in­ calcium. like PT, platelet, count, hemoglobin
halational general anesthetic, supplied electrophoresis, sickling, etc. are
in amber colored bottles. Its IUPAC INDICATIONS FOR GENERAL done if indicated in a particular case.
name is 2-bromo-2-chloro-1,1,1-trifluo­ • A thorough clinical examination is
ANESTHESIA
roethane. It is the only inhalational anes­ mandatory in every patient to evalu­
thetic agent containing a bromine atom. The indications for general anesthesia ate the general physical status of
It is colorless and pleasant-smelling, but are as follows: the patient and to identify other
unstable in light. It is available in dark- • The surgical procedures of larger associated diseases. Cardiovascular
colored bottles and contains 0.01 percent magnitude, which cannot be acco­ status is evaluated by clinical exami­
thymol as a stabilizing agent. Halothane mp­lished under local anes­thesia or nation and investigations like ECG,
is a core medicine in the World Health where the regional anesthesia and or echocar­ diography, Doppler, TMT,
Organization’s ‘Essential Drugs List’, sedation are inadequate to provide etc. when indicated in a particular
which is a list of minimum medical needs satisfactory analgesia. case. Similarly the pulmonary sta­
for a basic health care system.18 This ha­ • When the patients are uncooperative. tus is evaluated by clinical examina­
logenated hydrocarbon was first synthe­ • When patient compliance is not tion and posteroanterior (PA) X-ray
sized by CW Suckling19 of Imperial Chem­ required. of chest. Pulmonary diseases like
ical Industries (ICI) in 1951 and was first • Apprehensive patients where mus­ ‘chronic obstructive pulmonary dis­
used clinically by M Johnstone20 in Man­ cle relaxation is required for stabili­ ease’ (COPD), pulmonary tubercu­
chester in 1956. Its properties include zation. losis, plural fibrosis, consolidation or
cardiac depression at high levels, cardiac even active infection can complicate
sensitization to catecholamines such as PREANESTHETIC the administration of GA. The dis­
norepinephrine and potent bronchial re­ eases like arrythmias, ischemic heart
PREPARATION
laxation. Its lack of airway irritation made disease (IHD), hypertension (HT),
it a common inhalation induction agent For safe administration of the general cardiomyopathies can also make the
in pediatric anesthesia. Due to its cardiac anesthesia (GA) the patient is thoroughly administration of GA complicated
depressive effect, it was contraindicated evaluated and investigated and this unless controlled satisfactorily before
in patients with cardiac failure. Halothane procedure is called preanesthetic pre­ the administration of the anesthesia.
was also contraindicated in patients sus­ paration, which comprises of following The disorders like diabetes, thyroids
ceptible to cardiac arrythmias or in situa­ steps: disorders, Addison’s disease, etc.
tions related to high catecholamine levels • The patient is hospitalized 2 days must be adequately controlled before
such as pheochromocytoma. prior to the surgery to make him the procedure by giving appropriate
Repeated exposures to halothane in accustomed with environments to treatment. The patients are often re­
adults were, noted, in rare cases to result reduce the stress. ferred to physician for such evalua­
in severe liver injury. This occurred • Investigations comprising of Hb%, tion and management if required.
in about 1 in 35,000 exposures.21 The TLC, DLC, BT, CT routine urine • The preanesthetic check up is done
resulting syndrome was referred to as tests, asses­sment of blood sugar by the anesthetist, a day prior to the
halothane hepatitis and is thought to levels, are carried out to rule out surgery who evaluates the fitness for
General Anesthesia 181

the administration of the GA. The given and tight under garments are to make the induction pain free. The
anesthetist also evaluates the airway removed. side effect of the narcotic analgesics
anatomy, degree of mouth opening, • A written, informed consent of the pa­ is emesis, which may not be desir­
nasal patency, pharyngeal and lary­n­ tient is obtained and wherever neces­ able for oral surgical procedures
geal anatomy, cervical spine ano­ sary, risk consent is also obtained.24 especially where IMF is required and
malies and neck mobility, which hence should be avoided.
can pose difficulty in intubating the • Antihistaminics: The antihistamin­
patient.
PREANESTHETIC ics29 like phenergan (promethazine),
• The patient is kept nil by mouth/nil MEDICATION Avil (pheniramine maleate), are of­
per oral (NBM) 5 to 6 hours prior ten prescribed to counter any mild
to the surgery to ensure that the The drugs, which are prescribed prior allergic reactions. The IV fluids,
stomach is empty and the chances to the administration of the GA are IV sets may contain pyrogenes,
of vomiting and aspirations are called preanesthetic medication.25 The which may evoke mild allergic reac­
minimized. This much time is preanesthetic medication (Box 10.1) is tions like rigors, eruptions, pyrexic
required as it is the gastric emptying given: reaction, etc. mild to moderate reac­
time. If the patient comes for emer­ • To facilitate smooth administration/ tions can also occur during blood.
gency surgery where it is not possible induction of general anesthesia.26 The antihistaminics also have tran­
to the patient NBM for 5 hours, the • To ensure smooth recovery. quilizing effect.
gastric lavage is done to evacuate • To reduce the dose of general anes­ • Antiemetics: To prevent the vom­
the contents of the stomach before thetic. iting and thus, its aspiration in the
administration of the GA.22 • To prevent complications. tracheobronchial tree antiemetics
• Preparation of the bowel: The patient To achieve the above goals the fol­ are prescribed.30 The drugs like pro­
is prescribed laxatives a night before lowing drugs are administered intra­ methazine or metoclopromide are
surgery to ensure that the bowel and muscularly (IM) either 30 minutes prior used in a dose of 25 mg IM or IV.
rectum are evacuated. The commonly to the administration in the preanes­ • Vagolytic drugs: Atropine sulfate is
prescribed laxatives are bisacodyl thetic room or IV 5 to 10 minutes before vagolytic drug and helps in prevent­
(Dulcolax) 5 to 10 mg or liquid paraf­ the administration of GA. ing bradycardia31 also in reducing
fin about 5 to 10 mL orally. The former • Sedatives: The sedatives like diaze­ the salivary and tracheo­ bronchial
is an irritant cathartic and is not used pam,27 (5–10 mg), nitrazepam (5– secretions thus, keeping the airway
in patients with APD, ulcerative colitis, 10 mg), phenobarbitone (15–30 mg) patent. It is given in a dose of 0.6 mg
etc. The bowel preparation may not be are prescribed. These drugs reduce IM or IV.
relevant for maxillofacial procedures, the anxiety and stress and thus the • Antacids: The patients are kept NBM
but is vital for bowel, anorectal or ob­ levels of catecholamines. and are undergoing stress, both the
stetric and gynecological procedure. • Analgesics: The analgesics like For­ things can precipitate increased acid
In addition to the laxatives the patient twin (pentazocine lactate) 15 to secretion and gastritis. To prevent
is also given enema in the morning 30 mg, morphine28 10 to 15 mg or this, drugs like H2 blockers like Rani­
with either plain water, warm water or pethidine 40 to 60 mg are adminis­ tidine32 are prescribed in a dose of
soap water to ensure that the contents tered to potentiate the analgesia and 50 mg IM or IV.
are totally evacuated.23 • Corticosteroids: They help in inhi­
• Sedatives are often prescribed to Box 10.1: Preanesthetic medication biting antigen-antibody reaction,
ensure that the patient’s anxiety have anti-inflammatory property
Sedatives—diazepam
is alleviated and he has good rest and help in combating stress. The
Antihistaminics—promethazine
and sleep. The anxious patients hydrochloride (Phenergan), pheniramine drugs like sodium hydrocor­ tisone
have raised levels of catacolamines, maleate (Avil) succi­nate 100 mg or Dexamethasone
which make induction of anesthesia Antacids­—H2 blockers (Ranitidine) 4 to 8 mg are prescribed.
difficult. The agitated patient also Antiemetics—prochlorperazine (Stemetil),
metoclopramide (Perionorm)
tends to get exhausted easily.
Vagolytic drugs—atropine sulfate PHASES OF GENERAL
• The patient is prescribed bland diet Steroids—hydrocortisone, dexamethasone ANESTHESIA
to prevent any gastrointestinal (GI) Rationale
upset. To reduce anxiety There are three main phases of general
• Before shifting the patient the loose To facilitate smooth induction and recovery anesthesia:
operation theater (OT) garments are To prevent complications • Phase of induction
182 Neurological Disorders of Face and General Anesthesia

• Phase of maintenance • Involuntary micturation or defec­ L-Look for facial abnormality


• Phase of recovery. ation. E-evaluate 3-3-2
M-Mallampatti grade
STAGES OF GENERAL Stage III—Surgical Anesthesia O-obstruction
Extends from onset of regular respiration N-neck mobility
ANESTHESIA to cessation of spontaneous breathing. • Evaluation of the nasal cavity:
General anesthesia causes an irregularly This has been divided into four planes: For presence of polyps, deviated
descending depression of the central Plane 1—Roving eyeballs. This plane nasal septum and discharge as it
nervous system (CNS) in which the higher ends when eyes become fixed. may pose problems in nasotracheal
functions are lost first and progressively Plane 2—Loss of corneal and laryn­ intubation.
lower areas of the brain are involved,33 geal reflexes. • Oral examination: If the patient
but in the spinal cord lower segments Plane 3—Pupil starts dilating and has trismus, the laryngoscopy and
are affected somewhat earlier than light reflex is lost. intubation may become difficult.
the higher segments. The vital centers Plane 4—Intercostal paralysis, shal­ A large malignant growth over the
located in the medulla are paralyzed the low abdo­minal respiration, dilated pupil. anterior part of jaws may also make
last as the depth of anesthesia increases. As anesthesia passes to deeper the laryngoscopy difficult and the
Guedel34 in 1920 described four stages planes, progressively-muscle tone dec­ growth may bleed during laryngos­
with ether anesthesia, dividing the three reases, BP falls, HR increases with weak copy, leading to high chances of as­
stage into four planes. These clear-cut pulse, respiration decreases in depth piration. The loose teeth are likely to
stages are not seen now-a-days with the and later in frequency also t­horacic is be avulsed during larygoscopy and
use of faster acting general anesthetics, lagging behind abdominal. can get aspirated in the air passage.
premedication and employment of many Such teeth should be extracted be­
drugs together. The precise sequ­ence of Stage IV—Stage of Medullary fore hand. The presence of macro­
events differs somewhat with anesthetics glossia, grossly enlarged tonsils and
Paralysis
other than ether. presence of mandibular or maxillary
• There is cessation of breathing hypoplasia and the other hindering
Stage I—Stage of Analgesia leading to failure of circulation and factors.
• Starts from beginning of anesthetic death • Examination of neck: The neck
inhalation and lasts up to the loss of • Pupils are widely dilated should be inspected thoroughly. The
consciousness • Muscles are totally flaccid short necks are usually considered
• Pain is progressively abolished • Pulse is thready or imperceptible unfavorable for intubation. Similarly
• Patient remains conscious, can hear • BP is very low or unrecordable. presence of deformities of cervical
and see and feels a dream like state Many of the above indices have been spine, ankylosing cervical spine con­
• Amnesia develops by the end of this robbed by the use of atropine (pupillary, ditions preventing the neck move­
stage heart rate), mor­phine (respiration, pupi­ ments must be taken into consid­
• Reflexes and respiration remain nor­ llary), muscle relaxants (muscle tone, eration. The injuries to the cervical
mal. respiration, eye movements, reflexes), spine may require special precau­
Though some minor operations can etc. and the modern anesthetist has to tions during intubation.
be carried out during this stage, it is depend on several other observations to • The Mallampati score or Mallam­
rather difficult to maintain so the use is gauge the depth of anesthesia, such as pati classification: This score is
limited to short procedures. bispectral index (BIS). used to predict the ease of intu­
bation.35 It is determined by looking
Stage II—Stage of Excitement at the anatomy of the oral cavity;
• Stage starts from loss of consci­ PREANESTHETIC specifically, it is based on the visi­
ousness upto gain of rhythmical res­ EVALUATION bility of the base of uvula, faucial
piration pillars (the arches in front of and
• Respiration—Irregular and large in All the patients who are to be subjected behind the tonsils) and soft palate.
volume to general anesthesia are needed to be Scoring may be done with or without
• Heart rate (HR) and BP raises evaluated physically for ascertaining phonation. Higher Mallampati score
• Pupils—Large and divergent the fitness for anesthesia. The physical (Class 4) is associated with more
• Muscle tone increased—Jaw may be evaluation of the patient comprises of difficult intubation as well as a higher
tight LEMON criteria for evaluation of airway incidence of sleep apnea.36 (Fig. 10.1)
• Patient may shout or struggle which is as under: and (Box 10.2).
General Anesthesia 183

– Potential for airway contami­


nation (full stomach, gas­ troes­
ophageal [GE] reflux, GI or phar­
yngeal bleeding)
– Surgical need for muscle relax­
ation
– Predictable difficulty with endo­
tracheal intubation or where
anesthetist’s access to the airway
during the case will be difficult
(lateral or prone position). For
paralysis of vocal cord for intu­
bation a short acting muscle
Fig. 10.1: Mallampati classification relaxant such as suxamethonium
chloride is used.
Box 10.2: Mallampati classification/score • Adult patients and most children are – Surgery of the mouth or face
usually induced with intravenous – Prolonged procedure antici­pated.
Class 1: Full visibility of tonsils, uvula and drugs, this being a rapid and mini­ • Not all surgeries require muscle relax­
soft palate
Class 2: Visibility of hard and soft palate,
mally unpleasant experience for the ation.
upper portion of tonsils and uvula patient. However, the arrival of sevo­ • If surgery is taking place in muscle
Class 3: Soft and hard palate and base of flurane, a new and well-tole­rated an­ groups of the thorax and abdo­
the uvula are visible esthetic vapor, has led to something men areas, then in addition to the
Class 4: Only hard palate visible of a renaissance of elective inhalation induction agent and narcotic, an
induction of anes­thesia in adults. intermediate or long-acting muscle
• In addition to the induction drug, relaxant drug is administered. This
• Evaluate 3,3,2: Three of the pati­ most patients receive an injection paralyzes muscles indiscriminately,
ent’s fingers should be able to fit of narcotic analgesic. A wide range including the muscles of breathing.
into his/her mouth when open, of synthetic and naturally occurring Therefore, the patient’s lungs must
three fingers should comfortably narcotics with different properties be ventilated under pressure, neces­
fit between the chin and the throat are available. Induction agents and sitating an endotracheal tube.
and two fingers in the thyromental narcotics work synergistically to in­ • Persons who, for anatomic reasons,
distance (distance from thyroid car­ duce anesthesia. In addition, anti­ are likely to be difficult to intubate
tilage to chin). cipation of events that are about to are usually intubated electively at the
• Obstructions (stridorous breath occur, such as endotracheal intu­ beginning of the when the patient
sounds, wheezing, etc.). bation and incision of the skin, is awake using a fiberoptic bron­
• Cormack-Lehane grading sys­ generally raises the blood pressure choscope or other advanced airway
tem37,38 (according to the per­centage and heart rate of the patient. Nar­ tool. This prevents a situation in
of glottic opening on laryn­goscopy). cotic analgesia helps preempt this which attempts are made to manage
undesirable response. the airway with a lesser device, only
INDUCTION, MAINTENANCE • The next step of the induction pro­ for the anesthetist to discover that
cess is the securing of the airway. This oxygenation and ventilation are
AND REVERSAL OF GA may be a simple matter of manually inadequate. At that point during a
holding the patient’s jaw such that his surgical procedure, swift intubation
Induction or her natural breathing is unimpeded of the patient can be very difficult, if
Induction is usually the most critical by the tongue or may demand the not impossible.
part of the anesthesia process. insertion of a prosthetic airway device
• It is the stage of transformation of an such as a laryngeal mask airway or Maintenance Phase
awake patient into an anesthetized endo­tracheal tube. A variety of factors As the effect of the drugs used to initiate
one. are considered when making this the anes­thesia begin to wane off, the
• This can be achieved by intravenous deci­sion. The major issue is whether patient is kept anesthetized with a
injection of induction agents (drugs the patient requires an endotracheal maintenance agent. According to ASA
that work rapidly, such as thiopental tube. (American Society of Anesthesiologists)
and propofol), by the slower inhal­ • Indications for endotracheal intu­ monitoring of oxygenation, ventilation,
ation of anesthetic vapors from a bation under general anesthesia in­ circulation and temperature should be
face mask or a combination of both. clude the following: done by the anesthesiologist throughout
184 Neurological Disorders of Face and General Anesthesia

the procedures. The ETCO2, SPO2, pulse anesthetist a sim­plified output in real
rate, blood pressure, ECG and tem­ time, corres­ ponding to anesthetic
perature should be monitored. depth. These devices have yet to
• For the most part, this refers to the become univer­sally accepted as vital
delivery of anesthetic gases/vapors equipment.
into the patient’s lungs. These may • If muscle relaxants have not been
be inhaled as the patient breathes used, the depth of anesthesia is
himself (spontaneous respiration) inadequate. The patient will move,
or delivered under pressure by each cough or pupillary signs will be
mechanical breath of a ventilator. masked. Broncospasm will obstruct
A continuous infusion of muscle his airway if the anesthesia is too
relaxant is also required. light for the stimulus being given.
• The maintenance phase is usually • If muscle relaxants have been used,
the most stable part of the anesthe­ then clearly the patient is unable to
sia. However, understanding that demonstrate any of these phenome­
anes­thesia is a continuum of dif­ na. In these patients, the anesthesiol­
ferent depths is important. A level ogist must rely on careful observation
of anes­thesia that is satisfactory for of autonomic phenomena such as
surgery to the skin of an extremity, hypertension, tachycardia, sweating Fig. 10.2: Boyle’s machine
for example, would be inadequate and pupillary dilation to decide that
for manipulation of the bowel. the patient requires a deeper anes­
• Appropriate levels of anesthesia must thetic. switched off entirely to allow time
be chosen both for the plan­ned pro­ • This requires experience and judg­ for them to be excreted by the lungs.
cedure and for its various stages. In ment. It is from failure to recognize • Excess muscle relaxation is reversed
complex plastic surgery, for example, such signs that tragic and highly using specific drugs such as neostig­
a considerable period of time may publicized cases of awareness under mine and adequate long-acting nar­
elapse between the com­pletion of the anesthesia are caused. c­otic analgesic to keep the pati­ent
induction of anesthetic and the inci­ • Excessive anesthetic depth, on the comfortable in the recovery room.
sion of the skin. During the period other hand, is associated with decre­ • If a ventilator has been used, the
of skin pre­paration, urinary catheter ased heart rate and blood pres­ patient is restored to breathing by
inser­tion and marking incision lines sure and if carried to extremes, can himself (spontaneous) and as anes­
with a pen, the patient is not receiv­ jeopardize perfusion of vital organs thetic drugs dissipate, the patient
ing any noxious stimulus. This re­ or be fatal. Short of these serious emerges to consciousness.
quires a very light level of anesthesia, misadventures, excessive depth res­­ • Reversal agents—It is a combination
which must be converted rapidly to a ults in slower awakening and more of two drugs neostigmine + glyco­
dee­per level just before the incision is side effects. pylorrate in the ratio of 5:1, or Neo­
made. When the anesthesia pro­vider The controlled delivery of inhalant stigmine + atropine in a ratio of 5:2.
and surgeon are not accus­tomed to anesthetics and oxygen for maintenance Neo­ stigmine is categorized under
working together, good communica­ of the proper stage and plane of anes­ anti­cholinesterases group of drugs.
tion (e.g. warning of the start of new thesia and prevention of hypoxia, are Anti­cholinesterases are agents, which
stimuli, such as moving the head of ensured by the use of an anesthetic inhibit cholinesterase, protect acetyl­
an intubated patient or commencing machine (Boyle’s apparatus) is used choline from hydrolysis. Muscarinic
surgery facilitates preemptive deep­ (Fig. 10.2). side effects are minimized by con­
ening of the anesthetic). This maxi­ comitant adminis­tration of anticho­
mizes pati­ent safety and ultimately, Reversal linergic drug (glyco­pylorrate). The
saves everyone’s time. As the surgical procedure draws to a effect of neo­stigmine (0.04 mg/kg) is
As the procedure progresses, the close, the patient’s emergence from usually apparent in 5 to 10 minutes,
level of anesthesia is altered to give anesthesia is planned. Experience and and lasts for more than 1 hour. Pedi­
the minimum amount necessary to close communication with the surgeon atric and elderly patients appear to be
ensure adequate anesthetic depth. enable the anesthesiologist to predict more sensitive to it’s effects, experi­
Traditionally, this has been a matter the time at which the application of encing a more rapid onset and requir­
of clinical judgment, but new pro­ dressings and casts will be complete. ing smaller dose. The duration of ac­
cessed electro encephalograph (EEG) • In advance of that time, anesthetic tion is prolonged in geriatric patients.
machines (BIS monitors) give the vapors are decreased or even It has been reported that, neostigmine
General Anesthesia 185

crosses placental barrier resulting in aseptic precautions, can be a medium enzymes and can be used safely in
fetal bradycardia. Thus, atropine is a for rapid bacterial growth. partial or complete renal failure.
better choice than glycopyrrolate. • Anesthesia can also be induced by • Pancuronium is an established drug
• Emergence is not synonymous with inhalation of a vapor. This is how that is still in widespread use beca­
removal of the endotracheal tube or all anesthetics were once given and use of its low cost and fami­ liar­
ity,
other artificial airway device. This is a common and useful technique especially in intensive care units;
is only performed when the patient in uncooperative children. It is re- rocuronium, mivacurium and cisa­
has regained sufficient control of his emerging as a choice in adults. Halo­ tracurium are more likely to be used
or her airway reflexes. thane and sevoflurane are the most by contemporary anesthes­iologists.
• The patient must be watched for commonly used drugs for this pur­
respiratory distress and should be pose. Anesthetic Vapors
placed in lateral position and/or an • These are highly potent chlorofluoro­
oropharyngeal or nasopharyngeal Traditional Narcotic Analgesics carbons, which are delivered from
airway is placed, to prevent tongue • Morphine, meperidine and hydro­ precision vaporizers directly into the
fall and prevent aspiration of the mor­phone are widely used in anes­ patient’s inhaled gas stream. They
secretions even after extubation. In thesia as well as in emergency rooms, may be mixed with nitrous oxide,
cases of major cancer resections, surgical wards and obstetric suites. a much weaker, but nonetheless
especially extending across the mid­ • In addition, anesthesia providers useful anesthetic gas.
line, where the tongue control is have at their disposal a range of • The prototype of modern anesthetic
doubtful and the chances of tongue synthetic narcotics, which in general, vapors is halothane. It has an unpar­
fall or aspiration are high, in such cause less fluctuation in blood alleled track record of safety and effi­
cases the patient is not extubated pressure and are shorter acting. cacy, though it is associated with rare,
and the naso-tracheal tube is kept These include fentanyl, sufentanil, but devastating hepatic necrosis to a
indwelling for minimum 24 hours alfentanil and remifentanil. Remi­ greater extent than other agents.
until the patient has fully gained fentanil is the newest drug in this • In the 1980s, it was displaced by iso­
consciousness. class and has such a short duration of flurane and enflurane, agents that
action that it must be administered were cleared from the lungs faster
Induction Agents as a continuous infusion. and thus were associated with more
• For 50 years, the most commonly rapid anesthetic emergences.
used induction agents were rapidly Muscle Relaxants • In the late 1990s, two new vapors be­
acting, water-soluble barbiturates • Succinylcholine, a rapid-onset, short- came very popular, desflurane and
such as thiopental, methohexital and acting depolarizing muscle relaxant, sevoflurane. These drugs are much
thiamylal. is the drug of choice when rapid more maneuverable than their pre­
• These drugs are still commonly in muscle relaxation is needed. decessors and are associated with
use today, have an enormous record – For decades, anesthetists have much more rapid emergence.
of safety and reliability and are used it extensively despite a • Sevolurane can be used for volitile
econo­mical. number of predictable and un­ induction and maintenance of anes­
• More recently, propofol a non-bar­ predictable adverse effects asso­ thesia (VIMA).
biturate intravenous anesthetic, has ciated with its use.
displaced barbiturates in many an­ – The search for a drug that repli­
esthesia practices. cates its onset and offsets speed COMPLICATIONS OF
• The use of propofol is associated without its adverse effects is the GENERAL ANESTHESIA39:
with less postoperative nausea and holy grail of muscle relaxant
INTRA-ANESTHETIC
vomiting and a more rapid, clear- research.
headed recovery. • Other relaxants have durations of PROBLEMS
• In addition to being an excellent action ranging from 15 minutes to
induction agent, propofol can be more than 2 hours. Complications of general anesthetia are
administered by slow intravenous • Older drugs in this class were often described in Box 10.3.
infusion instead of vapor to maintain associated with changes in heart
the anesthesia (total intraveinous rate or blood pressure, but the newer Common Problems
anesthesia, TIVA). ones are devoid of these adverse • Hypotension—is a significant dec­
• Among its disadvantages are the facts properties. rease of arterial pressure less than
that it often causes pain on injection • Muscle relaxants generally are ex­ normal
and it is prepared in a lipid emulsion, creted by the kidney, but some prep­ – Decreased cardiac contractility
which if not handled using meticulous arations are broken down by plasma – Decreased systemic resistance
186 Neurological Disorders of Face and General Anesthesia

Box 10.3: Complications of general oropharyngeal and naso­ph­aryn­ – Spontaneous rupture of blebs or
anesthesia geal placement. bullae
Common
– Reflex closure of vocal cords – Accidental surgical entrance
Hypotension causing partial or total glottic – Alveolar rupture during excessive
Hypertension obs­truction positive pressure ventilation.
Dysrhythmias – Hypoxia, hypercarbia and aci­ Treatment
Hypoxia dosis – Discontinue nitrous oxide, venti­
Hypercarbia
Treatment late with 100 percent oxygen.
Oliguria
Hyperthermia – Deepening of anesthesia level – Introduce wide-bore needle with
Life-threatening – Remove the stimulus 10 mL syringe in 2nd or 3rd inter­
Laryngospasm – Continuous positive pressure costals space to confirm presence
Bronchospasm ventilation of air and place and chest tube in
Aspiration – Muscle relaxant—succinyl­cho­ 8th inter­costal space in posterior
Pneumothorax
line (10–20 mg IV in adults). axillary line.
MI
Air embolism • Bronchospasm40—may be centrally • Myocardial ischemia42—is the result
Malignant hyperthermia mediated or it may be a local res­ of imbalance between the oxygen
Anaphylactic reaction ponse to the airway. demand and supply.
– May be stimulated by histamine Features
releasing drugs (morphine, atra­ – Chest pain
– Inadequate venous return curium). – ECG – ST segment elevation
– Dysrrhythmias – Detected—Characteristic wheez­ Treatment
• Hypertension— ing, Tachypnea or dypnea in – Correction of hypoxia and ane­
– Excess catecholamine release awake patient. mia
– Pre-existing disease Treatment – Beta-adrenergic blockers like
– Systemic absorption of vasocon­ – Correction of endotracheal tube do­b­utamine, vasodilators like
strictors – Deepening anesthetic level—to nit­ro­glycerine.
• Dysrrhythmias pre­vent reverse bronchospam in • Air embolism—Venous air embo­
• Hypoxia—occurs when oxygen deli­ light anesthesia inhalational or lism (VAE) is a predominantly iatro­
very to the tissue is insufficient to IV agents are used. Ketamine has genic complication,43-44 which occurs
meet the metabolic demands advantage of causing broncho­ when atmospheric gas is introduced
– Inadequate oxygen supply dilation. into the systemic venous system.45 In
– Hypoventilation – Beta-2 adrenergic agonist—IV or the past, this medical condition was
– Ventilation perfusion shunt inhalational mostly associated with neurosur­
– Reduction of oxygen carrying – Adequate hydration and humidi­ gical procedures con­ducted in the
capacity fication of inspired gas. sitting position.46-47 More recently,
• Hypercarbia—is either due to inad­ • Aspiration—general anesthesia cau­ venous air embolism has been asso­
equate ventilation or increased car­ ses depression of the airway reflexes ciated with central venous catheter­
bon dioxide production that predisposes patient to aspirate. ization,48 high-pressure mecha­nical
• Oliguria—defined as urine output of Aspiration may cause bronchospasm, ventilation, thoracocentesis, hemo­
less than 0.5 mL/kg per hour. hypoxemia, atelectasia, tachypnea, dialysis, and several other invasive
• Hyperthermia—is the rise of tempe­ tachycardia and hypotension. vascular procedures (VAE is detailed
rature of 2 degree per hour or – Vomiting or regurgitation: below).
0.5 degree every 15 min. - Trendelenburg position
– Malignant hyperthermia - Head low position
– Inflammation - Face turned to one side VENOUS AIR EMBOLISM
– Hypermetabolic state. - Suctioning and endotracheal
tube placement Venous air emboli, pose a risk anytime
Life-threatening Problems - Cricoid pressure used to pre­ the surgical wound is elevated more
• Laryngospasm—is commonly cau­sed vent regurgitation.41 than 5 cm above the right atrium.2 The
by an irritative stimulus to the airway – Bronchoscopy presence of numerous, large, non-
during light plane of anes­thesia. – Aspiration of blood compressed, venous channels in the
– The common noxious stimuli – Antibiotic, if indicated surgical field (especially during cervical
to elicit reflex are secretion, – Close postoperative care. procedures and craniotomies that
vomitus and inhalation of pun­ • Pneumothorax—is the accumul­ation breach the dural sinuses) also increase
gent volatile anesthetic agents, of gas within the pleural space during: the risk of VAE.
General Anesthesia 187

Entrapment of air/gas facilitated ro­scopy, laparoscopy, urethral pro­ IV infusion tubing) that was injected
by the patient’s intraoperative position cedures and orogenital sexual activ­ intravenously. The injection of 2 or 3 mL
causing VAE, may result from other sur­ ity during pregnancy (by entering of air into the cerebral circulation can
gical procedures. These include, cranio­ veins of the myometrium during be fatal.52 Furthermore, as little as
facial surgery, dental implant surgery, pregnancy and/or after delivery). 0.5 mL of air in the left anterior des­
vascular procedures (e.g. endarterecto­ • Inadvertent infusion of air can also cending coronary artery has been shown
mies), liver transplan­tation, orthopedic occur during the injection of IV con­ to cause ventricular fibrillation. Basi­
pro­cedures (e.g. hip replacement, spine trast agents for CT scans. angiography cally, the closer the vein is to the right
surgery, arthroscopy), lateral decubitus and cardiac cathe­terization, as well as heart, the smaller the lethal volume is.
thoracotomy, genitourinary surgeries during cardiac ablation procedures. Rapid entry or large volumes of air
in the Trendelenburg position and sur­ Positive pressure ventilation during entering the systemic venous circulation
geries involving tumors/malformations mechanical ventilation places patients puts a substantial strain on the right ven­
with high degree of vascularity or com­ at risk for barotrauma and subsequently, tricle, especially if this results in a signifi­
promised vessels, as in the context of arterial and/or venous air emboli. Entry cant rise in pulmonary artery (PA) pres­
trauma. of gas into the circulation may result if sures. This increase in PA pressure can
Venous air embolism may also violation of pulmonary vascular integrity lead to right ventricular outflow obstruc­
result from the iatrogenic creation of a occurs at the same time alveoli rupture tion and further compromise pulmo­
pre­ssure gradient for air entry. Proce­ from overdistension of the airspaces. nary venous return to the left heart. The
dures causing such a pressure gradient This complication can occur in the diminished pulmonary venous return
include lumbar puncture, peri­ pheral setting of various diagnoses; however, it will lead to decreased left ventricular
intravenous lines and central venous is most frequently reported in patients preload with resultant decreased cardiac
cath­e­ters. with acute respiratory distress syndrome output and eventual systemic cardiovas­
Venous air embolism is a potentially and in premature neonates with hyaline cular collapse. With venous air embolism
life-threatening and under-recognized membrane disease. (VAE), resultant tachyarrhythmias are
complication of central venous cath­ The occurrence of venous air embo­ frequent, but bra­dyarrhythmias can also
eterization (CVC), including central lism (VAE) has also been described in occur.
lines, pulmonary catheters, hemodialy­ the setting of blunt and penetrating The rapid ingress of large volumes of
sis catheters and Hickman (long-term) chest and abdominal trauma as well as air (> 0.30 mL/kg/min) into the venous
catheters. A number of factors increase in neck and craniofacial injuries. circulatory system can overwhelm the
the risk of catheter-related VAE, includ­ air-filtering capacity of the pulmonary
ing the following: Pathophysiology vessels, resulting in a myriad of cellular
• Fracture or detachment of catheter Two preconditions must exist for venous changes. The air embolism effects on
connections (accounts for 60–90%) air embolism to occur: the pulmonary vasculature can lead to
• Failure to occlude the needle hub • A direct communication between a serious inflammatory changes in the
and/or catheter during insertion or source of air and the vasculature and pulmonary vessels; these include direct
removal • A pressure gradient favoring the endothelial damage and accumulation
• Dysfunction of self-sealing valves in passage of air into the circulation.49 of platelets, fibrin, neutrophils and lipid
plastic introducer sheaths The key factors determining the droplets.
• Presence of a persistent catheter degree of morbidity and mortality in Secondary injury as a result of the
tract following the removal of a cen­ venous air emboli are related to the acti­vation of complement and the
tral venous catheter volume of gas entrainment, the rate of release of mediators and free radicals
• Deep inspiration during insertion accumulation and the patient’s position can lead to capillary leakage and even­
or removal, which increases the at the time of the event.50 tual non-cardiogenic pulmonary edema.
magnitude of negative pressure Generally, small amounts of air Alteration in the resistance of the lung
• Hypovolemia, which reduces central are broken up in the capillary bed and vessels and ventilation-perfusion mis­
venous pressure absorbed from the circulation without matching can lead to intra­pulmonary
• Upright positioning of the patient, producing symptoms. Traditionally, right-to-left shun­ ting and increased
which reduces central venous pres­ it has been estimated that more than alveolar dead space with subsequent
sure. 5 mL/kg of air displaced into the intra­ arterial hypoxia and hypercapnea.
Mechanical insufflation or infusion venous space is required for significant Arterial embolism as a complication
is another cause of venous air emboli. injury (shock or cardiac arrest) to of VAE can occur through direct passage
• Several different procedures involve occur. However, complications have of air into the arterial system via ano­
the use of insufflation, including been reported with as little as 20 mL malous structures such as an atrial
arthroscopic procedures, CO2 hyste­ of air51 (the length of an unprimed or ventricular septal defect, a patent
188 Neurological Disorders of Face and General Anesthesia

foramen ovale or pulmonary arterial- organs, including, but not limited to the • Hypotension
venous malformations. This can cause brain, spinal cord, heart and skin. • Myocardial ischemia
paradoxical embolization into the arte­ Two additional contributing factors • Non-specific ST-segment and T-wave
rial tree. The risk for a paradoxical em­ include whether or not the patient is changes and/or evidence of right
bolus seems to be increased during spontaneously breathing (yielding neg­ heart strain
procedures performed in the sitting ative thoracic pressure) or is under • Pulmonary artery hypertension
posi­tion. controlled positive pressure ventilation. • Increased central venous pressure
Air embolism has also been des­ These two factors facilitate the entry of (CVP)
cribed as a potential cause of the systemic air down a pressure gradient. The clini­ • Circulatory shock/cardiovascular col­
inflammatory response syndrome (SIRS), cal presentation is also dependent on lapse
triggered by the release of endothelium the patient’s body position at the time of
derived cytokines.49 the event. Generally, if the patient is in a Pulmonary
sitting position, gas will travel retrograde • Adventitious sounds (rales, whee­zing)
Clinical Presentation via the internal jugular vein to the • Tachypnea
cerebral circulation, leading to neuro­ • Hemoptysis
History
logic symptoms secondary to increased • Cyanosis
Most VAE go unrecognized because intra­cranial pressure. In a recumbent • Decreased end-tidal carbon dioxide,
their presentations are protein and position, gas proceeds into the right arterial oxygen saturation and ten­sion
mimic other cardiac, pulmonary and ventricle and pulmonary circu­ lation, • Hypercapnia
neurologic dysfunctions. Because of the subsequently causing pul­monary hyper­ • Increased pulmonary vascular resis­
lack of specific signs and symptoms of tension and systemic hypotension. tance and airway pressures
VAE, a high index of suspicion is neces­ An arterial air embolism can also • Pulmonary edema
sary to establish the diagnosis and in­ form if passage of air occurred through • Apnea
stitute the appropriate treatment. The a right-to-left shunt, as in the case of a
number of procedures that place pa­ patent foramen ovale. The arterial air Neurological
tients at risk for VAE has increased, and emboli can then lodge in the coronary or • Acute altered mental status
these procedures occur across almost all cerebral circulation, causing myocardial • Seizures
clinical specialties. This must be consid­ infarction or stroke. • Transient/permanent focal deficits
ered to aid in the confirmation or ruling (weakness, paresthesias, paralysis of
out of VAE. If venous air embolism is Symptoms (Awake Patients) extremities)
suspected, inquiry about the following • Acute dyspnea • Loss of consciousness, collapse
key historical elements should be ob­ • Continuous cough • Coma (secondary to cerebral ede­ma)
tained: • ‘Gasp’ reflex (a classic gasp at times
• Invasive therapeutic and/or diag­ reported when a bolus of air enters Ophthalmologic
nostic procedures such as central the pulmonary circulation and causes Funduscopic examination may reveal
venous catheterization; lumbar acute hypoxemia) air bubbles in the retinal vessels.
puncture; high-pressure infusion of • Dizziness/lightheadedness/vertigo
medications, blood products and/or • Nausea Skin
IV contrast agents • Substernal chest pain Crepitus over superficial vessels (rarely
• Patients with hemodialysis access • Agitation / disorientation / sense of seen in setting of massive air embolus).
catheters or other indwelling central ‘im­­peding doom’ Livedo reticularis (vascular cond­
venous catheters ition characterized by purplish mottling
• Patients on positive pressure venti­ Signs of the skin).
lation. The above hemodynamic, pulm­
Cardiovascular onary, and neurologic complications
Physical Examination • Dysrhythmias (tachyarrhythmias/bra­ primarily result from gas gaining entry
dy­­cardias) into the systemic circulation, occluding
Clinical Features • ‘Mill wheel’ murmur—A temporary the micro­circulation and causing ische­
Many cases of VAE are subclinical and loud, machinery like, churning mic damage to these end organs.
do not result in untoward outcomes. sound due to blood mixing with air
However, severe cases are characterized in the right ventricle, best heard over Treatment
by cardiovascular collapse and/or acute the precordium (a late sign) The best management of this condition
vascular insufficiency of several specific • Jugular venous distention is precautions to avoid it and if it has
General Anesthesia 189

occurred inadvertently then it is treated undergoing mandibular resection


POSTANESTHETIC CARE56
symptomatically. across the midline. The tongue fall
The patient recovering from the GA of the tongue is prevented by lateral
Malignant Hyperthermia needs a good care as the patient is position of the head, extension of
It is hypermetabolic syndrome occur­ yet to regain full consciousness and neck, thrusting the angles of the jaw
ring in genetically susceptible patients53 the protective reflexes. The patient forwards.
when exposed to anesthetic triggering is susceptible to airway obstruction • The other modalities for preven­
agents. due to tongue fall, aspiration of secre­­­ ting the tongue fall are placing oro­
Triggering agents: Halothane, en­ tions, blood or vomitus in the tracheo­ pharyn­geal (Water’s oroph­aryn­geal
flurane, isoflurane, desflurane, sevoflu­ bronchial tree, thus requires good care. airway) or nasopharyngeal airway.
rane and succinylcholine. The care of the respiratory passage and Placing a tongue stitch to draw
The syndrome is thought to be due maintaining its patency is of paramount the tongue out and prevent fall is
to reduction of reuptake of calcium ions importance in oral and maxillofacial also practiced. The tongue stitch
by the sarcoplasmic reticulum leading surgery due to its intimate relation with is always placed using a thick silk
to sustained muscle contraction. This upper aerodigestive tract. Handling of suture and the needle bite is taken
results in signs of hypermetabolism like this part leads to bleeding, edema, loss horizontally deep in the tongue,
tachycardia, acidosis, hypercarbia, hypo­ of anchorage of tongue to the mandible as the vertical bite in the midline
xemia, and hyperthermia. in the cases where midline resection can lead to splitting of the tongue
has been done; enhance the chances of when it is drawn out by pulling.
Treatment respiratory obstruction and aspiration. The O2 saturation in the blood can
• Discontinue all anesthetic agents • The patient is kept nil per orally be monitored by pulse oxymetry.
• Administer—dantrolene54 2.5 mg/ till he regains full consciousness. • The vital parameters like pulse, tem­
kg/IV initially and repeat to a total Till such time the patient is kept perature and respiration (TPR) are
of 10 mg/kg (it inhibits the release of on parenteral therapy to fulfill the monitored periodically, initially in
calcium ions from sarcoplasmic reti­ nut­ri­ti­onal, fluid and electrolyte the immediate postoperative period
culum) requirement using appropriate IV the frequency of recoding could be
• Sodium bicarbonate administration fluids. every 1/2 hourly and as the pati­
• Hyperkalemia may be corrected with • The patient is kept in lateral position ent gets settled then 2 to 4 hourly
insulin and glucose with head low position to prevent recording of vitals could be enough.
• Dysrrhythmias can be treated with aspiration. The periodic suctioning In very critical patients conti­ nu­
procainamide of oral cavity, pharynx and nasal ous monitoring is warranted. All
• Treat hyperthermia by cold spon­ cavity are done to make them free the patients are monitored using
ging of secretions. However, vigorous multipara monitors now-a-days.
• Monitor urine output. deep suction using a catheter having • The periodic BP monitoring is done.
Anaphylactic reaction55—is an im­ opening at the tip should be avoided The continuous monitoring of the
mediate type of life-threatening allergic/ as it provokes gagging and may suck blood pressure is also possible using
hypersensitivity reaction. Characterized the friable mucosa and bleeding may the multipara monitors.
by severe hypotension and larygo-bron­ take place. Therefore recommended • Renal perfusion is monitored by
chospasms leading to severe hypoperfu­ to use plain rubber catheter with measuring the urine out put. Urine
sion of the tissue secondary to hypoxia. rounded end and opening at the out put less than 15 to 20 mL/hr is
It is initiated by IgE antibodies. side, which is less traumatic. In suggestive of oliguria and poor renal
the tracheostomized patients it is perfusion secondary to hypotension
Treatment desirable to use separate catheters or hypo­volmia. Appropriate action
• Discontinue anesthetic agents to suck oral cavity and tracheostomy should be taken to rectify the cause.
• Administer 100 percent oxygen tube to prevent conta­mination and The input and output chart is main­
• Epinephrine 5 to 100 µg IV/SC lower respiratory tract infections. tained.
• Steroids (sodium hydrocortisone • The tongue fall is the most common • Signs of respiratory distress should
hemisuccinate 250 mg – 1 gm IV) cause of respiratory obstruction in be checked and auscultation should
• Prophalactic drug to hypersensitivity– an unconscious patient. It is more be done to know air entry, signs of
h1 and h2 antagonist and cortico­ste­ common complication in oral and bronchospasm like ronchi/wheeze.
roids. maxillofacial surgery in patients In case, the tracheostomy has been
190 Neurological Disorders of Face and General Anesthesia

done or the endotracheal tube is kept and Other Vapors to Surgical Operations. 19. Suckling CW. Some chemical and physical
indewelling, the patency of the tube Hartford: J. Gaylord Wells, 1847.. factors in the development of fluothane.
must be ensured by periodic suc­ 3. Bigelow HJ. Insensibility during surgical Br J Anaesth. 1957;29(10):466-72.
tions and observing air blast. Saline operations produced by inhalation. 20. Johnstone M. The human cardiovascular
nebulization, few drops of soda bi­ Boston Med Surg J. 1846;35:309-17.. response to fluothane anaesthesia. Br J
carbonate or plain saline may be put 4. Atkinson RS, Rushman GB. A synopsis of Anaesth. 1956;28(9):392–410.
in the tubes to prevent crustation and anesthesia 8th edn. London, John Wright 21. Subcommitee on the National
drying of the secretions to prevent its and Son, Ltd. 1977.. Halothane Study of the Committee on
blockage due to thick, tenacious or 5. Wawersik J. History of chloroform anes­ Anesthesia, N. Summary of the national
dried secre­tions. thesia. Klinik fur Anasthesiologie und Halothane Study. Possible association
• Other care includes periodic change Operative Intensivmedizin, Klinikum der between halothane anesthesia and
of position (if permissible) to pre­ Christian-Albrechts-Universitat zu Kiel. postoperative hepatic necrosis. JAMA.
vent from a particular area of lung to Allerg Immunol (Paris). 1998;30(5):135-7.. 1966;197(10):775-88.
become dependent for a long-time. 6. Colton, Gardner Q. Anesthesia. New 22. Strunin L. How long should patients fast
Because the secretions stagnate and York: AG Sherwood and Company. 1886. before surgery? Time for new guidelines.
accumulate in that dependent part 7. Andrews, Edmund. The relative dangers (Editorial). Br. J. Anaesth. 1993;70:1-3.
by gravity and that part becomes hy­ of anaesthesia by chloroform and ether, 23. Nimmo WS. Gastric emptying and ana­es­
poperfused, increasing physiologic from statistics of 209893 cases. Chicago, thesia. Can J Anaesth, 1989;36(3): S45-S47.
dead space of respiration. The chest Robert Fergus’ Sons, 1870. 12 p. 24. McDonough JP, McMullen P, Philipsen N.
physiotherapy should be initiated to 8. Lucas GHW, Henderson VE. ‘A new Informed consent: an essential element of
prevent the same and facilitate drain­ anaesthetic gas: cyclopropane.’ Canad. safe anesthesia practice. CRNA, 1995;6(2):
age of stagnated secretions. The air­ Med. Assoc. Journ. 1929;xxi, 173. 64-9.
way, handling and irritation due to 9. Lundy JS. Intravenous Anesthesia: Preli­ 25. Alexander F, Cullen S. Preanesthetic
inhaled gases leads to mild inflam­ minary Report of the Use of the Two New medication. The American Journal of
mation and edema of airway and the Barbiturates, Proc. Staff Meet. Mayo Clin. Surgery. 1936;34(3):428-34.
secretions are enhanced. Steam neb­ 1935;10:536-43. 26. Cetina J. Smooth induction of anaes­thesia
ulizations are given to reduce airway 10. Dripps RD, et al. Introduction to anes­ in children by means of oral or rectal
congestion and liqu­efy the secretions thesia–The principle’s of safe practice, ketamine dehydrobenzperidol appli­
for their easy drainage. After a major 5th edn. Philadelphia WB: Saunder’s Co. cation. Anaesthesist. 1982;31(6):277-9.
surgery the patients remain confined 1977. 27. Aono K, Yoshinaga H. Use of intravenous
to the bed for long time without phys­ 11. Kay B, Rolly G. ICI 35868, a new intra­ diazepam for preanesthetic medication-
ical activity. In such cases, the chanc­ venous induction agent. Acta Anaes­the­ with special reference to sedative effects
es of venous stasis occur especially siol Belg. 1977;28:303. and changes in vital signs. Masui. 1971;
in the lower extremity due to lack 12. Irwin MG, Thompson M, Kenny GNC. 20(6):556-60.
of muscle activity and the chances Anesthesia; 1977;52:525-30. 28. Wilson DV, Evans AT, Miller R. Effects
of deep vein thrombosis and risk of 13. Ngan Kee WD, Khaw KS, Ma ML, et al. of preanesthetic administration of mor­
pulmonary embolism are increased, Postoperative analgesic requirement after phine on gastroesophageal reflux and
especially in elderly patients. In such cesarean section: a comparison of anes­ regurgitation during anesthesia in dogs.
patients calf physiotherapy should thetic induction with ketamine or thio­ Am J Vet Res. 2005;66(3):386-90.
be initiated. Similarly in cases of pental. Anesth Analg. 1997;85:1294–8. 29. Alfano G, Manicastri F. Meprobamate-
long-term non-ambulation, the back 14. Amiot JF, Bouju P, Palacci JH, et al. antihistaminic combination as a pre-
care is important to prevent pressure Intravenous regional anaesthesia with anesthetic medication for surgical patients.
sores (bed sores). A frequent change ketamine. Anaesthesia. 1985;40(9):899- Minerva Anestesiol. 1959;25:447-9.
in position, back massage, use of 901. 30. Saur P, Kazmaier S, Buhre W, et al.
ring air cushions or water beds is 15. Greenfield W. Neuroleptanalgesia and Clinical use of antiemetic drugs for
indicated. dissociative drugs. Dent Clin North Am. prevention and therapy of postoperative
1973;17(2):263–74. nausea and vomiting. Anaesthesiol
16. Guy K Tallmadge. The Third Part of the Reanim. 1996;21(6):153-8.
REFERENCES
De Extractione of Valerius Cordus. Isis. 31. Koichi Maruyama. Can intravenous
1. Priestley, Joseph. Experiments and Obser­ 1925;7(3):394-411. atropine prevent bradycardia and hypo­­
vations on Different Kinds of Air. London 17. Calderone, F.A. J. Pharmacology Experi­ tension during induction of total intra­
W. Bowyer and J. Nichols, 1774. Vol. 1 to 6.. mental Therapeutics, 1935;55(1): 24-39. venous anesthesia with propofol and
2. Wells, Horace. A History of the Discovery of 18. “WHO Model List of Essential Medicines”. remifentanil? Journal of Anesthesia. 2010:
the Application of Nitrous Oxide Gas, Ether, World Health Organization. 2005. 24:(2):293-96.
General Anesthesia 191

32. Kemmotsu O, Mizushima M, Morimoto Y, 40. Daniele RP. Pathophysiology of asthma. In: safety in the intensive care unit. Ann
et al. Effect of preanesthetic intramuscular Fishman ap, (Ed.). Pulmonary disea­ses, Vol Intern Med. 2004;140(12):1025-33.
ranitidine on gastric acidity and volume 1 New York, Mcgraw-Hill: 1998: 1055-68. 49. Kapoor T, Gutierrez G. Air embolism as
in children. J Clin Anesth. 1991;3(6): 41. Sellick BA, Cricoid pressure to control a cause of the systemic inflammatory
451-5. regurgitation of stomach contents during response syndrome: a case report. Crit
33. Barry Wyke. A neurological analysis of induction of anaesthesia. Lancet 2 (1961), Care. 2003;7(5):R98-R100.
the stages of anaesthesia. Irish Journal of pp. 404–6. 50. Sheasgreen J, Terry T, Mackey JR. Large-
Medical Science (1926-1967). 1960; 35(11). 42. Alpert JS, Francis GS. Handbook of coro­ volume air embolism as a complication of
34. Guedel AE. Third stage ether anesthesia. nary care, 6th edn. Lippincott Willi­ams augmented computed tomography: case
A subclassification regarding the signi­ and Wilkins, London, 2000. report. Can Assoc Radiol J. 2002;53(4):
ficance of the position and move­ments of 43. Mirski MA, Lele AV, Fitzsimmons L, et al. 199-201.
the eyeball. Am J Surg. 1920; 34:53-6. Diagnosis and treatment of vascular air 51. Moon R. Air or Gas Embolis. Hyperbaric
35. Mallampati S, Gatt S, Gugino L, et al. “A embolism. Anesthesiology. 2007; 106(1): Oxygen Committee Report. 2003;5-10.
clinical sign to predict difficult tracheal 164-77. 52. Ho AM. Is emergency thoracotomy
intubation: a prospective study.” Can 44. Sviri S, Woods WP, van Heerden PV. Air always the most appropriate immediate
Anaesth Soc J. 1985;32(4):429–34. embolism—a case series and review. Crit intervention for systemic air embolism after
36. Nuckton TJ, Glidden DV, Browner WS. Care Resusc. 2004;6(4):271-6. lung trauma?. Chest. 1999;116(1): 234-7.
“Physical examination: Mallampati score 45. van Hulst RA, Klein J, Lachmann B. 53. Denborough MA, Lovell RRH. Anaesthetic
as an independent predictor of obstructive Gas embolism: pathophysiology and deaths in a family, Lancet. 1960;2:45.
sleep apnea”. Sleep. 2006;29(7):903–8. treatment. Clin Physiol Funct Imaging. 54. Harrison GG. “Control of the malignant
37. Cormack RS, Lehane J. Difficult tracheal 2003;23(5):237-46. hyperpyrexic syndrome in MHS swine
intubation in obstetrics. Anaesthesia. 46. Muth CM, Shank ES. Gas embolism. N by dantrolene sodium”. British Journal of
1984;39:1105-11. Engl J Med. 2000;342(7):476-82. Anaesthesia. 1975;47(1):62–5.
38. Cormack R, Lehane J. Cormack-Lehane 47. Wong AY, Irwin MG. Large venous air em­ 55. Caranasos GJ. Drug reactions. In:
laryngoscopy grades. In Maltby JR (ed) No­ bolism in the sitting position despite moni­ Schwartz Gr (Ed). Principles and Practice
table names in anaesthesia. London, Royal toring with transoesophageal echocardiog­ of Emergency Medicine. Philadelphia,
Society of Medicine Press, pp. 43-5, 2002. raphy. Anaesthesia. 2005;60(8): 811-3. Lee and Febiger. 1992.
39. Gravenstein N, ed. Manual of Compli­ 48. Pronovost PJ, Wu AW, Sexton JB. Acute 56. Mcgrath B, Chung F. Post operative
cations during Anesthesia. Philadelphia. decompensation after removing a central recovery and discharge. Anesth Clin
USA: JB Lippincott, 1991. line: practical approaches to increasing North Am. 2003;21.
Section 3
Dentoalveolar Surgeries

n Exodontia
n Management of Impacted Teeth
n Preprosthetic Surgeries
11 Exodontia
Borle Rajiv M, Arora Aakash, Magarkar Shashwat D

extracting firmly rooted teeth, preferring are often more fragile and brittle due to
HISTORY to remove only those that were loose.1 carious undermining and desiccation
From the very earliest times, humans of the tooth structure due to loss of the
have been plagued by dental problems
DEFINITION OF EXODONTIA pulp and fracture readily during the
and have sort a variety of means to extraction and thus, require more careful
alleviate them. Egyptians, Greeks, Exodontia or tooth extraction is defined approach. The teeth have varying crown
Japanese, Indians and many more are as the painless removal of a whole tooth forms and varied root patterns and
associated with the history of dentistry. or tooth root, with minimal trauma to need to be assessed thoroughly before
Although the Ebers Papyrus from the investing tissues, so that the wound proceeding for the surgical procedure to
Egypt makes no mention of surgical in­ heals uneventfully and no postoperative prevent fracture of the tooth or its root.
tervention for dental ills, the Edwin Smith prosthetic problem is created.2 The bulbous crowns warrant selection
Papyrus, of the 17th century BC, cites of forceps with heavier beaks, while as
numerous operations of fractures and the tapering or peg-shaped crowned
dis­lo­cations of mandible, maxilla. Since APPLIED SURGICAL teeth require lighter beaked forceps. The
forceps are so prominently pic­tured in ANATOMY OF TEETH AND multirooted teeth offer more resistance
various caves and wall carvings, we can and cannot be luxated or extracted
JAW BONES
assume that extractions were indeed car­ with rotational force as the chances of
ried out. The teeth are firmly anchored in the root fracture are high. Similarly if the
Hippocrates (5th century BC) refer­red alveolar process of the jaw bone in roots are divergent, the delivery of the
dental forceps, made up of iron known as the alveolar sockets with the help of tooth becomes difficult and application
‘odontagra’, have been discovered sites of sharpey’s fibers of periodontal ligament. of excess force may lead to fracture of
Greece. The joint between the teeth and the the root or the alveolar bone. The roots
Pierre Fauchard, Father of modern alveolar bone is called a ‘gomphosis’. which are dilacerated thin and slender
dentistry in 16th century coined the The bones are more elastic and resi­ are also liable to fracture during the
term ‘Surgeon Dentist’. He devised lient in the younger individuals and are extraction. While the roots which are
many forceps for extraction of teeth. more amenable to pressure and expand fused, tapering and conical offer simple
He used to call it ‘pelican’, which had readily thus, the extractions are easier proposition.
a fixed part and a movable arm, with in the younger patients. In the elderly
hooked end. The hooked end was to patients, the bones become less vascular, Mandible
engage a tooth to be extracted, while the less cellular and become more compact The mandible is the only mobile bone
fixed ends presses against the adjacent and brittle and do not yield to pressure of the craniofacial skeleton and is the
teeth, acting as a brace and fulcrum. easily. Similarly, the teeth also become heaviest too. It has thick cortices, less
In Indian history, Sushruta has brittle owing to the regressive changes spongy bone and also has less vascular
described two kinds of surgical instru­ in them. As a result of this the tooth and supply as compared to maxilla (Fig. 11.1).
ments ‘yantra or blunt’ and ‘sastra or the alveolar bone can fracture during the Thus, the chances of complications
sharp’. Among yantra ‘dantasanka’—a extraction making, the extraction more are more and healing is also slower as
special forcep is described for extraction difficult and complicated. The non-vital compared to the maxillary sockets. The
of teeth. However, Sushruta disapproved and the endodontically treated teeth mandible is depressed during the jaw
196 Dentoalveolar Surgeries

the mandibular anterior teeth and molars and only thin bone separates the
their supporting alveolar bone and floor of the sinus and the root apices. Any
periodontal ligament fibers, up to the chronic periapical infection may lead
midline and never crosses over to the to destruction of this thin bone and the
other side. The mental nerve makes its periapical infection from the tooth may
exit from the mental foramen situated extend into the sinus causing odonto­
between the premolars and supplies the genic maxillary sinusitis. In the event of
labial mucoperiosteum and gingiva of fracture of the root and injudicious use
the mandibular anterior teeth, as well as of force or injudicious instrumentation
the lining of the lower lip. may displace the fractured root into the
The gingiva over the mandibular sinus.
molars is supplied by the long buccal The maxillary third molars are last
nerve, which also supplies the mucosa teeth to erupt and are invariably present
of the cheek up to the level of the corner in the maxillary tuberosity, which is the
of the mouth. structure having spongy bone. It has
The lingual gingiva of all the mandi­ been observed that in majority of cases,
Fig. 11.1: Mandibular alveolar bone showing bular teeth are supplied by the lingual the roots of the maxillary third molars
thick cortices and less spongy bone nerve up to the midline and the lingual are fused, conical and tapered and thus,
nerve also supplies the floor of the mouth the extraction of this tooth is a simple
opening and if the procedure is long and half of the tongue, ipsilaterally. procedure. However, when the roots
and the mandible is unsupported during are unfavorable and especially in elderly
the application of the forces during the Maxilla patients, where the bone becomes more
extraction, the chances of injuries to The maxillary bone has more spongy compact and brittle, the extraction of
the temporomandibular joint or its dis­ bone and thin cortical plates and the maxillary third molar may become a
location are very high. The cortical plates excellent vascularity (Fig. 11.2). Due difficult task and injudicious use of force
in relation to the mandibular incisors to the presence of the more spongy or use of heavy elevators for luxation of
are thinner as compared to the cortical bone, it is more amenable to expansion these teeth may lead to fracture of the
plates in the molar and premolar area when the pressure is applied during tuberosity and the formation of oroan­
and hence, local infiltrations with local extraction. Owing to its better vascula­rity tral communication.
anesthetic solution, may work in the as compared to the mandible and thus, As the maxillary alveolar bone has
anterior region but, fails to penetrate the healing is faster and less eventful. thin cortical plates simple paraperiosteal
the thick cortical plates around the However, maxilla being the weaker bone, infiltrations of local anesthetic solution
posterior teeth and local anesthetic effect heavy elevators like cross bar elevators can produce adequate anesthesia for
is inadequate and thus, nerve block is the cannot be used for luxating the teeth as facilitating the exodontias procedures.
modality of choice for anesthetizing the the chances of fracture of the alveolar However, to ensure proper anesthesia, it
mandibular teeth. The local infiltrations bone and the tuberosity are very high. is desirable to give nerve blocks, where
may work in the anterior area, but it is not The apices of the maxillary molars ever feasible.
a reliable method. are in close proximity to the floor of the
maxillary sinus. Sometimes due to the Nerve Supply of Maxillary Teeth
Nerve Supply of Mandibular Teeth anatomical variations, the sinus floor The maxillary teeth, alveolar bone and
The main nerve supply to the mandi­ extends deep between the roots of the the periodontal ligament fibers are sup­
bular teeth, the alveolar bone and the plied by the branches of the maxillary
periodontal ligament, is derived from nerve namely the posterior, middle and
the inferior alveolar bone, which enters the anterior superior alveolar branches.
the inferior alveolar canal through the The first and the second molars are sup­
mandibular foramen present on the plied by the posterior superior alveolar
lingual cortex of the ascending ramus. nerve. While the distobuccal and pala­
The nerve travels in the canal and tal roots of the first molar are supplied
supplies the mandibular molars and by the posterior superior alveolar nerve,
their supporting alveolar bone and its mesiobuccal root is supplied by the
periodontal ligament fibers. At the level middle superior alveolar nerve. Because
of the premolar, the inferior alveolar of this, separate infiltration is required
nerve divides into the incisive nerve and to be given for anesthetizing the middle
the mental nerve. The incisive nerve Fig. 11.2: Maxillary alveolar bone showing superior alveolar nerve in addition to
continues in the bone and supplies thin cortices and plenty of spongy bone the PSA nerve block, while extracting the
Exodontia 197

maxillary first molar. The middle and Box 11.1: Indications for exodontia lead to high chances of complicated
the anterior superior alveolar nerves are osteora­dion­ecrosis. However, due to
• Severe caries where the teeth are not
the branches originating from the infra­ restorable advent of better technology and care,
orbital nerve in the infra­orbital canal and • Pulpal necrosis now-a-days it is not practiced widely.
descend inferiorly in the maxillary bone • Severe periodontal disease • Supernumerary teeth.
to reach the teeth supplied by them, i.e. • Orthodontic reasons
• Malposed teeth which hinder with
the premolars and the anteriors respec­
the designing and fabrication of the CONTRAINDICATIONS
tively. The infra­ orbital nerve block is prosthesis or cause trauma from FOR EXTRACTION
good enough to block these two nerves. occlusion
All these three nerves form a plexus • Fractured teeth which cannot be All the patients undergoing the dental
in the maxillary alveolar bone called a conserved extractions need not be healthy and may
‘superior dental plexus’. • Preprosthetic extractions have associated medical disorders, which
• Teeth in fracture line
As the cortical plates are thin and can complicate the dental extraction.
• Teeth associated with pathologies
there is more spongy bone in maxilla, • Teeth in firing line of radiations Proper control of the underlying medical
even paraperiosteal infiltrations of local • Supernumerary teeth. or local pathology minimizes the chances
ane­­­sthetics work and produce adequate of complications and makes the surgical
ane­sthesia. However, in presence of lo­ procedure safe. The identification of the
cal infections or acute inflammatory • Malposed teeth which hinder with medical disorder, its evaluation, assess­
rea­ction the local infiltration may fail the designing and fabrication of ment and proper control is man­datory
and nerve block becomes the ultimate the prosthesis or cause trauma before the dental extraction is under­
choice of anesthesia. The local infiltra­ from occlusion causing recurrent taken. It requires adequate knowledge
tions can also fail in presence of osteo­ ulcers or lead to non-self cleansing of medical condition, proper history
sclerotic condi­ tions and thus, nerve areas thus leading to periodontal or taking, short but relevant general clinical
blocks are more reliable. carious disease. examination, appropriate and judicious
The buccal gingiva up to the molars is • Fractured teeth which cannot be investigations and timely referral to the
supplied by the posterior superior alveolar conserved. specialist for the treatment and advise.
nerve, in the premolar area by the middle • Preprosthetic extractions—total extra­­ In the medically compromised patients,
superior alveolar nerve and the labial gin­ ction for fabrication of complete where the chances of developing life-
gival of the anterior teeth are sup­plied by dentures or removal of undesirable threatening compli­cations are high, it
the anterior superior alveolar nerve. The teeth, which come in the way of fab­ becomes a teamwork for ensuring pro­
palatal gingival of molar and the premolar rication of proper dentures. per safety of the patients. Similarly,
area are supplied by the bran­ches of the • Teeth in fracture line—all the teeth undertaking this procedure under the
greater palatine nerve, while as the palatal in fracture line need not be removed, controlled environ­ ments is of para­
gingival of the anterior teeth is supplied by however, when the fracture occurs mount importance to provide necessary
the nasopalatine nerve. in dentate patient in the denture medical help and care to the patient
bearing area the fracture becomes promptly, if needed. In most of the dental
INDICATIONS FOR essentially a compound fracture and clinics the facilities and infrastructure
the chances of infection are very may not be available to combat the
EXTRACTION OF TOOTH high and thus, the teeth in fracture emergency and it is advisable that
The teeth can be extracted for either line may be removed. Similarly the such high risk patients be operated
therapeutic or prophylactic consider­ teeth which hinder with the proper under controlled environments, where
ations. The indications for extraction of reduction of the fracture may also be such facilities are available. The dental
the teeth can be enumerated as follows extracted. surgeon must be in position to suitably
(Box 11.1): • Teeth associated with pathologies alter the treatment plan or premedicate
• Severe caries where the teeth are not such as cysts, tumors, granulomas the patient during the perioperative
restorable. or chronic infections. phase to take adequate care to avoid
• Pulpal necrosis. • Teeth in firing line of radiations complications. Hence, it can be said that
• Severe periodontal disease leading the patients undergoing the radia­ the associated medical conditions are
to severe irreparable periodontal tion therapy for the management of only relative contraindications and not
loss and mobility. malignancies of the head neck area the ‘absolute contraindication’ for the
• Orthodontic reasons—for creation were usually subjected to prophy­ dental extraction in majority of cases,
of space, prevention of arch collapse, lactic extractions of the teeth in the if due care and control is established.
serial extractions and removal of way of radiations as the effects of Any medical condition which is uncon­
malposed teeth, which cannot be radiations on the bone (avascular­ trolled, severe or acute may become
corrected orthodontically. ity) and the teeth (radiation caries) absolute contraindication at a given
198 Dentoalveolar Surgeries

time, however the same patient may be blood, the tissues tend to bleed more3 therefore, be put on one side to allow
fit to undergo dental extraction, once and thus, the elective extractions should venous return to recover. Elective dental
the underlying medical condition is be avoided during the menstruation. care should be avoided in the last month
brought under control. One has to assess of pregnancy, as it is uncomfortable for
the severity of the condition, general Pregnancy the patient. Moreover, premature labor
condition of the patient and his ability to Pregnancy is a major event in any wo­­ or even abortion may also be ascribed.
withstand surgical stress as against the man's life and is associated with many The second trimester is supposed
advantages of dental extraction. Most physio­lo­gical changes affecting especially to be relatively safe for minor surgeries.
of the times there are conservative and the endocrine, cardiovascular and hema­ However, if the tooth is causing recurrent
less invasive options available for dental to­lo­gical systems. The levels of most of sepsis and infections and bacteremia/
extraction, e.g. simple opening of the the hormones rise, especially the sex septicemia, its extraction can be under­
root canal will decompress the periapical hormones, prolactin and thyroid hormo­ taken with due care as retaining it is
infection and provide temporary pain nes, but levels of luteinizing hor­mone and equally hazardous.
relief to the patient. One must weigh the follicle-stimulating hormone fall. Because of the risk of coincidental
advantages of dental extraction as against The first and the third trimesters of mishaps, it is wise to try to avoid giving
the chances of severe complications that the pregnancy are more risky. Fetal de­ any drugs, possibly even local anesthet­
can occur in a medically compromised velopment during the first 3 months is a ics, conscious sedation or general anes­
patient and should try to defer the pro­ complex process of organogenesis and thesia. As much treatment as possible
cedure by opting for conservative the fetus is at a risk of from developmental should be postponed until after parturi­
approach for time being. An extraction defect. The most critical period is the 3rd tion in those with bad obstetric history
must be regarded as a minor surgical week to 8th week, during differentiation. (the history of abortion). During first
procedure like any other surgical proce­ All drugs should be avoided unless a pot­ trimester the only safe course of action
dure on human body and thus, the focus en­tial benefit outweighs potential risk, as is to protect all patients from infections
should be on the patient as whole rather during the first trimester the organogen­ and avoid the use of drugs and radio­
than only on the local dental pathology. esis is taking place in the fetus and the graphs. Dental treatment is best carried
The contraindications (conditions drugs prescribed may have teratogenic out during the second trimester.
that warrant proper care) are (Table 11.1). effects. The patient may have severe tox­
e­mia and may not tolerate the procedure. Extreme Geriatric Patients
Physiological Contraindications During second and third trimesters, The physiologic compensatory mechani­
the fetus is growing and maturing, but sms are severely compromised and the
Menstruating Females can still be affected by infections, drugs stress combating capacity is very poor
Menstruation is a stressful condition and and possibly other factors. and such patients may not be able to cope
adding further surgical stress may not In the third trimester supine hypo­ up with minor surgical procedure and
be a good idea. Secondly, owing to high tension syndrome4 may result, if the thus they need to be avoided.
circulating levels of the estrogen in the patient is laid flat. The patient should,

Table 11.1: Contraindications for exodontia


Pathological Contraindications

Local Systemic Systemic Contraindications


• Acute infection Physiologic Unstable systemic disease:
• Tooth in malignant growth Menstruation • Unstable endocrine disorders like
• Tooth associated with vascular lesion Pregnancy myxedema, thyrotoxicosis, diabetes,
• Proximity with vital structures Extremely geriatric patients Addisons disease and patients on
• Irradiated jaw Pathological long term steroid therapy.
CVS—HT, IHD, CCF, valvular pathologies, con­
duction disorders • Renal disorders, e.g. chronic renal
Immunosuppression failure, glomerulonephritis, uremia.
Hepatic disorders • Cardiovascular, e.g. hypertension,
Endocrinal disorders—Addisons disease, hypo- ischemic heart diseases, cardiomyo­
and hyperthyroidism, diabetes pthia, valvular disorders, CCF, con­
Neurological—epilepsy, stroke
duction disorders.
Hematological—leukemia, agranulocytosis, ble­­e­
d­­ing disorders, coagulopathies, anticoagulant or • Pulmonary—bronchial asthma,
anti­platelet therapy COPD, active chest infections such
Renal disorders as tuber­culosis.
RS—asthema, pulmonary tuberculosis, COPD, • Hepatic disorders—cirrhosis of liver,
active chest infections acute liver infections.
Exodontia 199

• Neurological disorders—stroke, epi­ antibiotic prophylaxis in the form type of pathology he might be suffering
le­psy. of Amoxicillin, given intravenously from. It is therefore reemphasized that
• Hematologic disease—thrombocyto­­ half an hour before extraction in a relevant, concise history and brief rele-
penia, agranulocytosis, leuko­penia, dose of 500 mg or Ampicillin 500 mg vant general clinical examination is
leukemia, bleeding and clot­ting dis­ to 1 g IV, is given to prevent bacterial key to successful clinical practice. In
orders, patients on anticoa­gulants. endocarditis. As far as possible, the patients who are above 40 years of age,
• Immunosuppressed conditions. infection is controlled by antibiotic history of hypertension, diabetes, IHD
therapy and local measures for its must be obtained as these diseases are
Local Conditions drainage/decompression (e.g. open­ commonly seen due to urbanization
• Irradiated jaws—as the chances of ing the root canal) are under­taken and changing lifestyles in this age group.
osteoradionecrosis are very high to control it and relieve pain and Blood pressure should be recorded in
due to severe impairment of the discomfort to the patient. such patients, as they may be undetected
vascularity of the bone. hypertensive patients. The past history
• Vascular lesions, like AV malfor­ of dental treatment or extraction may
PRESURGICAL ASSESSMENT
mations, hemangiomas, aneurysms also give useful information and should
may lead to catastrophic bleeding. also be recorded.
• Malignant tumor—a malignant gro­ Medical Risk Assessment
wth in the region of the offending As already stated earlier a dental sur- Emotional Condition
tooth should be taken as an absolute geon must understand that he is ‘not By and large there are many misconcep­
contraindication for the dental extra­ treating a tooth, but he is treating tions prevailing in the society about the
ction as the tooth associated with an individual with a diseased tooth’. dental extractions, especially in rural
malignant lesions is mobile due to Therefore, the approach should not area, such as ‘weakening eye sight’ fol­
destruction of investing periodontal be localized and restricted to dental lowing the dental extraction. The patients
tissues. The extraction of such teeth pathology alone and the patient as are always very apprehensive to undergo
may lead to seeding of malignant a whole should be taken into consi­ dental extraction, as they often consider it
cells in the capillaries and may lead deration. Every dental extraction should to be a very painful procedure as it is nar­
to distant metastasis of the tumor to be consi­dered as a minor surgery and rated to them by someone. Such patients
viscera. The patients always tend to should be done with utmost care to are very anxious and are liable to go into
insist for the extraction of such teeth, prevent complications. All the patients a syncope or aggravation of their medical
which should not be done. walking in a dental surgery may not problems leading to complications, due
• Proximity to vital structures—the be absolutely healthy and may have to emotional stress. The anxious patients
teeth which are in close proximity associated medical conditions, which may be unnecessarily talkative, behave in
of vital structures such as inferior may lead to severe life-threatening a peculiar way and have palmar sweating.
alveolar nerve, maxillary sinus and complications and it is also true that Such anxious patients need to be identi­
extraction of such teeth can lead the complications do not occur with fied, counseled and premedicated prior
to damage to these structures thus prior warning, but effort must be made to the extraction as a part of anxiety re­
should not be extracted, unless it is to make the dental extractions safe duction protocol. Normally the counsel­
absolutely unavoidable. and uneventful for the patient. The ing is good enough, but in the patients
• Presence of acute infection—the patients are sometimes unaware of who are extremely anxious premedica­
tooth having acute infective patho­ their medical ailments and it is the test tion with tranquilizers/anxiolytics (Diaz­
logy should not be extracted as there of skill of history taking, where a dental epam) and atropine sulphate (vagolytic)
are chances of local extension of the surgeon should make comprehensive may be beneficial. The former reduces
infection in the deeper tissue planes effort to extract the desired information the anxiety and calms down the patient
due to handling and breaking the by direct or indirect questioning. It has and the latter prevents bradycardia by its
barriers during the surgery. At the been observed that even if the patient is vagolytic action, reducing the chances of
same time with the exposure of the aware of his medical illness, he will not syncope during the procedure.
capillaries, the microorganisms may reveal it to a dental surgeon as he often
get ingress into the bloodstream considers it unnecessary for undergoing Clinical Evaluation
and lead to bacteremia and com­ dental extraction due to illiteracy and Local clinical evaluation of the patient
pli­
cations associated with it. The ignorance. It is therefore, necessary for should be done thoroughly. Any extra­
most common complication apart a dental surgeon to establish a proper oral swelling, presence of cellulitis,
from pyrexia associated with bacte­ rapport with the patient, communicate abscess, lymphadenopathy and trismus
remia is bacterial endocarditis. well and should not resort to shortcuts, should be noted. The extraoral swelling
If the tooth is to be extracted in while obtaining the history. The drug is suggestive of extension of dental
presence of acute infection, suitable history can also indirectly suggest the infection to the soft tissue spaces around
200 Dentoalveolar Surgeries

the jaws and may warrant separate malposition, etc. as carious undermin­ both. It is also referred to as extraction
procedures apart from dental extraction ing and endodontic therapy may make by closed method.
such as, incision and drainage or deco­ the tooth structure brittle and the tooth Indications for intra-alveolar extrac­
mpression to bring about its resolution. may fracture, while extracting. The ad­ tion:
The presence of trismus is associated jacent tooth should also be evaluated • Loose teeth.
with inflammatory pathology is sugges­ for mobility, caries and presence of any • Firm teeth with intact crown.
tive of protective muscle spasm secon­ restoration. • Teeth facilitating proper access to
dary to pain and may obstruct the access forcep and/or elevators.
to the surgical site. Acuteness of these Radiographic Evaluation
clinical signs of infection should also be The tooth in question should be evaluated Transalveolar Extraction
assessed and the procedure should be radiographically. It is neces­sary to know Transalveolar extraction is practiced to
preferably carried out under antibiotic the normal radio­graphic landmarks on a remove the teeth, which are impacted or
cover to prevent bacteremia. The bac­ radiograph. The size, shape, form, num­ to remove the root pieces or teeth which
teremia related complications like ber of roots, pre­sence of dilacerations, have unfavorable roots. It is also called
bacterial endocarditis are more serious resorption and hyper­cementosis should a surgical extraction, which is misnomer
and should be prevented by antibiotic be noted. The condition of adjacent tooth as irrespective of the technique; the
prophylaxis. should also be evaluated. The condition extraction is a surgical procedure. In this
Intraoral examination should be car­ of the bone should also be evaluated as technique, the tooth is approached and
ried out to assess proper access to the sur­ the chronic infections make the bone accessed by removing the alveolar bone
gical site, bulky buccal fat of pad, trismus, sclerotic owing to the periosteal bone ap­ over it (transalveolar) (Box 11.2).
large tongue, hyperactive gag reflex usu­ position and such bone resists expansion
ally prevent proper access and handling during extraction. Presence of periapical
SEQUENCE OF PROCEDURES
of the intraoral structures. The condition patho­logies like cyst, granuloma should
of gingiva, acuteness of inflammation, also be noted and presence of any other TO BE UNDERTAKEN DURING
edema, congestion and pus discharge bony pathology associated with the tooth EXTRACTION
should be noted as such tissues are friable should be ruled out. The periapical cyst
and bleed during the surgery and their and granuloma needs to be curetted as Administration of Local
healing may be complicated. It is desir­ failure to do so may lead to residual cyst Anesthesia
able not to extract the tooth in presence of in the former case and prolonged oozing Most of the cases of exodontia are per­
acute infection as it may and lead to bac­ of the blood in latter case. The proximity formed effectively and successfully un­
teremia and spread of the infection to the of the tooth with vital structure like neu­ der local anesthesia. Hence, the first
deeper tissue planes. Such cases should rovascular bundle, maxillary sinus also step in the extraction of the tooth is ad­
be treated after proper control of infec­ needs to be evaluated radiographically. ministration of local anesthesia through
tion with antibiotics and local care. an appropriate agent and technique.
The dental arches should be evalu­ Overall Difficulty One must wait for the local anesthetic
ated. The periodontal condition of the When all the findings derived from the to act and verify the same by subjective
teeth, mobility, missing teeth, crowding history, general examination, local and and objective symptom evaluation.
should be noted. If the tooth in question is radiological examination are sum­med up,
crowded or malposed, the application the overall difficulty can be determined. Position of the Operator
of forceps or elevator may be difficult. Once the difficulty index is determined and the Patient
If the adjacent tooth is missing then the suitable preoperative evalu­ation, referral
inter­dental bone cannot be used as ful­ to consultant for control of underlying Position of the Operator
crum to luxate the tooth and the extrac­ medical condition, alteration in treatment • Standing or sitting.
tion may be carried out using forceps plan and preparation for surgery can be
only. Presence of generalized periodon­ undertaken to ensure smooth conduct
Box 11.2: Indications for transalveolar
tal disease asso­ciated with pockets and of the procedure and to minimize the
extraction
pus discharge render the teeth mobile, complications.
which are easy to extract, but the pres­ • Root pieces
ence of septic focus may cause wound • Severely undermined crowns
METHODS OF EXODONTIA • Fractured teeth
infection and requires antibiotic cover­
• Brittle teeth (RC treated)
age to prevent it. • Unfavorable root form
The tooth in question should be Intra-alveolar Extraction • Dense bone
thoroughly evaluated for its crown size, Intra-alveolar extraction is usually pra­ • Malposed teeth—crowding,
form, shape, carious undermining, pre­ cticed to extract an erupted, intact tooth incomplete eruption
• Proximity with vital structures
vious endodontic therapy, angulation, with the help of a forceps, elevator or
Exodontia 201

• In front or behind patient—for the •


Patient almost supine or semi- of operation, it is usual to remove
maxillary teeth and the mandibular sitting (back 20°–30° to ground) for man­ di­
bular teeth before the maxi­
teeth on the left side, the operator the mandibular teeth. llary. However, this sequence has dis­
should stand at 7 to 8° clock position
• Both the above positions are reco­ advantage as well, if the maxillary teeth
and for the mandibular posterior mmended when the operator is are extracted after the mandibular
teeth on the right side, the operator operating in sitting position. teeth, the loose fragments of calculus
should stand at 11° clock position • If the operator is standing then or fractured tooth fragments may fall in
(Figs 11.3A to C and 11.4A to C). the chair is raised and head of the the sockets of the extracted mandibular
• Be comfortable. Back straight. Head patient is tilted backwards, so that teeth. Such foreign bodies could hamper
not bent forward blocking light. the mandibular arch is parallel to the healing. Hence, it is recommended
• The operator should not lean over the floor and the maxillary arch is at by some authors to extract maxillary
the patient and contaminate the 45° angle to the floor. teeth before the extraction of the
sterile field created by draping and The level of the head of the patient mandibular teeth. The posterior teeth
isolation. should be at the level between the are extracted before the anterior teeth
shoulder and the elbow of the operator as it will not obstruct the access due to
Position of the Patient while the level of the head should be at placement of the pack. Unnecessary
• Patient should be kept in comfortable the level of elbow of the operator. movement to and fro around the chair is
position with head nicely supported avoided by starting multiple extractions
at the occiputs for maxillary teeth Sequence of Tooth Extraction with the right mandibular teeth, which
supine position (back 10° to ground) To prevent blood from the sockets are extracted from behind the sitting
is recommended. of extracted teeth obscuring the field patient.

A B C
Figs 11.3A to C: Position for mandibular anterior, right posterior, left posterior teeth

A B C
Figs 11.4A to C: Position of the operator for maxillary posteriors on left side, anteriors and right posterior teeth
202 Dentoalveolar Surgeries

It is wise to begin with the most Box 11.3: Fundamental requirements


painful tooth when undertaking multi­ To summarize the fundamental
ple extractions lest any surgical or anes­ requirements:
thetic difficulty prevents the completion • Adequate access
• Good visualization of the field
of the operation. Similarly, when wor­
• Unimpeded pathway of delivery of the
king under local anesthesia only one tooth
quadrant of the mouth should be injected • Controlled forces to retract adjacent
at a time. When the surgery in this area structures and remove tooth
has been successfully completed a new
quadrant may be injected. lt is better to
take out teeth from one side of the arch Fig. 11.5: Modified Austin’s retractor to be detached and retracted to facilitate
only, at one visit, thereby leaving the proper application of the forceps as api­
other for chewing. Austin/Minnesota retractors and Wie­der cally as possible below the CE junction
The extraction of many teeth at one tongue blade, respectively (Fig. 11.5). and to prevent laceration of the gingiva,
outpatient sitting is contraindicated as The mouth needs to be kept open during while performing extraction. The gingi­
it may produce significant inflamma­ the procedure to facilitate proper access val retraction should be lib­eral to facili­
tion and discomfort to the patient and to the surgical site and prevent accidental tate passive retraction (Figs 11.6A to C).
the blood loss can be considerable. It biting on the operator’s finger, especially The gingival papilla on either side of the
is not possible to standardize as to how while treating children and epileptic tooth should be reflected to expose the
many teeth should be extracted at a sin­ patients. Mouth props, bite block, side entire tooth to be extracted. The gingival
gle sitting as it depends on the surgical action mouth prop can be used for retraction can be done using a number
difficulty, patient’s health, morale and this purpose, but they are not usually 15 BP blade, Moon’s probe or a sharp
other factors relevant to the surgical pro­ required in an awake patient. The mouth periosteal elevator.
cedure. Where it is necessary to extract mirror can also be an effective tool in the
multiple teeth at one visit, the patient retraction of the cheek and the tongue Use of the Elevator5,6
should be kept in the recovery room for during the extraction. Elevators are single-bladed instruments
at least an hour postoperatively and then The visibility to the surgical site must
for extracting or luxating the teeth and
accompanied home by an attendant. be good and after retraction proper illu­
roots, which they do by moving them out
mination of the surgical site should beof the sockets along a path determined
Access ensured. Any secretions, blood should by the natural curvature of the roots.
An adequate access and visibility of the be readily sucked out to keep the sur­ They are applied on the cementum of
surgical site are important requirements gical site clear to impart uninterrupted
any surface, usually the mesial, distal or
for the uneventful extraction of the visibility. buccal, at a point.
tooth. Never try to apply the forceps The fundamental requirements for The dental elevators are used either
of elevators blindly as it may lead to the exodontia procedures are summa­ to elevate/luxate the tooth or to deliver
soft tissue injuries, slippage of the rized in Box 11.3. the tooth. The elevators are simple
instrument and fracture of the tooth. machines designed specially to suit
Proper access to the surgical site can Gingival Retraction different requirements and to deliver
be created by gently retracting the lips, Before proceeding for extraction, the maximum mechanical advantage with
cheek and the tongue using Bishops/ gingival attachment on the tooth needs minimum efforts. It is not necessary to

A B C
Figs 11.6A to C: Liberal gingival retraction
Exodontia 203

use elevators always, however, the teeth


which are firm and malposed and where
the forceps cannot be applied, the tooth
is luxated and then either delivered
using the elevator or with forceps.
The elevators are to be used judi­
ciously and following rules must be
followed, while using the elevators:
• Do not use heavy elevators like cross
bar elevators to luxate/deliver the A B
maxillary teeth, as it is a weak bone
Figs 11.7A and B: (A) Correct; (B) Incorrect method of application of elevator
and can get readily fractured.
• Do not use the adjacent tooth as a ful­
crum unless it is also to be extracted.
• Never use the buccal cortical plate at or mandible, fracturing the alveolar Work Principles in use of Elevators
the gingival line as a fulcrum, except process, slipping and plunging the point The work principle as for the use of the
where odontectomy is performed, or of the instrument into the soft tissue, elevators may be that of the lever, the
in the third molar areas. with the possible perforation of major wedge, the wheel and axle or the combin­
• Never use the lingual cortical plate vessels and nerves, penetrating the ation of the above mentioned principles
at the gingival line as a fulcrum. maxillary antrum or forcing the root into (Figs 11.8 to 11.10).
• Use controlled guided force and do the antrum, or forcing the apical third Lever principle: Elevators most
not use injudicious forces as it may of the root of the lower third molar into frequently make use of this principle.
lead to fracture of the tooth, alveolar the mandibular canal or through the The elevator is the lever of the first class-
bone or basal bone. lingual plate of the mandible into the position of the fulcrum is between the
• Engage the tip of the elevator on a submandibular or pterygomandibular effort and the resistance. In order to gain
natural undercut area such as below space depending upon the position of mechanical advantage in a lever of the
the cervical line (purchase groove) the third molar. first class, the effort arm, on one side of
or artificially created point on to the fulcrum must be longer than the
the tooth to be extracted ( purchase Parts of the Elevator resistance arm on the other side of the
point) to prevent slippage. • Handle—this may be a continuation fulcrum.
• Support the jaw and head to pre­ of the shank or at a right angle to it. Long arm is ¾ of the total length and
vent slippage of the elevator and • Shank. short arm is ¼ of the total length, to get
dislocation of the mandible, espe­ • Blade—part which engages the the mechanical advantage of 3.
cially while elevating the lower tooth. crown. The shape of blade differs for
• Use finger guard to prevent accide­ each elevator type and each is used
ntal soft tissue injury due to accide­ as the need dictates.
ntal slippage of the elevator, but According to form, elevators can be
make sure that the finger is protected classified as follows:
against the injury by the gauze piece • Straight: Wedge type.
as a wrapping (Figs 11.7A and B). • Angular: Right and left.
• When cutting through interseptal • Cross bar (handle at right angle to
bone, take care not to engage the shank).
root of an adjacent tooth. According to use, elevators can be
classified as:
Indications • Elevators designed to remove the
Elevator is generally used to luxate or entire tooth.
extract those teeth, which cannot be • Elevators designed to remove roots
engaged by the beaks of the forceps such broken off at the gingival line.
as in impactions, malposed teeth, to • Elevators designed to remove roots
remove roots, fractured or carious teeth. broken off halfway to the apex.
Elevator should be used with ut­ • Elevators designed to remove the
most caution at all times because of the apical at the apical third of the root.
dangers of damaging or even of extra­ • Elevators designed to reflect the
cting adjacent teeth, fracturing maxilla mucoperiosteum. Fig. 11.8: Straight elevator used as a lever
204 Dentoalveolar Surgeries

Fig. 11.9: Lever principle (Abbreviations:


R: Resistance; E : Effort, SA : Short arm; LA :
Long arm).

Fig. 11.12: Principle of wheel and axle


(Abbreviations: R : Resistance; E : Effort;
Rw : Radius of wheel; Ra : Radius of axle)

Surgical mallet can be used to drive


Fig. 11.10: Axo lever elevator
elevator along the route.
B Apexo elevator, with concavity
Wedge principle: Some elevators Figs 11.11A and B: Wedge principle— always turned towards root, is wedged
are designed to work on this principle apexo elevator in use (Abbreviations: R : Re­ into space occupied by periodontal
called wedge elevators. The wedge sistance; E : Effort; L : Length; H : Height). membrane. After forcing the tip along­
elevator is pushed between the root and side the root for approximately 5 mm,
the investing bony tissue parallel to long rotate the handle.
axis of the root, by hand pressure or by While the wheel and axle principle Caution:
mallet force. can be and is used as the sole work • Protect the surrounding tissue.
While the wedge principle can be principle in removing teeth, it is also • On the maxilla grasp the dental arch
and is used as the sole principle in used in conjunction with the wedge with the index finger and thumb,
removing teeth, it is used in conjunction principle and in some cases with the so that alveolus containing the root
with the lever principle. The wedge in its lever principle (Fig. 11.12). is between them. On the mandible
simplest form, as in a chisel, is a movable Effort × Radius of wheel = the first and second finger should
inclined plane, which overcomes a Resistance × Radius of Axle straddle the alveolus and the thumb
larger resistance at right angles to the Formula for the wheel and axle is placed beneath the mandible,
applied effort. The effort is applied at the principle: R/E= Rw/Ra supporting it, thus offsetting the
base of the plane and the resistance has downward pressure of the elevator,
its effect on the slant side. Some wedges Specific use of Certain Elevators which might otherwise dislocate
are movable double inclined planes. Straight apexo elevator no. 81 (Fig. 11.13A) the mandible. It is far better for the
Sharper the angle of the wedge less the is primarily used on the maxilla, where the dental surgeon to injure his own
effort that is required to overcome a upper central, lateral, cuspid or bicuspid finger than to run risk of seriously
given resistance (Figs 11.11A and B). has fractured at gingival line. injuring the patient, with a possible
Formula for wedge: E × I = R × h, or The straight apexo elevator is used lawsuit ensuing.
R/E = I/H as a wedge. Place this wedge on the Nos. 4 and 5 apexo elevators on the
Wheel and axle principle: The mesiolabial in the space occupied by mandible R and L:
wheel and axle is a simplest machine, the periodontal membrane. Apply In these apexo elevators, (Fig. 11.13B)
being really a modified form of a lever. apical pressure and a slight labiolingual the blade is at a 45° angle to the handle
The effort is applied to the circumference movement, then enter the elevator and the shank is at a angle to the handle
of a wheel, which turns the axle so as to on the distal and repeat; then enter 90°. The principle of their use is the same
raise a weight. the elevator at the mesial and repeat. as that for the straight apexo elevator, that
Exodontia 205

Fig. 11.13A: Straight apexo elevator no. 81 Fig. 11.13B: Apexo elevator Fig. 11.13C: Double apexo elevator
no. 4 (I) and no. 5 (II) technique

is, they are used as wedge. These elevators


may be used in on all lower teeth, where
fracture of the root has occurred at the
gingival line.
Insert, with a rotary motion and
simultaneous apical pressure, the point
of the no.4 apexo elevator along the
mesial surface of the root, until a depth Fig. 11.14: Apical fragment ejector
of 2 to 3 mm.
Next take the no. 5 apexo elevator
and repeat the procedure. Next insert
the point of the no. 4 apexo elevator on
the mesial surface of the root using more
and more rotary and apical pressure,
until a depth of 6 mm.
Double apexo elevator technique:
Place the no. 4 apexo elevator in the left
hand and the no. 5 in the right hand.
Then place the points of both elevators A B C
in against the root on opposite surfaces Figs 11.15A to C: Crossbar elevator
and using both elevators with lever
pressure occlusally, elevate the root to • To remove molar roots fractured at forceps have basically three components
the surface (Fig. 11.13C). or below the gingival line. (Fig. 11.16):
Apical fragment ejectors: Apical • To fracture off crown or split roots • The handle: It is longer as compare
fragment ejectors are shaped just like after a groove has been cut in with a to the beaks, which gives maximum
the straight and right and left apexo crosscut fissure bur. mechanical advantage. The handle
elevators, the only difference being that • In cases of impacted teeth. or the shaft is designed in such a
the apical fragment ejectors are smaller. way that it provides an unimpeded
Apical fragment ejectors are used to Forceps access to the tooth so as to prevent
remove roots, or parts of roots, fractured The forceps are based on the principles damage to the adjoining or opposing
at the apical third of the root (Fig. 11.14). of simple machine. They are designed in teeth and also prevents injury to the
Use of crossbar elevator on the such a way that the access to the tooth in lips and at the same time facilitates
mandible: Cross bar elevator are used question is unimpeded and the adjoin­ the application of the beaks parallel
on the mandible for the following ing structures are not damaged, while to the long axis of the tooth. The
purposes (Figs 11.15A to C). extra­cting the tooth with a forceps. The shaft of the forceps have serrations,
206 Dentoalveolar Surgeries

Mandibular Forceps
Mandibular forceps have beaks almost
perpendicular to the handle and are
illustrated in Figures 11.22A to E and
11.23A to C.
While extracting the maxillary teeth,
the operator grasps the maxillary al­
veolar pla­tes around the tooth to be ex­
tracted by a ‘pinch grip’ to support the
Fig. 11.16: Parts of forcep cortical plates, get a tactile feeling during
application of the force and to stabilize
which are away from the shank to the head (Fig. 11.24).
provide long arm of the lever and Similarly, while extracting the man­
thus, offer maximum mechanical dibular teeth, the mandible is grasped
advantage and it is the part where with ‘sling grip’ for the purposes men­
the ope­rator holds the forceps with tioned above and also for giving support
a palm grip. The serrations facilitate and counter traction to the mandible,
firm grip. while applying forces with the forceps to
• The shank: It is the area, where the prevent its dislocation (Figs 11.25A to C).
beaks unite with the handle. It also
corresponds to the fulcrum of the Forceps Extraction
lever. The forceps help in extraction of the
• The beaks: These are much shorter tooth by way of severing the periodontal
as compared to the shaft and provide ligament fibers and expanding the
short arm of the lever for optimum A B cortical plates. The pressures that are
mechanical advantage. The beaks of Figs 11.17A and B: Note the outer surface applied with a forceps to achieve the
the mandibular forceps are at almost of the beaks are tapered and smooth, while same are (Fig. 11.26):
90° angle to the shaft, while as the the inner surface is serrated • Apical pressure: For wedging the
beaks of the maxillary forceps are forceps beaks in the PDL space and
almost parallel to the handle of the to gain an apical seat.
forceps to facili­tate application of • Buccal pressure: It is the major move­
the beaks parallel to the long axis of ment as the buccal cortical plate is
the tooth to be extracted. The beaks thin and can be expanded easily. The
are of variable thickness, i.e. for the periodontal ligament fibers on the op­
posterior teeth, which are bulbous posite side get severed.
the beaks are thicker and for the • Lingual pressure: It is the minor
anterior teeth or roots, they are thin movement as the lingual cortical
and slender. The outer surface of plates are thick and do not expand
the beaks is smooth and tapering adequately when subjected to pres­
A B
to facilitate wedging of the beaks sure. The periodontal ligament fi­
Figs 11.18A and B: (A) Wedge principle;
between the alveolar bone and bers on the opposite side get severed.
(B) Bone expansion
the root surface in the periodontal Moreover, there are chances of frac­
ligament space to get an apical seat ture of the root, especially in cases
(beaks are applied apical to the CE • Unimpeded access. of maxillary molar extraction due to
junction). The inner surface of the • Application of the beaks apically and thick palatal bone. The fracture of
beaks has serration to facilitate firm parallel to the long axis of the tooth, the lingual cortical plate can lead to
grip on the tooth. (Figs 11.17A and without injuring adjacent structures. sublingual hematoma or damage to
B). The ideal contact between the • To get maximum mechanical advan­ the lingual nerve in cases of mandi­
tooth to be extracted and the beaks tage. bular molar extraction.
of the forceps is described as ‘two • To get firm grip. • Rotation: These forces are applied
point contact’ (Figs 11.18A and B). for breaking the PDL fibers. Rota­
The design of the forceps is variable Maxillary Forceps tional forces are not applied to the
for different teeth to achieve the objec­ Maxillary forceps are illustrated in multirooted teeth and the maxillary
tives of: Figures 11.19 to 11.21. lateral incisors as they have distal
Exodontia 207

A B C D
Figs 11.20A to D: Upper cowhorn forceps for
molars: (A) Left side; (B) Right side; (C) Bifurca­
ted palatal beak engages single palatal root;
(D) Pointed (horn like) buccal beak engages
A the bifurcation between two buccal roots.
The cowhorn forceps are used to extract the
teeth with severe carious undermining of the
crown

B I II III IV
Figs 11.19A and B: Maxillary molar forceps: (I) The rounded tip of the palatal beak;
(II) Buccal beak with a triangular projection, which engages the furcation area between
two buccal roots; (III) The maxillary molar forceps left side; (IV) The maxillary molar forceps
right side Fig. 11.21: Upper bionet forcep used for
the extraction of the root fragments

curvature of the root and there are


chances of fracture of the root. The
rotational forces are best suited for
the teeth having conical roots.
• Traction: It is applied to deliver the
tooth from the expanded socket and
with severed periodontal ligament
fibers.

Special Consideration while doing


an Orthodontic Extraction
The premolars are often extracted for
orthodontic considerations to create
space for correcting the crowding of
the teeth. When such an extraction is
planned, care must be taken to cause
minimal trauma to the bone. The ex­
pansion of the socket should be mini­ A B C D E
mal and the buccal cortical plate should Figs 11.22A to E: Mandibular forceps: (A) Anterior; (B) Premolar; (C) Molar;
not be fractured by application of the (D) Cowhorn for molars; (E) Third molar forceps
208 Dentoalveolar Surgeries

excessive force, nor the root should uneventfully. It is desirable to evaluate


fracture as removal of the residual root the roots of the premolar prior to extrac­
fragment may require transalveolar tion by obtaining intraoral periapical
technique resulting into damage to the X-rays to prevent the fracture of the root.
buccal cortical plate. Fortunately, the The use of elevator is avoided during the
A
patients requiring orthodontic extrac­ extraction for orthodontic reason, as it
tions are young and the bones have may create undue stresses in the bone
excellent elasticity and if proper preop­ and the indentations produced in the
erative evaluation is done and adequate bone used as fulcrum will resist move­
B
care is taken, the tooth is often extracted ment of tooth during orthodontic treat­
ment. Secondly, the socket should not
be compressed after the extraction as
the space is needed for movement of the
tooth in the socket.

C
Figs 11.23A to C: Mandibular extraction
What to Check During and After
forceps: (A) Lower molar, the pointed tips Extraction?
if the beaks engage the bifurcation area ‘See, hear and feel’ is the dictum.
buccolingually; (B) Lower anterior, the beaks While doing the extraction it is not only
are meeting as the crowns of anteriors are
necessary to visualize the field, but it is
less bulbous; (C) Lower premolar, the beaks
are heavy and have gap to accommodate also equally important to develop skills
the bulbous crown Fig. 11.24: Maxillary pinch grasp of tactile perception. When the forces

A B C
Figs 11.25A to C: Mandibular sling grasp

Fig. 11.26: Forcep extraction


Exodontia 209

are applied with the help of either the out. If the injury to the blood vessel is bleeding is the inside of the socket.
elevators or the forceps the movement suspected, pack the socket or use bone As the pack is kept on the top of the
of the tooth can be seen, but it is equally wax or gel foam to control the bleeding. socket and not inside the socket, to
important to feel the movement through The other cause of excessive bleeding is develop pressure on the inner walls
the tactile feeling that is perceived by gingival laceration and if it is present, and base of the socket is its filling with
the hand holding the forceps. This pressure pack or sutures are beneficial clotted blood, which gets compressed
skill needs to be developed purely by to control it. and exerts pressure on the bleeders
practice and cannot be explained in Palpate the edges of the socket for inside the socket thus, it requires more
the words. A skilled person will always any sharpness in the bony margins. If the time. Secondly the initial clot is soft,
know, which direction the forces are sharp bony margins are present nibble flabby and is unstable and liable to be
more effective and can be suitable to or file them off to make them smooth. dislodged readily with routine activities.
extract the tooth. The ears are also Such sharp margins irritate the gingival The clot retraction takes place in 30 to
required to be kept vigilant to hear the flap, cause pain and delay healing. The 45 minutes and the serum is expressed
sound, while luxating or extracting the patients always feel them with tongue out from the clot making it drier and
tooth as any clicking sound could be as a and complain of incomplete extraction more stable. The pressure pack should
result of fracture of the alveolar bone or of the tooth. thus, be kept for about 60 minutes.
the root of the tooth. As the cortical plates are expanded The sutures are not always indicated as
Once the tooth is delivered, the first during the extraction, they are gently the healing is by secondary intention,
thing that is to be done is to inspect the compressed with digital pressure to however, the suture help to stop bleed­
tooth and its root for their completeness. reduce the expanded cortical plates to ing, prevents food impaction. Generally
The roots normally taper and are conical their original position. This procedure dehiscence takes place even after placing
any incompleteness would suggest either is called a ‘simple alveoloplasty’. This the sutures as the flaps do not get properly
fracture or resorption of the root. Fracture is done to facilitate fabrication of sub­ approximated, unless the cortical plates
will always show a sharp line, while as the sequent prosthesis. Some clinicians do are trimmed significantly and the suture
resorption will show irregular margins. not recommend simple alveoloplasty if line lies on the defect. The sutures should
If the evidence of fracture is present an implant is planned. be loose approximating sutures.
determine, which root is fractured and The next step is application of pres­ The patient is given following post­
what would be its approximate length. sure using pressure pack to achieve operative instructions:
Never discard such tooth until the hemo­stasis. The material used for pres­ • To maintain pressure pack for
remaining fragment is also removed. sure pack is either rolled and moistened 60 minutes—for hemostasis.
The next step is to wipe the socket sterile gauze or a pressure pad prepared • Not to spit and swallow the saliva,
dry and make the field dry by sucking by rolling gauze over the absorbent as during the act of spitting the jaw
out the saliva or blood in the vicinity to cotton wool. The cotton wool absorbs moves and the pressure pack may
visualize the socket. Inspect the socket the blood and saliva and gauze prevents get disturbed.
thoroughly for any excessive bleeding, the sticking of the cotton fibers to the • Not to do forceful gargles or smoke—
foreign bodies like fragments of the raw surgical area. Never use cotton as the negative pressure generated,
tooth, calculus tags, granulation tissue wool to apply pressure directly over the while smoking may dislodge the clot
or any sharp or loose bony fragments. raw area, as the fibers may stick to the and lead to bleeding.
If they are present remove them by wound surface and may subsequently • Soft diet—as the pain may get aggra­
grasping with a mosquito artery forceps. interfere with the healing. The pressure vated, while making more mastica­
Any loose bony fragment which is devoid pack is placed on the top of the socket tory effort and the wound/clot does
of periosteal attachment is unlikely to and the patient is asked to bite on it not get disturbed.
survive and must be removed. Excessive for minimum 30 minutes to 1 hour to • No hot fomentations but to give
bleeding could be due to injury to blood achieve hemostasis. The normal clotting cold compressions—in the imme­
vessels (inferior alveolar or nutrient time is 8 to 12 minute, but still the pack diate post­operative phase, the vas­
vessels) or presence of the friable granu­ is maintained for longer time, because cular phase of inflammation is
lation tissue in the socket. In the latter one must remember the following the predominant and is mani­fested by
case, the blood will well out from in the extraction, the bleeding occurs from the vasodilatation, hot fomentations
socket steadily and in the former case, it gingival margins, severed periodontal may aggravate it and lead to excessive
will flow more forcefully. Pack the socket fibers and the apical vessels of the tooth. edema and discomfort. Hence, app­
with gauze and try to curette the socket The gingiva get compressed between li­cation of cold compressions helps
and remove all the residual granulation the pack and the alveolar bone and the in reducing the edema by inducing
tissue. The bleeding will not stop, until bleeding from the same stops rapidly vasoconstriction. Once the edema
all the granulation tissue is curetted due to direct pressure what keeps on sets in the mounting pressure within
210 Dentoalveolar Surgeries

the interstitial com­partment blocks the instrumentation and traumatizing


the lymphatics and venules, which the adjacent tissue.
are the draining channels and help Smaller root fragments may be
in reabsorbtion of the interstitial retained with due information to the
fluid to reduce the edema. It leads to patient. The patient should be advised
stasis of circulation. to report in case the root piece becomes
• Warm saline gargles after 48 hours: symptomatic. The criteria for retaining
These induce vasodilatation and faci­ the root fragment may be summarized
litates the reabsorption of interstitial as follows:
fluid and edema thus, improving • Small (≤ 5 mm in length). Fig. 11.27: Lone standing tooth with
local circulation, which also helps in • Root fragment must not be super­ grossly carious crown
faster healing and drug delivery. ficial.
• Tooth involved must not be infected
Policy for Leaving Root Fragments or have apical lesion on radiograph.
The roots that are fractured at the time of • If near vital structure, which may be
extraction should ideally be removed as injured.
the root fragment may serve as a septic • If has potential to be displaced into
focus or may give rise to pathologies sinus, inferior alveolar canal, or sub­
such as cyst. It is therefore imperative to mandibular space or would require
assess the root fragment for its length, excessive destruction of bone.
presence of any pathology, its proximity
Transalveolar Extraction Fig. 11.28: Destruction of crown
with vital structures and the depth of the
fragment in the bone. One has to evaluate The teeth when extracted by creating
the advantages of removing the root surgical access to it through the alveolar
fragment against the complications that bone, fall in the category of transalveolar
can be encountered, while attempting its extraction technique. As it requires
removal. It is not advisable to remove a reflection of the flap and removal of the
small root fragment of about 2 to 3 mm cortical bone, it is also called ‘extraction
by removing large quantity of bone, by open method’. The teeth which
while attempting a transalveolar removal cannot be removed by conventional
or damaging vital structures such as intra-alveolar method and require more
the neurovascular bundle or maxillary complex procedure for their removal are
sinus. Large root fragments, i.e. the roots termed a complicated exodontia. Fig. 11.29: Endodontically treated tooth
which are fractured at or below the CE The indications for the transalveolar
junction must be removed. They can be extraction are:
removed either using the intra-alveolar • Root pieces. instruments and therefore, the appli­
technique by using apexo or cryers • Severely undermined crowns. cation of forces. Such teeth fracture
elevators or by using the apical ejectors. • Fractured teeth. readily on application of forceps or the
The prerequisite is thorough evaluation • Brittle teeth (endodontically treated elevators.
including the radiographs and proper teeth, geriatric patients).
Roots
visibility. The procedure must not be • Unfavorable root form.
attempted blindly as the chances of • Dense bone. All those factors that result in unfavorable
displacement of the root fragment in • Malposed teeth—crowding, incom­ path of removal or increased resistance.
the maxillary sinus, sublingual space plete eruption. • Multiple roots
or trauma to the adjacent vital struc­ • Proximity with vital structures. • Bulbous roots
tures are more. In case of any doubts • Lone standing tooth with grossly • Endodontically treated teeth (Fig.
or difficulty in gaining proper access or carious crown (Fig. 11.27). 11.29)
visibility, it is better to resort to transal­ The factors that complicate the ex­ • Hypercementosis (Fig. 11.30)
veolar technique. Judicious removal traction of the tooth are: • Ankylosed teeth (Fig. 11.31)
of buccal cortical bone, splitting of the • Divergent/dilacerated roots (Figs 11.32
Crown
roots in case of multirooted teeth and and 11.33)
elevating the root with the help of an Destruction of the crown (Fig. 11.28) Bone: Increased density of the bone
elevator creating a purchase point on the (e.g. caries, complex restorations, fixed due to chronic periosteal reaction (osteo­
root is less traumatic than blindly doing prosthesis) prevents the application of con­­densation) and loss of resilience of the
Exodontia 211

like Paget’s disease and fibrous dysplasia, Prosthetic concerns:


the bone bulk increases making the • Preservation of alveolus
extraction more difficult. • Alveolar contour
Diminished access: The major cause • Preservation of attached gingiva.
of diminished access is due to trismus
Technique
and the common causes for the trismus
are: After a thorough preoperative evaluation
• Oral submucous fibrosis the decision of transalveolar extraction is
• Ankylosis taken. The patient should be explained
• Muscle spasm the treatment plan and the procedure is
Fig. 11.30: Hypercementosis • Scleroderma performed under local anesthesia.
• Microstomia To create proper access to the tooth
• Interferes with application of instru­ or the root fragment, an appropriate
ments due to crowding, supernumer­ muco­ periosteal flap is raised (details
ary, malposed teeth, hypertrophied of the basic principles of flap designing
buccal fat pad and macro­glossia. are given in Chapter 1) (Fig. 11.35).
The bone is removed from the buccal
Adjacent/nonadjacent teeth
cortical plate to expose the roots up to
• Highly carious adjacent teeth. cementoenamel junction in an intact
• Root canal on adjacent teeth. tooth or in case of the root fragment, the
• Heavily restored adjacent teeth. bone is removed to visualize the root,
Fig. 11.31: Ankylosis • Periodontally involved adjacent using burs or chisel (Fig. 11.36). The
teeth. bone should be removed judiciously.
• Lone maxillary molar or canine. Once the root fragment is exposed,
Malposed teeth: The teeth which are a hole is drilled in the root fragment,
positioned out of arch or are crowded which is used to engage the tip of the
the correct application of forceps may elevator. This point is called a ‘purchase
not be possible. Even the creation of the point’. While creating the purchase
‘purchase point’ for correct application
of elevators may not be available. The
transalveolar extraction may be the only
choice in such situations.
Adjacent vital structures: The close
proximity with vital anatomical struc­
Fig. 11.32: Divergent roots tures may lead to damage to these struc­
tures during the extraction, if due care is
not exercised. The structures which are
likely to be damaged are (Fig. 11.34):
• Inferior alveolar bundle
• Lingual nerve Fig. 11.35: Reflection of the mucoperiosteal
flap and removal of the bone to expose the
• Maxillary sinus.
furcation area

Fig. 11.33: Dilaceration roots

bone in the old age makes the bone less


amen­able to pressure and the expansion
of the socket is in adequate during the
extra­ction, which can lead to fracture of Fig. 11.36: Removal of the bone to expose
the cortical plates or the roots. During Fig. 11.34: Adjacent to vital structures, the root fragment and its removal by elev­
the extraction in some osteodystrophies i.e. inferior alveolar canal ation
212 Dentoalveolar Surgeries

A B
Fig. 11.37: The incorrect and correct way Figs 11.38A and B: Division of the roots at the bifurcation and delivering them
of creating the purchase point separately as per their curvature

point, care should be taken that it is Local Complications


created in healthy root area, so that it has
adequate strength to withstand the force Immediate Complications
applied through the elevator and does • Failure to secure local anesthesia.
not fracture easily. The purchase point • Failure to remove the tooth.
should be deep enough to engage the tip • Fracture of the tooth.
of the elevator securely (Fig. 11.37). A B • Fracture of the alveolus (including
In case of an intact tooth, the tooth maxillary tuberosity).
is sectioned and removed. If the crown • Oroantral communication.
is fragile, it can fracture in an unplanned • Displacement of the tooth or a root
manner, making the removal of remain­ into the adjacent tissues.
ing roots difficult. Hence, it is desirable C • Aspiration of the tooth or part of a
to section it (odontectomy) in a planned Figs 11.39A to C: Showing the direction tooth into the pharynx and hence to
manner, so that the remaining fragment of tooth elevation according to curvature the lung or stomach.
can be removed easily. The roots are of the root. The elevator is applied on the • Fracture or subluxation of an adja­
sectioned and removed separately in a convex side and the tooth is delivered cent tooth.
towards the concave side
multirooted tooth by creating purchase • Collateral damage to surrounding
point and elevating them with elevator. soft tissues.
The path of removal of the root piece is Exodontia is essentially a surgical • Thermal injury.
determined according to the curvature of procedure and warrants all the judicious • Bleeding.
the root (Figs 11.38A and B, 11.39A to C). precautions and the aseptic care to • Dislocation of the temporomandi­
After the tooth is removed comple­ prevent complications. Whenever the bu­lar joint.
tely, the wound is debrided and pre­pared basic principles of the surgery are vio­ • Fracture of mandible.
by curetting granulation tissue if any, lated, the relative chances of develop­ • Damage to branches of the trige­
removing loose and sharp bone fragment ing complications are increased signi­ minal nerve.
and rounding them off and finally ficantly. Similarly when the patients
irrigating the socket gently, with normal, are medically compromised and due Delayed Complications
sterile saline. The primary closure of the precautions are not taken; the likely • Excessive pain, swelling and trismus.
flap is done with sutures. hood of precipitating complications • Hemorrhage.
Postoperative care remains the is high. The complications can occur • Localized alvelolar osteitis (dry soc­
same as described for the intra-alveolar in spite of good care and precautions, ket).
extraction. but their incidence is minimized. It • Acute osteomyelitis.
therefore, necessitates the clinician to • Infection of soft tissues.
COMPLICATIONS take a comprehensive approach and • Oroantral fistula.
have sound knowledge of complications, • Failures of the socket to heal.
OF EXODONTIA their prevention and management. The • Nerve damage.
Dental extractions are commonly prac­ postdental extraction complications can
ticed and often considered as a minor be classified as: Late Complications
job, the clinicians tend to take it lightly. • Local complications • Chronic osteomyelitis.
No surgical procedure is guaranteed – Immediate • Osteoradionecrosis.
to be free of complications and tooth – Delayed. • Nerve damage.
extraction is no exception. • Systemic complications. • Chronic pain.
Exodontia 213

Failure to Secure Anesthesia nor­mally requires a surgical (trans­ When the fracture occurs, the
It is usually due to faulty technique, alveolar) approach. forceps are discarded and a large buccal
insufficient dosage of the anesthetic mucoperiosteal flap is raised. The frac­
agent, infection at the site of injection Fracture of the Alveolar Bone tured tuberosity and the tooth is then
or poor quality of local anesthetic Fracture of the alveolar bone is one of freed from the palatal soft tissues by
solution. A thorough evaluation of the the common complications of tooth blunt subperiosteal dissection and
anesthesia by subjective and objective extraction. It occurs due to accidental lifted from the wound. If the removal
methods is done to assess the effect of inclusion of alveolar bone within the of fractured fragment is tried without
local anesthetic. If the anesthesia is not forceps blades or to the configuration detaching its soft tissue attachment,
secured properly, additional dose of of roots. Exami­nation of extracted teeth the mucosa may get torn/lacerated
local anesthetic should be injected. reveals alveolar frag­ments adhering to and the lacerations might extend up
the teeth. The extraction of canines is to lateral pharyngeal wall. Once the
Failure to Remove the Tooth frequently complicated by fracture of fragment is removed, the oroantral
with Either Forceps or Elevators the labial plate, especially if the alveolar communication must be ruled out. The
If the tooth does not yield to reasonable bone has been weakened by extraction soft tissues flaps are then apposed with
displacing forces applied with forceps of the lateral incisor and/or the first mattress sutures, which evert the edges
or elevators, this normally indicates premolar prior to the removal of the and are left in situ for at least 10 days.
that either the bone texture is dense canine, hence, the canine should be If a large oroantral communication is
and inelastic, or that the root shape extracted prior to lateral incisor and present, which is unlikely to be closed
is obstructing its path of withdrawal. canine. It is advisable to remove any by suturing the flaps, proper plastic
Ankylosed teeth, abnormal root ana­ loose alveolar fragments, which are closure of the communication be done
tomy these also yield difficulty, while devoid of the periosteal attachment as using appropriate technique and flap.
removing the tooth. In such a situation, they tend to undergo avascular necrosis.
the cause of the obstruction should Oroantral Communication8
be sought, by taking a radiograph. Fracture of the Maxillary Oroantral communication is a patholo­
A mucoperiosteal flap should raise and Tuberosity7 gical communication between oral cavity
remove bone and/or divide the tooth Fracture of the maxillary tuberosity is a and the maxillary antrum. An oroantral
and remove the tooth. specific type of alveolar bone fracture fistula is an epithelized, patho­ logical,
(Fig. 11.40), which may be predisposed unnatural communication between
Fracture of the Tooth by: these two cavities. The root apices of the
The causes of crown or root fracture are: • The presence of a large antrum that maxillary cheek teeth are closely related
• Improper and excessive force ap­ weakens the maxillary alveolus. to the antral floor. With increasing age
plied to the tooth. • A large or splayed root mass of the the nasal sinuses slowly enlarge, so that
• A tooth weakened by caries or large upper second or third molar. the tooth roots often appear in a two-
restorations or endodontically trea­ • Fusion of an unerupted third molar dimensional radiographic view to be
ted teeth. to the root of the second molar. protruding into the antral cavity. In the
• Inappropriate application of force elderly patient, the bony barrier between
resulting from failure to grasp tooth and sinus is thin and brittle.
enough of the root mass or using As the tooth is manipulated in the
forceps with blades too wide to make forceps, there is a risk that the bone of
two point contacts on the root. the antral floor, which may be adherent
• Unfavorable root anatomy of dense to the roots, will fracture and be removed
and non-elastic bone. with the tooth, so leaving a defect and
• Inspection of the fractured tooth creating a communication from the
shows the likely size and position of mouth to the antrum via the socket. The
the retained root. detailed description of this condition
• If there is no preoperative radio­ is given in the Chapter 14 (Diseases of
graph, it should be taken at this Maxillary Sinus).
stage.
• When only the crown has been re­ Dislocation of the
moved, it may be possible to reapply Temporomandibular Joint
root forceps to remove the roots. Dislocation of the temporomandibular
• When the root itself has fractured, Fig. 11.40: Extracted tooth with fractured joint during forceps extraction is nor­
retrieval of the retained portion tuberosity mally the result of failure to support the
214 Dentoalveolar Surgeries

mandible, while a difficult lower tooth is • Do not apply forceps to a root below
being loosened. Dislocation may also be the antrum, unless there is sufficient
caused by the injudicious use of gags. To exposure of the root to allow the
avoid this complication, the operator’s blades to grasp the root securely
left hand should ideally stabilize the under direct vision.
jaw during this maneuver. If dislocation • Be content to leave the apical third of
occurs it should be reduced immediately. maxillary molar palatal roots, unless
To reduce the dislocation, the operator there is an overriding indication for
stands in front of the patient and places their removal.
his thumbs intraorally on the external • Never attempt to retrieve a root
oblique ridges lateral to any mandibular below the antrum by passing an
molars, which are present and his instrument up into the tooth socket.
fingers extraorally under the lower Any root in the antrum should be
border of the mandible (Fig. 11.41). This removed. The patient should be taken
complication of mandibular extractions for sinus exploration and root retrieval.
can usually be prevented if the lower Raise a buccal flap and remove bone
jaw is supported during extraction. An Fig. 11.41: Reduction of dislocated to allow adequate access for the root to
extraoral support to the joint should be condyle be elevated away from the antrum. The
applied and worn, until tenderness in remaining defect into the antrum from
the affected joint subsides. the socket also should be taken care of.
Certain situations make inadvertent
Fracture of the Mandible damage to other teeth more likely: Displacement of the Tooth
Fracture of the mandible is a rare event • Overhanging restorations in adjacent or a Root into the Tissues
during dental extraction. It usually sig­ teeth. Displacement of the tooth or a root
nifies that either there is some predi­ • Bulbous full crown restorations on into the tissues is a rare, but potentially
sposing weakness of the jaw, which then adjacent teeth. serious complication. The tooth or part
exhibits a pathological fracture when • If the tooth for extraction is a bridge of it may be lost under mucoperiosteal
‘normal’ forces are applied to a tooth, or abutment, the bridge must either be flap, into the lingual pouch through
that an excessive force, sufficient enough removed completely, or sectioned to the thin lingual cortex of bone in the
to break a ‘normal’ mandible has been isolate the tooth to be extracted. lower third molar region, or into the
used. • Lack of proper space between two infratemporal fossa around the back of
Examples of conditions predisposing teeth, i.e. crowding. the maxillary tuberosity from the upper
to pathological fracture include: Caries and loose or overhanging fill­ third molar region.
• Large cysts ings should be removed from an adjacent If a tooth or root is lost from view
• Tumors (including bone metastases) tooth and a temporary dressing inserted during the course of an extraction, it
• Impacted/buried teeth before the extraction. Extrac­tions under may be in one of the following sites:
• Generalized osteoporosis general anesthesia pose possible dan­ • Swallowed into the stomach or inha­
• Paget’s disease gers to the dentition from the injudicious led into the respiratory passage.
• Osteogenesis imperfect use of the mouth gags or props, laryngo­ If either of these is suspected, the
• Hyperparathyroidism. scopes, oral endotracheal tubes and air­ patient should be sent to hospital for
ways used during recovery of the patient. abdominal and chest radiographs.
• Pushed into the antrum.
Fracture or Subluxation Injury to Surrounding • Displaced into a soft tissue space.
of an Adjacent Tooth Structures • Collected inadvertently by the suc­
Fracture or subluxation of an adjacent tion apparatus (check the filter).
tooth complication should be avoidable Displacement of a Root • Still in the socket.
using appropriate techniques with into the Antrum9
forceps and elevators. The rule is that Displacement of a root into the antrum Collateral Damage to Surrounding
no force should be applied to teeth can occur following fracture of a maxil­ Soft Tissues
other than the one being removed. lary molar/premolar and ineffective at­ A certain amount of disruption to the
Careful preoperative examination will tempts to retrieve the retained palatal gingival tissues around an extracted
reveal, whether a tooth adjacent to that root. Inci­dence of this complication can tooth is to be expected. However, it
to be extracted is either carious, heavily be reduced, if the following basic rules can be minimized by judicious gingival
restored, or in the line of withdrawal. are observed. retraction.
Exodontia 215

The incidence of the following • Warn the patient’s guardians or par­ therapy in consultation with the physi­
modes of soft tissue injury can be ents against biting of lips and tongue. cian, at least 72 hours prior to the surgery,
reduced with care and forethought: • Also warn against eating and drin­ to allow new platelets to be produced by
• Gingival tissue lacerated by the king hot fluids; while the effect of the body, which would not be influenced
forceps blades. anesthesia is still present. by aspirin and help in the hemostasis.
• To avoid this complication, be sure • Gauze pack can be placed after The platelets once influenced by aspirin
to place the blades inside the gingival treat­ment to prevent lips trauma. do not recover.
crevice after liberal gingival retrac­ Precautions to minimize the risk of
tion. This is a particular dangerous Management hemorrhage include:
on the lingual aspect of lower teeth. Symptomatic: It comprises of analgesics • Proper medical history.
• Lower lip crushed against the lower and if necessary antibiotics. • Careful handling of the tissues to
teeth while extracting resistant up­ Topical application of petroleum avoid unnecessary trauma.
per molars: This is due to incorrect jelly or local anesthetic or antibiotic • Placing a gauze pack over the socket
angulations of the forceps and is cream to relieve the pain and achieve for at least 10 minutes.
more likely to happen under gen­ comfort during eating. • Avoiding vigorous mouth rinsing or
eral anesthesia or when the patient’s chewing.
lower lip is also anesthetized. The Thermal Injury • If hemorrhage is systemic then
best way for prevention of this com­ Thermal injury results from the conti­ proper case history should be taken,
plication is awareness of the patient. nued use of a handpiece with worn investigations like coagulation pro­
• Damage to the tongue, floor of bearings, so that the instrument over­ file done.
mouth or the palate due to elevator: heats. Awareness of the problem and If there is excessive bleeding at the
To avoid this complication, elevators regular maintenance of equipment will time of extraction:
should always be held with the index reduce the incidence of this unfortunate • Good suction apparatus should be
finger down the shank of the handle event. used.
towards the tip to act as a ‘stop’ in case • Injecting further local anesthetic so­
the instrument slips. The damage to Hemorrhage lution containing a vasoconstrictor.
the soft tissue can also occur due to • Primary hemorrhage—the bleeding • Inspecting the socket for the pres­
slippage of the bur if proper tissue may be at the time of surgery. ence of friable granulation tissue
retraction is not done and guards are • Reactionary hemorrhage—within a and if it is present it should be curet­
not placed. The poor maintenance few hours after surgery when the ted out.
of the rotary instruments like hand- vasoconstriction of damaged blood • Horizontal mattress/figure of 8—
pieces also leads to lot of frictional vessels ceases. suture is placed across the margins
heat during the use. As the patient • Secondary hemorrhage—present up of the socket.
is administered the local anesthesia to 14 days postoperatively as a result • A small pack of resorbable oxidized
and as the surgeon is wearing glo­ of infection. cellulose (Surgicel) or gelatin foam
ves, sometimes double gloves, the Excessive bleeding from the socket (Gelfoam) placed into the superficial
heating of the handpiece may go occurs not infrequently even in patients part of the socket. The Gelfoam is
unnoticed during the surgery and who have no pathological hemorrhagic made wet in saline before packing,
the patient may report subsequently tendency. To avoid this proper history while as the Surgicel is used in dry
with thermal injuries especially at (previous hemorrhagic episode; onset, form. They act as an artificial clot
the oral commissures. duration and amount of bleeding) should and provide scaffold for the clot
be taken. The drug history of the patient formation. With the absorption of
Self-inflicted Tissue Injury is also very important to find out, whether the blood/ fluid, they gain weight and
Self-inflicted tissue injury is common in the patient is on oral anticoagulants, hep­ seal the open ends of the capillaries.
children and mentally retarded adults. arin therapy. Most of the patients having The Gelfoam can be impregnated
It is seen in the form of self-inflicted hypertension, valvular pathologies, pros­ with adrenaline or thrombin before
trauma to lips, tongue and cheek. Dur­ thesis, CVA, neuroparalytic disorders are packing.
ing the postoperative phase when the often prescribed antiplatelet agents most • If a single blood vessel is seen to be
part is still anesthetized such patients common being acetyl salicylic acid (aspi­ the bleeding point then that can be
tend to bite heavily on the lips, tongue rin) in low doses of 75 to 150 milligrams tied off using a suture or coagulated
or cheeks producing severe lacerations. per day. By virtue of its antiplatelet effect, with diathermy.
it prevents the platelet aggregation and If there is persistent oozing from
Prevention such patients are at a risk of prolonged the cancellous bone then that can be
• Use minimum effective dose of local bleeding following surgery. It is there­ stopped by using bone wax in the bone
anesthetic agent. fore desirable to with hold the aspirin marrow. The bone wax mechanically
216 Dentoalveolar Surgeries

Box 11.4: Composition of bone wax ing bone union.10,11 Bone wax remains carried out for arresting the bleeding,
• Bees wax IP as a foreign body for many years, and simultaneously the blood samples
• White hard paraffin wax, IP can cause a giant cell reaction and local should be drawn to evaluate the sys­
• Isopropyl palmitate, USP inflammation.12 In skull base surgery, temic cause of the bleeding if any. The
bone wax has been reported to cause different investigations along with their
granuloma formation and CSF leak.13,14 interpretations are given in Table 11.2.
occludes the blood vessels. Bone wax is The bone wax is also known to inhibit When it is established that the pati­
made of beeswax containing a softening the osteoblast migration, retard the ent has a coagulopathy along side
agent such as paraffin (Box 11.4). Bone healing and may increase the chan­ces of the local measures mentioned above,
wax is used to mechanically stop bone infection. the systemic supportive therapy and
bleeding during surgical procedures. The The FDA has recently approved a definitive treat­ment should be under­
bone wax is smeared across the bleeding new water soluble bone hemostasis ma­ taken.
edge of the bone, blocking the holes and terial called Ostene, which is designed to Supportive treatment:
causing immediate bone hemostasis look and feel like bone wax. This mate­ • Monitor vitals for the signs of hypo­
through a tamponade effect. Bone wax rial comprises a sterile mixture of water- volemia periodically.
is supplied in sterile sticks and most soluble alkylene oxide copolymers, de­ • Intravenous administration of crys­
often requires softening before it can rived from ethylene oxide and pro­pylene talloids (Ringer’s lactate)/colloids
be applied. Once applied, it essentially oxide. These copolymers are considered (hexastarch solution as plasma ex­
never goes away. inert. These compounds are not me­ pander).
It is opaque in color and has a shelf tabolized, but eliminated from the body • IV calcium gluconate injection (should
life of 5 years. It can be sterilized with unchanged. It is anticipated that with the be given carefully as it can precipitate
gamma radiations. Although inexpen­ introduction of these new hemostatic cardiac arrythmias).
sive, easy to use and immediate, bone materials, the incidence of surgical bone • Administration of vitamin K and
wax has a number of adverse reactions infections, non-union and inflammatory vitamin C.
associated with it. Bone wax inhibits complications will decrease with time. The definitive treatment for the indi­
formation of new bone osteogenesis If the patient is an unknown bleeder, vidual coagulopathy is given in the table
and acts as a physical barrier prevent­ when the local measures are being (Table 11.3).

Table 11.2: Different investigations and their interpretation

S. No Test Method Reagent Normal value Causes of abnormality

1. Bleeding time Duke’s Ivy — 3.5 minutes Thrombocytopenia 70,000/mm3


5 minutes Thrombasthenia, thrombocytopathia—
asprin, uremia, cirrhosis of liver
2. Tourniquet test Rumple leed — 3–4 petechiae of — Capillary fragility
2.5 cm in diameter at — Vitamin C deficiency
40 mm of Hg
3. Platelet count Brecher and Phase contrast 160,000–3,5000/mm3
Cronkite microscope
4. Euglobulin clot — — 3–4 hours Platelet deficiency < 1,00,000/mm3
retraction time
5. Clotting time Lee-White — 9–14 minutes F VIII, IX, XI, XII rarely factor X deficiency
6. One stage PT Quick’s Tissue procoagulant, 15 seconds F IV, V, VII, X, fibrinogen, heparin
acetone, dehydrated (antithrombin action) deficiencies
rabbit brain, Ca++,
citrated plasma
7. Partial thromboplastin — Tissue procoagulant + Variable as per F VIII, IX, XI, XII and II, V,VII, X deficiencies
time blood product used
8. PTT + PT — — — PTT prolonged, PT Normal : PT
9. Thrombin time — Thrombin + plasma Variable Fibrinogen < 1,000 mg/dL
Exodontia 217

Table 11.3: Treatment for the individual coagulopathy

Component Contents Indications Approximate Amount of active Risk of Shelf life of


for use volume substance per hepatitis product
transfused unit

Platelet concentrate Platelets, few Bleeding resulting 30–50 3–5 × 1010 2 1–5 days depending
white blood from thrombocy­ on the storage and
cells, some topenia preperation
plasma
Whole blood
Cryprecipitate Coagulation Hemophilia, 10–25 80–100 units 2 12 Mo frozen,
factors I and VII Von-Willebrand factor VIII 2 hours thawed
disease, fibrinogen
deficiency

Factor Normal level Life span Fate during Level required Stability Ideal agent for
coagulation for safe in ACD replacing deficit
hemostasis hemostasis
Factor I 200–400 mg/ 72 hours Consumed 60–100 mg/100 mL Very stable Bank blood
100 mL concentrate
fibrinogen
Factor II 20 mg/100 mL 72 hours Consumed 15–20% Stable Bank blood,
(100%) concentrate
preparation
Factor V 100% 36 hours Consumed 5–30% Labile (40% Frozen fresh plasma,
at 1st week) blood under 7 days
Factor VII 100% 5 hours Survives 5–30% Stable Bank blood,
concentrate
preparation
Factor VIII concentrate 100% (50–150) 6–12 hours Consumed 30% Stable Fresh frozen
proconvertin plasma, bank blood,
serum prothrombin concentrated
conversion accelerator preparation
(SPCA) stable factor
Factor IX [Christmas 100% 24 hours Survives 20–30% Stable Bank blood,
factor, plasma concentrated
thromboplastin preparation
component (PTC),
Hemophilia B factor]
Factor X (Stuart 100% 40 hours Survives 15–20% Stable Bank blood,
Prower factor) concentrated
preparation
Factor XI [plasma 100% Probably 40–80 Survives 10% Probably
thromboplastin stable
antecedent] (PTA)
Factor XII (Hageman 100% Unknown Survives Deficit produces no Stable Replacement not
factor) bleeding tendency required
218 Dentoalveolar Surgeries

Table 11.4: Postdental extraction hemorrhage few days after an inferior dental nerve
block as the result of the development
Causes Management of a hematoma in the medical pterygoid
muscle. The hematoma may undergo
Local 1. Preventive
1. Trauma • History fibrosis. Trismus due to edema nor­
2. Laceration • Investigations mally resolves spon­taneously with the
3. Friable granulation tissue Local
2.
infla­mmation. The needle injury to the
4. Clot dislodgement: Mechanical infection • Curettage sphenomandibular ligament during the
5. Hemorrhagic lesions • Mechanical (sutures, ligatures, pterygomandibular block can also lead
clamps, pressure packs, bone wax) to pain and trismus.
• Thermal (application of hot and The patient can be made more
cold packs)
comfortable by the application of heat
• Electrocoagulation
• Chemical: to the affected area.
– Gel foam
– Topical thrombin Management
– Oxidized cellulose Management depends on the cause of
- Oxicell trismus and consists of the following:
- Surgicel
• Heat therapy (short waive diathermy)
- Methyl-2-cyanoacrylate
• Warm saline rinses
Systemic Systemic
• Analgesics
1. Coagulopathies 1. Supportive: Commercially available
2. Anticoagulant therapy nonspecific coagulants (Hemlock, • Anti-inflammatory
3. Antiplatelet drugs Botropase, Pause, etc.) • Muscle relaxants (role is question­
4. Liver dysfunction 2. Vitamin K able)
5. Chronic liver failure 3. Calcium gluconate • Application of glycerin magnesium
6. Uremia 4. Fluids, Hematocrit, monitoring sulfate dressing
7. LE 5. Investigations and definitive adequate
• Physiotherapy
8. Steroid therapy (prolonged) substitute.
9. Multiple myeloma • Surgical decompression
10. Leukemia • Antibiotics
11. HT
12. Thrombocytopenia. Nerve Damage
The following branches of the trigeminal
nerve may be at risk during tooth
Postdental Extraction the inflammation. Heavy dependence extraction.
Hemorrhage15,16 on the drugs can be avoided by following • The mental nerve—damaged by
The causes and management of post these principles. Suitable pharmacologi­ over­extension of relieving incisions
dental extraction bleeding are ill­u­str­a­ cal support using anti-inflammatory and in the depth of the buccal sulcus in
ted in Table 11.4. analgesic drugs can be prescribed. the lower premolar region.
• The inferior dental nerve—the roots
Excessive Pain, Swelling Causes for Trismus of the third molars are in close prox­
and Trismus17 • Muscle spasms. imity of the inferior alveolar nerve
Swelling and discomfort occurs after • Injury to ligament and medial ptery­ thus there are chances of damage to
any surgical procedure; tooth extrac­ goid muscle. the nerve during extraction. Similar­
tion is no exception. Appropriate post­ • Infection in pterygomandibular ly, injudicious instrumentation can
operative instructions and reassurance, space and/or submasseteric space. also lead to damage to the nerve.
is normally adequate management of Trismus is an inability to open the • The lingual nerve—nerve is at risk of
these symptoms. mouth to a normal gap, and is commonly crush injury during periosteal eleva­
The inflammatory edema can be min­ seen following extractions, particularly tion lingual to the lower third molar.
imized to a great extent by following the lower molars. Inflammation and edema
aseptic principles like aseptic care, gentle may spread from this region to affect the Management
tissue handling, judicious bone cutting powerful jaw closing muscles, masseter Most paresthesias resulting from the
and use of coolent and by placing sutures and medial pterygoid, which are then nerve damage, resolve within 8 weeks
loosely. Judicious use of physiotherapy painful when stretched and undergo without treatment.18 However, if the
in the form of cold com­pressions, warm protective myospasm. Severe and pro­ damage to the nerve is severe, then only
saline gargles can also help in reducing gres­sive trismus occasionally follows a the paresthesia may require longer time
Exodontia 219

or can be permanent.19 The recovery is fibrinolytic agent then dissolves the form of zinc oxide and oil of cloves
variable and depends upon the extent of blood clot and at the same time release on cotton wool or gauze, is loosely
the nerve injury. kinins from the kininogen, which is also tucked into the socket. This dressing
• Reassurance to the patient. in the clot, leading to severe pain. The is often referred to as ‘pom-pom’.
• Administer vitamins (vitamins B1, B6 loss of clot makes the bone bare and • The curettage of the socket to induce
and B12), parenteral and oral. leads to alveolitis and neuritis of the fresh bleeding is recommended,
• If dental treatment is to be contin­ free nerve endings in the bone, which is however, it is not advocated as the
ued, avoid readministration of the also the cause for the pain (Fig. 11.42). pain may get aggreviated and there
local anesthetic agent into the same are chances of the infection spread­
region of traumatized nerve. Clinical Features ing in the deeper tissue planes.
• Nerve decompression or anastomo­ The dry socket is characterized by: • Prophylactic use of antimicrobial
sis surgeries whenever indicated. • The onset of acute pain and a foul drugs such as metronidazole and
The details of nerve injuries are odor 3 to 4 days after the extraction. clindamycin has been shown to re­
covered under the Chapter on Neurolo­ • There is loss of blood clot in the duce its incidence though it is not
gical Disorders. socket, exposing vital bone, which is universal finding. The antibiotic
very tender to touch due to neuritis therapy with betalactum group of
Dry Socket in the exposed nerve endings. antibiotics with metronidazole is
(Synonym: Alveolar Osteitis)20 • The socket may have small quantity usually adequate. It must be un­
of grayish slough, but there is no derstood that it is not an infective
Definition suppuration. pathology as it is evident from the
Dry socket clinical entity is a localized • Similarly, the gingiva around the clinical and microbiologial finding.
osteitis involving either whole or part socket may not show the signs of The role of the antibiotics should not
of the condensed bone lining a tooth inflammation and the swelling is be overemphasized.
socket, the lamina dura. usually absent.
• The healing of the socket is delayed
process and pain normally continues Osteomyelitis
23
Causes
The exact etiology of the dry socket can­ for at least 10 to 14 days. Osteomyelitis is ‘an infection of the
not be ascertained; however, the follow­ bone and the bone marrow, which can
ing factors are believed to precipitate it: Management be caused by an infection in the body
• Excessive trauma to bone. • As the pain is severe the patient spreading in the blood stream from the
• Use of vasoconstrictor along with is given sedative dressings in the point of origin to the bone’.
the local anesthetic solution.
• Menstruating females and the pa­
tients on oral contraceptives.
• Infection (treponema denticola, fuso­
spirochetes, Borrelia vincentii)—al­
though these microorganisms have
been isolated from the lesions of the
dry socket, they are opportunistic and
anaerobic, which might grow in the
hypoperfused, sloughy tissue. The
other studies have shown that there
is a mixed infection and no single or­
ganism could be held responsible for
the dry socket. Moreover, the clini­
cal picture is not similar to that of the
other infective pathologies.
• Abnormal clot retraction.

Pathogenesis
Birn21,22 suggested that trauma and
infection cause inflammation of the
bone marrow with the resultant release
of tissue activators that convert the
plasminogen in the clot to plasmin. This Fig. 11.42: Etiology and pathogenesis of fibrinolytic alveolitis (Birn’s hypothesis22)
220 Dentoalveolar Surgeries

Etiology • These conditions ultimately lead to


REFERENCES
• Extractions done in presence of thrombosis, cellular death, progres­
acute infections. sive hypovascularity and fibrosis. 1. Malvin E King. Dentistry: An Illustrated
• Severe infection. • The radiated bed is hypocellular Histroy. New York: Abradale Press 1993.
• Immunocompromised patients, e.g. and devoid of fibroblasts and osteo­ 2. Geoffrey L. Howe. The Extraction of
unc­o­n­trolled diabetes. blasts. Teeth. 2nd edition revised. Bristol: J.
Contributing factors to the Develop­ Wright. 1974.
Symptoms of Osteomyelitis ment of ORN: 3. Kemal Findikcioglu. Effect of the men­
• Intense penetrating bone pain, pro­ • Dental trauma strual cycle on intraoperative bleeding
longed healing of the socket, anes­ • Tumor location in rhinoplasty patient. European Jour­
thesia of the lower lip and general • Radiation dosage nal of Plastic Surgery. 2009;32(2).
malaise. • Elapsed time since radiation 4. Beard RW, Gillian M Roberts. Supine
• Swelling and warmth in the infected • Nutrition hypotension syndrome. Br Med J. 1970;
area. • Alcohol and tobacco use 2(5704):297.
• Fever. • Concomitant surgery and chemo­ 5. William Harry Archer. Oral Surgery:
• Drainage of pus through the skin. therapy. A step-by-step atlas of operative tech­
Clinically there are three types of niques, 4th edn, WB Saunders Company.
Treatment ORN25,26 1966.
High dose of an appropriate antibiotic • Types I is trauma-induced ORN, 6. Moore US, Principles of Oral and
for an extended period, normally several which occurs when radiation or sur­ Maxillo­facial Surgery, 5th edn. Black­
weeks. Chronic suppurative osteomyeli­ gical wounding are coupled closely well Science Ltd, 2001.
tis demands surgical debridement of the together. 7. Norman JE Cannon PD: Fracture of
affected area to remove any sequestra of • Type II, also trauma-induced ORN, the maxillary tuberosity. Oral Surg.
dead bone. The details of this condition most common which occurs years 1967;24:459-67.
are described in the Chapter on Osteomy­ after radiation therapy. 8. Ehrl PA. Oroantral communications.
elitis. • Type III or spontaneous ORN can Int J Oral Surg.1980;9:351-8.
occur anytime after radiotherapy, 9. Fickling BW. Oral surgery involving the
Osteoradionecrosis24 but commonly occurs 6 months to maxillary sinus. Br Dent J. 1957;103:
Osteoradionecrosis was first described 2 years following radiotherapy, with­ 199-214. Ann R Coll Surg. 1957;20:13-
by Marx25 in 1983 as hypovascularity out any obvious preceding surgical 35.
hypocellularity, and local tissue hypoxia. or traumatic event. 10. Wang MY, Armstrong JK, Fisher TC,
It is an extremely serious complication Grading et al. ‘A new, pluronic-based, bone
of radiotherapy to the jaws that can be • Grade I: ORN is the most common hemostatic agent that does not impair
triggered by tooth extraction, biopsies, presentation. Exposed alveolar bone osteogenesis’. Neurosurgery. 2001;49:
related cancer surgery and periodontal is observed. 962-8.
procedures. The effect of radiation on • Grade II: Designated ORN that does 11. Schonauer C, Tessitore E, Barbagallo G,
the tissues, especially bone, is to reduce not respond to hyperbaric oxygen et al. ‘The use of local agents: bone wax,
dramatically their blood supply and therapy and sequestrectomy/sau­ gelatin, collagen, oxidized cellulose’.
therefore to increase vulnerability to cerization. Eur Spine J. 2004;13:S89-96.
infection and failure of normal healing. • Grade III: It is demonstrated by 12. Allison RT. ‘Foreign body reactions
All teeth in the anticipated radiation full thickness involvement and/or and an associated histological artefact
field that may require extraction patho­logic fracture. due to bone wax’. Br J Biomed Sci.
should ideally be removed before the 1994;51:14-7.
patient has radiotherapy treatment or Management 13. Patel RB, Kwatler JA, Hodosh RM.
within a few weeks of it. (The ischemic • Antibiotics. ‘Bone wax as a cause of foreign body
postirradiation effects on bone are • Thorough aseptic care during the granuloma in the cerebellopontine
slowly progressive over a period of extraction. angle: Case illustration’. J Neurosurg.
months). • Debridement and local care of the 2000;92:362.
extraction wound. 14. Bolger W, Tadros, M, Ellenbogen R, et al.
Pathophysiology • Segmental resection of the bone. ‘Endoscopic management of cerebro­
• The irradiated mandible, perios­ • Use of hyperbaric therapy. spinal fluid leak associated with the
teum and overlying soft tissue un­ Further details of this condition are use of bone wax in skull-base surgery’.
dergo hyperemia, inflammation and described in the Chapter 18 on Osteo­ Otolaryngol Head Neck Surg. 2000;132:
end­arteritis. myelitis of the Facial Bones. 418-20.
Exodontia 221

15. Milam SB, Cooper RL. Extensive bleed­ 19. Haas DA, Lennon D. A 21 year retro­ 24. Epstein J, van der Meij E, McKenzie M,
ing following extraction in a patients spective study reports of paresthesia et al. Postradiation Osteonecrosis of
under­going chronic hemodialysis. Oral following local anesthetic administra­ the mandible: a long-term follow-up
Surg. 1983;55:14. tion. J Can Dent Assoc. 1995; 61:961-7. study. Oral Sury Oral Med Oral Pathol
16. Olson RA, Roberts DL, Osbon DB. A 20. Krogh HW. Incidence of dry socket. J Oral Radiol Endod. 1997;83:657-62.
comparative study of polylactic acid, Am Dent. Assoc.1937;24:1829. 25. Marx RE. Osteoradionecrosis: a new
Gelfoam, and surgical in healing 21. Birn H. Fibrinolytic activity in dry socket. concept of its pathophysiology. J Oral
extrac­tion sites. Oral Surg. 1982;53:441. Acta Odont Scand. 1970;28:37-58. Maxillofac Surg. 1983;41(5):283-8.
17. Young HR. Resolution of postoperative 22. Birn H. Etiology and pathogenesis of 26. Marx RE, Johnson RP. Studies in the
swelling following oral surgery: chy­ fibrinolytic alveolitis (‘dry socket’). Int radiobiology of osteoradionecrosis and
moral. Oral Surg. 1967;23:12-8. J Oral Surg. 1973;2:211-63. their clinical significance. Oral Surg
18. Nickel AA, Jr. A retrospective study 23. Alling CC. Postextraction osteomyelitis Oral Med Oral Pathol. 1987;64(4):379-
of paresthesia of the dental alveolar syn­dr­ome. Dent Clin North Am. 1959; 90.
nerves. Anesth Prog. 1990; 37(1):42-5. 621.
12 Management of
Impacted Teeth
Borle Rajiv M, Arora Aakash, Magarkar Shashwat D

The tooth, which fails to erupt in the oral small size of the jaw which is not fully Systemic Factors
cavity due to obstruction to its path of grown at that age and secondly due to
eruption is called ‘impacted tooth’. The mesial drift phenomenon. The systemic factors are as follows:
obstruction could be due to adjacent • Prenatal causes—heredity.
tooth, thick bone, fibrous tissue, any cyst • Postnatal—rickets, anemia, tuber­
Theories of Impaction 2
or tumor. Archer1 has defined impaction culosis, congenital syphilis, mal­
as “The tooth, which fails to erupt in oral • Phylogenetic theory: Due to evolu­ nutrition.
cavity in its functional position and which tion, the human jaw size is becoming • Endocrinal disorders of thyroid, para­
has lost its further potential of eruption.” smaller and since the third molar thyroid, pituitary glands like hypo­
It should be differentiated from the tooth is the last to erupt there may thyroidism, achondroplasia, etc. Here
embedded tooth in which the tooth does not be room for it to emerge in the the primary retention of teeth is seen
not erupt in the oral cavity due to lack of oral cavity. due to lack of osteoclastic activity,
eruptive forces. • Mendelian’s theory: Here genetic which does not provide resorption
The man has evolved from apes variation plays a major role, if the of the bone overlying the developing
to the current civilized state. The food individual genetically receives a tooth.
habits have also changed from raw food small jaw from one parent and large • Heredity linked disorders—Down’s
to the cooked and processed food. The teeth from other parent. syndrome, Hurler’s syndrome, osteo-­
jaws have evolved due to the change in • Nodine theory: The modern diet petrosis, Cleidocranial dysostosis,
food habit and the need for heavy jaws (soft diet) does not require a decided cleft palate, etc. there is failure of
is no more felt. The size of the jaws has effort in mastication and hence, the overlying bone to resorb and
receded, but the number of teeth has according to Nodine et al.3; the development of an eruption pathway
remained constant, which resulted in growth stimulus of jaw is lost and is absent.
discrepancy between the size of the modern man has impacted teeth.
dentition and the space available to Impacted Mandibular
accommodate it in the jaws. Thus, the
Etiology Third Molars
teeth often get obstructed and fail to erupt
in the oral cavity, in the desired position. Apart from the above mentioned factors The mandibular third molars are the
The third molars are by far the most certain etiological factors have been most common teeth to be impacted4
commonly impacted as they are the last mentioned for impacted teeth. They are: and the most challenging impaction to
to be formed and erupt in the oral cavity. be treated.
By the time they start erupting in the Local Factors
oral cavity the other teeth have already The local factors are as follows: Applied Surgical
occupied the available space in the jaw • Micrognathia
and thus, the third molars face the space • Crowing of teeth
Anatomy
constraints. The second tooth commonly • Condensing osteitis • When the mandible is viewed super­
found impacted is maxillary canines and • Cysts oinferiorly it is noticed that the third
then the mandibular canines, as they • Tumors molars are located in the lingual shelf
also erupt later than their adjacent teeth • Thick fibrous bands under the of the bone and buccally a strong
and face the space problem due to the mucosa. buttressed bony ridge is present.
Management of Impacted Teeth 223

A B
Fig. 12.2: Showing the nutrient foramen in
Figs 12.1A and B: Lingual shelf for mandibular third molars the retromolar area

When viewed from inferior side the – The thin lingual cortical plate area in some mandibles. If the
lingual shelf is conspicuously seen may fracture readily and the vertical incision is taken lingually the
and it is noticed that the lingual shelf lingual nerve may get damaged. nutrient vessels may get traumatized
is thin as compared to the buccal The inferior alveolar nerve also and results into disturbing bleeding
bone (Figs 12.1A and B). lies close to the roots of the deeply during the surgery (Fig. 12.2).
• third molars are situated close to the placed impacted mandibular third • The Buccal fat pad is present laterally
junction of the thin vertical ramus molar.6 It may be in close proximity and superiorly to the ramus. If the
and thick body of the mandible. The of the apices, may pass between the vertical incision is placed too far
junction between the thick and the two roots or may groove the surface laterally to the ramus or taken too
thin portions of the bone constitutes of the root and pass through it. The long, the fat pad can get exposed
a line of weakness. The bone grains relation of the roots with the nerve and prolapse into the oral cavity. It
also change their course from vertical must be carefully assessed and the is difficult to reduce it to its original
to the horizontal direction in this treatment plan must be suitably position and may get necrosed and
area, which also makes the bone modified to prevent the damage to delay the healing.
weak in this area.5 When the third the nerve. • The bone grains in the ramus area
molars are impacted and placed deep • The facial artery lies at the ante­ are placed vertically. They change
in the bone, they occupy lot of space roinferior angle of the insertion of their course in the body and become
in the bone and undermine it making the masseter muscle and ascends horizontal. While removing the bone
it further weak. The reinforcement is anteriorly and upwards in the cheek. with the help of chisel and mallet,
provided to this area by the presence It is close to the buccal vestibule in first two stop cuts, which are cortex
of buttressed external and internal the molar area. During taking the deep, must be marked at the anterior
oblique ridges. If bone is removed vertical relieving incision if the knife and posterior ends of the proposed
injudiciously from this area during slips accidentally the vessel can get bone removal and then only the
the surgery or excessive force is damaged and lead to profuse hemor­ intervening bone should be removed.
applied the bone can fracture readily rhage. To stop the bleeding, firm If the chisel is directly used parallel
at the angle of the mandible. digital pressure may be applied at to the bone grains, without marking
• The lingual nerve lies very close to the anteroinferior angle of the insertion the vertical stop cuts, the whole bone
lingual cortical plate in the third molar of the masseter, over the inferior may get split along the bone grains.
area and can get damaged during the border of the mandible, exrtaorally.
surgery due to following reasons: The facial artery gets compressed
– If vertical incision at the anterior between the finger and the bone and Classification of the
border of the ramus is taken too the bleeding can be stopped, until impacted third molar
far lingually. the artery is ligated. To avoid such
impactions7
– If the soft tissues on the lingual accident, a beginner, while taking
side are not properly guarded the vertical relieving incision, must
direct the knife from the depth of the Winter’s Classification
8
by placing a guard then the ac­
cidental slippage of the sharp in­ vestibule to the gingival margin and The third molars are classified according
strument or clogging of the bur not the other way round. to the position of its long axis as follows
in the soft tissue may damage • There are small nutrient foramina (Figs 12.3A to G):
the nerve. on the lingual side of the retromolar • Mesioangular
224 Dentoalveolar Surgeries

A B C D

E F G
Figs 12.3A to G: Classification according to position: (A) Mesioangular; (B) Distoangular; (C) vertical; (D) horizontal;
(E) buccoversion; (F) linguoversion; (G) inverted

A B C
Figs 12.4A to C: Position A, B and C as per Pell and Gregory’s classification

• Horizontal According to the space available W—White line


• Vertical between the distal surface of the second A—Amber line
• Distoangular molar and the anterior border of the R—Red line
• Crown in buccoversion ramus of the mandible third molars can • White line—imaginary line joining
• Crown in the linguoversion be classified as: enamel cusps of erupted 2nd molar
• Inverted • Class I: When there is sufficient extending posteriorly over 3rd molar
space available between the distal • Amber line—imaginary line joining
Pell and Gregory’s surface of the second molar and crest of interdental septum between
Classification9 the anterior border of the ramus to molars
According to the relative depth of the third accommodate the third molar. • Red line—imaginary line perpendi­
molar in the bone in relation to the second • Class II: When the space is inade­ cular to amber line to an imaginary
molar, the third molars are classified as: quate and the third molar is partly point of application of elevator (usu­
• Position A: When the highest por­ present in the space between the ally on mesial side except for distoan­
tion of the impacted third molar is second molar and the anterior border gular molar) (Fig. 12.6).
at or above the occlusal level of the of the ramus and partly in the ramus.
second molar. • Class III: When the third molar is
Why the Classification
• Position B: When the highest por­ totally present in the ramus due to
tion of the impacted third molar is the lack of space (Figs 12.5A to C). is Important?
between the occlusal and cervical The third molar impactions should be
level of the second molar. Winter’s Lines classified for:
• Position C: When the highest por­ White, amber and red (WAR) lines given • Better understanding and communi­
tion of the impacted third molar is by George Winter8—based on ima­gi­nary cation.
below the cervical line of the second lines drawn on radiograph to determine • To assess the degree of difficulty in
molar (Figs 12.4A to C). position and depth of impaction: its surgical removal.
Management of Impacted Teeth 225

A B C
Figs 12.5A to C: Class I, II and III as per Pell and Gregory’s classification

• To assess the bone cover. • In acute condition due to surround­


• To assess the proximity with the vital ing cellulitis, mild extraoral swelling
structures. may be present.
• The patient experiences difficulty in
Sequelae of the mastication and swallowing.
• Due to the edema the tissue swells
Impacted Third Molars and the opposing tooth (upper third
The clinical problems caused by the molar) traumatizes this inflamed
impacted third molars are the sequel. In tissue. It results in inden­tations of
other words they are the indications for the cusp on the soft tissue opercu­lum
their removal.10 or sometimes traumatic ulceration.
• The acute inflammation localizes
Pericoronitis to form an abscess (pericoronal
Fig. 12.6: WAR lines Pericoronitis is defined as the inflam­ abscess), which is characterized by
mation of the soft tissue that covers or localized swelling, surrounded by
surrounds the crown of an unerupted inflamed and congested mucosa
tooth. When the third molars are and pus discharge.
not fully erupted or when they are • The acute stage may resolve or
abnormally placed, the area does not progress to a chronic stage, which is
remain self-cleansing. The food particles characterized by dull pain, fibrous
tend to accumulate and get degraded. tissue around the crown, which has
The micro­organisms get an opportunity a tendency to undergo acute exacer­
to proliferate. Due to the irritation and bation recurrently, especially when
infection the soft tissue under goes the tooth is impacted and non-self-
inflammation and pericoronitis ensues. cleansing. The infection may spread
Fig. 12.7: Pericoronitis The covering of the soft tissue on the along the soft tissue plane to the
crown of an unerupted tooth is called buccal space or submasseteric space
‘operculum’. The accumulation of food (Fig. 12.8).
particles below it or due to recurrent
trauma from occlusion, inflammation Management
sets in, resulting in pericoronitis. Secon­ The management of acute pericoronitis
dary infection worsens the condition is usually conservative, with antibiotics
(Fig. 12.7). and analgesics, anti-inflammatory drugs
and local measures like irrigations with
Clinical Features normal saline, warm saline gargles
The clinical features of the pericoronitis and soft diet, selective cuspal grinding
are: of the opposing tooth causing trauma
• In acute condition there is severe, from occlusion.11 The only surgical
persistent pain. intervention recom­mended at an acute
• Trismus due to protective myospasm state is drainage of the pericoronal
secondary to the pain. abscess. After the acute stage is subsided
Fig. 12.8: Buccal space infection • The pericoronal tissue is inflamed, and proper evaluation is completed,
secondary to pericoronitis congested and edematous. definitive surgical treatment comprising
226 Dentoalveolar Surgeries

of operculectomy or removal of offen­


ding tooth is recommended. The ope­r-­
cu­lectomy should be done in cases
where the tooth is in acceptable posi­­-
tion and if saved can function well. If
the tooth is likely to be non-functional
because of abnormal position it is
better that the tooth is removed as it
may cause recurrent attacks of pain
and operculectomy may not give lasting
relief to the patient. A B
Figs 12.9A and B: Carious involvement of (A) 3rd; (B) 2nd molars
Caries
Caries is generally observed as the tooth,
which is impacted and partially erupted
in the oral cavity fails to maintain good
contact with the adjacent tooth. Due to
this, the chronic food impaction results
and moreover it is not accessible site
for cleaning. This results in caries, not
only in the impacted tooth, but also
in the adjacent tooth, which like any
other carious tooth causes further
complications (Figs 12.9A and B).
Fig. 12.10: lack of contact, plunging of food
Periodontal Pocket Formation debris and pocket formation Fig. 12.11: Pressure resorption of the root
The food impaction leads to periodontal of second molar
pocket formation more commonly It is very important to note during the
between the second and the third orthodontic treatment, as drift can cause
molars. The food impaction distal to the anchorage loss and the orthodontic
third molar results in apical migration treatment can be complicated. Thus,
of the gingival attachment and results in the elective removal of the impacted
distal pocket formation. The periodontal third molars is advocated before the
pockets lead to recurrent attacks of orthodontic treatment (Fig. 12.12).
periodontitis and sensitivity to hot and
cold and cemental caries (Fig. 12.10). Cyst and Tumor Formation
The unerupted and impacted third mol­ Fig. 12.12: Mesial collapse of the arch due
Pressure Symptoms ars are covered with the reduced enamel to pressure from the third molar
The deep seated third molars impinge epithelium, which is the embryonic tissue
upon the neurovascular bundle and and has pleuripotentiality. Such emb­
produce pressure symptoms like dull ryonic tissues are capable of differen­
pain, hypoesthesia and tingling sensation. tiating in variety of other tissues and can
lead to patho­logical conditions like cyst,
ameloblastoma. The dentigerous cysts
Root Resorption of the are commonly seen to be associated
Second Molar with the impacted third molars, in which
Due to chronic pressure on the roots of the Ameloblastic transformations are a
the adjacent tooth (second molar), the common occurrence.12 To prevent such
roots of the second molar may undergo a development, prophylactic removal
resorption (Fig. 12.11). of the third molar is recommended. A
procedure called lateral trephnization13
Anchorage Loss is recommended in the literature in
The impacted third molars exert a which the developing bud of the third
mesial pressure on the arch, thus the molar is surgically removed to prevent Fig. 12.13: Dentigerous cyst associated
teeth have a tendency to drift mesially. further complications (Fig. 12.13). with the impacted third molar
Management of Impacted Teeth 227

Cheek Biting/Trauma Evaluation of the splitting (odontectomy) to prevent


damage to the adjacent tooth and to
from Occlusion patient for the third
prevent weakening of bone due to its
When the third molars are too far poste­ molar surgery14 removal during the surgery.
riorly and buccally placed they impinge The patients who are posted for surgery • Condition of the adjacent tooth: the
upon the soft tissue and traumatize it need a careful evaluation to ensure second molar should be evaluated
leading to traumatic ulceration. The smooth and uneventful procedure. Poor for caries, fractures, endodontic
upper third molars, which are buccally planning is one of the major causes for treat­­ment and prosthesis. The cari­
erupted and suprae­ru­pted due to lack encountering difficulties during the third ous exposure in the second molar or
of opposing tooth, often traumatize the molar surgery, increasing the surgical periapical infection may cause pain.
soft tissue in the retromolar area. The time and postoperative complications. Sometimes at the sight of an impacted
soft tissue is entrapped between the an­ The evaluation is as follows: tooth in the vicinity the clinician
terior border of the ramus and the cusps tends to jump to a conclusion that
of the third molar, it leads to ulceration, History the pain is due to impacted tooth and
pain and trismus. Although the pain is A short relevant medical history and its surgical removal is undertaken.
due to the trauma from upper molars, physical examination is mandatory to But, the pain persists as the cause lies
at the sight of impacted mandibular rule out any associated medical disor­ in adjacent tooth. Similar erroneous
molars the clinician tends to jump to a der, which will adversely affect the out­ planning can occur in the cases of
conclusion that the pain is due impact­ come of the surgery. A thorough local crack tooth syndrome associated with
ed mandibular molar and often remove examination is carried out and following second molar. If the second molar is
them although they may not be the points are noted. treated endodontically, it becomes
actual cause of pain. In such cases, both • Age of the patient: as the age of brittle and can readily frac­ture dur­
the upper and lower third molars, which the patient increases (more than ing elevation of the third molar if
are non-functional and cause recurrent 40 years) the bones tend to become the elevator is not used pro­ perly.
TFO are indicated for surgical removal. more compact and loose their Similarly, the filling or pro­ sthesis
resilience. Thus, the simple looking on second molar may be dam­ag­ed
Fracture of the mandible impactions are more difficult to during luxation of the third molar.
Impacted teeth occupy lot of space in remove in an elderly patient due • Relation with the adjacent tooth—
the bone and undermine the bone, to the compact bone. The removal the relation of the third molar with
making the bone weak and vulnerable of impacted teeth in younger indi­ the adjacent tooth must be assessed.
to fracture, in case of trauma (Fig. 12.14). viduals is easier to remove as the The crown of the third molars, which
When the mandibular third mol­ars are bones are more resilient and elastic. are mesioangularly or horizontally
in normal position or have been remo­ • Presence of acute infection. impacted may lie below the height
ved earlier prophylactically, the bone at • Presence of trismus of contour of the second molar and
the angle region is no more weak and • Level of eruption of the tooth, i.e. may require odontectomy for its
the chances of subcondylar fractures whether it is erupted, partially eru­ safe removal without damaging the
following trauma are increased. The pted or unerupted. second molar. These teeth are also
fractures at the angle are easier to treat • Condition of the soft tissue around known to cause resorption of the
than the subcondylar fractures and the crown as the inflamed and con­ interdental bone and the roots of
thus, it is recommended by some auth­ gested tissue oozes during the sur­ the second molar, due to chronic
ors not to remove the third molars pro­ gery and the healing in such tissue is pressure. Removal of the interdental
phylactically (Duan D H et al. 2008). retarded. bone during surgery should be avo­
• The size of the tongue, hyper­ ided as it may lead to pocket form­
trophied buccal pad of fat, excessive ation, cemental sensitivity and caries.
salivation, exaggerated gag reflex • Associated diseases like oral submu­
should also be noted as these fac­ cous fibrosis not only restrict the
tors interfere with access and the mouth opening, but also render
conduct of the procedure. the oral mucosa stiff. The removal
• Condition of the crown, the non of third molars in such patients is
vitality, carious undermining of the difficult as the access is difficult and
crown tends to make it fragile and the forceful retraction may lead to
lead to unplanned fracture of the tearing of the stiff buccal mucosa
Fig. 12.14: Fracture of mandible at angle. crown during the surgery. The size and significant bleeding. This is a
Note the third molar is unerupted occupy­ of the crown should also be assessed common occurrence in the patients
ing space in the bone as bulky crown needs removal by from this part of the world.
228 Dentoalveolar Surgeries

A B C
Figs 12.15A to C: (A) Improper; (B and C) Proper radiographs

• Position of the tooth in relation to Related to Changes in the Roots


the external oblique ridge, adjacent
tooth, presence of divergent ramus, • Darkening of the root (radiolucent)
should also be evaluated to facilitate • Dark and bifid root
the decision regarding the incision, • Narrowing of the root
bone removal, odontectomy. • Deflected root.

Radiological Evaluation Related with Changes in the Canal


The radiological evaluation is very • Interruption (loss) of white line
crucial for the third molar surgery.15 A • Converging canal (narrowing)
good quality periapical X-ray should • Diverted canal
normally be adequate to evaluate the Fig. 12.16: Classical ‘Bull’s eye’ image of
third molars properly. However, if they impacted mandibular third molar when it is Tube Shift Technique (Clark’s
are placed very deep or posteriorly their in linguoversion
Rule;16 Buccal Object Rule)
complete visualization on the periapical
radiograph is not possible, in such cases canal—the inferior alveolar canal
(Figs 12.18A to F)
an extraoral X-ray like lateral oblique starts lingually near the foramen The rationale of this procedure is deri­
view or panoramic view of mandible as it goes inferiorly and anteriorly ved from the manner in which the
should be taken and the complete tooth towards the mental foramen; it relative positions of radiographic ima­
should be visualized (Figs 12.15A to C). gradually curls to the buccal side. ges of two separate objects change when
The impacted mandibular third molar Normally, the roots of the third the projection angle at which the images
will produce a classical ‘Bull’s eye’ molar are present buccal to the were made is changed.
image on periapical radiograph when it canal, however, as the X-rays are If the tube is shifted and directed at
is in linguoversion (Fig. 12.16). two dimensional pictures, due to the reference object (e.g. the apex of a
The findings that should be studied superimposition it will appear as if tooth) from a more mesial angulation
on the X-ray are: the roots are in very close proximity and the object in question also moves
• The size of the crown and roots. of the canal. In some cases the roots mesially with respect to the reference
• The number and form of the roots, are really in a very close proximity object, then the object lies lingual to
i.e. fused, conical, divergent, dilacer­ of the canal and if proper care is not the reference object. Alternatively, if the
ated, hypercementosed, etc. taken may lead to damage to the tube is shifted mesially and the object
• The relation with the adjacent tooth, nerve. To avoid such accidents the in question appears to move distally, it
resorption of the roots of the adja­ following points must be critically lies on the buccal aspect of the reference
cent tooth. observed on the X-ray. The relation object. These relations can be easily
• Any carious undermining of the of the apices with the canal could be remembered by the acronym SLOB:
crown which can make the tooth as follows as per the JP Rood criteria same-lingual, opposite-buccal. Thus, if
structure fragile. (Figs 12.17A to E): the object in question appears to move
• Presence of any periapical path­ology. in the same direction with respect to the
• Associated pathologies like cyst or reference structures as the X-ray tube, it
Related but not Involving
tumor. is on the lingual aspect of the reference
• Depth of the tooth in the bone and the Canal object, if it appears to move in the
its angulations. • Separated opposite direction as the X-ray tube, it is
• Relation of the apices of the root of • Adjacent on the buccal aspect. If it does not move
the third molar with inferior alveolar • Superimposed. with respect to the reference object,
Management of Impacted Teeth 229

A B C

D E
Figs 12.17A to E: (A) Darkening of the roots; (B and E) Loss of cortication of the canal; (C) Deflection of the canal; (D) Narrowing of the
roots; (E) Break in continuity of the canal (Rood’s JP criteria 19906)

it lies at the same depth (in the same


vertical plane) as the reference object.
Examination of a conventional set
of full-mouth films with this rule in
mind will demonstrate that the incisive
foramen in indeed lingual (palatal) to
the roots of the central incisors and the
A B
mental foramen is buccal to the roots of
the premolars. This procedure will assist
in determining the position of impacted
teeth, foreign objects or other abnormal
conditions. It works just as well as when
the X-ray machine is moved in the
vertical plane as in the horizontal plane.
As sometimes happens, the surgeon
may have two radiographs of a region
C D of the dentition that were made at
different angles, but there is no record
of the orientation of the X-ray machine.
Comparison of the image fields (i.e. the
changed positions of the bony anatomy
with respect to the teeth) will help
distinguish changes in horizontal or
vertical angulations. For instance, the
E F image of lateral incisor on an incisor
Figs 12.18A to F: Tube shift technique
view will be projected from the mesial
230 Dentoalveolar Surgeries

than it will on a canine view. Similarly,


the relative positions of the osseous
landmarks—such as the inferior border
of the zygomatic process of the maxilla
or the anterior border of the mandibular
ramus, with respect to the teeth will help
identify changes in horizontal or vertical
angulations. These two structures lie
buccal to the teeth and will appear to
move mesially as the beam is oriented
more from the distal. Similarly, as the
angulation of the beam is increased
vertically, the zygomatic process will be
projected occlusally over the teeth.
The cone beam CT is a very useful
A B
facility as it gives accurate information
Figs 12.19A and B: Proper draping of the patient
regarding the apices of the roots and the
position of the inferior alveolar canal.
good prophylaxis as the organisms cient duration of anesthesia. The surgery
Investigations causing contamination are gram- posi­ under general anesthesia is indicated
Investigations that are desirable before tive and come from oral flora. Higher when the patient is uncooperative, ap­
any elective surgery. A complete hemo­ antibiotics are usually not required prehensive, mentally retarded or when
gram, urinalysis and coagulation pro­­ unless specifically indicated or the he impacted tooth is very deep and may
file (BT, CT) are the minimum required patient is immunocompromised. Immu­ require long and extensive surgery. The
investigations. Other relevant investi­ nization against the tetanus may be surgical trolley should be thoughtfully
gations should be done, whenever done by giving 0.5 mL tetanus toxoid, arranged and all the required instru­
indicated in a particular case. intramuscular, for the patients who are ments should be properly arranged and
previously not immunized. The sedatives checked by the surgeon before he goes
Part Preparation may be prescribed a night before the for scrubbing (Fig. 12.20).
As the surgery is performed intraorally surgery, to ensure good rest to the patient There is no universal protocol for
the mouth preparation should be done and the surgeries should be scheduled in surgical removal of wisdom tooth as
to prevent infections. It comprises of sca­ the morning as the patient is fresh and every case is different and the require­
ling, eradicating any active septic focus, can tolerate stress better.18 The patients ment of every patient is variable. The
preoperatively. The patient is prescribed who are extremely apprehensive, pre­ preferences and opinions of the surgeons
antiseptic mouth wash like chlorhexi­dine medication with dia­zepam 5 to 10 mg are also variable. Some dental surgeons
or povidine iodine to reduce the count of orally half an hour before the surgery wait to see the impacted tooth becoming
microorganisms, at least 24 hours prior or intramuscularly 15 minutes before sympto­ matic, while the others have
to the surgery. The final intraoral and the surgery should be given to relieve preventive approach. The preventive
extraoral part preparation is done imme­ anxiety. Atropine sulfate, in a dose of treatment com­prises of:
diately preceding the surgery. The skin of 0.6 mg. IM (vagolytic action) is helpful • Germectomy20 in late childhood
the perioral area needs to be prepared as in reducing the salivary secretions and • Lateral trephination and removal
the surgeon and assistant touch it dur­ preventing bradycardia and thus, the during adolescent.
ing the retraction of the tissue and during vasovagal attack during the surgery. • A curative approach involves expo­
supporting the mandible, while the The surgical procedure in most of sure of crown if tooth has good
elevators are used. The final preparation the cases can be performed under local position
can be done using 5 percent povidone anesthesia, in a dental chair. If the sur­ – To prevent the anticipated com­
iodine solution. After the part is prepared, gery is expected to be prolonged then pli­cations due to the impacted
the surgical field is isolated by draping lidocaine with adrenaline is a good third molars.
(Figs 12.19A and B). choice. It may be further complimented
with administration of pentazocine lac­ Early Prophylactic Removal
Premedication17 tate 15 to 30 mg IM. Long acting local The early prophylactic removal of the
The patient should be prescribed pre­ anesthetics like bupivacaine19 (sensor­ impacted third molar is recommended
operative prophylactic antibiotics. The caine, marcaine) 0.5 percent is also a by some clinicians to prevent the possible
Beta-lactam group of antibiotics give good anesthetic agent, which gives suffi­ complications related to the impac­ted
Management of Impacted Teeth 231

• Patient motivation is not a problem.


However, it is very difficult to moti­
vate the patients to undergo prophylactic
surgical removal of the third molar as
they are totally asymptomatic. Most of
the third molars are removed only when
they become symptomatic.

Surgical procedure
The surgical procedure will be discussed
under the following heads:
• Incision, designing and reflection of
the flap
• Removal of the bone
• Odontectomy
• Preparation of the wound for closure
Fig. 12.20: Armamentarium for the third molar surgery • Suturing
• Postoperative care.

Designing of the Flap


third molar such as pain, recur­ rent •
Morbidity of periodontal tissue is While designing the flap all the basic
pericoronitis, development of pathol­ reduced. principles of flap designing must be
ogies, etc. it is also argued that if the followed. The incisions and flaps recom­
impacted third molars are removed late Disadvantages mended for the third molar surgery are:
Excellent clinical judgment and moti­ • Envelope flap (Fig. 12.21A)
the surgery is more difficult and surgical
complications can occur. On the other vation for extraction in early age is • Three cornered flap
hand removal of developing tooth bud challenging to clinician. – Ward I incision21 (Fig. 12.21B)
before the root formation is complete, – Ward II incision (Fig. 12.21C)
the removal is easy and in the younger Late Therapeutic Removal – Modified ward incision
age the bones have excellent elasticity – L shaped incision.
Disadvantage of Advancing Age
and facilitate the surgical procedure. The The ward I and II incisions are more
healing is also faster and uneventful in• Unfavorable and bizarre root mor­ commonly practiced. The vertical leg of
younger patients. pho­logy the incision is placed along the anterior
• Bone becomes brittle and sclerosed border of the ramus. The incision follows
Advantages • Healing is not satisfactory the anterior border of the anterior border
The early prophylactic removal is easy: • More amount bone removal is requ­ of ramus and is slightly lateral to it. If
• Root formation not complete ired the incision is placed lingually there are
• Pericoronal space is wide • More discomfort to patient. chances of damage to the lingual nerve
• Bone is more elastic in early age and the nutrient vessels in the retromolar
• Operative and postoperative com­ Advantages area. The length of the incision is decided
pli­­cations are less • Therapeutic removal is done to treat as per the requirement in a given case.
• Healing is uneventful inflammatory component. One centimeter length of the incision is

A B C
Figs 12.21A to C: (A) Envelope incision; (B) Ward I incision; (C) Ward II incision
232 Dentoalveolar Surgeries

usually adequate. If the incision is too can be reflected and protected from
long and lateral, there may be exposure of accidental injury due to a sharp object. It
the buccal pad of fat. If the tooth is erupted is mandatory to be in the subperiosteal
then the incision extends anteriorly in plane to avoid damage to the lingual
the gingival crevice of the third molar up nerve as it lies supraperiosteally and
to the distal aspect of the second molar. is safely reflected along with the flap.
In ward I incision the vertical relieving (Figs 12.23A and B). The second reason
incision is placed distal to the second for reflecting the lingual flap is that
molar and in ward II incision it is mesial the bone on the distolingual aspect
to the second molar, which inclines over (distolingual lock) of the impacted third
the buccal alveolar bone at an angle of molar should be removed to facilitate the
45 degree to the horizontal incision in luxation of the third molar and without
the gingival crevice. If the third molar raising the lingual flap the bone removal
is unerupted then the vertical incision is difficult.
directly starts from distal of the second
molar. While taking the vertical relieving Removal of Bone
Fig. 12.22: Austin’s retractor, traumatic
incision if the knife slips the facial artery and atraumatic used for retraction of the As the third molars are covered with
may get injured and profuse bleeding mucoperiosteal flap bone, to create the access it is removed.
may take place. To avoid such an accident The bone cutting can be done with the
a beginner must direct the knife from help of a bur and dental motor or with
the depth of the vestibule to the gingival the help of a chisel and mallet.23 The
margin and not the other way round. chisel and mallet is not a preferred
The incision must be full thickness method as better and more effective
and the tissues must be incised in one rotary instruments are available. The
stroke. The flap should be designed in use of the chisel and mallet evokes more
such a way that the access to the surgical anxiety in a patient operated under local
site should be direct and passive. The anesthesia. If the chisel and mallet is
proposed surgical defect must be taken used two vertical stop cuts are first made
into account and the suture line should at the anterior and posterior boundaries
rest on the healthy bone and cover and of the proposed bony defect and then
defect adequately. Small incisions do not the intervening bone is removed to
A
facilitate free and passive access to the prevent the splitting of the bone along
surgical site and forceful retractions of the bone grains. The chisel should be
the tissue is required which enhances the sharp and heavy mallet blows should be
tissue handling, tissue trauma and thus, avoided to prevent fracture of the bone.
more postoperative edema. It is incorrect The chisel must have a good purchase
to think that the shorter incisions are less on the bone to prevent its slipping and
traumatic or they heal faster than the a guard must be kept to prevent damage
long incisions. The healing across the to the soft tissue. The mandible must be
incision is a simultaneous process and is supported, while applying the mallet
not affected by the length of the incision. B blows to prevent dislocation.
The degloving incision is recommended Figs 12.23A and B: Flap reflection—show­ The sharp stainless steel or carbide
only for the teeth, which are very deep ing reflection of (A) Buccal; (B) Lingual flaps burs should be used for the bone cutting.
in the bone or for lateral trephnization The diamond burs are not recommen­
procedure.22 the subperiosteal plane, without lacer­ ded for bone cutting as they do abrasive
The flap is reflected with the help ating the periosteum. The buccal flap cutting, generate more heat and the
of the sharp periosteal elevator as a full can be retracted using the Austin’s chances of the bone necrosis are more.
thickness mucoperiosteal flap. If any retractor to gain good access and prevent High speed cutting is not used as more
adhesions are present, they should be its laceration during the surgery due heat is produced and bone necrosis can
released with sharp dissection as it is less to injuries from burs and other sharp take place due to damage to osteocytes
traumatic and reduce tissue handling. instruments (Fig. 12.22). Many clinicians and release of alkaline phosphatase.
During the third molar surgery, do not prefer to raise the lingual flap The ideal speed of the bur should be
usually the buccal access is taken as the due to apprehension of lingual nerve 18000 to 20000 RPM and the motor
lingual split technique is complicated. damage. However, it is safe to reflect should have good torque to facilitate
the buccal flap is raised, necessarily in the lingual flap as well, as the tissue the bone removal at the lower speed.
Management of Impacted Teeth 233

Use of air rotors is contraindicated not is getting locked during the elevation. that “tooth belongs to surgeon and bone
only for the above reason, but due to The bone removal done blindly will belongs to patient” must be followed. As
the chances of surgical emphysema as invariably lead to unnecessary and the tooth is to be discarded it can be cut
air under pressure can enter in the open excessive bone removal. When the tooth as per the need but bone is precious and
tissue planes. During the bone cutting is placed deep in the bone, horizontally need to be dealt judiciously. If the tooth
with the help of a bur, first round bur is or mesioangularly impacted, the crown is sectioned in a planned manner the
used to mark the incision and then the is bulbous and lies very close and below operator will have good control over the
fissure bur is used. The round bur gets the height of contour of the second remaining portion of the roots and will
good purchase on the bone and does molar, it is advisable to split the crown be able to remove them with ease than
not slip. The soft tissues are protected by in pieces rather than doing excessive removing the fragments of the tooth,
retraction and by placing guard. Copious bone cutting or damaging the adjacent which fractures haphazardly during the
irrigation with normal saline is done tooth or bone. forceful elevation. The indications for
during the bone cutting to dissipate the After the removal of the bone a odontectomy are:
heat and to flush the bone particles to purchase point or groove is prepared • Large bulbous crown.
prevent the clogging of the bur.24 on the third molar for engaging the tip • Deep horizontal or mesioangular
The bone is removed judiciously as of the elevator. The purchase groove impactions.
the bone is to be preserved. The tooth should not be very superficial as proper • Disto angular impactions with plenty
is to be sacrificed and thus, the tooth purchase may not be obtained. It should of bone cover.
should be sectioned and removed be made with plenty of margin of tooth • Unfavorable root form like divergent,
in pieces to prevent excessive bone structure or else the thin tooth structure locking or dilacerated roots.
cutting. The bone in the area is weak due will fracture when the force is applied • Hyper cementosed roots.
to the reasons already discussed. It is with an elevator. The elevator should • Roots in close proximity of the
buttressed by the external oblique ridge not be wedged between the second inferior alveolar canal.
and if the excessive bone is removed and third molar for creating purchase • Badly carious and fragile tooth struc­
from this area it is rendered weaker and as the second molar may get damaged. ture.
may fracture during the surgery. The The bone in the younger individuals The other advantage of the odon­
bone removal should be just enough to is elastic and resilient and yields to the tectomy is that after the crown is sec­
expose the crown up to the CE junction pressure easily and thus, the younger tioned and removed it creates a space
(Figs 12.24A and B). The bone in the individuals the tooth can be easily for delivering/removal of the roots. This
distolingual area usually prevents the elevated and removed. The similar kind avoids the rotation of the roots in the
elevation of the tooth (distolingual of tooth will not be easily elevated in the bone, while elevating the tooth and pre­
lock) and hence, should be removed older patient as the bone tends to be vents the damage to the inferior alveolar
carefully. Usually the bone is removed more compact and brittle. nerve (Figs 12.25A to C). The odontec­
distobucally to expose the crown tomy may be performed with the help
and facilitates the application of the of the burs or sharp chisels. If straight
Odontectomy
elevator; it is called preparation of hand piece does not facilitate proper
the distobuccal gutter (Moore Gilby’s The splitting of the crown of the tooth is access then contra angled or modified
collar technique). The bone must be called odontectomy. It is done to facilitate contra angled handpiece may be used.
removed under the direct vision and removal of the tooth in pieces without The odontectomy cuts are marked with
after carefully observing where the tooth excessive bone cutting. The dictum stainless steel or carbide burs. The use
of diamond bur is very convenient for
this purpose. It is not necessary to split
the tooth by taking a full thickness cuts
with the help of bur. The tooth is split up
to two third of its thickness with the bur
and the remaining portion may be split
with a chisel or with the help of an eleva­
tor wedged in the cut and giving slight
leve­rage to fracture the remaining por­
tion. The tooth may be split in two, three
or four pieces, as shown in the figure,
depending upon the requirement in an
A B individual case7 (Figs 12.26A to E).
Figs 12.24A and B: (A) Bone removal for vertically impacted tooth; (B) Bone removal for Many a times in spite of all pre­
horizontally impacted tooth cautions the apical third of the root
234 Dentoalveolar Surgeries

A B C
Figs 12.25A to C: Arc of rotation of the third molar while elevation resulting in the damage to the nerve, odontectomy avoids the
damage to the nerve

Figs 12.26A to E: (A) Odontectomy for vertically


impacted tooth; (B) Odontectomy for mesioangularly
impacted tooth; (C) Odontec­tomy for distoangularly
impacted tooth; (D) Odontectomy for horizontally
E impacted tooth; (E) Odontectomy specimen
Management of Impacted Teeth 235

fractures, while delivering the roots. lining. The foreign bodies are picked Follow-up
Purposefully leaving the root fragment, up and the granulation tissue and the The patient is called periodically for the
root tip does not necessarily mean the residual cystic lining are curetted. The follow-up. The first visit is preferably
negligence of surgeon, but it could be alveolar bone margins are palpated and on subsequent day wherein apart from
deliberate decision and as a part of any loose bony fragments, devoid of edema, pain, trismus, wound condition
standard care.25 periosteal attachment, which can turn the evaluation of the lingual and
non-vital are removed. The sharp bony inferior alveolar nerves is carried out.
Criteria for Leaving the Root margins are filed off and made smooth The neurological evaluation is planned
Fragment as they can interfere with the healing by on first postoperative day because the
• When the root is free of any peria­ inducing irritation and inflammation of effect of local anesthesia totally wanes
pical pathology, which is true in the flap. Any lacerated margins of the off by then and early detection and
majority of cases of impacted third flap are carefully trimmed as they can get explanation to the patient can be done,
molars. necrosed and result in the dehiscence of if the neurological deficit is present. The
• When there is possibility of damage the wound. When the impacted third neurological examination is done by
to the vital structures, while attem­ molar is partially erupted in the oral assessing the perception of fine touch,
pting the removal of the root frag­ cavity, the gingival margin around it has prick and two point discrimination.
ments. reduplicated epithelial edge (gingival Similarly the taste sensation on the
• If the root is inaccessible to direct cuff ). It should be freshened up by exc­ tongue can also be ascertained.
vision or reflected vision with the is­ing the margin as the epithelium to
mouth mirror or when the root is epithelium contact can prevent healing. Postoperative Care
likely to be displaced in an inacces­ A pressure pack is given postoperatively,
sible area where it is going to be very Suturing which should be maintained for about an
difficult to remove. The closure of the prepared surgical hour to achieve adequate hemostasis. In
• If it is a minor fragment of about wound is done with 3’0’ silk or vicryl the immediate postoperative phase the
5 mm length. suture. The simple interrupted sutures vascular phase of the inflammation is
Usually the root tips remain harmless are placed. The first suture that should predominant which is characterized by
in and should be observed periodically be placed is the suture at the distal vasodilatation and increased capillary
for detecting any pathological changes end of the second molar, because if permeability. This leads to formation
in the bone and undergo some degree of there is dehiscence in the suture line, of inflammatory edema. To prevent the
resorption. As the alveolar bone recedes distal pocket formation will take place excessive edema formation, cold com­
following the removal of the tooth the with the second molar and recurrent pressions are advised, intermittently for
fragments often become superficial periodontal complications can occur. first 24 hours. The application of cold
and their removal becomes easy sub­ The sutures should not be placed too induces vasoconstriction and prevents
sequently, however this takes a long tightly, as it can result in strangulation excessive edema. The edema leads to
time. If the root becomes symptomatic of the wound edges and avascular raised interstitial fluid pressure, com­
due to infection, the root fragment necrosis of the wound edges leading pression of lymphatics, capillaries and
becomes loose due to inflammatory dehiscence. The tight closure will pre­ venules, stasis of circulation and may
process and its tracking and removal vent decompression of the wound and retard healing. The excessive edema
becomes easy. If the root fragment is left lead to excessive inflammatory edema. distends the tissue and generates
it must be informed to the patient. Hence, the sutures should be placed tension across the suture line, which
loosely. The purpose of the suture is can lead to dehiscence of the wound.
Debridement and Preparation to approximate the tissue and not to To reduce the edema and to correct
of the Wound for Closure achieve the water tight closure. The the stasis of circulation, the patient is
The key words to be remembered after sutures should be equidistant and prescribed anti-inflammatory drugs.
the tooth has been extracted are ‘see, should exert uniform pressure on the One should not heavily rely on the
feel and freshen, close’. The wound wound edge, throughout the length of drugs but, simpler things like warm
is thoroughly prepared for closure. the incision. The knots should be placed saline gargles and Glycerin-magnesium
The area is packed to achieve initial on one side and not on the incision line. sulfate dressings, given extra­ orally
hemostasis and then thoroughly inspec­ The sutures are removed on the seventh can be very helpful. The warm saline
ted for the presence of any foreign bodies postoperative day. Figures 12.27A to J gargles improve the circulation by
like fragments of the tooth, loose bony illu­strates step-by-step tech­ni­que for inducing vasodilatation and facilitate
fragments, granulation tissue or any the removal of an impacted mandibular the reabsorption of the interstitial
periapical pathological tissue like cystic third molar. fluid, thus reducing interstitial fluid
236 Dentoalveolar Surgeries

A B C

D E F

G H I J
Figs 12.27A to J: Step-by-step procedure for removal of impacted third molar: (A) Preoperative clinical photograph; (B) OPG; (C) Ward I
incision; (D) Reflection of the flap; (E) Removal of the bone by Gillby collar technique; (F) Odontectomy; (G) After odontectomy; (H) Removal
of the complete tooth; (I) Loose suturing; (J) Odontectomy specimen

pressure. The glycerin magnesium sul­ 24 hours, as by this time the vascular prescribed antibiotics and analgesics
fate dressing is hygroscopic in nature stage of inflammation settles and apart from anti-inflammatory drugs.
and thus draws the fluid across the cellular stage starts which is important Normally the edema increases up to
skin, which acts like a semipermeable to prevent infection and promote first 48 to 72 hours and then gradually
membrane. The reaction of glycerin healing. The use of steroids as anti- starts receding. The oral hygiene and
with magnesium sulfate is exothermic infla­mmatory drug has been mentioned the wound hygiene are maintained by
and works as hot fermen­ tations and in the literature and some clinicians antiseptic gargles using chlorhexidine or
induces vasodilatation and improves do recommend them but, it must be povidone iodine solution or by toileting
the circulation. The warm saline gargles remem­ bered that simpler things like (irrigation) of the wound with normal
have dual effect the warmth induces tissue respect (less tissue handling), saline solution. The patient obviously has
vasodilatation and improves the cir­ ­ sound surgical technique, less bone trismus, edema and pain and discomfort
culation, reduces stasis, mucosal con­ trauma, good wound preparation before postoperatively. The movements of
gestion, improves local drug delivery closure, loose sutures, aseptic techni­ jaw will further aggravate the pain and
and ensures that humoral factors nece­ que help in reducing the changes of discomfort, hence, the patient is pre­
ssary for promoting healing reach generation of excessive edema. The scribed soft and semisolid diet.
the site. The saline solution has more measures mentioned above help in
tonicity than the tissue fluid and thus, preventing and reducing the edema Alternative Technique
draws the fluid from the tissue across and should be tried rather than opting The above mentioned technique is a
the muc­osa. This should be done after for steroid therapy. The patient is standard surgical technique. As the
Management of Impacted Teeth 237

third molar is situated in the lingual placed to facilitate the drainage of spreads to ptery­ gomandibular or
shelf of bone, which is thin, William inflammatory exudates and collected buccal spaces. The incidence of
Kelsyfry recommended “Lingual split blood. The edema resolves fast in infection following the removal of
technique”.26 According to him it is easy, 72 hours and no vigorous treatment is third molars is very low.10
less traumatic to remove the thin lingual warranted. The other interventions • Osteomyelitis
bone and deliver the tooth lingually. In necessary to reduce the inflamm­ a­ • Fracture of the alveolar bone, espe­
this technique a good bucco-lingual flaps tory edema are discussed earlier. cially the lingual cortical plate
are raised. After guarding the lingual The suture line of vertical reliving • Fracture of the jaw—due to injudi­
soft tissues adequately, the lingual incision of Ward incision which cious application of excessive force
cortical bone is removed and the tooth rests on the alveolar bone may be with heavy elevators and injudi­cious
is delivered lingually. This technique left open without suturing to ensure bone removal.
is difficult to master and the chances of decompression and it helps in redu­ • Damage to the lingual nerve—the
lingual nerve damage are more. c­ing the edema. lingual nerve damage results from
• Trismus: The trismus is usually a injury to the lingual nerve due to
Coronectomy temporary phenomenon secondary fracture of the lingual cortical plate,
The removal of crown of the impacted to protective muscle spasm, secon­ sharp instruments or slipping of the
tooth and leaving behind the roots is a dary to pain at the site of surgery and burs. The taste fibers are relayed
procedure described as coronectomy. gets relieved within 4 to 5 days. But in the lingual nerve from chorda
It is indicated in the cases where the if it is severe and persists longer it tympani nerve and once they are
third molars are deep (position C) could be due to injury to the tendon damaged, the taste sensations are
and the roots are in proximity with the of temporalis muscle or injury to the very seldom restored.
inferior alveolar nerve. To prevent the medial pterygoid muscle or ligaments • Hemorrhage—damage to the facial
damge to the nerve it is recommended during the administration of the artery, inferior alveolar artery.
that the crown should be excised and inferior alveolar nerve block. If the • Dislodgements of the tooth in the
the roots should be left behind. As surgery is prolonged or if the lower sublingual space.
the tooth becomes non-functional jaw is not adequately supported • Damage to the second molar—distal
the roots become resorbed and with during elevation of the tooth, the pocket formation, sensitivity due to
the resorption of the alveolar bone and TMJ can get strained and arthritis can exposure of the root, luxation fracture.
its remodeling, they become superficial result leading to trismus, pain during
and are easy to remove and the chances mandibular movements and the Maxillary Canine
of damage to the inferior alveolar nerve tenderness over the joint. Such cases
are minimized. It is practiced with often require extended medicinal
Impactions
variable success by many clinicians. treatment with anti-inflammatory
The complications with this technique drugs and physiotherapy. The phy­ Introduction
could be infection and development of siotherapy comprises of short wave The permanent maxillary canines are
pathology with the re­tained root could diathermy, forceful jaw opening developed deep within the maxilla,
be late complication. using mouth gags after the acute complete their development late and
stage has subsided, followed by jaw emerge into the oral cavity after the
Complications of third exercises. neighboring teeth have erupted. Due
• Dry socket: The details of this to these circumstances, eruption dis­
molar surgery condition are described under the turbances are more common with
• Edema: Certain amount of inflam­m­ exodontias. maxillary canines than with other teeth,
atory edema is a normal occurrence • Infection: The infection could be except for third molars.
after the third molar surgery. The the exacerbation of the previous Mineralization of the primary canine
excessive edema is as a result of pericoronitis, which was not ade­ starts at 4 to 12 months of age and is
excessive tissue handling, excessive qua­­tely resolved or the infection complete by 6 to 7 years of age. Tooth
bone cutting, bone necrosis, tight acquired postoperatively. If the local germs are in close contact with apices of
wound closure preventing the signs of infection like congestion, primary canine as well as lateral incisor
drain­age of exudate or as a result of purulent discharge are evident in the and first premolar. During eruption the
secondary infection. wound, one suture may be removed canine moves down along the distal
The edema can be prevented by to decompress/drain the infective aspect of the lateral incisor, not in very
ensuring that the tissue is handled mate­ rial to prevent its spread. As close contact with it.
judiciously, bone is cooled dur­ the tissues are dissected during the Clinically, palpation of the buccal
ing removal with copious saline surgery and the anatomical barriers surface of the alveolar process distal
irrigation and the sutures are loosely are broken the infection rapidly to the lateral incisor may reveal the
238 Dentoalveolar Surgeries

position of the maxillary canine about 1 • Trauma, due to partial destruction • No treatment
to 1/2 years before its emergence. Dur­ of follicle and subsequent develop­ • Prophylactic space augmentation
ing the active phases of eruption, i.e. 1 to ment of ankylosis of tooth. • Extraction of primary canine (guided
2 years before oral emergence, the width eruption)
of the dental follicle increases, whereas • Surgical exposure and orthodontic
Diagnostic aids
the size of the follicle decreases in cases repositioning
of impacted teeth. Clinical inspection and palpation of the • Surgical repositioning-not useful
alveolar process in the canine region • Removal of canine.
Incidence should be performed every year from
The prevalence of non-eruption or ec­ the age of 8 years. Clinical examination
No treatment
topic eruption of maxillary canine is should include an evaluation of num­
reported to a range from 0.8 to 2.3 per­ ber of permanent teeth in position Few cases of initially ectopic positioned
cent. It is seen with a higher frequency and inclination of incisors as well as canines spontaneously upright and
in females as compared to males. Most asymmetries between eruption patterns show a normal eruption. The most
commonly, it is found unilaterally. The between both sides and its correlation common complication in absence of this
most common position of the impacted with age and somatic maturity. spontaneous correction is development
canine is palatal to the lateral incisor. In The alveolar process must be palpa­ of a follicular cyst. So also, development
only 15 percent of the cases the direction ted from both buccal and palatal sides to of odontogenic tumors from the follicle
of impaction is seen buccally. feel for the canine bulge. Normally a bulge is rarely seen. There is loss of attach­
appears in the buccal sulcus in the canine ment of the neighboring teeth with
Etiology27,28 region 1 to 1/2 years before eruption.29 which the impacted canine is in close
• Space loss: It can occur in dentition If the canine bulge cannot be pal­ approximation.
with severe crowding, but most fre­ pated between 8 and 10 years, a radio­
quently it is seen in dentitions with­ graphic investigation is indicated. A Prophylactic Space
out crowding. normal IOPA and occlusal radiograph Augmentation
• Ectopic position of tooth germ. must be taken to study the canine form Elimination of crowding in the dental
• Delayed resorption of root of and position. arch to make room for the eruption of
primary canine: It is most commonly the impacted canines in some cases may
a sequlae of impacted canine rather stimulate eruption.
Classification
than being an etiologic factor.
• Lack of guidance from gubernacu­ • Class I: Impacted canine located in Extraction of Primary Canine
lar canal: If the gubernacular canal the palate: Extraction of primary canines is carri­
does not widen normally during – Horizontal ed out to align a palatally erupting
develop­ment or if there is an oblit­ – Vertical maxillary canine wherein there is no
eration of the canal, impaction may – Semi-vertical. resorption of the incisor. This technique
result. • Class II: Impacted canine located in shows less favorable results with ectopic
• Root tip deflection. the buccal side: permanent canines.
• Heredity: An autosomal recessive – Horizontal
trait has been suggested for canine – Vertical Exposure and Orthodontic
impactions. – Semi-vertical. Repositioning
• Space augmentation: In cases of • Class III: Impacted canines located This is usually the treatment of choice
excessive space availability, the guid­ in both palatal as well as buccal in cases of ectopic positioning and
ance of the root of lateral incisor for alveolar bone. normally leads to a predictable and suc­
eruption of the canine is not avail­ • Class IV: Impacted canines located cessful result. However, the prognosis
able and may result into impaction. vertically between incisors and pre­ for orthodontic correction depends
• Obstruction to eruption pathway: molars. on several factors including age, space
The eruption may be prevented by • Class V: Impacted canines located conditions and sagittal and transverse
presence of supernumerary teeth and in edentulous maxilla. position of the canine crown and root.
odontomas. In addition; increased Even if there is a dentigerous cyst asso­
bone density, narrowed alveolar pro­ Management ciated with an impacted canine and the
cess and excessive fibrous mucosa Numerous treatment options exist for canine is in favorable position and likely
may restrict eruption of canine. the ectopically erupting or impacted to erupt in oral cavity, marsu­pialization of
• Cleft lip and palate cases. canines. These include: the cyst is carried to conserve the canine.
Management of Impacted Teeth 239

Surgical Removal bulge of the crown is located and a Impacted Maxillary


Surgical technique varies with the posi­ small access hole is made to visualize
tion of the canine. Either a labial or the crown and it is enlarged to uncover
Third Molar
palatal approach is used according to the entire crown and a part of the root.
the position of the crown. Damage to The crown is sectioned and elevated out. Introduction
adjacent tooth roots should be avoided. A purchase point is created in the root The maxillary third molar starts its
Labially positioned canines are and it is elevated out. Socket is irrigated development at the cervical neck of
accessed by raising a semilunar flap or and flap repositioned (Figs 12.29 and the second molar and with the occlusal
marginal flap according to the position of 12.30). When the tooth is placed in class surface facing posteriorly. Start of mine­
the crown. Pericoronal bone is removed III position a combined buccal and ralization can be seen radio­graphically
with burs/chisel until the widest part palatal approach is taken first the buccal at 8 to 10 years of age. The posteriorly
of the crown and half of the root has flap is raised and through the access tilted tooth gradually uprights during
been uncovered. Then the crown can be created in the bone the root is sectioned further crown and root formation and
sectioned and elevated out. A purchase from the crown and delivered buccally ends up with its axis being almost
point is created in the root and it is and then the crown is removed through vertical. Maxillary third molars erupt
elevated out. Socket is irrigated and flap the palatal access (Figs 12.31A to K). at approximate age of 20 years, being
repositioned (Figs 12.28A to F). 6 months late in females than males.
Palatally positioned crown is acce­ Complications However, extraction of any tooth ante­
ssed from palatal side. A palatal flap • Perforation of maxillary sinus floor rior to it, results in advancement of
is raised from premolar to premolar. forming an oroantral com­ muni­ eruption by 1.4 years and 1.3 years in
Palatal gingiva can be spared by giv­ cation. males and females, respectively.
ing an incision a few millimeters from • Perforation of nasal floor forming an The maxillary third molars are often
the marginal gingiva. Release incision oronasal communication. seen erupted in buccoversion. This
should be avoided on the palatal side • Hemorrhage from greater Palatine position results into impingement of the
to avoid damage to the greater palatine artery due to accidental damage, soft tissue between the cusps of the tooth
neurovascular bundle. However, a mid­ while using palatal approach. and the anterior border of coronoid
line palatal relieving incision can be • Damage to adjacent tooth roots process leading to traumatic ulcers and
given to manage unilateral impacted from bur/chisel or application of recurrent pain. The selective cuspal
canine. Once the palatal flap is raised, excessive forces with elevator. grinding of the third molar relieves the
trauma from occlusion temporarily. If
the clinician is not alert, it is observed
that many a times this condition is
labeled as pain due to pericoronitis
with mandibular third molars and the
lower third molars are subjected to
surgical removal. Sometimes the oper­
culum of the impacted mandibular
third molar is traumatized by the
upper third molar leading to pain. It is
therefore recommended that the exami­
nation of the third molar should be
A B comprehensive and both the upper and
lower third molars should be thoroughly
evaluated together. If one of the third
molars is in a non-functional position
and unlikely to be corrected in normal
functional position and if there is no
other consideration for their retention
the decision needs to be taken for their
removal simultaneously because if one
tooth is removed the other becomes
non-functional and supraerupts to
C D E F cause trauma from occlusion, abnor­
Figs 12.28A to F: Labial approach (Source: Archer HW, 1966) mal contact with adjacent tooth, food
240 Dentoalveolar Surgeries

A B C

Figs 12.29A to E: Palatal appro­


ach for unilateral impacted can­
D E ine (Source: Archer HW, 1966)

A B C

D E F

G H I
Figs 12.30A to I: Palatal approach with tooth sectioning (Source: Archer HW, 1966)
Management of Impacted Teeth 241

the age of 20 years although malposi­


tion and its sequelae are less frequent
in maxilla than mandible. The pan­
oramic radiograph is used frequently
for screening the patient for presence of
impacted maxillary third molars. How­
A B C ever, IOPA, oblique occlusal views are
also used for preoperative assessment
of the maxillary third molars. However,
no imaging technique can predict the
possibility of complications such as tu­
berosity fracture and perforation into
the maxillary sinus.

D E F Treatment
The treatment modalities for manage­
ment of impacted maxillary third molars
are:
• No treatment
• Surgical exposure
• Guidance into mesial eruption path
G H I • Surgical removal.

No Treatment
Treatment of a maxillary impacted third
molar can be deferred for some time in
any of the following two conditions.
Firstly, the tooth is so deeply impact­
J K ed that progression of marginal peri­
Figs 12.31A to K: Surgical approach for removing Class III impacted canine odontal inflammation from adjacent
2nd molar is not likely to occur.
Secondly, it can be left as it is when
impaction, caries or periodontal prob­ – Distoangular there is no radiographic sign of patho­
lems, subsequently. – Inverted logic changes such as cyst, tumors aris­
– Linguoangular ing from the impacted teeth.
Classification1 – Buccoangular
• Based on relative depth in bone These may also occur in bucco­ Surgical Exposure
(Figs 12.32A to C) version, linguoversion and torsover­ It is done very rarely, only if there is a
Class A: Lowest portion of the crown sion. need for functional third molars. In this
is in level with or below the occlusal • Based on relation to Sinus procedure, the mucosa covering the
surface of the maxillary second molar – Sinus approximation (SA): No crown is removed to allow for spontane­
Class B: Lowest portion of the crown bone or a thin partition of bone ous eruption of the molar.
is in between level of occlusal surface between impacted maxillary
and cervical line of the maxillary third molar and maxillary sinus. Guidance into a Mesial
second molar – No-sinus approximation (NSA): Eruption Path
Class C: Lowest portion of the crown 2 mm or more bone is present It is carried out if the prognosis of the
is at or above the cervical line of the between impacted maxillary second molar is poor and it is doubtful
maxillary second molar. third molar and maxillary sinus. that the 2nd molar will serve purpose for
• Based on position of long axis with a long time. In this procedure, the 2nd
relation to second molar: molar is extracted and the third molar
Diagnosis
– Vertical is allowed to erupt normally. It is found
– Horizontal The presence and position of maxillary that the 3rd molar will drift anteriorly
– Mesioangular third molars should be evaluated before such that it erupts upto the occlusal
242 Dentoalveolar Surgeries

C
Figs 12.32A to C: Classification of the impacted maxillary third molars.1 (A) Class-A; (B) Class B; (C) Class C
(Source: Archer WH. Oral and Maxillofacial Surgery, 5th edn.,1975. WB Saunders Co., Philadelphia).

level and achieves a normal proximal whether a buccal or palatal approach is gingival sulcus of the 2nd molar and
contact with the 1st molar. used. They include the following: 1st molar if required.
• Buccal sulcular incision: This inci­ • Buccal sulcular incision with vesti­
Surgical Removal sion starts from the distal part of the bular extension: This is similar
Several incisions can be used for removal tuberosity upto the distal surface of to the previous flap with the only
of the impacted 3rd molars based on the the 2nd molar and extends in the difference of having an additional
Management of Impacted Teeth 243

bur is less and the chances of injuring


the flap are more. Instead, a bone frac­
turing technique using a periosteal ele­
vator or chisel can be employed safely
(Figs 12.34A to F).
A B The tooth is then elevated out of
the socket by placing elevators mesio­
buccally between the 2nd and 3rd mo­
lars. The force is applied in the distal
and lateral direction with the retractor
placed distally to guard against the tooth
slipping into the pterygopalatine fossa.
C D E
In cases of divergent roots it might
be necessary to section the roots to
Figs 12.33A to E: Removal of the third molar by Buccal approach1 (1, 2, 3 depicts the
sites for placement of the three sutures) facilitate the elevation of the roots
separately. In case the tuberosity is
fractured, it should be repositioned
with the fingers and suturing done to
maintain the position.

Complications
• Resistance to removal: Resistance
to distobuccal removal is usually due
to a divergent palatal root. This can
be avoided by sectioning of the roots.
• Herniation of buccal fat pad
into surgical site: This complica­
tion arises due to damage to the
A B C
flap by burs or instrument slip­
page. The extruded fat can be re­
positioned or excised. However,
entire fat pad should not be removed.
• Displacement of tooth into infra­
temporal fossa: It can occur if distal
guard is not kept. The incision is
enlarged distally, to locate and ret­
rieve the tooth.
• Displacement into the sinus: This
may occur in sinus approximation
D E F impactions due to deficient bone in
Figs 12.34A to F: Removal of the third molar by Palatal approach1 (Source: Archer WH. the floor of the sinus. The tooth can
Oral and Maxillofacial Surgery, 5th edn., 1975. WB Saunders Co., Philadelphia) be retrieved by accessing the sinus
through the Caldwell Luc’s approach.
• Hemorrhage: Hemorrhage may
release incision at the anterior end of the tooth and surrounding bone easily. occur due to damage to posterior
the sulcular incision at 45° extending The most common direction of removal superior alveolar artery or the
onto the attached gingiva on the of the 3rd molar is distobuccal. Usually pterygoid plexus of veins.
buccal sulcus (Figs 12.33A to E). only a thin cortical plate covers the • Fracture of the tuberosity: It may
• Palatal incision: A palatal sulcular impacted maxillary tooth. Hence, most happen due to enlargement of sinus
incision is made from the distal of commonly bone covering the buccal into the tuberosity or divergent
the tuberosity to the mesial of the 1st and distal surface of the 3rd molar is roots of the 3rd molar (Fig. 12.35).
molar. removed with either with the periosteal Management of this complication
A mucoperiosteal flap is raised elevator, unibeveled chisel or a surgical can be by three ways:
irrespective of the incision and approach bur. The bur should be used cautiously 1. Immediate excision of the tube­
used. The flap is retracted to visualize as the space available for operating the rosity results into formation of
244 Dentoalveolar Surgeries

in clinical practice. Sb Ved Pr Lek Fak 17. Mehran Mehrabi. Therapeutic Agents
Karlovy Univerzity Hradci Kralove in Perioperative Third Molar Surgical
Suppl. 1974;17(5):451-65. Procedures. 2007;19(1):69-84.
5. Roman JF, Fernandez P, Moreno V, 18. Barclay JK. Diazepam and lorazepam
et al. The mechanical behaviour of hu­ compared as sedatives for outpatient
man mandibles studied by electronic third molar surgery. British Journal of
speckle pattern interferometry. Eur J Oral Surgery. 1980;18(2):41-9.
Orthod 21. 1999;413-21. 19. Sharif Nayyar M, Bupivacaine as
6. Rud J. Third molar surgery: relationship pre-emptive analgesia in third molar
of root to mandibular canal and injuries surgery: Randomised controlled trial.
to inferior dental nerve. Danish Dent J. British Journal of Oral and Maxillofacial
1983;87:619-31. Surgery. 2006;44(6):501-3.
7. Fonseca RJ. Surgical management of im­ 20. Matteo Chiapasco. Germectomy or de­
pacted teeth: oral and maxillofacial sur­ layed removal of mandibular impacted
Fig. 12.35: Specimen showing fractured gery, vol-1. 1st edn, Philadelphia, Penn­ third molars: The relation­ship between
tuberosity during maxillary third molar ex­ sylvania. Saunders comp, 2000.pp.256-9. age and incidence of complications.
traction
8. Winter GB. Principles of exodontia as 1995;53(4):418-22.
applied to the impacted mandibular 21. Ward TG. The split bone technique for
oroantral communication and third molar. St Louis (MO): American removal of lower third molars. Br Dent
this should be closed primarily. Medical Book Co; 1926. J. 1956;101:297.
2. Removal of third molar from 9. Pell GJ, Gregory GT. Impacted 22. Peter D. Waite Soft Tissue Incision De­
mobile tuberosity is performed mandibular third molars: classification sign. Symposium on Strategies Affecting
by sectioning the roots and con­ and modified technique for removal. the Outcome of Third Molar Surgery.
trolled removal of bone from the Dent Dig. 1933;39:330-8. Journal of Oral and Maxillofacial Sur­
tuberosity. The mobile tuberosity 10. Liedholm R, Knutsson K, Lysell L, gery. 2007;65(9): (Suppl), pp. 1-120.
is supported with finger pressure et al. Mandibular 3rd molars: Oral 23. Miloro M, Ghali GE, Larsen PE,
and primary suturing is done. surgeons assessment of the indications Waite PD. Impacted teeth: Peterson’s
3. Immobilization until bony heal­ for removal. British journal of OMFS. Principles of Oral and maxillofacial
ing and tooth removal is done 1999;37:440-3. surgery. 2nd edn. London, BC Decker
when prevention of oroantral fis­ 11. Gill Y, Scully C. British oral and maxil­ Inc. 2004.p.145.
tula may not be possible with the lofacial surgeons’ views on the aetiol­ 24. Sweet JB, Butler DP, Drager JL. Effects
previous two techniques. In this ogy and management of acute peri­ of lavage techniques with third molar
method the surgical procedure is coronitis. Br J Oral Maxillofac Surg. surgery. Oral Surg Oral Med Oral
stopped and tuberosity is immo­ 1991;29(3):180-22. Pathol. 1976;41(2):152-68.
bilized and the wound is closed 12. Guven O, Keskin A, Akal UK. The 25. Bowdler Henry C. Prophylactic odon­
with sutures. Fracture is allowed incidence of cysts and tumors around tectomy of the developing mandibular
to heal for 2 to 6 months after impacted third molars, International third molar : A new operation. Ameri­
which transalveolar extraction journal OMFS. 2000;29:131-5. can Journal of Orthodontics and Oral
is performed. However, it takes a 13. Henry C. Bowdler, Prophylactic Odon­ Surgery. 1938 ;24(1):72-84.
prolonged treatment time. tectomy of the Developing Mandibular 26. Ward TG. The Split Bone Technique
Third Molar. Am J Orthodontics and for Removal of Lower Third Molars. Br
Oral Surg. 1938;29:72. Dent J. 1956;101:297-304.
References
14. Shriniwasan B. Impacted teeth: Text 27. Marks SC Jr, Schroeder HE, Andreasen
1. Archer WH. Oral and Maxillofacial book of oral and Maxillofacial Surgery. JO. Theories and mechanisms of tooth
Surgery, 5th edn. WB Saunders Co., 2nd edn. New Delhi, Churchill Living­ eruption. In: Andreasen JO, Ko ¨lsen-
Philadelphia. 1975 pp.524-705. stone. 1996. p.68. Pedersen J, Laskin DM (Eds). Textbook
2. Archer WH. Impacted Teeth: Oral Sur­ 15. A Öhman. Preoperative radiographic and Color Atlas of Tooth Impactions.
gery—A Step by step Atlas of Operative evaluation of lower third molars with Copenhagen, Denmark: Munksgaard;
Techniques. 4th edn. Phil­adel­phia and computed tomography. Dentomaxil­ 1997. pp. 19-64.
London, WB Saunders Comp. 1966;122. lofacial Radiology. 2006;35:30-5. 28. Marks SC Jr, Schroeder HE. Tooth
3. Nodine AM. Aberrant teeth, their 16. Clark, CA. A method of ascertaining eruption: theories and facts. Anat Rec.
history, causes and treatment. Dent the relative position of unerupted 1996;245:374–93.
Items of Interest. 1943;65:440-51. teeth by means of film radiographs. 29. Williams BH. Diagnosis and prevention
4. Antalovská Z, Skalská H, György A. The Odont Sec Roy Soc Med Proc. 3:87- of maxillary cuspid impaction. Angle
significance of the lower third molar 90,1909-1910. Orthod 1981;51(1):30-40.
13 Preprosthetic Surgeries
Borle Rajiv M, Bhoyar Anjali, Garg Ketan

abnormal muscle attachments, flabby • Correction of soft tissue deformities.


Introduction soft tissue, hypertrophied maxillary tub­ • Implant supported restorations and
Preprosthetic surgery is a part of oral ero­sity, etc. which can come in the way adjuvant procedures.
and maxillofacial surgery that deals with of fabrication of a good prosthesis. The
preparation of oral tissues and struc­ surgical correction of such conditions
Anatomical and
tures favorable to placement of subse­ prior to the prosthesis enhances the
quent prosthesis for their proper place­ result outcome and the quality of the Physiological
ment, retention, stability, function and prosthesis and thus the quality of life for considerations
cosmesis. the patient.
The loss of teeth and their replace­ Willard (1853)1 was the first person Bone
ment by artificial dentures has always to recommend preprosthetic surgery In general, a loss of calcified tissue and a
been associated with many problems. as an aid in preparation of the patient concomitant increase in the porosity of
These may have existed before extra­ction, for complete dentures. Preprosthetic bone with age is seen, especially in wom­
but are exaggerated by the edentulous surgery emerged from a ridge trimming en. In addition, the bone is often more
state. An example is the loss of alveolar service to a truly reconstructive service. brittle due to myelofibrosis and dec­
bone through extensive periodontal dis­ It is essential for every member of the reased vascularity. On the microscopic
ease. Other abnormalities develop after dental profession to possess adequate level, a decreased number of lacunae
dentures have been worn for some time. knowledge of biologic considerations, and osteocytes are seen, along with an
Irritation of the soft tissues can occur, if which will aid in prosthodontic practice. associated decrease in the number of vi­
excessive resorption of the jaws occur; able precursor cells in the bone of elderly
as the alveolar process resorb further, Scope of Preprosthetic persons.2
the vestibule becomes shallow and The blood supply is impaired to
makes wearing of dentures difficult or
Surgery both the mandible and the maxilla
impossible. If excessive atrophy of the Preprosthetic surgeries includes the with age. Angiographic studies of the
entire bone occurs, grafts or implants foll­o­­wing: blood supply to the mandible have
may be the only solution for this difficult • Ridge preservation procedures. demonstrated that the inferior alveo­
problem. Finally, atrophy can become • Corrective recontouring procedures. lar artery is absent or reduced in size
so severe that a pathological fracture – Soft tissue corrective procedures. in older individuals.3 This finding may
may occur and then the only remedy is – Hard tissue corrective pro­ced­ures. be due to the atherosclerotic changes
a bone graft. Thus, the main functions of • Ridge extension procedures. in the artery itself or to loss of the teeth.
preprosthetic surgeries are elimination • Ridge augmentation procedures. Further investigation has demonstrated
of pathology in the denture-bearing soft – Alloplastic bone grafting mat­ the presence of a periosteal plexus of
and hard tissue, and making the eden­ erial. vessels along the inferior border of the
tulous ridges and supporting structures – Rib/Iliac crest bone grafting. mandible, which is composed of bran­
favorable for receiving pros­thesis. – Sinus lift techniques. ches from the buccal, lingual and facial
There may be many unfavorable – Implants. arteries. This plexus is contiguous with
situations such as high frenal attach­ • Correction of abnormal ridge rela­ the periosteum of the mandible and is
ments, sharp bony ridges, undercuts, tion­ships. thought to contribute to the major part
246 Dentoalveolar Surgeries

of the blood supply to the mandible Differences are found in the remo­­d­ the mandible occurs such that the resi­
as it ages. The maxilla has less age- eling pattern of alveolar and basilar bones dual ridge is located slightly to the
related vascular compromise than the of the jaws. Generalized remodeling anterior. The mental foramen, genial
mandible. The maxillary artery is more activity occurs at a much higher rate tubercles and muscle attachments are
prone to atheroma than any other in alveolar bone than in the adjacent all located nearer to the crest of the
artery,4 but because of the abundant basal bone in the mandible. This may ridge with continued resorption. With
collateral circulation of the midface, the be because the rate of deposition and severe resorption, the basilar bone of
maxilla remains well perfused. resorption in alveolar bone is greater the mandible can get affected, giving a
than that for the non-tooth-bearing concave shape to the superior surface
Bone Loss in the Edentulous bone tissues. This is thought to be of the mandible.6 The differential patt­
Jaw because alveolar bone is much more erns of resorption of maxilla and man­
Approximately 50 percent of the popu­ vascular and porous than basal bone. dible, coupled with autorotation of the
lation becomes edentulous by the age of Atwood (1986) gave a classification of mandible, place the residual alveolar
60. It is generally held that the alveolar resorption of residual alveolar ridges ridges in a pseudo-Class III relationship.7
bone relies on the presence of dentition (Fig. 13.1).
for its maintenance. The loss of the teeth The edentulous ridges are molded Facial Changes Associated
leads to lack of functional stresses on the by differential forces delivered onto the with Aging
bone and subsequently leads to disuse bone, determined by the timing and
atrophy of the bone, leading to tooth sequence of tooth loss, prosthesis wear Cutaneous Changes
loss accentuating the normal rate of and facial morphology (brachycephalic In addition to the effects of long-term
alveolar bone resorption in the jaws. The versus dolichocephalic). The usual patt­ exposure to the physical environment
physiology of this bone loss remains a ern is resorption of the maxilla on the (e.g. sun exposure), the skin has intrin­
mystery. However, biomechanical forces labial and inferior portions of the alveolar sic age changes that are thought by
are believed to be the control mechanism ridge. Consequently, the residual ridge many to be genetically controlled. These
for bone remodeling.5 Any imbalance moves posteriorly and superiorly. The changes begin at about 30 years of age
of forces applied to the bone stimulates palatal vault becomes shallow and the and progress to 80 to 90 years. Facial skin
both osteoblasts and osteoclasts. Tension residual ridge approaches the anterior thickness declines sharply at about age
forces result in bone deposition and nasal spine anteriorly and the hamulus of 60 years. As the skin becomes thinner,
pressure forces result in bone resorption. posteriorly. This is often accompanied underlying blood vessels become more
Remo­deling of the bone continues until by pneumatization of the maxillary sinus noticeable. Wrinkling of the facial skin is
the forces are balanced and the equili­ into the tuberosity regions of the maxilla. progressive, especially on the forehead,
brium returns. If resorption is allowed to continue, near the lateral canthus of the eyes, and
Once the teeth are extracted and the maxilla may become flat and ‘egg in the regions of nasolabial fold and
denture wearing commences, a differ­ shell’ thin. In contrast, resorption of perioral area. These perioral changes
ent pattern of force is applied onto the
alveolar bone. Certain areas are under­
loaded and other areas are overloaded,
causing bone remodeling. Denture wear
accentuates alveolar bone loss and this
bone loss is four times greater in the
mandible than in the maxilla or basal
bone. This may be due to the fact that
the stress bearing area of the maxilla is
1.8 times greater than that of the
mandible. Therefore, more compressive
forces per square centimeter are placed
on the mandible than on the maxilla
during normal function. Other factors
that may modulate the remodeling of
alveolar bone include heredity, hormonal Fig. 13.1: Atwood’s classification of ridge resorption. Order I—Pre-extraction; Order II—
factors, local pH, enzymatic agents, local Post-extraction ridge; Order III—High well rounded ridge; Order IV—Knife edge ridge;
oxygen tensions, bioelectric potentials Order V—Low-well rounded ridge; Order VI—Depressed ridge (Courtesy: Prosthodontics
and local induction phenomena. Department Museum, SPDC, Wardha, India)
Preprosthetic Surgeries 247

are magnified with tooth and alveolar • Poor cusp angles of artificial teeth. quire endodontic therapy to achieve app­
bone loss and with the loss of the vertical • The type of denture tooth materials ropriate crown-root length ratios, which
dimension of occlusion. This wrinkling used. adds to the cost of therapy along with the
is due to the loss of elastin fibers in the • Occlusal disharmonies. frequently required amalgam or gold cop­
facial skin and is exacerbated by dermal • Deformation of the denture bases. ings and attachments. In the final analysis
changes and loss of the subcutaneous Normally a mean alveolar bone loss the cost of over-dentures compares favor­
fat. There is also decreased function of of 0.1 mm per year is noted in the anterior ably with alternative treat­ment methods
the skin appendages, thought to be due maxilla and a 0.4 mm per year loss is because of the ease of maintenance and
to a loss of vascularity, causing a fibrosis found in the mandible.8 the low percentage of remakes.
of the glands of the skin. Collagen Alveolar ridge preservation can be
synthesis is reduced and fibroblasts are achieved through a variety of appro­aches: Submucosal Vital Root
relatively inactive in aged facial skin. • Supramucosal vital root retention. Retention
A decrease in hyaluronic acid produc­ • Submucosal vital root retention. Studies of human roots unintentionally
tion leads to a dehydration of the facial • Root cone implants. fractured at surgery and retained in
skin due to a decreased water-binding • Transcortical or endosseous implants. alveolar bone suggest that they generally
capacity. Subcutaneous fat is lost and remain asymptomatic until they break
the melanocytes appear to lose the Supramucosal Vital Root through the overlying mucosa and enter
ability to spread their melanin granules Retention the mouth.11 Clinical symptoms occur
evenly throughout the skin. The der­ Retained teeth and roots have been only with root exposure in the oral cavity
mis becomes relatively dehydrated and used for long periods to support a com­ and periradicular radiolucency.
loses vascularity, strength and elasticity. plete denture. Such prosthesis is called A series of early animal studies
In addition to wrinkling of the skin, an over­denture, telescopic denture or a showed that with roots appropriately
clinical facial changes associated with sleeve-coping denture. reduced to a level 2 mm below the
aging include a progressive weakening The advantages of a retained root alveolar crestal bone and with primary
of the orbital septum leading to down­ structure along with an expected decre­ watertight closure of the overlying mu­
slanting of the lateral canthus of the eye, ased ridge resorption include more favor­ cosa, roots would remain vital.12 The
resorption of adipose and subcutaneous able crown-to-root ratio (through crown severed root would be covered again
tissues of the cheeks and temporal areas, root disproportionate length red­uc­ tion), with regenerated bone with a structural
drooping of the nasal tip, downturning in­creased denture retention and stabil­ periodontal ligament and with a layer of
of the commissures of the mouth, and ity with intracoronal or intra­ radi­
cular cementoblast over cut dentin.
eversion of the lower lip with accen­ att­ach­­ments, increased pro­pri­o­ception, This was confirmed by early human
tuation of the labiomental fold. incre­ased masticatory effi­ci­ency and psy­ reports, although vitally submerged teeth
chological benefits to the patient.9,10 Ad­ appear to have a greater potential for
Sensory Changes ditionally, since the retained roots are the healing than those treated with root ca­
A generalized decrease in perception patients own tissues, there is no risk of nal filling prior to submerging.
of sensory nerves of the head and neck rejection as with the implanted materials. All teeth are to meet the following
occurs with age. This is due to senile The obvious disadvantages remain criteria for retention as proposed by
neuro­pathy in both, the central and those of caries and of periodontal Garver et al (1978).13,14
peripheral segments of the nervous disea­ses such that patient motivation • No more than 1 mm horizontal
system. The peripheral nervous system in the maintenance of a high level of mobility.
com­ ponent is due to accu­ mul­ated oral health and prosthodontic follow- • No infrabony pockets that could not
damage to the peripheral nerves and up care becomes bottom line in this be reduced at the time of surgery.
segmental demyelination. The central type of denture service. • Sufficient healthy mucogingival tis­
nervous system element is due mostly There are associated technical diffi­­ sues for watertight closure of the
to the central neuronal degeneration. culties in the more commonly retai­ned mucosa.
Breakdown in the alveolar ridge can lower teeth and roots such as the canines, • Remaining supporting tissue atleast
have various causes: where a buccal undercut is frequently one-third of the total root length.
• Disuse atrophy following the remo­ found. This may preclude denture fabri­ • Should be asymptomatic, test vital,
val of teeth. cation, but more often can be managed or show only calcific metamorphosis.
• An accelerated mucosal and bony by over-contouring the denture flange to
pathologic atrophy associated with assure relief on the tissue side or by the Technique of Submucosal Vital
faulty metabolism. use of resilient liners. Root Retention
• Pressures from the prosthesis. An additional potential disadvantage A full thickness mucoperiosteal flap is
• Overclosures. is that the retained teeth frequently will re­ raised using a reverse bevel incision
248 Dentoalveolar Surgeries

facially and lingually. Crown amputation Hydroxylapatite induces nei­ther an infla­ whenever the cavity is lined with
is done using either a high speed bur mmatory nor immune res­ ponse when remote grafted tissues or local flaps.
or chisel mallet. Following complete in contact with bone. It forms a nidus Contracture is usually prevented by
removal of crevicular epithelium and for new bone growth. It does not resorb overcorrection of the cavity defect
granulations, periosteal relaxing incisi­ and bonds chemically to bone without an without tension on the lining tissue.
ons are given to allow for tension-free intervening fibrous capsule.16 • The greater the thickness of split-
apposition of the flap. This is sutured skin graft the lesser the tendency for
with a running horizontal mattress su­ Ridge Extension Procedures contracture.
ture of nonwicking monofilament to The goal of ridge extension is to uncover
provide eversion closure, which is then existing basal bone of the jaws surgically Sulcoplasty
oversewn by a continuous running su­ by repositioning the overlying mucosa, Following removal of the natural teeth,
ture to effect a watertight closure.15 muscle attachments and muscle to a remodeling of the alveolar process
Denture placement is either at the lowered position in the mandible or results in a reduction in the height and
time of surgery with pressure paste relief to a superior position in the maxilla. width of the residual ridge. As the basal
and autopolymerizing treatment resin The resultant advantage is that a larger seat area becomes smaller, denture
reline inserted or is delayed until 6 weeks denture flange can be accommodated, stability and retention decrease.
after surgery. Conventional denture fab­ thus contributing to greater denture Ideally, it would seem desirable to
ri­­c­ation techniques are observed, with stability and retention. restore the alveolar ridge to its former
special emphasis placed on obtaining a All the cases of maxillary or mandi­ size by bone grafting. However, since
balanced occlusion without undue press­ bular basal bone atrophy cannot be several methods of sulcoplasty are
ure that could cause decubital ulcers and surgi­cally treated by sulcus extension. available to extend the denture foun­
subsequent root exposure in the mouth. There must be an adequate alveolar dation, bone grafting is indicated only
bone with sufficient height remaining when these methods of sulcoplasty
Complications to allow for repositioning of the mental cannot provide satisfactory results.
Immediate complications include tis­ nerves and the buccinator and myloh­ If a denture flange is overextended
sue dehiscence (due to closure under yoid muscles in the mandible. In the in an attempt to gain added resistance to
tension) or pressure dehiscence (due to maxilla the anterior nasal spine, the lateral displacing forces, the mucosa at
immediate denture). Immediate post- nasal cartilage and the malar buttresses the fornix of the vestibular or sublingual
surgical root exposure requires endo­ may interfere with repo­ sitioning the sulcus becomes traumatized, ulcerated
dontic therapy and conversion of the sulcus superiorly. and scarred and the denture gets easily
root to an overdenture abutment. Conversely not all cases require a displaced. Ultimately the flange must be
Delayed problems usually occur full skin or mucosal graft vestibuloplasty shortened to its physiologic limits.
14 to 20 days postoperatively and are with floor of the mouth lowering. Many If an incision is made at the fornix
usually related to a small dehiscence cases have success with a vestibular of the sulcus to accommodate a longer
into the mouth over individual roots extension anterior to the mental fora­ flange, granulation tissue and scar
that cannot easily be covered surgically miná or a lingual procedure to reduce tissues form around the flange and the
because of their small size, making tissue the genial tubercles or release the flange must be shortened. The incision
free grafts or flap closures questionable. mylohyoid muscle posteriorly in the heals and the sulcus returns to its former
The delayed dehiscence is usually not floor of the mouth, which may very well position with a scar in the fornix, making
pus production, but if persistent can solve the problem of lack of denture it even worse.
become fistulous and require root extra­ stability and retention. For successful extension of the
ction. These complications are related Ashley et al. (1953)17 gave the follow­ vestibular or sublingual sulcus both
to faulty prosthesis pressures, to alveolar ing principles of plastic revision of the osseous and the soft-tissue sides
bone resorption allowing sharp root tissues: must be lined with epithelium. If the
surfaces to penetrate the mucosa, or • Bare soft tissue should be covered extended sulcus is to be an aid in
to the presence of retained epithelium surgically with epithelium to prevent denture construction, the mucosa of
over the root. subsequent scars and contracture. the sulcus must be free of scar tissue.
• Whenever the local tissue is not To prevent relapse of the sulcus to
Root Cone Implants available to obtain the anticipated its former condition there must be a
Current studies have shown that porous final result or to cover the defect minimum of connective tissue between
and non-resorbable particulate and block without tension, distant tissue should the mucosa and the periosteum on
forms of hydroxylapatite can be used be used. the osseous side of the sulcus and the
clinically as tooth root, bone augmen­ • In creating a new cavity, allowance epithelial lining of the sulcus must be
tation and bone replacement materials. should be made for contracture free of tension.
Preprosthetic Surgeries 249

There are three general methods of advancement procedure. A similar test With the lip everted in the horizontal
sulcoplasty, as follows: can be used in the lower labial vestibule. plane, a scissor is introduced through
1. Mucosa adjacent to the sulcus can the incision and by blunt spreading
be advanced to line both sides of the Obwegeser’s Submucous dissection the mucosa is separated from
extended sulcus. Vestibuloplasty19 the submucosa on the right and left
2. Neighboring mucosa can be advan­ In many cases of a clinically short alveolar sides. A tunnel is formed between the
ced to line one side of the sulcus, while ridge there actually is enough bone mucosa and the submucosa, extending
the other side heals by granulation present. The difficulty lies in the fact that from the mucogingival junction well out
and secondary epitheli­zation. the mucosa and muscles of the sulcus are into the lip and cheek so that the mucosa
3. Epithelium, either skin or mucosa, attached too closely to the crest of the ridge. is completely undermined. The tunnel
can be transplanted as a free graft The objectives in this surgical procedure is carried posteriorly to the zygomatic
to line one or both sides of the are to extend the sulcus to provide buttresses of the maxilla and to the
extended sulcus. additional ridge height and to transfer mental foramen areas of the mandible.
the submucous connective tissue and When the submucosal tunnels have
the adjacent muscles to a position farther been created, the vertical incision is
Vestibuloplasty from the crest of the ridge.20 The purpose deepened to bone at the midline. If the
of the second objective is to prevent anterior nasal spine is prominent, it can
Procedures relapse of the sulcus to its preoperative be reduced through the median incision.
condition. This procedure is applicable Supraperiosteal tunnels are made to
Mucosal Advancement to the entire maxillary sulcus and to the the right and left with the scissors,
When the vestibular sulcus is to be anterior mandibular sulcus, but better separating the connective tissue and
extended, the first choice of procedure results are obtained in the maxillary muscles from the periosteum. The
should be the one whereby the neigh­ vestibule. This procedure is one that can sup­r­a­periosteal dissection should be
boring mucosa can be advanced to be performed with local anesthesia in extended as far as the proposed sulcus
line both sides of the sulcus. The prime the dental office. An important feature extension requires. A wedge-shaped
criterion for this type of procedure is of the operation takes place before the strip of connective tissue remains bet­
the presence of an adequate amount incision is made. A copious amount ween the two tunnels. This strip of
of healthy mucosa. Obwegeser18 used a of saline, or a dilute solution of local connective tissue may be cut close to
simple clinical test to determine whe­ anesthetic, is injected superficially in the the bone with the scissors. The tissue
ther or not there is sufficient mucosa submucosa of the sulcus, lip and cheek may be excised, or it may be permitted
available. With the lips in a relaxed to facilitate dissection of the mucosa to retract into the lip and cheek. The
position, a mouth mirror is inserted from the submucosa. A vertical incision freely movable mucosa is adapted into
into the sulcus to the required depth is made in the midline of the sulcus the deepened sulcus with finger pressure
required prosthetically. If the upper lip is through the mucosa only, extending and blood is milked out of the surgical
not displaced upward or drawn inward from the mucogingival junction to a field. The vertical incision is sutured.
by the maneuver, it can be assumed level in the lip corresponding to the pro­ A roll of gauze is placed into each sulcus
that there is sufficient mucosa for an posed sulcus extension (Figs 13.2A to D). to temporarily support the mucosa

A B C D

Figs 13.2A to D: Obwegeser’s submucous vestibuloplasty: (A) Incison in vestibule; (B) Blunt dissection by scissors; (C) Tunnel formed;
(D) Denture/splint with extended flanges secured to alveolar bone (Courtesy: Artist Kombe SPDC, Wardha, India)
250 Dentoalveolar Surgeries

and prevent hematoma formation, If the patient’s denture is lined with then performed a supraperiosteal dis­
while the denture is being prepared. a soft liner, sufficient retention can section to deepen the sulcus (Figs 13.3A
A compound impression is made of frequently be obtained so that osseous and B). The flap of mucosa was turned
the new sulcus with use of the patient’s fixation is unnecessary. downward from its attachment on
denture or a previously prepared splint. the alveolar ridge and placed directly
The compound is chilled and trimmed. Vestibuloplasty by Secondary against the periosteum to which it was
The denture or splint with the extended Epithelization sutured. A rubber catheter stent was
flanges is secured to the maxilla or The success of Obwegeser’s submucous placed in the deepened sulcus and
mandible for 1 week with peralveolar vestibuloplasty and Wallenius’ muco­ fixed through the lip to the outer surface
wires or pins or with circumzygomatic sal advan­cement operation depends on with percutaneous sutures. The catheter
or circummandibular wires. the presence of a sufficient amount of helped to hold the flap in its new position
The postoperative course is accom­ healthy mucosa in the vestibule. When and to maintain sulcus depth during the
panied by moderate pain and facial inflammatory hyperplasia and scar tis­ first stages of healing. The catheter was
swelling that subside after 4 or 5 days. sue are present, these muc­osal advan­ removed after 7 days. The labial donor
A new denture can usually be made after ce­ment procedures are contra­indi­cated. site was coated with tincture of benzoin
2 or 3 weeks. Secondary epitheli­zation techni­ques and was otherwise left raw to granulate
should be considered as the first alter­ and heal by secondary epithelization.
Wallenius’ (Open-View) Technique native. The basic disadvantage of this technique
Wallenius21 (1963) accomplished—the There are two basic techniques of is that the raw area is in the soft tissue,
same mucosa-lined sulcus extension vestibuloplasty by secondary epitheli­ which brings about scarring of the
as Obwegeser, but he used an ‘open zation with several variations. In one vestibule and relapse is common.
view’ procedure instead of a ‘tunneling’ technique (Kazanjian) a mucosal flap is
technique. An incision is made along raised in the lip and transferred to line Godwin Technique
the mucogingival junction through the the osseous side of the deepened sulcus. Godwin23 (1947) performed a similar
mucosa only. The supraperiosteal dis­ In the other (Clark) a flap of alveolar pro­cedure to deepen the lower vesti­
section is performed to the extent desired muc­ osa is raised and transferred to bular sulcus. Like Kazanjian, he raised
for the proposed sulcus extension. Care line the soft tissue side of the sulcus. a flap of labial mucosa, but he deep­
must be exercised not to cut or tear the Variations in the two basic techniques ened the sulcus by means of a sub­
periosteum. The mucosa is dissected relate to the periosteum. periosteal stripping. The periosteum
from the submucosa far out into the lip so and the attached connective tissue was
that a large flap of mucosa is mobilized. Kazanjian Technique either excised or pushed downward.
Stay sutures are placed in the flap to fix it Kazanjian22 (1935) made an incision in Godwin placed the flap of labial and
to the periosteum deep in the sulcus. The the mucosa of the lip and reflected a large vestibular mucosa directly against the
free margin of the flap is then returned to flap of labial and vestibular mucosa. He bone and sutured it to the connective
its original position and sutured.
Wallenius uses stay sutures to fix the
mucosa at the fornix of the sulcus to the
periosteum rather than use a stent or
percutaneous sutures.
Obwegeser also suggested an open-
view variation of his submucous vesti­
bulo­ plasty as an alternate procedure
for those who find the blind ‘tunnel’
technique difficult.
Obwegeser’s submucous vestibulo­
plasty is considerably easier to perform
in the maxillary sulcus than Wallenius’
technique. The intricate placement of
stay sutures deep in the sulcus to fix
the mucosa to the periosteum makes
Wallenius’ procedure difficult. Obwe­ A B
geser’s use of an extended denture
flange to hold the fornix of the sulcus in Figs 13.3A and B: Kazanjian’s technique: (A) Flap harvested from lip mucosa;
its new position is considerably easier. (B) Flap sutured to periosteum of bone
Preprosthetic Surgeries 251

tissue beyond the deepened sulcus, The advantages of Cooley technique to be the reverse of Kazanjian technique.
using absorbable suture. By stripping are as following: Clark based his operation on four prin­
the periosteum, Godwin exposed the • Bony irregularities on the crest and ciples of plastic surgery:
bone and was able to smoothen the labial surface of the ridge can be 1. Raw surfaces on connective tissue
bone with files, before the flap was corrected. contract, whereas the same surfaces
positioned in the sulcus. The raw tissues • The crest of the ridge is left raw to undergo minimal contraction when
healed by granulation and secondary granulate and heal by secondary covered with epithelium.
epithelization, with a contracture line epithelization. Since there can be 2. Raw surfaces overlying bone cannot
on the labial side of the sulcus. no scar contracture over bone, this contract.
Both Kazanjian’s and Godwin’s pro­ technique is an improvement over 3. Epithelial flaps must be undermined
ced­ures have the disadvantage of scar Kazanjian and Godwin techniques sufficiently to permit repositioning
contracture on the labial side of sulcus, in which a scar is formed on the and fixation without tension.
with a loss in sulcus depth. Godwin’s labial side of the sulcus. 4. Soft tissues undergoing plastic revi­
technique has the added disadvantage • The mental nerve can be repos­iti­ sion have a tendency to return to their
of inviting additional bone resorption by oned bilaterally, if indicated. former position so that over­correction
removing the periosteum. and firm fixation are necessary.
Collett Technique In Clark’s operation an incision is
Cooley Technique Collett25 (1954) used a previously pre­ made on the alveolar ridge and a supra­
Cooley (1952) presented a method for
24
pared denture with overextended flange periosteal dissection is done to the
deepening the mandibular and maxillary borders to support full-thickness labio­ depth desired. The mucosa of the lip
sulci. With his technique he was also able bu­ccal mucoperiosteal flaps. In his tech­ is undermined to the vermilion border
to smoothen any bony irregularities on nique the amount of sulcus extension is (Figs 13.4A and B). Three non-absor­
the crest of the ridge and reposition the determined preoperatively on a study bable mattress sutures are placed in the
mental nerve. He made an incision on cast and a clear surgical template with ap­ free margin of the mucosal flap and are
the crest of the mandibular ridge from propriately extended borders are made carried through the skin and tied over
second molar area on one side to the from the corrected cast. a cotton roll. The soft-tissue side of the
same position on the opposite side. Short An incision is made on the crest of sulcus is covered with mucosa, whereas,
lateral relaxing incisions were given at the maxillary ridge from one tuberosity on the osseous side, the raw periosteal
the posterior ends of the primary incision. to the other. The external mucoperios­ surface is left to granulate and epithelize.
A full thick­ness labiobuccal mucoperio­ teum and muscles are elevated and a Clark technique is particularly applicable
steal flap was reflected down to the level large full-thickness flap is reflected. for the mandibular labial sulcus.
of the pro­­posed sulcus extension. The The transparent template is inserted In 1953, Edlan27 recommended an
mental nerve was repositioned inferiorly and used to reposition the flaps higher inci­sion on the lip mucosa with full
on each side. The labial and buccal in the vestibular sulcus. The position of thick­­ness mucoperiosteal dissection
mucosa was undermined thoroughly. the flaps can be observed through the followed by incision of periosteum over
Three drill holes were placed through the template. No sutures are placed. The the crest of the ridge. The periosteum
alveolar ridge, one in the midline and one denture is inserted to support the newly was then used to cover the mucosal
in each cuspid area. The gingival margin deepened sulcus. The bone is protected wound over the lip. In 1954, Collett25
of the labial flap was sutured through the by the denture until granulation tissue described the procedure of secondary
peralveolar holes to the lingual muco­ forms and surface epithelization occurs. epithelization without suturing, which
periosteum leaving the crest of the ridge In Collett, Cooley, and Godwin pro­ resulted in scar contracture on the
bare. cedures the periosteum is stripped from labial aspect and finally there was loss
A previously prepared acrylic splint the bone. Godwin covered the bone with of vestibular depth. In 1955, Caldwell28
with extended flanges was secured to the mucosal flap. Cooley repositioned recommended that the incision should
the mandible for 6 days with circum­ the mucoperiosteal flap with only the be made on the top of the crest and that
ferential wires. This splint was worn by ridge crest remaining bare. In Collett pro­ it should extend from the retromolar
the patient after the immediate posto­ cedure the entire external surface of the pad to the bicuspid region through the
perative period until a new denture maxillary ridge is left bare, thus inviting periosteum down to the bone. It must
could be constructed. infection and additional bone resorption be carried sufficiently to the buccal
Cooley’s maxillary sulcoplasty pro­ of a previously resorbed ridge. side so as to assure a table of bone to
cedure was similar to the mandibular which the lingual periosteal flap can be
except that the primary incision, instead Clark’s Technique returned for closure of the wound. After
of being on the crest of the ridge, was Clark26 (1953) described a sulcus exten­ cutting the ridge and severance of all
made to the palatal side of the crest. sion procedure that can be considered muscle attachment the wound is closed.
252 Dentoalveolar Surgeries

• If the bony ridge is too small to per­


mit overcorrection, or if the raw
operative defect is large, a free
epithelial graft should be placed to
cover the wound.

Effects of Vestibuloplasty
Mechanical Resistance
to Displacement Forces
The vestibuloplasty with the skin
grafting (VSG) and lowering the floor
of the mouth (LFM) provides increased
sulcus depth, especially in the lingual
A B
flange area, which materially helps to
control lateral displacement.
Figs 13.4A and B: Clark’s technique: (A) Flap harvested from alveolar mucosa;
(B) Flap sutured to labial mucosa
Stable Denture Seating Area
The atrophic mandibular ridge has only
A rubber tube is sutured in position to the tissues have healed, usually in 3 or a small line of attached mucosa forming
maintain the sulcus depth. 4 weeks. the crest of the ridge. All the remaining
Obwegeser stated that within 3 years mucosa of the denture seating area can
Obwegeser Secondary 50 percent of the sulcus depth obtained be elevated by the movement of the
Epithelization Vestibuloplasty by secondary epithelization was lost by lips cheek and tongue. The vestibulo­
Obwegeser29 technique was published regression. As a result overcorrection is plasty with skin grafting and lowering of
in 1967, coauthored by Macintosh. It indicated. He stated that he had better the floor of the mouth (VSG and LFM)
is essentially a modification of Clark’s results with this procedure in cases of produces a non-displaceable tissue
technique. Obwegeser used secondary maxillary vestibuloplasty than in mandi­ cover­ing the entire denture-bearing area.
epithelization in cases in which there is bular. The skin’s firm attachment to the peri­
enough bone, but insufficient healthy osteum permits denture stability even in
mucosa for his submucous vestibulo­ Conclusion Regarding Secondary the severely atrophied mandible where
plasty technique. He used this proce­ Epithelization Vestibuloplasty no significant ridge height can be created.
dure primarily to extend the maxillary • The Clark procedure, which leaves
vestibule. The incision is made at the a raw periosteal surface that can­not Skin as a Load Bearing Tissue
mucogingival junction and the supra­ contract, is preferred to the Kaza­ Whereas mucosa tends to ulcerate in
periosteal dissection is extended quite njian procedure, which leaves a raw response to pressure, skin tends to
high, almost to the infraorbital fora­ lip that does contract. form a benign hyperkeratosis similar
men. The labial and buccal mucosa are • The mucosal flap must be free of ten­ to the callus response on the hand.
undermined. The free margin of the sion and must be fixed for a suffi­cient This hyperkeratosis is rarely painful.
mucosal flap is sutured to the perios­ period of time to prevent rela­pse. The pain threshold of grafted skin is
teum high in the extended sulcus with • Relapse can be further minimized, higher than that of mucosa and touch
000 chromic catgut sutures. Percutane­ if the periosteum is scarified at the perception is somewhat diminished.
ous sutures are not used in maxillary base of the sulcus. Patients are usually more comfortable
sulcoplasty operations. • The denture flange should not irri­tate with skin than mucosa as a load bearing
Obwegeser suggested that the den­ the granulating periosteal sur­face. tissue. Both skin and mucosa will rarely
ture flange be shortened so there is no • A new prosthesis may be made after exhibit problems like candidiasis.
contact with the raw periosteal surface. 4 to 5 weeks. The flange of the
Irritation from the flange that could denture should be of sufficient length Probable Slower Mandibular
cause proliferation of an excessive to maintain the new sulcus depth. Resorption Beneath Skin
amount of granulation tissue is thereby • Inspite of all the best efforts to avoid
avoided. 4 to 5 weeks postoperatively a a relapse, a 30 to 50 percent relapse Advantages of use of stents
flange is added to the denture. In such in sulcus depth can occur and so The stent is more versatile than the sut­
cases the denture is lined with a soft overcorrection of the sulcus should ur­ing method because the skin can be
acrylic resin that is changed weekly until be attempted whenever possible. adapted with accuracy to any contour
Preprosthetic Surgeries 253

of the labial-buccal area whereas with addition of a free skin or mucosal graft Morbidity, complications and side
suturing method, there should be mini­ may make the difference between suc­ effects of vestibuloplasty
mal depressions in the labial-buccal cess and failure.30 • Dysesthesia is a relatively frequent
contour. With the stent technique the Obwegeser31,32 (1963, 1967) used skin posto­perative complication. Avoi­
skin can be adapted to the lingual un­ grafting almost exclusively in mandibular dance of surgical error is of impor­
dercut via the Protaform-type adapta­ vestibuloplasty, usually combined with tance in reducing dysesthesia, i.e. the
tion material and poor crestal soft tissue a lowering of the floor of the mouth avoidance of physical injury to the
or sharp crestal bone can be dealt with (lingual sulcoplasty). The initial steps of nerve of the surgical area.
at the time of grafting. With the sutur­ the operative procedure are the same • Soft tissue profile changes of consi­
ing method, these problems need to be as those of secondary epithelization derable magnitude and uniform
dealt in with a separate procedure. vesti­­b­ulo­plasty in which a labiobuccal pattern have been found, even when
A graft with voids can be tolerated flap is sutured to the periosteum low in the surgical preparation is restricted.
using the stent method, as it can be the deepened sulcus (Figs 13.5A to C).
mani­pulated on the stent to give pro­ When ridge skin-grafting vestibuloplasty Lingual Sulcoplasty
per coverage. This allows a thinner is combined with lingual sulcoplasty, For the patient with a grossly resorbed
graft than may be used in the suturing the free margin of the labiobuccal flap mandible, extension of the lingual sul­
method, thus predisposing to better is sutured, not to the periosteum, but to cus, or lowering of the floor of the mouth,
donor site healing. the free margin of the lingual flap with can extend the denture found­ation and
chromic gut sutures that pass under improve the stability and retention of
Advantages of submucosal suturing the inferior border of the mandible. the mandibular denture. The mylohyoid
Without the stent the patient is more The split-thickness skin graft is placed and genioglossus muscles and the mu­
com­fortable for the first week postopera­ inside a previously prepared stent and cosa of the floor of the mouth can be
tively. In addition, no stent cons­truction secured with an adhesive. The stent and repositioned inferiorly without un­ due
or adaptation materials are required. skin graft are secured to the mandible impairment of function. Cooley24 (1952)
for 1 week by circumferential wires or suggested lingual frenotomy and trans­
Skin Graft heavy nylon sutures. After a week the plantation of the superficial fibers of the
Skin grafts have been used for years to stent is removed. The graft has healed genioglossus muscles to improve the
cover wounds of the oral tissues in the to the raw periosteum. Excess skin may contour of the anterior lingual sulcus.
plastic repair of trauma and in tumor be removed with a scissor. The stent or
surgery. In preprosthetic oral surgery temporary denture should be replaced to Trauner Technique
when there is an inadequate amount of prevent contracture and loss of the newly Trauner33 (1970) stated that lingual
oral mucosa that can be repositioned deepened sulcus. After 4 to 5 weeks a new sulcus extension was indicated when
to deepen the vestibular sulcus, the denture may be constructed. the mucosa of the floor of the mouth

A B C
Figs 13.5A to C: Obwegeser’s secondary epithelization vestibuloplasty: (A) Flap harvested from alveolar mucosa; (B) Flap sutured to lip
and skin graft secured; (C) Temporary denture placed as stent
254 Dentoalveolar Surgeries

A B C
Figs 13.6A to C: Lingual sulcoplasty (Trauner’s technique): (A) Incision near lingual crest of ridge; (B) Release of periosteum and
genioglossus muscle; (C) Mucosa sutured to skin under the mandible

rose as high as the mandibular ridge grafting vestibuloplasty with a lingual progressively more unstable. As the alve­
when the tongue is elevated and when sulcoplasty (Figs 13.7A to D). olar ridge resorbs and becomes shorter,
the mylohyoid muscle is attached at the Moore34 (1970) suggested a modi­ the denture flange must be shortened a
level of the ridge. fication of Obwegeser technique. Moore little amount to prevent the formation
Trauner made an incision in the used a soft silicone lining in the splint. of decubiti and hyper­ plastic folds of
mucosa of the floor of the mouth close He sutured the mucosal flaps to the stent vestibular mucosa. As the denture flan­
to the mandible from the third molar and fixed the stent to the mandible with ges are shortened, both stability and
region on one side to the same location Steinman pins. With this modification, retention decrease. This situation can
on the opposite side (Figs 13.6A to C). By Moore was able to avoid making the ten be partly overcome by certain surgical
blunt dissection the connective tissue submandibular awl punctures that are procedures designed to deepen the vesti­
was separated from the periosteum until part of Obwegeser procedure. bule and the sublingual sulcus.
the inferior border of the mandible was
encountered. The mucosa of the floor Corrective Surgical Labial Frenectomy
of the mouth and the mylohyoid muscle One of the easiest corrective surgical
were sutured with heavy nylon mattress
Procedures procedures to perform is the excision of
sutures through the skin to buttons ­un­ a hypertrophic labial frenum. The labial
der the mandible. The medial periosteal Soft tissue Corrective frenum is a band of fibrous connective
surface of the mandible was left bare Surgeries35 tissue, covered with mucous membrane
to granulate and epithelize. Since this Surgical correction of various normal that binds the lip to the alveolar process.
process took as long as 2 months and and abnormal soft tissue conditions The upper labial frenum is usually more
the floor of the mouth was quite tender can aid in denture construction for the prominent and more fibrous than the
until healing was complete, Trauner alsodentist and make denture wearing more lower, which often is reduced to a mere
suggested that split-thickness skin grafts
successful for the patient. Included here vestige. When a frenum is attached at
could be used on a stent to cover the raw
are correction of hypertrophic frenii, or near the crest of the alveolar ridge, it
periosteal surfaces. The results of the double lip, papillary hyperplasia of the may be subjected to repeated irritation
skin grafts were favorable. The total time
palate and submucosal hyperplasia of from a denture flange. The procedure
for healing was shortened to a few weeks.
the maxillary tuberosities, the palate, can be performed with local or general
A considerable amount of posto­ the mandibular retromolar pads and the anesthesia in just a few minutes.
perative swelling and difficulty in swal­
vestibule. The lip is elevated, everted and
lowing occurs, but these symptoms usua­ The grossly resorbed alveolar pro­cess tensed so that the frenum becomes pro­
lly subside after a week. Antibiotics and
presents several problems. Press­ ures minent. Before making the incisions,
analgesics are usually prescribed. from the denture flanges on the mental it should be recalled that the purpose
nerve can produce pain or num­bness. for performing the frenectomy is the
Obwegeser technique for skin grafting As the alveolar bone resorbs, the gingiva elimination of the fibrous part of the
Obwegeser (1963, 1967) modified Trauner loses its bony support and becomes soft frenum and that the mucosa should be
technique. He combined a ridge skin- and mobile and the denture becomes repositioned to cover the surgical defect.
Preprosthetic Surgeries 255

The incisions are given in the muc­


ous membrane around the frenum and
are carried down to the bone (Figs 13.8A
to D). If the frenectomy is performed to
aid the orthodontic closure of a median
diastema, the apex of the V should be at
or near the incisive papilla on the palate.
The two limbs of the V incision should
be closely placed and often are nearly
parallel. When the frenum is detached
from the bone with a periosteal elevator,
most of the connective tissue fibers
A B retract upward into the lip. The small
tag of labial mucosa and any surplus
connective tissue can be removed eas­
ily with scissors. The margins of the
result­ing diamond-shaped defect can
be undermined with a scissor and
closed with interrupted sutures. The
first suture should be placed across the
middle of the wound (usually the widest
part) and should engage both mucosal
margins and the periosteum at the
midline. This deeply fixed suture helps
to maintain the height of the vestibular
C D sulcus in the midline and to minimize
the formation of a hematoma under the
Figs 13.7A to D: Obwegeser’s modified linguosulcoplasty: (A) Incision sparing mucosa alveolar mucosa. Additional sutures are
at crest of ridge; (B) Labial and lingual ridge extensions; (C) Raw bone is skin grafted and placed to close the wound in a vertical
covered with surgical stent; (D) Final result line. Sutures should be removed in
7 days.

Buccal Frenectomy
Buccal frena are composed mainly of
folds of mucous membrane with only a
thin fibrous stroma. They occur in the
first bicuspid regions of the mandible
and the maxilla. Their correction can
be accomplished by a V-Y plasty or
a V-diamond plasty if the frena are
large. Since most buccal frena are
A B
small, a transverse incision through
the frenum with a scalpel or scissors
is all that is required to produce a
diamond-shaped wound, the margins
of which are under­mined and closed
longitudinally, or perpendicular to the
original incision (Figs 13.9A and B).
When correcting a lower buccal fre­
num, the surgeon should rem­ em­ ber
that the mental neu­ro­vascular bundle
C D is often found in the connective tissue
Figs 13.8A to D: Labial frenectomy: (A) V shaped incision; (B) Frenum detached from and trauma to the mental nerve should
bone; (C) Diamond shaped defect; (D) Closure be avoided.
256 Dentoalveolar Surgeries

binds the tip of the tongue to the alveolar


process. It may be merely a short fibrous
frenum that restricts movements of the
tongue, or it may contain fibers of the
genioglossus muscles.
As a simple test of lingual function,
the patient can be asked to touch his
upper lip with the tip of his tongue. When
a patient is unable to move the tip of his
tongue adequately or when the ventral
A B
surface or tip of the tongue is bound to the
Figs 13.9A and B: Buccal frenectomy alveolar process, frenotomy is indicated.
The procedure can be performed
with local or general anesthesia. When
local is used, bilateral lingual nerve
blocks are performed and supple­mented
with minimal amounts of infiltration to
avoid distortion of the sublingual tissues.
A traction suture is placed through the
muscles of the tip of the tongue so that the
tongue may be elevated and the frenum
tensed. A transverse incision is made in
the mucous membrane of the frenum
midway between the ventral surface of
A B the tongue and the sublingual caruncles
(Figs 13.10A to D). Deeper dissection is
performed with scissors in the midline,
avoiding the ducts of the submandibular
salivary glands and the sublingual veins,
which are usually found lateral to the
surgical field. If fibers of the genioglossus
muscles are found to be in the field, they
may be cut as needed. The dissection
is continued until the tip of the tongue
can be retracted sufficiently to touch
C D the maxillary incisor teeth or alveolar
process, while the mouth is open. The
Figs 13.10A to D: Lingual frenectomy: (A) Preoperative limited tongue protrusion;
(B) Transverse incision along lingual frenum; (C) Approximation of mucosa and suture; mucosal flaps are undermined with
(D) Preoperative free tongue movement scissors and closed as a longitudinal
linear incision with interrupted sutures.

Correction of Scar performed with a scissor until the tissue is Double Lip
freely movable. The wound margins are Double lip is an accessory fold of
Contractures of the Lips
undermined and closed with sutures. redundant mucous membrane that
and Buccal Mucosa Large scars can be corrected by is situated just inside the vermilion
Depending on the size of the scar con­ Z-pla­sty, V-Y plasty or other tissue-rep­ border of the lip. It is an uncommon
tracture and its location, a variety of o­si­tioning procedures. congenital anomaly and may also be
corrective procedures can be performed. acquired by sucking the lip between the
Thin scars can be corrected by a simple Lingual Frenotomy teeth. Usually the upper lip is involved,
transverse incision across the scar similar Ankyloglossia, or tongue-tie, is observed although it can occur on the lower one.
to that made for a buccal frenum. The most often in children and is usually Double lip is especially noticeable when
wound is converted from a transverse corrected while the child is young. the lip is tensed in smiling.
incision to a longitudinal diamond-sha­ The lingual frenum may consist of The procedure is performed in the
ped wound by tensing the tissue. Deeper a fold of mucous membrane only, or it dental office with local anesthesia.
dissection of the fibrous scar band can be may contain a dense fibrous septum that Bilateral infraorbital nerve blocks are
Preprosthetic Surgeries 257

i ii iii
Figs 13.11A: Diagrammatic representation of the double lip surgery: (i) presurgical;
(ii) intraoperative excision with knife; (iii) closure

i ii iii

Figs 13.11B: Double lip excision: (i) Preoper­


ative photograph of double lip; (ii) Inci­sion;
(iii) Surgical defect following exci­sion; (iv) sut­
ur­ing of the surgical wound; (v) post­operative
iv v photograph

commonly on the hard palate, although it


administered so that infiltration into the verify the benign nature of the disease.
is not restricted to this location. It has been
lip, producing distortion of the contour, Removal of the denture for several days
can be avoided. The redundant folds of observed primarily, but not exclusively, in helps to reduce the inflammation, but
labial mucosa are grasped gently with patients who wear a complete maxillary does not eradicate the lesions.
denture.36 It also occurs in patients who
Allis forceps and elliptical incisions are Split-thickness, supraperiosteal exci­
made around the masses (Figs 13.11A wear a maxillary partial denture and sion is the treatment of choice for most
and B). The incisions are carried deep in patients with natural teeth and no lesions of inflammatory papillary hyper­
into the submucosa so that one or prosthetic dental appliances. plasia. Small lesions can be removed with
two blocks of tissue, wedge-shaped in The etiology is obscure. However, sharp curettes or by mucoa­brasion with a
cross section, are removed. A few small many authors agree, at least in part, on rotary instrument. Use of electrocautery38
bleeders are ligated/cauterized. The a number of contributing factors:37 and cryosurgery39 by liquid nitrogen have
wounds are closed in layers with 4 ‘0’ • Poorly fitting denture. also been reported. They have found that
absorbable sutures. • Wearing the denture 24 hours a day. 2 to 4 treatments at weekly intervals are
• Poor oral hygiene. necessary, but the postoperative pain
Inflammatory Papillary • Use of palatal relief. reportedly is less than that occurring
Hyperplasia of the Palate • Predisposing factors. after other methods of treatment. In all
Inflammatory papillary hyperplasia is Treatment of this disease can be cases the patient’s denture or a specially
a painless, irreversible disease of the accomplished in a variety of ways. prepared surgical splint should be used
oral mucous membrane. It occurs most In every case a biopsy is indicated to to cover the raw wound.
258 Dentoalveolar Surgeries

Fibrous Hyperplasia mandibular retromolar pad, the opera­


of the Oral Tissues40 tion should be performed on the maxil­
lary ridge.
Palatal Gingiva and Maxillary If the retromolar pad must be redu­
Ridge ced, the operation can be performed
Fibrous hyperplasia of the palatal with local anesthesia in the dental office.
gingiva is not uncommon. When this Elliptical incisions are made around the
condition is present, the palatal gingiva soft tissue mass. The incisions should
often is enlarged to the extent that it converge and be carried to bone so
actually extends below the maxillary that a block of mandibular gingiva
occlusal plane. This condition should be can be removed. The gingival flaps are
corrected for the following reasons: approximated and sutured. Trauma to Fig. 13.12: Mental nerve repositioning
• Removal of the soft or hypermobile the lingual nerve should be avoided lost
gingiva leaves a firm maxillary ridge taste and sensation to the anterior two-
for good denture stability. thirds of the tongue be interrupted. A vertical groove should be made in
• The palatal gingiva is recontoured to the bone beneath the mental foramen
remove soft-tissue undercuts. Surgical Repositioning with a dental drill (Fig. 13.12). When
• The crest of the maxillary ridge is of the Mental Nerve the osseous preparation has been
shortened, thus providing space for In patients with gross atrophy of the completed, the neurovascular bundle
a denture base. mandibular alveolar process the mental may be care­ fully positioned in the
Surgical reduction of the hyper­plastic foramen may be found at or near the crest newly formed foramen. Surgicel may be
submucosa of the posterior maxillary of the residual ridge. When this occurs, placed over the neurovascular struct­
ridge and tuberosity can be performed the mental nerve may be subjected to ures to maintain them in their new
in the dental office with local anesthesia. pressure from a denture during masti­ position. The soft tissue flap should be
Elliptical incisions are made around the cation. Patients with this condition often repositioned and sutured.
gingival masses. These incisions should complain of sudden, sharp, severe pain
be carried to bone, so that a full thickness of short duration similar to the pain of Unsupported and Hypermobile
block of gingiva can be removed with trigeminal neuralgia. The pain may be Gingiva41
a rongeur forceps. The buccal and initiated during functional loading of In cases of severe atrophy of the residual
palatal soft tissues should be thinned. the denture during mastication. Some ridge, the gingiva loses its bony support
Submucous incisions are made in the patients complain of both pain and and becomes freely movable. As a
buccal and palatal connective tissue, numbness in the lower lip. result, the denture becomes increasingly
parallel with the mucosal surface, and are For many patients the symptoms can more unstable. Treatment is directed
carried to bone. The blocks of submucous be eliminated by relieving the denture to towards providing a firm basal seat area
connective tissue are removed, leaving avoid pressure on the mental fora­men. for the denture. The operation may be
buccal and palatal flaps of appropriate This method is successful when, there performed with local anesthesia. Two
thickness, which are repositioned and is sufficient support provi­ ded by the incisions are made along the crest of the
sutured. remaining denture-bearing area. When residual maxillary ridge, one to the labial
the denture support is insufficient, the and the other to the palatal side. The two
Mandibular Retromolar Pad denture should not be relieved, as this incisions converge at the right and left
Reduction would reduce the support even more. ends of the surgical field and are carried
Fibrous hyperplasia of the mandibu­ Instead, the mental neurovascular bun­ to bone so that a long strip of gingiva
lar retro­molar pad occurs infrequently. dl­e should be surgically repositioned. may be removed. The wound margins
When it does occur, the retromolar pad The surgical procedure can be per­ are approximated and sutured. A soft
may contact the maxillary tuberosity or formed with local anesthesia in the den­ denture-lining material may be placed
teeth. The fibrous portion of the retro­ tal office. A long incision is made on the inside the denture to compensate for the
molar pad supports the posterior border crest of the residual ridge. If the mental change in tissue contour.
of the mandibular denture. Complete ex­ foramen has been found by palpation to The excision of hypermobile mandi­
cision of the retromolar pad deprives the be located on the crest of the ridge, the in­ bular gingiva usually is complicated by
mandibular ridge of a valuable protective cision should be curved lingually to avoid the presence of a very thin and short
covering and permits exces­sive settling the foramen. The mucoperiosteal flap is residual ridge. Since there is a deficiency
of the denture and ridge resorption. If a carefully reflected to expose the mental of mandibular gingiva, it is desirable
choice is available between surgical re­ foramen and the neurovascular bundle, not to excise too much when the hyper­
duction of the maxillary gingiva and the which should be carefully retracted. mobile gingival crest is removed. Sutures
Preprosthetic Surgeries 259

are rarely necessary. A soft denture- hyperplastic masses are com­­ posed of in the oral cavity. Overerupted teeth
lining material may be placed inside the fibrous connective tissue with a mucous have elongated alveolar process so
denture to improve the tissue-denture membrane covering and occ­­asi­onally that vertical reduction of bony margins
contact and to protect the tender mandi­ some labial mucous glands in the stro­ of socket often is indicated when
bular ridge, which heals in a week with ma. Inflammation is a common fea­ture. such teeth are removed. An envelope
minimal postoperative pain and swel­ling. These masses should be excised in flap is generally enough for access to
Excision of hypermobile gingiva, such a way that minimal scarring of the the cortical plates, when indicated a
whether maxillary or mandibular, does ves­ti­
bule occurs and the depth of the trapezoidal flap can be used with one or
not consistently produce good results. sulcus is maintained. Usually the wound two releasing incisions. With a rongeur
In some cases of extreme alveolar atro­ mar­gins cannot be sutured together with­ bone-cutting forceps held parallel to
phy, rem­o­val of the hypermobile gin­ out reducing the depth of the sulcus. As bony margin of alveolar process, just
giva res­ults in a short ridge with a soft a result, many of these wounds heal by right amount of bone can be removed.
mucosal cov­ ering. Sulcus-deepening granulation and secondary epitheli­zation. Schram suggested that only one-half the
pro­cedures are necessary to permit con­ desired amount of bone be removed, as
struction of a den­­ture with a flange of this amount would be enough.
Hard Tissue Procedures
sufficient length to pro­vide some mea­
sure of denture sta­bi­lity. Cortical Alveoloplasty
Recognizing the limitations of sur­ Alveoloplasty In normal circumstances the residual
gical reduction of the hypermobile Alveolectomy has been defined by alveolar ridge is allowed to resorb and
ridge, Laskin (1970) had injected a Boucher42 as the excision of a portion mould itself after extraction, without
sclerosing solution into the hypermobile of the alveolar process. Only recently any additional surgical procedures.
gingiva in an effort to produce fibrosis ‘alveoloplasty’ has been adopted to However, if the denture construction
within the soft tissue and a resultant signify recontouring of the alveolar pro­ is more urgent, cortical alveoloplasty is
reduction in the mobility of the ridge. cess rather than its removal. Alveolo­ indicated. Cortical alveoloplasty may
He recommends that the patient should plasty is generally performed to facilitate be performed after extraction of a single
not wear his denture after the injections the removal of one or more teeth, and tooth, multiple teeth and teeth in the
lest tissue movement interfere with the to prepare the residual ridge for the entire arch.
fibrosis of the ridge. After 4 to 6 weeks, reception of artificial dentures. A crestal incision is made through
the ridge should be sufficiently rigid that Willard1 AT first reported (1853) a the extraction site. The projecting bone
a new denture may be made. case of alveolectomy, where he removed is removed with rongeur or surgical bur
the interdental papilla and alveolar and smoothed with a bone file. Soft tissue
Inflammatory Hyperplasia margin, permitting edge-to-edge clos­ure can be removed from the mesial and
of the Vestibular Mucosa of the soft tissues. Dean43 (1936) intro­ distal sides of the socket to facilitate linear
Chronic irritation from a poorly fit­ duced ‘Intra-Septal Alveolectomy’ a closure of the wound. The wound is closed
ting denture frequently results in the procedure he had been using since 1916. with interrupted or mattress sutures.
for­mation of areas of hyperplastic He advocated preservation of labial Dean alveoloplasty: Dean43 gave
enlar­ gement of the alveolar mucosa cortex at the expense of inter radicular this successful technique for preparing
(Fig. 13.13) and the mucous mem­brane medullary bone. the alveolar ridge for dentures. Thoma
of the vestibular sulcus. The terms ‘epu- described this procedure as inter-cortical
lis fissurata’ and ‘denture fib­roma’ have Types of Alveoloplasty rather than interseptal to describe the
been used to describe this lesion. These Alveolar compression: The easiest and removal of inter-radicular bone.44 ‘Crush
quickest form of alveoloplasty is the technique’ is also a common term used
compression of outer and inner corti­ for the same procedure. Regardless
cal plates between the fingers. This of the descriptive terminology, Dean
procedure should be done for all the technique and its results are based on
extra­ctions in which considerable mani­ sound biological principles:
pulation of the tooth with expansion of • The prominence of the labial and
buccal cortex was necessary. Compre­ buccal alveolar margin is reduced to
ssion reduces the width of the socket and facilitate the reception of dentures.
eliminates many otherwise troublesome • The muscle attachments are undis­
bony undercuts. Suture may or may not turbed.
be used to maintain soft tissues. • The periosteum remains intact.
Simple alveoloplasty: It is used to • The cortical plate is preserved as
trim the buccal or palatal cortical mar­ a viable onlay bone graft with an
Fig. 13.13: gingival hyperplasia gins after extraction of isolated tooth intact blood supply.
260 Dentoalveolar Surgeries

so the labial cortex became a freely


movable bone graft attached to only the
mucoperiosteum from which it received
its blood supply. The horizontal fracture
line in the apical area was smoothened
with a bone file from within the socket
to produce a smooth labial surface.
Dean used this technique on posterior
A B ridges as well as anterior ridges, making
a buccal cortical relief at the most
posterior socket.

Obwegeser Technique
for Alveoloplasty
Obwegeser29 suggested further modifi­
cation of Dean’s technique. In cases
of extreme premaxillary protrusion,
C D Dean’s technique would produce a
V-shaped anterior ridge instead of the
Figs 13.14A to D: Dean’s alveoloplasty: (A) Cross-sectional view prior to extraction;
(B) Removal of interdental bone; (C) Fracturing of labial cortex; (D) Approximation and desired U-shaped ridge. To avoid such
suturing of mucosa a ridge, Obwegeser fractured both the
labial and the palatal cortices.
Removal of teeth is done as usual.
Sockets are connected using rongeurs
or burs to remove the medullary inter-
radicular bone. Both the labial and
palatal plates are cut with burs in the
cuspid area to weaken the bone and
to form the three-sided bone flaps in
both cortical plates (Figs 13.15A to D).
A small mounted disk is inserted into
A B the sockets and through to score or
groove the labial and palatal plates,
horizontally weakening them along the
proposed fracture lines. Finger pressure
is then used to mold the alveolar process
into its desired shape. Sutures close the
gingiva over the sockets and help to hold
the bone in position. A denture on splint
is used to stabilize the fractured alveolar
process, which heals in 4 to 6 weeks.
C D The operation should be ‘performed’
Figs 13.15A to D: Obwegeser’s technique: (A) Cross-sectional view of ridge prior to on the plaster or stone model in the
extraction; (B) Scoring of labial and palatal cortex; (C) Both cortical plates fractured; labo­ratory first, and then a splint or
(D) Approximation of cortices and closure the denture should be constructed on
the ‘operated’ model. By planning the
procedure on plaster in the laboratory,
• Because the cortical bone is spar­ed, sary to permit the telescoping of the the surgery can be performed more
postoperative resorption is minimized. labial cortex, Dean used a chisel to accurately in the dental office or opera­
After removal of the teeth the inter­ make an inverted V-shaped excision of ting room.
radicular bony septa should be removed bone in the labial cortex of the cuspid
with a rongeur forceps (some operators socket. Thus, three sides of the labial Buccal and Labial Alveoloplasty
prefer chisels or burs) (Figs 13.14A to D). cortical flap were freed. At this point Reduction of the outer cortical plates is
To permit the labial cortex to be finger pressure usually was sufficient the oldest and most popular method of
moved palatally, some relief is neces­ to compress the cortex palatally. Doing alveoloplasty.
Preprosthetic Surgeries 261

An incision is made in gingival and and prominences can be removed with level as or at a higher level than the
a full thickness muco-periosteal flap a side-cutting rongeur. The ridge is then alveolar process. Frequently, the lingual
that extends at least one tooth on either smoothed with a bone file. Care must mucoperiosteum overlying the mylo­
side of area of bony surgery is elevated. be taken to avoid removing too much hyoid ridge becomes traumatized,
A sharp side cutting ronguer forceps is bone, since there is a deficiency of bone ulcerates, and fails to heal. In such a
held with one beak beneath the bony to begin with. The incision is closed case the bony shelf must be removed in
rim of the socket and other on the crest without tension by interrupted sutures, order to permit closure of the ulcerated
of the ridge. Small pieces of the bone can with caution exercised not to reduce the tissue with sutures.
be nibbled off the ridge. After the bone depth of the vestibular sulcus. Howe49 states that reduction of
is removed, a bone file can be used to the mylohyoid ridge is the most useful
smooth and perfect the bony contour. Maxillary Tuberosity Reduction single operation available for the grossly
This type of alveoloplasty is most An increase in the vertical dimension resor­bed mandible, for not only is the
suited in cases in which minimal bone of the maxillary tuberosity is frequently painfully sharp bony edge reduced, but
reduction is indicated. encountered. When of sufficient degree, the lingual sulcus is also lowered at the
this increase will impinge upon the inter­ same time.
Alveolectomy maxillary space required for successful The incision is made in the residual
and Alveolotomy45 denture construction. It may also be gingiva on the crest of the alveolar
The extraction of isolated posterior teeth pendulous, inhibiting denture stability process from the bicuspid to the third
commonly leaves prominent cortical and palatal bony undercuts may be molar region. In cases in which a mucosal
bone with superficial buccal undercuts. present. Pneumatization of the maxillary ulcer overlies the bony prominence the
A single longitudinal crestal or a narrow sinus may proceed into the elongated incision is adapted to include the ulcer.
elliptical subperiosteal incision permits tuberosity.46 In this way the lingual flap does not
access to these and their removal where have a ‘button hole’ perforation. The
indicated. Causes lingual mucoperiosteum is reflected
Troublesome undercuts are frequ­ • Gingival fibromatosis. care­fully, exposing the mylohyoid ridge
ently found on the labial surfaces of both • Loss of the lower molar teeth per­ and muscle. The mylohyoid muscle is
upper and lower anterior regions, some mit­ting over eruption of the upper attached to the edge and inferior surface
patient for unknown reason undergo molar teeth with an accompanying of the mylohyoid ridge and must be
grossly uneven alveolar resorption parti­ bony alveolar hyperplasia when carefully incised with a scalpel, keeping
cu­l­
arly of the labial or buccal plates, the teeth are extracted the enlarged the blade directed laterally toward the
which produces multiple irregular hori­ bony tuberosity may remain. mandible. Once the muscle has been
zontal bony protuberance on which it is • The resection of a maxillary 3rd reflected, the bony ridge can be reduced
impossible to fit satisfactorily denture. molar. with rongeurs and bone file. Interrupted
• An enlarged maxillary antrum. sutures close the wound and complete
Reduction of the Knife-edged Hyperplastic tuberosity is recon­ the operation. The detached mylohyoid
or Saw-tooth Ridge toured by wedge resection.47 Two elli­ muscle will reattach to the mandible at
Extreme alveolar atrophy of the mandi­ ptical incisions are made over the crest a lower level. If the patient already has a
bular ridge and occasionally of the of the tuberosity and carried down to denture, the lingual flange can be border
maxillary ridge often results in a sharp bone. The resulting wedge of tissue is trimmed with impression compound
residual alveolar crest that literally cuts grasped with a hemostat and dissected and relined temporarily with a soft
into the mucoperiosteum from the deep free and sutured in position. denture-lining material. The recon­tou­
surface whenever pressure is brought red denture flange serves to hold down
to bear on the area. Denture wearing Reduction of the Mylohyoid Ridge the mylohyoid muscle, resulting in a
becomes extremely painful in this situ­ Extreme alveolar atrophy sometimes deeper lingual sulcus.
ation. The pain is usually relieved when accentuates the mylohyoid ridge, which
the denture is removed, but mere finger can be palpated along the lingual surface Elimination of Labial Mandibular
pressure on the tender area will produce of the mandible in the second and third Undercut
the pain again. molar area. Occasionally the mylohyoid Many patients experience resorption
The incision should be made hori­ ridge and external oblique ridge are the of the mandibular alveolar process,
zontally in the gingiva just apical to highest points of the atrophic mandible, resulting in a marked labial and buccal
the alveolar crest, with a small relaxing since the alveolar process has been undercut due to more resorption in
incision at each end. The labial and reduced to a groove by resorption. the apical areas than at the alveolar
lingual flaps are reflected just far Gillies48 states that the mylohyoid crest. With such a ridge it is extremely
enough to expose the sharp bone at the ridge should be reduced whenever difficult for a patient to wear a denture
crest. Any sharp or rough bony edges the ridge is found to be at the same successfully.
262 Dentoalveolar Surgeries

Two methods of treatment are avail­ bilaterally along the median suture on If the torus extends to the posterior
able: the oral surface of the hard palate. The border of the hard palate, care must
1. Excision of the overhanging bone at etiology is unknown. Heredity, sup­er­ be exercised to avoid penetration thro­
the alveolar crest can be performed. ficial trauma, malocclusion, and fun­ ugh the soft palate into the nasal cavity
2. The undercut area can be filled and ctional response to mastication have (Figs 13.16A to D). Each flap is reflected
recontoured with a bone graft or some been suggested as possible factors.51 with a periosteal elevator and is sutured
biologically inert foreign material. Palatal tori serve no useful purpose. to the mucosa of the alveolar process to
If the alveolar process is broad, the Generally no treatment is indicated un­ keep it out of the operative field.
pati­­ent usually can afford to sacrifice a less: If the torus is small and pedun­culated
little buccal overhanging bone. Even if • They become as large as to interfere and if the palatal bone is thick, it is possible
the posterior ridge is narrow, the support with speech. to cleave the torus from the palate with a
offered by the oblique line will compensate • The mucosa becomes traumatized sharp blow of a mallet on a sharp, single-
for the narrow ridge. Anteriorly the prob­ due to trauma from occlusion, ulcer­ beveled chisel. In a broad based torus,
lem is more acute, if the anterior ridge is ates, and fails to heal because of its a no. 703 carbide fissure bur or another
reduced in size, it must bear a larger share poor vascularity. bone bur of comparable size, can be used
of the masti­catory load per unit area and • The patient cannot otherwise be to cut crisscross grooves, dividing the
eventually undergo additional resorption. convinced that he or she does not torus in multiple small segments, giving
In such cases it is useful to fill out the have a malignant tumor. it the appearance of a waffle. Once the
undercut rather than reduce the surface • The torus interferes with the design torus has been divided, the pieces can be
area. Tantalum mesh and cartilage have and construction of a removable removed with rongeur forceps or with a
been used to fill an undercut extending dental prosthesis. mallet and chisel, without the hazard of
from the right molar area around to the A median palatal incision is made in fracturing the palate.
left molar area with favorable results.50 the mucosa the full length of the torus The stump of the torus then is smoo­
Transplantation of autogenous al­ with two short, obliquely diverging thed with bone files, chisels or large bone
veolar bone can produce very satisfying incisi­ons at the anterior and posterior burs. The torus need not be reduced to
results and should be considered when­ ends, avoiding the vascular foramina. the extent that a concave palatal contour
ever bone is being removed for alveolo­
plasty.

Genial Tubercle Reduction


Genial tubercles give attachment to
genioglossus superiorly and geniohy­
oid inferiorly. One may note that the
separ­a­tion between the genioglossi and
genio­hyoids can often be identified by
a layer of fat between these muscles.
Approximately one-half or less of the
genioglossi are sectioned at the genial
tubercle on the superior and lateral
portions. Obwegeser reported that diffi­ A B
culty in swallowing will occur for several
months, if the genioglossi are sectioned
completely. The dimensions of the
genial tubercle are highly variable. Like
the mylohyoid ridge, sharp edges may be
trimmed, but do not require trimming
as they will usually resorb.

Torus Palatinus
Torus palatinus, or palatal torus, is a
benign, slowly growing, bony projection
of the palatine processes of the maxillae C D
and occasionally of the horizontal pla­ Figs 13.16A to D: Removal of palatal tor: (A) Transverse incision; (B) Division of large tori
tes of the palatine bones. It occurs into multiple fragments; (C) Smoothening the palatal bed; (D) Closure
Preprosthetic Surgeries 263

results. A flat palate, or even one with a • When the covering mucosa ulcerates
slight residual median ridge, is adequate as a result of trauma and fails to heal.
in most cases. • To facilitate the construction of re­
There is often a surplus of palatal mo­­­vable partial and complete den­
muc­ osa that can be trimmed with tures.
scissors, if desired and then the mucosa Removal of mandibular tori is not
is closed over the bony wound with non- difficult. It is easily accomplished in the
absorbable suture. Great care must be office with local anesthesia, frequently
exercised in suturing, as the thin mucosa at the same time as the removal of the
tears quite easily. Some surgeons prefer posterior teeth.
to save all or most of the surplus mucosa. The incision is made on the crest of
In such cases, the mucosa is replaced Fig. 13.17 : Torus mandibularis as seen on the alveolar process from the molar to
with the edges everted and held with occlusal radiograph the incisor region (Figs 13.18A and B).
mattress sutures so that the raw surfaces Most mandibular tori can be removed
of the two flaps are in contact. This chisel. After removal of the exostosis the by a sharp blow of a mallet on a sharp
results in a thicker mucosal covering in alveolar process is smoothened, and the chisel. In the case of a large, fusiform
the midline of palate. mucosa replaced and sutured. Only rou­ torus, it is helpful to use a dental bur
The most important postoperative t­ine post­operative care is necessary. to establish a plane of cleavage before
care is prevention of hematoma forma­ using the mallet. Water tight closure is
tion by the use of a rubber drain or Torus Mandibularis done to prevent any hematoma form­
by a splint or stent. A stent is used to Torus mandibularis, or mandibular ation. A stent can also be used to protect
adapt and support the mucosal flaps in torus, is an exostosis, usually occurring the thin lingual mucosa.
contact with the bone, thus eliminating bilaterally on the medial surface of the
dead space into which blood and serum body and alveolar process in canine- Ridge Augmentation Procedures
can accumulate. premolar region (Fig. 13.17). Mandibular Patients suitable for ridge augmentation
Several complications of torus remo­ tori are composed of dense, cortical bone should:
val are possible and all can be avoid or with minimal amounts of a medullary • Have gross mandibular atrophy, that
controlled.52 core. The overlying mucoperiosteum is the vertical symphyseal height of
• Hemorrhage. is very thin, as it is on the entire medial 2 cm or less.
• Hematoma. sur­face of the mandible. Laceration or • Be middle aged or younger and
• Sloughing of the palatal mucosa. traumatic ulceration of the mucosa is not medi­cally fit.
• Perforation of the floor of the nose. uncommon. Mandibular tori are remo­ved. • Be aware that a subsequent vesti­
• Fracture of the palate. • When they become so large that they buloplasty may be required.
cause speech impairment or diffi­ • Be grossly dissatisfied with their
Buccal Exostoses culty in eating. existing dentures.
For the prosthetic patient there are
two problems. Reduction of the buccal
exostosis is necessary for the accuracy
of the denture impression and the
stability and retention of the denture;
and yet this bone reduction could result
in excessive loss of cortical bone, thus
leaving the cancellous bone covered
only by mucosa. As a result, excessive
resorption of the alveolar process could
occur, substantially reducing not only
the size of the alveolar process, but also
the transverse width of the entire maxilla.
The incision is placed on the crest
of the ridge. An anterior, oblique or
relaxing, incision is made, if necessary,
to gain sufficient access to the area. The
mucosal flap is reflected to a level imm­ A B
edi­ately above the exostosis, which is Figs 13.18A and B: Lingual tori excision: (A) Incision and flap elevation; (B) Removal
removed with rongeurs, burs, or a sharp of tori using chisel/bur
264 Dentoalveolar Surgeries

Maxillary Ridge Augmentation


Surgical preprosthetic reconstruction of
the maxilla is complicated by several uni­
que anatomic features. The proximity
of the maxillary sinus to the nasal cavity,
the contour of the zygomatic buttress, the
position of the hamulus, and the nature
of the alveolar bone of the maxi­lla make
surgical augmentation more difficult than
it is in the mandi­ble. Con­tri­buting aspects
(such as peri­od­ ontal disease, malnutrition,
and men­­o­­pause) and systemic disease
Figs 13.19: total maxillary onlay bone Fig. 13.20: total maxillary interpositional
states (such as osteoporosis) should be grafting bone graft
evalu­ ated and corrected preoperatively
whenever possible. Once the ribs have been harvested, with onlay bone grafts by allowing for
Clinical examination should be con­ the orofacial region is approached. An earlier and better functional loading of
ducted systematically. Radiographic incision is made through the crestal the bone graft.55
examination will require panoramic tissue from tuberosity to tuberosity.
radio­­­graphs to evaluate the jaws for path­ A facial mucoperiosteal flap is reflected, Total Interpositional Bone
o­logy, sinusitis, retained teeth and roots, exposing the zygomatic crest of the Graft (Fig. 13.20)
residual bone height of the mandible, maxilla, the piriform apertures and, if Owing to the rapid resorption of the
proximity of the maxillary antrum to necessary, the infraorbital foramen. onlay graft system, Farrell et al.56 pre­
the alveolus, and position of the inferior Depending on the amount of facial tissue ferred the interpositional bone graft for
alveolar neurovascular bundle. Lateral available for closure, a limited palatal the atrophic maxilla with good palatal
cephalograms with the head in a natural flap may be developed. The rib graft vault form.
position and the lips in an unrestrained may be fixed by a variety of techniques, Patients with Class III relationships,
position will allow for evaluation of the including stainless steel wires and usually secondary to the edentulous
anteroposterior relationship of the max­ miniplates. Preparation of the rib for alveolar bone loss of both the maxilla
illa and the mandible as well as general grafting is performed on a separate table, and the mandible, can also benefit from
shape of the anterior maxilla and mandi­ while the maxilla is prepared. Using a anterior repositioning of the mobilized
ble. Vertical height, position of the genial cast of the maxilla, poured in acrylic and segment.
tubercles, and proximity of the sinuses gas sterilized for use in the surgical field, After the maxilla is down fractured,
and nasal floor can also be evaluated. An one rib is despined and kerfed (notched) an interpositional bone graft is per­
occlusal radiograph of the mandible can on the inner aspect (lesser curvature), formed with an allogeneic strut of bone
permit evaluation of mandibular width.53 allowing it to bend to the contour of the between the lateral antral walls. The
When a nearly flat surface exists between residual maxilla. The notching should bone graft, which has been shaped to the
the palate and the vestibule, replacement extend 270° around the rib cortex, allow­ proper height and dumbbell-mortised
of the supportive bone should be under­ ing for ease of bending. The rib is cut to for insertion along the lateral antral
taken. the appropriate length and shaped in wall, is positioned and retained in place
the posterior region to conform to the with transosseous wires through the
Onlay Bone Graft (Fig. 13.19) tuberosity. The rib is then stabilized as previously placed bur holes.
When resorption of the edentulous necessary and the rib strut is fitted to the
maxillary ridge is symmetric and the maxillary ridge. Once the rib strut has Total Maxillary Osteotomy
alveolar bone loss has been so extreme been stabilized, the flaps are mobilized with Advancement (Fig. 13.21)
as to reduce the maxilla to a nearly flat and evaluated to ensure adequate rela­ Maxilla has a natural tendency to resorb
surface between the palate and the x­ation of the closure. Closure is com­ to a smaller more posterior position,
vestibule, an onlay grafting procedure pleted with a horizontal mattress suture while the mandible seems to become
may be considered. Maxillary onlay and followed by oversewing with a more prominent with edentulous alveo­
bone grafting is indicated in cases of continuous suture for good wound edge lar bone loss. This combined with verti­
severe maxillary alveolar atrophy, flat eversion and a ‘belt and braces’ closure.54 cal over closure, gives the appearance
pala­tal vault form, mild to moderate It is believed that combining the of mandibular prognathism. If patient
antero­ posterior ridge relation discre­ onlay bone graft with the implants at the is deemed to have a deficiency in the
pancy and also used in isolated anterior time of the grafting procedure may retard an­teri­oposterior relationship or in the
ridge loss. the bone resorption often associated tran­sverse dimension, it can be corrected
Preprosthetic Surgeries 265

Fig. 13.21: Advancement of total Fig. 13.22: total mandibular onlay bone
osteotomized maxilla grafting

at the time of vertical augmentation with • Improvement of the maxillomandi­ Fig. 13.23: horizontal osteotomy for
inter positional bone grafting. bular relationship. interpositional bone graft augmentation
The maxilla can be positioned for­ • Increasing the bony bulk of the man­
ward for a predetermined distance and dible.
stabilized with the transosseous wires and • Providing adequate bone for implant surface. If ileum is used, the graft should
interpositional bone grafts. Graft should placement in selected patient. fit over the basal bone of the mandible.
be used if the advancement is greater Several procedures are available for
than 5 mm or if there is an anomaly that augmentation of edentulous mandible.58 Alternative Method
would increase the chan­ces of relapse. There is less chance of infection from By splitting both ribs and removing the
Stabilization is easily accomplished an autogenously bone graft because of cancellous bone, four sections of ribs
by placing a block of allogeneic bone, rapid healing. are placed so that each inner cortex is
hydroxyapatite,57 or autologous bone in next to an outer cortex. The cancellous
the posterior section and wedging the Total Onlay Graft (Fig. 13.22) bone and any chips from the excess
posterior aspects of the maxilla apart. For the mandible with generalized length of rib may be packed around the
However, this amount of movement is atrophy that measures less than 3 to rib. The total on lay graft to augment the
generally not necessary in these patients. 6 mm at the mental foramen region, mandible can achieve an immediate
there are few viable treatment altern­ increase in the mandible height equal to
Mandibular Procedures atives. The patient usually is unable to the height of the graft place.
A common pattern of mandibular EBL wear a lower prosthesis, has Class III
involves the generalized loss of alveolar ridge relationships, and is at risk for Augmentation to Inferior Border
bone, uniformly throughout the arch. injury from minor trauma. The total of Mandible (Fig. 13.23)
This tends to produce a mandi­ ble in onlay graft is one of the few surgical The procedure was suggested by Saun­
which the genial tubercles and mylohyoid options feasible for these patients. ders and Cox59 (1976). While as Beu­
ridges remain elevated and the rest of The graft material of choice for the to­ mer60 (1979), in their study showed that
the ridge is flat. The basal bone is all tal onlay graft should be auto­lo­­gous bone. inferior border grafting is superior to
that remains, leaving a mandible that Rib or ileum is satis­fac­tory. Pulmonary superior border grafting. Quinn61 (1992)
may appear pencil-thin on panoramic disease is a relative contradiction for gave a new technique for inferior border
radio­graphs. Clinically, a ‘negative ridge’ removal of an endogenous rib use as a augmentation and gave following indi­
exists where the muscle attachments graft. The sharp spine on the superior cati­ons:
have actually elevated above the region edge of rib is removed by nears of • Augmentation of severely atrophic
available for denture bearing. rongeur. If ileum is to be used, the medial edentulous mandible.
The height of remaining mandibular cortex and cancel­ lous marrow can be • Prevention of pathologic fracture.
bone may be measured at the mental harvested and contoured to appropriate • Management of non-union/mal-
foramen region. The area should be shape. The placement of the rib should union of severely atrophic mandible.
evaluated for height and width. be slightly toward the lingual surface Ribs are harvested and kerfing of ribs
The goal of surgical treatment to of the mandible, this is an attempt to is done. A deep submandibular incision
augment the mandibular ridge include: reproduce the position of the resorbed on both sides is taken. Subplatysmal
• Providing optimum ridge from for alveolar ridge. Anteriorly the rib should dissection is done to expose lower border
the support of a prosthesis. rest on the mandible toward the lingual done protecting the mental bundle.
266 Dentoalveolar Surgeries

The placement of one rib along lingual part of the mandible via a horizontal osteo­ the main fragment, fixing it with anterior
aspect and one along buccal aspect tomy below the alveolar nerve from one mattress and posterior circumferential
of inferior border done, space filled retromolar pad to the other. The cranial wires.
up with pieces of bone. Stabilization fragment was raised and supported by The incision is closed by one layer of
carried out using circumferential and interpositional plaster of paris or deprot­ buried absorbable sutures, which hold
interosseous wiring. Closure is done einized bovine bone 3 weeks later. He the raw surface together and the top layer
using non-resorbable sutures. later developed a one-stage technique.63 of continous or mattress sutures, which
must avert the mucosa. As the sutures
Advantages Visor Osteotomy (Figs 13.24A to F) are inserted, autogenous cancellous
• Does not obliterate the vestibule like An incision is made through the muco­ bone chips from the iliac crest are packed
intraoral onlay graft technique. periosteum of the alveolar crest and under the mucosa against the cancellous
• No chance of mucosal dehiscence. flaps raised. surface of the lingual bone as far back as
• Little orofacial pain and oral feeding Harle64 made the osteotomy cut the ramus.
is permitted. midway between the labial and buccal Dentures may be inserted three mon­
• Does not alter vertical dimension of cortices between the mental foramina ths postoperatively and, if necessary,
occlusion. and on the lingual third posteriorly to either a vestibuloplasty or a skin graft may
• Secondary lingual sulcoplasty is them so as to avoid the inferior dental be completed as soon there is radiological
not needed as mylohyoid muscle is canal. This produces a weak and often evidence of the consolidation of the
lowered in initial surgery. small lingual portion of bone, which bone graft. The procedure has the two
• Excellent for fracture stabilization is easily fractured. The inferior dental important drawbacks—width of mandible
and splints are not needed. bundle should be mobilized adequately. is reduced to half, no more than twice
• Lesser bone resorption as direct A groove is cut in the posterior molar its height can be gained and a potential
masticatory forces are not applied. area in the external oblique ridge and damage to inferior alveolar nerve (IAN).
• Patients with a history of sulcoplasty the bundle is reflected laterally and fixed
with skin graft placement—no viola­ onto the soft tissues of the cheek adjacent Visor Osteotomy with Bone
tion of the SSG. to the mandible by a loose catgut suture. Grafting
• Patients with a functioning sub­peri­ There are disadvantages to bundle The visor osteotomy doubles the mandi­
o­steal implant with atrophic ridge— mobilization: bular height and is therefore suitable,
strengthening of mandible with sal­ • The blood supply of the mandible is where the mandible is approxi­ mately
vage of implant. further reduced (Oikarinen65). How­ 2 cm or more in height. However, if
• Augmentation of pencil thin mandi­ ever, there is evidence that the supply the vertical height of the jaw is less or
bles where interpositional grafting/ may not have been of significance there is subsequent resorption the long
visor osteotomy is not possible. (Bradley3). term gain will not be sufficient. In this
• Skin graft vestibuloplasty is easier in • The bundle is attached to the lateral event the required gain can be achi­
inferior border grafting than super­ surface of the mandible by scar eved by the interposition of blocks of
ior border grafting. tissue after wound closure. This may corticocancellous bone.
increase the difficulty of subsequent
Disadvantages vesti­buloplasty. Sandwich Osteotomy (Fig. 13.25)
• Large extraoral incision with extra­ After reflection of the bundle, a A corticocancellous bone graft is har­
oral scarring. con­ti­
nuous vertical cut through the vested from iliac crest (5 cm2 cortical
• Redundant, loose tissue required to mandible is made by a surgical burr or and 15 mL cancellous). The recipient site
avoid distortion of facial appearance. oscillating saw midway between the preparation is as usual. Full thickness
• Does not correct superior border lingual and labial cortices from one side mucoperiosteal flap elevated by giving
irregularities. to the other as far as the reflected nerve incision between two retromolar pad
bundle. The assistant’s finger placed areas. Mental nerve is identified and
Interpositional Bone Graft beneath the jaw give warning that the freed. A lingual sub­periosteal tunnel in
Augmentation lower border has been reached. After retromolar region is made. A horizontal
In an attempt to overcome the disadvan­ completion of the vertical section, two osteotomy inferior to inferior alveolar
tage of subperiosteal onlay grafting (i.e. cuts are made with the oblique saw canal (IAC) with inferior angulation
rapid resorption), inter­ posi­
tional bone blade at right angles through the lingual of saw is done lingually. Superior seg­
graft techniques were developed. Barros- cortices in the vertical plane to complete ment is fractured upwards. Bone flap is
Saint-Pasteur,62 a pioneer in the field, the osteotomy. pedicled to genioglossus and supra­hyoid
initially described a two-stage procedure. Harle64 advised placing the lower muscles. Superior segment is reposi­
This involved mobilization of the alveolar 20% of the lingual bone in contact with tioned super­iorly. Cortical bone from
Preprosthetic Surgeries 267

A B C D

E F

Figs 13.24A to F: technique for visor osteotomy

packed around cortical struts and a water


tight closure of soft tissue is achieved.
The procedure suffers in that not
enough space is present between the
crest and foramina for horizontal cut,
if only anterior area is addressed the
posterior remains deficient and if done
below mental nerve, the risk of fracture
and damage to mental nerve from
overlying denture is present.

Modified ‘Visor’ Osteotomy


(Fig. 13.26)
The combination of the ‘visor’ and the Fig. 13.26: ostetomy cut for modified
‘sandwich’ techniques was designed visor osteotomy

Fig. 13.25: sandwich technique for to overcome the aforementioned dis­


mandibular ridge augmentation ad­vantages of both methods. A modi­
fication of the visor osteotomy has been the same position on the opposite side.
recom­mended for patients with at least The lingually pedicled segment is raised
ilium is harvested and placed in canine 8 mm of bone height as measured at the in visor fashion and wired into position.
and molar areas on both sides. Superior mental nerve region. This procedure This procedure has been modi­ fied in
segment is secured to inferior with thick involves a parasagittal split of the man­ various reports. Peterson and Slade,66
resorbable sutures. Cancellous marrow is dible from the midbody on one side to raised the lingual segment along a
268 Dentoalveolar Surgeries

greater length of the mandibular body Procedure osteo­tomy superiorly with the membrane
and added free chips of bone to the Local anesthesia is used by blocking to provide a roof for the graft material
lateral aspect of the raised bony segment. posterior superior alveolar and greater and the subsequent implants. Small
Frost et al.67 used a sagittal cut in the palatine nerves, plus infiltration. Use no perforations of the underlying memb­
body region of the mandible, but changed 15 scalpel blade, a palatocrestal incision rane do not require suturing and collapse
to a horizontal cut anteriorly. This allows is made extending from the canine area inward on themselves. Other perforat­ions
for use of a block of grafted bone in an posteriorly to vertical releasing incisions may be covered by placing a resorbable
interpositional fashion in the anterior in the tuberosity and canine fossa areas collagen wound dressing below the per­
region and for easy mobilization of the beyond the bony margins of the planned foration. This provides an interface bet­
pedicled segments, firm stabilization osteotomy. A full-thickness flap is ref­le­ ween the membrane and the graft.
with a corticocancellous block of bone in cted exposing the lateral maxilla, pro­ Various materials are used for bone
the anterior, and maintenance of the full viding access to the maxillary sinus. grafting such as autologous cancellous
width of the alveolar ridge. Using a high-torque rotary drill and a or corticocancellous bone from the iliac
The visor and modified visor osteo­ small round bur, a rectangular or oval crest, porous non-resorbable hydro­
tomies have largely been abandoned osteotomy or window is made through xyapatite, porous and non-porous re­
due to there drawbacks. the cortical bone, avoiding perforation sorbable hydroxyapatite, mineralized
of serous membrane. The inferior bor­ and non-mineralized freeze dried and
Sinus lift and Bone Grafting der of the osteotomy is located 2 to various combination of graft materials.
of the Atrophic Maxilla 3 mm above the alveolar crest and is The graft materials, after packing is con­
(Figs 13.27A to G) generally 10 to 20 mm in length. The tained by the sinus floor inferiorly, the
The loss of maxillary posterior dentition superior osteotomy of this window is 10 superiorly positioned bony window or
at an early age enhances sinus enlarge­ to 15 mm above the inferior osteotomy. resorbable collagen dressing, if placed
ment at the expense of the alveolus and Two vertical osteotomies connect the superiorly, the elevated Schneiderian
an increased sinus pneum­ ati­
zation superior and inferior osteotomy. membrane medially and the resutured
decre­ases the amount of available bone The sinus membrane is gently teased mucoperiosteal flap laterally.
in this area of the maxilla with ardent from the sinus floor and lateral wall and Stage I implant surgery is generally
of dental implants it is now possible to the bony osteotomy is gently pushed performed 6 to 9 months following the
improve prosthetic reconstruction by inward or medially at the inferior border, bone grafting procedure. Stage I implant
lifting the sinus membrane prior to bone hinging on its superior border, keeping surgery may be performed at the time of
grafting of this region and subsequently the sinus membrane away from the sinus bone grafting, if adequate residual bone
placing dental implants. floor at the same time, elevating the is available prior to grafting (3–6 mm).

A B C D

E F G
Figs 13.27A to G: Sinus lift procedure
Preprosthetic Surgeries 269

A B C D

E F G
Figs 13.28A to G: Sinus lifting procedure with autogenous bone graft and coverage with allographic membrane: (A) Incision; (B) Flap
reflection; (C) Exposure of the wall of sinus; (D) Bone grafting; (E) Membrane to cover the area; (F) Membrane fixed with titanium track;
(G) Closure

Sinus lifting procedure with auto­ and distractor is removed. Osteotomy After desired amount of distraction
genous bone graft and coverage with allo­ is performed with divergent vertical is achieved, the consolidation period is
graphic membrane (Figs 13.28A to G). cuts to prevent undercuts at the inferior initiated and continued for 8 to 12 weeks.
osteo­tomy margins. After completion After completion distractor is removed,
Alveolar Ridge Distraction of cuts the transport segment should be preferably under local anesthesia.
The Russian orthopedic surgeon, Gavriel mobilized carefully using an osteotome. The complications of this procedure
Ilizarov, pioneered the recon­ struction The distractor is then placed and secured are as follows:
technique of distraction osteo­genesis for with screws and acute activation of • There are chances of mandibular
managing a variety of limb deformities.68 distractor is done to check for functioning fracture in severely resorbed mandi­
In distraction osteogenesis bone trans­ of distractor. Then mucosa is closed with ble, while distraction.
port is done with help of distractor. nut of distractor exposed so that it can be • If during surgery the osteotomy cuts
Reten­tion of complete denture in patient used later to transport the segment. result in improper vector for distrac­
with severe atrophy of alveolar processes After 5 to 7 days of latency, distra­ tion, then it will lead to formation of
is extremely difficult (Figs 13.29A and ction begins at the rate of 0.5 mm two undesirable shape of alveolar process.
B). It overcomes the disadvantages of times per day, thereby displacing the • If blood supply of the transport
autogenous grafting such as additional upper segment to desired height. The segment is hampered during surgery
surgical site morbidity and graft failure amount of augmentation can be asse­ by accidental stripping of lingual
due to infection or improper healing. ssed radiographically at regular intervals mucosa attached then necrosis of
intervals (Figs 13.30 and 13.31). bone segment can occur.
Technique
In this procedure a horizontal incision on
the vestibular surface is made followed by
exposure of alveolar process by reflecting
mucoperiosteal flap. Lin­g­­u­­ally mucosa
remains attached to the bone, providing
blood supply to trans­port bone segment
during distr­action. After identification of
mental ner­ves bilaterally and preparation
of adeq­uate space in soft tissues, vertical
distraction system is fitted submucosally A B
and temporarily attached with single Figs 13.29A and B: resorbed mandible (Source: craniofacial distraction osteogenesis
screw. Then osteotomy site is marked 2001 mosby)
270 Dentoalveolar Surgeries

14. Garver DG, Fenster RK. Vital root


reten­ tion in humans: A final report.
The Journal of Prosthetic Dentistry.
1980;43(4):368-73.
15. Garver DG, Theodore E. Muir: The
retention of vital submucosal roots
under immediate dentures: A surgical
procedure. The Journal of Prosthetic
Dentistry. 1983;50(6):753-6.
16. Boyne PJ, Rothstein SS, Gumaer Kl,
et al. Long-term study of hydroxylapatite
A B
implants in canine alveolar bone.
Figs 13.30A and B: Surgical procedure with distraction in situ and activated distraction.
Journal of Oral and maxillofac Surg.
(Source: craniofacial distraction osteogenesis 2001 Mosby)
September 1984;42(9):589-94.
17. Ashley, et al. Preprosthetic Surgeries.
3. Bradley JC. Age changes in the vascular In: Carl Kruger (Ed). Textbook of
supply of the mandible. British Dental Oral and Maxillofacial Surgery. WB
Journal. 1972;132:142. Saunders.
4. Branzi A, Quintarelli G. Ulteriore contri­ 18. Obwegeser H. On the indication for
bute allo studio anastomois­tolo­gico delle the various methods of vestibuloplasty
modificazioni dellarteria muscellare and plastic surgery of the floor of the
interna nelle varie eta dell’uomo. Riv Ital mouth. Fortschr Kiefer Gesichtschir.
Stomat. 1956;11:1. 1965;10:1-8.
5. Robling AG, Castillo AB, Turner CH. 19. Obwegeser H. Die submukoese Ves­
Biomechanical and molecular regulation tibulumplastik Dtsch Zahnaerztl Z
of bone remodeling. Annu Rev Biomed 1959;14: 629-39.
Eng. 2006;8:455-98. 20. Fouad Al-Mahdy Al-Belasy. Mandi­
6. Enlow DH. The remodeling of the bular Anterior Ridge Extension: A
eden­­tulous mandible. The Journal of modification of the kazanjian vestibulo­
Pro­sthetic Dentistry. 1976;36(6):685-93. plasty technique. Oral Maxillofacial
7. Jaime Pietrokovski, et al. Morphologic Surgery. 1997;55.
Fig. 13.31: postoperative radiograph with chara­cteristics of bony edentulous jaws. 21. Wallenius K. Ridge extension: A modi­
distractor placed anteriorly on mandi­ ble.
Jour­nal of Prosthodontics. 2007;16(2): fied operative technique. J Oral Surg
(Source: craniofacial distraction osteogenesis
2001 Mosby) 141-7. Anesth Hosp Dent Serv. 1963;21:54.
8. Lammie GA. The reduction of the eden­ 22. Kazanjian VH. Surgery as an aid to
tulous ridges. The Journal of Prosthetic more efficient service with prosthetic
• In severely resorbed ridge there are Dentistry. 1960;10(4):605-11. dentures. J Am Dent Assoc.1935;22:
chances of damage to the inferior 9. Schweitzer JM. The telescoped com­ 566.
alveolar nerve. plete denture: A research report at the 23. Godwin JG. Submucous surgery for
Distraction osteogenesis is a valuable clinical level. The Journal of Prosthetic better denture service. J Am Dent
method of augmentation of the alveolar Dentistry. 1971;26(4):357-72. Assoc. 1947;34:678.
process when performing preprosthetic 10. Dhir RC. Clinical assessment of the 24. Cooley DO. A method for deepening
surgery, even in cases of extremely resor­ overdenture therapy. J Indian Prostho­ the mandibular and maxillary sulci to
bed mandible. In addition, it decreases dont Soc. 2005;5:187-92. correct deficient edentulous ridges. J
additional morbidity and requires only 11. Helsham RW. Some observations on Oral Surg. 1952;10:279-89.
single operation. the subject of roots of teeth retained 25. Collett HA. Immediate maxillary ridge
in the jaws as a result of incomplete extension. Dent Digest. 1954;60:104-6.
exodontia Aust Dent J. 1960; 5:70-7. 26. Clark HB Jr. Deepening of labial sulcus
References
12. Casey DM, Lauciello FR. A review of by mucosal flap and vancement: Report
1. Willard AT. Ridge preparation for the submerged root concept. J Prosthet of a case. J Oral Surg. 1953;11:165.
eden­­tulous cases. Am J Dental Science. Dent. 1980;43:128-32. 27. Edlan A. Prosthetic repair of the vesti­
1853;4:134. 13. Garver DG, Fenster RK, Baker RD, et al. bule of the maxilla. Cesk Stomatol.
2. Atwood DA. Bone loss of edentulous Vital root retention in humans: a preli­ 1953;53(5):271-6.
alveolar ridges. J Periodontol. 1979;50: min­ary report. J Prosthet Dent. 1978; 28. Caldwell JB. Lingual Ridge Extension. J
11 (4 Special Issue). 40(1). Oral Surg. 1955;13:287.
Preprosthetic Surgeries 271

29. MacIntosh RB, Obwegeser HL. Prepro­ 42. Hickey JC, Zarb GA. Boucher’s prosth­ vestibuloplasty of the atrophic maxilla.
sth­etic surgery: A scheme for its effec­ odontic treatment for edentulous pa­ J Oral Surg. 1976;34(10):901-6.
tive employment. J Oral Surg. 1967; tients (8 edn). The CV Mosby Co., St 57. Albert RM. Wittkampf: Augmentation
25;397-413. Louis (1980). of the Maxillary Alveolar Ridge With
30. In: Fonseca R, Davis W, (Eds): Recon­ 43. Dean OT. Surgery for the denture Hydroxylapatite and Fibrin Glue;
structive preprosthetic oral and patient. J Am Dent Assoc. 1936;23:2124. JOMS. 1988;46.
maxillo­ facial surgery, Philadelphia, 44. Thoma KH, Holland DJ: Atrophy of the 58. Mercier P. A comparative study of the
WB Saunders. 1985;64-9. mandible. Oral Surg. 1951; 4:1477. efficacy and morbidity of five tech­
31. Obwegeser HL. Die Totale Mund­ 45. Hopkins R. Alveolectomy and alveolot­ niques for ridge augmentation of the
bodenplastik. Schweiz Mschwr Zahn­ omy, in Moore JR: Surgery of the Mouth mandible; JOMS. 1952;50.
heilk. 1963;73(7):565-72. and Jaws. Oxford, Blackwell Scientific, 59. Sanders, Cox R. Inferior border rib
32. Steinhauser E, Obwegeser H. Rebuil­ 1985. pp. 449-50. graft­ing for augmentation of the atro­
ding the alveolar ridge with bone and 46. Leonard M. The maxillary tuberosity: phic edentulous mandible. J Oral Surg.
cartilage autografts. Trans Congr Int indi­ cations and simple technique for 1976;34:897.
Assoc Oral Surg. 1967. pp. 203-8. red­­u­­c­tion. Dent Today. 2001;20(2):52-5. 60. Beumer J. Complete dentures for pati­
33. Trauner R, Eskici A, Kurhajec P. Alveo­ 47. Hernandez A. Maxillary tuberosity ridge ents with mandibular inferior border
plasty with ridge extension. British reduction. Dent Surv. 1978;54(3): 43-4. rib grafts. J Oral Surg. 1979;37:301.
Journal of Oral Surgery. 1970;8(1):70-6. 48. Gillies RJ. A surgical aid to a prosthetic 61. Quinn PD, Kent K, MacAfee KA. Recon­
34. Black EE, Moore JR. Modified technics problem. Aust dent J. 1956;1:329. structing the atrophic mandible with
in mandibular pre prosthetic surgery. J 49. Thomas J. Starshak, Bruce Sanders inferior border grafting and implants: A
Oral Surg. 1970;28:184. editors: Preprosthetic oral and maxi­ preliminary report. Int J Oral Maxillofac
35. Miller EL. Sometimes overlooked: pre­ llo­­facial surgery. pp. 99-101. Implants. 1992;7(1):87-93.
pr­o­­sthetic surgery. JPD. 1976;36. 50. Guernsey LH. Preprosthetic surgery 62. Barros-Saint-Pasteur J. Plastic restor­
36. Cutright DE. Morphogenesis of inflam­ in Textbook of Oral and Maxillofacial ation of the alveolar crest of the mandi­
m­ atory papillary hyperplasia. The Surgery Gustav O Kruger. 5th edn. ble. Acta Odontol Venez. 1966;4(1):3-21.
Jour­nal of Prosthetic Dentistry. 1975; St Louis, Toronto, London, The CV 63. Barros-Saint-Pasteur J. Plastic recon­
33(4):380-5. Mosby Company, 1979. struction of the alveolar crest. Clinico-
37. Ettinger RL. The etiology of inflamm­ 51. Rezai RF, Jackson JT, Salamat K. Torus surgical investigation. Acta Odontol
atory papillary hyperplasia. The palatinus, an exostosis of unknown Venez. 1970;8(2):168-82.
Journal of Prosthetic Dentistry. 1975; etiology: review of the literature. 64. Harle F. Visor osteotomy to increase
34(3):254-61. Compend Contin Educ Dent. 1985; the absolute height of the atrophied
38. Steven A, Rathofe. A comparison of 6(2):149-52,147. mandible. J Maxillofac Surg. 1975;3:257.
healing and pain following excision 52. Ghalichebaf M, Bycroft B, Graves R. An 65. Ylikontiola L, Kinnunen J, Oikarinen K.
of inflammatory papillary hyperplasia unpredictable result from a torus pala­ Factors effecting neurosensory distur­­
with electrosurgery and blade-loop tinus removal and its treatment: a clini­­cal bance after mandibular bilateral sagi­
knives in human patients. Oral Surgery, report. J Prosthet Dent. 1992; 68(3):397-8. ttal split osteotomy. J Oral Maxill­ofac
Oral Medicine, Oral Pathology. 1985; 53. MacIntosh RB, Obwegeser HL. Pre­ Surg. 2000;58:1234.
(2):130-5. prosthetic surgery: a scheme for its 66. Peterson LJ, Slade EW. Mandibular
39. Getter L, Perez B. Controlled cryoth­ effective employment, J Oral Surg. ridge augmentation by a modified visor
erapy in the treatment of inflammatory 1967;25:397-413. osteotomy: A preliminary report. J Oral
papillary hyperplasia. Oral Surgery, 54. Terry BC, Albright JE, Baker RD. Alve­­olar Surg. 1977;35:999.
Oral Medicine, Oral Pathology. 1972; ridge augmentation in the edentulous 67. Frost DE, Gregg JM, Terry BC, et
34:178-86. maxilla with use of auto­genous ribs, J al. Mandibular interpositional and
40. Desjardins RP. Etiology and manage­ Oral Surg. 1974;32: 429-34. onlay bone grafting for treatment of
ment of hypermobile mucosa overlying 55. Kahnberg KE, Nystrom E, Bartholdsson mandibular bony deficiency in the
the residual alveolar ridge. JPD. 1974; L. Combined use of bone grafts and edentulous patient. J Oral Maxillofac
32. Branemark fixtures in the treatment of Surg. 1982;40(6):353-60.
41. Gongloff RK, Woodard KL. A surgical severely resorbed maxillae. Int J Oral 68. Samchukov ML, Cope JB, Cherkashin
technique for the correction of the Maxillofac Surg. 1989;4:297-304. AM. Craniofacial diteraction osteo­
hypermobile anterior maxillary ridge. J 56. Farrell CD, Kent JN, Guerra LR. One- gensis, 2001, Mosby.
Oral Surg. 1981;39:340-2. stage interpositional bone grafting and
Section 4
Maxillary Sinus

n Diseases of Maxillary Sinus


14 Diseases of
Maxillary Sinus
Borle Rajiv M, Arora Aakash, Nimonkar Pranali V

The maxillary sinus is of great applied maxillary sinus is variable even in two have incomplete bony septae. It opens
importance to an oral surgeon due to sides of a same skull. It has an average in the middle meatus of the nose in the
its anatomical proximity to the teeth. It height of about 3.5 cm in molar area, hiatus semilunaris, through an opening
is commonly involved in inflammatory an average transverse width of about called ostium maxillare, which is present
disorders of dental origin, especially 2.5 cm and an average anteroposterior in anteriosuperior part of the base of
from the upper premolars and molars. depth of about 3.2 cm.3 The maxillary hiatus semilunaris (Fig. 14.2). The clinical
Injudicious instrumentation in this sinus is pyramidal in shape with its base osti­um is smaller than the bony ostium.
area during the exodontia procedures towards the lateral nasal wall and apex Thus, its opening is situated at a higher
can lead to oroantral communications. directed towards the zygomatic process level than the base of the sinus. The sinus
The malignant lesions originating from of maxilla. It is the largest and the most is lined by pseudostratified, columnar,
maxillary sinus involve the teeth. Simi­ important of all the paranasal sinuses. ciliated epithelium and gob­ let cells,
larly, pain originating from the sinus It has got a roof, which is the floor of which secrete the mucous. The rhythmic
may be referred to the teeth (referred the orbit and is ridged by the presence of beat­ing of the cilia is res­ponsible for the
odontalgia) and can be mistaken as infraorbital canal, floor (alveolar pro­cess) drainage of the sinus against the gravity.
dental pain. The dental surgeon may be which is about 1.25 cm below the nasal The posterosuperior part of lateral wall
the first person to see the patient in both floor, anterolateral wall, post­erol­ateral wall of inferior meatus is the thinnest area
the latter conditions and is expected to and the posterior wall. The posterolateral and is the preferred site for the nasal
diagnose these conditions correctly. wall forms the medial boundry of the antrostomy.
infra­temporal fossa. The roof of the sinus
APPLIED SURGICAL is very thin and the infraorbital nerve AGE CHANGES IN THE
may lay hanging in the sinus (Figs 14.1A
ANATOMY1,2 MAXILLARY SINUS
and B). The floor has several bony pro­
The maxillary sinus is the largest of all jections, which correspond to the roots At birth the maxillary sinus is an oblong
the paranasal sinuses. The size of the of the maxillary teeth and the sinus may cavity longer anteroposteriorly than

A B
Figs 14.1A and B: Various walls of the maxillary sinus
276 Maxillary Sinus

process takes place and the floor also upper airway, including the maxillary
starts descending down, (Fig. 14.3). At sinus.6 The sinus lining becomes edema­
around 12 years, the floor of the sinus is tous, inflamed and congested. This leads
at level with the floor of the nose. to excessive secretion of mucous, loss
In the elderly persons, as there is a loss of ciliary action, stasis of secretions and
of the teeth and atrophy of the alveolar secondary infection. The primary infec­
process occurs, the bone separating the tion of the sinus occurs when the sinus
oral cavity and the floor of maxillary sinus gets exposed to the exogenous mic­ro­
becomes thin and the chances of oroantral organisms, e.g. when there is an oroantral
fistula are incre­ased (Fig. 14.4). fistula or a foreign body in the sinus.7
The sinus depends on the action of The exposure of the sinus during tra­
Fig. 14.2: Conchi and meati on the lateral the cilia for its drainage. The lack of ciliary u­ma may also lead to the sinusitis. The
nasal wall with ostium maxillary in the
action leads to stasis of secre­tions, which sinus can also get infected secondary to
middle meatus
leads to infections. The blood supply of the odontogenic pathology. The apices
the sinus is from facial, infraorbital and of maxillary molars and the premolars
greater palatine vessels4 and its lymphatic are very close to the floor of the sinus.
drainage is to sub­ mandibular lymph A chronic periapical infection leads to
nodes. The nerve supply to the sinus is destruction of intervening bone and the
from infraorbital, anterior, middle and infection enters the sinus (odontogenic
posterior superior alveolar nerves. The sinusitis). The destruction of the floor of
sinus attains its full growth with the the sinus by tumors can also lead to the
eruption of permanent teeth. At the old infection of the sinus.
age, the teeth are exfoliated and the alve­
olar process becomes resorbed and atro­ Etiology of Maxillary Sinusitis
phic and thus the floor is close to the oral • Overwhelming infection.
cavity. The diseases of the maxillary sinus • Interference with antral drainage:
can be classified as shown in (Box 14.1). – Congenital anatomical abnor­
Fig. 14.3: Fetal skull showing floor of malities leading to decreased
maxillary sinus above the floor of nose due dra­i­­­nage.
to underdeveloped alveolar process MAXILLARY SINUSITIS
– Deviated nasal septum (DNS),
The maxillary sinusitis is usually secon­ cau­­s­ing obstruction to the drain­
dary to allergy or infection.5 The inhaled age.
pollens get deposited on the lining of the – Paradoxical turbinates.
– Malformed uncinate process.
• Alteration in quality of mucosa—
Box 14.1: The classification of the cystic fibrosis.
diseases of the maxillary sinus • Ciliary dysfunction:
– Kartagener syndrome8—combi­
• Developmental disorders nation of situs inversus, chronic
• Inflammatory diseases sinusitis and bronchiectasis.
– Allergic – Smooth cilia syndrome
– Infective – Young syndrome9—bronchi­ec­
– Odontogenic
ta­­sis, rhinosinusitis and reduced
– Degenerative
– Traumatic fertility.
• Neoplastic diseases – Samter’s triad10—combination
– Primary tumors – carcinoma, of asthma, aspirin sensitivity and
Fig. 14.4: Skull of an elderly person show­
papillomas na­sal/ethmoidal polyposis.
ing thin bone in the floor of sinus due to – Tumors, originating from oral
atrophy of alveolar process – Rhi­nitis medicamentosa.
cavity and secondarily involving
the sinus, like oral squamous cell
• Nasal obstruction:
carcinoma, odontogenic tumors – Choanal atresia.
sup­­
er­
oinferiorly with the floor above and cysts, minor salivary gland • Odontogenic sinusitis:
the level of floor of the nose. In the early tumors, etc. – Dentoalveolar abscess.
childhood, the floor of the maxillary • Cysts—mucoceles – Periapical granuloma or infected
• Granulomatous diseases—Hansen’s
sinus is above the floor of the nose and as periapical cyst communicating
disease, Wegener’s granuloma
the teeth develop, the growth of alveolar with the sinus.
Diseases of Maxillary Sinus 277

Box 14.2: Classification of the Box 14.3: Clinical signs of sinusitis • Cough: The trickling of secretions to
sinusitis as per duration the lower respiratory passage (no­c­
• Pain turnal postnasal drip) leads to infe­
• Acute (< 4 weeks) • Fever
c­­tion of lower respiratory tract and
• Subacute (4–12 weeks) • Headache aggrevated on bending
• Chronic (> 12 weeks) • Nasal stuffiness productive cough.
• Nasal discharge–mucoid, purulent, foul • Spread of infection to other para­na­
smelling sal sinuses leads to signs of pansinu­
• Anosmia sitis. The maxillary sinus is usually
• Involvement of the sinus during sur­ • Negative transillumination test the first to be involved as its opening
• Haziness of sinus on X–ray
geries (OAF): is at a higher level than the floor. As
• Epistaxis
– Facial trauma. • Referred odontalgia the drainage is nondependent, the
– Tumors of maxillary sinus or na­ • Cough drainage basically depends on the
sal cavity. functioning of cilia. The inflamm­
• Fungal sinusitis:11 ation of the sinus lining leads to loss
– Common fungal infections are of ciliary function, stasis of secretions
Aspergillus, mucormycosis, can­ smel­ling secretions from the nose and and secondary infection.
di­­di­asis. presence of congestion in the nasal • Radiological examination reveals
– Aspergillus infection occurs in mucous membrane, which are absent haz­­i­­­ness of the maxillary sinus (Fig.
he­althy patients without rela­ti­on­­­­ in dental pains. Classical tenderness 14.5A) on X-ray paranasal sinu­ ses
ship to pulmonary asper­gill­osis. can be elicited over the involved (PNS also called PA Water’s sinus
– Mucormycosis occurs in uncon­ sinus and all the maxillary posterior view). In the cases of chronic sinusitis
trolled diabetes mellitus. teeth may be tender to percussion in the entire sinus appears hazy and
– Candidal infection occurs in pati­ absence of any obvious pathology. the sinus lining may show thickening
ents with long-term anti­biotics. The sinus tenderness is associated (Figs 14.5B and C). When poly­poi­dal
The maxillary sinusitis can be fur­ with erythema and flushing of the growth is present, a soft tissue shadow
ther class­ified according to duration as cheek and the patient often complains of the polyps may be seen. In case of
(Box 14.2). of heaviness over the sinus. Thus, the empyema antri, when the X-ray PNS
In the chronic sinusitis although clinician must be careful while exam­ is taken in sitting position, a clear cut
the clinical signs and symptoms are ining such cases (Box 14.3). fluid level is seen, which is not seen if
mild, there are degenerative changes in • Nasal discharge: The mucous dis­ the X-ray is taken in the lying position
the lining which leads to loss of ciliary charge from the nose on the involved as the fluid spreads in the sinus in this
action, stasis of secretions and acute side increases. The discharge is position13 (Figs 14.6A and B). The fluid
exacerbation of the infection. increasingly foul smelling in chronic level also shifts on tilting of the head.
cases and purulent in nature in cases • Antroscopy done using an endoscope
Clinical Features where there is suppuration (empy­ passed through a nasal antrostomy
•Pain and tenderness over the maxi­­ ema antri).12 The edema of the nasal could be useful in studying the poly­­
llary sinus, which is usually asso­ lining and the thick secretions lead to poid growths, mucoceles or for­eign
ciated with headache. The head­ache nasal stuffiness and blockade. bodies in the sinus and for taking
is often due to involvement of other • Epistaxis: The inflamed sinus lining biopsies of the intra-antral gro­wths.14
sinuses, especially the frontal and bleeds on blowing of nose or spon­ • Transillumination test is negative when
sphenoid sinuses. In pansi­ nusitis, taneously. In chronic sinusitis, polyp the sinus is grossly inflamed, occup­ied
the headache is a consistent feature. formation occurs which also bleeds with pus, hematoma or tumor.
The headache often gets aggravated readily.
on bending forward and radiates • Fever: In acute sinusitis the patient Management
to the eye. The pain also radiates to has fever, malaise, bodyache and The management of sinusitis can be
the teeth and is often mistaken as other systemic signs of infection. divided into (Flow chart 14.1):
den­tal pain (referred odotalgia) and • Anosmia: The temporary loss of • Medicinal treatment.
the dental surgeon may be the first smell sensation results due to edema • Surgical treatment.
person to be consulted by the patient of the nasal lining and nasal blockade
for the same. due to secretions. Medicinal Treatment15
This pain can be differentiated • Nasal stuffiness due to edema, sec­ • In cases with allergic sinusitis, anti­
from dental pain by absence of acute re­­tions or polyps. histaminics and decongestants are
septic focus in the area, tenderness • Purulent/foul smelling discharge prescribed. Antibiotics are often
over the sinus, increased and foul due to infection. pre­s­cri­bed to prevent secondary
278 Maxillary Sinus

A B C
Figs 14.5A to C: (A) Early sinusitis showing mild haziness of the left sinus; (B) Chronic sinusitis showing thickening of the left
sinus lining; (C) Chronic sinusitis showing complete haziness of right sinus

further stasis. Hence, mucolytic drugs


like bromhexine in a dose of 8 mg,
three times a day can be prescribed.
The steam inhalation is particularly
useful as it has decongestant and
mu­ co­lytic action. Mucolytics and
decongestants like tinc­ture benzoin,
cam­ phor, chlorbutol and menthol
are commonly used. How­­ever, some
A B clinicians believe that these agents
may cause rebound con­ge­stion.
Figs 14.6A and B: Fluid level note the shifting of the fluid level on tilting of the head
• The topical decongestants (Ephed­
rine sulfate 0.5% or 1% in normal
saline, Xylometazoline HCl 0.1%)
Flow chart 14.1: Treatment of maxillary sinusitis should be used judiciously as their
excessive use can lead to rhinitis
medicamentosa and lead to further
loss of ciliary action. Instead the
plain normal saline drops are safe.
The systemic decongestants like
phenylpropanolamine and pseudo­
ephidrine are often useful.
The above mentioned treatment
comprising of antibiotics, antihis­
taminics and decongestants and
steam inhalation are collectively
called ‘sinus regime’.

Surgical Treatment
Nasal Antrostomy
The nasal antrostomy done in the infer­
ior turbinate is very useful in establi­shing
infection. Macrolide of antibiotics losporins, peni­­­­cillin group of antibi­ a dependent drainage for the sinus,
are pre­ ferred as they cover gram otics are also commonly used drugs. especially when the ciliary function is
positive orga­nisms, which are com­ The anal­g­­esics and antipyretic drugs comprised and the normal opening is
monly seen in upper respiratory are pre­scribed to relieve the pain blocked by edema, congestion or by
tract infections. Erythromycin, Roxi­ and fever. a polyp or a tumor. It helps in clearing
thromycine or Azithromycin are the • The use of antihistaminic tends to the stasis, drainage and in relieving
commonly used macrolaids. Cepha­ dry up the secretions and can lead to the pain. It is a simple procedure done
Diseases of Maxillary Sinus 279

under local anesthesia using a trochar • Foreign bodies in the sinus. achieved by packing with roller gauze.
and cannula on outdoor basis. Antral • For diagnostic purpose As the lining is removed, the ciliary
lavage can also be done through this site • For elevating the fractures of zygoma action is absent due to removal of
with the help of normal saline solution. and the floor of the orbit. the lining. So to facilitate free gravity
The resolution should occur nor­ dependent drainage nasal antrostomy
Procedure
mally with medicinal treatment and the is done. The pack left in situ for
antrostomy. The resistant cases, which The Caldwell-Luc operation is per­ achieving hemostasis, the end of the
do not respond to this treatment and formed under general anesthesia. An pack is taken out through the nasal
change to a chronic sinusitis require intraoral degloving incision is taken antrostomy site and intraoral incision
further surgical treatment in the form of in the labial vestibule over the can­ is closed primarily. The sinus regimen
Caldwell-Luc operation. ine fossa (Fig. 14.7B1). The bone is is started and continued for 8 to 10
exposed. The round bony cut is mar­ days. The excised lining is submitted
Caldwell-Luc Operation16 ked over the canine fossa using a for histopathological examination.
It is the surgical procedure for access­ round bur (post stamp incision) and The alternative procedure for the
ing the maxillary sinus. It can be done the incision is completed with a fissure Caldwell-Luc operation is Denker’s pro­
for dia­gnostic (biopsies of intra-antral bur or an ossisector. When a pre- cedure in which in addition to Caldwell-
gro­wths) or for therapeutic purposes exis­
ting oroantral fistula is present, Luc surgery a slit of bone is removed from
(Fig. 14.7A). the same bony defect is widened to the anterior bony angle of the antrum
create an access to the sinus. The right up to the lateral nasal aperture so as
Indications
opening should be wide enough to to render continuous, free, unimpeded
• Chronic sinusitis with severe dege­ permit adequate access to the sinus drainage of the sinus from the canine
ne­ration of lining, polypoid growths, (approximately of the size of the index fossa and the nasal cavity (Fig. 14.7B2).
mucoceles in the lining. finger). Under good illumination the
sinus lining is inspected. Any foreign CARCINOMA OF MAXILLARY
body present should be picked up. The
SINUS17,18
diseased lining is gently curetted. As
the lining is inflamed, it tends to bleed The carcinoma of maxillary sinus is
on provocation, which is cleared by the tumor classically originating from
suction or intermittent packing using its lining. The oral squamous cell
roller gauze. Care should be taken carcinoma originating from the maxi­
while curetting the posterior and the llary gingiva or the malignant minor
supe­rior walls, as they are thin and fra­ salivary gland tumors originating from
gile and may further be eroded by the the palatal minor salivary glands may
pathology. If these walls are perforated secondarily involve the sinus, but are
accidentally, hemorrhage and damage not true carcinomas originating from
to the orbital contents can occur, the antral lining. In advanced cases, it
res­
pec­tively. After all the diseased is difficult to say where the tumor has
Fig. 14.7A: A Caldwell–Luc operation lining is curetted out, hemostasis is originally started from.

B1 B2
Fig. 14.7B: (B1) Incisions for Caldwell-Luc operation; (B2) Denker’s procedure
280 Maxillary Sinus

Etiology cal area posteriorly below the


• Smoking. zygomatic bone.
• Snuff inhalation. iii. Trismus due to muscle infil­
• People working in hardwood furni­ tration.
ture industry, nickel refining, leather The X-ray picture on the X-ray PNS
work and manufacture of mustard shows haziness and irregular destruction
gas. of the walls. The CT scans are very useful
• Chronic maxillary sinusitis. in giving complete information about the
• In some cases no etiological factor is extent of the tumor (Figs 14.10A to C).
detected.
Management19,20
Fig. 14.9: Involvement of anterolateral wall
Clinical Features The diagnosis must be established by
• General taking a biopsy and histopathological
– Signs of chronic sinusitis. ii. The involvement of the infer­­ exam­ination. The carcinoma of maxi­llary
– Foul smelling nasal discharge. ior rectus and inferior obli­ sinus is usually less radio respon­ sive.
– Nasal stuffiness. ques muscles will produce Surgery is the most preferred treatment
– Epistaxis. di­p­­­lo­­pia. modality when the tumor is operable
– Loss of transillumination. iii. As the tumor encroaches and the patient is fit to undergo surgery.
• The clinical features depending upon the orbital cavity initi­ The contraindications for the surgery
upon the wall involved: ally there is proptosis and de­ are, tumor extending to infratemporal
– If the floor is involved. s­tr­u­­c­tion of the eyeball. fossa by perforating the posterior wall,
i. Loosening of the teeth. – If the medial wall is involved full thickness involve­­­ment of anter­
ii. Spontaneous exfoliation of i. Bulging of the lateral nasal ior wall including the overlying skin,
teeth and fungation of tumor, wall towards the septum. nasoethmoidal exten­ sions and medi­
intr­aor­ally. ii. Nasal blockage. cally compromised pati­ents. The carcin­
iii. Pain on mastication as the iii. Obstruction to the drainage of omas of the sinus are not known to
teeth are loose. the sinus as the opening gets metastasize to the cervical lymphatics
iv. Heaviness in the teeth due to blocked, leading to recurrent in the earlier stage of the disease, but in
the involvement of the super­ sinusitis. advanced cases neck node metastasis
ior dental plexus. – If the anterolateral wall is invol­ must be carefully evaluated and treated.
– If the roof is involved (Fig. 14.8) ved (Fig. 14.9)
i. Neurological deficit in the dis­ i. Involvement of the infraor­ Surgical Treatment21
tribution of infraorbital ner­ve, bital nerve leads to neurolo­ • Segmental maxillectomy: In this
anterior and middle sup­ er­ gical deficit in the distribution lower level of the maxilla or only the
ior alveolar nerves as they are of its branches, i.e. inferior involved segment is excised. The pro­
present in the floor of the orbit. palpebral, superior labial and cedure can be accomplished intra­
lateral nasal nerves. orally, through a degloving incision
ii. Swelling in the infraorbital in the buccal vestibule (Figs 14.11A
area, which gets adherent to to C). Some surgeons prefer the extr­
the overlying skin. The skin a­oral lateral rhinotomy or Weber-Fer­
becomes erythematous, with gusson app­ro­­ach (Figs 14.12A and B).
orange peel appearance and • Partial maxillectomy: Excision of
finally fungates through the the maxilla sparing the infraorbital
skin. floor (Figs 14.12A and B).
– If the posterior or posterolateral • Total maxillectomy: Excision of
wall is involved the maxilla with the orbital floor
i. The clinical features are mani­­ but sparing the orbital contents
fested late and initially only (Fig. 14.13).
general features may be pre­ • Radical or extended maxillectomy:
sent. The unilateral maxilla is excised
ii. The tumor perforates the along with the eyeball, or including
bony wall and infiltrates the eth­moidectomy, sphenoidectomy
infra­temporal fossa and may in the procedure. These procedures
Fig. 14.8: Involvement of roof of sinus produce a swelling in the buc­ are done by appropriately modifying
Diseases of Maxillary Sinus 281

A B C
Figs 14.10A to C: CT scans showing growth in the maxillary sinus: (A and B) Malignant tumors causing destruction of the walls;
(C) Benign tumor causing expansion of the walls

Fig. 14.13: Total maxillectomy, orbital floor


removed

flap, laterally rotated nasal septal flap,


free fibular flap or by placing obturators
B C which cover the defect.

Figs 14.11A to C: Intraoral degloving incision


OROANTRAL FISTULA
The oroantral fistula (OAF) is a path­
ological communication between the
oral cavity and the maxillary sinus, which
is lined by epithelium. It is the chronic
version of the acute communication of
the maxillary sinus into the oral cavity.
It facilitates the regurgitation of fluids
from the oral cavity into the maxillary
sinus and contamination of the sinus
with the oral microbial flora, which
A B leads to chronic sinusitis.
Figs 14.12A and B: Weber-Fergusson incision for partial maxillectomy
Etiology
the Weber-Fergusson incision (Figs dissection along with the maxillectomy • Traumatic extraction of maxillary
14.14A to F). is required. molars or premolars teeth, which
When the tumor shows metastasis The reconstruction of the defect is are in close anatomical proximity
in the cervical lymph nodes, neck done with temporalis muscle-fascia with the sinus.
282 Maxillary Sinus

A B C

D E F
Figs 14.14A to F: Extended maxillectomy with orbital exenteration

• Accidental dislodgement of a root in


the maxillary sinus.
• Fracture of maxilla passing through
the wall of the sinus (dentoalveolar
Le-Fort I, II).
• Malignant tumors of sinus or oral
cavity.
• Gummatous lesions of the maxilla
like tuberculosis and leprosy.
• Osteomyelitis of maxilla.
• Wegener’s or Stuart’s granulo­ma­t­
osis.
Fig. 14.16: Deflection of the cotton wool
• Following the resection of the cysts filaments
and tumors of the maxilla.
Fig. 14.15: Nasal regurgitation of fluid
Clinical Features of the cotton wool filaments held
• Regurgitation of fluid in the sinus below the socket and cause the fogg­
when the patient tries to drink the fro­
thing or bubbling in the blood ing of the mouth mirror held below
water (Fig. 14.15). present in the socket of the extracted the socket (Fig. 14.16). This will occur
• Loss of resonance and nasal twang tooth, when the bleeding stops or due to escape of air into the oral cavity
to the voice. the patient reports late, the same through the communication/fistula.
• When the patient’s nostrils are procedure will produce abnormal • Unilateral epistaxis following the
com­­pressed and he is asked to leakage of the air in the oral cavity, tra­uma.
blow through the nose it produces which is demonstrated by deflection • Transillumination test is positive.
Diseases of Maxillary Sinus 283

• In chronic cases unilateral, foul sme­ • To follow Do’s and Don’ts like: Box 14.4: Different methods of
l­l­ing pus discharge may be present – Do not ask the patient to blow the closure of OAF
and signs of maxillary sinusitis are nose forcefully and repeatedly.
Management of OAF
pre­sent due to secondary infection – Do not probe the sinus with sharp If the OAF is small (< 5 mm)
from the oral flora. instruments. Advancement of buccal and palatal gingiva
• Inability to whistle. – Do not curette the socket. and closure
– Place loose wet gauze pack in If the OAF is large
Diagnosis the socket and place a suture Buccal flaps
The diagnosis is based on the clinical across the socket engaging the Burger’s flap
Rehrmann’s flap
history, demonstration of above menti­ buccopalatal gingival.
Moczair’s flap
oned signs and symptoms and on the – Prescribe antibiotics and other Palatal flaps
X-ray findings. The X-ray PNS shows sym­ptomatic treatment. Ashley’s pedicle flap
hazi­ness of the sinus when the sinusitis – Refer the patient to the compe­ Others
sets in or when there is bleeding in the tent person for the further mana­ Schuchardt’s Transversal flap
sinus. Dislodged foreign body, if it is ge­­ment. Regional flaps
large may also be seen on the X-ray. The Tongue flaps
Definitive Management22 Buccal fat pad
intraoral peri­apical radiographs show Randomized cheek flaps
the defect in the bone above the apices The small communications do not Distant flaps
of the roots with loss of cortication of the require any specific treatment as the Temporal muscle fascia flaps
floor of the sinus. If the fistula is large, blood clot seals off the communication. Bone grafts
clear cut comm­unication between the The surgeon must ensure that the clot Alloplastic material–silastic, titanium
socket and the sinus is seen. is not dislodged. It can be achieved by Obturators
approximating the buccal and pala­
General Management tal gingiva, across the socket with
Once the diagnosis is established, the sutures after reducing the height of the • Distant flaps like lingual pedicle flap.
treatment should be started as early alveolar bone (Fig. 14.17). Instructions Buccal mucosal pedicle flaps, Buc­­cal
as possible to prevent infection in the should be given to the patient against fat pad graft,26 etc.
sinus. An average dental surgeon lacks blowing the nose forcefully, vigorous • Bone grafts.
adequate skill and training to deal with gargling and smoking. The moderate • Alloplastic implants like titanium,
such problems and hence, it is desirable and large-sized fistulas require defini­ silastic, silicon or membranes.
that he gives the first aid treatment and tive treatment. • Simple procedures like providing an
refers the patient to the maxillofacial The definitive treatment comprises obturator fabricated in acrylic resin
surgeon for definitive treatment. The of plastic closure of the OAF by taking to cover the defect (Box 14.4).
first aid treatment comprises of – various flaps. The flaps can be classified When the oroantral fistula is asso­ci­
• Gentle packing of the socket with as follows: ated with the displacement of the root
wet gauze to control the bleeding. • Buccal flap (Burger’s flap, Moczair’s fragment into the sinus simple mane­
This is effective in controlling the flap,23 Rherman’s flap24). uvers can be performed in an attempt
bleeding from the socket only. The • Palatal flap (Ashley’s palatal pedicle to remove it. These are compressing the
antral bleeding needs the packing flap25). nostrils and asking the patient to blow
of the sinus with roller gauze and • Combition of buccal and palatal flap forcefully through the nose. The pressure
sometimes anterior nasal packing. (advancement flaps). of the air may sometimes drive the root
piece out through the same fistula. The
antrum is packed with a roller gauze and
then the gauze is pulled out abruptly,
the root piece may get entangled with
it and come out along with the gauze.
The root piece can sometimes enter in
the plane between the bone and the
antral lining, rather than entering into
the sinus and remain asymptomatic
for time. However, the root fragments
which are in the antrum serve as source
of infection and should be removed by
performing Cardwell-Luc operation, if
Fig. 14.17: Simple closure of small OAC by approximating buccal and palatal flaps the simpler methods described earlier
284 Maxillary Sinus

Fig. 14.18: Burger’s flap

A B C
Figs 14.19A to C: Rehrmann’s technique used to close OAF

fail. The indications for Caldwell-Luc is done to advance the flap. This results
operation in OAF are root piece in the into obliteration of the buccal vestibular
sinus and chronic OAF causing chronic depth.
sinusitis and producing polypoid degen­ Moczair’s flap23: It is also described as
er­ative changes in the lining. a buccal sliding trapezoidal flap pro­cedure
for closure of alveolar fistulas. The change
Buccal Flaps in the vestibular sulcus is negligible by
shifting the flap one tooth distally. The
Burger’s flap
main disadvantage of this flap being that
The edges of the socket are trimmed it necessitates greater amount of dento­
and rounded off. A full thickness muco­ gingival detachment in order to facilitate
peri­osteal trapezoid flap is designed and the shift (Fig. 14.20). The distal shifting of
reflected on the buccal side. The peri­ the flap covers the OAF but leaves gap/ Fig. 14.20: Moczair’s flap
osteum is tough and nonelastic and thus, defect, medially on the buccal alveolus.
limits the advancement of the flap. The As the raw area lies on the healthy bone of the fistula adequately. Thus, this
periosteum is selectively incised from it heals uneventfully by granulation and flap is called island pedicle flap. The
inside of the flap carefully. This enhances subsequent epithelization. island derives its blood supply from the
the elasticity of the flap as the mucosa is pedicle. The edges of the fistula and
elastic. The flap is then advanced to the Palatal Flap the fistulous tract are excised to get the
palatal side and sutured with the palatal freshened edges. The flap is then rotated
Ashley’s palatal pedicle flap 25
gingival margin. This flap is an example of and sutured to the freshened edges of
advancement flap (Fig. 14.18). The similar A pedicle flap based on greater palatine the fistula with absorbable material
procedure was described by Rehrmann vessels is designed and reflected full (vicryl) using vertical mattress sutures,
(Figs 14.19A to C). thickness from the bone to avoid injury preferably. The raw area on the palate
However, the Rehermann’s flap is to the vessels. At the end of the flap an from where the flap is raised, is covered
a broad based flap and rather than the island is designed in such way that is with a gauze soaked in antiseptic
periosteal scoring, liberal undermining covers the defect created by excision solution like acriflavin or povidone
Diseases of Maxillary Sinus 285

well established. The Ashley’s flap is an


example of rotation flap (Fig. 14.21).
Palatal rotational-advancement flap:
This technique in contrast, provides
adequate mobility and tissue bulk to the
flap (Figs 14.22A to C). It requires the
mobilization of large amount of palatal
tissue. The flap often kinks following the
rotation of the flap and can cause venous
congestion. Kruger suggested a V-shaped
excision of the lesser curva­ture of the flap
to minimize folding (Fig. 14.23).
Fig. 14.21: Straight advancement flap (A). Pedicle island flap: Its use for clo­
Pal­atal rotational-advancement flap (B); sure of oroantral defect was menti­oned Fig. 14.23: Kruger’s modification
(Ashley’s palatal flap) by Hendersen in 1974.
Advantages: It can be used in closure
iodine, which is secured in place using of large fistula. It is a one-stage local
stay sutures. This pack is removed after procedure that provides a flap with an
24 hours as contamination with food excellent bulk, blood supply and mobility.
makes it foul smelling and unhygienic. Necrosis of the palatal bone of the donor
It is preferable to use a nonadhesive site is not a problem with this procedure,
material like Vaseline gauze but, it is as there is ample blood supply from the
not well-accepted by the patient when nasal mucosa. This procedure is suitable
used intra-orally owing to its unpleasant for closure of posterior fistula, which is
taste. The island heals and unites with pedicled on the greater palatine vessels
the edges of the fistula. The palatal raw (Fig. 14.24). Its application is limited
bone gradually gets epithelized. Once in closure of anterior defect. Gullan
the flap heals and the fistula gets closed, and Arena described a modification
the pedicle can be detached from the of island flap to obtain appro­ ximately Fig. 14.24: Island flap based on greater
palatal end and can be returned back 1 cm extra length of the flap by freeing the palatine vessel
to the palate and sutured back in its vessels at the greater palatine foramen.
original position after freshening the This provides an additional mobility for
edges of the palatal raw area and curet­ anterior advancement of the flap. Both island and hinged flaps leave a
ting the underlying granulation tissue. Palatal hinged flap: This flap is small raw area for granulation.
This second stage procedure is usually utilized for closure of small to moderate
done after two weeks, as early attempt size fistulas (Fig. 14.25). Combined Local Flaps
may lead to avascular necrosis of the The procedure is simple to perform These include the combination of inver­­
flap as the collateral circulation is not with minimum morbidity. sion and rotational-advancement flaps,

A B C
Figs 14.22A to C: Closure of fistula by palatal rotational-advancement flap
286 Maxillary Sinus

may compromise its vascularity as the


vascular pedicle gets compressed. This
flap is myomucosal and thus an example
of composite flap with randomized
blood supply as it does not have any
feeding vessel in it (Figs 14.28A and B).
The buccal mucosal random pedicle
flaps are also used for closing the OAF.
The pedicle must be sufficiently broad
to ensure good afferent and efferent
blood supply, to prevent a vascular
necrosis. The disadvantage with the
Fig. 14.25: Palatal hinged flap lingual pedicle flap is its instability as
Fig. 14.27: Schuchardt’s transversal flap (A),
the movements of the tongue tend to
Modification by Egyedi (B)
cause dehiscence of its margins.
Use of buccal pad of fat: The buccal
doubled overlapping hinged flaps, dou­ Advantages fat pad can be effectively used to close
bled island flaps and superi­mposi­tion • Bilateral blood supply. moderate sized oroantral communi­
of reverse palatal and buccal flaps. All • Donor site closed by primary closure. cations, especially in the posterior areas.
these procedures preserve the buccal • Favorable for closure of minor ante­ The buccal fat pad is easy to harvest
vestibular height (Figs 14.26A to C). r­ior fistula in association with miss­ and provides adequate tissue to cover
ing anterior teeth. moderate defects. The buccal fat pad
Other Procedures can reach anteriorly up to the premolar
Schuchardt’s transversal flap27: In this Disadvantages area. It is reliable and heals by secondary
technique, the mucoperiosteum over­­ • Reduces the labial sulcular height. epithelization. The morbidity to the do­
ly­ing an edentulous ridge in the vici­ • Presence of two pedicles on top of nor site is negligible (Figs 14.29A and B).
nity of the fistula has been utilized in the alveolus. Use of temporalis muscle fascia: The
the form of transversal flap. The basic temporalis muscle fascia flaps can be
Distant flaps
advantage of this technique is the used for the repair of large oroantral
buccal vestibular height is not affected The most commonly used distant flap is fistulas, which generally result following
following the closure. However, it does lingual myomucosal pedicle flap. This ablative tumor surgeries or tissue loss
not offer greater mobility and results in a flap could be either on anteriorly or secondary to trauma. The temporalis
raw area over the donor site (Fig. 14.27). posteriorly based pedicle. The anteri­ muscle fascia flap is pedicled on the deep
Modification of Schuchardt method was orly based pedicle flap is preferable due temporal vessels. The flap is tunneled
described by Egyedi. He utilized a labial to its ease in handling. The posteriorly below the zygomatic arch and drawn into
vestibular bipedicle flap to close a fistula based pedicle flaps are required to be the oral cavity. The reach of the flap is not
in the anterior region. rotated for proper placement which adequate anteriorly and can be used to
close the defects in the molar area.

A B C
Figs 14.26A to C: Combined local flaps
Diseases of Maxillary Sinus 287

oral mucosa. The use of an autogenous


cancellous bone in the closure of
palatal defect is a well known procedure
(Figs 14.30A and B). Cockerham et al.
in 1976 suggested that, when a con­
servative method fails or when the size
of the defect is too large, bone graft
should be indicated in the closure.
Whitney et al. advocated bone grafts in
cases where there is need to recontour
the alveolar ridge. The disadvantage
with this tech­nique is that an additional
A B
surgical procedure is needed to obtain
Figs 14.28A and B: Posteriorly and anteriorly based tongue flaps the bone graft, this increases the length
of the procedure and morbidity.
A single stage and simpler surgical
pro­cedure was given by Brusati in
1982. In this, he took the bone from
the lateral wall of the antrum and
pedicled on the periosteum to close
the alveolar defect (Figs 14.30A and B).
The disadvantage with this procedure
was that the buc­cal vestibular height
was reduced as a result of the use of
the buccal flap as a soft tissue coverage
and in case of dehiscence chances of
A B addi­ti­onal oro­antral communication
Figs 14.29A and B: Use of buccal fat pad for the closure of OAF are there.

Acrylic Obturators
When the fistula is very large, e.g. due
to tumor is fabricated to rehabilitate the
patient.

Alloplastic Material
Alloplastic material can be used in con­
junction with the soft tissue flaps. They
are placed below the flap to cover the
bony defect.
Various alloplastic materials used
are:
A B
• Gold foil
Figs 14.30A and B: Bone grafting to close OAF; • Gold plate
(A) Bone graft; (B) Buccal osteoperiosteal flap
• Tantalum plate
• Soft polymethylmethacrylate
Use of bone grafts28: The OAF has two defect is large then in the primary state • Lyophilized collagen.
ways compounding, i.e. in oral cavity attempt should be made to close the By using alloplastic materials, it does
and the maxillary sinus. Hence, primary OAF using a soft tissue flap and once the not require raising of a large amount of
bone grafting is not advisable as good antral lining is healed and established, local tissue. The procedure does not
soft tissue cover cannot be provided second surgery should be performed affect the buccal vestibular height and
on both the ends in spite of using any for bone grafting. The bone graft is there is no raw area left behind for gran­
technique for closure of OAF. If the placed between the antral lining and ul­ation following the closure.
288 Maxillary Sinus

10. McMains KC, Kountakis SE. “Medical retrospective analysis of treatment


REFERENCES
and surgical considerations in patients methods, J Otolaryngol.1984;13:141-6.
1. McGowan DA, Baxter PW, James. The with Samter’s triad”. American journal 20. Macnab T, Flores AD, Anderson DW.
maxillary sinus and its Dental impli­ of rhinology. 2006;20(6):573-6. Treatment of paranasal sinus mali­
cations. Oxford: Wright, Butter­worth- 11. Ferreiro JA, Carlson BA, Cody T. Par­ gnancy: the BCCA experience, J Otol­
Heinemann Ltd. Chapter 1. 1993. a­nasal sinus Fungal Balls. Head Neck; ary­ngol. 1992; 21:244-48.
2. Ritter FN, Lee D. The para­nasal sinuses, 1997. p. 19. 21. Yucel A, Cinar C, Aydin Y, et al. Malig­
Anatomy and surgical techniques. 12. Roughton EW. Empyema of the antrum nant tumors requiring maxillec­tomy. J
St Louis, The Mosby company. 1978. of highmore. The Laryngoscope. 1898; Cranio­fac Surg. 2000;11:418-29.
3. Harneja NK, Hukmani P: A study of 4(3):159-63. 22. Sokler K, Vuksan V, Lauc T. Treatment
the maxillary sinus in Indian subjects; 13. Kuhn JP. Imaging of the paranasal of oroantral fistula. Acta Stomat Croat.
Indian Journal of Otolaryngology. sinuses: Current status. J Allergy Clin 2002;36:135-40.
1980; 32(4):101–2. Immunol;1986. p. 77. 23. Moczair L. Nuovo methodo operati­
4. Traxler H, Windisch A, Geyerhofer U, et 14. Menlhelm ER, Oliverio TJ, Benson opela chisura delle fistole del seno
al. Arterial blood supply of the maxillary ML, et al. Optimal CT evaluation for mascellase di origina dentale. Stomatol
sinus. Clin Anat. 1999;14(6):417-21. functional endoscopic sinus surgery. (Roma). 1930;28:1087-88.
5. Aust R, Drettner B. Oxygentension in Am J Neuro Radiol;1991. p. 12. 24. Rehrmann A. Eine methode zur Schlies­
human maxillary sinus under normal 15. Benninger MS, Anon J, Mabry RS. The sung von Kieferhohlenperforationen.
and pathological conditions. Acta Otol­ medical management of rhino sinu­sitis. Dtsch. Zahnarztl. Z. 1936:39:1136-9.
aryngol; 1973. p. 78. Otolaryngol Head Neck Surg. 1997;117 25. Ashley REA. A method of closing antro­
6. Furukawa CT. The role of allergy in sin­ (3 Pt 2):S41-9. alveolar fistulae. Ann. Otol Rhi­nol.
u­sitis in children. J Allergy Clin Imm­ 16. Mabry RL, Marple BF. Open maxillary Laryngol. 1939;48:632-5.
unol;1992. p. 90. sinus procedures. In: Kennedy DW, 26. Poeschl PW, Baumann A, Russmmeller
7. Brook I. Microbiology and manage­me­nt Bol­ker WE, Zinreich SJ, (Eds). Diseases G, Poeschl E, Klug C, Ewers R. Closure
of sinusitis. J Otolaryngol;1996. p. 25. of sinuses: Diagnosis in management. of Oroantral Communications with
8. Kartagener M. Zur pathogenese der Hami­l­ton: BC Decker. Inc 2001. Bichat’s Buccal Fat Pad. J Oral and
bronchiectasien. I Mitteilung: bron­ 17. Lewis JS, Castro EB: Cancer of the nasal Maxillofac Surg. 2009;67(7):1460-6.
chiectasien bei situs viscerum inver­ cavity and paranasal sinuses. J Laryn­ 27. Schuchardt K. Methodik des Vers­chl­
sus. Betr Klin Tuberk. 1933;83:498- gol Otol. 1972;86:255-62. usses von Defekten im alveolar­ for­
501. 18. Weber AL, Stanton AC. Malignant tum­ors sate zalm lose oberkiefer. Dtsch. Zahn
9. Handelsman DJ, Conway AJ, Boylan of the nasal sinuses: radiologic, clinical, Mund Kieferheilk. 1953;17:366-69.
LM, Turtle JR. “Young’s syndrome. and histopathologic evalu­ ation of 200 28. Brusati R. The use of an autogenous
Obstr­­u­c­tive azoospermia and chronic cases, Head Neck Surg. 1984;6:761-76. osteoperiosteal flap to close oroantral
sinopul­­ monary infections”. N Engl J 19. Flores AD, Anderson DW, Doyle PJ, fistulas. J Oral Maxillofac Surg. 1982;40:
Med. 1984;310(1):3-9. et al. Paranasal sinus malignancy: a 250-51.
Section 5
Salivary Glands Pathologies

n Diseases of Salivary Glands


15 Diseases of
Salivary Glands
Borle Rajiv M, Agni Nishit, Arora Aakash

Salivary glands may be classified as as a proliferation of oral epithelial cells have hypothesized that apoptosis of
major and minor glands. Major glands forming a focal thickening that grows centrally located cells in the cell cords
are paired glands. They include parotid, into the underlying ectomesenchyme. may be responsible for lumen formation.
submandibular and sublingual salivary Conti­ nued growth results in the for­ Following the development of the
glands. There are numerous minor sali­ mation of a small bud connected to the lumen in the terminal buds, the epith­
vary glands that are widely distributed in surface by a trailing cord of epithe­lial elium consists of two layers of cells. The
the oral cavity in the submucosal layer. cells, with mesenchymal cells conden­ cells of the inner layer differentiate into
They include labial, buccal, palatine, sing around the bud. Clefts develop secretory cells of the mature gland. They
lingual and incisive glands. Based on in the bud, forming two or more new may be mucous or serous depending
the type of secretions, salivary glands buds and this process is continued and on the gland type. Few cells of the outer
are classified as: is known as branching morphogenesis. layer form contractile myoepithelial cells
• Mucous salivary glands This pro­duces successive generations of that are present around the secretory
• Serous salivary glands buds and a hierarchical ramification of end pieces and intercalated ducts. As
• Mixed salivary glands. the gland. the epithelial parenchymal component
Salivary glands are often involved in a Several factors control the branch increases in size and number, there is a
wide variety of disorders that frequently points and the overall structure of the decrease in the associated mesenchyme.
require surgical treatment. These glands glands. Members of the fibroblast gro­ However, a thin layer of connective
can be involved with acute and chronic wth factor protein family along with tissue remains around each secretory
inflammatory processes, give rise to transforming growth factor-β play a end piece and duct of the adult gland.
benign and malignant tumors, manifest major role in the branching. The differ­ Thicker partitions of connective tissue
congenital abnormalities or represent ential contraction of actin fila­ments at (septa), which are continuous with the
involvement of a systemic disorder. the basal and apical ends of the epithe­ capsule invest the excretory ducts and
Amo­ ngst all the disorders, the most lial cells probably provides the physical divide the gland into lobes and lobules.
comm­on are problems with neoplasms mechanism underlying cleft forma­ They contain the nerves and blood
and infections. tion. The deposition of extra­cellular vessels, which supply the gland.
The rate of secretion of individual mat­rix com­ponents within the clefts The parotid gland is the first to
glands ranges from barely perceptible apparently serves to stabilize them. The appear and begins development at 4th
during sleep to as high as 4 mL/min on specific mesen­ chyme associated with to 6th week of intrauterine life. They
maximal stimulation. In a 24 hours per­ the salivary glands seems to provide develop from the buds that arise from
iod, the submandibular gland produces the optimum environ­­ ment for gland the oral ectodermal lining near the
70 per­cent of the saliva, parotid gland development. angle of the stomodeum and later grow
25 percent and minor glands another The development of lumen within towards the ear. The ducts are formed by
5 percent. the branched epithelium occurs first in 10 weeks of intra uterine life. Secretions
the distal end of the main cord and in commence by 18 weeks. The capsule
EMBRYOLOGICAL branch cords, then in proximal end of and connective tissue develop from the
the main cord and finally in the central surrounding mesenchyme.
DEVELOPMENT portion of the main cord. Lumina form The submandibular glands appear
The salivary glands arise from the epith­ within the ducts before they develop late in the 6th week. They develop from
elial lining of the oral cavity.1 They arise within the terminal buds. A few studies the endodermal buds in the floor of the
292 Salivary Glands Pathologies

stomodeum. Acini begin forming at acoustic meatus, which is situated in is non-fluctuant due to the presence
12 weeks and secretory activity begins a groove of the gland. Sur­ rounding of the tough fascial covering, once the
at 16 weeks. The growth continues after the acoustic meatus on its inferior sur­ abscess is diagnosed one should not
birth also. face, the gland reaches posteriorly to wait for the fluctuations to develop and
The sublingual glands appear in the mastoid process and sterno­ clei­ then drain the abscess, but drain it at the
the 8th week. They develop from endo­ domastoid mus­cle. Anteriorly, it is in earliest. The delay tends to mount more
dermal buds in the paralingual sulcus. contact with the posterior border of pressure and induces ischemic necrosis
The minor salivary glands too develop medial pterygoid muscle and mandi­ of the gland parenchyma, which can
at 8 to 12 weeks of gestation. bular ramus. A part of the gland extends be avoided by early drainage/decom­
The cells of the secretory end pieces anteriorly on the outer surface of the pression. If the drainage is delayed the
and ducts attain maturity during last mandibular ramus and masseter muscle chances of bursting the abscess in the
2 weeks of intrauterine life. The glands as thin, triangular layer.3 Outer surface external auditory canal are high. Simi­
continue to grow postnatally with the of the gland is situated superficially larly, the benign tumors are slow to
volume proportion of acinar tissue inc­ covered by capsule, superficial fascia project outwards to any great extent
reasing and that of ducts, connective and skin. Upper lobules of the superficial and hence take years to present as
tissue and vascular tissue decreasing up part of gland cover the craniomandi­ conspicuous bulges. The parotid fascia
to 2 years of life. bular articulation in front of the ear, but continues anteriorly as the masseteric
never transgress the lower border of the fascia and thus it is collectively referred
SURGICAL ANATOMY zygomatic arch (Fig. 15.1). to as parotidomasseteric fascia.
A dense fibrous capsule derived Parotid gland is like an inverted, flat,
OF PAROTID GLAND from the investing layer of the deep three-sided pyramid, presenting a small
The parotid gland is the largest of the cervical fascia and incompletely invests superior and superficial, anteromedial
salivary glands weighing approxima- the gland. The capsule is tight and firmly and posteromedial surfaces. It tapers
tely about 15 to 30 g (avg. 25 g).2 It is connected with strong septa dividing inferiorly into a blunt apex. The facial
an irregular, lobulated, yellowish mass the lobes and lobules of the gland from nerve and its branches pass within the
lying largely below the external acous­ one another. It is closely adherent to parotid gland and divide it into super­
tic meatus in a deep hollow between the gland. The toughness of the fascia/ ficial and deep parts or lobes. About
the mandible and sternocleidomastoid capsule on the external surface of the 80 percent of the Parotid gland lies
muscle. It lies in the retromandibu­lar gland restricts a massive swelling in superficial to the nerve, thus comprising
fossa and reaches medially to the sty­ parotid space infections, which are very the bulk of the gland and 20 percent of the
loid process and muscles ari­sing from painful due to the unyielding nature gland lies deep to the nerve entering the
it. Upwards it extends up to external of the capsule. As the parotid abscess parapharyngeal space. A narrow isthmus
connects the superficial and deep lobes.
The other structures that lie within the
gland are lymph nodes, external carotid
artery and retromandibular vein. The
tumors of the parotid involving both the
superficial lobe and the deep lobe are
often described as ‘dumbbell tumor’ due
to its peculiar appearance.
Duct of the parotid gland, i.e.
the Stensen’s duct is about 5 cm
(2 inches) long and passes forward
across the masseter about a finger
breadth below the zygomatic arch.4
It crosses the masseter at junction of
upper and middle one-third. At its
anterior bor­der it turns medially almost
at right angle, traversing the buccal
fat pad and the buccinator muscle.
It then runs obliquely forwards for a
short distance between the buccinator
and oral mu­cosa to open upon a small
papilla (salivary caruncle) opposite the
Fig. 15.1: Relation of parotid gland with surrounding structures crown of 2nd maxillary molar. The duct
Diseases of Salivary Glands 293

is relatively straighter and the secretions of the facial nerve is carried out in three of the mastoid process on the other.
are serous in nature thus, the chances of ways: The tym­pano­mastoid sulcus lies at
the salivary calculus are very low in the • Early direct identification of the the apex of the vaginomastoid angle,
Stensen’s duct. If the calculus is formed main trunk where it exits through which is formed by meeting of the
in the duct it is usually found near the the stylomastoid foramen. vaginal process of tympanic portion
point where the duct bends acutely • Retrograde approach to the trunk of the temporal bone and mastoid
at the anterior border of the masseter from either the mandibular branch, process. The nerve emerges from
muscle. The duct can be palpated over where it passes over the retro­mandi­ the stylomastoid foramen some 3 to
the clenched masseter muscle. During bular vein or the peri­pheral branches 4 mm deep to the outer edge of the
the inflammatory pathologies the duct is alongside the parotid duct. bony external canal. However; the
well felt and is chord-like in consistency • Supravital staining of the parotid groove is filled with fibrofatty lobules
and tender. gland, contrasting the blue normal that mimic the trunk of the facial
The structures passing through the gland from the unstained tumor nerve, which may lie as deep as 1 cm
gland are the terminal part of the external and the gleaming white facial nerve to this landmark.
carotid artery, retromandibular vein and bran­ches. 3. The most reliable landmark for find­
the lymph nodes. Hence the pathologies There are four facial nerve pointers ing the nerve is the posterior belly of
of the gland could be parenchymal or at the stylomastoid foramen. the digastric muscle, which lies just
non-parenchymal in origin. 1. The cartilaginous pointer described inferior to the nerve. The anterior
by Conley5 (1978) is an artificially cre­ superior aspect of the poster­ior belly
IDENTIFICATION OF THE ated landmark at its anterior-inferior of the digastric mus­cle is inserted
border formed by posterior traction just behind the stylo­mastoid fora­
FACIAL NERVE on the external auditory canal. The men.
Isthmus of the gland (part behind the ra­ backward pull on the cartilage causes 4. The styloid process is a useful con­
mus of the mandible joining the superfi­ the meatus to assume the shape of a firmatory landmark. The facial nerve
cial and deep lobes) is most often found horn, the curved extremity of which courses lateral to the styloid pro­
in the bifurcation of the facial nerve into allegedly points to the position of the cess near the base of the styloid.
upper temporofacial and lower cervico­ facial nerve (Fig. 15.3). The nerve is However, to depend on it for finding
facial divisions. There can be anatomical located medial and inferior to the the nerve is to court trouble, since it
variations in the branching of the nerve pointer. This is probably the least re­ lies medial and anterior to the point
(Fig. 15.2). liable as it depends on the configura­ of emergence of the nerve from the
The facial nerve can be identified tion of the cartilaginous meatus. mastoid. The posterior auricular
either proximally or distally. Proximally 2. The segment of the nerve, which lies in artery bleeds fre­quently, while look­
the main trunk of the nerve is identified the interval between the sty­lo­mastoid ing for the facial nerve, since it lies
before it enters the gland. Distally it is foramen and parotid gland is extre­ below and just lateral to the nerve.
identified as branches after the nerve mely short, but is an ideal location
leaves the gland. It is ressected only to find the facial nerve before the SURGICAL ANATOMY OF
when function is impaired preopera­ parotidectomy comm­ences. It is best
SUBMANDIBULAR GLAND
tively. Identification for the preservation found by searching in the tympano­
mastoid sulcus, which is formed by Submandibular gland is irregular in
the edge of the bony external meatus shape and of the size of a walnut. It has
on one hand and the anterior face a mixture of serous and mucous acini,
but is chiefly serous. The upper pole lies
on the medial surface of the mandible
in the submandibular fossa and lower
pole extends beyond boundaries of the
digastric triangle covering intermediate
tendon of the digastric muscle. The
gland is palpable between the index
finger placed on the floor of the mouth
and thumb placed anteromedial to the
angle of mandible below the floor.
Inferiorly the gland approaches the
greater cornu of the hyoid, which ser­
Fig. 15.2: Branches of facial nerve Fig. 15.3: Cartilaginous pointer of Conley ves as a useful landmark when marking
294 Salivary Glands Pathologies

Fig. 15.4: Submandibular gland and its relation to deeper structure

the incision for the operation to remove risk when the deep part of the gland release short ducts 5 to 15 in number,
the gland. The marginal mandi­ bular is being mobilized. The duct of the which open at the crest of sublingual
branch of the facial nerve and its submandibular gland is longer and has eminence on the floor of the oral cavity.
subsidiary branches lie plastered to a tortuous course. In addition, it has an These minor ducts are known as ducts
the outer aspect of the deep cervical uphill course. Thus the secretions have of Rivinus. The excretory ducts of the
fascia and never make contact with the to be emptied against gravity and there sublingual glands are very superficially
gland or its capsule. So the dissection are increased chances of retention. Also, located and hence easily get damaged.
should be done in a plane deep to the the mineral content of the secretion They result into mucous retention cysts
fascia overlying the submandibular is high, especially calcium content,6 the ‘ranula’.
gland. Any dissection limited to a plane which along with increased retention of
within the capsule does not harm these secretions result into higher incidence Incidence
structures. However, most inferior of the of calculus formation and inflammatory In most parts of the world the incidence
branches of the marginal mandibular pathologies. of salivary gland tumors, both benign
nerve lies close to the lower border of and malignant, varies from 1 to 2 per
the submandibular gland and could SURGICAL ANATOMY 100,000 populations per year.7 Because
be damaged when gaining entry to the of the rarity of tumors of the salivary
plane of dissection at the beginning
OF SUBLINGUAL GLAND glands, they are often included as
of the surgery. The hypoglossal nerve Sublingual glands are the smallest of the “miscellaneous” or “other” head and
with its venae comitantes lies on the major salivary glands. They lie beneath neck tumors in epidemio­logic surveys
hyoglossus, but is separated from the the mucosa of the floor of the mouth of neoplasia. The annual incidence of
deep aspect of the gland by a potential causing an elevation, salivary eminence, salivary gland tumors varies around
space (Fig. 15.4). Escape of disease from on the floor of the oral cavity. The gland is the world from approximately 0.4 to
the deep aspect of the gland would be narrow, flat, shaped like an almond and 13.5 cases per 100,000 people.8
the only likely circumstance to put the weighs 3 to 4 g.4 There are 8 to 20 ducts Salivary gland neoplasms do not
nerve at risk when removing benign of the sublingual gland. The smaller exhibit any strong predilection for a
tumors. The lingual nerve arches gently ducts mostly open separately on the parti­cular sex nor is there any distinct
downwards just above the deep part summit of the sublingual fold and a few racial incidence pattern. Patients of
of the gland to which it is attached by into submandibular duct. From anterior all ages can be affected.9 However, the
a ganglionic connection, alongside part of the gland, small rami arise from majority of salivary gland tumors are
which is a small blood vessel. The the major salivary duct and known diagnosed between fourth and seventh
nerve subsequently passes below the as Bartholin’s duct. Smaller or minor decade.
duct then round its outer aspect in sublingual glands may be subdivided Historically, an exception to the low
the form of a broad loop before heading into two groups. One group lies at the incidence of salivary gland neo­plasms is
for the mucosa of the tongue. It is at superior surface of the gland. They its incidence in Inuit population living in
Diseases of Salivary Glands 295

the western and central Canadian Artic. 1 percent of all registered malignancies. Box 15.1: Classification of the salivary
From 1950 to 1966 salivary gland neo­ Table 15.1 gives the site-wise incidence gland pathologies
plasms, predominantly lymphoe­pithelial of salivary gland tumors.
• Developmental
carci­noma accounted for appro­ximately
– Aplasia—absence of gland
25 percent of all cancers affecting this Incidence of Salivary Gland – Atresia—absence of duct
population. These tumors were so preva­
Tumors According to Site10 – Aberrancy—ectopic gland
lent that the term ‘Eskimomas’ was coi­
• Enlargement of gland
ned to denote them. The mortality rate Age and sex predilection for major sali­
– Inflammatory
arising from these tumors was 100 and vary gland tumors is as follows: Benign:
i. Viral: Mumps, Coxsackie-A, CMV,
400 times greater among Inuit men and 40 years and Malignant: 55 years. Male influenza, parainfluenza virus
women respectively as compared to Can­ predominance is seen in Warthin’s tu­ ii. Bacterial
a­dian men and women. mor and female predominance in Aci­nic iii. Allergic
In the United States, data on salivary cell tumors. iv. Sarcoidosis
gland tumors is limited to incidence of v. Obstructive
salivary gland carcinomas. In 1959, Dorn Site Wise Distribution11 – Non-inflammatory
and Cutler reported a higher inci­dence The site-wise distribution of the salivary i.  Autoimmune: Sjögren’s
of salivary gland carcinoma in nonwhites gland tumors is tabulated in Table 15.2.12 syndrome, Mikulicz’s disease
than whites. Recent data (May 1989) ii. Alcoholic cirrhosis
from surveillance, epid­emiology and end General Classification of Salivary iii. Diabetes mellitus
iv. Nutritional deficiency
results (SEER) regis­tries of the National Gland Pathologies
v. HIV associated
Cancer Insti­tute show the age-adjusted The salivary gland pathologies can be bro­­
• Cysts
incidence of sali­vary gland cancer from adly classified as shown in the Box 15.1.
– Extravasation cysts
1982 to 1986 in all races and both sexes
to be 0.9 cases per 100,000 people. Since WHO Histological Classification – Retention cysts
– Ranula
malignant tumors comprise between 35 of Tumors of the Salivary Glands
• Tumors of salivary glands
to 40 per­cent of all salivary gland tumors, 2005 – Benign
it is estimated that annual inci­ dence Because of the low incidence of the – Malignant
of sali­vary gland tumors in the United salivary gland tumors their classification
• Necrotizing sialometaplasia
States is between 2.2 and 2.5 cases per has emerged slowly. The WHO classified
• Salivary gland dysfunction
100,000 people. It accounts for 650 the salivary gland tumors first in 2002,
– Sialorrhea
deaths per year in the USA. In USA 3 to which was subsequently modified in the
– Xerostomia
4 percent of all neoplasms of the Head year 2005 as shown in Box 15.2.
and Neck are salivary gland neoplasms.
In UK it comprises of 40 cases per year. TNM Classification and Staging
AT CRI, Varanasi; 1 to 4 new cases of the Salivary Gland Neoplasms
per year are diagnosed as salivary gland The first clinical staging system was the Memorial Hospital. The TN (Tumor,
tumors. They account for less than deve­l­oped by Spiro and co-workers at Nodes) system and TNM modification
(Tumor, Nodes, Metastases) was deve­
Table 15.1: Site wise incidence of salivary gland tumors loped for the parotid gland and gland
neoplasms.
Type Parotid Submandibular Sublingual Minor glands11 (Palate) The American Joint Commission on
Benign 80% 60% 30% 53% Cancer in 2002, staged the salivary gland
neoplasms. The staging system follows
Malignant 20% 40% 70% 47%
the tumor, node, metastasis (TNM)
system of staging like other parts of the
body. Primary tumor stage depends
Table 15.2: Site wise distribution of the salivary gland tumors
primarily on: (a) the size of the primary
Site Distribution % Malignant % tumor, (b) extraparenchymal extension
and (c) involvement of the seventh
Parotid 75–80 17–20 cranial nerve or skull base. Minor salivary
Submandibular 5–10 50 gland tumors staged according to the
Sublingual 1–2 80 system used to classify primary tumors
of the particular sites of origin, e.g. oral
Minor glands 10–20 50
cavity, oropharynx, etc.
296 Salivary Glands Pathologies

Box 15.2: WHO classification of salivary gland tumors 2005 Primary Tumor (T) (Box 15.3)
Tumor categories Code Box 15.3: Primary tumor (T)
• Malignant epithelial tumors
– Acinic cell carcinoma 8550/3 • TX—Primary tumor cannot be assessed
– Mucoepidermoid carcinoma 8430/3 • T0—No evidence of primary tumor
– Adenoid cystic carcinoma 8200/3 • T1—Tumor 2 cm or less in greatest dimen-
– Polymorphous low-grade adenocarcinoma 8525/3 sion without extraparenchymal extension
– Epithelial–myoepithelial carcinoma 8562/3
• T2—Tumor > 2 cm but not > 4 cm in gre­
– Clear cell carcinoma, not otherwise specified 8310/3
a­test dimension without extraparen­chy­
– Basal cell adenocarcinoma 8147/3 mal extension
– Sebaceous carcinoma 8410/3
– Sebaceous lymphadenocarcinoma 8410/3 • T3—Tumor > 4 cm and/or tumor having
extraparenchymal extension
– Cystadenocarcinoma 8440/3
– Low-grade cribriform adenocarcinoma • T4a—Tumor invades skin, mandible, ear
– Mucinous adenocarcinoma 8480/3 canal, and/or facial nerve
– Oncocytic carcinoma 8290/3 • T4b—Tumor invades skull base and/or
– Salivary duct carcinoma 8500/3 pterygoid plates and/or encases carotid
– Adenocarcinoma, not otherwise specified 8140/3 artery.
– Myoepithelial carcinoma 8982/3 (Extraparenchymal extension—clinical or
– Carcinoma ex-pleomorphic adenoma 8941/3 macroscopic evidence of invasion of soft
– Carcinosarcoma 8980/3 tissues or nerve, except those listed under
– Metastasizing pleomorphic adenoma 8940/1 T4a and T4b. Microscopic evidence alone
– Squamous cell carcinoma 8070/3 does not constitute extraparenchymal
– Small cell carcinoma 8041/3 extension for classification purposes)
– Large cell carcinoma 8012/3
– Lymphoepithelial carcinoma 8082/3
– Sialoblastoma 8974/1
Regional Lymph Nodes (N)
• Benign epithelial tumors (Box 15.4)
– Pleomorphic adenoma 8940/0
Box 15.4: Nodal metastasis N
– Myoepithelioma 8982/0
– Basal cell adenoma 8147/0 • NX—Regional lymph nodes cannot be
– Warthin’s tumor 8561/0 assessed
– Oncocytoma 8290/0 • N0—No regional lymph node metastasis
– Canalicular adenoma 8149/0 • N1—Metastasis in single ipsilateral lymph
– Sebaceous adenoma 8410/0 node, 3 cm or less in greatest dimension
– Lymphadenoma • N2—Metastasis in single ipsilateral lymph
i. Sebaceous 8410/0 node, > 3 cm but not > 6 cm in greatest
ii. Non-sebaceous 8410/0 dimension; or in multiple ipsilateral lymph
– Ductal papillomas nodes, none > 6 cm in greatest dimension;
i. Inverted ductal papilloma 8503/0 or in bilateral or contralateral lymph
ii. Intraductal papilloma 8503/0 nodes, none > 6 cm in greatest dimension
iii. Sialadenoma papilliferum 8406/0 • N2a—Metastasis in single ipsilateral
– Cystadenoma 8440/0 lymph node, > 3 cm but not > 6 cm in
i. Soft tissue tumors greatest dimension
– Hemangioma 9120/0 • N2b—Metastasis in multiple ipsilateral
lymph nodes, none more than 6 cm in
i. Hematolymphoid tumors
greatest dimension
ii. Hodgkin lymphoma
• N2c—Metastasis in bilateral or contra-
– Diffuse large B-cell lymphoma 9680/3
lateral lymph nodes, none more than
– Extranodal marginal zone B-cell lymphoma 9699/3 6 cm in greatest dimension
i. Secondary tumors • N3—Metastasis in a lymph node more
Behavior is coded as follows: than 6 cm in greatest dimension
0- benign tumors (Regional nodes are the cervical nodes. Mid-
1-borderline or uncertain behavior line nodes are considered ipsilateral nodes.)
3-malignant tumors
Diseases of Salivary Glands 297

Distant Metastasis (M)(Box 15.5) gland enlargements are not seen


on plain radiographs.
Box 15.5: Distant metastasis (M) – Ultrasonography: It is a non-in­
vasive technique, utilizes non-
• MX—Presence of distant metastasis
cannot be assessed ionizing radiation, gives good
• M0—No distant metastasis
soft-tissue discrimination, has
exce­llent sensitivity for mass le­
• M1—Distant metastasis
sions and can be repeated as
frequently as required. It helps
The malignant salivary gland neoplasms to distinguish a cystic lesion
can be staged as shown in Table 15.3. from a solid mass in space oc­
cupying lesion. Normal salivary
gland is homogeneously rela­
DIAGNOSTIC AIDS tively hyperechogenic on USG
than adjacent muscle. Tumors
In salivary gland disease a careful history and cysts are more hypoechoic
and exam­ination will usually provide a than normal parenchyma.13 It is
correct diagnosis, but the major salivary Fig. 15.5: Bimanual palpation of the a more sensitive scan than CT
glands may pose a diagnostic chal­lenge submandibular gland and its duct for identification of small lesions
because they are not only affected by less than 1 cm in diameter. Neo­
specific local pathology, but also by plasms appear as solid masses.
systemic disease. A meticulous history orifices of the ducts are observed for A relatively well-defined capsule
leads to the determination of the nature saliva output. Bimanual palpation is with a homogeneous central
of the lesion in the salivary glands. It must done to differentiate the major salivary area is indicative of a benign or
include the onset, duration, progress glands from lymph node enlargement low-grade malignant tumor. An
and rapidity of growth, extent of growth, (Fig. 15.5). irregular or ill-defined capsule
presence of associated symptoms like Mobility denotes that the lesion has with complicated heterogeneous
paresthesia, pain, cystic enlargement, not infiltrated the surrounding tissues. A center indicates malignant or in­
infection. A history of sudden growth or malignant tumor and its lymphatic spread flammatory changes.14 Overall
ulceration usually suggests malignancy. except early lymph node metastasis sensitivity of USG in detecting
Inspection and palpation are most are not readily movable. If the tumor is parotid tumors is very high. The
important diagnostically. Any palpable fluctuant, the tumor probably is cystic. drawbacks of USG include its in­
enlargement is abnormal. The major However regardless of the sites both ability to demonstrate the facial
salivary glands are palpated and the benign and malignant tumors resemble nerve in relation to the parotid
each other clinically. Histopathology is gland and to define the extent
Table 15.3: Staging of the malignant the gold standard to final diagnosis. It of tumors extending outside the
salivary gland neoplasms is impor­ tant to document function of deep surface or of extraglandular
the facial nerve when evaluating paro­ lesions such as nasopharyngeal
Stage 1 T1 N0 M0
tid tumors, because the nerve runs tumors invading the deep aspect
Stage 2 T2 N0 M0
through the gland and evidence of of the gland. In addition, it is dif­
Stage 3 T3 N0 M0 decre­ased motor function of the nerve ficult to image the deep lobes of
T1 N1 M0 thus has diagnostic significance. Facial the major salivary glands.
T2 N1 M0 nerve paralysis (Bell’s palsy) is usually – Doppler ultrasound and color-
T3 N1 M0 indicative of malignancy. flow imaging: It enables imme­
Stage 4A T4a N0 M0 diate recognition of vascular
T4a N1 M0
Investigations structures and allows confident
T1 N2 M0
The investigations that can be performed discrimination between small
to aid in diagnosing the salivary gland vessels and ducts and rapid as­
T2 N2 M0
neoplasms are as follows: sessment of the vascularity of the
T3 N2 M0
• Diagnostic imaging: mass lesions.
T4a N2 M0 – Routine radiographs: It is not of – Sialography: It involves intub­
Stage 4B T4b Any N M0 much value except for diagnos­ ation of the principal duct of the
Any T N3 M0 ing radiopaque sialoliths and pa­ salivary gland and instillation of
Stage 4C Any T Any N M1 renchymal calcification. Salivary radiopaque contrast medium to
298 Salivary Glands Pathologies

delineate the ductal system and be diagnosed early on MRI due the needle tract. However, the
any other spaces in continuity. to better soft tissue delineation. aspi­rate may show limited his­
Its chief value is in assessment of The criteria of nerve involvement tolo­
gical architectural features
obstructive pathology. include replacement of normal and the tumor–stroma interface,
– Radionucleotide scanning: It perineural fat with tumor, en­ which is of importance in diag­
is a valuable diagnostic tool in hancement with gadolinium (re­ nosis of many salivary tumors.
the evaluation of salivary gland gardless of size) and increased Also, the status of invasion by
physiology and pathology. These size of the nerve in question (re­ the tumor, which is the most im­
scans are useful in differentiat­ gardless of enhancement). portant criteria in predicting bi­
ing between acute obstructive – Arteriography: It not only defines ologic behavior, is not disclosed
and non-obstructive sialadenitis, the vasculature of the tumor, but by FNA.
showing presence of parenchy­ also delineates the origin of the – Incisional biopsy: It plays a minor
mal masses greater than 1 cm vascular supply, which can aid the role in diagnosis of salivary gland
in diameter and in few cases in surgeon in preoperative planning lesions. The tumors of the parotid
identification of specific types of of the surgical procedure. are seldom biopsied as there are
tumors. It includes static and dy­ – Positron emission tomography15: chances of seeding of the tumor
namic scanning. It is not a routinely used modality cells and fungation through the
– CT scan: It provides excellent soft for diagnosis of salivary gland skin at the site of biopsy.
tissue details that show not only disorders because salivary glands – Frozen sections during surgery
the lesion, but also involvement have a variable and inconsistent are helpful to determine the be­
of the surrounding structures. It uptake of Fluorodeoxyglucose nign or malignant nature of the
can be used to evaluate masses (FDG), which is a radiotracer tumor, surgical clearance, how­
involving the parotid gland and most commonly used with posi­ ever the accurate histopatho­
adjacent structures and their tron emission tomography (PET) logical diagnosis of the tumor
relation to the facial nerve. The scans. Hence, FDG-PET is unreli­ may not be possible on frozen
criteria of nerve involvement in able both in tumor detec­tion and sections.
parotid neoplasms on CT rely on in distinguishing benign from Histopathological diagnosis of sali­
bony changes along the course mali­ gn
­ant tumors. The FDG- vary gland tumors is often challen­ging,
of the facial nerve, which include PET is too expensive and is not especially when it is done with FNAC.
bone erosion, sclerotic margins cost-­ effective. However FDG- Clinicians make fanatic efforts to diag­
and widening of the normal PET measures the metabolic nose these lesions preoperatively. It is
diameter of the fallopian canal acti­­vity in various tissues and often difficult to make the subtyping
or stylomastoid foramen. hence is superior to CT and MRI of the salivary tumors on the basis of
– MRI scan: MRI differs from CT in in diagnosing recurrence and cytology or histopathology alone but
its apparent sensitivity to calci­ differentiating it from post-oper­ may require special immunohisto­
fication. The soft tissue contrast ative fibrosis.16 Since it can mea­ pathological techniques. Open biopsies
obtained with MRI allows very sure tumor metabolism, it can are not always indicated. The salivary
good assessment of majority of be used to evaluate tumor proli­ gland contains parenchyma and non­
the salivary masses. Benign or feration rates or tumor hypo­ salivary inclusions such as lymphatic
low-grade neoplasms have well xia, which can be used to opti­ tissue, blood vessels and nerves. The
defined margins with relatively mize treatment strategy such as tumors of parenchymal origin comprise
homogeneous low signal inten­ fractionation scheme for radio­ of 95 to 96 percent of salivary tumors
sity on T1-weighted images and therapy or sequence for combi­ and the tumors of the interstitial tissue
high signal on T2-weighted im­ ned therapy. origin comprise of 4 to 5 percent salivary
ages, which is thought to reflect • Histopathology: tumors. The salivary gland swellings
high proportion of serous and – Fine needle aspiration cytopa­ could be inflammatory or neoplastic
mucinous products present. By thology (FNAC): It has a fairly in origin. Hence, the clinician needs
contrast, high-grade malignan­ high accu­racy in the diagnosis to know preoperatively the nature of
cies have poorly defined mar­ of salivary gland lesions. The the swelling rather than the subtyping.
gins and tend to have heteroge­ diagnostic accuracy of FNAC is A simple approach to salivary gland
neous low signal on both T1 and 98 percent for benign tumors, swellings can simplify the approach
T2-weighted images, reflecting 93 percent for malignant tumors to their diagnosis and management.
the high nuclear-cytoplasm ratio and 88 per­cent for meta­static tu­ The clinician should try to know if
and lack of serous and mucinous mors. It has a minimal chance the swelling is salivary or nonsalivary
material. Perineural spread can of tumor implantation along in origin. If it is salivary in origin,
Diseases of Salivary Glands 299

Occupation
People in occupations such as asbestos
mining,15 manufacturing of rubber pro­
ducts leading to increased exposure to
nitrosamines, industries that use these
rubber products such as shoe manu­fact­
uring, plumbing (exposure to metals) and
woodworking in the automobile industry
are more prone to develop salivary gland
carcinoma. Similarly people associated
with an increased exposure to silica dust
are more prone to salivary gland tumors.19

Lifestyle
Researchers could demonstrate no asso­
ciation of salivary gland tumors with
heavy smoking or heavy alcohol con­
Fig. 15.6: The diagnosis and evaluation of salivary gland swellings
sum­­ption. However, cigarette smok­ing
may play a causative role in the develop­
then whether it is inflammatory or gland neoplasms to etiologic factors like ment of epidermoid carcinomas. War­
neoplastic. If it is neoplastic, then it viruses, radiation, occupation, lifestyle, thin’s tumor is strongly associated with
should be known whether it is benign hormones, etc. cigarette smoking.20 Although sev­ ere
or malignant. A subtyping beyond mal­nutrition such as kwashiorkor causes
this need not be known because it will Viruses enlargement of salivary glands, incre­
usually not affect the treatment plan. All Epstein-Barr viruses have been impli­ ased incidence of salivary gland tumors
malignant tumors are locally infiltrative cated in the etiology of malignant lym­p­ have not been observed.
and tend to metastasize to the regional ho­­epithelial lesion,17 a form of malig­nant
lymph nodes. It may be argued that salivary gland carcinoma. The inter- Endogenous Hormones
the Adenoid cystic carcinoma spreads relationships of immunity, environ­ They have a role in carcinogenesis of
perinurally, but the fact remains that mental factors and genetic constitution salivary gland tumors. Studies have indi­
several other malignant tumors are of the host may all play a role in malig­ cated the presence of estrogen recep­tors
also known to spread perinurally and nant transformation of salivary gland in 80 percent of normal salivary glands
perivascularly (Fig. 15.6). epithelial cells. The other viruses sus­ and prolactin-binding activity in both
Salivary gland swelling chronology for pected as possible etiologic agents are normal and neoplastic salivary gland
diagnosis should be as shown in Fig. 15.6. Polyomavirus, Cytomegalovirus, type C tissue. There has been an increased inci­
If the tumor is malignant, then the particles similar to those associated with dence of salivary gland tumors in patients
clinician should know the extent of the murine leukemia, type B particles similar with breast cancer.21
tumor, whether facial nerve is involved to those associated with murine breast
or not and if the regional lymph node tumors and human papilloma virus types COMMON SALIVARY
metastasis or distant metastasis is pre­ 16 and 18.
sent or not. These factors will guide the
GLAND NEOPLASM
surgeon about the operability of the Radiation
tumor, reconstruction modalities, pre­­Evidence exists for the relationship Pleomorphic Adenoma or Benign
servation or sacrifice of the facial ner­ve,
between exposure to ionizing radiation Mixed Tumor
regional lymph node dissection req­u­­ and the later development of salivary Definition: It is a tumor of variable/in­
gland tumors.18 The substantial lym­
ired or not. It will also prompt the choice complete, encapsulation, chara­cteri­zed
phoid component of the parotid gland
of the treatment as to whether it should microscopically by architectural rather
be surgery alone or surgery plus che­ may be more susceptible to low-dose than cellular pleomorphism. Epith­elial
moradiations or just chemoradiation. radiation damage than the parenchyma. and myoepithelial elements inter­mingle
It seems that doses as low as 140 Rad most commonly with tissue of mucoid,
may increase the risk of developing myxoid or chondroid appe­arance.
ETIOLOGY OF TUMORS
salivary gland neoplasms. Ultraviolet It is also called mixed salivary gland
The etiology of salivary gland tumors radiation may also be associated with tumor due to presence of variety of com­
is unknown. However, investigations an increased risk of salivary gland ponents such as mucoid, myxoid, chon­
have been carried out to link salivary can­cer. droid and sometimes osseous tissue.
300 Salivary Glands Pathologies

Epidemiology: Most common salivary Clinical features: It presents a slow tail of the superficial lobe of the parotid.
gland tumor (60% of all salivary gland growing, well defined, ovoid, round or It can also arise from deep lobe. When
tumors).22 Mean age of presentation is multilobulated, painless mass. Small the tumor involves both, the superfi­
46 years (ranges from 1st–10th). Slight tumors are typically smooth, immobile, cial lobe and the deep lobe of parotid,
female preponderance. firm lumps but larger tumors become it is described as a Dumbbell tumor
Localization: 84 percent in parotid, 8 bosselated. In a very large tumor fluc­ (Figs 15.8A and B). The pleomorphic
percent in submandibular gland and 0.5 tuant areas may be present due to cystic ade­no­mas are usually solitary but syn­
percent in sublingual gland.23 Lower pole degeneration of the stroma (Figs 15.7A ch­ro­nous/meta­chronous presen­tati ons
of parotid is most common location. to J). The common site of origin is the can be seen. The size of the tumor is

A B C

D E F

G H I J
Figs 15.7A to J: Various presentations of pleomorphic adenomas in major and minor salivary glands
Diseases of Salivary Glands 301

is increased among tobacco smok­


ers.25 Warthin’s tumors are bilateral in
12 percent of cases. Warthin’s tumors
have a smooth capsule. When incised,
multiple cystic spaces that contain mu­
cinous material are appreciated. On
microscopic evalu­ ation, multiple pa­
pillae are present, projecting into the
cystic spaces. The papillae consist of
double-layered epithelium. The outer
layer consists of granular eosinophilic
A B cells. The stroma beneath the epithe­
Figs 15.8A and B: CT scan of extensive pleomorphic adenoma of parotid involving the lium is lymphoid, often containing ger­
superficial and deep lobes (Dumbbell tumor) minal centers.26
Warthin’s tumors are best treated
by means of superficial parotidectomy,
variable at the time of first diagnosis. which spares the facial nerve.27,28
The tumor is usually asymptomatic and
thus, the patients tend to ignore it and Oncocytoma
the tumor grows slowly, but steadily Oncocytomas are unusual benign neo­
to a large size. Inspite of large size the plasm that arises from the granular
involvement of the facial nerve does not oncocytes within the salivary glands.
occur. The larger tumors have a typical These tumors account for less than
mul­tilobulated appearance and it does 1 percent of all salivary gland tumors.
not sag down, but stands out inspite They occur more commonly in older
of its large size and weight due to the patients and affect men and women equ­
presence of the chondroid tissue. The ally. Malignant oncocytomas do occur,
facial nerve is not involved in benign but they are extremely rare.29
variants even if the tumor is large Benign oncocytomas are smooth
(Fig. 15.9). The encapsulation is incom­ and firm with a rubbery consistency. The
plete and thus the tumor tends to recur tumors are cellular, containing round
even after surgery, if the resection is not eosinophilic cells with a granular cyto­
adeq­uate. plasm. The nuclei are small and have in­
Histopathology: The pleomorphic ade­­n­­ dentations. The granular appearance of
oma has remarkable degree of mor­phol­ Fig. 15.9: Large lipoma in the parotid area this electron microscopy is used to iden­
ogical diversity. The essential compo­ note the tumor surface is not lobulated and tify this ultrastructural feature, which
nents are capsule (usually inco­mp ­ lete), is sagging down. The tumor is not standing can be diagnostically helpful.
epithelial and myoepithelial cells and out like the pleomorphic adenoma These tumors most commonly arise
mesenchymal or stromal elements. The in the superficial portion of the parotid
epithelial component shows a wide va­ stroma can be striking feature of some gland, they are best treated with superficial
riety of cells including cuboidal, basa­ tumor. parotidectomy with preservation of the
loid, squamous, spindle, plasmacytoid facial nerve. Tumors that occur outside
and clear cells. The cells are cytologically Warthin’s Tumor (Papillary the parotid gland should be excised with
bland and have vacuolated nuclei with­ Cystadenoma Lymphomatosum) a cuff of normal tissue.
out prominent nucleoli and low mitotic Warthin’s tumor represents the second
frequency. The epithelium usually forms most common benign salivary gland Monomorphic Adenoma
sheets or duct like structures, duct show neoplasm, comprising approximately Monomorphic adenomas are often
cuboidal luminal cells and there may be 6 to 10 percent of all parotid tumors. grouped with pleomorphic adenomas.
abluminal layer of myoepithelial cells. War­thin’s tumors rarely occur in the These are distance tumors histologically,
Mesenchymal component is usually mu­ sub­man­ dibular or minor salivary however and lack pleomorphic features.
coid/myxoid, cartilaginous or hyalinized. glands. Warthin’s tumors affect men Basal cell adenomas and clear cell
Due to the presence of diversified tissue more commonly than women, with a adenomas are included in this group
it is often called a mixed tumor. Deposi­ male-to-female ratio of 5:124 and they to tumors. Monomorphic adenomas
tion of homogeneous eosinophilic hyaline typically appear between the 4th and are benign, slow growing and the least
material between tumor cells and within 7th decades of life. The prevalence aggressive of the salivary gland tumors.
302 Salivary Glands Pathologies

They probably represent fewer than 3. Neoplastic transformation of the configuration varies in and between
2 percent of salivary gland neoplasms.30 mucus secreting cells commonly tumors. They are usually multicystic
The most common variety of mono­ found in the pluripotential epithelial with solid component and sometime the
mor­ phic adenomas is the basal cell lining of dentigerous cysts associated latter predominates. According to the
adenoma. Basal cell adenomas occur with impacted third molars. clinical behavior and the severity of the
most commonly in the minor salivary 4. Neoplastic transformation and inva­ dysplasia the tumor can be subgraded
glands, usually the upper lip.31 Of the s­ion from the lining of the maxil­ as low grade, moderate grade or severe
major salivary glands, the parotid gland lary sinus. Our patient gave a prior grade tumors.
is the usual location of occurrence. history of cyst enucleation in the
Macroscopy: The tumors are encap­ same regi­ on as the tumor, which Adenoid Cystic Carcinoma
sulated and are smooth. may indi­cate the possibility of neo­ Adenoid cystic carcinoma (ACC) is the
Microscopic appearance: The tumors plastic tran­sf­ormation of the cyst second most common malignant sali­
con­ tain epithelial parenchyma, which wall into a mali­gnant non-odonto­ vary gland tumor, representing appro­
is sharply demarcated from the scant genic tumor. ximately 10 percent of all salivary gland
stroma by a thick, prominent basement Clinical features: Most tumors pre­­sent as neoplasms.36 It is the most common
membrane. The epithelial cells have a firm, fixed and painless swellings. Subli­ malignancy in the submandibular gland
palisading appearance at the periphery of ngual gland lesions may demonstrate pain and usually appears as slow-growing
the tumor parenchyma. The appearance in spite of small size. Superficial intraoral painless mass. It has a tendency for early
can be confused with adenoid cystic neoplasms may exhibit a blue-red color ulceration (Figs 15.11 to 15.14).
carcinoma, but the distinction is clearly and mimic a mucocele or vascular lesion. The most common symptom is a slow
important, as the biologic behavior of the The mucosa overlying palatal tumors can growing mass followed by pain due to the
two tumors is vastly different. be papillary. Cortical bone is sometimes propensity of these tumors for perineural
Treatment: It consists of surgical exci­ superficially eroded. Sym­ptoms can incl­ invasion. Facial nerve paralysis may also
sion with a margin of normal tissue for ude pain, otorrhea, paresthesia, facial occur in parotid tumors.
these benign and non-aggressive tumors. nerve palsy, dysphagia, bleeding and tri­ Metastasis to regional lymph nodes
smus (Figs 15.10A and B). is uncommon, but distant metastasis,
Mucoepidermoid Carcinoma Macroscopy: Firm, smooth often cystic, (usually to the lung) is more common.
Definition: It is a malignant glandular tan or pink, well defined or infiltrative Adenoid cystic carcinoma is unique in
epith­e­lial tumor, characterized by mucus, edges.35 The tumor often has slimy stroma. the survival at 5 years is approximately
inter­mediate and epidermoid cells with Tumor spread: Paro­­tid g­l­­­and tumors 65 percent, but 15-year survival is only
colu­­ mnar, clear cells and onco­ cytoid spread to adjacent prea­uri­­cular lymph 12 percent. Because of the slow growth
fea­tu
­ res. nodes, then to sub­man­di­bular region. of this tumor, patients may remain
Epidemiology: Most common primary Submandibular gland neo­plasms spread free of disease after initial treatment
salivary gland malignancy in both adults to submandi­ bular and upper jugular for 10 years or longer, only to develop
and children. Mean patient age is ap­ lymphatic chain. metas­tases.37-39 Local recurrence is
prox 45 years. The M: F ratio is 3:2. Histopathology: Mucoepidermoid car­ also common. The tendency for this
Localization: Half of the tumors occur ci­­­n­oma is characterized by squamoid tumor to grow along perineural40 and
in major glands, 89.6 percent involved (epi­­d­er­moid) mucus producing cells and perivascular planes, often with skip les­
the parotid, 8.4 percent submandibular cells of intermediate type. Proportion of ions, helps explain the generally poor
and 0.4 percent sublingual gland.32 The different cell types and their architectural success of treatment.
central mucoepidermoid carcinomas in
the mandible, especially at the angle due
to entrapment of glandular tissue during
embryonic fusion have been reported.
The mucoepidermoid carcinoma is also
seen in the tongue.33
Pathogenesis: Four possible origins
have been described:34
1. Entrapment of retromolar mucous
glands within the mandible, which
sub­sequently undergo neoplastic
trans­­formation.
2. Developmentally included embry­ A B
onic remnants of the submaxillary Figs 15.10A and B: Mucoepidermoid carcinoma of the submandibular salivary gland
gland within the mandible. treated with excision of the affected gland
Diseases of Salivary Glands 303

Gross findings: Adenoid cystic carci­no­ and Solid.41 The cribriform pattern has the propensity for perineural invasion.42
mas are usually monolobular and non- the classic ‘swiss cheese’ appearance with Perineural extension accounts for the
encapsulated. They have a gray-pink basophilic mucinous substance filling difficulty in eradicating adenoid cystic
color and infiltrate the surrounding nor­ the cystic spaces. In the tubular pattern, carcinoma despite extent of excision.
mal tissue. the cells are arranged in smaller ducts
Microscopically: The tumors consist of and tubules with less prominent cystic Acinic Cell Carcinoma
basaloid epithelial elements that from spaces. The solid type is characterized by Definition: Malignant epithelial neopl­
cylindrical structures. Tumors are class­ sheets of neoplastic cells with few cystic asm of salivary glands characterized by
ified by the general architecture into the spaces. Any given, tumor may contain all cyto­plasmic zymogen granules.
following three type: Cribriform, Tubular three patterns, but common to all types is Epidemiology: Slightly more women are
affected than men.43 Affected patients
are ranging from young children to
elderly adults, but is seen especially in
2nd decade.
Localization: Overwhelming majority 80
percent parotid gland 17 percent intraoral
salivary gland, 4 percent submandibular
gland, 1 percent submental gland.44
Clinical features: Slowly enlarging/
solitary unfixed mass, some patients
experience pain which is often described
as vague and intermittent.
A B
Macroscopy: 1 to 3 largest dimension,
Figs 15.11A and B: ACC involving the sublingual salivary gland circumscribed solitary nodules, lobular
and tan red. Firm to soft, solid to cystic.
Tumor spread: Acinic cell carcinoma
initially metastasizes to cervical lymph
nodes.
Histopathology: Several cell types and
growth patterns are recognized. Acinar,
intercalated ductal, vacuolated, clear,
glandular, solid/lobular, microcystic,
papi­­
llary, follicular, (solid, solid-lobu­
lar, aci­nar-microcystic, papillary cystic,
tubulo­ductal, follicular/macrocystic and
A B dedifferentiated45).
Figs 15.12A and B: ACC involving minor salivary gland of palate

A B C
Figs 15.13A to C: ACC CT scan showing extension of the tumor to the skull base
304 Salivary Glands Pathologies

Clinical features: Long-standing mass


(> 3 years) with recent history of rapid
growth over previous few months.52 The
earliest sign could be paresthesia of the
overlying skin and subsequently the signs
of involvement of the nerves in the area53
(facial nerve in case of the parotid gland)
may follow (Figs 15.15A to H and 15.16A
and B). Like other carcinomas it has
tendency to metastasize to the cervical
lymph nodes.
A B Macroscopy: The size is twice that of its
benign counterpart (1.5–2.5 cm), poorly
circumscribed and many are extensively
infiltrative. Occasionally are well circu­m­
scribed scar-like or completely capsulated.
Histopathology: Proportion of benign vs.
malignant components are quite variable.
Malignant component is most frequently
a poorly differentiated adenocarcinoma
or an undifferentiated carcinoma.54 An
infiltrative, destructive growth pattern is
C D most reliable diagnostic criteria. Nuclear
hyperchromatism and pleomorphism are
important diagnostic criteria.

Squamous Cell Carcinoma


Primary squamous cell carcinoma of the
salivary glands is rare. Ruling out high-
grade mucoepidermoid carcinoma,
which may appear similar to squamous
cell carcinoma, is important. Similarly,
E F G the differential diagnosis must exclude
a primary squamous cell carcinoma of
Figs 15.14A to G: Case of ACC involving minor salivary gland, extending to orbit, sphenoidal
and ethmoidal air sinuses: (A) Approach to tumor with Weber Fergusson incision; (B) Intraoral the skin or upper respiratory squamous
presentation of the tumor; (C) Intraoperative photograph showing hemi-maxillectomy with mucosa with regional metastasis to the
ethmoid and sphenoidal sinus clearance; (D) Removal of the orbital contents; (E) Surgical salivary glands. Excluding these two
defect created after wide local excision of tumor; (F and G) Excised specimen possibilities, true primary squamous
cell carcinomas likely represent 0.3 to
1.5 percent of salivary gland tumors.
Acinar cells are large polygonal with cent of all salivary malignancy and As in other head and neck squa­
light basophilic, granular cytoplasm, 6.2 percent of all pleomorphic adeno­ mous cell carcinomas, local and regional
round eccentric nuclei, cells are enlar­ mas.47 recurrence occurs frequently. Treatment
ged in sheets nodules/lobules, cystic Etiology: Accumulation of genetic insta­ comprised of wide local excision, cervical
micro­cystic, papillary projections, lym­ bilities in long-standing pleomorphic neck dissection where ever merited and
phoid infiltrate positive.46 adenomas.48 Carcinoma ex-PA usually chemoradiations, if needed.
presents in 6th to 7th decades,49 approxi­
Carcinoma Ex-pleomorphic mately 1 decade later than patients of Adenocarcinoma (Not Otherwise
Adenoma pleo­morphic adenoma. Specified)
Definition: Pleomorphic adenoma (PA) Localization: Carcinoma ex-pleomor­ Definition: Malignant salivary gland tu­
from which an epithelial malignancy phic adenoma most frequently arises in mor that exhibits ductal differ­en­tia­tion,
has derived. the parotid gland, may originate in sub­ but lacks any of the histomor­phological
Epidemiology: They comprise 3.6 per­ mandibular gland and minor salivary features that characterize the other de­
cent of all salivary gland tumors, 12 per­­- glands.50,51 fined types of salivary carcinoma.
Diseases of Salivary Glands 305

A B C

D E F

Figs 15.15A to H: Malignant pleomorphic adenoma of left parotid gland:


(A) Bell’s palsy due to facial nerve involvement; (B) Fixity to skin; (C) CT
scan; (D) Marking of incision; (E) Exposed tumor; (F) Tumor excision with
G H radical neck dissection; (G and H) Reconstruction with PMMC flap

Clinical features: Most patients with


tumors of major glands present with
solitary, asymptomatic masses, but
20 percent have pain or facial weak­
ness. Pain is often associated with
submandibular glands. Minor salivary
glands are often ulcerated and about
20 percent of palatal tumors involve the
underlying bone.
Macroscopy: Adenocarcinoma partially
circumscribed, but in many areas the
A B periphery is irregular and ill defined.
Figs 15.16A and B: Carcinoma ex-pleomorphic adenoma Areas of hemorrhage and necrosis may
contract with white or yellowish cut sur­
face.
Epidemiology: It is second only to mu­ Localization: About 60 and 40 percent Histopathology: All tumors have pres­
coepidermoid carcinoma in occurrence, respectively occur in major and minor ence of glandular or duct like structures,
accounts for 17 percent of salivary carci­ glands. Major gland involved is parotid, infiltrative growth into parenchyma or
nomas. Women outnumber men slight­ minor glands are from the hard palate, surrounding tissues. Tumor cells are in
ly. Average patient age is 58 years. buccal mucosa. nests and cords or large discrete islands
306 Salivary Glands Pathologies

with intervening trabeculae of fibrous Histopathology: It is characterized by Localization: Approximately 90 percent


connective tissue. cytologic uniformity, histologic diversity arise in the parotid area, with occasional
Prognosis: Minor salivary gland tumors and an infiltrative growth pattern. The tumors in the oral cavity, vallecula, sub­
have better survival than major gland tumor cells are small to medium size and lingual gland, submandibular gland and
tumors. Fifteen years survival rate for uniform in shape with bland, minimally epiglottis.
low intermediate and high-grade tumor hyperchromatic oval nuclei and occasion­ Clinical features: Patients typically pre­
was 54, 31, and 3 percent respectively.55 ally nucleoli. Main microscopic features sent with a painful mass with varying
are lobular, papillary, papillary-cystic, degrees of facial nerve paralysis and
Polymorphous Low-grade cribri­form, trabecular or small duct-like occasional fixation to the skin.
Adenocarcinoma structures. Cells form concentric whorls Macroscopy: Tumors have ranged from
Definition: A malignant epithelial tu­ or targetoid arrangements around blood 0.6 to 8.5 cm in greatest dimension and
mor characterized by cytologic unifor­ vessels or nerves. Stroma may show areas vary from yellow, tan-white, grayish-
mity, morphologic diversity, an infiltra­ of hyalination or mucinosis. white, white, to pale pink. They are well
tive growth pattern and low metastatic Prognosis: Overall survival rate of circum­scribed or partially encap­sulated,
potential. pati­­ents with PLGA is excellent. Local with pushing or locally infiltrating mar­
Epidemiology: Polymorphous low-grade recu­r­rence rate varies between 9 and gins.
adenocarcinoma (PLGA) is the most 17 percent and a regional metastasis rate Histopathology: Tumors are composed
common intraoral malignant salivary is 9 to 15 percent. The distant metastasis of multiple large foci and nests or sheets
gland tumor56 accounting for 26 percent have been seldom reported. of cells with hyperchromatic nuclei and
of all carcinomas. Male:Female ratio is abundant clear to eosinophilic cyto­pla­
2:1. Patient age ranges from 16 to 94 years. Sebaceous Carcinoma sm. Cellular pleomorphism and cy­to­­logic
Mean age is 59 years. (Figs 15.17A to C) atypia are present to varying deg­rees and
Localization: Approximately 60 percent Definition: Sebaceous carcinoma is a are much more prevalent than in seba­
of the cases involve palate. Other intra­ malignant tumor composed of seba­ ceous adenomas. Squamous diff­ eren­
oral localization are buccal mucosa, ceous cells of varying maturity. They are tiation is common. There may be areas
retro­molar region, upper lip and base of arranged in sheets and/or nests with of basaloid differentiation, parti­ cularly
tongue.57 different deg­ rees of pleomorphism, at the periphery of cellular nests. Areas of
Clinical features: It presents as a pain­ nuclear atypia and invasiveness. necrosis and fibrosis are common. Peri­
less mass in the palate. Duration of Epidemiology: There is a bimodal age neural invasion is seen in greater than 20
lesion varies from weeks to as much as distribution with a peak incidence in the percent of tumors; vas­cular invasion is
40 years. Bleeding telangiectasia or ulc­ third decade and the 7th and 8th decades infrequent. Rare oncocytes and foreign
er­ation of the overlying mucosa occ­asi­ of life (range 17–93 years). The male and body giant cells with histiocytes may be
on­ally occurs. female incidence is almost equal. Unlike observed, but lymphoid tissue with fol­
Macroscopy: PLGA usually appear as a sebaceous neoplasms of the skin there is licles or subcapsular sinuses is not seen.
firm circumscribed, but nonencapsu­ no increased risk of developing a visceral Prognosis and predictive factors:
lated, yellow-tan lobulated nodule up to carcinoma in patients with a salivary The treatment of choice is wide surgi­
several centimeter. gland sebaceous tumor. cal excision for low stage carcinomas.

A B C
Figs 15.17A to C: Sebacious carcinoma of parotid gland: (A) Preoperative photograph; (B) Intraoperative photograph showing excision
of tumor with neck dissection; (C) Closure and reconstruction with PMMC flap
Diseases of Salivary Glands 307

Adjunctive radiation therapy is recom­ patient preparation is done such as subcutaneous fat should be left to cover
mended for higher-stage and grade tu­ shaving of the hair, i.e. one fingerbreadth it as the flap is raised. Penetration on the
mors. The overall 5-year survival rate is all around the pinna followed by deep surface will bring it into contact
62 percent, slightly less than the survival shampoo bath and scrubbing of the with the muscle such as masseter or
for similar tumors arising in the skin and surgical site. It is preferred that the side loose connective tissue. The former can
orbit. of the face to be operated is not covered be excised in continuity with the mass;
by drapes to visualize the twitching of the latter should be divided under direct
the facial muscles. Adrenaline diluted vision some little distance from the
APPROACH TO THE
with saline is infiltrated locally along tumor and allowed to collapse on to its
MANAGEMENT OF the incision site to reduce bleeding. surface. Filamentous structures passing
SALIVARY GLAND TUMORS Blair’s incision is commonly used for horizontally or radiating from the region
access. The incision in the neck crease of the main trunk are likely to be nerves
• Try to know whether it is benign or is deepened first exposing and dividing and should be conserved. The branches
malignant—Usually clinical exami­ the platysma and identifying the thick decrease in diameter as they are traced
nation and FNAC is adequate to deep fascia, at the angle of the mandible. peripherally in contrast to the main
determine the same. The subtyping The greater auricular nerve is identified duct that increases in size to reach 2 to
of the tumor does not affect the and preserved. Facial nerve injury is 3 mm in cross-section as it emerges from
treatment planning and thus it is not avoided at this stage due to its position the gland anteriorly. Further it passes
necessary. deep to the deep fascia but some diagonally upwards and forwards. Blood
• If it is malignant the grade, i.e. whe­ subcutaneous fat should be left on the vessels, except for the transverse facial
ther it is low, intermediate or high- fascia near the zygomatic bone due to generally run up from below and unlike
grade malignancy. superficial location of the facial nerve. nerves, have elasticity, so that with care
• If it is malignant remove the total The branches of the facial nerve are they can be distinguished. Branches
gland. Address the neck nodes if indi­ visible through the translucent fascia as from the great auricular nerve differ
cated. they emerge from the anterior border from those of the facial by remaining
• The facial nerve should be preserved of the gland. Facial nerve identification on the surface of the gland as they are
unless it is distinctly indicated to be is carried out using the various facial traced posteriorly. The branches of the
sacrificed in cases where: nerve pointers58 or using facial nerve facial nerve should be preserved as
– There is clinical evidence of monitoring. As each branch is identified, far as possible until visible infiltration
nerve involvement. it is labeled by under running it with a by malignancy is seen or facial nerve
– It is difficult to dissect the nerve length of black silk, the ends of which weakness is present preoperatively. In
free due to the tumor infiltration. are clamped in mosquito artery forceps. general, the nerves pass superficial to
– Tumors known to spread perin­ The facial nerve and its branches are the retromandibular vein, but some may
urally, e.g. adenoid cystic carci­ invested by loose connective tissue pass deep to it.59 Careful mobilization of
noma. and lie in tunnels within the parotid both nerve and vein with division and
into which the tips of the blades of ligation of the latter is necessary. Tiny
Management of Parotid curved mosquito artery forceps may be vessels should be sealed with diathermy
Tumors insinuated. The blades are then opened by accurately grasping them with fine
The various procedures that are comm­ a little to stretch the tissues and raised, artery forceps and touching briefly
only practiced are: so as to lift the gland substance off the with the electrode, avoiding damage to
• Local excision of the parotid gland surface of the nerve, a short length of adjacent nerves. The mobilization and
• Superficial parotidectomy with pre­ which may then be exposed by cutting excision of the superficial lobe containing
ser­­vation of the facial nerve through the gland with scissors. At all the tumor mass is carried out.
• Functional superficial parotid­ectomy times when a cut is made the adjacent
• Total parotidectomy with preser­ nerve must be seen clearly. The facial Complications
vation of the facial nerve nerve splits into an upper temporofacial • Facial paresis or paralysis often result
• Radical parotidectomy with or with­ and a lower cervicofacial division at the from poor technique and failure to
out neck dissection in continuity level of the condylar neck. Each branch preserve small nerve branches
• Parotidomandibulectomy is dissected free of the parotid gland so • Bleeding and hematoma formation,
• Temporoparotidectomy. as to mobilize the entire gland. Tissue which can significantly compromise
Surgical technique most commonly adjacent to tumor is compressed into a the airway
used is partial or total parotidectomy thin capsule. Where the tumor, reaches • Rarely, persistent salivary leakage or
with facial nerve preservation. Routine the surface of the gland some overlying sialocele formation occurs
308 Salivary Glands Pathologies

• Frey’s syndrome plete excision of the entire gland pare­ procedure is being carried out for a
• Skin flap necrosis. n­­chyma with preservation of the facial neoplastic growth. The gland is removed
nerve wherever possible (Figs 15.19A together with its investing fascia, which
Functional Superficial to E, 15.20A and B). The nerve is sacri­ is separated from the anterior and
Parotidectomy ficed only if there is malignant infiltration posterior bellies of the digastric and the
Functional superficial parotidectomy or preoperative facial nerve paresis. stylohyoid muscle. The facial artery and
involves preservation of the stensen’s However, in such a situation it is imm­ vein are identified early in their course
duct and its connection to the deep edi­ately reconstructed with micro­neuro­ as close to the inferior posterior pole of
lobe. This is possible if the duct is deep surgical transfer from greater auri­cular the gland and deep to it and are ligated
to the facial nerve and does not obstruct nerve or sural nerve. (Figs 15.21A and B). After transection
dissection of the nerve. Here, the fun­ Other extended surgeries such as pa­ of these vessels they are elevated supe­
ction of the gland is preserved. rotidomandibulectomy or temporopar­ riorly to identify and reflect the marginal
otidectomy or parotidectomy with neck mandibular nerve from the field. After
Advantages of functional superficial dissection can be performed depending safeguarding the mandibular nerve,
parotidectomy:
on the extent of local or regional inva­ the fascia is divided at the inferior
• It is a simpler surgery than conser­ sion by the tumor. mandibular border. The superficial part
vative superficial parotidectomy. of the gland is dissected from the muscle
• It preserves partial function of the Management of up to the posterolateral border where
parotid gland. Submandibular and three vital structures are identified here
• It avoids the influence of subsequent Sublingual Gland Tumors viz. lingual nerve, hypoglossal nerve and
gland atrophy on facial contour. Extracapsular excision of the submandi­ Wharton’s duct. When the free edge of
• It decreases postoperative compli­ bular gland is done, if tumor is confined the mylohyoid is retracted medially the
cations. to the gland proper. If the tumor has attachment of the lingual nerve to the
spread beyond the confines of the gland, gland that represents its parasympathetic
Partial Superficial Parotidectomy an extended surgical procedure for re­ supply is evident. The Wharton’s duct
It is excision of only that portion of the section of the involved areas of the floor is inferior to lingual nerve and is often
super­ ficial lobe containing the tumor of the mouth should be carried out with surrounded by sublingual glands. As
with preservation of the facial nerve. It marginal or segmental mandibulectomy, fascia and gland are mobilized upwards
results into lesser incidence of Frey’s depending on the extent of the tumor. from the surface of the hyoglossus, the
syndrome. So also, gland function is An approximately 7 cm long incision hypoglossal nerve is identified more
preserved due to more parenchyma is made in the submandibular skin inferiorly. It is accompanied by ranine
being preserved (Figs 15.18A to C). crease around two finger breadths be­ vein, which may aid in its identification.
low the lower border of the mandible The vena comitans that accompany the
Total Parotidectomy with Facial and a subplatysmal dissection is done nerve are inevitably damaged. Post­
Nerve Preservation to raise a flap. The capsule of the gland eriorly the angular tract of fascia has to
Total parotidectomy with facial nerve and surrounding soft tissue must be left be cut with scissors to allow the gland in
pre­servation or sacrifice involves com­ intact over the gland when the surgical its fascial envelope to be drawn down.

A B C
Figs 15.18A to C: Partial superficial parotidectomy
Diseases of Salivary Glands 309

This step is the most difficult because


it is important not to grasp the gland
with instruments, particularly tissue
forceps lest the tumor be ruptured.
Where necessary the upper pole may be
mobilized via the mouth. An assistant
can then depress the gland towards the
submandibular wound to enable the
operation to be concluded. The duct and
the branch of the lingual nerve supplying
the submandibular gland are ligated and
A B
transected. The duct is divided close
behind the papilla. During excision for
inflamma­tory disease the nerve is always
separated from the gland with knife or
scissors. However, if the nerve appears to
be involved in a tumor it is sectioned in
front of and behind the gland and the cut
ends sutured. Should a greater margin
of tissue than the immediate capsule
C D be required laterally, the periosteum
of the mandible is divided along the
lower border and stripped up from the
submandibular fossa. It must be divided
at the level of the mylohyoid line, so that
the lingual nerve can be found and freed
as described above. The wound is closed
in layers with drainage in the usual way
(Figs 15.22A and B).
For the sublingual gland excision
intraoral incision is placed parallel to
the floor of the mouth lateral to the
submandibular duct, with care taken not
to extend the incision more posteriorly
E than the first molar tooth, so as to avoid
Figs 15.19A to E: Pleomorphic adenoma involving both deep and superficial lobes of damage to the lingual nerve. When
parotid (Dumbbell tumor). Note the tumor has also involved the submandibular gland. sublin­gual gland excision is necessary
Treated by parotidectomy and excision of the submandibular glands. Preserving the facial for a tumor, it should be removed with
nerve a wide margin including a rim resection
of the mandi­ble. The larger tumors may
require the extraoral submandibular
incision for their excision.

Complications
• Hematoma in the dead space is
avo­ided by proper hemostasis and
compression dressing or placement
of drain in the postoperative period.
• Trismus is a result of masseter muscle
spasm or inflammation of the TMJ
capsule secondary to trauma. It is
A B self-limiting, but long-standing cases
Figs 15.20A and B: Pleomorphic adenoma of the parotid. Tumor removed by performing may require intra-articular steroid
total paratidectomy, preserving the facial nerve injections.
310 Salivary Glands Pathologies

glands traveling in the same nerve


are transected. During regener­ ation
there is cross-innervation of the nerve
endings. Hence, while eating food
due to activity of the secretomotor
para­sympathetic nerves, which now
supply the sweat glands, there is swea­
ting.

Management of Minor Salivary


A B Gland Tumors
Figs 15.21A and B: (A) Pleomorphic adenoma involving submandibular gland; The minor salivary glands of the palate
(B) Intraoperative photograph are the most commonly involved glands
due to salivary gland tumors. Majority
of the minor salivary gland tumors are
malignant. Thus, they involve the invest­
ing bone and due to the spongy nature
of maxilla spread fast into the adjoining
vital anatomical structures like paranasal
sinuses, orbit, infra-temporal fossa and
subsequently the skull base and can
produce intracranial involvement. The
tumor seen outside may be small but
rapidly infiltrates the deeper structures.
They often require radical excision.
A B
The benign tumors like pleomorphic
Figs 15.22A and B: (A) Pleomorphic adenoma involving submandibular gland;
adenomas are also present in the minor
(B) Mobilization of the gland superficially to identify the facial artery
salivary glands and may require less
radical excision without compromising
the surgical margins (Figs 15.23A and
B and 15.24A to D). Various surgical
procedures like shelling of the tumor,
segmental rese­ction of the maxilla, low
level maxi­ll­e­ctomy, hemimaxillectomy
and radical/extended maxillectomy may
be required to treat the neoplasm depen­
ding on their size, site of involvement,
type of underlying pathology.

RADIOTHERAPY AND
A B CHEMOTHERAPY IN THE
Figs 15.23A and B: Pleomorphic adenoma of the palate treated with wide local excision MANAGEMENT OF SALIVARY
GLAND TUMORS
• Salivary fistula or a sialocele occurs praxia due to stretching and handl­
due to discontinuity between the re­ ing of the nerve during surgery. Per­
maining gland parenchyma and the manent damage occurs usually if the Radiotherapy
duct. It is self-limiting and is man­ nerve is transected or sacrificed. Traditionally salivary gland tumors
aged by repeated aspiration, pre­ssure • Frey’s syndrome60 is associated with were considered to be radioresistant,
dressing, wound care and patience. gus­tatory sweating. During sur­gery if however management of malignant
The patient can even be prescribed the auriculotemporal nerve is dam­ sali­vary gland neoplasms has changed
antisialagogue medication. aged, secretomotor para­sym­­­pa­th­ in recent years. Research over a period
• Facial nerve paresis can be temporary etic nerves from the otic gang­ lion of years suggests that postoperative
or permanent. Temporaray facial supply­ing the parotid gland and sym­ pho­ ton irradiation improves local
ner­ve paresis results from neuro­ path­etic nerves supplying the sweat con­ trol rates in patients with high
Diseases of Salivary Glands 311

Chemotherapy
The role of chemotherapy in the manage­
ment of salivary gland cancers is under
study and in the budding stages.65,66 Vari­­
ous chemotherapeutic regimens are
used currently for palliation of advan­ced
tumors and there is no benefit for use in the
induction or adjuvant setti­ng. The overall
response rate to chemotherapy is found
to be 42 percent. Generally combination
therapy is more effective against salivary
A B gland tumors as compared to single-drug
therapy. The most effective drug regimens
include cisplatin, paclitaxel, doxorubicin,
5-fluo­ro­uracil and epirubicin in different
com­­­­bin­­ations. Although salivary gl­and
cancers show some response to vari­ous
chemotherapeutic agents, these res­
ponses are rarely complete, are usua­
lly short-lived, and have not resulted in
signifi­cant improvement in long-term
sur­vival. A recent study indicated that the
frequent expression of multidrug resistant
genes by carcinoma of the salivary glands
might be responsible for the low response
C D rates to conventional chemotherapy.
Figs 15.24A to D: (A) Pleomorphic adenoma of palate; (B) Intraoperative photograph
showing excision of the tumor and harvestion buccal pad of fat (BFP); (C) Excised specimen;
(D) Reconstruction of the surgical defect with BFP CYSTIC CONDITIONS
The mucocele (mucus retention cyst)
is the most common cystic lesion of
risk of residual microscopic disease. complications, including severe xerosto­ the minor salivary glands (Figs 15.25A
Postoperative radiotherapy has shown mia, sensorineural hearing loss, osteora­ and B). The vast majority presents the
to improve locoregional control for dionecrosis of the temporal bone and extra­vasation phenomenon and has
patients with advanced-stage gland radiation injury to the temporal lobe. Re­ no epithelial lining. The common site
cancer. Reports suggest that use of cent advances in the delivery of radiation is lower lips of young people and the
adju­vant radiotherapy in conjunction therapy including three-dimensional con­ etiology is usually minor trauma.67 Up
with surgery is superior to surgery formal radiotherapy (3DCRT) and intensi­ to 20 percent lesions may represent true
alone in treatment of high-grade ty-modulated radiotherapy (IMRT) have retention cyst secondary to obstruction
and/or advanced cancers of the parotid led to better tumor dosimetry and relative or microliths. The cyst may burst and
gland.61 Adenoid cystic carcinoma has sparing of surrounding normal structures drain spontaneously and occasionally
been reported to be the most consistent such as the oral cavity, cochlea and brain. lead to complete resolution following
radio­responsive tumor type. In cases Neutron beam therapy has also scarring. The simple removal of cyst leads
of adenoid cystic carcinoma wherein shown to improve locoregional control to recurrence of mucocele. The vertical
there is perineural spread radiotherapy rates (67%) for advanced stage tumors.62,63 incision over the cyst and complete
should also be directed along the Frac­tion­
ated neutron irradiation has removal of the underlying mucus gland is
path of the cranial nerve at risk for high relative biologic effectiveness in almost always curative.
involvement. A postoperative radiation many salivary gland histologic types as In the sublingual salivary gland,
dose of 60 Gy (50 – 75 Gy) in 30 fractions com­pared to conventional radiation. the mucous retention cyst occurs due
to the operative bed is thought to be In cases of inoperable tumors, fast- to retention of the saliva beneath the
beneficial. In cases of named nerve neutron radiation therapy provides thin mucous membrane of the floor of
invasion, the path of the nerve should higher rates of locoregional control of the mouth, which is called ranula. The
be treated electively up to its ganglion. the unresectable salivary gland cancer as bluish color gives it is resemblance
Wide-field radiation therapy to the compared to photon or electron radia­ to the belly of the frog and thus the
parotid glands may result in significant tion therapy.64 name, ranula (Fig. 15.26). The cyst is
312 Salivary Glands Pathologies

A B
Figs 15.25A and B: Mucoceles of tongue and lower lip

fungal. The bacterial diseases are further


Fig. 15.27: A case of parotitis
classified into specific (Tuberculosis Acti­
nomycosis) or no-specific like suppurative
infections. The bacterial diseases can be the parotid area. The skin becomes
secondary to the following: tense, glossy and erythematous.
• Ductal anamolies The ear lobule gets lifted, which is
• Obstructive ductal conditions like the pathognomonic sign of paro­
sialolithiasis (calculus) or strictures. tid swelling as there is no other
• Hematogenous infections. anatomical structure in this region
• Secondary to dehydration (uremia, except the parotid, which can cause
liver failure, diabetes, exanthe­mat­ this sign (Fig. 15.27).
Fig. 15.26: Sublingual ‘ranula’ ous fevers) • The salivary caruncle situated on the
• Immunosuppressed states buccal mucosa opposite the maxil­
usually present above the mylohyoid • Secondary to viral infections like lary second molar is inflamed and
curtain, but then mylohyoid does not mumps. milking of the gland leads to puru­
always from a complete diaphram and The infections result secondary to lent discharge from the orifice. The
allows the leakage of the saliva below stasis of salivary flow, which in turn salivary flow is diminished.
the mylohyoid allowing the lesion facilitates the retrograde spread of the • Due to the presence of the dense
to present in the upper part of neck, bacteria from oral cavity in the gland fascia the swelling are not fluctuant
which is called a ‘plunging ranula’. The through the duct. Poor oral hygiene is and are extremely painful due to
treatment modalities are deroofing the one of the predisposing factors for the the mounting pressure as the fascia
cyst and marsupialization to the over suppurative sialadenitis. is non-yielding. The mounting
lying oral mucosa or total excision of pressure leads to ischemic necrosis
the sublingual salivary gland. Suppurative Parotitis of the gland parenchyma and the
The cystic lesions are uncommon in Suppurative parotitis is the acute bac­ abscess may spontaneously burst in
the submandibular salivary gland. The terial infection of the parotid gland the external auditory canal.
cystic lesions involving the parotid gland, (Fig. 15.27). The predisposing factors are • The duct when palpated over the clen­
the hereditary polycystic disease, parotid mentioned above. The causative organ­ ched masseter muscle feels cord like.
duct cyst, retention cyst, lymphoepithelial isms are staphylococci or streptococci. The investigations comprise of plain
cyst. The later is most common and warr­ The predisposing factors are states of X-ray to rule out calculus. Sialography is
ants differentiation from solitary tum­ors dehydration, strictures of the duct, cal­ strictly contraindicated in acute parotitis
like cystic pleomorphic adenoma, muco­ culus, exanthematous fevers and immu­ as it may aggravate the infection and
epidermoid tumor. Multiple, bila­ nosuppression.
teral lead to the necrosis of the gland. The
lym­phoepithelial cysts of the parotid gland The clinical features are as follows: culture of the pus from the duct by taking
are seen in AIDS. • General constitutional signs and a swab after milking the gland may help
sym­ ptoms like, high-grade fever, in planning the antibiotic therapy.
malaise, body ache, leukocytosis. The
INFLAMMATORY DISEASES
signs of dehydration may be present. Management
The inflammatory disorders (sialad­enitis) • The local signs are diffuse inflam­ The management comprises of the medi­
can be classified into bacterial, viral and matory swelling and tenderness over cinal treatment, supportive treat­
ment
Diseases of Salivary Glands 313

and the surgical treatment. The medicinal bimanual palpation effort should be the meals and the salivary clearance
treatment comprises of prescription of made to feel any hard calculus in the is slow. It leads to distension of the
parenteral antibiotics like ampicillin 1 gland or its duct. The milking of the gland and feeling of discomfort,
to 2 g/day or crystalline penicillin 10 to gland results in purulent discharge from tightness in the gland. The gland gets
20 Lac IU, 6 hourly.68 Anti-inflammatory the opening of the duct. swollen due to salivary retention.
and analgesics may be prescribed for The investigations are plain occlusal The phenomenon is labeled as sialo­
sympto­ matic relief. The supportive X-ray of the mandibular arch to rule out angiectasis (dilation of the salivary
treatment in the form of maintaining the any calculus in the duct or the gland. duct) (Figs 15.28 to 15.30).
hydration of patient by oral or parenteral The treatment is similar to that of acute • The obstruction invariably leads to
rehydration therapy is given. Maintenance parotitis, however if the calculus is retrograde infection in the gland
of good oral hygiene by antiseptic gargles present it should be removed once the and the clinical signs of chronic
is advocated. The infection may resolve acute symptoms subside. sialadenitis like, purulent discharge,
with this treatment. One should not wait diminished flow of saliva are present.
for the localizing signs of the infection such Obstructive Pathologies • On palpation calcified, hard calculus
as fluctuations to occur and the prompt may be palpable. In the sub­mandibular
drainage/decompression should be und­ Sialolithiasis gland bimanual palpation of the
er­­­taken to prevent ischemic necrosis of Sialolithiasis is the condition chara­ gland and duct may show presence
the gland. The best way of draining the cterized by formation of the calculus in of calculus. In cases of the parotid,
paro­tid abscess is by placing an incision the gland or the duct. It is commonly on palpation of the gland and the
parallel to the branches of the facial nerve seen in the submandibular gland than duct over the clenched masseter the
to avoid injury to them. The preauricular the parotid. It is also reported rarely in the calculus may be felt.
incision and blunt dissection to drain the sublingual gland, but almost non-existing • Plain radiographs show the calcified
abscess gives good cosmetic results. in the minor salivary glands. The calculus body in the gland or the duct. The
The infection if not managed may or a sialolith causes obstruction to the calculus in the submandibular duct is
get suppressed and pass into subacute flow of the saliva, stasis and paves the best seen on the mandibular occlusal
or chronic form. The gland becomes way for retrograde spread of the infection radiographs and the calculus in the
fibrotic and degenerated. in the gland from the oral cavity and thus phylum is seen on lateral oblique
Once the acute stage has resolved infection secondary to the obstruction view of mandible. The calculus in the
then dilatation of duct by using blunt is hall mark of the sialolithiasis. In the parotid superficial lobe is seen on
probe may help in removing any mucus submandibular gland 85 percent stones the PA view of the skull and mandible
plug and facilitates the free flow of the are radiopaque and more commonly and that in the deep lobe are seen
saliva. Sialogogue may also be helpful. present in the duct. Sometimes the sub­ on the lateral oblique view of the
mandi­ bular gland calculus is present mandible. The calculi in the parotid
Submandibular Gland in the promotion of the duct that lies duct can be visualized by placing
The cause of sialadenitis of the sub­ posterior to the mylohyoid muscle, i.e. the dental film in the upper buccal
mandi­bular salivary gland is more com­ in the hilum of the gland. On the other vestibule (Figs 15.31A to C).
m­only due to obstructive pathology, as hand 85 percent of the parotid stones
the sialolithiasis is more common in it. are radiolucent (mucus plugs) in nature
The gland becomes inflamed, painful and are commonly present in the duct
and tender. A swelling appears below the distal to its bend where it turns acutely
lower border of the mandible. The skin at the anterior border of the masseter
becomes tense, glossy and erythematous, and pierces the buccinator muscle. The
the constitutional signs and symptoms cause for larger incidence of the calculus
are present. The gland becomes palpable in the submandibular gland is the mixed
on bimanual examination be placing and viscid nature of the secretions, more
one finger on the external surface and inorganic contents, uphill and tor­tuous
the other in the lingual sulcus intraorally. course of the duct. The clinical mani­
This examination helps in differentiating festations of sialolithiasis are:
the salivary gland swelling from the • Pain and swelling: The pain has
lymph node swelling. The lymph nodes classical relation with the meals. The
are not commonly palpable bimanually, pain is aggrevated during the meals Fig. 15.28: Sialolith in the orifice of the
unless they are sizably enlarged, during as the salivary flow increases during Stensen’s duct
314 Salivary Glands Pathologies

transorally under local anesthesia


(Figs 15.32A and B). A suture is placed
around the duct distal to the calculus to
prevent posterior slipping of the calculus.
An incision is placed directly on the
calculus in the floor of mouth, parallel
to the lingual vestibule. The duct is also
incised over the stone and the stone is
A B removed. The duct is irrigated to remove
microliths. The incised ends of the duct
Figs 15.29A and B: Submandibular swelling in a case of sialolithiasis, occlusal view
shows sialolith are sutured to the mucosa of the floor of
mouth to create new opening. The stones,
which are situated posteriorly to the
mylohyoid, i.e. in the phylum of the gland
are difficult to be removed transorally and
such stones are managed by existing the
gland itself through the submandibular
incision. The duct of the excised gland is
traced above the masseter as anteriorly
as possible and then ligated. The ligation
of the duct prevents communication bet­
ween the oral cavity and neck. If the duct
is ligated too far posteriorly, the back-
flow of saliva from the sublingual gland,
on rare occasions may lead to formation
of calculus in it.
A B The calculus in the parotid duct in
the portion that lies below the buccin­
Figs 15.30A and B: Inflamed duct due to calculus
ator can be removed transorally. But, the
calculus that lies in the part of the duct
• The hypocalcified calculi or the Management over the masseter is removed through an
mucus plugs may not be seen on The calculus needs to be removed sur­ extraoral incision placed on the skin. The
plain radiographs and sialography gically in order to relieve the obstruction incision is placed parallel to the branches
in such cases may show a classical and prevent infection. The small stones of the facial nerve to avoid damage to
filling defect. may get ejected spontaneously. The them. After the calculus is removed, the
• The chronic infection in the gland small stones situated near the orifice of duct is repaired over the canula.
secondary to obstruction may lead the duct can be removed by massaging The stones can also be removed by
to degenerative changes and fibr­osis and milking of the gland. The calculus other modalities like, endoscopic remo­
in the gland. in the submandibular duct is removed val, lithotripsy.

A B C
Figs 15.31A to C: Radiographs showing sialolith in the Warton’s duct
Diseases of Salivary Glands 315

• The duct is cannulated using a 22 no.


cannula and the cannula is secured
in place with a circumferential suture
around the duct.
• The dye is loaded in a Luer lock
syringe and the syringe is attached to
the cannula. The dye is slowly pushed,
with simultaneously mass­ aging the
A B gland. The injection is continued
Figs 15.32A and B: Transoral removal of calculus in the duct of the submandibular until the patient feels discomfort due
salivary gland to pressure.
• If the piston, the syringe is released
Sialography • Obstructive pathologies like stric­ the dye tends to flow back due to
Sialography is a specialized radiologi­ ture, mucus plugs, hypocalcified increased pressure in the gland,
cal technique for visualizing the sali­ calculi, external compressions. to prevent back flow of the dye the
vary gland with a contrast medium. This • Degenerative conditions. piston is held in place with the help
tech­­­­nique is no more popular due to ad­ • Chronic inflammatory conditions of adhesive tape.
vent of newer technology like ultra­sono­­ (chro­nic sialodentis, Sjögren’s syn­ • The X-rays are taken at regular inter­
graphy and MRI scans. drome). val as the die is filled and flows out of

Intra and extraglandular tumors. the duct.
Contrast Medium •
Ductal anamolies (perforations, sia­ • The salivation is stimulated to em­
Contrast medium are iodine based l­o­­­celes, fistulas). pty the gland of the dye after the
solutions. They are classified as follows: procedure.
• Ionic aqueous solution: This is an Contraindications
aque­ous (water soluble) solution and The contraindications for sialography are: Interpretation
is available in two types viz. loth­al­­ • Allergy to the dye. • The normal salivary gland shows
amate (Conray 480) and metri­zoate • Acute inflammatory conditions. The a ‘winter tree’ or ‘leaf less tree’ ap­
(Triosil). injection of dye in acute inflam­ pearance, because in the functional
• Oil-based solution: This is water mation will cause severe pain and gland the saliva present in the acini
inso­ luble and is available in two can lead to necrosis of the gland. prevents the entry of the dye in them
types: Iodized poppy seed oil–lipio­ and thus only the ductules and the
dol and water insoluble organic Procedure duct are seen (Figs 15.33A to E).
iodine compounds such as panto­ • The orifice of the duct is identified • In case of the chronically inflamed
paque (Table 15.4). and isolated. gland and in Sjögrens syndrome,
• Local anesthesia is infiltrated around the gland has the ‘leafy tree’ or the
Indications the opening. ‘blossom tree appearance’ as the
The indications for sialography are as • The duct opening is dilated by non-functional acini are empty and
follows: probing with a blunt probe like a the eye enters in them and thus at
lacrimal probe. the end of the ductules a round ball
is seen.
Table 15.4: Various dye agents, their advantages and disadvantages • When there is a stricture of mucus
plug in the duct a filling defect is
Dye type Advantages Disadvantages seen. In case of multiple strictures, a
sausage-string appearance is seen.
Oil based Densely radiopaque Extravasated dye may remain in • In case of intraglandular tumors the
tissues for months
normal glandular structure surrounds
Good contrast Foreign body reaction the tumor and thus a ‘cannon ball’
High viscosity – slow excretion Requires increased pressure for appearance is produced.
from gland – adequate time for the introduction into duct—may force • The extraglandular tumor displaces
procedure calculi deeper into the duct
the glandular structure is displaced
Water based Less viscosity – easily introduced Less radiopaque—less contrast to one side and produces a ‘ball in
medium is needed
hand appearance’.
Rapidly excreted Rapid excretion • In case of perforation of the duct or
Easily absorbed and excreted if sialocele the spillage of the dye in
extravasated
the soft tissue is seen.
316 Salivary Glands Pathologies

a classical relation to the meals as it is


aggravated during the meals. Secondary
infection can set in and in such event
the condition becomes symptomatic
and the discharge becomes purulent
in nature. Depending on the nature of
the duct that is damaged the salivary
fistula can be labeled as major or minor
fistula. If the main duct is damaged, the
A B
major fistula is formed and if the small
collecting duct is severed then the minor
salivary fistula results.
The management of this condition
comprises the following:
• Conservative management: It is
gen­­erally done for the minor fistulas.
A compression dressing is given,
which prevents the cutaneous drai­
C D nage of the saliva and the mounting
pressure of saliva within the tissue
finds a way out in the oral cavity
through the transected distal end of
the duct. The pressure is maintained
till the tract is formed between the
E two severed ends of the duct. The
Figs 15.33A to E: Diagrammatic representation of the different sialographic pictures: minor salivary fistulas close with
(A) Winter tree appearance; (B) Blossom tree appearance; (C) Ball in hand appearance; the conservative treatment and the
(D) Cannon ball appearance; (E) Sausage string appearance cutaneous drainage of the saliva
stops spontaneously.
• Anastomosis of the severed duct: If
the fistula is of recent onset then the
area is explored surgically and the
two severed ends are identified and
anastomosed over the peripheral
venous catheter (PVC) cannula
(Fig. 15.35).
• Total excision of the involved
gland in case of the persistent major
fistula which fails to respond to
conservative treatment and where
the anastomosis of the duct is not
A B
possible due to loss of tissue, the
Figs 15.34A and B: Sialocele following ablative tumor surgery involved gland may be excised.

saliva collects in the adjoining soft tissue


SALIVARY FISTULA
and produces asymptomatic swelling
The injuries to the duct of the salivary unless there is secondary infection.
gland lead to extravasation of the saliva The collection of the saliva is the soft
in the soft tissue. The saliva fails to drain tissue plane is termed as sialocele
in the oral cavity. The injuries could be (Figs 15.34A and B). The swelling gradu­
due to penetrating injuries on the check ally erodes the overlying skin and
or as a result of the accidental damage forms a fistula, which drains saliva. The Fig. 15.35: Anastomosis of the duct over
during the surgical procedure. The discharge is watery in nature and has the canula
Diseases of Salivary Glands 317

• Irradiation of the gland: Irradiation 12. Cornog JL, Gray SR. Surgical and clinical 24. Chung YFA. Epidemiology of Warthin’s
renders the gland fibrotic and pathology of salivary gland tumors. tumor of the parotid gland in an Asian
non-functional and the fistula gets Rankow RM, Polayes IM, (Eds). Diseases population. British Journal of Surgery.
obliterated. of Salivary glands. WB Saunders, 1999;86(5):661-4.
Philadelphia. Chap 5. 1976.pp. 99-142. 25. Jens Peter Klussmann. High risk for
13. Bialek EJ, et al. US of the Major bilateral Warthin’s tumor in heavy
REFERENCES
Salivary Glands: Anatomy and Spatial smokers – review of 185 cases. Acta Oto-
1. Antonio Nanci. Ten Cate’s Oral Relationships, Pathologic Conditions, laryngologica. 2006;126(11): 1213-7.
Histology: Development, Structure, and Pitfalls. RadioGraphics. 2006;26: 26. Kumar V, Abbas AK, Fausto N. Robbins
and Function. Mosby. Missouri; chap 745-63. and Cotran pathologic basis of disease,
11. 2005. pp. 299-328.. 14. Lee YYP, Wong KT, King AD, Ahuja 7 edn. St. Louis, MO: Elsevier Saunders
2. Berkovitz S, Hackney BKB, Ruskell CM. AT. Imaging of salivary gland tumors. 2005.
IGL Gra’s Anatomy. The anatomical European journal of radiology. 2008; 27. Nussbaum M. Superficial paro­tidec­
basis of clinical practice. 39th Churchill 66(3):419-36. tomy with facial nerve prese­rvation. In:
and Livingtone, Edinburg. 2005,pp.1290.. 15. Graham S, Blanchet M, Rohrer T. Cancer Nuss­baum M, (Ed), Modern Technics in
3. DuBrul EL. The oral viscera. In: DuBrul in asbestos-mining and other areas of Surgery, Futura, Mount Kisco, NY (1981).
EL (Ed). Sicher and DuBrul’s Oral Ana­ Quebec. J Natl Cancer Inst. 1977;59(4): 28. Moshe Harell. Superficial paroti­
to­my, 8th edn. Ishiyaku Eouro­America, 1139-45. dectomy for benign parotid lesions.
St Louis. Chapt 6. 1988. pp. 161-78.. 16. Jong-Lyel Roh. Clinical Utility of 18F- Operative techniques in otolaryngology.
4. Snell RS. Clinical anatomy. 7th edn. FDG PET for Patients with Salivary 1996; 7(4): 315-22.
Philadelphia (PA): Lippincott Williams Gland Malignancies. Journal of Nucle­ 29. Mahnke, Christoph, Janig, et al.
and Wilkins. 2004; Chapter 11:719-922.. ar Medicine. 2007;48(2):240-6. Malignant oncocytoma of the parotid
5. Conley J. Search for and identification 17. Tsai CC, Chen CL, Hsu HC. Expression gland: Case report and review of the
of the facial nerve. Laryngoscope. of Epstein-Barr virus in carcinomas of literature. Australian Journal of Oto-
1978;88: 172-6.. major salivary glands: a strong associa­ Laryngology, 1998.
6. Harrison JD. Histochemical and bioc­ tion with lymphoepithelioma-like carci­ 30. Batsakis JG, Brannon RB, Sciubba JJ.
he­­
mical determination of calcium in noma. Hum Pathol. 1996;2 7(3):258-62. Monomorphic adenomas of major
salivary glands with particular reference 18. Schneider AB, Favus MJ, Stachura salivary glands: a histologic study of
to chronic submandibular sialadenitis. ME, et al. Salivary gland neoplasms 96 tumors. Clin Otolaryngol Allied Sci.
Virchows Archiv. 1993;423(1). as a late consequence of head and 1981;6(2):129-43.
7. I Van Der Waal. Salivary gland neo­ neck irradiation. Ann Intern Med. 31. Minicucci EM, de Campos EB, Weber
plasms. I Van Der Waal, Prabhu SR, 1977;87(2):160–4. SA, et al. Basal cell adenoma of the
Wilson DF, Daftary DK, Johnson NW, 19. Zheng W, Shu XO, Ji BT, et al. Diet upper lip from minor salivary gland
(Eds). Oral diseases in the Tropics. and other risk factors for cancer of the origin. Eur J Dent. 2008;2(3):213-6.
Oxford University Press, Delhi; Chap 41. salivary glands:a population-based 32. Eversole LR. Mucoepidermoid Car­
1993. pp. 478-486. case-control study. Int J Cancer. 1996 cinoma: Review of 815 reported cas­
8. Spitz MR, Batsakis JG. Major salivary 17;67(2):194-8. es. Oral Surg Oral Med Oral Pathol.
gland carcinoma. Arch Otolaryngol. 20. Sadetzki S, Oberman B, Mandelzweig L, 1970;28:490–5.
1984;110:45. et al. Smoking and risk of parotid gland 33. Heidelberger KP, Batsakis JG. Muco­
9. Sharma D. Salivary gland tumors. tumors: a nationwide case-control epidermoid carcinoma of the ton­gue.
Text of Smt. Radha Devi Memorial study. Cancer. 2008;112(9):1974-82. J Laryngol Otol. 1973;87(12):1239-42.
Oration delivered on 29th December, 21. In der Maur CD, Klokman WJ, van 34. Shafer WG, Hine MK, Levy BM. Text
99 at Madurai during ASICON. Indian Leeuwen FE, et al. Increased risk book of Oral Pathology. Philadelphia
association of surgical oncology. of breast cancer development after WB Saunders, 3 edn. 1974. pp. 225-31.
(www.indiandoctors.com/iaso/htm. diagnosis of salivary gland tumor. Eur 35. Luna, Mario A. Salivary Mucoepid­ermoid
Accessed on 18th July,05) J Cancer. 2005;41(9):1311-5. Carcinoma: Revisited. Advances in
10. Eneroth CM. Salivary gland tumors 22. Johns M, Nachlas N. Salivary gland Anatomic Pathology. 2006;13(6):293-307.
in the parotid gland, submandibular tumors Paperella. Shumrick, Gluck­ 36. Spiro RH, Huvos AG, Strong EW.
gland and the palate region. Cancer. man, Meyerhoff editors. Otolaryn­ Adenoid cystic carcinoma of salivary
1971;27:1415-8. gology; WB Saunders Company. Phila­ origin. A clinicopathologic study of 242
11. Walker NI, Gobe GC. Cell death and dephia. 3rd edn. 1991;3:2099-127. cases. Am J Surg. 1974;128(4):512-20.
cell proliferation during atrophy of 23. Rankow RM, Polayes IM. Diseases of 37. Spiro RH. The controversial adenoid
the rat parotid gland induced by duct the Salivary Glands Pennsylvania: WB cystic carcinoma. Clinical consi­ der­
obstruction. J Pathol. 1987;152:333-44. Saunders. Chapter 5: 1976. pp. 99-142. ations. In: McGurk M, Renehan AG
318 Salivary Glands Pathologies

(Eds). Controversies in the Manage­ 47. Olsen KD, Lewis JE. Carcinoma ex ple­ and Neck Tumors. World Health
ment of Salivary Gland Disease. Ox­ omorphic adenoma: a clinicopatho­logic Organization Classification of Tumors.
ford, UK: Oxford University Press. 2001. review. Head Neck. 2001;23: 705-12. Lyon: IARC Press; 2005.pp. 223-4.
pp. 207-11. 48. Eneroth CM, Zetterberg A. Malignancy 58. Pather N. Landmarks of the facial ner­ve:
38. Speight PM, Barrett AW. Salivary gland in pleomorphic adenoma. A clinical implications for parotidectomy. Sur­­gical
tumors. Oral Dis. 2002;8(5):229-40. and microspectrophotometric study. and Radiologic Anatomy. 2006; 28(2).
39. Friedrich RE, Bleckmann V. Adenoid Acta Otolaryngol. 1974;77(6):426-32. 59. Neil Bhattacharyya. Anomalous rela­
cystic carcinoma of salivary and 49. Beahrs OH, Woolner LB, Kirklin JW, tion­­
ship of the facial nerve and the
lacri­mal gland origin: localization, et al. Carcinomatous transformation retromandibular vein: A case report.
classifi­cation, clinical pathological of mixed tumors of the parotid gland. JOMS. 1999;57(1):75-6.
correlation, treatment results and long- ALH. AMA Arch Surg. 1957;75(4):605- 60. Frey L. Le syndrome du nerf auriculo-
term follow-up control in 84 patients. 13; discussion 613-4. temporal. Rev Neurol. 1923;2:92-104.
Anticancer Res. 2003;23(2A):931-40. 50. Gnepp DR. Malignant mixed tumors 61. Guillamondegui OM, Byers RM,
40. Hoffman H, Funk G, Endres D. of the salivary glands: a review. Pathol Luna MA, et al. Aggressive surgery in
Evaluation and surgical treatment Annu. 1993;28 Pt 1:279-328. treatment for parotid cancer: the role of
of tumors of the salivary gland. In: 51. Gnepp DR, Wenig BM. Malignant adjunctive postoperative radiotherapy.
Comprehensive management of head mixed tumors. In: Ellis GL, Auclair Am J Roent­genol Radium Ther Nucl
and neck tumors Thawley SE, Panje PL, Gnepp DR. Surgical pathology Med. 1975;123(1):49-54.
WR, Batsakis JG, Lindberg RD (Eds). of salivary the glands. Philadelphia: 62. Krüll A, Schwarz R, Engenhart R, et al.
Philadelphia: WB Saunders Company; Saun­ders; 1991. pp. 350-68. Euro­pean results in neutron therapy of
1999. pp. 1147-81. 52. LiVolsi VA, Perzin KH. Malignant malignant salivary gland tumors. Bull
41. Batsakis JG, Luna MA, el-Naggar A. mixed tumors arising in salivary Cancer Radiother 1996; 83 (Suppl):
Histopathologic grading of salivary glands. I. Carcinomas arising in benign 125-9s, 1996.
gland neoplasms: III. Adenoid cystic mixed tumors: a clinicopathologic 63. Douglas JG, Lee S, Laramore GE, et al.
carcinomas. Ann Otol Rhinol Laryngol. study. Cancer. 1977;39(5):2209-30. Neutron radiotherapy for the treat­ment
1990;99(12):1007-9. 53. Seifert G, Mehlkle A, Haubrich J, et al. of locally advanced major sali­vary gland
42. Dale H Rice. Malignant Salivary Gland Diseases of the Salivary Glands: Diag­ tumors. Head Neck. 1999;21(3): 255-63.
Neoplasms. Otolaryngologic Clinics of nosis, Treatment, Facial Nerve Surgery. 64. Wang CC, Goodman M. Photon irra­
North America. 1999;32(5). Stuttgart: Georg Theime Verlag; 1986. diation of unresectable carcinomas of
43. Abrams AM, Corayn J, Scofield HH pp. 222-81. salivary glands. Int J Radiat Oncol Biol
and Hansen LS. Acinic cell adeno­car­ 54. Gnepp DR. Malignant mixed tumors Phys. 1991;21(3):569-76.
cinoma of the major salivary glands—a of the salivary glands: a review. Pathol 65. Suen JY, Johns ME. Chemotherapy for
clinicop­ athologic study of 77 cases, Annu. 1993;28 Pt 1:279-328. sali­
vary gland cancer. Laryngoscope
Cancer. 1965;18:1145-62. 55. Spiro RH. Factors affecting survival 1982;92(3):235-9.
44. Hoffman HI, Kannell LH, Robinson RA, in salivary gland cancers. In: McGurk 66. Posner MR, Ervin TJ, Weichselbaum
Pinkston JA, Menck HR. National Cancer M, Renehan AG (Eds). Controversies RR, et al. Chemotherapy of advanced
Data Base Report on cancer of the head in the Management of Salivary Gland salivary gland neoplasms. Cancer.
and neck—ACC (Multi-institution rep­ Disease. Oxford, UK: Oxford University 1982; 50(11):2261-4.
ort). Head and Neck, 1999. Press; 2001.pp. 143-50. 67. Re-Cecconi D, Achilli A, Tarozzi M, et al.
45. Amisha Shah. Acinic cell carcinoma, 56. Yih WY, Kratochvil FJ, Stewart JC. Mucoceles of the oral cavity: a large case
papillary-cystic variant of the parotid Intraoral minor salivary gland neo­ series (1994-2008) and a literature rev­­i­
gland: A case report with review of plasms: review of 213 cases. J Oral ew. Med Oral Patol Oral Cir Bucal. 2009.
litera­ture. Oral Oncology Extra. 2005; Maxillofac Surg. 2005;63(6):805-10. 68. Schmitt W, Ortel S, Blume H. Clinical
41(7):137-41. 57. Luna MA, Wenig BM. Polymorphous and experimental contribution to the
46. Lewis JE, Olsen KD, Weiland LH. Acinic low-grade adenocarcinoma. In: Barnes penicillin therapy of acute suppurative
cell carcinoma Clinicopathologic L, Eveson JW, Reichart P, Sidransky parotitis. Zentralbl Chir. 1954;79(38):
review. Cancer. 1991;67(1):172–9. D(Eds). Pathology and Genetics Head 1589-1601.
Section 6
Infections of Maxillofacial Region

n Management of Periapical Infections


n Odontogenic Infections
n Osteomyelitis of the Facial Bones
16 Management of
Periapical Infections
Borle Rajiv M, Garg Ketan

The periapical infections are commonly and/or relieving factors for the pain in
Causes
seen in the clinical practice. The peria­ this condition. The mounting pressure
pical infections result secondary to within the pulp chamber compresses The common causes of the pulpal
pulpal pathologies and the involved the periapical blood vessels and the pathologies are:
tooth is invariably non-vital and disco­ lymphatics and the ischemic necrosis • Carious lesions leading to pulp expo­
lored. The exposure of the pulp to the of the pulp takes place. The tooth which sure and infection.
external (oral) environments secon­ had pulpitis and was very painful and • Regressive conditions like abrasion,
dary to caries, attrition/abrasion leads sensitive to hot and cold becomes less attrition, erosion leading to pulp
to contamination and subseq­ uently painful and insen­ sitive owing to the expo­sure.
infection of the pulp (Box 16.1). Simi­ necrosis of the pulp. The necrotic pulp • Fractures of the tooth involving the
larly, the thermal or chemical insult serves as a good nidus for the microbial pulp.
of the pulp also leads to inflammatory proliferation. The infection leads to • Dentoalveolar injuries which lead
changes in the pulp. The pulp is enclosed liquefactive necrosis of the pulp and the to luxation of the tooth and render it
in an inexpansile chamber (tooth) and necrotic, infected material escapes into non-vital, which serves as a nidus for
inflammation and edema of the pulp the peri­apical area of the tooth leading the infection.
leads to increased pressure within the to peri­apical infection. The mounting • Extension of the periodontal infecti­
chamber leading to its compression peri­apical pressure due to infection and ons to the periapical area.
and ischemia. The pain of pulpitis is inflammation causes extrusion of the
very severe and the involved tooth tooth. The tooth has premature contact Fate of the Periapical
becomes to hot and cold. In fact, the due to extrusion and patient feels pain
hot and cold could be the aggravating during mastication. The tooth also
Infection
becomes tender on vertical percussion • Complete resolution, if the cause is
and the mobility sets in due to lysis of treated.
periodontal fibers. The infection initi­ • Transition to the chronic form
Box 16.1: The common causes of the
ally produces widening of lamina dura leading to PA granuloma or cyst
pulpal pathologies
and mild periapical rarefaction on formation.
radio­graphs and endodontic therapy is • Spread to adjoining bone.
• Carious lesions leading to pulp exposure
and infection. good enough to drain and manage the • Extension in the adjacent soft-tissue
• Regressive conditions like abrasion, periapical infection. However, the long spaces.
attrition, erosion leading to pulp standing periapical infection leads to The periapical infection (abscess)
exposure. changes like chronic periapical gran­ can be drained through the root canal
• Fractures of the tooth involving the uloma, periapical cyst and it may not be or through the socket of the tooth by
pulp.
amenable to the endodontic treatment extracting the offending tooth. This is
• Dentoalveolar injuries which lead to
luxation of the tooth and render it non alone and to prevent recurrent episodes very important in the management of
vital which serves as a nidus for the of infection and to remove the periapical the pain due to acute periapical infec­
infection. pathological tissue completely, the end­ tion/abscess. The common mistake
• Extension of the periodontal infections o­dontic treatment needs to be followed done by the clinician is the attempt
to the periapical area. by the periapical surgery. to treat the periapical infection by
322 Infections of Maxillofacial Region

prescribing heavy doses of analgesics down products or exotoxins). Pre­val­


and antibiotics. The pain never gets ence of lymphocytes was noted. Auto­
relieved satisfactorily with medication lytic death of bone cells with empty
as the cause of the pain is pressure and lacunae is seen.
the decompression of the area will give
lasting relief to the patients rather than Zone of Irritation
the antibiotics and analgesics alone. This zone is characterized by macro­
The history of the periapical sur­ phages and osteoclasts. Fish found irrit­
geries also reveals the procedure called ation evidences further from the central
‘trephination’ (creating the hole in the lesion as the toxins became more
buccal cortical plate) to decompress diluted. In this zone, normal bone cells
the infection.1 The infection should be and osteoclasts just managed to survive
Fig. 16.1: Case of periapical abscess
promptly drained by opening the root in the presence of small, round cells.
canal and then the drugs should be These osteoclasts activated the bone
prescribed. Endodontic therapy will lead tissue, while the collagen framework
to satisfactory remission of the infection. was destroyed by macrophages. This
However, the chronic infections may opens up a gap in the bone around the
not be treated by endodontic therapy center of the lesion; as trees are felled
alone. The periapical cyst, granuloma to isolate a forest fire, and this space
or the extension of the infection in soft is then subsequently filled with poly­
tissue leading to a chronic cutaneous morphonuclear lymphocytes and until
or gingival sinus may require further this has taken places a danger of wide­
sur­gical intervention in the form of spread of necrosis remains. The histo­
periapical curettage, apicoectomy and logic picture is of starting of repar­ative
excision of cutaneous sinus along with activity.
the tract (Figs 16.1 to 16.3).
Zone of Stimulation
Pathogenesis of This zone is characterized by fibroblasts
and osteoblasts. At the periphery, the
Periapical Lesions toxin is mild enough to be stimulant
Fish2 described the reaction of perira­ according to Fish’s observations. Fibro­
dicular tissues to noxious products of blasts lay down collagen fibers, which
tissue necrosis, bacterial products and act like a wall of defense around the zone
antigenic agents from root canal by Fig. 16.2: Radiological picture of irritation and act like a scaffold on
establishing experimental foci of infec­ which osteoblasts build new bone. This
tion in the jaws of guinea pigs by drilling newly built bone is deposited in irregular
openings in the bone and packing in fashion.
wool fibers saturated with broth culture
of microorganisms. Four well-defined
zones of reaction were found: Apicoectomy/
Zone of Infection Apisectomy
This zone was found in the center of Apicoectomy is the surgical procedure
the lesion and characterized by poly­ done to resect the diseased apex of
morphonuclear leukocytes. The micro­ an infected root of a tooth. This term
organisms not disposed off by poly­ is often interchanged with the term
morphonuclear leukocytes are found in apicoectomy. The history of this surgery
Haversian canals. Fig. 16.3: Peridontal abscess dates back to late 18th century when a
hole was drilled in the buccal cortex of
Zone of Contamination the alveolar bone to drain the periapical
This zone is characterized by round cell by the toxins released from the central abscess. The surgery is often done to
infiltration around the central zone. Fish zone. The nature of the toxins how­ever eliminate the periapical pathology,
observed an area of cellular destruction could not be established (tissue-brea­k­­­ which can not be treated by endodontic
Management of Periapical Infections 323

Box 16.2: The indications for the obturated by anterograde method


periapical surgery or the apicoectomy and remain under filled.
• Periapical cysts
• Periapical granulomas Indications and
• Over extended root canal fillings Contraindications for
• Dilacerated, calcified or curved root
canals, which can not be adequately
Periradicular Surgery
obturated by anterograde method and
remain under filled. Indications for Periradicular
Surgery (According to Europian
Society of Endodontics 1994)3
Box 16.3: Indications for periradicular sur­
gery (According to Europian Society of • Obstructed canal with radiologic
Fig. 16.4: Maxillary sinus
Endodontics 1994)3 findings and/or clinical symptoms.
• Extruded material with radiologic
• Obstructed canal with radiologic find­ findings and/or clinical symptoms. • Nasopalatine nerve and vessels
ings and/or clinical symptoms. • Failed root canal treatment when • Greater palatine neurovascular bun­
• Extruded material with radiologic find­ retreatment is inappropriate (isth­mus dle
ings and/or clinical symptoms.
• Failed root canal treatment when
tissue, persistent acute sym­ptoms or • Floor of the mouth.
retreat­ment is inappropriate (isthmus flare-ups, risk of root frac­ture). Each of these should be kept in mind
tissue, persistent acute symptoms or • Perforations with radiologic findings and taken into consideration, while per­
flare-ups, risk of root fracture). and/or clinical symptoms and where forming surgery in the involved region
• Perforations with radiologic findings it is impossible to treat from within so as to avoid damage to them.
and/or clinical symptoms, and where
the pulp cavity. The standard armamentarium req­
it is impossible to treat from within the
pulp cavity uired for the periapical surgery is shown
Contraindications for in Box 16.5 and Figure 16.5.
Periradicular Surgery (According
Box 16.4: Contraindications for periradi­ to Europian Society of Box 16.5: Instruments required
cular surgery (According to Europian Soci­
ety of Endodontics 1994)2
Endodontics 1994)2
• Local anatomical factors (e.g. inacc­ • Local anesthetic solution containing vas­­
o­constrictor
• Local anatomical factors (e.g. inaccess­ e­s­sible root end).
ible root end). • No. 3 BP handle with No. 15 Surgical
• Tooth with inadequate periodontal blade
• Tooth with inadequate periodontal sup­ support.
port. • Molt periosteal elevator
• Nonrestorable tooth, without function
• Nonrestorable tooth, tooth without • Cawood-Minnesota retractor
(no antagonist, no pillar for removable function (no antagonist, no pillar for • Standard dental high speed handpiece
or fixed prothesis). removable or fixed prosthesis). No. 6 round bur and No. 557 long fissure
• Uncooperative patient. • Uncooperative patient. bur
• Compromised medical history. • Compromised medical history. • Mayo-Hegar needle holder
• Dean’s surgical dissecting scissors
• Black silk or Vicryl suture (3 ’0’ or 4 ’0’)
Anatomical on cutting needle. The instruments
means alone. The indications and
contraindications for the periapical
Considerations required for periapical surgery are
shown in the Figure 16.5.
surgery are summarized in Box 16.2 to The anatomical structures, which are to
16.4. be considered while performing peri­
apical procedures include: Steps
Indications for the Periapical • Maxillary sinus4 (Fig. 16.4) • Soft tissue access via a muco­peri­
Surgery or the Apicoectomy • Inferior alveolar neurovascular bun­ osteal flap
• Periapical cysts dle and mental nerve as it emerges • Cortical ostectomy to approach the
• Periapical granulomas from the mental foramen5 root apex
• Over extended root canal fillings • Facial artery • Apical curettage
• Dilacerated, calcified or curved root • Floor of the nose with anterior nasal • Apicoectomy
canals, which can not be adequately spine • Retrofilling.
324 Infections of Maxillofacial Region

Flap Designing
Basic principles to be followed, while
refl­e­c­ting the mucoperisteal flap. The
flap should be wider at the base than the
apex to ensure proper blood supply and
drainage of the flap (Figs 16.6A and B,
Fig. 16.7).
The incisions recommended for this
procedure are6,7
• Degloving incision (Figs 16.8A and B)
• Submarginal flap (Figs 16.9A to C)
• Semilunar incision (Figs 16.10A and
B)
• Trapezoid incision (Figs 16.11 and
16.12)
• Triangular incision (Figs 16.13A and
B)
• Envelope incision (Figs 16.14A and B)
• Palatal flap for maxillary posteriors
Fig. 16.5: Instruments required for periapical surgery
(rare) (Fig. 16.15).

Surgical Procedure
The routine patient preparation is done
prior to the surgery. Good quality post
root canal treatment (RCT) radiographs
are obtained to assess the size of the
lesion to facilitate proper planning and
reflection of the mucoperiosteal flap.
Under all aspectic precautions like part A B
preparation, draping, etc. the proce­ Figs 16.6A and B: Flap designing: (A) Dimensions of flap (x>y); (B) Correct and incorrect
dure is usually carried out under the way of designing of flap
local anesthesia. The general anesthesia
is indicated in extensive lesions and
where the patient compliance is poor.
After taking one of the above mentioned
incisions suitable in the given case a
full thickness mucoperiosteal flap is
designed and reflected. Selection of the
appropriate flap design should be based
on the following principles:
• Incision should lie on healthy bone so
that after closure the suture line lies Fig. 16.7: Direction of blood supply in the anterior maxillary region
on solid healthy bone, as incisions
closed over a dead space tend to
break­­down.
• Healing is initiated by epithelial
migration across the suture line and
this is four times faster in attached
gingiva as compared to alveolar
mucosa and this advantage should
be taken by placing horizontal inci­
sion over the attached gingival.
• The horizontal incision should ext­ A B
end atleast one tooth on the either Figs 16.8A and B: Flap design for lower anteriors degloving incision
Management of Periapical Infections 325

A B C
Figs 16.9A to C: luebke-ochsenbein (scalloped) submarginal flap

A B
Figs 16.10A and B: Semilunar incision Fig. 16.11: Trapezoid flap

Fig. 16.12: Triangular/trapezoidal flap for


posterior mandible with release in the
A B
lateral incisor-canine area to avoid damage
to the mental nerve and vessels Figs 16.13A and B: Triangular incision

A B
Figs 16.14A and B: Envelope flap Fig. 16.15: Palatal flap design
326 Infections of Maxillofacial Region

side of the tooth/teeth on which ior release in the lateral incisor-canine through the bone then the intact cortical
apico­ectomy is to be performed. area are indicated. Never place the plate is seen. If the cortical perforation
• The flap must provide adequate incision in the buccal mandibular is present, the same is widened with the
access and visualization of the sur­ vesti­bule. If additional access is req­ help of the flat fissure bur to expose the
gical site without tearing/bruising of uired then a posterior release incision periapical pathology. If the cortex is intact
the flap and damage to the adjacent can be given. a post stamp incision is taken in the bone
structures. with a number 8 round bur and the holes
• Retracting instrument of the flap Technique are joined with the flat fissure bur and
must rest on healthy bone to avoid • Horizontal incision is made first the intervening bone is removed to
trauma so as provide healing with with a sharp, clean stroke avoiding expose the periapical pathology and the
minimal inflammation, pain and multiple incisions. apex of the involved tooth. The purpose
subsequent scarring of tissues and • The vertical arm or arms are then of creating a window in the bone is to gain
subsequent carrying of the tissue. added to it. working access to the tooth being treated.
• The primary blood supply for the • Intactness of papilla should be main­­­ The size of the bone window should
free alveolar mucosa is derived from tained as it will serve as an ancho­ring be large enough to provide complete
the supraperiosteal vasculature that point for sutures. removal of the periapical pathology.
runs parallel to the long axis of the • The entire length of the incision The root apex of the offending tooth
tooth and any horizontal incision in should then be scored with a peri­ should be located precisely to prevent
this unattached mucosa will greatly o­steal elevator to assure its com­ injury to the apices of the adjacent teeth.
compromise the blood supply of the pleteness to the bone and avoid Three methods may be used to locate
flap, which will result in compromised accidental tearing of the flap. the tooth apex and thus the area of
healing. Therefore, only vertical • The flap is then raised with the sharp ostectomy:
release incisions should be made in end of the periosteal elevator starting 1. In most cases the cortical plate may
the alveolar mucosa (see Fig. 16.7). with the horizontal incision and the be thin because of underlying path­
• The vertical release incision should blunt end is then used to reflect the flap. ology and may show fene­strations
be made at an obtuse angle to the • With the sulcular incision, the elev­ or fistulae. A periosteal elevator or
horizontal one so as to have a flap with ation is started at the incisal papilla curette is used to start the access
a broad base with respect to the apex. farthest from the release incision. window in such situations.
• Horizontal incision is to be placed in • If two release incisions are used then 2. In cases of posterior teeth with thic­
the gingival sulcus in cases of severe flap reflection is started from the ker overlying bone root apices can
periodontal disease. crestal gingival and taken to each be located by establishing wor­king
• Fixed and removable prosthetic vertical arm. length of the tooth over a radio­
res­torations if present should be • If the cystic lesion is adherent to the graph and then transposing the
considered with the incision being mucoperiosteal flap then a scissors measurement with a file or curette,
placed on the attached gingival in should be used to dissect the flap approximate site of root apex is
visible smile zones and under the from the cystic lining. Often a layer of located by this technique.
denture base, in cases of presence of thick tissue is present, this should be 3. If still not located as in cases of
removable prostheses. left attached to the cyst wall and the mandible molars then it can be done
• In cases of mandibular anterior teeth, free mucosa sharply dissected from it. by using a round bur to drill a hole
the sulcular incision is considered To access the palatal root of the into the buccal cortical plate as close
to be best because of a presence of maxillary molars a sulcular incision with a to the estimated apex as possible; a
a narrow band of attached gingival vertical release in the region of the canine medium sized gutta-percha point
and a high incidence of dehiscence is indicated. These areas require a large is then placed into the hole and a
of vestibular incisions. The incision soft-tissue flap to provide adequate access periapical X-ray is now taken to loc­
can also be placed in the lip 1 to through the dense palatal bone. The ate the apex accurately.
1.5 cm anterior to the mucobuccal vertical releasing incision should extend After the apex is located, the surgical
fold, this incision goes for 2 mm just short of midline and be tapered window is prepared depending on the
into the orbicularis oris muscle posteriorly. It may involve the terminal size of the pathology (Figs 16.16A and
and a myocutaneous flap is made, branches of the greater palatine artery. B) and all unsupported bone is removed
the periosteum is then incised and The buccal cortical plate is exposed. since it has a poor vascular supply and
the superior flap is then elevated to If a sinus is present previously, then fails to heal. The root apex is particularly
expose the root apex. perforation in the cortex is noticed along difficult to locate in cases, where very
• For mandibular molar and premolar with the gingival sinus tract. If the lesion small/abs­ ent periapical lesions are
regions sulcular incisions with anter­ is within the bone and has not perforated present.
Management of Periapical Infections 327

the periapical surgery will be reduced


and morbid complications can also be
avoided. All the tissue that are removed
should be submitted to the pathologist
for histopathological examination.

Apicoectomy
Purpose
A B
To create an apical bevel permitting the
Figs 16.16A and B: Preparation of the bony window
operator to access the apex
The angle of bevel should be kept
minimum to minimize leakage through
dentinal tubules. The ideal angle of
resection is flat (0°) cut since it mini­mizes
apical leakage (Fig. 16.19).8 The technical
requirement for good surgical access
to place a retrograde filling means that
some bevel is necessary, which should be
kept to the smallest angle possible.

Factors
The factors affecting inclination of bevel
A B C are9:
Figs 16.17A to C: Apical curettage (periapical cyst) • Anatomy of the root.
• Surgical visibility and access to the
site.
Apical Curettage • Size of instrument used to prepare
to gently disengage the sac from the the root end for retrofilling.
Two types of pathosis are associated with bone by placing the sharp edge against The cut through the apex should
endodontically treated teeth (Figs 16.17A the bone and convex surface against the bevel the root so that it gives a lateral/
to C): cystic membrane to avoid perforation of forward inclination toward the operator.
• Granulation tissue the cystic lining (Figs 16.17A to C, 16.18A This permits an adequate view of the
• Radicular cyst to D). On the other hand the granuloma apical foramen. The projecting Gutta-
Granulation tissue is removed with is composed of fragile, friable tissue, percha point should be identified while
curette (see Figs 16.16A and B). Complete which bleeds and fragments readily on performing apicoectomy.
removal is advised in cases of smaller instrumentation. It is often removed
radiographically confined lesions. In cas­ in piece meal. The stoppage of the Retrograde Filling10
es of large lesions, any com­m­unications bleeding from the bone should be If the apical seal of the root canal filling
with the nasal cavity, maxi­llary sinus, taken as a sign of complete removal of is inadequate then the chances of micro­
lingual plate defects, adjacent roots, the granuloma. The lining of the cyst leakage and the recurrent infections are
inferior alveolar neurovascular bundle also tends to fragment and bleed if it is very high. To avoid these complications,
should be ruled out. grossly infected. apical seal can be achieved by doing the
If no communications are present In cases of large lesions, which are retrograde filling.
then complete removal of the lesion close to the vital structures and are
should be done. likely to result in large defects and dam­ Wound Closure and Postoperative
A periapical cyst differs from gran­ age to the adjacent vital stru­ctures, an Care
ul­­­ation tissue in terms of tissue chara­ alternative treatment plan compri­sing of • Wound should be thoroughly irrig­
cteristics, organization and struc­ ture. elimination of the source of infection and ated with sterile normal saline
The cysts are well-encap­ sulated stru­ creation of an effective periapical seal by solution before closure.
ctures and should be removed in toto endodontic therapy, preoperatively, then • Closure should not be too tight.
as a single unit. After delineation of the the residual cystic lining or granulation • First suture after repositioning the
bony soft-tissue border, a curette is used tissue will resolve and the magnitude of flap in proper alignment is to be
328 Infections of Maxillofacial Region

Suture Removal
Mucoperiosteal flap reattaches within
48 hours and incisions in the attached
gingiva heal within 4 to 5 days. However,
suture removal is done on 7th day,
depending upon clinical judgement and
patient comfort.

References
A B
1. Brian M. Henry. Trephination for acute
pain management. Journal of endo­
dontics. 2003;29(2):144-6.
2. Fish EW. The physiology of dentine
and its reaction to injury and disease.
Br Dent J. 1928;49:593.
3. ESE/European Society of Endodon­
tology: Consensus report of the Euro­pean
Soci­ety of Endodontology on quality gui­
C D de­ lines for endodontic treatment. Int
Figs 16.18A to D: Curettage of the cystic lining Endod J. 1994;27:115.
4. Garcia, et al. Periapical Surgery in
arch bar for a period of 4 to 6 weeks Maxi­llary Premolars and Molars. J Oral
till the healing has taken place. Maxillofac Surg. 2008.
5. Martí, et al. Distance Between Peri­
Pain apical Lesion and Mandibular Canal as
The postoperative pain is managed by a Factor in Periapical Surgery in Man­
non-steroidal anti-inflammatory drugs di­­bular Molars. J Oral Maxillofac Surg.
(NSAID’s) or any other suitable anal­ 2008.
gesic. 6. Gutmann JL, Harrison JW. Surgical
Endodontics. 1994;123-299.
Antibiotics11 7. Vreeland DL, Tidwell E. Flap design for
Generally not required, but depends on: surgical endodontics. Oral Surg. 1982;
• Medical history. 54:461-5.
• Length of time the wound was open. 8. Gagliani M, Taschieri S, Molinari R. Ultra­
• Surgical contamination. sonic root-end preparation: influ­ence of
• Clinical findings. cutting angle on the apical seal. J. Endod.,
Usually the beta lactum group of anti­ Baltimore, 1998. v.24, n.11, pp.726-30.
Fig. 16.19: Direction of the bevel
biotics are adequate to provide good cover 9. Hirsch JM, Ahlstrom U, Hendrikson
(e.g. penicillin, amoxicillin, ampi­c­illin and PA, Periapical surgery. Int J Oral Surg.
placed at the point of convergence of cephalosporins). 1979;8:173-85.
the vertical and horizontal incisions. 10. Obón-Arroyave, SI, et al. Ex vivo micro­
This is the positional suture, once this Swelling scopic assessment of factors affecting
is done, then the vertical and lastly A mild to moderate postoperative swe­ the quality of apical seal created by
the horizontal incisions are closed. lling is expected and can be managed by root-end fillings. Int. Endod. J. 2007;
• Periodontal sling or simple interr­ use of icepacks and anti-inflammatory 40(8):590-602.
upted sutures can be placed. drugs. Routine use of steroids is not 11. Baumgartner JG, Bakland LK, Sugita
• Some portion of the vertical incision advocated for periapical procedures. EI. Microbiology of endo­dontics and
can be left open to facilitate drainage Application of the cold packs in first asepsis in endodontic practice. In John
of the collected hematoma/exudate. 24 hours of surgery help in reducing Ingle, Leif Bakland (Eds) Endodontics,
• If the teeth are found to be mobile the inflammatory edema by inducing 5th edn, BC Becker, London, Chapter 3,
then they can be splinted using an vasoconstriction. pp. 63-94.
17 Odontogenic Infections
Borle Rajiv M, Angik Richa

The infections of the maxillofacial area are required in health, but this number periosteum, raising the pressure and
are of great importance to the oral and gets reduced in patients with immuno­ the periosteum is forcefully stripped
maxillofacial surgeon. They are not only suppression. out producing severe pain. As the perio­
common in clinical practice, but are The tissues around the teeth, bone, steum is eroded and perforated, the
also challenging and can lead to fatal periosteum, muscles and fascia serve as infection comes in the soft tissue around
complications if not treated timely. The the anatomical barriers for the spread the bone which is elastic and resilient
common causes of odontogenic infec­ of the infection to the adjoining tissue and the pressure drops and the severity
tions are dental caries and periodontal planes. The maxillofacial infections of the pain also drops. The next barrier is
infections. The oral cavity is a highly are restricted to the particular area by the muscle attachment to the bone and
contaminated cavity. The oral flora exists these anatomical barriers; however the fascia, investing layer of the cervical
in such a way that some microorganisms more virulent organisms are capable fascia and they try to limit the further
suppress the growth of the others. The of breaking these anatomical barriers spread of the infection. However, if they
fungal growth is usually suppressed. by producing toxins and the infection are also broken the infection spreads
However, with long-term antibiotic spreads to the other adjacent areas. further to the adjoining tissue planes.
therapy the bacterial flora gets disturbed The odontogenic infection arises from The infection has two fates; first it
and the fungi get an opportunity to the tooth and is initially confined to the will localize, suppurate and form an
proliferate and produce fungal infect­ alveolar bone, which serves as the first abscess and the second it may spread
ions, e.g. candidiasis (opp­or­tunistic infec­ barrier. The spongy bone offers least locally and systemically. It is usually
tion). The saliva and its composition resistance and the infection spreads seen that the staphylococcal infections
also keep in con­ trol the growth and along this path of least resistance to the have tendency for early localization
pathogenicity of microorganisms by cortical plates which are the second and the streptococcal infections tend to
virtue of its pH and secreted antibodies. barrier, which get eroded and perforated spread without getting localized as the
There is a delicate balance between the more readily where they are thin. If the microorganisms produce hyaluronidase
virulence of the microbes and the host cortical plate gets perforated above the which breaks down the intercellular
resistance. Whenever there is imbalance muscle attachment, the infection forms cementing substance and facilitate the
between these two factors, the infection intraoral abscess on the gingiva called further spread without suppuration
is caused by the normal oral inhabitants. gingival abscess or the parulis, e.g. (cellulitis). The anaerobic infections
The infection may remain confined mandibular anterior teeth. If the cortical are not primary in occurrence and will
to the dentoalveolar area in a healthy plates are eroded below the muscle be precipitated if the environ­ ments
host, but when the microorganisms are attachment then an extraoral swelling is are favorable to the growth of anerobic
highly virulent and the host resistance is produced, e.g. the mandibular posterior organisms such as hypoxic tissue,
severely depleted, the infection spreads teeth. The third barrier is the periosteum large hypoperfused cavities, slough or
to the adjoining tissue planes. The covering the bone which is tough, non- necrotic material. They occur as oppor­
lymphatic and hematogenous spread elastic and firmly adherent to the bone. tunistic infections. The oro­facial infec­
of the infection can lead to the systemic The infection after perforating the tions are usually gram positive and
complications which could be fatal. cortex forms the subperiosteal infection the causative organisms are usually
Usually it is being said that to cause the which leads to the accumulation of the sta­phylococci or streptococci. The
infection 106 million microorganisms inflammatory edema or pus below the staphylococci are the inhabitants of
330 Infections of Maxillofacial Region

the skin, while as streptococci are the


primary organisms of the oral cavity.
The bacteroids and the Escherichia coli
are the next in frequency. The gram-
negative infections are commonly seen
in the peritonial cavity, genitourinary
passage, but they can occasionally occur
in oral cavity as a result of nosocomial
or hospital acquired infections. The
odontogenic infections spread to the
adjoining fascial spaces formed by
the deep cervical fascia.
A B
APPLIED SURGICAL Figs 17.1A and B: Gingival abscess or a ‘Parulis’
ANATOMY
The bacterial quantity and virulence
determine the clinical course of the fascia attached to it. As the infection Anatomy of the Cervical
infection. The microorganisms produce progresses within the bone, it spreads in Fascia
lytic enzymes, potent endotoxins and the radial manner through the spongy The fibrous connective tissue that consti­
exotoxins and interference with or bone and extends to the cortical plates. tutes the cervical fascia varies from loose
resistance to host humoral and cellular Once the cortical plates are perforated areolar tissue to dense fibrous bands.
defences. the infection comes to lie below the This fascia serves to envelope the mus­
The infection once set has three periosteum to form the subperiosteal cles, nerves, vessels and viscera of the
fates: abscess. If the cortex is perforated above neck, thereby forming planes and poten­
1. The body’s defence systems over­ the muscle attachment (e.g. mandibular tial spaces that serve to divide the neck
power the microorganisms and anterior teeth) then the infection into functional units. The cervical fascia
either completely eliminate them or localizes intraorally to form a gingival functions to both direct and limit the
the infection gets localized to form an abscess (parulis) (Figs 17.1A and B). If spread of disease processes in the neck.
abscess which drains spontaneously the infection perforates the cortex below The cervical fascia was first descri­
on the surface. the muscle attachment (e.g. mandibular bed by Burns in 1811. It is now generally
2. The infection changes from acute to posterior teeth), then the infection agreed upon that the cervical fascia can
chronic form and persists. It under­ extends in the anatomical spaces around be divided into a simpler superficial
goes acute exacerbations intermit­ the bone and presents extraorally. layer and a more complex deep layer that
tently whenever the environments is further subdivided into superficial,
are conductive. Periosteum middle and deep layers.
3. It spreads in an aggressive manner Periosteum is the next local barrier. This
and produces local and systemic structure is better developed in mandible Superficial Fascia
complications which could be life and hence can delay further spread of The superficial layer of cervical fascia
threatening. infection leading to development of a ensheaths the platysma in the neck and
The anatomical barriers present in subperiosteal abscess. The periosteum extends superiorly to the face to cover the
the body tend to restrict the spread of is tough, non-elastic and is tenaciously muscles of facial expression. Below the
the infection and try to localize it. adherent to the bone and thus when the mouth, the muscles of facial expression
pressure mounts due to subperiosteal are deep to it whereas above the mouth
infection; it gets stripped from the bone. they are superficial to this layer. It is
LOCAL BARRIERS
As the periosteum is non-yielding, the the equivalent of subcutaneous tissue
pressure does not get relieved and the elsewhere in the body and forms a
Alveolar Bone subperiosteal abscess is very painful. continuous sheet from the head and
Most of the odontogenic infections It does not provide much resistance neck to the chest, shoulders and axilla.
origi­
nate in the alveolar bone, which and the infection spreads into adjacent
forms the first barrier for the spread of surrounding soft tissues. Deep Cervical Fascia
the infection. The alveolar bone has The adjacent Muscles and Fascia are The deep cervical fascia can be divided
components like spongy bone, cortical the next barriers for the localization of into anterior, middle and posterior layer
bone, periosteum and the muscles and infection. (Fig. 17.2).
Odontogenic Infections 331

forming the floor of the submandibular


space. At the mandible, the fascia splits
into an internal layer, which covers the
medial surface of the medial pterygoid
and attaches to the skull base and an
outer layer that covers the masseter and
inserts on the zygomatic arch.

Middle Layer
The middle layer of the deep cervical
Fig. 17.2: Different layers of the cervical fascia is also known as the visceral
fascia in cross section of the neck fascia, the prethyroid fascia and the
pretracheal fascia. It can be thought of in
two subdivisions, the muscular division,
A. Anterior layer: which surrounds the infrahyoid strap
• Parotidomassetric fascia muscles and the visceral division, which
• Temporal fascia envelops the pharynx, larynx, esophagus,
B. Middle layer: trachea and thyroid gland. The superior
• Muscular division: extent of the muscular division is the
– Sternohyoid—omohyoid hyoid and thyroid cartilage, inferiorly Fig. 17.3: Posterior Lincoln’s highway
– Sterothyroid—thyrohyoid it inserts on the sternum and clavicle.
• Visceral: Its surgical significance is that this
– Buccopharyngeal fascia. layer of deep cervical fascia should of the cervical vertebra and the
C. Posterior layer: be divided in the midline to approach ligamentum nuchae. At the transverse
Anterior—Alar fascia the thyroid gland and trachea. It does processes of the cervical vertebra, it
Posterior—Prevertebral layer. not have any significance regarding divides into an anterior alar layer and a
spread of infection from orofacial posterior prevertebral layer.
Anterior Layer region. However, it is responsible for The alar fascia extends from the
The anterior layer of the deep cervical the movement of the thyroid swelling on base of the skull to the second thoracic
fascia is also known as the investing deglutition. vertebra (T2). It lies between the
layer or the enveloping layer or the The visceral division attaches to the visceral layer of the middle fascia and
external layer or the superficial layer of hyoid bone above and surrounds the the prevertebral layer. It fuses with the
the deep fascia. It has been described trachea, esophagus and thyroid gland. retropharyngeal fascia between C6 and
using the ‘rule of twos’—it envelops Above the hyoid, the fascia surrounds T4. This fusion forms the bottom of the
two muscles, two glands and forms the pharynx on the lateral and posterior retropharyngeal space and infections
two spaces. This layer originates from sides lying on the superficial side of the of the retropharyngeal space may
the spinous processes of the vertebral constrictor muscles of the pharynx where rupture the alar fascia and enter the
column and spreads circumferentially it is known as the buccopharyngeal danger space which is continuous with
around the neck and splits to cover the fascia. It extends inferiorly into the upper the posterior mediastinum (Posterior
sternocleiodomastoid and trapezius medi­ astinum where it is continuous Lincoln’s highway) (Fig. 17.3).
muscles. In the midline, inferiorly it splits with the fibrous pericardium and covers The prevertebral fascia lies just
2 centimeters above the manubrium the thoracic trachea and esophagus. anterior to the vertebral bodies and ext­
forming the suprasternal space of Burns. The retropharyngeal, pretracheal and ends the entire length of the vertebral
The space of burns contains anterior lateral pharyngeal spaces lie superficial column. It travels circumferentially
jugular vein, lymph nodes and the loose to this layer. A specialized condensation around the neck and covers the para­
connective tissue. Superiorly, it attaches of the fascia forms around the carotid vertebral muscles, the deep muscles
to the hyoid bone and continues arteries on either side which is called of the posterior triangle of the neck
superiorly to enclose the submandibular carotid sheath which encloses common and the scalene muscles. This layer of
and parotid glands. The portion of the carotid artery, internal jugular vein and fascia surrounds the brachial plexus
fascia covering the masseter muscle and the vagus nerve. and subclavian vessels and continues
enclosing the parotid gland is known laterally as the axillary sheath. It may
as the ‘Parotideomassetric fascia’. It Posterior Layer be involved by infections of the ver­
also covers the anterior bellies of the The deep layer of the deep cervical fascia tebral bodies and is not involved in
digastrics and the mylohyoid, thereby originates from the spinous processes maxillofacial infections.
332 Infections of Maxillofacial Region

Carotid Sheath from the tooth spreads to various fascial spaces, pter­ygomandibular space or the
The carotid sheath is a specialized fascial spaces adjacent to the jaw (Table 17.4). lateral pharyngeal space are from the
condensation of cervical fascia, that alth­ Commonly the infections from the man­ mandi­bular third molars (Figs 17.5A and
ough associated with, but anatomi­cally dibular molars spread to the sublingual B). The infections from the mandibular
separate from the other layers of the deep or sub­mandi­bular space. While as the anteriors either produce the gin­­gival ab­
cervical fascia. It receives con­tributions infec­tion to the buccal, submasseteric scess or a submental space abs­cess.
from all three layers of deep cervical
fascia and contains the carotid artery, Table 17.1: Differences between cellulitis and abscess
internal jugular vein and vagus nerve. It
continues from the skull base through Characteristics Cellulitis Abscess
the neck along the anterior surface of the
Duration Acute phase Chronic phase
prevertebral fascia and enters the chest Pain Severe and generalized Localized
behind the clavicle. The infections from Size Large Small
the neck region can descend through it Localization Diffuse borders Well-circumscribed
into the anterior mediastenum and thus Palpation Doughy to indurated, pitting edema Fluctuant
it is called ‘Anterior Lincoln’s highway’. Presence of pus Absent Present
Degree of seriousness Greater Less
Bacteria Aerobic Mixed
Relative Terms in the Infection
• Abscess: It is defined as ‘a localized
collection of the pus’ or an abscess
is ‘a pathological cavity lined by
gran­ul­
ation tissue and contains
pus’. The suppuration is a hallmark
of an abscess and the common
orga­nisms that are responsible to
form an abscess are staphylococci,
predominantly pre­sent in the skin.
Differences between cellulitis and
abscess is given in Table 17.1.
• Cellulitis: It is in literal sense the in­
flammation of the cells. A cellulitis
is a nonsuppurative, spreading in­
flammation (Figs 17.4A and B). The A B
causative microorganisms are strep­ Figs 17.4A and B: Cellulitis. (A) Note the pitting edema; (B) Localized abscess.
tococci, predominantly present in
the oral flora. Table 17.2: Various stages of infection
• Bacteremia: Transient presence
of viable bacteria in the circulating Characteristic Inoculation Cellulitis Abscess
blood.
Time 0–3 days 3–7 days > 5 days
• Septicemia: Systemic toxicity due to Pain Mild-moderate Severe and Moderate-severe and
invasion by virulent microorganisms generalized localized
or their toxins in the bloodstream Size Small Large Small
coming from a local seat of infection. Localization Diffuse Diffuse Circumscribed
The clinical presentation of the Palpation Soft, doughy, Hard, exquisitely Fluctuant, tender
infec­tion changes with the duration as mildly tender tender
depicted in the Table 17.2. Presentation Normal color Reddened Peripherally reddened
Skin quality Normal Thickened Centrally undermined and
shiny
FASCIAL SPACES Temperature Slightly heated Hot Moderately heated
Loss of function Minimal or none Severe Moderately severe
The fascial spaces are divided into: Tissue fluid Edema Serosanguineous, Pus
• Those around the mandible. flecks of pus
• Those around the maxilla. Levels of malaise Mild Severe Moderate-severe
The facial spaces are also named Severity Mild Severe Moderate-severe
by other names and the synonyms are Percutaneous Aerobic Mixed Anaerobic
summarized in Table 17.3. The infection bacteria
Odontogenic Infections 333

Table 17.3: Different spaces around the jaw bones The infections originating from
the maxillary anterior teeth spread to
Spaces around the mandible Spaces around the maxilla the infraorbital space while as that
from the molars spread to the buccal
Submasseteric space Buccal space
space, the infratemporal space and
Submandibular space Canine fossa/infraorbital space
Submental space Infratemporal space the maxillary sinus. The infections
Sublingual space Lateral pharyngeal space originating from the palatal root of the
Masticator space Retropharyngeal space maxillary molars may form a localized
Superficial and deep temporal pouches palatal abscess. (Fig. 17.6).

Table 17.4: Probable etiology, contents and the related spaces

Space Likely causes Contents Neighbouring spaces

Buccal Upper premolars Parotid duct Infraorbital


Upper molars Anterior facial artery and vein Pterygomandibular
Lower premolars Transverse facial artery and vein Infratemporal
Buccal fat pad
Infraorbital Upper canine Angular artery and vein Buccal
Infraorbital nerve
Submandibular Lower molars Submandibular gland Sublingual
Facial artery and vein Submental
Lymph nodes Lateral pharyngeal
Buccal
Submental Lower anteriors Anterior jugular vein Submandibular (on either side)
Symphysis fracture Lymph nodes
Sublingual Lower premolars Sublingual glands Submandibular
Lower molars Whartson’s duct Lateral pharyngeal
Direct trauma Lingual nerve Visceral (trachea and esophagus)
Sublingual artery and vein
Pterygomandibular Lower third molars Mandibular division of trigeminal Buccal
Fracture of mandible angle nerve Lateral pharyngeal
Inferior alveolar artery and vein Submasseteric
Deep temporal
Parotid
Submasseteric Lower third molars Masseteric artery and vein Buccal
Fracture of mandible angle Pterygomandibular
Superficial temporal
Parotid
Infratemporal and Upper molars Pterygoid plexus Buccal
deep temporal Interior maxillary artery and vein Superficial temporal
Mandibular division of trigeminal Inferior petrosal sinus
nerve
Skull base foramina
Superficial temporal Upper molars Temporal fat pad Buccal
Lower molars Temporal branch of facial nerve Deep temporal
Lateral pharyngeal Lower third molars Carotid artery Pterygomandibular
Tonsils Internal jugular vein Submandibular
Infections in neighboring Vagus nerve Sublingual
spaces Cervical sympathetic vein Peritonsillar
Retropharyngeal
334 Infections of Maxillofacial Region

from one space extends to the other


from the posterior border of this muscle.
In short although these anatomical
compart­ments try to limit the spread
of the infection, they are liable to
breakdown and the infection can still
spread to the adjacent area by breaking
down of these barriers. Apart from the
virulence of the microorganisms and
the effects of their toxins on the inter­
cellular cementing substance, the other
major determinant is pressure generated
within the tissue by inflammatory
edema, which causes breakdown of
these barriers and facilitates the lateral
spread of the infection.
Fig. 17.5A: Spread of infection from the teeth to various spaces

SPACES AROUND THE


MANDIBLE

Submandibular Space
Infection
Surgical Anatomy
The submandibular space is present
below the mandible. It is also called
as the digastric triangle as it is bound
anteroposteoriorly by the anterior and
the posterior bellies of the digastric
Fig. 17.5B: Palatal abscess due to periapical Fig. 17.6: Spread of infection from sublin­ muscle, respectively. The medial wall
infection originating from the palatal root gual to submandibular space behind the is formed by the mylohyoid muscle and
of maxillary molar mylohyoid muscle
the hyoglossus muscle while the lateral

Although the involvement of the Table 17.5: Various space infection and their synonyms
parti­
cular space commonly occurs
due to a specific tooth, it is not a rule Name Synonym
of thumb (Table 17.5). Moreover, the
Space of the body of the mandible Mandibular space
infec­
tion when aggressive rapidly
spreads to the adjacent spaces. If we Submandibular space Submaxillary space
Submylohyoid space
carefully look at the spaces it will be
Masticator space Masticatory space
noticed that the superficial temporal
Masseteric space
pouch freely communicates with the
Temporal space Temporal pouches
submasseteric space, inferiorly, while as
the deep temporal pouch communicates Infratemporal spaces Postzygomatic space
inferiorly with infratemporal fossa, the Buccal space Buccinator space
lateral pharyngeal space and with the Infraorbital space Canine space
ptery­gomandibular space. Similarly due Lateral pharyngeal space Parapharyngeal space
to the presence of loose spaces between Pharygomaxillary space
the instrinsic muscles of the tongue, Retropharyngeal space Retroesophageal space
a unilateral sublingual space infec­ Pretracheal space Perivisceral spaces
tion rapidly beco­mes bilateral. As the Paravisceral spaces
sublingual space is separated from the Paratracheal spaces
submandibular space by an incomplete Carotid space Visceral vascular space
partition of the mylohyoid, the infection Anterior Lincoln’s highway
Odontogenic Infections 335

Box 17.1: Boundaries of the space sublingual space can also lead to the
submandi­bular space infection.
Anterior Anterior belly of digastric muscle
Posterior Posterior belly of digastric muscle, stylohyoid muscle Clinical Features
stylopharyngeous muscle • There is a swelling involving the
Superior Medial aspect of mandible and attachment of mylohyoid muscle submandibular area, which is diffuse
Inferior Anterior and posterior bellies of digastric muscle in the beginning and tends to get
localized and extends from the lower
Medial Mylohyoid, hyoglossus, styloglossus
border of the mandible to the hyoid
Lateral Skin, superficial fascia, platysma, superficial, layer of deep cervical fascia
bone, superioinferiorly. More virulent
Anterior bellies of digastric muscles
infections break the tissue barriers
and spread to the adjoining space.
• The muscles become spastic and
wall is formed by the skin, superficial there may be trismus.
fascia and the platysma. The base of the • The swelling shows all the classical
submandibular space is situated at signs of inflammatory swelling like
the lower border of the mandible and redness, raised local temperature,
the apex is at the common tendon of the tenderness and pain. Initially, the
digastric muscle at the greater cornu of diffuse swelling is firm in consis­
the hyoid bone (Box 17.1). The contents tency and pits on pressure due to
are the submandibular lymph nodes, cellulites, but as the abscess gets
the submandibular salivary gland, facial localized bimanual palpation elicits
artery and anterior facial vein. fluctuations.
• Constitutional sign and symptoms
Applied Anatomy are present in the acute phase.
The space lies between the anterior and • The submandibular lymph nodes
posterior bellies of digastric muscles. are enlarged, tender and firm in
The mylohyoid muscle which forms consistency, but they are difficult to
the floor of the oral cavity separates assess in presence of swelling.
this space from the sublingual space Fig. 17.7: Spread of periapical infection
below, is the key to diagnosis and from the molar to submandibular space Management
below the mylohyoid line
surgical management of this space The primary management is surgical
infections. This muscle attaches to the drainage. The incision and drainage is
lingual surface of mandible along the done through a standard submandibular
mylohyoid ridge which runs obliquely Source of Infection incision taken 1 cm below and behind
and downward from posterior to • The common sources of infection are the inferior border of the mandible
anterior. Odontogenic infections of this the odontogenic infections from the to avoid the damage to the marginal
space are commonly caused by 2nd mandibular posterior teeth,1 either mandibular branch of facial nerve
and 3rd molar teeth and rarely by 1st by direct spread or spread through (Figs 17.8A and B). Superficial abscesses
molar as their root apices lie inferior to the lymphatics. The involved lymph are drained through a stab incision, but
mylohyoid line of muscle attachment. nodes breakdown due to suppur­ation the deep seated abscess is drained by
Only loose connective tissues separate and the septic material is discharged dissecting the tissue layer wise to open
one side of floor of mouth from other in the adjoining tissue space. the skin, superficial fascia, platysma
permitting bilateral spread of infection • Septic fractures of the mandible,2 and deep fascia. In deep seated abscess,
with ease (Figs 17.6 and 17.7). osteomyelitis of mandible. sometimes the fluctuations are difficult
Diagnosis is established by brawny • The infections originating from to be elicited and thus to confirm the
or soft swelling in the submandibu­ the submandibular salivary gland presence of the pus in deeper planes
lar region along with an associated due to sialoithiasis and the other it is a good idea to insert a wide bore
diseased mandibular molar. Infectious suppurative glandular pathologies.3 needle and aspirate. The incision is
process commonly spreads across the • Rarely hematogenous infections, always placed on the dependent part
midline into contralateral submandi­ extension from adjacent tissue to facilitate gravity assisted drainage,
bular space. spaces like submasseteric space, however when the abscess is pointing
336 Infections of Maxillofacial Region

A B
Figs 17.8A and B: A case of submandibular abscess drained by incision and drainage,
A
corrugated rubber dam drain in place

Box 17.2: Boundaries of submental space

Anterior Inferior border of mandible


Posterior Hyoid bone
Superior Mylohyoid muscle
Inferior Skin, superficial fascia, platysma,
deep cervical fascia
Medial Anterior bellies of digastric
mus­cles
Lateral Investing fascia

B
Figs 17.10A and B: Submental space
infection drained by incision and drainage
tal space gets involved (Box 17.2 and
Fig. 17.9). The chin appears grossly
Fig. 17.9: Anatomical boundaries of the
submental space swollen and is quite firm and erythe­ Management
matous. Submental infection may spread Percutaneous surgical drainage is the
on skin, the incision may be placed easily to either or both submandi­bular most effective approach. Transverse
on the most prominent part to drain spaces (see Fig. 17.6). incision is given in the skin below the
the abscess and to achieve the gravity symphysis of the mandible provides
assisted drainage, especially in the Source of Infection dependent drainage and the most
large abscess cavities, another counter • Infections from the lower anterior cosmetically acceptable scar. Blunt
incision is placed at the dependent site. teeth dissection is carried out by inserting a
The drainage of the septic material helps • Infected symphyseal or parasym­ sinus forceps in upward and backward
in reducing the edema, prevent further physeal fractures direction. Drain is inserted. Space may
spread of infection due to reduced • Extension of submandibular space be drained orally through the mentalis
tension in the tissue planes and prevent infection muscle through the labial vestibule,
further absorption of the septic material. • Suppuration in the submental lymph but dependent drainage cannot be
The septic focus like offending tooth nodes. established (Figs 17.11A and B).
should also be removed simultaneously
to prevent the infection from slipping Clinical Features Sublingual Space Infection
into chronic phase from the acute phase • The submental space infection pro­ The sublingual space is located with­
(Fig. 17.9). duces a swelling below the chin in the mandibular body, extending
producing a classical double chin from the genial tubercles anteriorly up
Submental Space appearance (Figs 17.10A and B). to the base of the tongue, at the body of
• The skin is erythematous, tense, the hyoid bone. It is a ‘V’-shaped space
A potential space exists in the chin. If the glossy and tender to touch. lying lateral to muscles of tongue, in­
infection from the incisors exits labially • The local temperature is raised. cluding hyoglossus, genioglossus and
through the mandibular bone, inferior • Once the infection gets localized, the geniohyoid. The roof is formed by the
to the muscle attachments, the submen­ fluctuations may be elicited. mucosa of the floor of the mouth. The
Odontogenic Infections 337

Management
An incision is made close to the lingual
cortical plate, lateral to the sublingual
plica, as lingual nerve, which is deeply
placed, is less likely to be damaged by
this approach. The other important
structures lie medial to the plica is
Whar­ton’s duct, sublingual artery and
veins (Figs 17.12E). The sinus forceps is
then inser­ted and opened to evacuate the
pus. If the space is drained extraorally, a
submandibular incision is taken and a
sinus forcep is introduced to pierce the
mylohyoid muscle, which forms the floor
A B
of the sublingual space. This approach
pro­vides gravity dependent drainage.
Figs 17.11A and B: Sublingual space infection: (A) Showing sublingual spread of
the infection through the perforation of the lingual cortex, as the root tip is above the
attachment of mylohyoid resulting in sublingual space infection; (B) Loose spaces in the Masticatory Space
floor of mouth (2) and around the intrinsic muscles (1) of the tongue facilitate the bilateral
spread of the infection. (3) Geniohyoid muscle and (4) Deep cervical facial Masticatory space is formed by splitting
of investing fascia into superficial and
floor is formed by the mylohyoid an­ Elevation of tongue is clinical hallmark deep layers. The superficial layer lies
teriorly and the hyoglossus posteri­ of sublingual space infection. Patient is along lateral surfaces of masseter and
orly (Box 17.3). The space contains the usually unable to protrude his tongue lower half of temporalis muscles.
duct of the submandibular gland and to or beyond vermillion border of upper
the part of the gland which lies supe­ lip. Applied Anatomy
rior to the mylohyoid. The sublingual Superiorly the superficial layer fuses
gland is also enclosed in this place. Source of Infection with periosteum of zygoma and tempo­
The lingual nerve and the submandi­ • Odontogenic infections from man­ ralis fascia. The deep layer passes along
bular ganglion are also present within di­­bular teeth which drain above the the medial surface of pterygoid mus­cles
this space. mylohyoid muscle (Fig. 17.11). before attaching to base of skull supe­
• Infection of the sublingual or sub­ riorly. Like the perimandibular spaces,
Applied Anatomy man­di­bular salivary glands. masticatory space is one anato­ mical
Anteriorly the sublingual space comm­ • Extension of the submandibular, sub­­ compartment enclosed by splitting of
uni­cates with submental space. In mental or pterygomandibular spaces. the anterior layer of deep cervical fas­
this area, the sublingual space may be cia around the muscles of mastication
invaded by infection from incisor teeth Clinical Features (Fig. 17.13). Infections of this space oc­
especially from periodontal infections. The initial clinical feature of the sub­ cur more frequently from third mo­
Posteriorly, it is continuous with the lingual space infection is the congestion lars, the pericoronitis associated with
submandibular space at posterior edge and edema of the floor of the mouth it and caries induced dental abscesses,
of mylohyoid muscle and the infection (Figs 17.12C and D). The edema incre­ contaminated inferior alveolar nerve
can traverse into submandibular space. ases rapidly to cause elev­ation and pro­ blocks, direct trauma or through surgery
trusion of the tongue (Figs 17.12A to C). in the area.
Box 17.3: Boundaries of the sublingual This sign is the warning sign of the im­ The clinical features comprise of
space pending laryngeal edema as the sublin­ swelling around the ramus of mandible,
gual space extends right up to the hyoid pain, tenderness, fever and difficulty in
Anterior Lingual aspect of mandible bone and can induce the laryngeal ede­ deglution. The hallmark of masticatory
Posterior Body of hyoid ma. This emergency drainage must be space infection is trismus.
Superior Mucosa of floor of mouth undertaken to prevent respiratory em­ The masticatory space comprises of
barrassment due to the laryngeal edema. following four spaces:
Inferior Mylohyoid muscle
The earliest warning sign of the laryngeal 1. Pterygomandibular space.
Medial Anterior bellies of digastric
edema is complaint of breathlessness in 2. Submasseteric space.
muscles
supine position and the patient prefers to 3. Temporal space.
Lateral Investing fascia stay in the sitting position. 4. Infratemporal space.
338 Infections of Maxillofacial Region

A B C

D E
Figs 17.12A to E: Sublingual space infection: (A and B) Protrusion and lifting of the tongue; (C and D) Elevation of the floor of mouth;
(E) The space drained by a transoral incision

molar. Trismus caused by edema and


inflammation of the medial ptery­
goid muscle hinders the view of
swollen anterior tonsilar pillar and
the deviation of uvula to opposite side
that are characteristic of infection in
this space. Infection may spread into
infratemporal portion of the deep
tem­poral space by passing superiorly
around lateral pterygoid muscle. More
com­ m­only infection spreads to the
lateral phar­yn­geal space.
The pterygomandibular space lies
Fig. 17.13: Masticator space and its communicating spaces medial to the ramus of the mandible
and its boun­ daries are shown in
mandibular angle. Extraoral incision Box 17.4 and Fig. 17.14.
Management and drainage is a more technical and
Masseteric and pterygoid compart­ prudent than intraoral approach. Contents
ments may be entered by superficial, Mandibular nerve, lingual nerve, inferior
sharp and deep blunt dissection at the Pterygomandibular Space alveolar artery and vein mylohyoid
external angle of the mandible avoiding Of all the severe odontogenic infec­ nerve and vessels.
the mandibular branch of facial nerve. tions, it is the most frequently affected • Teeth involved: Buccal roots of
This approach allows dependent drain­ anatomical compartment. Infections maxi­llary second and third molars.
age of both the spaces at the insertion of this space are correlated highly • Spread: Superficial temporal, par­
of muscle sling on inferior border at with pericoronitis of mandibular 3rd otid spaces.
Odontogenic Infections 339

Box 17.4: Boundaries of pterygomandibular space

Laterally Anterior border of ramus of mandible


Medially Medial pterygoid muscle
Superiorly Infratemporal surface of greater wing of sphenoid and zygomatic arch, lateral
pterygoid muscle
Inferiorly Pterygomasseteric sling
Anteriorly Buccinator and superior pharyngeal constrictor muscles as they meet at the
pterygomandibular raphe
Posteriorly Deep portion of parotid gland

Fig. 17.16: Anatomic boundaries of the


submasseteric space

Fig. 17.14: Boundaries of the


pterigomandibular space Source of Infection5,6
• Mandibular third molar infections
are the most common source of
Applied Anatomy Fig. 17.15: Drainage of pterygomandibular
infection as the infection can extend
space through Risdon’s approach
Needle track infections occur most often subperi­osteally in the submasseteric
in the pterygomandibular space because space. The infections from the man­
of attempts to anesthetize inferior alve­ an extraoral subman­dibular ‘Risdon’s in­ di­bular posterior teeth can also lead
olar nerve before dental procedures. cision’ is placed and the dissection is car­ to the submasseteric space infections.
Incision is given in the buccal vestibule ried out medially to detach the insertion • Septic fractures at the angle of the
opposite second and third molars. The of the medial pterygoid muscle from the mandible are also the cause of the
exploration is carried out medial to angle of the mandible to drain the ptery­ submasseteric space infection.
coronoid process and temporalis muscle gomandibular space (Fig. 17.15). The • The minor causes are the extension of
upwards and backwards with a sinus drain is placed in situ. Jaw exercises (ac­ the infection from the adjoining tis­
forceps. The space is entered and drained tive moth opening) are necessary to pre­ sue planes in the infratemporal space,
and drain is secured. vent the trismus post operatively. temporal pouch abscess, sublingual
space infection, etc. Suppurative par­
Sources of Infection Submasseteric Space Infection o­titis can also secondarily inv­olve the
• Due to contaminated needles/solu­ submasseteric space as the parotid
tion used while giving pterygoman­ Surgical Anatomy fascia after covering the parotid gland
dibular block. The submasseteric space is present goes on to cover the masseter muscle
• Septic fractures of mandibular lateral to the ascending ramus of the (parotidomasseteric fascia) and the
ramus. mandible (Figs 17.16 and 17.17A). It infection can extend into the sub
• Infections from mandibular third is bounded laterally by the masseter masseteric space.
molars. muscle and the fascia covering it, • Hematogenous spread of the inf­ec­
medially by the lateral surface of the tion can also lead to subma­sseteric
Management ascending ramus. Inferiorly, it extends space infection in cases of septi­cemia.
An incision is placed along the anterior up to the insertion of the masseter at the
border of the coronoid process and the si­ angle of the mandible and superiorly it Clinical Presentation
nus forcep is passed medial to the ramus extends up to the origin of the masseter • The first sign of the submasseteric
of the mandible to enter and drain the at the inferior border of the zygomatic space infection is trismus due to the
pterygomandibular space, transorally. arch and thus the submasseteric space spasm of the masseter.7 The swelling
However, in presence of severe trismus infection can also extend to the infra­ is inconspicuous as the infection lies
when transoral drainage is not possible temporal fossa.­4 below the muscle. The mild swelling
340 Infections of Maxillofacial Region

A B C

D E F
Figs 17.17A to F: Submasseteric space abscess, note the trismus, the abscess is superficial plane leading to dusky appearance to skin,
treated with incision and drainage

over the angle of the mandible which touch the local temperature is also Management
is relatively a late occurrence and raised. The medicinal treatment comprises
is diffuse in nature. The infection • When the infection gets localized of prescription of antibiotics and anti-
gets localized due to the anatomi­ and still present below the masseter, inflammatory drugs which help in
cal barrier formed by the muscle deep seated fluctuations can be elic­ locali­zing the infection. The appli­cation
(Figs 17.17B and C). The swelling ited by bimaunal palpation. When of glycerine and magsulf dres­sing dur­
some­times mimics the parotitis and the infection becomes super­ficial by ing the diffuse state of the infection is
may be misdiagnosed as parotitis. perforating through the fibers of the also helpful in localizing the infection.
The differentiating feature is that masseter and comes to lie below the Once the infection is localized, surgical
classical parotid swelling is post­ superficial fascia and the skin, the treatment like drainage is indicated.
eri­
orly present over the parotid swelling becomes fluctuant due to
area and is associated with lifting laudable pus. Surgical Management
of the ear lob­ule. The more virulent • The intraoral septic focus in the The surgical treatment comprises of
infections rapidly breakdown the form of carious tooth, pericoronitis incision and drainage of the abscess. The
tissue barriers and extend to the is usually present. submassertic space infection/abscess
adjacent tissue planes. • General constitutional signs and can be drained intraorally as well as
• The infection leads to irritation and symptoms like fever, malaise, body extra­orally. In the intraoral procedure,
spa­sm of the muscle and leads to tri­ ache, etc. are present. an incision is placed in the retromolar
s­mus. The submasseteric space infec­ area along the anterior border of the
• The infection when diffuse is firm tion can extend to the submandibu­ ramus and the dissection is done along
in consistency and tender to lar space due to the direct extension. the lateral border of the ramus. An
Odontogenic Infections 341

artery forcep is introduced between the Box 17.5: Boundaries of buccal space
ramus and the masseter muscle to drain
the abscess. A guaze drain is placed to Superior Zygomatic arch, infraorbital space
Inferior Lower border of mandible
facilitate the drainage of the pus along
Anterior Zygomaticus major muscle above and depressor anguli oris muscle
it. The disadvantage of this procedure Posterior Anterior edge of masseter muscle, pterygomandibular space
is that the incision site is not dependent Medial Buccinator muscle, buccopharyngeal fascia
and the gravity assisted drainage is not Lateral Skin, subcutaneous tissue
present.
The extraoral procedure consists of
placing a standard Risdon’s submandi­ Clinical Features
bular incision 1 cm below and behind
the inferior border of the mandible • Extraoral swelling of the cheek
and curling around the angle. The from lower border of mandible to
incision avoids damage to the marginal infra­orbital rim (Figs 17.19A and
mandibular branch of the facial nerve 17.20) and from anterior border of
and the scar is hidden. The superficial masseter to corner of mouth when
abscess gets drained with only a stab the lower compartment is involved.
incision. But, the deep seated abscess When the upper compartment is
is drained by dissecting the tissue layer involved (due to maxillary teeth)
by layer and after incising and reflecting the swelling extends from the
the fibers of the masseter muscle at its Fig. 17.18: Buccal spread of infection via zygomatic bone to the corner of
insertion at the angle of the mandible, periapical infection of maxillary and man- the mouth. As the face has plenty of
taking precaution not to damage the dibular teeth loose areolar spaces the adjoining
facial artery (Figs 17.17D to F). area is edematous and presents like
A sinus forceps or a gloved finger is a diffuse cellulitis.
passed through the incision and moved in this spread may confuse the diagnosis of • The obliteration of the buccal vesti­
different directions to break all the loculi submandi­bular space abscess. bule occurs due to bulging swel­
and achieve full drainage. A corrugated ling in the buccal vestibule of the
rubber dam drain is inserted and kept Source of Infection9 maxilla or the mandible, depending
in place to facilitate drainage. If there is • Maxillary premolars and molars if on whether the upper or lower
bleeding from the absess cavity then an root apices are above the attachment compartment is involved.
iodoform, acriflavine or the glycerine- of the buccinator muscle.
magsulf tape gauze is gently packed in • Mandibular premolars and molars if Management
abscess cavity to achieve the hemostasis root apices are below the attachment The management comprises of drainage
and keep the drainage site patent. of the buccinator muscle. of the abscess transorally, by placing

SPACES AROUND MAXILLA

Buccal Space
Buccal space is the potential space
between buccinator muscle and mass­
eter muscle8 (Box 17.5 and Fig. 17.18).
Infection of this space is identified
easily because of marked cheek swelling
associated with a diseased molar or
premolar tooth. Because the buccal space
is a portion of the subcutaneous space,
buccal infections can spread through the
subcutaneous space into the periorbital
space and pass the inferior border of A B
mandible to the subcutaneous tissue lying Figs 17.19A and B: (A) Localized buccal space abscess; (B) Drained intraorally at
superficial to the submandibular space, dependent site although the prominent part was extraorally
342 Infections of Maxillofacial Region

Box 17.6: Boundaries of canine space

Superior Levator labii superioris alaeque nasi, levator labii superioris, zygomaticus
minor
Inferior Caninus (Levator anguli oris), oral mucosa
Anterior Orbicularis oris, nasal cartilages
Posterior Buccinator and buccal space
Medial Anterolateral surface of maxilla

Fig. 17.20: Diffuse cellulitis due to buccal


space infection

the incision in the respective buccal


vestibule (Fig. 17.19B). Even if the abs­
cess is localized and the prominent part
is on the skin incision should be avoided Fig. 17.21: Anatomical boundaries of the
to prevent unsightly scar on the face. The canine space
drain is left in situ. The maxillary buccal
space drains passively with a vestibular Fig. 17.22: Infraorbital space infection,
incision as it is facilitated by gravity. But levator of the upper lip (quadratus labii note edema of eyelids
for the mandibular buccal space as the superioris) originates from the face of
gravity assisted drainage is not possible, the maxilla by several heads to insert •
Cheek swelling and redness.
libral incision should be taken and into the angle of the mouth. Medially, •
Obliteration of nasolabial folds.
the collection should be periodically a potential space exists between the •
Obliteration of the labial vestibule
evaculated by compressing the tissue infraorbital and zygomatic heads, as well due to the swelling.
extraorally. Even if the infection is not as between it and the caninus muscle • Edema of upper and lower eyelid.
localized and is in the stage of cellulitis arising from the bone above the canine • Tenderness and severe pain secon­
decompression by way of placing inci­ fossa. This represents a plane along dary to infraorbital nerve edema and
sion produces rewarding results by which an infec­tion from the canine tooth inflam­mations.
causing early resolution. can track superiorly. Alternatively, there The swelling of the eyelids is
may be direct extension from maxillary a common occurrence due to the
vestibular infections and from buccal presence of the loose areolar tissue.
Canine Space or Infraorbial space infection that pass freely into the The edema is more conspicuous in
Space Infection canine space. the morning when the patient gets up
The canine space or infraorbital space from sleep (dependent edema) and it
is situ­ated over the anterior surface of Source of Infection gradually gets reduced over a period
the maxilla in the infra orbital area and • Upper anterior teeth and bicuspid of time, as the patient is upright. The
its boundaries are as shown in (Box 17.6 • Skin infection from nose and upper edema sometimes extends to upper
and Fig. 17.21). lip. eyelid closing the eye completely. The
abscess tends to point intraorally in the
Clinical Features Signs and Symptoms labial vestibule.
Odontogenic infection enter the canine • Swelling is present from lateral nasal
space from the periapical abscess of the groove to the anterior boundary of Surgical Treatment
maxillary canine that erode through the the buccal space and from upper Treatment is by dependent drainage
buccal cortex superior to the attachment lip to the preseptal area of the lower intra­orally or percutaneously if the ab­
of the levator anguli oris muscle. The eyelid (Fig. 17.22). scess is pointing there. The tran­ soral
Odontogenic Infections 343

Box 17.7: Boundaries of the superficial temporal space

Laterally Skin, temporal fascia


Medially Squamous temporal bone and skull base
Inferiorly Superior surface of lateral pterygoid muscle
Superiorly and Attachment of temporalis to cranium, anterior border
posteriorly
Anteriorly Posterior wall of maxillary sinus, pterygomandibular fissure

Box 17.8: Boundaries of the deep temporal space


Fig. 17.23: Aspiration of the blood stained,
purulent material in a case of canine space
Laterally Temporalis muscle
infection Medially Lateral surface of the temporalis muscle
Inferiorly Superior surface of lateral pterygoid muscle
dissection is preferred as the percu­ Superiorly and Attachment of temporal fascia to cranium, anterior border
taneous drainage leaves an unsightly posteriorly
scar on the face. As with all infections Anteriorly Attachment of the fascia to the orbital process of the zygoma
from pulpally involved teeth, extraction
or root-canal therapy of the offending
tooth is also necessary.
Boundaries (Boxes 17.7 and 17.8) Deep Temporal Space
Drainage of the canine space ab­ Anteriorly: Posterior surface of lateral Deep temporal space lies deep to
scess is made by making incision paral­ orbital rim. temporalis muscle and skull. Below the
lel to and in depth of the maxillary ves­ Posteriorly: Fusion of temporal level of zygomatic arch, superficial and
tibule adjacent to the abscessed tooth fascia with pericranium. deep space communicate directly with
(Fig. 17.23). Blunt dissection is carried Inferiorly: Zygomatic arch (Fig. 17.24). the infratemporal and pterygopalatine
superiorly through the levator anguli fossa.
Applied anatomy
oris muscle into the canine space. Care­
Contents
ful dissection is necessary to preserve Temporal fascia splits into two layers
the infraorbital nerve and its branches. that pass lateral and medial to zygomatic Terminal division of internal maxillary
A drain is positioned into the infected arch. This compartment contains leaflet artery and mandibular division of trige­
space and secured in position by suture. of buccal fat pad and three small veins minal nerve
Aggressive antibiotic therapy is that drain temporal region. Buccal space
important to aid in resolution of the local infection may follow buccal fat pad into Clinical Features
infection and to prevent the extension this space. The temporal space infections produce
into the orbit and the brain as it lies in a mild swelling in the temporal area
the ‘Danger zone’ of the face. (Fig. 17.25A). The swelling is not very
Angular vein, an ascending branch conspicuous due to the presence of
of the facial vein, courses through the the tenacious temporal fascia in case
canine space. Canine space infection of superficial pouch involvement and
may give rise to septic thrombi in the in case of the deep pouch, due to the
angular vein, which can travel to the presence of the temporalis muscle and
cavernous sinus by way of superior and overlying fascia. The hallmark of the
inferior ophthalmic vein of the orbit.10 temporal pouch infection is trismus due
to the spasm of the temporalis muscle.11
Temporal Space The superficial pouch infection extents
Temporal pouches are fascial spaces in below the zygomatic arch in the massetric
relation to ternporalis muscle. They are area producing a classical ‘dumbbell’-
two in number—superficial and deep shaped swelling (Fig. 17.25C). The deep
temporal space. pouch infections can extend to the
infratemporal, lateral pharyngeal and
Superficial Temporal Space pterigomandibular spaces.
Superficial temporal space lies between
the deep temporal fascia which is conti­ Management
nuation of parotideomasseteric fascia Fig. 17.24: Anatomical boundaries of the Extraoral incision is placed in the
and the temporalis muscle. temporal pouches temporal region, well above the hairline,
344 Infections of Maxillofacial Region

A B C
Figs 17.25A to C: Typical dumbbell-shaped swelling in temporal pouch infection

45 degrees to zygomatic arch. The hem­ Box 17.9: Boundaries and contents of the Applied anatomy
lateral pharyngeal space
ostat is inserted above and below the Relations of lateral pharyngeal space ex­
temporalis muscle. The care should be Superiorly Base of skull, petrous part of plain its most common involvement in
taken not to damage the branches of temporal bone with maxillofacial infections. Infections may
facial nerve. The incision can be placed Inferiorly foramen lacerum and jugular encircle the airway by spreading from
above and parallel to the zygomatic arch Anteriorly foramen one lateral pharyngeal space to other
(Fig. 17.25B). The temporal fascia is divi­ Laterally Hyoid bone through retropharyngeal space. Con­
ded to evacuate the contents of the super­ Pterygomandibular raphe trast enhanced CT is valuable aid in con­
ficial pouch and the temporalis muscle is Medially Ascending ramus of mandible, firmation of diagnosis, deter­mination of
pierced open to drain the contents of the medial pterygoid muscle, extent and stage of deep cervical space
Posteriorly
deep pouch. As the abscess cavity heals medial surface of deep lobe of infections.
by fibrosis there can be persistant trismus parotid gland. Infections in the parapharyngeal
and hence postoperative physiotherapy Pharyngeal wall, superior spaces have sometimes been associated
and middle constrictors and
should be given to prevent the muscle with morbid vascular or neurologic prob­
stylopharyngeus Stylohyoid
fibrosis and trismus. muscle, upper part of carotid lems and occasionally with mortality.
sheath, prevertebral fascia Knowledge of the anatomy of the discrete
Parapharyngeal Spaces with foramen lacerum and anterior and posterior compartments
Parapharyngeal spaces include lateral jugular foramen of the lateral pharyngeal space provides
pharyngeal and retropharyngeal spaces. Contents Anterior compartment: Lymph infor­mation for accurate diagnosis,
They form a ring around pharynx and nodes, ascending pharyngeal, ensures correct treatment and thus, af­
together form a pathway for spread of facial artery, loose areolar fects eventual outcome of the infection.
connective tissue.
orofacial infections in neck and media­ The styloid process divides the space
Posterior compartment:
stinum. into an anterior muscular compartment
Carotid sheath,
glossopharyngeal nerve, closely related to the tonsillar fossa and
Lateral Pharyngeal Space spinal accessory nerve, a posterior vascular compartment.12
(Pharyngomaxillary Space) hypoglossal nerve and The anterior compartment contains
Lateral pharyngeal space is a poten­ cervical sympathetic trunk. fat, muscle, lymph nodes and connective
tial, inverted cone, shaped space with tissue.
its base at the skull and its apex at the The posterior compartment, also
greater cornu of hyoid bone (Box 17.9). called the post-styloid or retro-styloid
It is divided into anterior and posterior geal wall, deviated uvula, dysphagia and compartment, contains cranial nerves
com­ partments by styloid process and trismus. IX to XII13,14 and the carotid sheath and
a short layer of condensed fascia called If the posterior compartment beco­ its contents (the internal carotid artery,
aponeurosis of Zuckercandl and Testut. mes infected, there is absence of tris­ internal jugular vein, vagus nerve and
If the anterior compartment becomes mus along with visible swelling, but lymph nodes). The carotid sheath
infected, the patient exhibits pain, fever, respiratory obstruction, septic thromo­ extends from the base of the skull down
chills, medial bulging of lateral pharyn­ phlebitis of IJV may ensue in late stages. through the lateral pharyngeal space,
Odontogenic Infections 345

runs along the prevertebral fascia below involvement is by direct extension over compartment of the lateral pharyngeal
the hyoid bone, and then enters the chest the mylo­hyoid muscle and into the an­ space may be secondary to rupture of
below the clavicle. The sympathetic terior lateral pharyngeal space, although lymph nodes draining an odontogenic
trunk lies behind the sheath in a fascial sometimes infection may first occur in infection. Theoretically, in such cases,
reflection from the deep surface of the the pterygomandibular space and sub­ the anterior compartment may not
posterior wall.15 sequently spread to the lateral phar­yn­ become involved in the infection. With
The possibility that the strongest geal space (Fig. 17.26). inflammatory swelling of the lymph
fascial plane in the head and neck is the Every peritonsillar space abscess glands for more than several weeks, an
stylopharyngeal aponeurosis of Zucker­ (quincy) can become a lateral pharyn­ abscess frequently results. Suppuration
kandel and Testut, formed by the conflu­ geal space abscess by local spread. without high fever may develop.
ence of the alar, buccopharyngeal and Infection in such a patient is much more Middle ear infections with associated
stylomuscular fascia. This aponeurosis is severe than the classic peritonsillar mastoiditis can develop into an internal
a barrier against direct spread of anterior abscess in that it not only presents with Bezold’ s abscess,21 the result of the
compartment infections to the vital struc­ tonsillar inflammation and swelling infection breaking through the bone
tures of the posterior compartment.16 of the lateral pharyngeal wall, but also and creating a subperiosteal abscess on
extreme trismus and occasional parotid the inner aspect of the mastoid tip in the
Pathophysiology and etiology swelling. region of the digastric groove. Further
of infection The deep fascia of the parotid gland progression of this abscess will directly
Common sites of origin of paraphar­ is not complete at the base of the skull involve the lateral pharyngeal space.
yngeal infection include the teeth, tonsils and it fails to cover the upper inner
Clinical features
and adenoids; parotid gland and lymph surface of the gland.19 On the other
glands draining the nose and the phar­ hand, the lateral aspect of the gland The symptoms of lateral pharyngeal
ynx.17 Thrombosis of the internal jugular forms a rather dense capsule. Therefore, infections will vary according to whe­
vein or of peritonsillar veins, metastatic parotid infections readily pass medially ther the anterior, posterior or both com­
tumors with secondary infection of the into the lateral pharyngeal space.20 partments are involved.
internal jugular lymph node chain, iat­ Parapharyngeal infections may occur There are four cardinal signs of
rogenic introduction of organisms dur­ from lymphatic drainage of surrou­nding invol­ve­ment of the anterior lateral phar­
ing infiltration for a mandibular nerve tissues such as the periodontal region. yngeal compartment:22
block18 or adminis­tration of an anesthet­ Idiopathic cervical abscesses may spread 1. Trismus.
ic during tonsillec­tomy are documented across fairly large areas of uninvolved 2. Induration and swelling at the angle
causes of spread of infection. The most tissues through lymph vessels from the of the jaw.
common origin of a lateral pharyngeal portal of entrance directly to the lymph 3. Fever.
space infection, however, is odontogen­ nodes of the neck. In such cases, the 4. Pharyngeal bulging (Fig. 17.27).
ic, secondary to a grossly carious molar, glands may breakdown and form an Trismus is the most important sign
pericoronitis or tooth extraction. Usually abscess. Involvement of the posterior and results from the close relationship
of the infection to the medial pterygoid
muscle.23
Because the anterior compartment
ends at the level of the angle of the

Fig. 17.26: Spread of odontogenic infection from pterygomandibular space to the lateral Fig. 17.27: Medial displacement of lateral
pharyngeal space pharyngeal wall
346 Infections of Maxillofacial Region

jaw, induration and swelling is evident of the lateral posterior pharyngeal sion and drainage, maintenance of air­
medial to the angle of the mandible. wall and the parotid space do occur. way, removal of the causative agent and
At this point, the most superficial part antibiotic therapy initiated empirically
Complications
in the neck, the anterior compartment and adjusted when results of culture
is separated from the skin surface by Shapiro26 lists a number of complica­ and antibiotic sensitivity tests have been
two thick complete fascial layers—the tions that may ensue with any para­ obtained.
superficial layer of the deep cervical pharyngeal space infection, including Incision and drainage is most im­
fascia, and the blind end of the anterior mediastini­ tis, jugular thrombosis, portant to decompress the lateral pha­
lateral pharyngeal space or fascial fold.22 edema of the larynx, Ludwig’s angina, ryngeal space and avoid the dreaded
Fluctuation, therefore, can be felt late or hem­o­rrhage from erosion and blowout complications of major vessel erosion,
may not be detected at all. the large vessels, osteomyelitis of the airway embarrassment, and sepsis.
Fever usually occurs concomitantly mandible, pneumonia, vagus involve­ There are multiple approaches to
with infection that is localized in the ment (sudden death), meningitis and the lateral pharyngeal space: intraoral,28
fascial space. Pharyngeal bulging is due parotid abscess. extraoral and a combination of both
to the thin fasciomuscular wall between Lifschutz27 states that the blood (Figs 17.28A and B). The intraoral
the pharynx and the compartment. vessels are usually the last to yield in the incisions can be either transpharyngeal13
Because of the relation to the tonsil­ case of an abscess or sloughing infection or lateral.29
lar area, there is usually bulging of the in the deep cervical space. Sudden The transpharyngeal approach is
posterolateral pharyngeal wall and ton­ spontaneous rupture of the abscess made through the tonsillar fossa. This
sillar region as well. It is relatively easy to into the throat may rarely produce fatal approach is not recommended because
differentiate isolated peritonsillar infec­ consequences due to aspiration. adequate drainage is very difficult to
tions from lateral pharyngeal space infec­ The erosion and rupture of major obtain and because there is absolutely
tions. A hoarse voice and a usual lack of vessels like internal jugular vein and the no exposure of the vessels.
trismus are associated with peritonsillar internal carotid artery in the posterior The lateral approach is most easily
abscess.24 It is often difficult to differenti­ compartment leads to fulminating hem­ performed by making an incision lateral
ate a pterygomandibular space abscess orrhage which is invariably fatal. to the pterygomandibular raphe and
from lateral pharyngeal space abscess. The infection can spread upwards dissecting bluntly with a Kelly clamp
Sometimes they are confluent. through foramen lacerum, ovale, jugular medial to the medial pterygoid muscle
Infections in the posterior compart­ foramen producing brain absc­ess, men­ into the parapharyngeal space.
ment will show: ingitis or sinus thrombosis. It spreads All peroral incisions are contrain­
• Posterior tonsillar pillar deviation downward into carotid sheath towards dicated when there has been prior
and retropharyngeal swelling due to mediastinum, a pathway called ‘anterior hemorrhage.
the proximity of the two areas. Lincoln’s highway’ of the neck. The extraoral submandibular incisi­
• May show neurologic involvement of on is the safest approach and should
cranial nerves IX through XII and of Management be used if there is any involvement of
the cervical sympathetic chain, with Treatment of parapharyngeal infection the posterior compartment. A verti­
ipsilateral Horner’s syndrome.25 requ­ires immediate hospitalization, inci­ cal exten­ sion to the submandibular
• Thrombosis of the internal jugular
vein with sepsis may cause abrupt
rises and falls in temperature and
chills.
• Blood cultures are often positive.
• Venous blowouts are more common
than arterial. Even though the tight­
ness of the vascular sheath resists
intrusion, erosion of the common,
external, or internal carotid artery
may occur within the carotid sheath.
• In infections limited to the posterior
compartment, the muscles of masti­
cation are not involved and minimal
trismus or tonsillar prolapse occurs. A B
• Because of the close relationship with Figs 17.28A and B: Incision and drainage of lateral pharyngeal space: (A) Intraoral
the parotid space, however, swelling mucosal incision; (B) Kelly clamp anterior to the sternocleidomastoid muscle
Odontogenic Infections 347

inci­sion may be given to form a T shaped of major vessel erosion and subsequent Box 17.10: Boundaries of retropharyngeal
inci­­sion, which may rarely be necessary severe hemorrhage. Examination by space
to have adequate exposure for control of vascular surgeon and an arteriogram Laterally Carotid sheath, lateral
major vessels.30 should be obtained. If one encoun­ pharyngeal space
In the combined intraoral and ex­ ters only purulent material, the wound Superiorly Base of the skull
Inferiorly Fusion of retropharyngeal
traoral approach, the mucosal incision should be irrigated and a large drain is
fascia
is made lateral to the pterygomandibu­ inserted. Anteriorly Deep cervical fascia and
lar raphe.29 A large curved Kelly clamp is Intubation, elective tracheostomy or and alar fascia
then passed lateral to the superior con­ cricothyrotomy should be contem­plated post­eriorly
strictor muscle and medial to the me­ in cases involving airway compromise Medially Midline septum
dial pterygoid muscle. The blunt dissec­ or vascular com­ plications. Significant
tion is carried posteroinferiorly below tongue elevation, severe dysphagia
the angle of the mandible. When the tip and rapid speed of infection, all sug­ Infections of these spaces may prove
of the instrument is palpated extraor­ gest need for airway protection. Should fatal owing to their ability to impinge
ally anterior to the sterno­cleidomastoid, these signs present prior to elective tra­ on the airway directly and potential
a cutaneous incision is made over the cheostomy, muscle relaxants should not involvement of danger space.31
tip (Fig. 17.29). This technique affords be given, because intubation via the oral The deep layer of the deep investing
direct access into the lateral pharyn­ route may not be impossible.29 Fiberop­ fascia encloses the vertebra and para­
geal space and aids correct placement tic lary­ngoscopy, with the patient awake vertebral musculature. This deep layer is
of the external incision in a patient with and comfortable, may be a useful ad­ further subdivided into the prevertebral
gross edema. Blunt dissection behind junct. Should doubt occur during con­ and alar layers.
the posteriorly retracted sternocleido­ trol of the airway, emergency cricothy­ • The prevertebral layer lies anterior
mastoid allows direct entrance into the roid puncture may be difficult, because to the vertebral column from the
inferior aspect of the posterior compart­ land­marks are masked by the swelling. base of the skull to the coccyx.
ment. Finger dissection is carried out If the anesthesiologist wishes to attempt • The alar layer of the deep layer of
to identify such landmarks as the hyoid intubation, the neck should be marked the deep cervical fascia lies posterior
bone and the posterior belly of the di­ for a tracheotomy incision and injected to the middle layer and pharynx
gastric muscle. Loculations of pus are with local anesthesia prior to such at­ and fuses with the transverse pro­
broken up. The presence of old blood tempts. If an immediate trache­otomy is cesses. This fascia extends from the
clots should alert one to the possibility needed, a vertical mid­line incision will base of the skull to the posterior
provide the quick­est and most bloodless mediastinum (Fig. 17.30).
access. The retropharyngeal abscess is an
abscess in the potential space of loose
connective tissue posterior to the pha­
Retropharyngeal Space ryngeal wall and anterior to the middle
Retropharyngeal space is a potential layer of the deep investing fascia; or be­
midline space between the pharyn­ tween the middle layer of the deep in­
gobasilar fascia, which attaches the pha­ vesting fascia and the alar layer of the
ryngeal constrictors to the base of the investing fascia, or between the alar and
skull and prevertebral fascia. This space prevertebral layers of the deep layer of
is continuous with retroesophageal the deep investing fascia. This extends
space into the posterior mediastinum to from the base of the skull to the mediasti­
the level of sixth thoracic vertebra. The num. Because of the interconnecting na­
anatomical boundries of the retropha­ ture of the layers of the deep fascia, retro­
ryngeal space are as shown in Box 17.10. pharyngeal abscesses may communicate
Dyspnea, dysphagia, nuchal rigidity, with the lateral pharyngeal space, the
esophageal regurgitation and fever char­ pretracheal space and the mediastinum.
acterize retropharyngeal space infections.
Pathophysiology and etiology
Applied anatomy The incidence of retropharyngeal abscess
Fig. 17.29: Various incisions for draining Retropharyngeal and lateral pharyngeal is greatest in the 3 to 4 year-old age group.
the fascial space infections; A For tem­ spaces contain a rich supply of lymph Even though only a low incidence has
poral pouches; B Submandibular, sub­
nodes that drain Waldeyer’s ring. When been reported since the introduction of
masseteric and pterigomandibular space;
these nodes necrose, fascial space antibiotics, the retropharyngeal abscess
C Submental space; D Lateral pha­ ry­
ngeal space infection may develop. does occur in adults.
348 Infections of Maxillofacial Region

and 1.9 mm in females, with a range


in both from 1.5 to 4.0 mm. Wholey
et al.39 in 1958 reviewed 480 soft tissue
radiographs of the neck in adults. Retro­
pharyngeal region was identified from
the base of the skull to C5. The repre­
sentative distance between C2 and the
posterior pharyngeal wall was used
as a standard. This distance averaged
3.4 mm in adults and ranged from
1.0 to 7.0 mm. The representative dis­
tance for the retrotracheal region was
from C6 to the posterior tracheal wall
and this average was 14.0 mm with a
range of 9.0 to 22.0 mm. Using these
studies as standards, soft tissue radio­
graphs of the neck in adults that lie
beyond the accepted range and are
correlated clinically will be diagnostic.
The use of the CT scan40 has proved
Fig. 17.30: Retropharyngeal space and fascial boundaries to be more effective in diagnosing the
retropharyngeal region abscess.

These are usually due to32-35 implicated in retropharyngeal abscesses Treatment


• Otologic secondary to vertebral osteomyelitis.35,36 The most important initial considera­
• Pharyngeal or nasopharyngeal infe­c-­­­­­­ tion is maintenance of a patent airway.
tions can directly spread to the Clinical Features Possible airway compromise must be ad­
ret­­ro­­­pharyngeal space The signs and symptoms of retropha­ dressed early in the treatment plan. Elec­
• Upper respiratory infections ryngeal abscess include:32,33,35,37 tive tracheostomy, fiberoptic intubation
• Odontogenic infections • Fever or blind, awake nasotracheal intubation
• Cervical osteomyelitis • Sialorrhea are all viable alternatives for initial airway
• Foreign body introduction • Stiff neck maintenance. Consider­ ation must be
• Regional trauma • Sore throat given to the possible necessity for long-
• Spread by the lymphatics. • Dysphagia term intubation post­operatively.
It is well known that the parotid, sub­ • Possible stridor Initial antibiotic therapy should be
mandibular and masticator spaces com­ • Leukocytosis aggressive and based on the gram stain
municate with the lateral pharyngeal • Occasional lateral neck erythema from an aspirate or a productive inci­
space. Infections originating in any of and swelling. sion and drainage. There have been a
these spaces may then ultimately prog­ Each of these, however, are not number of surgical approaches reported
ress to affect the retro­pharyngeal region diagnostic and must be correlated with to the retropharyngeal region. Some in­
via the lateral pharyngeal space.36 radiographic findings. Soft tissue radio­ corporate an intraoral midline incision
The organisms identified with in­ graphs are invaluable in identifying through the anterior wall of the pharynx.
fections of the retropharyngeal space abnormalities of the retropharyngeal The constant drainage of purulent mate­
are consistent with the specific etiology. region. Hay38 in 1930 was the first to rial and blood can leave the patient open
Odontogenic or oropharyngeal infec­ correlate soft tissue radiographs and to aspiration and respiratory obstruction
tions frequently yield combinations or posterior pharyngeal pathosis. In his utilizing this approach.
anaerobic and aerobic gram-positive review of 50 ‘soft tissue lateral neck’ The extraoral approach affords the
and gram-negative bacteria, predomi­ radiographs of adults, he measured the greatest control and manipulation of the
nantly Bacteroides fragilis or Strepto­ distance between cervical vertebrae and affected spaces. An incision transcutane­
coccus species. Sinusitis, otitis media the posterior pharyngeal wall from C1 to ously anterior to the sternocleidomastoid
and mastoiditis most frequently reveal C5 as being representative of the thick­ muscle from the level of the angle of the
anaerobes of a mixed variety. Staphylo­ ness of soft tissue in the retropharyngeal mandible to the level of the hyoid bone
coccus aureus, Coccidioides immitis and region. The retropharyngeal soft tissue will allow retraction of the sternocleido­
Mycobacterium tuberculosis are most regional average was 2.0 mm in males mastoid muscle. The carotid sheath with
Odontogenic Infections 349

its contents can then be inspected for But the primary line of treatment for abscess, the incision must be placed
possible erosion. Retraction of both the the pyogenic infection is surgical, com­ on the most dependent site to facilitate
muscle and the sheath allows for a blunt prising of decompression or drain­age. gravity assisted drainage. However,
dissection into the lateral pharyngeal and One should not always wait for the signs if the most prominent part of the
retropharyngeal space, the latter verified of the localization of the infection and abscess is chosen and it is not the most
by palpation of the anterior processes formation of the localized abscess, but dependent part then a counter incision
of the cervical spine posteriorly and the should proceed with surgical decom­ should be placed on the dependent site
endotracheal tube anteriorly. Appropri­ pression at the earliest. The decom­ to facilitate gravity assisted drainage.
ate drains may then be placed. These pression helps in reducing the mounting The incisions taken for the drainage
drains are then irrigated and advanced in pressure within the tissue planes and of an abscess or the decompression of
accordance with the individual postop­ thus helps in: the cellulitis should always be liberal
erative course. • Preventing lateral spread of the infe­ to achieve free and passive drainage.
ction due to pressure. While draining large abscess or multiple
Complications • Prevents pressure/ischemic necrosis fascial space involvement, the incision
The most frequent complication of the of the tissue. should be liberal enough to allow pass­
retropharyngeal abscess is dissection to • Improves the local circulation by age of the index finger. When the index
the posterior mediastinum with resultant decompressing the pressure. finger is introduced in an abscess the
medi­ astinitis, pleuritis and pericardi­ • Improves the drainage of the part finger being blunt does not damage
tis.34,41 Spontaneous rupture of the abscess by opening up the lymphatic and the vital structures and palpates the
into the pharynx may result in aspiration venous cannels which were blocked anatomical landmarks, simultaneously.
pneumonia or empyema.32,33 Erosion of by edema and pressure and thus It also breaks the locules in the abscess
the great vessels of the neck have been reduces tissue edema, congestion and converts a multiloculated abscess
reported and are potentially fatal.42 Upper and stasis of local circulation due to into a uniloculated cavity thus helps in
airway obstruction is a potential threat reabsorption of interstitial edema. complete drainage of the septic material
and close observation is required. • Improves delivery of the antibiotics and reduces further absorption of the
to the local site and thus helps in bacterial toxins. The chances of missing
controlling the infection rapidly. any pocket or locules are minimum as
GENERAL PRINCIPLES OF • Prevents further complications like the infected tissue is often fragile and
INFECTION MANAGEMENT laryngeal edema, mediastenitis, etc. easily gives way with pressure applied
(BOX 17.11) If the signs of localization such as by the inserted finger. The healthy tissue
fluctuations are present, the drainage offers resistance to the finger and thus
Although the antibiotics are useful in must be undertaken promptly. In the the operator is in position to know the
the management of the infections, the maxillofacial area due to presence completeness of the procedure.
role of surgical intervention is very of loose areolar tissue a deep seated While draining any abscess one
important, in the early resolution and abscess will invariably be accompanied must remember three golden rules:
preventing further complications. The by the edema or cellulitis of the overlying 1. The incision should be at dependant
specific infections like tuberculosis, skin. Thus, classical fluctuations may site.
syphilis, typhoid, etc. are primarily sometimes get masked. It is particularly 2. It should be liberal.
treated with drugs and surgery has a true in cases of submasseteric, deep 3. It should facilitate, free passive
minor role in specific situations only. temporal pouch and the parotid abscess drainage.
where the overlying muscle or thick If the presence of necrotic granulation
Box 17.11: Principles of abscess drainage fascia will mask the fluctuations. In tissue is noticed lining the abscess, such
such cases, diagnostic aspirations with tissue should be gently curetted out. If
•  lace the incision on the most depen-
P the help of wide-bore needle may be the infected, necrotic granulation tissue
dent part done to demonstrate a deep seated pus is left in situ, it will bleed for a long time
• If the incision is placed on the prominent pocket. The USG or CT scan may also be being friable in nature. Secondly, such
part, place the counter incision on the helpful in locating pus pockets so that tissue will breakdown and liquify to
dependent part the drainage can be adequately planned produce pus subsequently and thirdly
• Liberal, dependent, passive drainage
and undertaken. Once the diagnosis of leaving such tissue will increase the
should be achieved
• Use sinus forcep or index finger to break an abscess is arrived at, the drainage load on the scavenging mechanisms
the locules can be done by any of the documented of the body. The abscess cavity should
• Break all locules to change multiloculated methods, i.e. Hiltons method or modified be gently irrigated with normal saline
cavity into a uniloculated one Hiltons method. The surgical procedure or diluted povidone iodine solution to
• Use drain is often referred to as an Incision and flush out the septic material and necrotic
• Send the sample for C and ST.
Drainage (I and D). While incising the tissue tags. Use of hydrogen peroxide is
350 Infections of Maxillofacial Region

debated as some clinicians feel that the infection getting controlled or it could be When the cellulitis is present the use
effervescence produced by it will drive due to blockade of the corrugations due of glycerin magnesium sulfate (glycerin
out the debris of necrotic tissue and to fibrin. In such cases, the drain should magsulf) dressing is helpful (Figs 17.31A
deliver the nascent oxygen which helps be displaced to break adhesions and to C). It is the gauze soaked in the
in inhibiting the growth of anaerobic the soakage should again be observed saturated solution of the magnesium
microorganisms and facilitate for­mation for next 24 hours and if the soakage is sulfate in glycerine. It has following
of the granulation tissue, while others still minimal then the drain should be effects:
feel that the effervescence will drive the discontinued. It is also recommended • The magsulf is hygroscopic and thus
microorganisms in deeper tissue planes to withdraw the drain gradually daily so helps in drawing the interstitial fluid
to cause flaring of the infection. that thus reduces edema, reduces tissue
The drained pus should be carefully • The drain does not get blocked due pressure, improves local circulation
colle­c­ted in a sterile bulb and should be to fibrinous adhesions. and drainage and facilitates healing.
submitted to microbiology lab for culture • The abscess cavity and gets filled • The glycerin magsulf produces exo­
and sensitivity to determine specific anti­ gradually from the base and shrinks. th­er­mic reaction and produces heat
biotic therapy. Usually the midstream of • While doing the gradual withdrawal which causes vasodilatation and
the drained pus is collec­ted. the fixing stitch is removed which reduces congestion due to improve­­
After the drainage the most suitable may lead to falling of the drain in the ment of local circulation.
material used as a drain is a corrugated cavity to prevent this, a sterile safety • Glycerin has soothing action on
rubber dam drain. The tube drains or pin is used to fix the drain. tissue.
vacuum drains are not ideal unless the Similarly the drain should not be
irrigation of the abscess cavity is planned kept for long after the purpose of drai­ MEDICINAL TREATMENT IN
subsequently. The drain facilitates the nage is achieved as:
OROFACIAL INFECTIONS
free drainage of pus and exudates and • It can introduce retrograde infection.
keeps the opening (incision) patent. • It may be in contact with major The supportive management comprises
Gauze drains should not be used ideally vessel and may erode it. of antibiotics and anti-inflammatory
as the gauze has capillarity. It absorbs • It may get biodegraded and may drugs. The antibiotics usually prescribed
fluid, swells and impedes the drainage. become difficult to remove. in the management of the odontogenic
It should be used as a pack cum drain The local care of the incision wound infection are penicillin or cephalosporin
to achieve hemostasis, only when the and the abscess cavity is required follow­ group of antibiotics (beta-lactam group)
abscess cavity bleeds and should be ing the drainage. Although abscess is as the infection of odontogenic origin
removed after 24 hours and replaced an infected cavity, the daily dressings is caused by the oral microorganisms,
by rubber dam drain. The appropriate must be done under aseptic care. The which predominantly are gram-positive
time for removal of the drain is variable abscess cavity may be gently irrigated and respond well to the penicillin group
and depends on the given case and with sterile normal saline to flush out of antibiotics. In severe infections or
condition. If the pus discharge gets the necrotic tissue tags, thick pus, etc. where the patient has compromised
reduced and is minimal in last 24 hours Povidon iodine 5 percent solution can immunity, higher doses should be
then it could be either because of the be used for irri­gation. prescribed. Cloxacillin can be added

A B C
Figs 17.31A to C: Glycerine and magsulf dressing is used in the diffuse and acute stage
Odontogenic Infections 351

to ampicillin or amoxicillin as the later are more common in the genitourinary conductive environments for their
two may not be effective in the presence and lower gastrointestinal tract infec­ growth and proliferation are present
of (penicillinase) beta-lactamase pro­ tions and hence the aminoglycosides such as, hypoperfused cavities, dead or
ducing organisms. Cloxacillin has a are of limited value in the management devitalized tissue.
property of resisting the beta-lactamase of odontogenic infections. The amino­ Definitive antibiotic therapy can be
(penicillinase) and thus is more effective glycosides may be added to beta-lactam started after the culture and sensitivity
in such situation and is known to antibiotics, if the gram-negative micro­ test. Glycerine and magsulf dressing is
potentiate the action of the ampicillin organisms are detected on the culture used in the diffuse and acute stage.
and amoxicillin. The addition of the of the pus sample. The gram-negative
clavulanic acid also potentiate the organisms may some­times be present in
SELECTION OF ANESTHESIA
action of amoxicillin (Augmentin) in the postoperative nosocomial infections
presence of beta-lactamase-producing in the maxillofacial area. The superficial, minor abscess can
microorganisms (Table 17.6). When evidence of anaerobic infec­ be drained comfortably under the lo­
In the mixed infections, to give wider tion like slough, crepitus, gas, foul- cal anesthesia. However, deep seated
spectrum of coverage against the gram- smelling, thick greenish black pus is abs­cess cannot be drained completely
negative organisms aminoglycosides present, then metronidazole in appro­ under local anesthesia alone. The skin
(gentamycin, amicacin) may be given. priate dose should be added. The anae­ can be infilterated with local anes­
However, gram-negative infections are robes are facultative organisms and thetic and the incision may be painless,
seldom present in the orofacial area and will cause the infection only when the but while draining large, deep seated,

Table 17.6: Various antibiotics used in the management of odontogenic infection

Name Group Dose Adverse effects

Amoxicillin Penicillin 40–45 upto 80–95 mg/kg/wt • Bone marrow depression


Ampicillin Penicillin Used orally and injection • Granulocytopenia
Ampiclox/Amoxyclox Penicillinase resistant With clavulanate it is 1.2 g • Rarely hepatitis
Clavulanate Penicillin in which 1 g is ampicillin and • Pain at site of IM injection
Beta lactamase inhibitor 0.2 g is clavulanic acid • P
 hlebitis/thromobophlebitis at site of IV
injection
• Hypersensitivity
Cefazolin Cephalosporin first 1–1.5 g every 6 hourly • Nephrotoxic, but not as aminoglycosides
Cephalexin generation 1 g every 6 hourly • Diarrhea
Cefadroxil 1 g every 12 hourly • Hypersensitivity
Cefoxitin Cephalosporin second 2 g every 4 hourly or
generation 3 g every 6 hourly
Cefaclor 1 g every 8 hourly
Cefotaxime Cephalosporin third 2 g every 4–8 hours
generation
Ceftriaxone 2 g every 12–48 hours
Cefepime Cephalosporin fourth 2 g every 8 hourly
generation
Gentamicin Aminoglycoside 2 mg/kg loading and then • Ototoxicity
3–5 mg/kg/day in adults • Nephrotoxicity
For children upto 2 years
2–2.5 mg/kg every 8 hours
Amikacin 15 mg/kg/day
Clindamycin Lincosamide 150–600 mg in divided doses for adults • Abdominal pain
10–30 mg/kg in 4–6 divided doses • Diarrhea
• Blood in stools
Metronidazole Nitroimidazole 750 mg to 2 g/day in divided doses • Headache
• Nausea
• Metallic taste
• Dry mouth
• Rarely vomiting, diarrhea
352 Infections of Maxillofacial Region

multi­lucolated abscess drainage will be the septic material is discharged in the nidus for proliferation of the anerobic
very painful while draining. Moreover that tissue plane which spreads to the organisms. However, the predominant
just the placement of the incision is not adjacent tissue planes. organisms are the streptococci.
synonymous with drainage, the loculi • Septic fractures
within are required to be broken to • Salivary gland infections Clinical Features
achieve complete drainage. Attemp­ting • Hematogenous infections. • It is characterized by acute course
to drain such abscess under local anes­ producing, bilateral swelling due
thesia may be incomplete job. Sedating Predisposing Factors to cellulites of the submandibular,
the patient, giving intra­ venous anes­ • Immunosuppression sublingual and submental spaces.
thetic agents like thiopen­tal sodium and • Steroid therapy The skin is tense, glossy and hypere­
ketamine carry a high risk of aspiration • Diabetes mic. The consistency is often descri­
of pus as the airway is often unguarded. • Debilitating conditions bed as ‘wood like’ or called brawny
Although the abs­cess is drained by ex­ • Due to advent of the antibiotics induration.43
traoral incision during the manipula­ the occurrences of this condition is • The swelling of the submental space
tion, the eroded or thinned out loculi uncommon, but in the above menti­ produces a classical double chinned
may rupture intra­orally leading to as­ oned patients the Ludwig’s angina appearance.
piration. The cases of trismus, large ab­ can be precipitated. • Skin is tense due to accumulation
scesses, lateral or retropharyngeal ab­ of the inflammatory exudates in
scesses pose a great threat of aspiration. Causative Organisms the interstitial compartment which
It is therefore advis­able to guard the It is primarily caused by the beta- makes the tissue to pit and blanch
airway by intubation and packing of the hemolytic streptococci.43 The hallmark on pressure (Fig. 17.32A and B).
pharynx. Most of the perianal abscess­ of the streptococcal infection is that the • Tenderness on palpation is present.
es produce pro­ nounced trismus and infection tends to spread rather than • Due to mounting interstitial fluid
endotracheal intubation may be dif­ localizing, due to liberation of exotoxins pressure, the edema rapidly spreads
ficult. In such cases blind intubation is by the streptococci which breakdown the along the fascial plane, breaking the
risky. Thus, intubating fiberoptic bron­ intercellular cementing substance which tissue barriers and go on to involve
choscope or laryngoscopically guided facilitates the spread of the infection along the adjoining spaces.
intuba­tion should be attempted. If there the tissue planes. Apart from streptocci, • The involvement of the sublingual
is prono­unced laryngeal edema as in E. coli has also been isolated from the space leads to edema and congestion
cases of Ludwig’s angina, cricothyroid­ cultures taken in the cases of Ludwig’s of the floor of mouth and the ton­
otomy or tracheostomy should be done angina.44 Anaerobic organisms are also gue gets lifted and protrudes out
to secure the airway and intubate the isolated when there are gangrenous (Figs 17.33A to D, 17.34A to C).
patient for administration of anesthesia. changes in the tissue due to combined • The infection of the sublingual space
effect of increased interstitial pressure, rapidly spreads along it to its base
hypoxia and the effects of the bacterial which is present at the hyoid bone.
COMPLICATIONS OF exotoxins. The devitalized tissue serves as Posterior inferior to the base of the
MAXILLOFACIAL
INFECTIONS

Ludwig’s Angina
Ludwig’s angina is defined as acute,
‘non-suppurating, necrotising cellulitis’
involving the submandibular, sublingual
and submental spaces, bilaterally. It is a
life-threatening complication caused
due to infection.

Etiology
• Odontogenic infections are by far the
most common cause of this condition,
the infection spreads to the adjoining A B
tissue planes either by direct spread Figs 17.32A and B: (A) Unilateral submandibular, submental and sublingual space
or through the lymphatics, which in infection not falling in definition of Ludwig’s angina, but it is potentially dangerous;
turn suppurate and breakdown and (B) Surgical decompression accomplished and drains in place
Odontogenic Infections 353

nearly impossible in these patients due


to severe laryngeal edema, elevation of
the tongue and trismus (Fig. 17.34D).
Even if the signs of laryngeal edema
and the respiratory embarrassment are
not conspicuously present, the surgical
decompression of the tissue planes must
be undertaken immediately, to relieve
the pressure within the tissue so that the
edema does not increase further and
does not spread laterally. This is achieved
by giving a liberal incision on the skin
and opening the tissue planes—layer-by-
layer dissection. In the older literature, a
A B horse shoe-shaped incision is described
in the submandi­bular area along infe­
rior border of the mandible.45 Two sepa­
rate incisions are given bilaterally in the
submandibular area and one in the
sub­mental area is commonly practiced
(Fig. 17.34E). The decompression of the
sublingual space is most important which
is achieved by piercing open the mylohy­
oid muscle, which in fact is a must in case
of Ludwig’s angina. The subl­ingual space
can also be decompressed by placing an
C D incision on the floor of the mouth; paral­
Figs 17.33A to D: (A and B) Ludwig’s angina clinical picture, patient looks toxic, tongue is lel to the lingual vestibule. The term de­
elevated, tracheostomy in place; (C) X-ray shows distended neck shadow due to cellulitis; compression is often used as the purpose
(D) Separate incisions for decompression of the submandibular, sublingual and submental of the incision is to open the tissue plane
spaces to reduce the mounting pressure within
the tissue planes and to prevent the fur­
ther spread of the edema. As the condi­
sublingual space lays the larynx and • The patient has often dysphagia and tion is usually non-suppurating, the pus is
the edema extends to the larynx caus­ saliva may dribble from the corner of absent. In some cases, there may be deep
ing the edema of the epiglottis and the the mouth. seated small pocket of pus, which is sur­
cords, which leads to acute respira­ • The patient is extremely toxic with rounded by area of cellulites. After placing
tory obstruction, due to which death high-grade fever (> 104°F), malaise, the incision, a corrugated rubber drain
can occur due to asphyxia. Thus, an body aches, leukocytosis and all the may be left in situ to keep the inci­
acute respi­ratory emergency situation classical constitutional features of sions pat­ ent and to drain the exudate
is crea­ted which warrants immedi­ septicemia are present. The periph­ (see Fig. 17.32B). The decompression ser­
ate attention. The early signs of the eral blood smear may show intracel­ ves three purposes:
laryngeal edema are dyspnea which lular eosinophilic toxic granules and 1. It reduces the tension within the
gets aggravated when the patient lies pre­sence of band cells. tissue plane and prevents the further
down. The dyspnea in supine position spread of the edema and infection.
should be regarded as the warning Management 2. As the pressure in the tissue drops
sign of impending laryn­geal edema. The treatment of Ludwig’s angina is the circulation of the tissue improves
As the edema increases the dyspnea primarily surgical. The first priority which facilitates reabsorption of the
worsens and progresses into as­phyxia. in the management is always the life- edema.
The lateral X-ray of the neck shows saving measures. If the patient has signs 3. It drains the septic material, if any
edematous soft tissue shadow and if of the laryngeal edema like dyspnea, to and prevents further bacteremia.
the laryngeal edema is present then save the life of the patient emergency The edema reduces gradually.
the epiglottis may look like a raised tracheostomy should be performed The medicinal supportive treatment
thumb (thumb sign of epiglotitis). promptly. Endotracheal intubation is comprises of prescription of parenteral
354 Infections of Maxillofacial Region

should be maintained until the edema


regress substantially. The septic focus
precipitating this complication should
be eliminated either simultaneously or
subsequently.

Cavernous Sinus Thrombosis


The cavernous sinuses are the venous
sinuses situated in the middle cranial
fossa, which are situated on either side
of sella turcica. They are formed by
splitting of dura and are traversed with
numerous fibrous septae, thus giving
A B
it a cave-like appearance and thus the
name, ‘cavernous sinus’. The cavernous
sinuses on either side communicate
freely with each other by anterior and
posterior intercavernous sinuses they
also communicate with other venous
sinuses like sagital sinus, transverse
sinus and sigmoid sinus either directly
or indirectly. The internal carotid artery
C and the VIth carnial nerve, i.e. abducent
nerve pass through this sinus. It is the
only anatomical location in the human
body where an artery passes through the
vein. The 3rd and 4th cranial nerves and
the mandibular and maxillary branches
of the 5th cranial nerve pass through the
lateral wall of the cavernous sinus.48 The
cavernous sinus communicates extra
cranially with the neck veins.
E D • The ophthalmic and angular veins
Figs 17.34A to E: Ludwig’s angina: (A) Cellulitis of submental and submandibular into the anterior facial vein (anterior
spaces with elevation of the tongue; (B) Lateral view; (C) Congestion and swelling of the connection).
floor of mouth; (D) Intubated with fiberoptic broncoscope; (E) Marking of incisions for • Through emissary veins with the
decompression pteygoid plexus of veins (posterior
connection).
antibiotics. As the patient has dysphagia, unless gangrenous tissue is present. The facial veins, unlike the veins of
oral antibiotics are not prescribed. The As the circulatory impairment occurs the extremities lack valves as the blood
choice of the antibiotic is usually the and the environments are ischemic flow through these veins is along the
penicillin group of antibiotics is high and hypoxic, due to mounting pressure gravity and the valves are not required to
therapeutic doses, as the infection is within the tissue plains, as prophylactic prevent the back flow of the blood. Due to
caused by streptococci. Crystalline peni­ major against the anaerobic infec­ this, any septic thrombophlebitis in these
cillin in a dose of 10 to 20 lacs IU IV, tion metronidazole may be prescribed. veins is capable to travel in a retrograde
every 6 hourly is given. Alternatively, Intravenous fluids are administered to manner and can extend intercranially
ampicillin 2 to 4 g/day is divided doses or maintain proper fluid and electrolyte through them in the cavernous sinus.
third generation cephalosporins can be balance and to fulfill the nutritio­ The area of the face between the inner
prescribed to make the spectrum of the nal requirement of the patient as the canthi of the eye and the corners of the
antibiotics wider aminoglyconsides like patient has difficulty in deglutition. mouth is called ‘danger triangle’ of the
gentamycin 1 to 4 mg/kg of body weight Other symptomatic treatments like ana­ face as severe sepsis in this area can
or amikacin 500 mg every 8 hourly may lgesics, anti inflammatory drugs may lead to septic thrombophlebitis and the
be prescribed.46,47 Metronidazole is be prescribed. The local care of the infection can spread in the retrograde
not the primarily prescribed antibiotic wound is taken by dressings. The drain manner and can extend in the cavernous
Odontogenic Infections 355

sinus through the angular and the


ophthalmic veins into the carvernous
sinus49 (Fig. 17.35A). This is the anterior
root of spread of infection. The other
route is through the emissary veins at
the base of the skull which communicate
with cavernous sinus. Any infection in
the infratemporal fossa at the base of
the skull can lead to spread of infection
to the cavernous sinus.50 The third route
is direct spread of extra cranial infection
into the cavernous sinus as a result
of osteomyelitis of the base of the skull
(Fig. 17.35B).
The carvernous sinus thrombosis
is a rare complication of maxillofacial
infections.51,52 The predisposing factors A
are:
• Immunocompromised patients
• Malnourishment
• Diabetes
• Leukemia
• Angranulocytosis
• HIV infection.

Clinical Features
• The patient is fibrile with body
temperature elevated to 104°F to
105°F and the patient is extremely
toxic.
• The level of consciousness is altered
as a result of increased intracranial
pressure.
• There is severe infection in the above
mentioned sites in the form of canine
space infection, boil, cellulites or
carbuncle in the nasal area, etc.
• The veins are blocked due to septic
thrombophlebitis and the ensuing
venous stasis leads to the edema of
B
the face especially around the eyes
(Figs 17.36A and B). Figs 17.35A and B: (A) Danger triangle’ of the face; (B) Venous network connecting with
• The fundus appears congested on the cavernous sinus;
fundoscopy and it could be the
initial sign of the cavernous sinus
thrombosis. Sometimes, the edema paralysis of the lateral rectus muscle superior orbital fissure syndrome is
of the eyelids is so severe that and diplopia results. precipitated.
fundoscopy may not be possible. • The 3rd and the 4th cranial nerves • Next due to thrombosis of the cavern­
• The eyeball is pushed out due to lie in the lateral wall of the sinus ous sinus spreads intracranially in the
increased intraorbital pressure owing and are involved later, producing other venous sinuses producing se­
to the edema and proptosis results. complete external opthalmoplagia, vere venous stasis and cerebral ede­
• The 6th cranial nerve passes through diplopia on all gazes. The pupil ma is precipitated. The signs of the
the cavernous sinus and thus it is the becomes fixed and dilated and raised intracranial pressure develop.
first nerve to be involved producing does not respond to light. Thus, a The papilledema developes.
356 Infections of Maxillofacial Region

Pathophysiology
Necrotizing fasciitis is a severe and
potentially fatal infection of the dermal,
fascial and subcutaneous layers of the
skin. These infections are marked by
the absence of clear local boundaries
or palpable limits. This explains the
frequent delay in recognizing the sur­
gical nature of the infection. These
infections could be clostridial or non-
clostridial.
It is classically associated with clos­
A B
tridial infections, but organisms such as
Escherichia coli, Klebsiella, Peptostrep­
Figs 17.36A and B: Cavernous sinus thrombosis, note massive facial edema and severe
tococcus and Bacteroides may also pro­
chemosis of conjuctiva
duce subcutaneous emphysema. The
more common anaerobic organisms
seen in necrotizing fasciitis of the head
• Further complications are as result to barrier). Clindamycin, third-generation and neck include Peptostreptococcus,
the raised intracranial pressure and cephlo­sporins, aminoglycosides are star­ Bacteroides melaninogenicus and Fuso­
severe intracranial sepsis like pyo­ ted in high therapeutic doses. The raised bacterium.55
genic meningitis, frank brain abscess. intracranial pressure is reduced by giving The most common cause of cervical
The erosion of the internal carotid IV manniotol. The role of steroids for necrotizing fasciitis (CNF) is dental infec­
artery leads to its rupture leading to reducing the raised intra cranial pressure tions. Immunocompromised patients
fatal intracranial hemorrhage or ca­ is controversial and there is risk of spread and those suffering from systemic ill­
rotid—cavernous fistula. The later is of infection. Neurosurgical intervention nesses such as diabetes mellitus are
characterized by proptosis and pulsa­ is mandatory. at an increased risk of developing this
tion of the eyeball corresponding to infection. It may also affect previously
heart beats. The death results due to Cervical Necrotizing Fasciitis healthy individuals (13–31%). It is in
either of these complications. Necrotizing fasciitis has various epony­ these patients who are infected with
The clinical signs are diagnostic ms. It has been called hospital gangrene Group A beta hemolytic streptococci
enough. However, initially fundos­ copy (Brooks,53 1966), Meleney’s gangrene that the infection spreads with a speed
may give important clue. The papill­ (Meleney54 1924), hemolytic streptococ­ to produce massive tissue infection. The
edema is suggestive of raised intracranial cal gangrene and synergestic necrotizing causative organism may be a single agent,
tension. CT scans and MRI are of great cellulitis. These infections can spread commonly Group A beta hemolytic
diagnostic value. Blood cultures can rapidly and cause significant morbidity streptococci or Staphylococcal Aureus
lead to identification of micro organisms and mortality. Aerobic and anaerobic or may be a polymicrobial infections.
leading to this infection and their sensi­ microorganisms resulting in massive Polymicrobial infections are caused by
tivity to the antibiotics. tissue destruction and toxic shock mixed aerobic and anaerobic pathogens.
syndrome cause necrotizing fasciitis. Synergy between them contributes to the
Immunocompromised pati­ ents are at pathogenesis of polymicrobial fasciitis,
Management an increased risk of developing necro­ i.e. synergistic gangrene.
The best management is prevention. In tizing fasciitis. Necrotizing fasciitis may In most cases, the pathogen gains
the patients who have the predisposition affect any part of the body; however it entry through a disruption of the skin
to this condition or spread of infection, most commonly affects the extremities, caused by trauma or surgery. Initially,
the infections in the anterior facial area abdominal wall and the perineum. there is cellulitis which leads to inva­
and at the base of the skull should be sion of the deeper tissues. Clinically,
managed with broad spectrum anti­ Definition at this stage skin changes of erythema
biotics and active surgical intervention Necrotizing fasciitis is an uncommon and edema are seen. Progressive tissue
in time. Once the cavernous sinus rapidly spreading soft tissue infection necrosis causes an invasion by the
thrombosis sets in, the mortality is high. of polymicrobial origin characterized by normal flora. Continuous bact­erial over­
The patient is given broad spectrum extensive necrosis and gas formation in growth and synergy, cau­ses a decrease
parenteral antibiotics preferable those the subcutaneous tissue and superficial in oxygen tension and development
which cross the BBB (blood brain fascia. of local ischemia and proliferation of
Odontogenic Infections 357

anaerobic organisms. In 4 to 5 days gan­ • Gas formation under the skin other supportive treatment57 (Figs 17.38
grene is evident and after 8 to 10 days • Frank gangrene of skin with slough­ to 17.40). It is essential that all areas of
necrotic tissue separ­ ates from the ing, exposing the underlying necroti­ necr­otic tissue be debrided. Excision to
underlying ischemic, but viable tissue. zing fascia and subcutaneous fat the point of bleeding tissue is a useful
Staphylococci and streptococci pro­ (Fig. 17.37B). guide for debridement. There are cer­
duce extracellular enzymes that damage Diagnosis: Is made on the basis of: tain centers which advocate the use
connective tissue. Bacterial metabo­ • Clinical history/features of hyperbaric oxygen for treating this
lism may produce insoluble hydrogen, • Radiographs condition.58
nitrogen, nitrous oxide and hydrogen • CT scan
sulfide gases that result in subcutaneous • Frozen section.
emphysema. Obliterative endarteritis FUNGAL INFECTIONS OF
and thrombosis of the subcutaneous Investigations THE MAXILLOFACIAL AREA
vessels along with necrotic superficial The routine investigations show leuko­
fascia and microbial colonization of the cytosis, band cells and toxic granules
skin and fascia is seen. The necrosis of in the leukocytes. The USG of the neck Mucormycosis
the fascia and obliteration of the blood shows the collection in the superficial Mucormycosis represents most fatal,
vessels renders the overlying skin ische­ planes and the superficial necrotic foci acute, opportunistic fungal infection.
mic and undergoes gangrenous changes and the CT scans are useful in detecting It is caused by fungi belonging to Mu­
and sloughing. Myonecrosis is rarely the deep seated collections and the coraceae family and includes Rhizopus,
seen except in clostridia infections. necrosis. Mucor, and Absidia; the Mucor is the
most common. The terms phycomyco­
Clinical Features sis and mucormycosis are used inter­
Management changeably to denote infec­tion by class
Systemic
The critical step in management is the phycomycetes. Mucor is found in soil
• High fever recognition of the condition and early, like Aspergillus, but the source of infec­
• Tachycardia aggressive surgical intervention.56 These tion in mucormycosis is mucor found in
• Weakness infections require a rapid diag­nosis as oral cavity, which is a part of normal oral
• Nausea mortality rates up to 76 percent have microbial flora.
• Sepsis been reported without early intervention. It presents in six clinical forms:59
• Hemolysis Mortality is higher in patients over 1. Rhinoparanasal and rhinocereberal:
• Intravascular volume depletion.
50 years of age, those with associated The entry portals of this variant are
syste­mic illnesses like diabetes mellitus mucosa of mouth, nose, paranasal
Local
or peripheral vascular diseases and when sinuses.
• Affected area becomes swollen and there is a delay in diagnosis. Pain out of 2. Pulmonary: It is seen in patients
erythematous proportion to other clinical findings is with malignancy.
• Sudden pain, edema and generalized an important clue to the diagnosis of this 3. GIT: It is seen in malnourished
toxicity (Fig. 17.37A) condition. Treatment involves wide local patients.
• The skin overlying becomes dusky and serial surgical debridement supp­ 4. Cutaneous: It is most often seen in
with purple mottling orted by intravenous antibiotics and burns patients.
5. CNS.
6. Disemminated: It is rare, but very
severe.

Pathogenesis
Mucormycosis is a rare opportunistic
infection that usually affects patients
who have a depleted immunological
status or uncontrolled diabetes. Depen­
ding on the immunological status of the
host it may present in any of the above
six forms. Rhinicerebral and pulmonary
variants are most commonly seen
A B in diabetic patients whereas the GIT
Figs 17.37A and B: CNF: (A) Pitting edema due to extensive cellulitis; variant is seen in malnourished patient.
(B) Subsequently resulting into gangrene of the skin Inhalation of spores of this fungus is
358 Infections of Maxillofacial Region

the primary portal of entry. However, the periorbital fat leads to widespread Rhinocerebral Mucormycosis
in cases of cutaneous variant, the entry maxillary and orbital involvement. Once
portal is breach in the skin. After its the infection enters the orbit, it can Symptoms
entry, the fungus grows and invades enter the cranial cavity either through • Facial pain/headache.
the tissues, especially blood vessels and the blood vessels or by direct extension • Impaired mental state.
elastic lamina of arterioles which further through the superior orbital fissure. • Fever.
leads to thrombosis and tissue necrosis. Disseminated disease is due to ex­ • Orbital involvement: Orbital cell­
The fungus has affinity for adipose tissue tension of the primary disease in severely ulitis, loss of extraoccular muscle
and spreads along the buccal fat pad and immunocompromised patients. function followed by proptosis, con­
junctival swelling, loss of vision due
to retinal artery stenosis (Figs 17.41A
to F).
• Cranial nerve involvement mani­
fested as pupillary dilation, ptosis.
This is a marker of poor prognosis.
• CNS involvement: Meningoen­
cephalitis, brain abscess, cavernous
sinus thrombosis.
• Involvement of nasal cavity: Rhi­
norrhea, bloody discharge, necrosis
of nasal turbinates and septum, ne­
crotic lesions of hard and soft pal­
ate which appear as sharply demar­
cated black eschars on mucosa. The
A B mucosa might also appear ischemic
and cyanotic before ulceration is
produced. Anesthesia of the mucosa
might also be present.

Pulmonary Mucormycosis
Pulmonary mucormycosis is predomin­
antly seen in patients with malignan­
cies. It shows a significant neutropenia
due to the chemotherapy taken for
C D E the hematologic malignancies. Many
patients are on broad-spectrum antibi­
Figs 17.38A to E: CNF managed with decompression,
serial debridement and skin grafting otics.

A B C
Fig. 17.39A to C: CNF treated with serial debridement and skin grafting
Odontogenic Infections 359

A B C

D E F
Figs 17.40A to F: CNF treated with liberal fasciotomy incision (surgical decompression) and debridement of necrotic fascia

A B C

D E F
Figs 17.41A to F: Rhinocerebral mucormycosis in a 55-year-old, diabetic woman,
treated with surgical debridement and amphotericin B
360 Infections of Maxillofacial Region

They present with fever, dyspnea, include the study of intracranial con­ 5. Mandel L, Baurmash H. Submasse­
cough followed by hemoptysis and tents in case of changes in mental status. teric abscess. Oral Surg Oral Med Oral
pulmonary infarcts. Fatal pulmonary Angiography of ICA can be done if its Pathol. 1958;11:1210–9.
hemorrhage due to erosion of major involvement is suspected. However, 6. Balatsouras DG, Kloutsos GM, Proto­
blood vessels can also occur. Pulmonary its involvement is associated with an papas D, et al. Submasseteric abscess.
infiltration, consolidation and cavitation increased mortality rate. J Laryngol Otol. 2001;115:68-70.
occur in high percentage of patients. 7. Nishimura T, Okabe Y, Furukawa M.
Management A chronic organized masseter abscess
Cutaneous Mucormycosis • Debridement of all necrotic tissue causing trismus resolved by hemimas­
Primary lesion appears as superficial, (see Figs 17.41A to F). seter myotomy. Auris Nasus Larynx.
painful, erythematous patches with • Orbital excenteration if the signs 1996;23:140-2.
central necrosis showing pustules and of orbital involvement are present, 8. Tart RP, Kotzur IM, Mancuso AA, et al.
papules. Secondary lesions are a result i.e. ophthalmoplegia, retinal artery CT and MR imaging of the buccal
of diss­emi­nated disease. stenosis, invasion of periorbital soft space and buccal space masses.
tissue, orbital apex syndrome. RadioGraphics. 1995;15:531-50.
GIT Mucormycosis • Correct acidosis and neutropenia 9. Smoker WRK. Oral cavity. In: Som PM,
This arises from organisms that enter • After the identification of fungus, Curtin HD, (Eds). Head and neck imag­
GIT through contaminated food. All start IV amphotericin B. After givi­ ing. 3rd edn. St. Louis: Mosby. 1996; pp.
portions of the GIT are susceptible to ng a test dose of 0.3 mg/kg, a daily 488–544.
contracting this lesion. Usually, this dose of 0.5 to 0.7 mg/kg and a total 10. Felice O’ryan. Orbital infections: Clini­
disease presents in the acute form and dose of 2500 to 4000 mg can be cal and radiographic diagnosis and
is rapidly fatal. Initial manifestations given. surgical treatment. 1988;46(11):991-7.
include abdominal pain and distension, • Monitor renal function periodically 11. Ash C, Cohen MA. Temporal-space
nausea, vomiting and fever. as renal toxicity is the complication infec­tions: report of three cases. J
of prolonged therapy with ampho­ Otolaryngol. 1996;25(6):416-20.
CNS Mucormycosis tericine. Lipid formulation of am­ 12. Mattucci K, Samet C. Pterygomaxillary
Usually it occurs due to primary disease photericin B causes increased blood space abscess. New York State Journal of
of nasal cavity and paranasal sinuses. It levels of the drug with decreased re­ Medicine. NY State J Med. 1974;74: 1409.
is characterized by decreasing level of nal toxicity. 13. Zangenbrunner DJ, Dajani S. Pharyn­
consciousness, focal neurological signs, • Concomitant use of 5 fluorocytosine gomaxillary space abscess with ca­
hemiplegia, hemiparesis and cranial acts as synergistic and has a kidney rotid artery erosion. Arch Otolaryngol.
nerve involvement. sparing effect. 1971;94:447.
Isolated brain involvement is repo­ • Hyperbaric oxygen can be used. 14. Granite EL. Anatomic considerations
r­ted in IV drug abusers in patients • Overall survival is poor, i.e. less than in infections of the face and neck:
suffering from AIDS and leukemia. 50 percent. review of the literature. J Oral Surg.
Hemiplegia and facial necrosis are 1976;34:34.
indicators of poor prognosis. The most 15. Levitt GW. Cervical fascia and deep
commonly involved paranasal sinus is REFERENCES neck infections. Laryngoscope. 1970;
the ethmoid sinus followed by sphenoid 80:409.
and maxillary sinus. 1. Aya Ohshima. Anatomical consider­ 16. Paonessa DF, Goldstein JC. Anatomy
ations for the spread of odontogenic and physiology of head and neck
Diagnostic Procedures infection originating from the pericoro­ infections (with emphasis on the fascia
“Early diagnosis is key to saving patient” nitis of impacted mandibular third mo­ of the face and neck). Otolaryngol Clin
Hallmark of diagnosis is demonstra­tion lar: Computed tomographic analyses. North Am. 1976;9561.
of organisms on biopsy specimens. The OOOOE. 2004;98(5):589-97. 17. Schwarti HC, Bauer RA, Davis NJ, et al.
specimen is stained immediately with 2. Parhiscar A, Har-El G. Deep neck Ludwig’s angina: use of fiberoptic
Hematoxylin and Eosin stain. However, abscess: A retrospective review of laryngoscopy to avoid tracheostomy. J
more specific staining is done by Gomori 210 cases. Ann Otol Rhinol Laryngol. Oral Surg. 1974;32:608.
Methanamine Silver (GMS) stain. Culture 2001;110(11):1051-4. 18. Kitay D, Ferraro N, Sonis ST. Lateral
of the fungus is done using Saboraud’s 3. Joacim Stalfors. Deep neck space pharyngeal space abscess as a conse­
glucose agar. The mucor shows irregularly infections remain a surgical challenge. quence of regional anesthesia. J Am
shaped, non-septate hyphae with bran­ A study of 72 patients. Acta Oto-laryn­ Dent Assoc. 122(6):56-9.
ching at 90 degree angle. gologica. 2004;124(10):1191-6. 19. Mosher HP. Submaxillary fossa appro­ach
Diagnostic tools include CT scan 4. Bransby-Zachary GM. The submass­ to deep pus in the neck. Trans Am Acad
of paranasal sinuses, which might also eteric space. Br Dent J. 1948;84:10-3. Opthalmol Otolaryngol. 1929;34: 19.
Odontogenic Infections 361

20. Collier FA, Yglesias L. The relation of the 34. Janecka IP, Rankow RM. Fatal mediasti­ 47. Daniel Bross-Soriano. Management of
spread of infection to fascial planes in the nitis following retro­pharyn­geal abscess. Ludwig’s angina with small neck inci­
neck and thorax. Surgery. 1937;1:323. Arch Otol­aryn­gol. 1971; 93(6): 630-3. sions: 18 years experience. Otojournal.
21. Bezold F. Ein neuer Weg fFCr die Aus­ 35. Bryan CS, King BG, Bryant RE. Retro­ 2004;130(6):712-7.
breitung eitriger EntzFCndung aus den pharyngeal infection in adults. Arch Int 48. Ramanand Y. An atypical presentation
RE4umen des Mittelohrs aus die Nach­ Med. 1974;134:127. of cavernous sinus thrombosis. Indian
barschaft. Deutsche medi­ zinische. 36. Dzyak WR, Zide MR. Diagnosis and J Otolaryngol Head and Neck Surg.
Woch­enschrift. 1881;28:381-4. treat­ment of lateral pharyngeal space 2007;59:2.
22. Hall C. The parapharyngeal space: an infections. J Oral Maxillofac Surg. 1984; 49. David Goldenberg. Facial vein throm­
anatomical and clinical study. Ann 42:243. bophlebitis: A rare but potentially
Otol Rhinoi Laryngol. 1939;43:793. 37. Greene JS, Asher IM. Retro­pharyngeal lethal entity. Otolaryngol Head Neck
23. Alaani A. Parapharyngeal abscess: di­ abscess: a previously unreported symp­ Surg. 2000;122(5):769-71.
agnosis, complications and manage­ tom. Annal Emerg Med. 1984;13:615. 50. Herbert G Childs Jr. Thrombosis of the
ment in adults. European Archives of 38. Hay PD. The neck. Annal Roentgeono­ cavernous sinus secondary to dental
Oto-Rhino-Laryngology. 2005;262(4). lo. 1930;9:5. infection. Am J Orthodont Oral Surg.
24. William R. Dzyak. Diagnosis and treat­ 39. Wholey MH, Bruwer AJ, Baker HL. The 1942;28(7):B402-B413.
ment of lateral pharyngeal space infec­ lateralm roentgenogram of the neck. 51. Deji A. Ogundiya. Cavernous sinus
tions. 1984;42(4):243-9. Radiology. 1958;71:350. thrombosis and blindness as compli­
25. Petri Koivunen. Internal carotid artery 40. Endicott JN, Nelson RJ, Saraceno CA. cations of an odontogenic infection:
thrombosis and Horner’s syn­ drome Diagnosis and management deci­ si­ report of a case and review of literature.
as complications of paraph­ aryngeal ons in infections of the deep fascial JOMS. 1989;47(12):1317-21.
abscess. 1999;121(1): 160-2. spaces of the head and neck utilizing 52. M Wen-Der Yun. Cavernous sinus thr­o­
26. Shapiro SL. Deep cervical infection computerized tomography. Laryngo­ m­bosis following odontogenic and cer­
following tonsillectomy. Arch Otolarv­ scope. 1982;92:630. vicofacial infection. European Arc­hi­­ves
nuol. 1930;11:701. 41. Levine TM, Wurster CF, Krespi YP. of Oto-Rhino-Laryngology. 1991; 248:7.
27. Lifschutz J. Fatal hemorrhage resulting |Mediastinitis occurring as a complica­ 53. Brooks S. Civil War Medicine. Spring­
from retropharyngeal abscess. Arch tion of odontogenic infec­tions. Laryn­ field, 111, Charles C Thomas Co. 1966.
Oto­laryngol. 1931;14:149. goscope. 1986;96:747. 54. Meleney FL. Hemolytic streptococcus
28. Yannick G Amar. Intraoral drainage: 42. Alexander DW, Leonard JR, Trail ML. gangrene. Arch Surg. 1924;9:317-64.
recommended as the initial approach Vascular complications of deep neck 55. Dunbar NM. Necrotizing fasciitis:
for the treatment of parapharyngeal abscesses. Laryngoscope. 1968;78:361. mani­festations, microbiology and con­
abscesses. 2004;130(6):676-80. 43. Srirompotong Somchai. Ludwig’s an­ nection with black tar heroin. J Foren­
29. Archer WH. Oral Surgery. Philadelphia: gina: A clinical review. European Ar­ sic Sci. 2007;52(4):920-3.
WB Saunders, 1966; pp. 362. chives of Oto-Rhino-Laryngology. 2003; 56. John D Urschel. Necrotizing soft
30. Mosher HP. Submaxillary fossa appro­ 260(7):401-3. tissue infections. Postgrad Med J.
ach to deep pus in the neck. Trans Am 44. Burt R. Meyers Ludwig’s angina: Case 1999;75:645-9.
Acad Opthalmol Otolaryngol. 1929; report, with review of bacteriology and 57. De Backe. Management of necro­tizing
34:19. current therapy. AMJ Med. 1972;53(2): fasciitis in the neck. J Cranio Maxillofac
31. Ridder GJ, Technau-Ihling K, Sander 257-60. Surg. 1996; 24(6): 366-71.
A, et al. Spectrum and management of 45. Lieutenant Colonel Thomas R. Gaines. 58. Jallali N, Withey S, Butler P. Hyper­
deep neck space infections: an 8-year Penicillin in the treatment of patients baric oxygen as adjuvant therapy in the
experience of 234 cases. Otolaryngol with deep infections of the neck. Arch manage­ ment of necrotizing fasciitis.
Head Neck Surg. 2005;133(5):709-14. Otolaryngol. 1945;42(1):1-5. Am J Surg. 189(4):462-6.
32. Frank I. Retropharyngeal abscess. J Am 46. Esquivel Bonilla D, Huerta Ayala S, 59. Baker RD, Seabury JH, Schneidau JD Jr.
Med Assoc. 1921;77:517. Molina Moguel JL. Report of 16 cases of Subcutaneous and cutaneous mucor­
33. Richards L. Retropharyngeal abscess. Ludwig’s angina: 5-year review. Pract mycosis and subcutaneous phycomy­
New England J Med. 1936; 215:1120. Odontol. 1991;12(4):23-4, 28. cosis. Lab Invest. 1962;11:1091-1102.
18 Osteomyelitis of the
Facial Bones
Borle Rajiv M, Yadav Abhilasha, Arora Aakash

Osteomyelitis is defined1 as ‘an inflam­ helps in reparative and remodeling all the facial bones, the mandible is the
matory condition of bone that begins functions. As the age progresses the most common bone to be involved by
as an infection of medullary cavity and periosteum becomes less cellular and osteomyelitis due to the presence of
Haversian systems of the cortex and fibrosed thus, the periosteal source of more of compact bone and relatively
extends to involve the periosteum of the blood supply diminishes and so is the less cancellous bone. The lesser amount
affected area’. The meaning of the word reparative potential. The bone, marrow of cancellous bone leads to lesser blood
osteomyelitis is ‘osteon’ meaning bony, is enclosed in the cancellous bone. The supply unlike the other facial bones. The
‘myelos’ is marrow and the word ‘itis’ bone, marrow is made up of cancellous other facial bones (e.g. the maxilla) have
means inflammation. bone which is rich in osteoblastic thin cortical bone and more cancellous
precursor cells, reticuloendothelial cells, bone leading to more blood supply
APPLIED SURGICAL erythrocytes, granulocytes and platelets and less chances of the osteomyelitis.
and is highly vascular. The cortical The osteomyelitis of maxilla or other
ANATOMY
bone is made up of dense bone, which facial bones is very rare and whenever
The bone has essentially three struc­ contains a well-organized trabecular it occurs, the other predisposing condi­
tures, a cortical bone, a cancellous bone system connecting the bone marrow tions like immunosuppression,2 un­con­­
and the periosteum. The cortical bone with the cortical bone. It consists of trolled diabetes,3 sickle cell disorders,4
is present outside and is covered by the longitudinally oriented canals, the etc. are usually present and they should
periosteum, while the cancellous bone Haversian system, which is the central always be ruled out. The osteomyelitis
lies within the cortical bone. The facial canal having nutrient blood vessel. It of the jaw bones is more common as
bones are the flat bones and unlike the gives blood supply to osteocytes, which compared to rest of the facial bones
long bones the blood supply to these are lodged in lacunae (Figs 18.1A and B). as the odontogenic infections are the
bones is predominantly through the There are communicating canals most common source of infections in
nutrient vessels that enter the bone called the Volkmann’s canals. The Volk­ the maxillofacial area. The jaw bones
through the foramina and then they mann’s canals connect the Haversian provide anchorage to the teeth and are
branch out to form a network in the systems with each other. The Volkmann’s also commonly affected by odontogenic
cancellous bone. The other source of the canals also connect the bone marrow infections and the osteomyelitis.
blood supply is through the periosteum. to the periosteum, which envelops the
The periosteum has two layers, the outer cortical bone (Figs 18.1C and D). These PATHOPHYSIOLOGY
is fibrosed and provide the attachment well organized complex interconnected
to the muscles and derives blood supply systems provide nourishment for repair
OF OSTEOMYELITIS
through these attachments. The vessels and regeneration of bone. As the age pro­ The process leading to osteomyelitis
giving the periosteal supply run parallel gresses the bone marrow becomes less (OML) is initiated by acute inflamma­
to cortical surface of bone giving off cellular and fibrosed and its vascularity tion, hyperemia, increased capillary
nutrient vessels, which penetrate is also diminished. This brings down the permeability and infiltration of granulo­
cortical bone and anastomose with reparative potential of the bone. cytes. Tissue necrosis occurs as proteo­
the dominant nutrient vessel (e.g. the The facial bones by and large have lytic enzymes are released and vascular
inferior alveolar artery in mandible). The an excellent vascularity and thus, the thrombosis ensues. As the pus accumu­
inner layer of the periosteum is cellular incidence of osteomyelitis is fairly less lates, the intramedullary pressure increas­
and is called cambium. The cambium as compared to the long bones. Out of es resulting in vascular collapse, venous
Osteomyelitis of the Facial Bones 363

A B

C D

Figs 18.1A to D: Haversian system of the bone

stasis and ischemia. Pus travels through necrotic bone (sequestra) from viable Secondly, the calcium mobilization
the Haversian and nutrient canals and bone (Flow chart 18.1). Small sections of from the devitalized bone does not take
accumulates beneath the periosteum, el­ bone may be lysed completely, whereas place and hence, the sequestrated bone
evating it from the bone and thereby fur­ larger ones may be isolated by a bed of appears more opaque on the X-ray. As
ther reducing the vascular supply. granulation tissue encased in a sheath reparative mechanism the periosteal
Compression of the neurovascu­ of new bone (involucrum). Sequ­estra bone apposition also takes place and the
lar bundle accelerates thrombosis and may be revasularized, remain quies­ periosteal reaction is evident on the X-
isch­emia and results in osteomyelitis in­ cent, reab­sorb or be infected chronically ray. The lifting of the periosteum at the
duced (inferior alveolar in case of mandi­ and require surgical removal before the edges of the bony defect produces a tri­
ble) nerve dysfunction. Extensive perios­ infec­
tion subsides completely. Occa­ angular elevation called the Codman’s
teal elevation occurs more frequently in sionally the involucrum is penetrated by triangle.5 The initial radiological picture
children, presumably because the peri­ channels (cloacae), through which pus of an acute osteomyelitis is alteration
osteum is bound less firmly to bone than escapes to an epithelial surface. Bone and thinning of the trabecular pattern.
in adults. If pus continues to accumulate, surrounding a sequestrum sometimes While as the more opaque sequestrum
the periosteum is pene­trated and muco­ appears radiographically as less densely is separated from normal bone by ra­
sal and cutaneous abscesses and fistulas mineralized than the seque­strum itself, diolucent area (involucrum) and asso­
may develop. If this condition is treated because increased vascularity of adja­ ciated periosteal reaction is the picture
with antibiotics alone, without appropri­ cent vital bone creates a relative demi­ in chronic osteomyelitis. The sequestra
ate surgical intervention, the condition neralization. Ischemia causes increase formation leads to undermining of the
may progress to chronic form. in CO2 level, which attracts calcium due bone and renders it weak. Such a weak
Inflammation regresses, granulation to change in pH. The calcium deposition bone is liable to fracture even during
tissue forms, and new blood vessels lyse leads to increase in mineralization of the functional movements or on application
the bone, thus separating fragments of sequestrum (dystrophic calcification). of mild stress (pathological fracture).
364 Infections of Maxillofacial Region

Flow chart 18.1: Pathogenesis of acute and secondary chronic osteomyelitis of the jaws. – Anemia/sickle cell anemia
Pathway A shows the role of inflammation and pathway B the role of pus formation in – Tuberculosis
compromising blood supply of the infected bone, which can be considered as the final
– Malnutrition
common pathway in the formation of sequestra
– Agranulocytosis
A B – Leukemia
– Chronic alcoholism
– Febrile illness.
• Conditions compromising jaw vas­
cularity are:
– Radiation
– Paget’s disease, osteopetrosis, os­
teoporosis
– Fibrous dysplasia
– Peripheral vascular disease
– Malignancy
– Sickle cell anemia.

ETIOLOGY
The etiological factors for the oste­
omyelitis are6:
• Odontogenic infections
• Trauma
• Infections derived from periosti­
tis following gingival ulceration,
lymph nodes infected from furun­
Table 18.1: Factors-predisposing osteomyelitis cles, lacerations and peritonsillar
abscess.
Systemic factors compromising the host immunity • Infections derived by hematogenous
route—furuncle on face, wound
Diabetes mellitus Malnutrition
on the skin, upper respiratory tract
Autoimmune disorders Chemotherapy
infection, middle ear infection, mas­
AIDS Corticosteroid and other imm­uno­suppressive therapy
toiditis, systemic tuberculosis.
Agranulocytosis Alcohol and tobacco
The mechanisms of systemic diseas­
Anemia (especially sickle cell) Drug abuse
es/conditions predisposing to osteomy­
Leukemia Prior major surgery elitis (Adapted from Marx 1991) are as
Syphilis Herpes simplex virus (zoster) and cytomegalovirus under (Box 18.1).
infection
Many authors have tried to classify
Local and systemic factors altering bone vascularity the osteomyelitis in different ways. The
Smoking Osteoporosis basic classification as per the duration is
Diabetes mellitus Bisphosphonate-induced osteochemonecrosis acute, sub acute or chronic osteomyelitis.
Florid osseous dysplasia Other forms of osteonecrosis (mercury, bismuth, arsenic) The osteomyelitis can also be classified as
Fibrous dysplasia Tobacco per the specific or non specific infective
Paget’s disease Radiation therapy and osteoradionecrosis organisms precipitating infection and
Osteopetrosis (Albers-Schonberg Bone malignancy (primary or metastatic)
subsequently the osteomyelitis, as speci­
disease) fic or non specific infective osteo­myelitis
(Box 18.2).
Huddson’s classification is as given
in (Box 18.3).
PREDISPOSING FACTORS are enhanced if there is an underlying
local or systemic pathological of con­
CLINICAL FEATURES
The odontogenic infections are common dition (Table 18.1).
in occurrence, however majority of • Conditions compromising the Host The clinical features of osteomyelitis
them do not lead to osteomyelitis. The defense are (Fig. 18.2): can be enumerated as per the type of
chances of precipitation of osteomyelitis – Diabetes osteo­myelitis as follows:
Osteomyelitis of the Facial Bones 365

Box 18.3: Hudson’s classification7


• Acute forms of OML (suppurative and
non-suppurative include:
– Contiguous focus:
i. Trauma
ii. Surgery
iii. Odontogenic infections
– Progressive:
i. Burns
ii. Sinusitis
iii. Vascular insufficiency
– Hematogenous (metastatic): Develo­
p­ing skeleton (children)
Fig. 18.2: Interaction of host and pathogens. If the balance is shifted to the advantage of • Chronic forms of OML
the aggressor, deep bone infection will be established – Recurrent multifocal:
i. Developing skeleton (children)
ii. Escalated osteogenic activity
Box 18.1: Mechanism of precipitation of osteomyelitis due to various factors (age < 25 years)
– Garre’s:
Disease Mechanism facilitating bone infection i. Unique proliferative subperio­
steal reaction
Diabetes Diminished leukocyte chemotaxis, phagocytosis
ii. Developing skeleton (children
and lifespan; diminished vascularity of tissue due to
to young adults)
vasculopathy thus reducing perfusion and the ability for
– Suppurative or non-suppurative:
an effective inflammatory response; slower healing rate
i. Inadequately treated forms
due to reduced tissue perfusion and defective glucose
ii. Systematically compromised pati­­
utilization
ents
Leukemia Deficient leukocyte function and associated anemia iii. Chronic refractory OML
Malnutrition Reduced wound healing and reduction of immunological – Diffuse sclerosing:
response i. Fastidious organism
ii. Compromised host/pathogen
Cancer Reduced wound healing and reduction of immunological inter­­­face
response
Osteopetrosis (Albers- Reduction of bone vascularization due to enhanced
Schonberg disease) mineralization, replacement of hematopoietic marrow
causing anemia and leukopenia • Pus discharge from the gingival cre­
vice.
Severe anemia (particularly Systemic debilitation, reduced tissue oxygenation, bone
sickle-cell anemia) infarction (sickle cell anemia), especially in patients with
• Mobility of the teeth in the involved
a homozygous anemia trait area.
• Acute osteomyelitis may not show
IV drug abuse Repeated septic injections, spreading of septic emboli
(especially with harboring septic vegetation on heart pronounced radiological features,
valves, in skin or within veins) because to develop the same more
AIDS Impaired immune response than 30 percent calcium has to
be mobilized from the bone. The
Immunosuppression (steroids, Impaired immune response
cytostatic drugs)
radiological picture may range
from simple rarefaction of the bony
trabeculae (Fig. 18.3) to ‘moth
Box 18.2: Classification Acute Suppurative eaten’ radiolucency (Fig. 18.4). The
Historically accepted classification
Osteomyelitis offending tooth is present, which
based on clinical course • Deep intense pain. may show periapical rarefaction.
• Acute • High grade, intermittent fever. • A strongly positive radionucleotide
• Subacute • Constitutional signs of the acute scan along with the above.
• Chronic infection such as bodyache, malaise,
Infective leukocytosis, raised ESR, etc.
– Specific
• Paresthesia or anesthesia of lower
Subacute Suppurative
i. Tuberculosis
ii. Syphillis lip due to involvement of the inferior Osteomyelitis
iii. Actinomycosis alveolar nerve. The clinical signs and symptoms are
– Non-specific • The cause is usually, clearly identi­ less severe as compared to the acute
i. Pyogenic fiable in the form of acute infection condition and some of the signs are well
ii. Necrosis
associated with the tooth. established. The duration of the disease
366 Infections of Maxillofacial Region

A B

Fig. 18.3: Patchy rarefied radiolucent


lesion

C D
Figs 18.5A to D: Cutaneous sinus secondary to chronic osteomyelitis

ment or due to the immunity contr­o­lling stage for the first time and where the past
the infection, the condition slips into a history is not reliable.
Fig. 18.4: Osteomyelitis moth-eaten chronic form wherein the symptoms are The surrounding soft tissue is indur­
appearance on X-ray less severe, intermittent and persistent ated, thickened or woody in consistency.
unless comprehensive treatment is un­ Pain and tenderness are usually mild
is longer as compared to the acute dertaken. The abscess drains spontane­ and non-significant.
variety. ously on the skin or gin­gival surface lead­
• There is a deep seated, dull, pain, ing to a chronic pus discharging sinus,
RADIOLOGICAL FEATURES
anorexia and fever (101°F to 102°F). which is adherent to the bone through
• The teeth in the involved area an epithelized sinus tract and drains pus
Worth’s Criteria (1969)8
become loose and are tender on intermittently (Figs 18.5A to D). The in­
percussion. fected bone undergoes necrosis and gets • ‘Moth-eaten’ appearance (enlarge­
• The pus exudates through gingival separated from the normal bone, the ne­ ment of medullary spaces and
and cutaneous fistulas. crotic bone is called as the sequestrum. widening of Volkmann’s canals)
• Fetid oral odor may be present due It serves as the nidus of infection and the (Fig. 18.4)
to pus. pus collects inside the bone and the tis­ • Islands that is ‘seqeustrum’ (avascu­
• The cellulitis of the cheek may be sue plane intermittently. When sufficient lar necrotic bone, which har­ bors
present over the involved area. pressure is generated, it drains through micro­­organisms) with evidence
• The expansion of the bone due to the sinus. As the pus is drained out, the of trabecular pattern and marrow
periosteal reaction. sinus becomes non-draining. The sinus spaces (Figs 18.6A and B).
• The infection gets localized to form opening shows exuberant granulation The computerized tomography scans
an abscess in the adjoining soft tissue and as the sinus tract is epithe­ are very informative and useful in dete­
tissue. lized, it fails to heal even after the septic cting and assessing the osteomye­litis. It
• The regional lymph nodes get enla­ focus is eliminated. The cutaneous sinus gives accurate indication of:
rged and are discrete, soft and may sometimes be formed at a distance i. Bone destruction
tender. from the bony lesion. Sometimes more ii. Periosteal reaction (Fig. 18.7)
• Leukocytosis is not a consistent find­ than one sinus tracts are present. As iii. Medullary destruction
ing. the surrounding soft tissue is indurated, iv. Cortical involvement.
sometimes it becomes difficult to differ­ The MRI scan is more accurate
Chronic Osteomyelitis entiate between fungating malignancy, com­ pared to CT scans, which gives
As the acute symptoms subside, due to which is secondarily infected and an information about the bone marrow
antibiotic therapy without surgical treat­ osteomy­elitis if the patient is seen in this changes and the soft tissue changes.
Osteomyelitis of the Facial Bones 367

to diagnose OML. When the patient’s age


and clinical findings make the diagnosis
equivocal, as when a neoplasm is sus­
pected, the Tc scan may be followed by
a gallium scan (Ga). Positive findings on
both tests usually confirm the infectious
nature of the disease. When the Tc scan
result is positive and the Ga scan results
A B are negative, OML probably is not the
Figs 18.6A and B: Radiopaque seque­strum primary disease. Ga uptake that exceeds
Tc uptake indicates active inflammatory
disease. In chronic OML reduced Ga
lide that emits light, is then used to accumulation in the follow-up scan
obtain images of the isotope containing is useful indicator for termination of
areas. The resulting image shows the therapy in OML.
distribution of radionuclide in areas of Recently positron emission tomo­
increased bone activity. The complete graphy (Figs 18.8A and B) using radio­
bone scan has three phases: isotopes of phy­siologically active com­
• Flow study consists of serial images pounds such as glucose,11 ammonia and
at the intervals of 3 to 4 seconds flouride have shown greater promise
during 1 to 2 minutes after injection in mapping out varying margins of
of the drug. metabolic activity.
• Blood pool study consists of a single
Fig. 18.7: Periosteal reaction image obtained 5 to 10 minutes after
PRINCIPLES OF TREATMENT
injection.
• Delayed study includes multiple OF OSTEOMYELITIS
Specialized Investigations views obtained 2 to 4 hours after • Thorough clinical evaluation and
In the borderline cases, the specialized injection. correction of host defense deficien­
investigations are carried out to de­ Positive Tc scan results can be useful cies.
tect the bony changes at an early stage, in confirming the diagnosis of acute • Administration of empirical antibiot­
which helps in detection of the osteomy­ OML, although bone scan findings may ics.
elitis, vascularity and reparative activity be negative very early in the disease. • Imaging to rule out bone tumors.
in the bone. Addition of gallium 67 to technetium • Removal of the septic foci such as
(Tc) 99 aids in distinguishing OML from loose teeth and sequestra.
Bone Scintigraphy malignancy and trauma.10 • Administration of culture guided
Bone scanning (scintigraphy), radion­ If neoplastic disease is not suspec­ted antibiotics; repeated cultures
uclide imaging, or skeletal scintigraphy as the cause of symptoms due to the age, • Possible placement of irrigating
is useful in determining the presence clinical findings or laboratory studies, a drains/polymethylmethacrilate–an­
of reactive bone thus, it is particularly positive Tc scan result alone is sufficient tibiotic beads
helpful in the diagnosis of bone disease. It
helps in the diagnosis and management
of osteomyelitis of the jaws, which is
based on reactive bone formation rather
than demineralization. The changes are
seen as early as 3 days after the onset of
symptoms of OML.
In this bone is scanned using Tc-lab­
eled ethylene diphosphonate,9 which
is administered intravenously. The
radioi­sotope is distributed to the entire
skeleton and concentrated in areas
of increased blood flow and osteo­
blastic activity. A rectilinear scanner
or scintillation camera, both of which A B
contain sodium iodide, a crystal nuc­ Figs 18.8A and B: Positron emission tomographic scan in case of osteomyelitis
368 Infections of Maxillofacial Region

• Surgical management by seques­ Flow chart 18.2: Decision tree for diagnosis of osteomyelitis
trectomy, debridement, decortica­
tion, resection, reconstruction
• Hyperbaric oxygen therapy
Marx (1992) has proposed certain
guidelines for three management of
osteomyelitis as given in Box 18.4.
By and large the diagnosis of osteo­
myelitis on clinical and radiological find­
ings is easy. But, in the early, borderline
and cases with atypical presentation the
evaluation of the cases should be under­
taken as depicted in the Box 18.5.

Decision Tree12
Decision tree for diagnosis of osteo­my­
elities is illustrated in Flow chart 18.2.

Medicinal Treatment
The medicinal treatment of osteomye­
litis comprises of administration of an­
tibiotics, supportive treatment, dietry
suppliments and other symptomatic

Box 18.4: Treatment guidelines for acute


and chronic osteomyelitis (Marx 1992)

•  isrupt the infectious foci


D
interventions such as administration fractures of the jaw, hospital acquired
• Debride any foreign bodies, necrotic
tissues, or sequestra
of analgesics, antipyretics and anti in­ infections or hematogenous infections
• Culture and identify specific pathogens flammatory drugs. The osteomye­litis of in a compromised host. The selection
for eventual definitive antibiotic treat­ the jaw bones is commonly secondary of the specific antibiotics depends upon
ment to odontogenic infections and thus, the the culture and sensitivity report of the
• Drain and irrigate the region microbial flora is similar to oral flora pus samples taken from the lesion. The
• Begin empiric antibiotics based on comprising of gram positive microor­ antibiotic regimen for osteomyelitis of
Gram’s stain ganisms such as streptococci, staphy­ the jaws recommended by Topazian13
• Stabilize calcified tissue regionally lococci. These organisms are sensitive is as shown in Box 18.6.
• Consider adjunctive treatments to en-
to beta lactam antibiotics. Owing to
hance microvascular reperfusion: Treph-
ination, decortication, vascular flaps the hypoperfused environments and Local Antibiotic Therapy
HBO therapy the necrotic tissue, the facultative an­ Closed wound irrigation suction: After
• Reconstruction: as necessary following erobes also invade making it a mixed intraoral debridement, sequestrectomy
resolution of infection. infection. Thus, routinely the beta lac­ and saucerization or decortications,
tam antibiotics (Penicillin, amoxicillin, two small pediatric nasogastric feed­
ampicillin and cephalosporins) along ing tubes, catheters or polyethylene
Box 18.5: Decision tree
with the drugs like metronidazole (for drain tubes, 3 to 4 mm in diameter and
• Conventional radiograph-Positive-OML anerobic infections) are suited for em­ 6 to 10 inches long in length are placed
stop pirical antibiotic therapy. However, against the bony bed through separate
Negative OML highly suspected upon the culture and sensitivity if other skin incisions at some distance and se­
• Technetium bone scan Positive-OML- organisms such as gram negative are cured with sutures.
stop
detected then aminoglycosides can be One tube is connected to low pres­
Negative OML highly suspected
• Ga67 or IN111 WBC scan-Positive-OML administered. The chances of infec­ sure suction to allow drainage of pus
stop tions from the other organisms apart and serum and another is kept patent
Negative OML highly suspected then from those which are the part of oral to provide a route through which local
• MRI or CT-Positive-OML stop flora, increase in case of osteomyeli­ antibiotics are instilled in very high con­
Negative-OML stop tis secondary to grossly contaminated centrations.14
Osteomyelitis of the Facial Bones 369

Box 18.6: Topazian protocol for antibiotic regimen for osteomyelitis

Regimen I For hospitalized/medically com­­pro­ Aqueous penicillin, 2 million units IV q4h, plus metronidazole, 500 mg IV q6h.
mised patients or when intravenous When improved for 48–72 hours, switch to:
therapy is indicated Penicillin V, 500 mg PO q4h, plus metronidazole 500 mg PO q6h, for an
additional 4–6 weeks.
OR
Ampicillin/salbactum 1.5–3 g IV q6h,
When improved for 48–72 hours switch to:
Amoxicillin/clavulanic acid (Augmentin) 875/125 mg PO bid, for an additional
4–6 weeks.
Regimen II For out patient treatment Penicillin V 2 g, plus metronidazole 0.5 g q8h PO, for 2–4 weeks after last
sequestrum removed and patient without symptoms.
OR
Clindamycin, 600–900 mg q6h IV; then clindamycin 300–450 mg q6h PO
OR
Cefoxitin 1 g q8h IV or 2 g q4h IM or IV, until no symptoms, then switch to:
Cephalexin 500 mg q6h PO, for 2–4 weeks
For penicillin allergic patients:
Clindamycin (as above)
Cefoxitin as above, for allergy not of anaphylactoid type.

Negative Pressure Healing15 Antibiotic should be bacteriostatic, Sequestrectomy and


Negative pressure healing occurs by or preferably bactericidal and be Saucerization
three mechanisms: sufficiently stable in the face of high
Sequestrum formation is a classical sign
1. Altered blood flow: Vacuum inc­ temperatures to prevent degradation of secondary chronic and advanced
reases the vascularity of wound during the curing the pro­cess of theacute osteomyelitis cases. Usually a time
edges by increasing blood flow cement. frame of at least 2 weeks after onset of
diameter, velocity, blood volume, Indications for using beads: infection is necessary until presenta­tion.
endothelial proliferation and angio­ • Infection that is refractory to tradi­
In general, sequestra are confined to the
genesis and thus promotes healing. tional treatment. cortical bone, but may also be cancellous
2. Mechanical deformation: Because • Decreased blood flow to the infected
or cortico-cancellous. Once a sequestrum
of the negative pressure there is area. is fully formed, it may persist for several
stretching of the cells which causes • Immunocompromised host. months in untreated cases before be­
disturbances in the extracellular and • Medically compromised patient. ing resorbed or spontaneously expelled
intracellular skeleton. To overcome through the oral mucosa or the facial skin.
this there is increased mitotic acti­ Surgical Management Resorption of sequestrum is achieved by
vity, which in turn promotes healing. Surgical management of acute and lytic activity of the osteoclast cells in the
3. Pressure gradient: Pressure itself chronic osteomyelitis is depicted in surrounding granulation tissue. Gradual­
pulls cytotoxic substances, bacteria, Fig. 18.9. ly the granulation tissue may ingrow the
normal cells towards infected site,
reduces interstitial edema and thus
promotes healing.

Antibiotic Impregnated Beads


Used in the treatment of OML to deliver
high concentrations of antibiotics
into the wound bed and in immediate
proximity to the infected bone.
Gentamycin-PMMA beads16: The
unique advantage of using antibiotic
impregnated PMMA beads is in the fact
that a very high local concentration Fig. 18.9: Surgical management of acute and secondary chronic
of antibiotics can be delivered with osteomyelitis. Dep­en­­ding on the extent of the infected bone,
minimal concomitant systemic levels. surgery has to be adapted, resulting in a smaller or larger procedure
370 Infections of Maxillofacial Region

medullary cavity. This allows direct ac­


cess to be formed and forming seques­
tra, granulation tissue, and affected
bone (Box 18.7).
Saucerization can be useful in early
acute osteomyelitis cases and cases
of limited extent. In early stages of the
infection, it helps in decompression of
the medullary cavity and allow ready
A B extrusion of pus, debris, granulation
tissue and avascular fragments. Since
the removal of bone by this procedure is
limited, the strength of the mandible is
not critically jeopardized and healing by
secondary intention is suffcient. While
the saucerization procedure is frequently
used in mandibular osteomyelitis, it is
rarely needed in the maxilla. Because
of its thin cortex, sequestra usually
form more rapidly and are exposed to
C D the oral cavity, creating wider defects
Figs 18.10A to D: Maxillary osteomyelitis in an uncontrolled diabetic patient treated and possibly causing oroantral fistulas
with sequestrectomy (Figs 18.11, 18.12 and 18.13).
• Surgical removal of dead necrotic
bone is sequestrectomy.
sequestrum and promote its degrada­ Saucerization describes the ‘unro­ • Helps in establishment of local
tion. If sequestra are not fully removed ofing’ of the oral-faced jawbone to ex­ micro­vascular proliferation.
in treatment, partial, superficial heal­ pose the medullary cavity for subse­ • Saucerization is the unroofing of the
ing may occur. Because sequestrum are quent thorough debridement. The bone to expose the medullary cavity
avascular, they are poorly penetrated by mar­gins of necrotic bone overlying the for thorough debridement (Box 18.5).
antibiotics or HBO and hence, are ideal focus of osteomyelitis are excised creat­ • Permits removal of formed and
bread­ ing grounds for bacteria. They ing direct visualization of the infected forming sequestra.
serve as sources of exacerbations of the
osteomyelitis when pus and granula­ Box 18.7: Surgical technique for saucerization
tion tissue accumulates around them. In
rare cases of osteomyelitis of the jaws, a • Access to the bone by creating a mucoperiosteal flap, usually using a gingival crest
sterile abscess formation around the se­ incision
questrum (Brodie’s abscess), common • Refection of fap should be as limited as possible to preserve local blood supply
• Affected teeth (loosened and other dental foci within the affected area) are extracted
to long bone osteomyelitis, occurs.13
• The lateral cortex of the mandible is reduced using burs or rongeurs, until the sufficient
Once the sequestrum is formed com­
bleeding bone is encountered at all margins, approximately to the level of the unattached
pletely, it may be removed with minimal mucosa, thus producing a saucer-like defect
surgical trauma (Figs 18.10A to D). This • Local debridement is performed by removing granulation tissue and loose bone
minimally invasive procedure reduces fragments from the bone bed using curettes
subsequent bone and tooth loss. While • The debrided area is thoroughly irrigated with sterile saline solution with or without
this approach may be applicable in additional antibiotic such as neomycin
cases of localized osteomyelitis with • If there is substantial local bleeding due to hyperemia caused by the inflammatory
process, a medicated pack may be placed and serve as local compression device
superficial sequestrum formation, it is
• The buccal flap is trimmed and a medicated pack (such as iodoform gauze lightly covered
contraindicated in advan­ced cases with with antibiotic and local steroid ointment is placed for hemostasis and to maintain the
protracted spreading of the infection flap in a retracted position. The pack is placed firmly without pressure and retained by
and sequestrum formation in more several non-resorbable sutures, extending over the pack from the lingual to the buccal
profound regions of the bone. Here a flap
more aggressive surgical debridement • The pack is remained in situ for several days up to 2 weeks or even more in some instances
is necessary, which clearly must exceed and may be replaced several times, until the surface of the bed of granulation tissue is
epithelialized and the margins have healed
the sole removal of sequestrum.
Osteomyelitis of the Facial Bones 371

Decortication
Decortication was first advocated
for treatment of osteomyelitis of the
mandible in 1917 and further described
by Mowlem.17 In advanced acute and
secondary chronic osteomyelitis of
the jaws, especially the mandible, use
of decortication promotes resolution
based on the premise that the affected
cortical bone is avascular and harbors
microorganisms. The medullary cavity
A B C
shows destruction and is largely replaced
Figs 18.11A to C: Sequestrectomy and saucerization by granulation tissue and pus. Parenteral
or per oral administered antibiotics
cannot reach the affected region. Wait­
ing for sequestrum formation and
reducing surgery to sequestrectomy is
not an option because of the advanced
stage of the infection with risk for further
spread, abscess formation and cellulitis.
Furthermore, the disadvantages asso­
ciated with prolonged antibiotic therapy
A B
may become more prominent with
time.
The major purpose of the decorti­
cation procedure is to remove the chron­
ically infected cortex of the jaw­bone and
gain access to affected medullary cavity
to allow a sufficient decompression of
intramedullary pressure and meticulous
surgical debridement under direct visu­
alization (Figs 18.14 to 18.16). Further­
more, this procedure allows bringing
C D well-perfused tissue (e.g. masseter mus­
Figs 18.12A to D: Chronic osteomyelitis treated with sequestrectomy and curettage (Case 1) cle) into contact with bone, promoting
further healing.
• Lateral and inferior cortex removed.
• Irrigation and debridement.
• Trimming up to bleeding point in
vital bone.
• Refers to removal of chronically
infected cortex of bone.
• The lateral and inferior border cor­
tex is removed 1 to 2 cm beyond the
A B C
affected area, thus providing access
to the medullary cavity.
• Used as initial treatment of primary
and secondary chronic OML or
when initial conservative regimens
have failed.
After the surgical procedures such
as sequestrectomy, saucerization or
D E cortico­tomy are undertaken, the ensu­
Figs 18.13A to E: Chronic osteomyelitis treated with sequestrectomy and ing surgical defect is not closed primar­
curettage (Case 2) ily and is packed open leaving in situ the
372 Infections of Maxillofacial Region

gauze pack impregnated in the 5 percent only wound hygiene maintenance is in­
povidone iodine solution or acriflavine. dicated (Figs 18.15 and 18.16).
The wound is an infected wound and
is unlikely to heal by primary intention Resection and Reconstruction
and heals by secondary epithelization. In the resistant cases of OML, which do
Daily care of the wound comprises of ir­ not respond to the routine treatment
rigation with saline, 5 percent povidone or if there are associated conditions
iodine solution and hydrogen peroxide. like osteopetrosis, irradiated bone, for
The pack is changed daily and its size is complete, elimination of the infective
A B reduced gradually. After the base gets process resection of the involved segment
Figs 18.14A and B: Lateral and inferior granulated and the epithelization be­ of the bone and then reconstruction of
cortex removal gins, the pack may be discontinued and the defect by autologous bone grafts and

A B C
Figs 18.15A to C: Decortication: The margins of the intended area of decortication are marked with a burr. Note that the distal and mesial
borders are selected in an area, where well-vascularized and healthy bone are assumed, usually 1–2 cm beyond the affected area. When
performing the osteotomies, it should be stressed that they are strictly limited to the buccal cortex of the mandible to avoid damage to
the inferior alveolar nerve

A B
Figs 18.16A and B: Mandible after completed decortication and surgical debridement. The remaining bone represents the remaining
vital bone tissue
Osteomyelitis of the Facial Bones 373

the reconstruction plates is advocated. do not have protective intracellular Box 18.9: Complications of HBO therapy
However, unless the infection has totally superoxide scavenging enzymes.
• Most of the complications associated
resolved the reconstruction should be • Many exotoxins liberated by the with HBO delivery result from barometric
differed as the chances of rejection of pathophysiologic activity of micro­ pressure changes or oxygen toxicity
the graft or the implant due to infection organisms are rendered inert by ex­ • Eustachian tube dysfunction
are optimum.18 posure to elevated partial pres­sures • Tympanic membrane rupture
of oxygen. • Oxygen toxicity
Trephination • Tissue hypoxia is intermittently • Ear sinus, or tooth pain
Trephination is the creation of holes or reversed by the HBO therapy, mimi­ • Decompression sickness
windows in the overlying cortical bone cking the tissue level during wound • Pneumothorax
adjacent to the infectious pro­cess for the healing by saturating the interstitial
decompression of the medullary com­ plasma above the normal levels Box 18.10: Contraindication for hyperbaric
partment. It provides multiple surgical produced by the hemoglobin oxygen oxygen (HBO) therapy
transcortical ports that allow transuda­ transport mechanism.
• Pneumothorax
tive weeping and vascular communica­ • Positive enhancement of neoan­
• COPD
tion between the periosteum and the giogenesis in the aerobic portion
• Optic neuritis
medullary cavity.19 of the proliferative phase of wound • Acute viral infection
healing. • Acute seizures
Hyperbaric Oxygen Therapy • URI
The hyperbaric oxygen (HBO) thera­ Hyperbaric Oxygen Chamber • Pregnancy
py is indicated in the cases of osteo­ The patient is placed in a chamber. Oxygen • Thoracic surgery
myelitis, which do not respond to is given by mask or by hood. It is given for • Ear surgery
routine treatment due to presence of 5 days per week for 30, 60, or more dives • Malignant disease
certain associated conditions like irradi­ at 2.4 ATA for 90 minutes, while breathing
ated jaw, osteosclerosis, osteope­trosis, 100 percent oxygen twice daily. Box 18.11: Types of osteomyelitis
and geriatric patients. It facilitates the Hart and Mainous22 (1976) and Marx23
healing of the bone and also helps in (1983) protocol (Box 18.8) recommends • Infantile osteomyelitis
combating the infection. The HBO 60 sessions with 2 ATA of oxygen. • Acute pyogenic osteomyelitis
therapy involves the intermittent, twice The complications of hyperbaric oxy­ • Chronic suppurative
daily, inhalation of 100 percent humidi­ gen therapy are summarized in Box 18.9. • Chronic non-suppurative
fied oxygen under 2 atmospheric pres­ The hyperbaric oxygen therapy is • Garre’s osteomyelitis
sure (ATA) for 90 minutes. HBO reduces contraindicted in the conditions men­ • Actinomycosis
• Tubercular osteomyelitis
the hypoxia within the affected tissues tioned in the Box 18.10.
• Syphilitic osteomyelitis
and stimulates angiogenesis in the hy­
povascular tissues.20 It enhances phago­
cytic activity of leuko­cytes to stimulate DIFFERENT TYPES OF
fibroblast growth, increase in collagen OSTEOMYELITIS AND THEIR Infantile Osteomyelitis
formation and promote growth of new (Synonym: Osteomyelitis maxillaries neo­
capillaries.
CLINICAL PRESENTATIONS natorum)
Five aspects of HBO beneficial in the Different types of osteomyelitis and Infantile osteomyelitis was first des­
treat­ment of OML of jaws.21 their clinical presentations is given in cribed by Rees24 in 1847. It can occur
• Enhances the lysosomal degradation Box 18.11. within first 9 months of life and as early
pot­ential by enhancing the develop­ as 1 week after birth.
ment of intracellular halides in
PMN’s and oxygen radicals that are Box 18.8: Marx protocol (1983) Etiology
major components of the catabolic • Hematogenous infection.
enzymes of the macrophage lyso­ • 30 initial dives, if improved then 60 dives • Perinatal trauma to the oral mucosa
completed
some. Formation of these enzymes from obstetrician’s finger, mucus
• Otherwise, sequestrectomy + 30 dives
is depressed in hypoxic environment • If wound dehiscence, resection + 60 suction bulb and unhygienic condi­
such as found in osteomyelitic foci. dives and 20 dives after 10 weeks tion during the child birth.
• Free radicals of oxygen are formed • Patient with pathological fracture, oro­ • Infection involving maxillary sinus.
during HBO therapy that is toxic to cu­taneous fistula are given 30 dives • Unhygienic human or artificial nip­
many pathogenic anaerobes that more prior going to resection. ples.
374 Infections of Maxillofacial Region

Clinical Features Chronic Sclerosing Differential Diagnosis


• Sudden onset, very acute course. Osteomyelitis • Infantile cortical hyperostosis:29 It
• General constitutional symptoms, occurs in young infants and involves
high grade fever. Chronic sclerosing osteomyelitis is an a number of bones. The clavicles
• Facial cellulitis centered around inflammatory, non-suppurative, painful and ulnae are usually involved, but
orbit, intercanthal swelling, palpebral disease with a protracted course. It the mandible is invariably involved.
edema, closure of eye, conjunctivitis, commonly affects basal bone and The condition is uninfluenced with
proptosis. alveolar process of mandible. It is usu­ antibiotics. The disease usually is
• Inability to suckle and signs of dehy­ ally unilateral and produces recurrent self- limiting and eventually regres­
dration. swelling and pain.25 It is usually caused ses.
• Subperiosteal abscess in alveolar by a low-grade infection. • Ewing sarcoma.
region. • Osteosarcoma.
• Fistulae or pus draining tracts on Radiographic Findings • Fibrous dysplasia: Clinically it is indi­
alveolar mucosa. Diffuse intramedullary sclerosis with sting­uishable from Garre’s osteo­
• Sloughing out of bone and teeth poorly defined margins is noted with myelitis. The only differentiating
buds. occasional focal areas of radiolucency feature is radiological appearance of
and radiopacity. ‘onion skin appearance’ in Garre’s
Microorganisms osteomyelitis.
• Staphylococcus aureus Treatment
• Haemophilus influenzae • Antibiotics Treatment
• Streptococci • Removal of source of infection The treatment comprises of removal
• Pneumococci • Wound irrigation of infected tooth and curettage of the
• Neisseria gonorrhoeae • Debridement. socket. Surgical recontouring of the
• Coliform bacilli expanded bone is undertaken at a later
Radiographic findings are noticed in stage. If the teeth are to be conserved
late stages, sequestra and necrotic tooth Garre’s Osteomyelitis then the endodontic therapy should be
germs. Garre’s osteomyelitis is irritation indu­ started to treat the offending teeth.30 As it
ced focal thickening of periosteum and is the low-grade infection, the antibiotic
Differential Diagnosis cortical bone. It is usually caused in therapy is not aggressive unlike the
The condition needs be differentiated the children as a result of low-grade pyogenic osteomyelitis.
from the infantile cortical hyperostosis. infection.26 The infection leads to perios­
teal irritation and it stimulates the pro­ Actinomyces Osteomyelitis
Treatment liferation and bone apposition.27 The
• Broad spectrum antibiotics. characteristics of this type of osteo­ Introduction
• Culture and sensitivity test for myelitis are: Actinomycosis is an infectious disease
specific antibiotic therapy. • It is a non-suppurative inflammatory caused by a slender gram positive, rod-
• Incision and drainage of fluctuant process. shaped bacterium, Actinomyces israelii,
abscess. • It is characterized by peripheral sub­ that exhibits a number of simple fungus
• Irrigations of sinus tracts with nor­ periosteal bone deposition. like characteristics, such as tendency
mal saline, 5 percent povidone io­ • It occurs primarily in children and to grow as a mass of rounded bodies
dine and hydrogen peroxide. young adults. (clubs) and filaments in tissues (hence
• Supportive therapy such as paren­ • The common etiological factors are the term ray fungus), low virulence
teral feeding. carious tooth, soft tissue infections. and a property of eliciting suppuration,
• Sequestrectomy as indicated by • It produces a localized, hard, non- necrosis and a chronic granulomatous
clinical and radiographic findings. tender swelling of lateral and inferior response.
• Two weeks postoperative intrave­ cortices of the mandible.
nous antibiotics, followed by an ad­ • As it is a low-grade infection, the lym­ Clinical Presentation
ditional 6 weeks administration of ph­ad­enopathy, hyperpyrexia and • It may involve soft tissue or bone
oral anti­biotics. leukocytosis are seldom present. (actinomyces osteomyelitis) or both.
• Children, who have undergone • It presents as a chronic, persistent,
sequ­estrectomy, should be followed Radiological Features infection with induration and nodu­
up by an orthodontist to aid in the A focal area of well-calcified bone proli­ larity of the tissues due to fibrosis and
development of arch and mainte­ feration may be seen that is smooth and intermittent, spontaneous occurring
nance of occlusion. has ‘onion skin’ appearance.28 draining sinuses.
Osteomyelitis of the Facial Bones 375

• A variation of this description is A. israelii is mostly responsible for organism is Nocardia asteroides. It
another presentation in which the the human actinomycosis. A. naeslundii, can occur without a dental injury. It
most prominent finding is limited A. odontolyticus and A. meyeri are less presents as suppurative lesion with
mouth opening, often months or common causes of the disease. Most necrosis and abscess formation. The
years after removal of posterior infections are accompanied by other treatment is incision and drainage and
tooth or after some trauma. This is organisms, such as Actinobacillus actino­ sulphonamides for 6 to 8 weeks.
mainly attributed to fibrosis of one mycetemcomitans, Bacteroides species,
of the muscles of mastication or Eikenella corrodens, Enterobacteriaceae, Tuberculous Osteomyelitis
from chronic deep seated focus of Fusobacterium species, Porphyromonas Tuberculosis of bone is an uncommon
infection. This presentation is often species, Prevotella species, staphylocci form of chronic osteomyelitis, occurring
termed as ‘Lumpy jaw’. (Lumpy jaw and streptococci, and may be potential more often in young individuals and
is more common in cattle’s than copathogens that aid in the inhibition of usually in late stages of the disease. The
humans). host defenses or reduce oxygen tension.32 sites of predilection are dorsal and lum­
• The disease forms external sinuses bar vertebrae and epiphysis and diaphy­
that discharge distinctive ‘sulfur Investigations sis of long bones and the flat bones, in­
granules’ (the colonies of the orga­ Radiolucency of varying size can be seen cluding those of the skull and mandible,
nism) and spread unimpeded by on radiographs (OPG). The focus of in­ which are rarely affected. Tubercular
anatomic barriers when endogenous fection may be difficult to locate. Ortho­ osteomyelitis of the mandible is found
oral commensals invade the tissues of pan­tomogram may be supplemented to be more among children than adults.
the oral-cervicofacial, thoracic, pelvic by a CT scan or MRI. Sometimes a scan Tuberculosis in the oral and maxillofa­
and abdominal regions.31 Tissues with 67Ga, which is taken up by inflam­ cial region is five times more prevalent
may be invaded by direct extension matory cells, or a scan using 99-techne­ in males than in females. However, iso­
or by hematogenous spread. tium methylene diphosphonate, which is lated tuberculosis of mandible in the ab­
• Cervicofacial disease may affect the taken up by osteoblasts, will locate the fo­ sence of active pulmonary tuberculosis
mandible and overlying soft tissues, cus of infection, which CT scan and plain is an uncommon clinical entity. Due to
parotid gland, tongue and maxillary radiographs cannot detect. Laboratory the rarity of tuberculosis of mandible,
sinus. Nearly every structure and investigations show increased ESR and it seldom arises clinical suspicion, es­
space of head and neck may be leukocytosis. pecially when a positive history of a
an initial site of involvement. systemic infection or therapy is denied.
Secondary spread to other areas of Treatment The diagnosis, therefore, is variable and
the head and neck readily occur. The management comprises of surgical established after biopsy.35 The involve­
• Firm soft tissue masses are present management with incision and drain­ ment of the mandible by tuberculous
on the skin; they have purplish, dark age and debridement. The administra­ infection is extremely rare as it contains
red, oily areas with occasional small tion of the antibiotics and supportive less cancellous bone though the man­
zones of fluctuations. Spontaneous treatment are recommended. The peni­ dibular involvement is more frequent
drainage of serous fluids containing cillin group of antibiotics are the drug of than maxilla and the alveolar and angle
granular material may occur. choice like crystalline penicillin 5 to 10 regions have greater affinity. The infec­
• Regional lymph nodes may be occ­ lac U 6 hourly or penicillin V 1 g 6 hourly tion may extend to the mandible by:36
asionally involved. or ampicillin 500 mg to 1 g 6 hourly or • Direct transfer from infected sputum
• The patient usually has no fever and amoxicillin 500 mg 8 hourly can be giv­ or infected raw milk of cow through
constitutional symptoms. en.33 Anti­biotics must be administered – An open pulp in carious tooth.
• Delayed healing of extraction soc­ for a pro­longed period as the condition – An extraction wound.
kets can be noted. may recur. For patients who are allergic – Gingival margin or perforation
to penicillin, Doxycillin 100 mg twice a of an erupting tooth.
Microbiology day for 6 months can be used. Imaging • Regional extension of soft tissue
Actionomyces is not a fungus, but rather should be done intermittently, through­ lesion to involve the underlying
a gram positive, microaerophilic, non- out the treatment to monitor healing of bone.
spore forming, non-acid-fast bacteria. bone and possible need of additional • Hematogenous route: Bacilli are
The morphologic characteristics vary surgical procedures like sequestrectomy possibly transferred from a primary
with filamentous cocci or bacillary forms. and saucerization. focus in another part of the body
They are not sensitive to antifungal and localized in the jaw, after trau­
drugs and unlike fungi, are sensitive Nocardial Osteomyelitis ma. Tuberculosis of the jaw causes
to antibiotics. The cell wall electron Nocardial osteomyelitis resembles the slow necrosis of the bone and
microscopy and other studies confirm actinomycosis to a large extent in its may involve the entire mandible.
their bacterial nature. clinical presentation.34 The causative The destruction of the bone in
376 Infections of Maxillofacial Region

radiographs appears as blurring can lead to reversal of all destruc­ is not so common now-a-days. The
of trabecular details with irregular tive bony changes. maxilla is more affected than mandible
areas of radiolucency. Two types of in this condition. The gummatous
clinical presentation of the disease Diagnosis and Management per­
foration of the palate can lead to
are seen, closed lesions, which The hematological picture is of lym­ oroantral or oronasal communication.
is devoid of any draining sinuses phocytosis, monocytosis, raised ESR The sequestra are called filiary sequestra,
and is not open to oral environ­ and the Montoux test may be positive. because they are fine.
ment and open lesions, presence of In case of open jaw lesions, AFB may be
multiple draining sinuses. There is positive in saliva. Age Incidence
erosion of the cortex with little ten­ Diagnosis of the lesion is generally Syphilitic osteomyelitis can be conge­
dency to repair. Gradually the bone con­firmed on aspiration for smears, nital, but it usually occurs between the
is replaced by soft tuberculous biopsy and culture studies. Radiography, ages of 30 to 40 years.
granulation tissue without seques­ scintigraphy, CT scan aid in diagnosis.
tra formation as is typically seen in However, histopathology is the most Site
other bacterial and viral osteomy­ common modality of reaching the Syphilitic osteomyelitis usually occurs
elitis. Caseation appears at places confirmatory diagnosis. in shaft of long bones and it affects
followed by softening and liquefac­ Management consists of surgical the skull. In majority of cases, there is
tion. A subperiosteal abscess then treatment based on pathological studies. hyperostosis.
forms presenting as a painless, soft Unlike the pyogenic osteomyelitis, the
and cold (devoid of signs of inflam­ management of tubercular osteomyelitis Radiographic Features
mation) swelling. This cold abscess is primarily with chemotherapy with The affected bone shows marked
may burst either intraorally or ex­ antitubercular (anti-Koch’s) drugs such periosteal changes, the outline of medu­
traorally forming single or multiple as streptomycin, isoniazide, rifampicin, lla becomes obliterated.37 In old cases,
sinuses. Pathological fracture of ethambutol and pyrazinamide. The sur­ gumma may be formed or in the form of
mandible and sequestration may gical management is marginal and filiary sequestra may be present.
also occur. Usually tuberculosis of restricted to debridements and drainage
the mandible presents as multifocal after the chemotherapy is started. Clinical Features
lesion elsewhere in body, involving • Closed lesions: Positive aspirate Gummatous osteomyelitis forms bone
other bones and lungs. The diagno­ for AFB: In these cases, patient is dependent bone destruction and new
sis of a case of tuberculosis of man­ started on a suitable anti-tubercular bone formation in which there are areas
dible is extremely difficult as there regimen, that is, isoniazid, rifampicin, of mottling.
are no specific signs pathognomic etham­butol and pyrazinamide. The diagnosis is the basis of history of
of infection. The only manifesta­ Negative aspirate for AFB: A com­plete exposure, presence of primary chancre
tion may be a localized swelling of excisional biopsy and debridement previously, positive KTVDRL test. The
the jaw and it may be misdiagnosed is advocated. treat­ment comprises of crystalline peni­
as a pyogenic abscess or if sinuses • Open lesions: For open lesions, cillin 10 to 20 lacs IU 6 hourly for 2 weeks
are present, or it may be confused inci­sional biopsy is done for histo­ and later with long acting penicillin
with actinomycosis. The diagnosis pathological studies. If found posi­ (Penidure) 6 to 12 lac IU, once in a week or
must be established by histologi­ tive for tuberculosis, anti-tubercular biweekly for 3 to 4 months. Surgery
cal examination of tissue and dem­ regimen is started and no surgery is has marginal role in the management
onstration of the organisms in the performed immediately to prevent condition.
lesion. Although it is rare, the dif­ dissemination of the disease, that
ferential diagnosis of tubercular is, miliary spread of tuberculosis by Osteomyelitis of Mandible
osteomyelitis must always be kept hematogenous route. After 6 to 9 in Sickle Cell Disease
in mind by clinicians, when routine weeks of anti-tubercular treatment,
therapy fails to bring about an im­ patient is reassessed clini­ cally, as Pathogenesis
provement in the lesions of mandi­ well as radiographically to decide Sickle cell disease is an inherited hemo­
ble. Since the involvement of bone upon the need for surgery. globinopathy. It occurs when hemoglobin
occurs in late stages of the disease, SS is deoxygenated and the molecules
the prognosis is poor and death Syphilitic Osteomyelitis polymerize to form pseudocrystalline
from involvement of internal or­ The syphilitic osteomyelitis or the structures known as ‘tactoids’. This leads
gans or from tubercular meningitis gumma is commonly seen in the tertiary to the characteristic sickle-shaped red
is common. However, if the lesion syphilis. With the advent of better cell. The polymerization is reversible
is primary and detected early, the modalities of diagnosis, awareness and when reoxygenation occurs. However,
disease is completely curable and better treatment modalities, the disease distortion of the red cell membrane may
Osteomyelitis of the Facial Bones 377

be permanent (irreversible sickling). The factors that precipitate the


The greater the concentrations of sickle cell osteomyelitis of the bone are
sickled hemoglobin, the more easily the periapical infection and periodontal
tactoids are formed. This process may infections.39 In the event of sickling,
be enhanced or retarded by the presence if the avascular necrosis of the bone
of other hemoglobins. Because of the occurs, it can get secondarily infected
sickled cells, there is increased viscosity and the osteomyelitis is the end result.
and loss of plasticity. Sludging occurs The sickle cell osteomyelitis follows
in the microvasculature, which causes the pattern of osteomyelitis of the jaws
obstruction to blood flow and leads to in patient with normal hemoglobin
tissue ischemia (Flow chart 18.3). The concentration and rest of the course of
ischemic tissue subsequently becomes the disease is similar to that of pyogenic
edematous and painful.4 Involvement of osteomyelitis. The mandible is the Fig. 18.17A: Case of sickle cell OM
the bones in sickle cell disease has been common bone to be involved in this of maxilla
reported in the literature.38 In the long condition, however, the involvement
bones, the head of femur is commonly of maxilla can also occur. As the
involved and facial bone involvement maxilla is not commonly involved in
may occur on rare occasions. The osteomyelitis, whenever it is seen other
pathophysiology for such involvement predisposing conditions should be
involves trauma or infection in bone, suspected and ruled out. In the central
which leads to inflammatory changes, India, sickle cell disorders are common
stasis of circulation and hypoxia. The amongst the tribal population and so
hypoxia serves as a stimulus for inducing is the incidence of sickle cell related
sickling, which clogs the lumena of the complications, including osteomyelitis.
capillaries and the tissues are rendered Hence, all maxillary osteo­myelitis cases
ischemic, with subsequent infarction. must be thoroughly eval­ uated and
Such ischemic bones become necrotic predisposing medical condi­tions such
and can become secondarily infected. In as diabetes (due to micro­an­gio­pathies) Fig. 18.17B: Total maxillary sequestration
the long bones, this secondary infection and sickle cell disease must be ruled out in a patient with sickle cell anemia
is usually caused by various strains (Figs 18.17A and B).
of salmonella. However, in the jaw Treatment
bones, the organisms that are cultured Diagnosis Treatment of sickle cell osteomyelitist
from such lesions belong to the flora The diagnosis of sickle cell disease can comprises of40:
of the oral cavity such as streptococci, be made on the basis of: • Antibiotic therapy.
staphylococci and Escherichia coli. • Demonstration of early and late • Surgery comprising of sequestrecto­
sickling on the peripheral blood my, saucerization or decortications.
Flow chart 18.3: Pathophysiology of sickle smear. • Precautions during the anesthesia as
cell osteomyelitis • Hemoglobin electrophoresis to de­ mentioned above.
tect SS pattern. • Prevention of infection.
Whenever a patient with sickle cell • Gentle tissue handling.
disorder needs the surgery follow­ing
precautions must be taken during Post-traumatic Osteomyelitis
the surgery and anesthesia. Post-traumatic osteomyelitis is the
– Maintain proper hydration and osteo­myelitis of the mandible following
prevent dehydration. an infected fracture.
– Prevent hypoxia and acidosis.
– Prevention of hypothermia. Risk Factors41
– Follow aseptic principle and • Ineffective fixation, reduction and
avoid infection. imm­o­bilization.
– Tissue to be handled gently – Delay in treatment (old fracture).
and excessive trauma should – Delay in administration of anti­
be avoided as these factors can biotic therapy or inadequate
precipitate the sickling. antibiotic therapy.
378 Infections of Maxillofacial Region

• More than 50 percent of a tooth root absorbs more energy than soft tissue and sion. Irradiation induces inflammatory
exposed in a fracture. is more susceptible to secondary radia­ response in soft tissue erythema, des­
• Devitalized segments of bone in the tion. The effects of radiation on bone quamation and pigmentation of
fracture site because of excessive depend on the following four factors, viz: overlying skin. Radiation results in
stripping of periosteum, overzealous 1. Quality of radiation progressive obliterative arteritis (endar­
use of transosseous wiring, or over­ 2. Quantity of radiation teritis, periarteritis, hyalinization and
heating of bone by burs. 3. The location and extent of lesion fibrosis and thrombosis of vessels),
• Decreased host resistance or in­ 4. Condition of teeth and periodon­ devitalization of tissues. The periosteal
creased susceptibility to infection. tium. vessels and larger vessels such as
Mucositis, atrophic mucosa, xero­ inferior alveolar artery are markedly
Signs and Symptoms sto­mia, and radiation caries are com­ affected. As long as overlying soft tissues
mon. An additional late and major com­ do not breakdown, irradiated bone may
Early signs:
plication of therapeutic radiotherapy function normally.48 Previously ORN
• Deep, intense pain. for head and neck cancer is osteoradio­ was thought to be a triad of radiation,
• High, intermittent fever. necrosis. For many years osteoradione­ trauma and infection. Marx et al.48 have
• Paresthesia or anesthesia of the crosis was considered an infection initi­ shown that microorganisms are merely
mental nerve (arising after trauma ated by injury to irradiated bone leading contaminants and trauma is only one of
and reduction of fracture). to marked pain, bone loss, functional several factors involved in the disease.
• A clearly defined cause. and cosmetic disability. In recent times
studies by Marx43,44 (1983) has shown Definition
Late signs:
that it is a chronic, non-healing wound Osteoradionecrosis is the exposure of
• Cellulitis over the involved portion caused by hypoxia, hypocellularity and nonviable, nonhealing, nonseptic lesion
of mandible. hypovascularity of irradiated tissue. of irradiated bone, which fails to heal
• Intraoral or extraoral draining Before 1960s, orthovoltage was rou­ without intervention.49
sinuses. tinely used for therapeutic radiation, The ORN is a radiation induced, non-
• Mild leukocytosis. but was found to be highly deleterious healing, hypoxic wound rather than true
• Fever. to bone and resulting in incidence of osteomyelitis of irradiated bone. The
Radiologically, a moth-eaten appea­ jaw bone necrosis ranging from 17 to viable, radiation damaged cells are not
rance and sequestrum formation may 37 percent.45 In recent years orthovolt­ replaced by cells of similar type resulting
be present. age has been replaced by megavoltage in less cellular and more of collagen.
and other techniques such as dose frac­ This fibrotic and poorly vascularized
Treatment42 tionization, collimation, shielding of tissue has reduced or absent healing
• Removal of non-vital tissue, foreign normal tissues and maintenance of pre­ ability. Tissue breakdown occurs due to
bodies and associated teeth. irradiation and postirradiation health, inability of tissues to maintain normal
• Debridement of infected areas. which are found to be bone sparing cell turnover and collagen synthesis
• Establishing drainage. reduced the incidence of osteoradione­ and such tissues are susceptible to
• Continuous irrigation and drainage crosis to 2 to 5 percent.46 spontaneous breakdown from minor
systems. Complication of osteoradionecrosis injury.50
• Local and systemic antibiotics. (ORN) is dependent on the radiation Clinically ORN may appear as a
• Immobilization of the mandible. dose to bone. Radiation dose in excess seque­strum of dead bone, osteopenic
• HBO therapy. of 50 Gy have been seen to elevate the fibrotic in nature. Lesions may be
The rigid fixation of the fracture and risk of ORN.47 Radioactive implants infected, but this is usually secondary.
bone grafts is not advisable, until the within a tissue tumor also show a higher Exposed bone need not necessarily
infection is controlled for the fear of loss incidence of ORN. dead. It is usually due to encasing soft
of graft due to infection and rejection of The mandible is affected more com­ tissue insult.
the implant. monly than maxilla, because most oral
tumors are perimandibular, moreover Incidence
the absence of dense cortical plates and There is wide variation of reported inci­
OSTEORADIONECROSIS
the presence of a dense vascular net­ dence of ORN of facial bones. Incidence
Malignancies of maxillofacial region are work in maxilla lessens the likelihood of involvement of mandible (Figs 18.18A
treated by (i) radiation therapy, (ii) sur­ of radiation necrosis effects compared and B) ranges from 2 to 3 percent.51 ORN
gery, (iii) chemotherapy, (iv) combina­ with the mandible. of maxilla is extremely rare. The second
tion therapy. Radiation often has serious Ionizing radiation destroys neo­ most common facial bone to be involved
effects on hard and soft tissues. Because plastic cells by damaging chromo­somes is temporal bone. Tooth extraction is
of its inorganic composition, bone and thus, causing impaired cell divi­ reported to be a triggering factor for
Osteomyelitis of the Facial Bones 379

• Selective rinsing with topical anti­


septics.
• Removal of small sequestra.
• Local debridement.
• Use of narcotic analgesics and nerve
blocks (bupivacaine or alcohol),
nerve avulsion or rhizotomy for
effective pain control.
• Other supportive care such as ade­
quate hydration and nutrition.
A B
• Maintenance of good oral hygiene
Figs 18.18A and B: Osteoradionecrosis of the mandible
by oral rinses of 1 percent sodium
fluoride gel, 1 percent chlorhexidine
ORN in 60 to 89 percent of cases.52-54 • There is slow sequestration, because gluconate and plain water help
The mean time period between RT and not only osteoblastic, but also, ost­ reduce xerostomia, mucositis and
development of ORN has been reported eo­­clastic activity is destroyed. radiation caries.
to be between 7.5 to up to 20 years. • Pathologic fractures may also occur. Ultrasound therapy: Use of ultra­
• The tissues surrounding exposed sound combined with local debri­de­ment.
Effects of Radiation bone may be indurated or ulcerated. Ultra­sound treatment is non-inva­ sive
Effects of radiations on various tissues is • If induration persists after infection and reportedly promotes neo­­va­scularity
illustrated in Table 18.2. has been controlled by irrigation and and neocellularity of ischemic tissues
antibiotics, or if ulceration is present, and has been used succ­ess­fully in treat­
Clinical Features a biopsy should be performed. ing ORN of jaws.55 An ultrasound pro­
The ORN has varied clinical presen­ gram of 1 watt/cm2, 3 mega Hz, pulsed
tations. It is usually painful, debilitating Radiographic Features 1:4, 15 min a day for 60 days is proposed
and frequ­ently refractory to treatment. Little radiographic change occurs in to be optimum.
The signs and symptoms vary depen­ early stages of disease. The characteri­
ding upon the condition: stic changes seen in osteomyelitis of Radical Method
• Pain (severe, deep and boring) and non-irradiated bone (sequestra and
evidence of exposed bone are the involucra) occur late or not at all in Treatment methodology is aimed at
chief presenting features. irradiated bone because of severely supp­ or­
ting and salvaging viable, but
• Initially patient may develop tris­ compromised blood supply. compromised tissue and not attempting
mus, fetid breath, pyrexia, soft tissue to resurrect dead tissue. The treatment
absce­sses and persistently draining Treatment is directed at reversing the hypoxia and
sinuses. There is no universally accepted increasing the vascularity and cellularity
• Exposed bone with intraoral/extra­ protocol for management of ORN. Two of tissues.
oral fistulae (Figs 18.18A and B). treatment modalities are: Definitive treatment should be dire­
The exposed bone often has rough cted towards either revascularization of
surface that abrades adjacent soft Conservative Method bone or excision of affected bone, with
tissue and causes further discom­ • Administration of systemic anti­ or without reconstruction. Adjunctive
fort. biotics. treat­­ment with HBO or other modalities

Table 18.2: Effects of radiations on various tissues

Tissue Radiation induced changes Complications

Oral mucosa Atrophy Mucositis, recurrent ulcerations, intolerance to hot and spicy
food, loss of taste sensation
Skin Atrophy, inflammation Diminished healing potential, painful ulceration
Bone marrow Hypovascularity, diminished cellularity, mye­l­ofi­brosis Diminished healing potential
Periosteum Hypovascularity, fibrosis, diminished cell­ul­arity Diminished healing potential
Dental pulp Hypovascularity, fibrosis, diminished cellul­arity Brittleness of tooth structure, diminished reparative potential
Salivary gland Atrophy, diminished salivary flow Burning sensation in oral cavity, radiation caries, increased
chances of odontogenic infections
380 Infections of Maxillofacial Region

may be necessary and feasible in select susceptible to lower antibiotic concentr­ Vudiniabola S, Goss AN et al.58
patients. ation and by enhancing phago­ cytic modified Marx protocol and proposed
The overall treatment comprises of: killing. In addition, neoangiogenesis, staging depending upon its clinical
• Local debridement fibroblastic prolif­er­
ation and collagen presentation plus response to treatment
• Adequate pain control: Use of narc­ synthesis occur. As resorption and with HBO as follows:
otic analgesics and nerve blocks replacement of devitalized bone with Stage I: Exposed bone with non-
(bupivacaine or alcohol), nerve healthy tissue progresses, formation healing wound 30 HBO sessions and
avulsion or rhizotomy of sequestra that undergo resorption is review. Those patient who respond
• Control of infection by adminis­ enhanced. well, further 10 HBO sessions. Non-
tration of systemic antibiotics (as Marx44,56 described a protocol for respondents considered as stage II ORN.
decided on culture and sensitivity) its effective use in several situations, Stage II: Local debridement to induce
and local irrigation of wounds by especially for prevention, treatment, fresh bleeding, followed by 10 HBO
topical antibiotics reco­n­­struction of mandible, where sessions.
• Supportive treatment such as ade­ reconstruction is indicated. It accounts Stage III: Non-respondent stage II
quate hydration, nutritional supple­ for marked decrease in pain, trismus, ORN or those with orocutaneous fistula,
ments and closure of fistulas. path­ologic fracture or inferior border
• Hospitalization, if required resor­ption, total 30 HBO sessions,
• Maintenance of good oral hygiene followed by resection and stabilization
by oral rinses of 1 percent sodium
Marx-University of Miami of remaining jaw by external fixation or
fluoride gel, 1 percent chlorhexidine Protocol57 IMF.
gluconate and plain water help All patients entering this protocol receive Stage III R: If reconstruction is
reduce xerostomia, mucositis and 30 sessions of HBO (stage I). Those with required, then they are reclassified as
radiation caries a pathological fracture, orocutaneous stage III R with 10 sessions of HBO further.
• Sequestrectomy fistula or osteolysis of inferior border
• Pathologic fractures: These do not of mandible (as viewed by panoramic Prevention of
heal readily. The best form of treat­ radiographs or a CT scan) are placed in
Osteoradionecrosis
ment is excision of necrotic ends group III category and have a continuity
of both fragments with or without resection of mandible. Preirradiation Dental Care
reconstruction Stage I: If individuals with ORN
• Bone resection: It is performed have none of the criteria to place them • Extraction of teeth: The teeth in
when there is persistent pain, infec­ in stage III, they undergo initial 30 HBO direct beam of radiation, non-
tion or pathological fractures. Pref­ sessions. If softening of the exposed restorable, periodontally compro­
erentially done intraorally to avoid bone results (an attempt at spontaneous mised should be extracted. Radi­
orocutaneous fistula in radiation sequestration and formation of healthy ation therapy is delayed by 10 to
compromised skin granulation), the wound is debrided and 14 days to allow initial healing.
• Adjunctive therapy with hyperbaric 10 more HBO sessions provided. If no • Alveoloplasty.
oxygen (HBO) (Flow chart 18.4). changes occur in exposed bone, patients • Restoration of teeth, topical fluoride
are reclassified as stage II. application and periodontal therapy
Stage II: Non-continuity resection should be completed.
Hyperbaric Oxygen Therapy in
of exposed bone to bleeding margins by • During therapy: Mouth rinses with
Osteo­radionecrosis alveolar bone resection or decortication 0.2 percent aqueous chlorhexidine,
The HBO therapy consists of breathing followed by 10 HBO sessions. If the tissue supervised cleaning of all teeth,
100 percent oxygen through a face mask heals spontaneously with no exposed oral hygiene instructions, dietary
or hood of monoplace or large chamber bone, the patient is considered a stage II counseling.
at 2.4 absolute atmospheric pressure for respondent. If wound dehiscence results
90 minutes session or dives for as many in exposure of non-viable bone, the Postirradiation Dental Care
as 5 days a week totaling 30 or more individual is considered a stage II non- • Avoidance of denture use.
sessions, often followed by another 10 respondent and together with stage I non- • Use of saliva substitutes.
or more sessions. responders enters stage III treatment. • Restoration of teeth with postirr­
The HBO treatment causes increase Stage III: Patients whose condition adiation pulpitis.
in arterial and venous oxygen tension. does not respond to either stage I or II, • Limit any extractions (if needed)
Oxy­gen under increased tension enhan­ treatment undergo a continuity resec­ to 1 or 2 per appointment under
ces healing by direct bacteriostatic effect tion and 10 postoperative sessions of proper antibiotic cover followed by
on microorganisms that renders them HBO and reconstruction after 3 months. meticulous wound care.
Osteomyelitis of the Facial Bones 381

Flow chart 18.4: Treatment of ORN

REFERENCES 6. Koorbusch GF, Fotos P, Gall KT. imaging for the assessment of chronic
Retrospective assessment of osteo­ osteomyelitis: a systematic review and
1. Richard G Topazian, Morton H Gold­ myelitis: Etiology, demo­graphics, risk meta-analysis. J Bone Joint Surg Am.
berg, James R Hupp. Oral and Maxil­ factors, and management in 35 cases. 2005;87(11):2464-71.
lofacial Infections, 4th subedition. WB. Oral Surg, Oral Medi, Oral Pathol. 12. Aliabadi P, Nikpoor N. Imaging
Saunders Company; 2002; p. 214. 1992;74(2):149-54. osteomyelitis. Arthritis Rheum. 1994;
2. Hovi L, Saarinen UM, Donner U, et al. 7. Hudson JW. Osteomyelitis of the jaws: 37(5):617-22.
Opportunistic Osteomyelitis in the jaws a 50-year perspective. J Oral Maxillofac 13. Richard G Topazian, Morton H Gold­
of children on immuno­ suppressive Surg. 1993;51(12):1294-1301. berg, James R Hupp. Osteo­myelitis of
chemotherapy. Pediat Hematol/Oncol. 8. Worth HM. Principles and Practice of jaws in Oral and Maxillofacial Infec­
1996; 18(1):90-94. Oral Radiologic Interpretation. Chicago: tions, 4th subed­ ition. WB Saunders
3. Bachalli PS. Incidence of chronic Year book Medical Publi­sher Inc. 1969. Company; 2002.
non-suppurative osteomyelitis of the 9. Gold R. Diagnosis of osteomyelitis. 14. Turlington EG. Transactions of the
maxilla in diabetic adult patients and Pediatr Rev. 1991;12:292. IV International Conference on Oral
its management. Int J Oral Maxillofac 10. Tsuchimochi M, Higashino N, Okano Surgery. Copen hagen, Denmark:
Surg. 2007;36(11):1039. A, et al. Study of combined technetium Munksgaard; 1973.
4. Borle RM, Prasant MC, Badjate SJ, et al. 99m methylene dipho­ sphonate and 15. Wee Leon Lam, Anselmo Garrido, Paul
Sickle cell osteomyelitis of the maxilla: gallium 67 citrate scintigraphy in RW Stanley. Use of topical negative
a case report. J Oral Maxillofac Surg. diffuse sclerozing osteomyelitis of pressure in the treatment of chronic
2001;59(11):1371-73. the mandible: case reports. J Oral osteomyelitis. J Bone Joint Surg Am.
5. Desai RV, Jain V, Katariya S. Cod­man’s Maxillofac Surg. 1991;49:887-97. 2005;87:622-24.
triangle in tubercular osteo­myelitis. J 11. Termaat MF, Raijmakers PG, Scho­lten 16. Grime PD, Bowerman JE, Weller
Postgrad Med. 2002;48(2):157-8. HJ, et al. The accuracy of diagnostic PJ. Gentamicin impregnated poly­
382 Infections of Maxillofacial Region

meth­yl­methacrylate (PMMA) beads 31. Thisted E, Poulsen P, Christensen PO. 44. Marx RE. A new concept in the treat­
in the treatment of primary chronic Actinomycotic osteomyelitis in a child. ment of osteoradionecrosis. J Oral
osteomyelitis of the mandible. Br J Oral J Laryngol Otol. 1987;101(7): 746-8. Maxillofac Surg. 1983;41(6):351-7.
Maxillofac Surg. 1990;28(6):367-74. 32. Russo TA. Agents of actinomycosis. In: 45. Mark A Engleman, Gayle Woloschak,
17. Mowlem R. Osteomyelitis of the jaws. Mandell GL, Bennett JE, Dolin R (Eds). William Small Jr. Radiation-induced
Proc R Soc Med. 1945;38:452. Principles and Practice of Infectious skeletal injury. In: William Small Jr,
18. Marx RE. Chronic osteomyelitis of the Diseases, 6th edition. Philadelphia Gayle W (Eds). Radiation Toxicity:
jaws. Oral Maxillofac Surg Clin North Elsevier Churchill Livingstone 2005. A practical Guide, Volume 128. US:
Am. 1991;3(2):367-81. pp. 2924-34. Springer. 2006.pp.155-69.
19. Laube J, Honscha W, Franke W. 33. Smego RA, Foglia G. Actinomycosis. 46. Lauren O’Malley, et al. Improvement
Trephination and antibiotic irrigation- Clin Infect Dis. 1998;26(6):1255-61. of radiological penumbra using inter­
drainage as a possible treatment of 34. Schwartz JG, Tio FO. Nocardial osteo­ mediate energy photons (IEP) for ste­
the septic phase of acute hematogenic myelitis: a case report and review of the reotactic radiosurgery. Phys Med Biol.
osteomyelitis. Z Arztl Fortbild (Jena). literature. Diagn Microbiol Infect Dis. 2006;51:2537-48.
1973;67(19):972-73. 1987;8:37. 47. Marx RE. Osteoradionecrosis: a new
20. Coviello V, Stevens MR, Contem­porary 35. Chaudhary S, Kalra N, Gomber S. concept of its pathophysiology. J Oral
Concepts in the treatment of chronic Tuberculous osteomyelitis of the Maxillofac Surg. 1983;41(5):283-8.
osteomyelitis. Oral Maxillofac Surg mandible: a case report in a 4-year-old 48. Marx RE, Carlson ER, Smith BR, et al.
Clin North Am. 2007;19(4):523-34. child. Oral Surg Oral Med Oral Pathol isolation of actinomyces species and
21. Jörg Schmutz. Osteomyelitis The­rapy- Oral Radiol Endod. 2004;97:603-6. Eiikenella corrodens from patients
Hyperbaric Oxygen as an Adjunct in 36. Mishra YC, Bhoyar SC. Primary tuber­ with chronic diffuse scelerosing osteo­
Treatment of Osteo­myelitis of the Jaws. culous osteomyelitis of mandi­ ble. J myelitis. JOMS. 1994;52:26.
Heidel­berg, Berlin: Springer;2008. pp. Indian Dental Assoc. 1986; 58:335-9. 49. Clayman L. Clinical controversies in
191-204. 37. Thomason HA, Mayoral A. Syphilitic oral and maxillofacial surgery: Part
22. Hart GB, Mainous EG. The treatment osteomyelitis. J Bone Joint Surg Am. II. Management of dental extractions
of radiation necrosis with hyperbaric 1940;22:203-6. in irradiated jaws: a protocol without
oxygen. Cancer. 1976;37(6):2580-85. 38. Shroyer JV III, Lew D, Abreo F, et al. hyperbaric oxygen therapy. J Oral
23. Marx RE. Osteoradionecrosis: a new Osteomyelitis of the mandible as a Maxillofac Surg. 1997;55:275-81.
concept of its pathophysiology. J Oral result of sickle cell disease. Report and 50. Tompach PC, et al. Cell response to
Maxillofac Surg. 1983;41:282-88. literature review. Oral Surg Oral Med hyperbaric oxygen treatment. Int J Oral
24. Rees GA. On uncommon forms of Oral Pathol. 1991;72(1):25-8. Maxillofac Surg. 1997;26:82-86.
abscess in childhood. London Med 39. Girasole RV, Lyon ED. Sickle cell osteo­ 51. Bras J, de Jonge HK, van Merkesteyn
Gaz. 1847;4:859. myelitis of the mandible: report of three JP. Osteoradionecrosis of the mandi­
25. Shafer WG. Chronic sclerosing osteo­m­ cases. J Oral Surg. 1977;35(3):231-34. ble: pathogenesis. Am J Otol­aryngol.
yelitis. Oral Surg. 1957;15:138-42. 40. Dietrich R Lawrenz. Sickle cell disease: 1990;11(4):244-50.
26. Oulis C, Berdousis E, Vadiakas G, et al. a review and update of current therapy. 52. Marx RE, Johnson SP. Studies in the
Garre’s osteomyelitis of an unusual ori­ J Oral Maxillofac Surg. 1999;57(2):171- radiobiology of ORN and their clinical
gin in a 8-year-old child. A case report. 78. significance. Oral Surg Oral Med Oral
Int J Pediatr Dent. 2000;10:240-44. 41. Merritt K. Factors increasing the risk Pathol. 1987;64:379-90.
27. Eversole LR, Leider AS, Corwin JO, et al. of infection in patients with open 53. Beumer J III, Silverman S Jr, Berak
Proliferative periostitis of Garre’s: its dif­ fractures. J Trauma. 1988;28:823. SB Jr. Hard and soft tissue necrosis
ferentiation from other neoperiostoses. 42. Robert M Kellman, Darin L Wright. following radiation therapy for oral
J Oral Surg. 1979;37: 725-31. Management of post-traumatic osteo­ cancer. J Prosthet Dent. 1972;27:640-
28. Eswar N. Garré’s osteomyelitis: a case myelitis of the mandible. In: Alex M 7.
report. J Indian Soc Pedod Prev Dent. Greenberg, Joachim Prein (Eds). Cra­ 54. Murray CG, Daly TE, Zimmerman
2001;19(4)157-59. niomaxillofacial Reconstructive and SO. The relationship between dental
29. Caffey J. Infantile cortical hypero­ Corrective Bone Surgery; Principles of disease and radiation necrosis of the
stoses. J Pediatr. 1946;29:541-59. Internal Fixation Using the AO/ASIF mandible. Oral Surg Oral Med Oral
30. Batcheldor GD Jr, Giansanti JS, Hibbard Technique. Springers; 2002. pp. 433-8. Pathol. 1980;49:99-104.
ED, et al. Garré’s osteo­myelitis of the 43. Marx RE. Chronic osteomyelitis of 55. Harris M. The conservative mana­
jaws: a review and report of two cases. jaws, Oral Maxillofac Surg Clin North gement of osteoradionecrosis of the
J Am Dent Assoc. 1973;87(4):892-7. Am. 1991;3:367. mandible with ultrasound therapy.
Osteomyelitis of the Facial Bones 383

Br J Oral Maxillofac Surg. 1992; myelitis of the temporal bone. JOMS.


BIBLIOGRAPHY
30:313. 1998;56:1364-52.
56. Marx RE. Hyperbaric oxygen: its role 1. Hudson JW. Osteomyelitis of the jaws. 5. Sato M, Yamaguchi S. Osteomyelitis of
after radiotherapy. In: Booth PW, JOMS. 1993;51:1294-1301. the mandible in a patient with acquired
Schendel SA, Hausamen JE (Eds). 2. Laskin DM. Oral and Maxillofacial systemic analgia. JOMS. 1997;55:97-9.
Maxillofacial Surgery. New York: Surgery, Illinois, Chicago. Mosby CV. 6. Topazian RG, Goldbery MH. Oral
Churchill Livingstone; 1999. 1999;256-76. and Maxillofacial Infections, USA,
57. Marx RE. Osteoradionecrosis of the 3. Olaitan AA, Amuda JT. Osteomyelitis of Saunders WB. 2002;214-42.
jaws: Review and update. HB02 Rev. mandible in sickle cell disease. BJOMS.
1984;5:78-128. 1997;35:190-2.
58. Vudiniabola S, Pirone C, Williams J, 4. Sano K, Yoshida Shin-ichi. Preauricu­
et al. Hyperbaric oxygen in the preven­ lar mass presenting as a sign of osteo­
tion of osteoradionecrosis of the jaws.
Aust Dent J. 1999;44(4):243-7.
Section 7
Maxillofacial Trauma

n Management of Soft Tissue Injuries


n Fractures of Mandible
n Fractures of Middle Third of Facial Skeleton
n Facial Burns
n Medicolegal Aspects of Injury
19 Management of Soft
Tissue Injuries
Jajoo Suhas N, Yadav Abhilasha, Garg Rajat

to the facial injuries like the injuries to


Introduction Examination and brow, eyelid, nose; lip and ear require
Injuries to the face commonly result in History careful assessment and treatment to av­
a significant psychological response. oid defor­­­mity and potential inter­ference
The face is the most prime possession The time spent in the examination of the with function. Injuries to eyelid and
of an individual and everybody wants injury and treatment planning is never orbit require ophthalmic evalu­ation to
to look good and presentable. The dis­ wasted and is ultimately beneficial for the esta­blish visual status and presence of
figurement of the face due to injuries patient. In the soft tissue injuries, which any corneal damage. Facial injuries can
or ablative surgeries causes a big are without bony injuries, the minimal be superficial, but may extend to involve
psychological dent and undermines and esthetically acceptable scar can be adjacent structures includ­ ing bones,
the self-esteem of the person. The achieved if the wound is first thoroughly nerves, ducts, muscles, vessels, glands
management of the facial hard and soft cleaned, debri­ ded and meticulously and/or dentoalveolar structures. A thor­
tissue injuries is often very challenging sutured, using an appropriate technique ough head and neck examination deter­
as the patients are very demanding and and material. But, when there is a bony mines the extent of associated facial
want the function and the esthetics injury treatment plan changes, hence, wounds.
to be restored to its preinjury status, a careful examination and evaluation is The involvement of cranial nerves
which may not be always possible. warranted. Apart from general aspects (Vth and VIIth) may be associated with
Injuries to the head occur in over of the history that are common to all lacerations that involve the face. The
70 percent of all automobile accidents trauma patients, a com­ plete history facial nerve exits the stylomastoid fora­
and nearly 70 percent cases of assaults. of the incidence leading to the injury men and divides into five branches
the management of facial lacerations should be taken. A careful history reveals within the parotid gland dividing the
is not the priority, especially if it is presence of any foreign bodies in wounds gland into superficial and deep lobes.
associated with grievous injuries by understanding the mechanism of the Any injury to the gland, preauricular
like head injury or acute res­ piratory injury (such as splinters, glass pieces). area or cheek should arouse suspicion
obstruction. Particular attention should be paid to the for associated facial nerve injury. Facial
wounds, which have been in contact with nerve is deep when it exits stylomastoid
caustic substances such as the wounds foramen then gradually become super­
Definition of Wound
during the industrial accidents. In a typical ficial, that is why involvement of facial
The acute wound is a breakdown of road traffic accident (RTA) injury the nerve injury depends on location of
the integrity of the soft tissue envelope dirt, foreign bodies are embedded in the wound and extent of wound (Fig. 19.1).
surrounding any portion of the body. It wound, but are obscure initially because Injury to the parotid gland or its main duct
is defined by size, depth and involved of blood. Foreign bodies in automobile can lead to salivary fistula. The parotid
anatomic structures. The time course accidents may be glass, plastic or metal. duct is approximately 5 cm in length and
between an acute versus chronic wound A careful examination should be done for 5 mm in diameter. It exits the gland and
is a continuum between 4 and 6 weeks. It the presence of any foreign body such as runs along the superficial surface of the
is during this time that if an acute wound glass, which not detected on radiographs. masseter muscle and then penetrates
has not healed spontaneously, it is likely The specialized nature of the diff­ the buccinator muscle to enter the oral
to become a chronic, ‘problem wound’ erent anatomical structures of the face cavity opposite the upper second molar.
that requires further intervention. dem­ands special attention to be paid The treatment of parotid duct injuries
388 Maxillofacial Trauma

Types of Injury
Wounds can be classified into tidy and
untidy wounds (Box 19.1). The surgeons
aim is to convert untidy wounds to tidy
wounds by removing all contaminated
and devitalized tissue.
Primary repair is possible with tidy
wounds, but contaminated wounds
require debridement on one or several
occasions before definitive repair can be
carried out.
It also can be classified according to
level of tissue insult:
Abrasions
• Contusions
Incised wounds
• Lacerations
Fig. 19.1: Facial nerve and its branches
• Avulsions
• Bites (animals and humans)
depends upon the location of the injury. • Crush injury
If the injury involves the proximal • Penetrating injuries
duct, while it is still in the gland, the These all types may be associated
parotid capsule should be closed and with or without tissue loss.
a pressure dressing is placed. If the
injury is present in the mid-region of Abrasions
the duct, the duct should be repaired. Shear forces that remove a superficial
Injuries involving the terminal portion layer of skin cause abrasions such as
of the duct should be drained directly sliding along pavement, dirt or glass that
into the mouth. Lacerations are closed removes the epithelial layer and papillary
primarily and a pressure dressing is layer of dermis leaving the raw bleeding
placed to prevent fluid accumulation. If reticular layer of dermis exposed. This
the deep soft tissue injuries are present Fig. 19.2: Lines of minimal tension seen on type of wound may be painful because
in the infraorbital area the branches of face in old age of exposed free nerve endings. Abrasions
the infraorbital nerve may get involved can be superficial and deep. The age of the
producing sensory deficit in the area of caused by the contraction of the frontalis abrasion can be ascertained by clinical
distribution of the nerve. muscles, which is inserted into the skin of appearance of the wound as depicted in
If the penetrating injuries are pre­ the lower forehead. In the upper eyelids, Figs 19.3A to C. The wound should be
sent on the neck, face and temporal many fine perpendicular strands of fibers gently cleansed with a mild soap solution
bone, critical evaluation of the wound of the elevator aponeurosis terminate and irrigated with normal saline. These
should be done to rule out injuries to the in the dermis of the skin and along the superficial injuries usually heal with local
underlying vital structures. tarsus to form the supratarsal fold. Similar wound care and can be left exposed for
The lines of minimal tension, also insertions in the lower lid create fine healing, but deep abrasions are never left
called relaxed skin tension lines, are result horizontal lines, which are accentuated open as it can lead to contamination of
of the adaptation of the skin to the function by the circumferential contraction of the the wound. It is important to determine
and are also related to the elastic nature of orbicularis oculi muscle. whether foreign bodies have been
the underlying dermis. The intermittent Incision should be preferably made
and chronic contractions of the muscles of along or within the lines of mini­ mal Box 19.1: Types of wound
facial expression create depressed creases tension as the ensuing scar is incon­
in the skin of the face. These creases spicuous and gives excellent esthetic Tidy wounds Untidy wounds
become more visible and deepen with results. Any incision or portion of an Incised Crushed or avulsed
the growing age (Fig. 19.2). For instance, incision that crosses such a crease often Clean Contaminated
the supraorbital wrinkle lines and the produces unsightly and conspi­ cuous Healthy tissue Devitalized tissue
Seldom tissue loss Often tissue loss
transverse lines of the forehead are scars.
Management of Soft Tissue Injuries 389

A B C
Figs 19.3A to C: Healing of abrasion: (A) On 1st day with dark red scab; (B) After 3–5 days brownish red scab; (C) After 5–7 days falling
off of scab

em­ be­dded in the wound. Failure to mucosa are intact, but if the contusion
remove all foreign material can lead to is associated with a laceration, the con­
permanent ‘tattooing’ of the soft tissue. tused margins should be excised before
After the wound is cleansed the abrasion closure. If contused margins involve vi­
is covered with a thin layer of topical tal structures like eye than delayed clo­
antibiotic ointment like bacitracin to sure should be done until the contusion
minimize desiccation and secondary resolves. In general there is no specific
crusting of the wound and dressed with treatment for most facial contusions
cotton gauze or covered with antibiotic with the exception of ear or septal he­
coated cellulose acetate gauze. matomas, which req­ uires immediate
The epithelialization without signifi­ evacuation.
cant scarring is complete in 7 to 10
days, if the epidermal pegs have not Incised Wound
been completely removed. At 14 days, These wounds have sharp and clear
fibroblast and capillary formation in the cut margins and are caused by a sharp
dermis increases and new elastic fibers object drawn across the skin/mucosa.
develop by 3 months. If the abrasions Fig. 19.4: Abrasion on cheek region with Sharp instruments may be like knife,
significantly extend into the reticular laceration on lip and infraorbital region razor, scissors or sword, axe, hatchet.
dermal layer, significant scarring from Incised wound is always broader than
granulation tissue formation will result the edge of the weapon causing it ow­
(Fig. 19.4). For this compression can be ing to the retraction of the divided tis­
given over injury to avoid hypertrophy of sues. It is somewhat spindle shaped; it’s
the granulation tissue. length greater than depth and width. as
the edges of the wound are sharp and
Contusions healthy, without any devitalization they
Contusions are caused by blunt trauma can be closed primarily after irrigation
that causes edema and hematoma for­ with sterile normal saline solution and
mation in the subcutaneous tissues diluted antiseptics line 5 percent po­
Fig. 19.5: Contusion on chest due to blunt
(Fig. 19.5). It occurs variably depending vidone iodine solution. They heal fast
injury
upon the area involved (eyelids or lip) and the ensuing scars are acceptable
will develop a relatively greater amo­unt (Figs 19.6A to D).
of swelling than forehead or cheek, as occur, but is rarely permanent. Large
it has more loose aerolar tissue. Small hematomas should be drained (evacu­ Lacerations
hematomas usually resolve with­ out ated) to prevent perma­nent pig­men­tary Lacerations are caused by blunt to
treatment; hypopigme­ntation or hyper­ changes and secondary subcu­taneous semi sharp and hard objects to the soft
pigmentation of the involved tiss­ue can atrophy. Usually the over­lying skin and tissue. Lacerations can have sharp,
390 Maxillofacial Trauma

A B C D
Figs 19.6A to D: (A) Incised wound over the nose and eyelid caused by a razor; (B) Clear division of the alar and septal cartilages;
(C) Primary closure of the wound; (D) Clinical photograph on 8th postoperative day showing good healing and minimum scarring

A B C
Figs 19.7A to C: Different types of simple laceration seen: (A) On forehead; (B) On lip with nasal injury; (C) On upper eyelid

if necessary for 5 to 7 days. Similarly,


contused wounds should be evaluated if
enough tissue is available after excising
the margins it should be closed primarily
with loose, approximating sutures, other­
wise treatment should be delayed until
contusion resolves (Figs 19.7A to C).

Stellate Laceration
If the margins are bevelled or ragged they
should be conservatively excised to provide
A B perpendicular skin edges to prevent exce­
Figs 19.8A and B: (A) Laceration with ragged borders; (B) Scar of stellate laceration ssive scar formation1 (Figs 19.8A and B).
Undermining of the soft tissue wound
contused, ragged or stel­late margins as margins is help­ful in suturing of tissue
Simple Laceration
seen in crushing type of injury or they without exce­ssive tension at the wound
may involve partial avulsion of tissues Simple laceration may be clean, conta­ margin. But, extensive undermining leads
that remain pedicled to surrounding minated or contused. Clean lacerations to contraction of wound and scarring.
structures. Closure is performed using may be repaired with little debridement. Interrupted sutures should be used to
a layered technique. Laceration can be Con­taminated wounds should be clean­ close the wound as far as the stellate
simple, stellate or flap-like. sed and closed primarily; it can be delayed portion of the wound margin. Rarely there
Management of Soft Tissue Injuries 391

A B C
Figs 19.9A to C: Flap-like laceration: (A) Preoperative; (B) After debridement; (C) Closure

animal and human bites. Animal bites


particularly from dogs, are polymi­
crobial and are more avulsive due to the
‘pull back’ response of the victim where
as human bites are mostly on lip, nose
and ear. Most wounds are thor­ou­ghly
irrigated with minimal debri­ dement
and primary closure, but when wounds
are more than 24 hours old than closure
A B is controversial. Some prefer primary
Figs 19.10A and B: Avulsions: (A) Cheek; (B) Forearm closure so that minimal risks of infection,
but other prefer dela­yed primary closure.
An adjunctive broad­spec­trum antibiotic
with tetanus and rabies pro­phylaxis is
is an indication for changing the direction injuries are relatively uncommon, occu­ necessary (Figs 19.11 and 19.12).
of the wound margins by Z-plasty at the r­­­ring mostly due to gunshot wou­nds or
time of primary wound repair. These weapon injuries3 (Figs 19.10A and B). Crush Injury Syndrome
procedures should be done as secondary Some­times initial examination may show Crush injury syndrome can be described
revision procedures if indicated. Use of apparent loss of tissue, but thorough as prolonged severe compression of one
adhesive strips can assist in relieving ten­ exam­in ­ ation reveals that the tissue mar­ or several compartments of the body
sion on the wound margin. gins have been retracted or rolled under (Fig. 19.13). As a consequence of multi­ple
the wound margin. Undermining the compartment involvement and exten­sive
Flap-like Lacerations adjacent tissue, followed by primary myonecrosis, there is excessive formation
It is a laceration with significant under­ closure, can close small defects. When of myoglobin and potassium, which
min­ing of the soft tissues without loss primary closure is not possible, other enters into the systemic circul­ation and
of tissue (Figs 19.9A to C). Debris is options are considered. These include cause hyperkalemia, cardiac arrhythmia,
very commonly found in deep tissues local flaps, skin grafts or apposition of the shock, renal failure and death.
under the flap. Pressure dressings play skin margin to the mucous membrane.
an important role in minimizing dead Facial wounds should not be allowed to Clinical Features
space and limiting hematoma formation heal by secondary intention (granulation In patients those are subjected to mas­
or fluid collection within the deep tissue formation) because of excessive sive crush injury that has been prol­
tissue.2 The use of drains may be helpful scar formation. onged for several hours, following feat­
in achieving the desirable cosmetic ures can be seen:
results and ensuring proper healing. • Sudden massive swelling, marked
Animal and Human Bites edema with variable degree of local
Avulsions Animal and human bite wounds have hemorrhage.
Avulsive injures are characterized by a significant risk of infection as they • Paralysis of involved limb is seen.
the loss of segments of soft tissue. These are highly contaminated. These can be The peripheral pulses may be
392 Maxillofacial Trauma

A B C
Figs 19.11A to C: Human bite of lower lip: (A and B) Preoperative; (C) Postoperative

extravasation of plasma and electrolyte characteristics of the penetrating object


bearing fluid. This is the first phase and the amount of energy transmitted to
of shock, which is compensated by the tissues. Assessment of the penetrating
peripheral vaso­ constriction; this com­ injury may involve X-rays or computed
pensatory mech­ anism is capable to tomography (CT) scans and treatment
keep up with the fluid loss. But, once com­prises of repair of the damaged struc­
blood pressure falls then the second tures and removal of foreign objects.
stage of shock will develop, which is a As a missile passes through tissue, it
life-threatening situation. To prevent decelerates, dissipating and transferring
hypovolemic shock in patients with kinetic energy to the tissues; which
crush injuries intravenous (IV) isotonic causes the injury. The velocity of the
saline and crystalloids solution is most projectile is a more important factor
Fig. 19.12: Pig bite present on upper lip important to prevent shock. than its mass in determining how
much damage is done; kinetic energy
increases with the square of the velocity.
Penetrating Injuries The amount of energy transferred to
Penetrating injury occurs when an tissue by a missile depends on the
object pierces the skin and enters the square of its velocity, the density of
deeper tissues of the body, creating an the tissue and the presenting area of
open wound. The penetrating object the missile, for example the denser the
may remain embedded in the tissues, tissue, the greater the amount of energy
come out the way it entered in, or may transmitted to it.4 The path of a projectile
Fig. 19.13: Crush injury of a hand pass through the tissues and exit from can be estimated by imagining a line
another area (surface) like knife, bullet from the entrance wound to the exit
or splinters of the blast injuries. The wound, but the actual trajectory may
bullet injuries may look simple or the vary due to differences in tissue density.
misleading as the main arte­ rial entry wound at the penetrating site While penetrating facial trauma can
supply is damaged due to exten­sive may look small, but it may have an exit pose a risk of airway obstruction due to
involvement of muscle. wound site on the other side, which will edema or bleeding. Penetrating injury to
• Patient will have pale, cold and be massive due to rotation of the bullet the eye can cause the rupture of the globe
moist skin, while maintaining in the tissues in concentric manner. or leakage of the vitreous humor posing
normal blood pressure. Penetrating trauma can be serious a serious threat to eyesight. Penetrating
Due to prolonged compression because it can damage internal organs, head injury accounts for only a small
there will be anoxia, which will lead vital organs and presents a risk of shock percentage of all traumatic brain injur­
to increased capillary permeability and infection. The severity of the injury ies and it is associated with a high mort­
and massive tran­ su­­
dation, leading to varies widely depending on its site, the ality rate. Penetrating head trauma can
Management of Soft Tissue Injuries 393

cause cerebral contusions and lacer­ cer­vical spine and head injuries before get disrupted. Prophylactic antibiotics
ations, intra­cranial hematomas, pseu­ evaluation of facial soft tissue wounds. should be given in all contaminated
do­aneurysms and arteriovenous fistulas. The fractures of supporting facial bones wounds as well as for clean wounds, if
Assessment can be difficult because must be excluded by careful clinical there is any delay in repair. Betalactlam
much of the damage is often internal and and radiographic examination. Facial antibiotics are mostly used as a pro­phyl­
not visible. The patient is thoroughly lacerations do not require immediate actic antibiotic, but when the wounds
examined. X-ray and CT scanning may treatment because of the excellent are deep, soiled and have plenty of
be used to identify the type and location blood supply to the facial region. During crushed or devitalized tissue, Metr­oni­
of potentially lethal injuries. Sometimes the assessment of other injuries, the dazole should be added to cover the
before an X-ray is performed on a wounds should be kept moist with ster­ anaerobic microorganism. The amino­
person with penetrating trauma from ile dressings of gauze soaked in an anti­ glycosides can also be used along with
a projectile, a paper clip is taped over biotic solution until final mana­ge­ment. beta-lactam antibiotics, if the wounds
entry and exit wounds to show their It is important to simultaneously are badly soiled and likely to be invaded
location on the film. ach­i­eve hemostasis, while stabilizing by gram negative organisms to provide
and evaluating the patient who has sus­ broader spectrum of coverage.
Management of Soft tained trauma. The bleeding from most A history of tetanus immunization
of the sites will respond to application of status is essential as part of medical history.
Tissue Injuries a pressure dressing. The bleeding from Facial wounds often appear clean, but they
Before the 17th century, it was a the lacerations involving the scalp can are at risk and require tetanus prophylaxis.
common practice to pour hot oil on the occ­asi­onally be difficult to control with Although the face has excellent vascularity
wounds in order to cauterize damaged pre­ssure and may require clamping, and the anaerobic environments are rare,
blood vessels to achieve the hemostasis, ligation or electrocautery. The face is the badly soiled wounds with devitalized
but the French surgeon Ambroise Pare5 well supplied with blood vessels, which tissue require prophylaxis against tetanus
challenged the use of this method in are generally small in diameter and with administration of tetanus toxoid (ac­
1545 and he was the first to propose supp­lied with elastic fibers. When blood tive immunity).
using ligature to control the bleeding. vessels of face are completely transected, The American College of Surgeons
During the American Civil War, they tend to contract and collapse and Comm­­ittee on Trauma Recomm­en­dat­
chloro­form was used during surgery to bleeding stops spontaneously because the ions on Tetanus Care6 (1987) are as foll­
reduce pain and allow more time for vessels become occluded with thrombi ows Box 19.2.
operations. As the sterile technique was and compressed by the enve­ lop­
ing However, in Indian circumstances
not practiced in the hospitals, infection hematoma. However, partially tran­se­ cted as the immunization status of the pati­
was the leading cause of death for woun­ vessels have a propensity for continued ent is not known or reliable due to
ded soldiers. During the World War I, hemorrhage. Tough tissues of scalp do not
doctors began replacing patients lost allow vessels to retract due to the presence
fluid with salt with parenteral fluid ther­ of aponeurosis and the scalp lacerations Box 19.2: Tetanus prophylaxis
apy. The practice of blood trans­fusion can bleed excessively for a long time.
became more popular dur­ing the World In the soft tissue injuries other Fully immunized individuals
War II to replace lost fluids. The use than those involving the face, the time- If the last dose of tetanus toxoid was given
within 10 years, administer 0.5 mL absorbed
of antibiotics also came into practice lapse from initial injury to treatment is
tetanus toxoid for tetanus prone wounds. If
during World War II. important. Secondary risk of infection < 5 years have elapsed since last dose, then
The management of the soft tissue increases with the lapse of time. Because this booster may be omitted.
injury can be divided as: of the rich vascularity of the face there is Partially immunized individuals
• Primary general management no ‘golden period’ for the suturing or When the patient has received two or
• Specific/definitive management. repair of facial wounds and the healing more injections of tetanus toxoid and last
of facial wounds is unaffected by the dose was received more than 10 years ago,
Primary General Management interval between injury and repair. That 0.5 mL absorbed toxoid is administered for
both tetanus prone and nontetanus prone
The initial examination involves evalu­ is why primary closure of facial wounds, wounds.
at­ing and stabilizing the trauma patient. can be delayed, if there is underlying
Individuals not adequately immunized
Any life-threatening conditions should bone fracture. Treatment of the fracture For nontetanus prone wounds administer
be identified and managed immediately. should be completed before final soft 0.5 mL of absorbed toxoid.
The assessment of airway, breathing tissue closure, because the wound For tetanus prone wounds
and circulation is made, which is itself may provide an access to the • Administer 0.5 mL absorbed toxoid
follo­wed by a general neurologic ass- fracture site and if is undertaken prior • Administer 250 units TIG
• Administer antibiotics.
es­
­ s­
ment with particular attention to to fracture reduction the suture line may
394 Maxillofacial Trauma

ignorance and illiteracy, especially in amount of local anesthesia required and With respect to infection rates, studies
rural population it is always safe to also prevent distortion of the tissues. have shown no statistical difference in
admi­nister tetanus toxoid, prophyl­acti­ How­ever, the local infilteration of local wounds irrigated with normal saline
cally following an injury. anesthetic solution containing adren­ when compared to other antimicrobial
aline provides good hemostasis and dry solutions.
Specific Management field during the surgery. Soaps do not harm the intact skin
for Wounds surfaces when used in proper concen­
The decision is made first whether to tration, as the thick layer of epidermis
Wound Debridement
repair the wound in the casualty depart­ protects the underlying tissue, but
ment under local anesthesia or to per­ Debridement is the most fundamental soaps may enter the wound and cause
form the repair in the operating room principle in surgical wound preparation cellular damage and necrosis. Hydrogen
under a general anesthesia. Large com­ before the closure. Inadequate debride­ peroxide produces effervescence and is
plicated, extensive lacerations involv­ ment is the surgical corollary to a post­ known to flush out small dirt particles
ing deep structures demand ideal light­ operative infectious complication after from the wound bed. It also releases
ing and patient cooperation. General acute wound bed closure.7 It is a plastic nascent oxygen however; it impedes
anes­thesia offers the best opportunity surgery dictum. wound healing and has poor bactericidal
for exp­l­­or­­ation and repair. The patient Under adequate anesthesia the wou­ activity. A good rule is to avoid irrigating
may req­uire repair of other traumatic nd is thoroughly debrided (Figs 19.14A to the wound with any solution that would
injur­ies in the operating room and on C). All the nonvital tissue is exci­­sed with not be suitable for irrigating the eye.
many occasions, definitive repair of asso­ an attempt to salvage the tissue as much Toxic materials like alcohol, hydro­
ciated facial soft tissue injuries can be per­ as possible, as radical deb­ride­ment on gen per­o­xide, benzalkonium chloride,
formed at the same time. Facial injuries in the face is not recommended due to stro­ng soaps like hexachlorophene and
pedi­atric patients must be repaired under the excellent vascularity. Devitalized povi­done-iodine should not have direct
general anesthesia as the patients do not tissue impedes phagocytosis and often contact with open wound as these agents
cooperate. works as a nidus of infection. Persistent induce cellular necrosis on contact. If
A thorough evaluation of the 7th infection at a wound site leads to the these agents are used around the wound,
cranial nerve should be undertaken prior release of inflammatory cytokines from they should be used in dilute form
to injection of local anesthetic or admini­ monocytes and macrophages, which (povidone-iodine 1 mL/l can be used)
stration of a general anes­thetic. Injecting delays wound healing. An anaero­ bic and the wound should be thoroughly
local anesthetic prior to cleaning the environment results and limits leukocyte irrigated with bal­ an­­
ced salt solutions.
wound will allow more effective wound function. Soft tissue wounds are often Normally, 0.5 per­cent cetrimide or savl­
cleaning and pre­ paration. One should contaminated with bacteria and foreign on is considered to be best solutions for
avoid injecting the local anesthetic dir­ material. Treatment of these injuries wounds.
ectly into the wound as important land­­ involves copious irrigation and is aimed Lacerations that are extending
marks could get distorted. Regional nerve at minimizing the bacterial wound into the scalp or any hair bearing area
blocks are beneficial in minimizing the flora and removing any foreign bodies. that should be shaved to provide good

A B C
Figs 19.14A to C: Wound debridement: (A) Preoperative laceration; (B) Thoroughly debrided laceration; (C) Closure
Management of Soft Tissue Injuries 395

access for debridement and repair. the skin flap margins, but invariably
How­­ever, areas such as eyebrows and strangulate the wound edges producing
eyelashes should never be shaved rather ischemic necrosis of the wound margins
clipped closely to provide landmark for and dehiscence (gaping) of the suture
positioning of soft tissues during closure. line. The sutures should be tied loose,
Careful and meticulous cleaning so that the suture line itself should serve
of the wounds primarily will avoid un­ as drainage channel for the collected
favorable results such as ‘tattooing,’ exudates under the skin flaps. In case
infection, hypertrophic scarring and gross collection is detected below the
granulomas. A pulsatile type of irrigat­ skin flaps it is advisable to open one or
ing device is useful for removing de­ two sutures to drain the collection. Fig. 19.15: Rotational flap technique
bris, necrotic tissue and loose mate­ In the grossly contaminated wounds
rial. An abrasive wound having debris ideal material for closure of the deeper are advancement, rotational, transposi­
and dirt should be scrubbed with a soft tissue is not catgut, but material like tion and free vascularized flaps.
scrub brush and detergent soap to re­ vicryl should be used. Similarly, multifil­
move deeply imbedded foreign mate­ a­ment material is having capillarity like Rotational Flap
rial. However, soaps may cause cellular linen or silk are not ideal for the clos­ure Basic rotation flap is a simple pivotal flap,
damage and necrosis. A surgical blade of the skin and in such situation mono­ which is curvilinear in shape and which
may be help­ful to scrape foreign mate­ filament, inert material having mini­ rotates around a pivotal point near the
rial that is deeply embedded. Polymyxin mum capillarity like prolene should be defect (Fig. 19.15). It is best suited for
B sulfate can be used to remove residual used for better cosmetic results. triangular defects, designed immediately
grease or tar in wounds. Proper clean­ If the wound cannot be closed pri­ adjacent to defect—so one side of the
ing and good surgical technique are im­ marily due to tissue loss then closure with defect is the advancing edge of the flap.
perative in minimizing infection. Infec­ the help of local flaps should be planned.
Advantages
tions are rare when the wound is closed
so that no dead space, devitalized tis­ Local Flaps • The flap has two sides, both edges
sue, or foreign bodies remain beneath A flap is a unit of tissue that may be can be placed in borders of esthetic
the sutured skin. transferred from a donor to a recipient units of face
Conservation should be the rule site, while maintaining its blood supply.8 • It has broad base and reliable vascul­
in debridement of facial wounds and A flap is different from a graft; it has arity
debri­dement should be limited to devi­ an intrinsic blood supply that is respon­ • It has great flexibility in design and
talized tissue that either is stained by sible for its viability. A graft must rely on positioning
road tar or contains dirt or other parti­ diffusion until its vascularity becomes • Arterial and venous disruptions may
cles that cannot be removed with meti­ re-established. The anatomy of macro­ be minimized and sensory inner­
culous scrubbing. circulation is used to define and design vations can be maximized by good
a flap. The major arterial inflow and positioning of flap base.
Primary Closure venous outflow of a flap constitute the
Disadvantages
After meticulous cleaning and debri­ foundation from which the microcircu­
dement the closure/repair of the wound latory beds then provide nutrition and • Defect has to be triangular.
is undertaken. If there is no tiss­ue loss oxygen and carry away CO2 and waste • It creates a right angle at the distal
or if with mobilization of the tissue by products, thus forming the basis of cel­ tip thus, care should be taken, while
undermining of the skin or mucosa, if lular metabolism throughout the flap. positioning the tip to avoid compro­
the wounds can be closed primarily it Vascularity of a flap can be determined mised vascularity.
should be undertaken. Care must be either by excising small margin of flap • Effective length becomes progressi­
taken not to approximate the tissue un­ or by needle prick method at various vely less as flap moves through its
der tension as the incision line can break sites of flap to check bleeding. If bleed­ arc of rotation; hence, care should
producing dehiscence of the wound. ing is present it means flap is having be taken, while designing.
One has to anticipate the subsequent good vascularity. The major disadvan­
inflammatory edema that can ensue in tages of flap are additional incision and Advancement Flaps
these wounds due to trauma and heavy later more scar formation on face, but at Advancement flaps it involves making
contamination. Thus, the closure should the same time local flaps are the best to of two parallel incisions from the defect
be passive and tension free and should close the avulsive defect. Facial flaps do and undermining the tissue until the flap
be able to accommodate the edema. The best when the pedicle is based laterally can be advanced into the defect under
too tight sutures may stop bleeding from and inferiorly. Basic flaps used on face minimal tension. The various types of
396 Maxillofacial Trauma

Box 19.3: Different advancement flaps

Type Location
• Single and Forehead, eyebrow,
bilateral (U-and helical rim
H-plasty)
• O-T, A-T plasty Forehead, lower
eyelid, lip, chin
• Island pedicle Upper lip, cheek,
nasal sidewall
• Cheek Medial cheek A
advancement
• Mucosal Lower lip
advancement
• Wedge Lip, ear
resection with
advancement

advan­cement flaps and their utility in


different anatomical regions is shown in
Box 19.3. B
• Single-pedicle advancement flap:
Figs 19.16A and B: U-plasty
It is the most basic flap, also called
U-plasty. Ratio of defect the length
to the flap length is 3:1 (Figs 19.16A
and B).
• Bilateral advancement (H-plasty):
It is typically made when a single-
pedicle advancement flap does not
allow sufficient tissue for closure of
the defect. The major disadvantage
of this flap is the potentially long
suture line (Figs 19.17A and B).
• O-T plasty or A-T plasty: This flap
represents a type of bilateral advance­
ment flap where a triangular defect
is closed by advancing tissue from A B
either side of the defect (Figs 19.18A Figs 19.17A and B: Bilateral advancement flap on forehead
and B). The advantage of this flap is
that the defect can be divided in half
by the use of the two flaps allowing
placement of the incisions in natural
creases, junctions of esthetic units
or in the hairline. It works very well
in the forehead and temple with the
horizontal component placed in
the hairline and along the lip with the
horizontal limb at the vermilion. A B
• V-Y plasty: This is a unique flap Figs 19.18A and B: O-T plasty to close defect on upper lip
where a V-shaped flap is moved into
a defect with primary closure of the
donor area leaving a final Y-shaped mobility of the skin allows wide Transposition Flaps
suture line (Figs 19.19 and 19.20). undermining and closure of medi­ Transposition flaps involves swinging
• Cheek advancement flap: These um to large defects along the lat­ the flaps into areas of defect over heal­
flaps are optimally used in the cheek eral nasal wall and infra­orbital area thy tissue, with a secondary defect at
where the increased elasticity and (Figs 19.21 and 19.22). the donor site that is closed primarily
Management of Soft Tissue Injuries 397

by undermining adjacent tissue or by tension line. The middle segment of


coverage with a free skin graft. the Z-shaped incision is made along
Various transposition flaps are: the line of greatest tension or con­
• Z-plasty: Z-plasty is a method of sur­ traction and the flaps are raised on
gical revision of a scar or closure of a opposite sides of the two ends and
wound using a Z-shaped incision to then transposed, the length and an­
reduce contractures of the adjacent gle of each flap must be precisely the
skin. A straight line closure may re­ same to avoid mismatched flaps that
sult into more scar contracture and may produce bad scar. It requires
hence a Z-closure is useful to mini­ a proper skin thickness, a thin flap
mize contractures when used pri­ contracts read­ ily and give unes­
Fig. 19.19: V-Y plasty in which V- shaped marily (Figs 19.23A to C). It can elon­ thetic scar and a flap with too much
defect is created and sutured to form a gate a contracted scar or rotate scar subcutaneous tissue is difficult to
Y-shape

A B C
Figs 19.20A to C: A defect on finger in which V-shaped defect is created and sutured to form a Y-shape

A B C
Figs 19.21A to C: Cheek advancement flap

A B C
Figs 19.22A to C: Cracker burst injury: (A) After debridement; (B) Canulation of parotid duct; (C) Final closure
398 Maxillofacial Trauma

position beca­use of limited rotation.


The plane of dissection should al­
ways be deve­loped between subder­
mal ple­xus and sub­cutaneous fat for
pro­per thic­k­ness.
The three stages of the Z-plasty
tech­nique are given in Figures 19.23A
to C.
• Rhombic flap: It is very versatile
A B C flap, highly reliable, allows precise
incisions and wound closures result­
ing in predictable straight line sc­
Figs 19.23A to C: Stages of Z-plasty technique ars. Major disadvantage is risk of
necrosis is more with this flap. It
consists of two equilateral triangles
placed base to base to form a rhom­
bus (Fig. 19.24).
• Bilobed flap: It is a double trans­
positioned flap that shares a single
base. It is used extensively for nasal
reconstructions. The primary flap is
to repair the surgical defect and the
secondary flap is used to repair the
flap donor site. The secondary flap
defect is then closed primarily. It is
used extensively for nasal recon­
Fig. 19.24: Marking for rhombic flap to Fig. 19.25: Marking for bilobed flap to struction (Fig. 19.25).
close defect close the defect • Nasolabial flap: It is an axial pattern
flap based on angular artery. It can
be used for reconstruction of lower
two-third of nose, perinasal area,
upper lip and minor intraoral defects
in the anterior area. The flap could
be on inferiorly based, superiorly
based or central pedical (Figs 19.26
to 19.28). The flap is reliable but
the area of average is limited. The
nasolabial flap based on the central
pedicle has good length but the
A B
width is limited.
Figs 19.26A and B: Inferiorly based nasolabial flap Whenever tissue loss is extensive,
which cannot be repaired using local flaps,
distant flaps can be taken in such cases–
such as pectoralis major myo­cu­taneous
flap, deltopectoral flap, trap­ e­zius flap.
Free tissue transfer using microvascular
ana­stomosis have increased the flexi­bility
in the soft tissue and osseous recon­
struction, e.g. radial forearm flap, fibular
flaps, lateral scapular flap.

Free Grafts
A B Graft is something that is potentially dead
Figs 19.27A and B: Superiorly based nasolabial flap and its survival depends on recipient site
Management of Soft Tissue Injuries 399

Salient Features for Harvesting


Skin Graft
• Skin graft should have a good vas­
cular bed at the recipient site for
better uptake and support.
• Donor site and recipient site should
be free of pathogens deleterious for
graft.
• Graft should be in closest possible
con­ tact with the bed to prevent
A B hema­­toma, air bubble, which does
Figs 19.28A and B: Bi-peddled nasolabial flap for intraoral closure not allow proper healing.
• Graft should be totally immobile
over the bed for which it should be
covered with pressure dressing for
first 5 days till anchorage of graft has
occurred at the recipient site.
• The raw surface of donor site after
graft harvesting should be covered
with vaseline gauze pieces, then
with burn pads and then tightly tied
roller bandage. Dressing is kept for
A B 15 days till it gets loose its own.
Figs 19.29A and B: Humby knife used for harvesting the skin grafts
Injuries Require Special
Consideration
whereas flap is attached to a pedicle, skin graft will preserve the original size
which provides an arterial blood supply and shape of the defect, which can be Lip
with venous and lymphatic drainage. repaired later, till then it will provide Injuries of lip require special care be­
Following are some of the free grafts: sterile cover and minimize fibrosis. cause of the peculiar anatomy of the
• Split-thickness skin grafts A skin graft adheres to its new bed region of the vermilion border. Even a
• Full-thickness skin grafts (Wolf graft) by fibrin. This diffuses from the plasma mismatch of 1 mm of vermilion border
• Composite full-thickness skin and bed and supplies the immediate nutri­ can be noti­ceable. After the trauma as
cartilage grafts ti­onal requirements in the form of plas­ the edema sets in and approximation of
• Pinch grafts (Free skin grafts) matic circulation. This is enhanced by margins may result in irregular vermil­
• Dermal and fat grafts the outgrowth of capillary buds such ion margin, which may become con­
• Fascial grafts that a circulation of blood in the graft spicuous after the edema subsides. The
• Chondromucosal grafts. can be demonstrated at 48 hours. At the nerve blocks for establishing local an­
The first four receive their blood sup­ same time, fibers grow into the fibrin, esthesia are preferred rather local infil­
ply from recipient site and last three are which convert the adhesive clot into a tration to avoid distortion of the tissue.
avascular. more definite fibrous tissue attachment The wound on the lip should be closed
A free skin graft consists of entire that increases over the ensuing days, so in layers; the re-approximation of orbi­
thickness of the epidermis and a vari­ that by 5 days reasonable anchorage has cularis oris mu­scle is very important as
able amount of the dermis. A split skin occurred and that is why we keep pressure any disr­up­tion will leads to scar forma­
graft consists of entire epidermis with dressing over skin grafts for at least 5 days tion and compromised function.
variable amount of dermis, where as full after which anchorage has occurred and
thickness skin grafts consists of entire chances of any hematoma formation Ear
epidermis and dermis. When there is beneath the graft would be minimal. The ear has a very good blood supply
full thickness defect of the cheek or lip, Instrument required for split skin and can maintain large portion of tissue
mucosa can be closed to the skin. Split gra­­­fts is Humby knife (Figs 19.29A and B). on very small pedicles. Injuries on ear
400 Maxillofacial Trauma

A B
Figs 19.30A and B: Ear lobule repair

A B C
Figs 19.31A to C: Injury of eyebrow closed primarily

A B C
Figs 19.32A to C: Injury of eyebrow and upper eyelid

require conservative debridement and defects and the sutures should be placed fun­­ctional deformity. Eyebrows are never
manipulation to maintain as much through the skin establishing good skin shaved for part preparation and inci­sion
tissue as possible. The cartilage of the closure (Figs 19.30A and B). given on eyebrows should be oblique
ear does not require suturing as the and parallel to the hair follicles to avoid
mani­pulation and undermining of skin Eyebrow injury to hair follicle, which leads to loss
over it can devitalize the cartilage. Mini­ Reconstruction of eyebrows is extremely of hair and unsighty scar (Figs 19.31 and
mal sutures should be used to close ear difficult as it can lead to esthetic and 19.32). Sutures should not be secured
Management of Soft Tissue Injuries 401

A B C D
Figs 19.33A to D: Correction of post-trauma ectropion: (A) Preoperative view; (B) V-shaped incision given; (C) V to Y closure done;
(D) Postoperative view showing corrected ectropion

tightly as it causes decrease blood supply 2. Maxillofacial Surgery Vol. 2, 2nd edit­ 2. Singer AJ, Hollander JE, Quinn JV.
to hair follicles. Single layer closure is ion-Peter Ward Booth. Evalu­ation and Management of Trau­
never justified for eyebrows. 3. Maxillofacial Trauma and Esthetics matic Lacerations. N Engl J Med.
Facial Reconstruction by Peter Ward 1997;337:1142–8.
Eyelid Booth. 3. Haug RH. Etiology, Distribution, and
Eyelids are composed of very thin skin, 4. Oral and Maxillofacial Trauma 3rd Classification of Craniomaxillofacial
alveolar tissue, orbicularis oculi muscle, edition Vol. 2 edited by Raymond J. De­formities: Traumatic Defects. Cra­
tarsus, tarsal glands and conjunctiva. Fonseca. niomaxillofacial reconstructive and
Eyelid is thin and contains containing so 5. Peterson’s Principles of Oral and corrective bone surgery. Springer New
many structures and during reconstruc­ Maxillofacial Surgery 2nd edition Vol. 1 York. 2002.
tion these all should be sutured indi­ edited by Michael Miloro. 4. Bartlett, et al. Ballistics and Gunshot
vidually. Levator muscle inserts in skin 6. Rowe and William’s Maxillofacial Inju­ Wounds: Effects on Musculoskel­
of upper lid and is responsible for eleva­ ries edited by William’s JLI Vol. 1. etal Tissues. J Am Acad Orthop Surg.
tion of the eyelid. If closure is not done 7. Stell and Maran’s Head and Neck Sur­ 2000;8:21-36.
in layers it can lead to formation of scar gery 4th edition by John C Watkinson. 5. Ambroise Pare La Méthod de traicter
and ectropion (Figs 19.33A to D). Inju­ 8. Surgical Clinics of North America. les playes faites par les arquebuses et
ries to the nasolacrimal apparatus must 9. Textbook of Plastic surgery 6th edition aultres bastons à feu 1545.
be addressed properly facing to which Grabb and Smith. 6. Advisory Committee: Centers for Disease
epiphora may result. Hence, a careful 10. Textbook of Plastic Surgery Vol 2-Mc­ Control: Tetanus—United States, 1987
examination and these special consider­ Carthy. and 1988. MMWR. 1990; 39:7-41.
ations should be taken during any man­ 7. Lee C, Hansen S. Management of Acute
agement of soft tissue injury on face. Wounds. Clinics in Plastic Surgery.
References
2007; 34(4):685-96.
1. Ochs M, Tucker M. Current concepts in 8. Charles H Thorne. Grabb and Smith’s
Suggested Reading
mana­gement of facial trauma. Journal Plastic Surgery. Lippincott Williams
1. Craniomaxillofacial Trauma by David of Oral and Maxillofacial Surgery. 1993; and Wilkins. 2002.
DJ and Simpson DA. 51(1):42-55.
20 Fractures of Mandible
Borle Rajiv M, Arora Aakash, Yadav Abhilasha

The mandible forms the lower third of the they strike against the glenoid fossa. The a bilateral fracture at the parasymphysis
face. It is the most prominent part of the condylar neck fractures readily, owing to area, the tongue tends to loose its anchor­
lower third of the face at the symphyseal its weakness and absorbs all the shock and age on the bone and the patient looses
area and thus, most vulnerable site to prevents it from being transmitted to the control and the tongue tends to fall back.
be traumatized during the road traffic base of the skull. It is especially true for the unconscious
accidents (RTA). Similarly it is the most The ramus of the mandible is thin as patient, where the tongue fall blocks the
tempting site to be hit during the assault compared to the body. Whenever a thick airway and it could be fatal if not prevent­
and thus, the fractures of the mandible are portion of the bone unites with the thin ed. The inferior alveolar neurovascular
most common in the symphyseal or the portion, it constitutes a line of weakness. bundle passes through the bone and in
para symphyseal area. Further, the third molars are located case of fracture it may get traumatized and
in the angle region and when they are can lead to hematoma and neurological
APPLIED SURGICAL impacted they occupy lot of space in the deficit.
bone and undermine it. The bone grains,
ANATOMY OF MANDIBLE which are oriented vertically in the ramus CLASSIFICATION OF
The mandible is the strongest of all the change their course at the angle of mandi­
FRACTURE MANDIBLE
facial bones and it is the only mobile bone ble as they enter the body of mandible.
of the facial skeleton. It is roughly horseshoe This abrupt change in the course of the The fracture is defined as a breach in
shaped with the symphysis being its most bone grains also makes the bone weak. All the continuity of the bone. The general
prominent part. It has thick cortical plates. these factors make the mandible vulner­ classification of fractures of the bone is as
The condyles articulate with the glenoid able for fracture at this site. follows:
fossa of the temporal bone, superior to In the canine area also the mandible is • Simple fracture: Simple fracture is
which the middle cranial fossa is located. weaker as the canine has a longest and the the fracture of the bone, where the
The condylar neck is thin, slender and stoutest root and it occupies lot of space fracture line is not exposed to external
weak. This is a natural protection provided in the bone and undermines and weakens environments as the overlying soft
by the nature. When there is trauma to the it. Thus, the mandible has a tendency to tissue cover is intact (Figs 20.1A and B).
symphyseal area, the forces are transmitted fracture at this site. • Compound fracture: Compound frac­
to the condyle and the base of glenoid fossa The symphyseal area as stated earlier ture is that, where the fracture line is
along the bone, if the condylar necks were is most prominent and most vulnerable to exposed to the external environments
strong structures, the forces would have trauma. There is compression of the outer (Internal—oral cavity, external—atmo­
been transmitted to the base of the glenoid cortex and expansion of the inner cortex sphere) (Figs 20.2A and B).
fossa, resulting in the fracture and the and the fracture will result when the forces • Comminuted fracture: Comminuted
condyles would have entered in the middle are beyond the capacity of the bone to fracture is that fracture, where there
cranial fossa creating a grievous head withstand them. are multiple fracture lines and more
injury. To prevent such grievous injuries, There is a pair of genial tubercles on than two fragments of the bone are
the nature has made the condylar process the lingual cortical plate in the midline, present (Fig. 20.3).
thin, slender and weak. Whenever there is situated superoinferiorly, which give ori­ • Simple comminuted fracture: When
trauma to the symphysis, the condyles tend gin to the genioglossus and geniohyoid the comminuted fracture is not ex­
to get pushed upwards and posteriorly and muscles, respectively. Whenever there is posed to the external environments.
Fractures of Mandible 403

• Symphyseal fractures and parasym­


physeal fractures (including the canine
area fracture) (14%)
• Body fractures (21%)
• Gonial area or angle fractures (20%)
• Condylar fractures (intracapsular) and
subcondylar fractures (high and low)
(36%)
• Coronoid process fractures (2%)
• Dentoalveolar fractures (3%).

According to Displacement
and Ability to Prevent
A B Displacement due to
Figs 20.1A and B: Simple fracture, in figure A although the tooth is involved the fracture Muscle Pull
is simple because the tooth is unerrupted
The fracture fragments are liable to dis­
placement according to unfavorable
muscle pull leading to difficulty in the
management of these displaced frac­
tures. The elevators of the mandible are
attached to the ramus (masseter, tempo­
ralis, lateral pterygoid), while as the de­
pressors of the mandible, i.e. the supra­
hyoid muscles (digastricus, geni­ohyoid)
are attached to the body and the genial
tubercles, respectively. The lateral ptery­
goid is attached on the pterygoid fovea at
the neck of the condyle, which common­
ly displaces the subcondylar frac­ tures
medially and sometimes the fractured
A B
condyle gets dislocated in the infratem­
Figs 20.2A and B: (A) Compound fracture due to involvement of the erupted tooth and poral fossa (Fig. 20.7).
fracture of the tooth; (B) Degloving laceration is present, compounding the fracture
intraorally
Vertically Favorable
seen in the children, where the bones When the fracture line is viewed from the
are elastic and resilient. The children superior aspect of the mandible (alveolar
are susceptible to fall and thus this is a border) and is passing from buccal cor­
natural protection against the fracture. tical plate to the lingual cortical plate
This type of fracture is commonly seen with the buccal end lying mesially and
in the long bones. In the facial skeleton the lingual end of the line lying distally. In
the condylar neck is the most common such a situation, the distal fragment will
site to show this fracture (Figs 20.4A be drawn closer to the proximal fragment
and B). due to the pull of the medial pterygoid
• Pathological fracture: When the bone muscle and the fracture segments will
is undermined by any pathology and has come closer rather than getting separated
Fig. 20.3: Comminuted fracture become significantly weak, can fra­cture in bucco-lingual plane and thus the
readily with physiological fun­ction, trifle fracture is called vertically favorable
• Compound comminuted fracture: trauma or normal functional pressure or (BALP).
When the comminuted fracture is movement (Figs 20.5A and B).
exposed to the external environment. Vertically Unfavorable
• Green stick fracture: Green stick According to the Site In vertically unfavorable case, the fracture
fracture is the incomplete fracture and The fractures can be classified according line passes buccolingual with the buccal
often presents like a cortical bending to the site of fracture and its incidence as end lying mesially, when viewed from
rather than breaking. It is commonly follows1 (Figs 20.6A and B): superior border. The distal fragment
404 Maxillofacial Trauma

lying posteriorly than its inferior end. In


this situation the muscle pull from the
temporalis and masseter muscle will pull
the distal segment superiorly and the
suprahyoid muscles will put the proximal
segment inferiorly, thus drawing both the
segments closer to each other. This type
A
of fracture is called horizontally favorable
fracture.

Horizontally Unfavorable
When viewed horizontally, the fracture line
runs superoinferiorly with its superior and
lying anteriorly and the inferior end lying
posteriorly thus, the muscle pull becomes
unfavorable and drifts the proxi­mal and
distal fracture segments apart. This is
B described as a horizontally unfavorable
Figs 20.4A and B: Green stick fracture fracture (Figs 20.9 and 20.10).

Direct and Indirect Fracture


When the force is applied to the bone,
the cortex (buccal cortex) at the site
of application of the force undergoes
compression and the other cortex (lingual
cortex) of the bone undergoes tension. If
the force is greater than the compressive
and the tensile strength of the bone a
fracture ensues.
A B Similarly, when the force is applied to
Figs 20.5A and B: Pathological fracture the mandible, the point of application of
the force is compressed and the resultant
vector travels along the bone and applies
tensile force on the point intersected by
this vector. The fracture occurs at the site
of direct application of the force and the
fracture occurs at this site due to compres­
sion of the bone (direct fracture). A fracture
also occurs at the site intersection of the
resultant vector by tensile forces (indirect
fracture). For example, the force applied
to the symphysis menti results in a direct
fracture at the symphysis. The vector trav­
els to the condylar necks bilaterally and
A B induce indirect fractures of subcondylar
Figs 20.6A and B: Fracture sites and incidence areas bilaterally, as the condylar necks are
weak. This is called ‘Tripod fracture’ (as
the fracture is at three points) or ‘parade
in this case will be easily viewed from fracture is said to be vertically unfavorable ground fracture’ or ‘guardsman’s fracture’.
superior border. The distal fragment in (Figs 20.8A and B). The later terms are used because when the
this case will easily get drifted lingually soldier at the parade ground stand upright
due to the pull of the medial pterygoid Horizontally Favorable for a long time and faints, falls on the chin
muscle, thus there will be separation of the When viewed from the buccal side and the fracture occurs at symphysis and
fragments in the buccolingual plane due (horizontally), the fracture line runs condylar necks, bilaterally (Figs 20.11A
to the unfavorable muscle pull, and the superoinferiorly with its superior end and B).
Fractures of Mandible 405

Fig. 20.10: Horizontally unfavorable frac­


ture of the proximal segment has been
displaced superiorly
Fig. 20.7: Muscle attachments of the mandible, causing displacement of the Box 20.1: Combination of direct and
fractured segments due to unfavorable pull indirect fractures
Direct Indirect
Symphysis Bilateral subcondylar
Parasymphysis Contralateral
subcondylar fracture
Canine region Contralateral angle
Body Contralateral angle or
subcondylar

The other common examples of direct


and indirect fractures are shown in Box 20.1
and Fig. 20.11C.
It is necessary to know this combi­nation
because as a rule of thumb, when ever a
direct fracture is seen at the site of primary
impact, one must examine the correspond­
A B
ing indir­ect fracture site and rule out the
Figs 20.8A and B: Vertically favorable and unfavorable fractures
indirect fracture. If this principle is followed
dur­ing the examin­ation of the patient, the
chances of missing the indirect fracture are
minimized. Although, no two traumas are
identical, no two fractures are identical.
These are the standard combinations, which
are comm­only encountered in the clinical
practice, but occasionally different patterns
of injuries can be seen due to varied nature
of the trauma (Figs 20.11B).

CLINICAL FEATURES OF THE


FRACTURE
The clinical features of the fractures are as
follows:
• Pain, inability to masticate and swallow
A B leading to dribbling of saliva.
Figs 20.9A and B: Horizontally favorable fracture (A); Unfavorable fracture (B) • Swelling and hematoma.
406 Maxillofacial Trauma

A B C
Figs 20.11A to C: (A and B) Direct and indirect fracture due to the vector (canine and opposite angle); (C) Various combinations of the
direct and indirect fractures

A B C
Figs 20.12A to C: (A) Sublingual hematoma (Colman’s sign); (B and C) Step deformity

• Facial asymmetry due to edema and pterygoid muscle. In case of unilateral • Derangement of occlusion due to dis­
hematoma. subcondylar fracture, the opposite placement of the fracture segments.
• Bleeding per orally from the fracture sided lateral excursion is lost. • Step deformity in the arch (Figs 20.12B
site. • Tenderness over the fracture site. and C).
• The skin may show contusion, abra­ • Crepitus over the fracture site due • Sublingual hematoma, especially
sion or laceration with discoloration to grating of the segments over each during the fracture involving the den­
due to injury. In case of symphyseal during the palpation. ture bearing area. This sign is called
fracture or subcondylar fracture, lac­ • Abnormal mobility across the fracture ‘Colman’s sign’. It should be taken as
eration is usually present on the chin. site. a pathognomonic sign of fracture, as
• Trismus and limited excursions of the • Step deformity palpable at the site due the sublingual hematoma cannot be
mandible. The trismus is produced to the displacement of the fracture formed unless the lingual cortex is
as a result of protective myospasm segments. fractured and it is unlikely that direct
secondary to pain. The movements • Injury to the inferior alveolar nerve injury to the lingual cortex will occur
increase the pain. When the there is in the bony canal during the fracture to the lingual tissue by an external
swelling and hematoma, the affected may lead to neurological deficit in the object (Fig. 20.12A).
part becomes heavy and the fractured distribution of the mental nerve. • The teeth may show luxation, displace­
jaw is unable to offer support to • In case of bilateral subcondylar frac­ ment, avulsion with laceration of the
the part. Normal movements while ture, when the proximal segment gets gingiva. There may be laceration, ecchy­
speaking, chewing and even the jerks displaced medially due to the pull of mosis in the buccal vestibule. The teeth
during walking precipitate pain. lateral pterygoid and the distal seg­ are sometimes involved in fracture line.
Thus, the body induces its protective ment is pulled superiorly, shortening When the fracture line passes through
mechanism by inducing myospasm to of the ramus takes place. This phe­ the dentate area of the dentulous
restrict the movements. The protrusive nomenon is called ‘telescoping of patient; the teeth are always involved
and lateral excursions are lost when the fracture’ which results in the an­ in the fracture line. This fracture is
there is a subcondylar fracture, owing terior open bite with gagging of the essentially a compound fracture as the
to the lack of function of the lateral last molars. intraoral compounding, if the fracture
Fractures of Mandible 407

takes place intraorally, through the canal gets traumatized between the to perform various excursions of
periodontal ligament or the pulp of the condyle and the posterior wall of the the mandible and the condylar
fractured tooth. The injury to the teeth bony canal and leads to its laceration, movements are felt, which are
should be carefully evaluated as such resulting into bleeding from the ear. diminished when the mandible is
teeth may infect the fracture and delay It should be carefully examined and fractured. They are move severely
the healing. All the teeth involved in the laceration should be visualized by hampered when the subcondylar
the fracture line need not be extracted, mopping the blood. The laceration is fractures are present. If there
especially when they are firm, intact, largely present over the anterior wall. is a fracture dislocation of the
unerupted and do not interfere with In absence of such laceration, the condyle, the glenoid fossa appears
the proper reduction or are required other causes for bleeding per ear, like empty. Then the palpating finger
to be preserved for esthetic reasons, fracture of base of the skull, which are is passed over the posterior
especially in case of young patients more grievous, should be ruled out. border of the mandible, angle,
with involvement of the anterior teeth. inferior border up to the midline,
The teeth, which are grossly luxated, EXAMINATION OF THE bilaterally to note any ten­derness,
fractured beyond conservation, badly crepitus, step deformity or abno­r-­­
PATIENT
carious or obstruct proper reduction mal mobility (Figs 20.14A to D).
should be extracted (Fig. 20.13). The examination of the patient with Bima­ nual examination should
• When the mandible is held bimanu­ally, suspected fracture of the mandible is done also be carried out to reach a
keeping index fingers on the occlusal in a methodical ways as follows: clinical diagnosis. A clinician must
surface on the teeth across the sus­ • General examination comprising of follow certain basic rules as a rule
pected fracture line and the mandible examination of vital signs, and for of thumb that:
is moved superoinferiorly and antero­ ruling out other injuries, visceral • When a fracture or even a laceration
posteriorly, abnormal movements are injuries, other bone fractures, head is detected in the symphyseal area,
elicited. injury, spine injury, fractures of ribs, bilateral subcondylar area must be
• The bilateral parasymphyseal fractures flail chest, etc. to decide priorities in thoroughly examined to rule out any
make the genioglossus muscle loose the management as the life-saving indirect fracture.
its anchorage onto the bone and the measures are undoubtedly the first • Whenever a parasymphyseal fracture
fractured segment tends to collapse priority. is detected, contralateral subcondylar
lingually, making the tongue to fall • Local examination comprises of: area must be examined to rule out
back. This is very dangerous in an – Inspection: To note swelling, de­ indirect fracture.
unconscious patient as it can lead to formity, soft-tissue injuries, limi­ • Whenever a fracture is detected at the
respiratory embarrassment. tation of mandibular excursions, canine area an indirect fracture must
• During the injuries to the chin, which derangement of occlusion, step be ruled out at the opposite angle of
may result in the symphyseal or sub­ deformity in the arch, Col­man’s the mandible. The teeth involved in
condylar fracture, the mandible gets sign, bleeding per orally, bleeding the fracture line must be carefully
pushed backwards and superiorly. per ear, etc. examined.
The cartilage of the external auditory – Palpation: The palpation of the – Bimanual palpation: The bima­
mandible starts with the condyles. nual palpation is done to elicit
Even though there is no fracture abnormal mobility across the frac­
of the condyle, contusion of ture line in cases of the fractures
the condyle will also produce involving denture bearing areas,
tenderness over the condyle. The i.e. the symphysis, parasymphysis
condyle is palpated by placing and the body. The man­ dible
the fingers over them anterior to is grasped on either side of the
the tragus. If there is excessive suspected fracture line in such a
of edema, the condyles and way that the index finger is on the
their movements will be poorly occlusal surface of the teeth and the
felt in such cases thus, the little thumbs are on the inferior border.
fingers are hooked in the external The proximal and distal segments
auditory meatus with their pulp are moved in superoinferior and
placed towards the anterior wall. anteroposterior direction, to elicit
Fig. 20.13: Fracture line passing through This will allow the operator to abnormal mobility (Fig. 20.15). This
the tooth which is also fractured, necessi­ feel the posterosuperior aspect of examination is useful in detecting
tating its extraction the condyle. The patient is asked the fractures which are undisplaced
408 Maxillofacial Trauma

X-rays of the mandible as they show


the complete mandible. The specific
views can be advised on the basis
of the findings of these screening
radiographs to visualize the fracture
line properly and to obtain further
details. As a rule in orthopedics, the
X-ray must be taken in two planes
perpendicular to each other, i.e. in
the anteroposterior and mediolateral.
A B
Thus, apart from the PA view, lateral
oblique view is taken for body, angle,
ramus and subcondylar fractures.
The symphyseal area is poorly seen
on PA or panoramic view due to the
spinal super imposition (Figs 20.17A
to D). In such cases IOPA X-ray or an
occlusal film should be taken for better
visualization. The condylar head is
seen well on transcranial view for
C D intracapsular fractures and the high
Figs 20.14A to D: Palpatory examination of patient. Start from the condyles and follow subcondylar fractures are visualized
through posteriors borders and inferior border on the transpharyngeal view. When
the fracture line runs obliquely on
and the fractures of the symphysis/ the operator, elicits tenderness, the bone or due to angulation of the
parasymphysis which are not pro­ which may suggest the fracture X-rays, two images of buccal and
perly visualized on routine radio­ (Figs 20.16A and B). lingual cortical plates fracture are
graphs due to superimposition of • Radiographic examination is the most seen giving a false picture of a comm­
the shadow of the spine. conclusive evidence of the fracture, united fracture. The computed tomo­
– Compression test: When there is however it must be remembered that graphy (CT) scans are very help­ful and
a hairline, undisplaced fracture it is not the substitute for the clinical give excellent information (Figs 20.18A
of the mandible especially at examination. Even for advising proper to G).
the symphysis, angle or in the radiographic views, the clinical diag­
subcondylar areas and it is not nosis of the fracture is essential. The MANAGEMENT OF THE
conspicuous clinically and radio­ X-rays are the concrete evidence of
FRACTURE
logically, a compression of the the fracture and thus, mandatory to
mandible at the symphysis area be taken and preserved in medicolegal The management of the fracture of man­di­
and over both the sides over the cases. The PA view of mandible and ble can be discussed under following heads:
body, using both the palms by the panoramic X-ray are the screening • General supportive treatment.

A B
Fig. 20.15: Bimanual palpation of the Figs 20.16A and B: Compression test for the undisplaced mandibular fractures at
mandible to elicit abnormal mobility subcondylar, symphyseal (A) and angle region (B)
Fractures of Mandible 409

• First aid management. GENERAL SUPPORTIVE with other injuries. The polytrauma
• Definitive management. patients require priority wise treatment,
TREATMENT
• Special consideration for manage­ i.e. the life-saving treatment must be done
ment of pediatric, geriatric edentulous The fractures of the mandible do not always on priority basis and the management of
fractures and condylar fractures. occur in isolation, but can be associated minor injuries and fractures can be delayed
until the patient is stabilized. The priorities
in the management are as follows:
• The vital parameters should be criti­
cally monitored and airway patency
and respiratory support must be
given whenever required, to prevent
the hypoxia. The circulatory effi­
ciency must be assessed by monitor­
ing pulse, blood pressure (BP) and
organ perfusion must be monitored.
When there is blood loss, the pulse
becomes rapid and thready depending
upon the amount of blood loss. When
the patient is in hypotension, the periph­
eral pulse is lost. When the BP is around
A B
60 mm Hg the radial pulse is absent
and only carotid pulse is felt. If the BP
is around 70 mm Hg, the femoral pulse
is palpable and when the BP is around
80 mm Hg, the radial pulse is palpable.
The hypotension results in inadequate
organ perfusion due to selective periph­
eral vasoconstriction and fall in mean
arterial pressure. The measurement of
the urinary output is reliable marker for
C D
assessing the organ perfusion. It should
Figs 20.17A to D: PA view, lateral oblique view and panoramic view of the mandible be more than 0.5 mL/kg of body weight
showing fracture

A B C D

E F G
Figs 20.18A to G: CT scans on axial (B, C) and coronal (A, D, E) sections along with
3D reconstruction (F, G) showing fracture of mandible
410 Maxillofacial Trauma

per minute in adults, 1 mL/kg of body further bleeding, hematoma, pain and Management of Soft-tissue
weight/hour in children and 1.5 mL/kg/ inflammatory edema. The fractured part Injuries
hour in infants (around 20 mL/hour). lacks support and becomes heavy due to
If it is less, then replacement of blood edema and hematoma. The movement The fractures of the mandible are asso­
volume by parenteral administration aggravates pain, inflammation, bleeding ciated with soft-tissue injuries such as
of crystalloid solution should be done. and in case of compound fractures, the abra­sions, lacerations of skin, intraoral
The further bleeding should be arrested infection gets pumped in due to the deglo­ving lacerations (Figs 20.21 and
by sutures, ligatures, pressure packs movement, all these things are prevented 20.22). The fracture line sometimes gets
or surgical exploration, before blood by temporary splinting. com­­pounded to intraoral or extraoral
transfusion is started. Due consider­ The patient is given nutritional support environments increasing the chances of
ation should be given to the head injury by administering parenteral fluids, if he is contamination/infection of the fracture.
and periodical neurological examina­ unconscious or unable to take orally. The An adequate and timely management
tion should be carried out to assess the patients often have trismus and difficulty in of the soft-tissue injuries around the
level of consciousness, posture, neuro­ swallowing who they should be prescribed fracture line is very important as it helps
logical deterioration and alteration in liquid diet or are fed through the nasogastric preventing the infection of the fracture.
vital signs. The Glasgow coma scale2 is tube if there is no contraindication for It is famous quote in orthopedics that
assessed periodically to assess the head passing the nasogastric tube. The local ‘The bone is like a plant, which has the
injury. In the suspected cases, CT scan wound hygiene is maintained. The defini­ roots in the soft-tissue’. The endosteal
should be taken and relevant treatment tive treatment is under taken as early blood supply of the bone gets disrupted
should be started immediately. The as possible because the delay will only when it is fractured and if the soft-tissue
neck splinting should be done in case of increase the chances of infection. infection sets in it may interfere with the
spinal injuries as the movements may
aggravate the injury.
The patient is given prophylaxis
against tetanus by administering teta­
nus toxoid. In severe trauma, where
the wounds are badly soiled or there is
crushed or devitalized tissue, antitetanus
serum (ATS) was administered in the past.
If the horse’s serum is used, then 1,500 to
3,000 IU of ATS is given IM after the test
dose of 200 IU intradermally. The human
diploid cell vaccines are available, which
have better efficacy and compliance.
The long bone fracture is temporarily
immobilized by giving plaster of Paris
(POP) casts. The mandibular fractures
are also temporarily splinted using the
extraoral barrel bandage or the ‘four A B
tailed bandage using a crape bandage’ Figs 20.19A and B: Support to the fractured lower jaw using the four tailed bandage
(Figs 20.19A and B). Alternatively, inter­
maxillary fixation may be done by inser­
ting at least one Ivy loop on either side of
the fracture line. In the dentulous patient
if the fracture is present in the denture
bearing area, then a horizontal wire is
passed in the embrasure between the
adjacent sound, standing teeth and the
wire is tightened, this is called horizontal
fixation (Figs 20.20A and B). The purpose
of the temporary immobilization is not
to reduce the fracture but to splint and A B
immobilize the part to provide rest to Figs 20.20A and B: Temporary fixation of the fracture with horizontal stay wire across
the part, prevent movement to prevent the fracture line
Fractures of Mandible 411

Advantages of the Closed


Reduction (Box 20.3)
Box 20.3: Advantages of closed reduction

1. Non-invasive, simple, easy to master.


2. Does not require exposure to general
anesthesia.
3. Economical.
4. Less chances of infection.

Disadvantages of Closed
Reduction
A B • The reduction is not 100% perfect, as
Figs 20.21A and B: Laceration on the chin only superior segment alignment is
done by achieving good occlusal rela­
tion­ship. The inferior border may not
DEFINITIVE TREATMENT be adequately reduced.
• The immobilization may not be ad­
The definitive treatment comprises of equate which delays the healing. It
following steps: is especially true in case of fractures
• Reduction—closed reduction and open involving the angle and subcondylar
reduction area where the control over the proxi­
• Immobilization mal segment is not established and
• Fixation (usually applied to the open can get displaced with unfavorable
reduction when the fracture fragments muscle pull.
are fixed with implant). • The healing of bone is by secondary
The reduction is done to bring the intention, i.e. callous formation. The
fractured segments together in approxi­ hyperplastic callous may not be esthe­
mation close to their previous anatomical tically or functionally acceptable.
Fig. 20.22: Degloving injury position so that the healing is proper and • The treatment induces lot of morbidity
rapid. This can be done with: to the patient as the intermaxillary
periosteal blood supply as well, leading • Manual reduction fixation is kept for long period affecting
to devitalization. And hence, proper • By elastic traction feeding, speech of the patient.
management of the soft-tissue injuries is • During open reduction with bone • The closed reduction is especially
warranted. holding forceps or the bone levers. problematic when the fracture of
The other importance of the lacerated The indications for closed reduction mandi­ble is associated with the con­
wounds pertaining to fractures of the are summarized in Box 20.2: dylar injuries. For the management
mandible is that a laceration on the chin of frac­tures at other sites than the
is usually associated with fracture at the condylar areas, the immobilization is
Box 20.2: Indications for closed reduction
symphysis and/or the indirect fracture at required for a longer period of time.
the subcondylar area (see Figs 20.21A and 1. Undisplaced fractures. If the associ­ ated condylar injury is
B). Even if there is no symphyseal fracture, 2. Where skill and facilities for open present, a long-term immobilization
the subcondylar fracture could be seen reduction are not available. increases the risk of fibrous adhesions
in some patients. Whenever there is an 3. Medically compromised patients and ankylosis. If the inadequate
injury to chin, an indirect injury to the where conservative line of treatment is immo­ bilization is done, the healing
temporomandibular joint (TMJ) may be required. of the other fracture is compromised.
present due to pushing back of condyles 4. Poor financial status where patient does The rigid internal fixa­ tion has over
against the glenoid fossa and if fracture not afford the cost of treatment. come this draw back to a large extent.
is not present other injuries such as the 5. Grossly infected fractures where the • Closed reduction is not safe in epil­ep­
implants are likely to be infected.
contusion, effusion or hemarthrosis may tic patients as during the epileptic
be present, which warrants careful eva­ 6. Pediatric fractures with mixed dentition seizures the wired teeth can be avulsed
phase.
luation and management to prevent or the patient may aspirate during the
7. Geriatric fracture with edentulous jaws.
further com­plications like ankylosis. post convulsive phase.
412 Maxillofacial Trauma

Modalities of Immobilization • Figure-of-eight wiring: This is the the teeth. Finally, the incompletely
Once the fracture segments are reduced in simple wiring technique often used to tightened ends of the stay wire are
acceptable position, the segments are held temporarily splint the luxated teeth. It tightened fully, to complete the wiring.
and immobilized in the same position by is not used for doing the intermaxillary The cut ends of the wires are bent away
means of wiring or splints. The reduction is fixation. It has got inherent draw from the soft tissue so that they do not
done either by manipulation or the elastic back that it does not offer good three- irritate the soft tissue.
traction. The best example of the use of dimensional stability. • Risdon’s wiring: In this technique, a
elastic traction is the subcondylar fracture • Essig’s wiring: This wiring technique long piece of 24 gauge stay wire is taken
with telescoping of the fracture segments. is also used in the management and passed through the embrasure
In this case, the patient will have anterior of dentoalveolar fractures and for between the last two standing teeth
open bite and gagging of the last molars. splinting the luxated teeth. This is a in the arch from buccal to the lingual
The fracture is not reducible due to muscle better technique as compared to the side. The lingual end is now taken cir­
spasm. This unfavorable muscle pull can figure-of-eight wiring as it gives better cum­ferentially around the last tooth in
be countered by gradual elastic traction stability. In this technique, a piece of the arch and both the ends are firmly
by placing heavy intermaxillary elastics, 24 gauge stainless steel wire is taken twisted over each other. The same
anteriorly. In closed reduction, the guidance and passed through the distal embra­ exercise is done on the other side also
to the proper reduction is achievement sure between the adjacent healthy teeth the twister wires from both the sides
of good occlusal relationship, thus, only to the site of dentoalveolar fracture, i.e. are now twisted together in the midline.
superior segment alignment is given if the incisors are traumatized then The twisted stay wire is ligated to all the
important. The upper and the lower jaws the stay wire is passed through the teeth in the arch using separate pieces
are immobilized by fixing them together embrasure between the healthy canine of number 26 tie wires like it is done
in occlusal relationship (intermaxillary and the first premolar tooth. The wire for legating the arch bar (Figs 20.23A to
fixation or maxillo-mandibular fixation) is passed from buccal side and is drawn C). The Risdon’s wiring can be used for
using wires or splints. The wires, which are from the lingual side. The lingual end is splinting the dentoalveolar fractures and
passed between the teeth of the same jaw passed through the embrasure between for intermaxillary fixa­tion by passing the
through the embrasure spaces are called the distal embrasures of the sound intermaxillary wires inferior to the stay
interdental wires which are the means for adjacent tooth present on the other wires placed in both the arches.
doing the intermaxillary wiring. side of the traumatized segment from • Ivy loop wiring: It is the most com­
The various modalities used for inter­ the lingual to the buccal side and then monly used by practiced wiring tech­
maxillary fixation are: both the ends are tightened by twisting nique. The Ivy loops are prepared from
i. Wiring over each other using a wire twister number 24 to 26 SS wire, depending
• Figure-of-eight wiring or heavy straight artery forceps. The upon the size of the interdental embra­
• Essig’s wiring wires are always tightened by twisting sure. To prepare the Ivy loop a 4″ piece
• Continuous wiring in a clockwise direction and loosened of the temporized wire is taken and
• Risdon’s wiring by twisting in anticlockwise direction. the loops are prepared as shown in
• Ivy loop wiring The wire ends are not tightened fully. Figures 20.24A to C. The free ends of
• Continuous Ivy loop wiring This wire is called a stay wire. Then the loop should be of equal length.
• Gilmour’s wiring pieces of (about 4″ long) number 26
ii. Arch bars tie wire are taken, which are passed Adaptation of the Ivy Loop
iii. Splints through the embrasure, between the The Ivy loop is adapted to teeth in the arch
• Cap splints in pediatric patients traumatized teeth from the labial to as follows:
• Gunning splints in edentulous patients the lingual side, first superior to the • Both the ends of the Ivy loop are passed
• External fixators. labial and lingual stay wire and then buccolingually through the gingival
drawn lingual to labial side through embrasure and drawn lingually.
Dental Wiring the same embrasure, but inferior to One end is taken circumferentially
Usually the high quality stainless steel the stay wires, thus the stay wires are around the distal tooth and drawn
wires are used for this purpose. They have encircled by the tie wire. The tie wire to the buccal side through the distal
good elasticity and do not break readily. ends are now tightened by twisting embrasure. The other end is taken
The number 26 and number 24 wires are fully. The twisting adapts the labial and circumferentially around the mesial
commonly used. The wires are sterilized lingual stay wires to the contour of the tooth and drawn buccally through
by autoclaving. The wires are stretched to traumatized teeth. This procedure is the mesial embrasure. The distal end
10 percent of its original length before use repeated in all the adjacent embrasures is now passed through the loop and
this is called hardening or temporization in the traumatized segment, thus the both the ends are tied by twisting on
of the wire, which makes the wire stiff. stay wire gets nicely adapted to all the mesial/anterior side. The wires are
Fractures of Mandible 413

A B C
Figs 20.23A to C: Step in Risdon’s wiring

the teeth have unfavorable conical


shape.
• Continuous Ivy loop wiring: The Ivy
loops are similar to that of the inter­
rupted Ivy loop wiring only difference
being that they are prepared in the oral
cavity, while doing the wiring. Like in
case of the continuous wiring one long
26 number wire is taken and passed
through the last interdental embrasure
A B
in the arch, from buccal to lingual side.
The buccal sided wire stays as a stay
wire. The lingual wire is drawn through
the adjacent embrasure above the buc­
cal stay wire and passed again to the lin­
gual side through the same embrasure
below the stay wire, keeping the mirror
top handle or a probe in between. The
handle is now rotated to twist the wire
C D and an Ivy loop is prepared. The mirror
top/probe is remo­ved. The same exer­
Figs 20.24A to D: Ligation of the Erich’s arch bars along with IMF with wires and elastics,
cise is repeated in all the adjacent em­
note the brackets are facing gingivally
brasures to prepare multiple Ivy loops.
The disadvantage of this technique is
never tied distally as it is difficult to do tightened to achieve the intermaxillary that if the wire breaks at one point the
so. The loop should be tight enough to fixation (Figs 20.25A to C). whole wiring becomes loose.
prevent its slipping or loosening. The • Gilmour’s wiring:3 It is also called sin­
twisted ends are cut and bent away Limitation of Ivy Loop Wiring gle tooth wiring. It is very useful when
from the gingiva to prevent irritation. • It cannot be done in partially edentu­ the adjacent tooth is missing and the
The Ivy loops are evenly distributed lous patients. Ivy loop wiring is not possible. In this
along the arch to give adequate • It cannot be done if the teeth are technique, a piece of 26 stainless steel
anchorage. If the fracture is present periodontally compromised. wire is taken and passed around a
in the denture bearing area then the • It is not possible to adapt the loop if tooth circumferentially mesiodistally
distribution of the Ivy loops should the adjacent tooth is absent. and the two ends are twisted till it gets
be adequate on either side of the • It cannot be done in mixed dentition tightly adapted to the tooth near its
fracture line. The Ivy loops are placed phase or when the teeth are partially cervical line, below the height of con­
in both the arches. The intermaxillary erupted. tour. The wires are ligated to all the
wires are passed through the loops • It does not have proper stability when teeth in both the arches and then
in the upper and lower jaws and are the teeth have wide diastema or when the maxillary wires are tied with the
414 Maxillofacial Trauma

A
B C
Figs 20.25A to C: Ivy loop wiring

A B C
Figs 20.26A to C: Gilmour’s wiring

mandibular wires to achieve the inter­ • They can be used in presence of should be ligated on right and the left side
maxillary fixation (Figs 20.26A to C). teeth having diastema or unfavorable leaving the gap at the fracture site. If a
forms. The wires tend to slip when the single arch bar is ligated, it will splint the
diastema are present and the contacts fractured segments and hamper proper
Arch Bars between the teeth are absent. reduction.
The arch bars are more effective means for • They can be used when the teeth
the intermaxillary fixation. The wires tend are periodontally compromised and Intermaxillary Fixation
to get loose over a period of time, while the loose. The arch bar splints the teeth Using Screws
arch bars provide more stable fixation. The and provides stable anchorage. The wiring and the arch bar fixation is time
arch bars are of two basic types: • The arch bar has brackets and these consuming and painful procedure for the
• Rigid arch bars: They are not comm­ brackets are very useful for applying patient inspite of local anesthesia. Ligation
only used. These arch bars are adapted intermaxillary elastics. of the arch bar or interdental wiring in the
to the patients cast in the laboratory • The arch bar while providing assistance operating room, while the patient is under
and then transferred to the patient’s in achieving the intermaxillary fixation general anesthesia prolongs the duration
mouth for ligation to the dental arch. simultaneously helps in reducing and of surgery and anesthesia. Moreover, these
• Soft of flexible arch bars: They are splinting the associated dentoalveolar techniques are uncomfortable for the
commonly used. They can be adapted injury. patient due to excess of hardware in the oral
and contoured to the patient’s dental While ligating the arch bar it must be cavity and it is often difficult to maintain
arch directly due to their flexibility, e.g. ensured that the brackets of the arch bar proper oral hygiene. The intermaxillary
Erich’s arch bar (see Figs 20.24A to D). face gingivally to facilitate the application screws are another option for achieving the
of the intermaxillary wires or elastics intermaxillary fixation (IMF). These screws
Advantages of the Arch Bar
(see Figs 20.24A to D). Similarly, the are directly fixed into the alveolar bone
• They can be used in a patient who is arch bar should never be ligated across through the stab incision in the region
partially edentulous or has uneven the fracture line, i.e. if the fracture of of the labial vestibule avoiding injury to
distribution of the teeth in upper and mandible is in the symphysis area, rather the apices of the teeth (Fig. 20.27). If the
lower arches, where wiring is difficult than ligating a single arch bar to entire IMF is planned for long-term then screws
to be done. mandibular arch, two separate arch bars are not a suitable option as the fixation is
Fractures of Mandible 415

a short period of 10 to 15 days and an early


mobilization of the jaw is ensured to prevent
fibrous adhesions and subsequently, anky­
losis. The preferred way of IMF is applica­
tion of the intermaxillary elastics. Even if the
proximal segment of the fracture in subcon­
dylar fracture is medially displaced and the
fracture is high subcondylar, conservative
line of treatment in form of short-term im­ A
Fig. 20.27: Intermaxillary screws mobilization followed by physiotherapy is
used for IMF advocated. The fracture segments are not
reduced and the healing occurs as ‘pseudo-
not adequate. The intermaxillary screws arthrosis’ (false joint).
should only be used in cases, where only
short-term immobilization is required, Splints
e.g. while doing open reduction or during The splints are effective modalities of treat­
the orthognathic surgical procedure. ing the fracture of mandible in edentulous
All the wiring techniques can be done patients and the pediatric patients with de­
under local anesthesia. The indications for ciduous dentition or mixed dentition.
general anesthesia (GA) are uncooperative
patients, limited access due to trismus Cap Splints B
or multiple injuries, severe pain or when The pediatric jaw fractures are treated Figs 20.28A and B: Cap splint along with
the unfavorable muscle spasm or pain with specially fabricated cap splints. The circum-mandibular wiring used to reduce
prevents adequate reduction of the deciduous teeth have unfavorable size pediatric mandibular fracture
fracture. Administration of the GA brings shape and which does not facilitate the
about the muscle relaxation and facilitates wiring. The teeth are sometimes mobile splint is secured to the mandible with the
proper reduction. When the patient is due to the root resorption or during the help of circum-mandibular wiring, using
operated under GA and IMF is done, there mixed dentition some teeth are partially a bone awl or long hypodermic needle
is always a risk of aspiration of vomitus erupted and are not favorable for wiring. In (Figs 20.28A and B).
in the respiratory passage, if the patient such circumstances, the splint becomes the
vomits during the postoperative recovery obvious choice. The open reduction with Procedure for Circum-
period. Hence, the patient should be kept rigid internal fixation is also not possible as mandibular Wiring
in the head low position with head turned the jaw is occupied with developing teeth Under all aseptic precautions, a stab
to one side. A wire cutter should be kept buds, which can get traumatized due to the incision is placed below the inferior
readily available bed side to cut open placement of screws or wires. The splint is border of the mandible up to the bone.
the intermaxillary wires in the event of fabricated by making an impression of the The incision should be taken at the site
vomiting to prevent the aspiration. fractured jaw and preparation of the cast. avoiding the facial vessels at the anterior
The intermaxillary wiring is main­ The cast of the upper jaw is also made. The border of the masseter and avoiding the
tained for a period of 6 to 8 weeks as this cast of the lower arch is split across the mental nerve in the deciduous molar area.
is a period required for healing of the fracture line, where the step is present. The The bone awl (Kelsy Fry) is introduced
fracture. In the younger patients, it is kept split halves of the lower cast are articulated through the incision along the bone and
for shorter time as the healing occurs fast with the upper cast in pre-existing occlusal drawn in the buccal vestibule. A 26 gauge
due to excellent healing potential. In the relationship, thus the fracture gets reduced stainless steel wire is passed through
geriatric patients it is kept longer as the in vitro. Now the base is poured so that the the eye of the awl and then the awl is
healing potential is reduced. Similarly cast is obtained in the reduced position. withdrawn and without withdrawing
when the jaws are sclerosed, irradiated, The acrylic cap splint is fabricated on completely from the skin incision passed
having osteodystrophies-like osteogenesis this cast, which is finished and sterilized along the inferior border to the lingual
imperfecta, are present the immobilization by chemical sterilization. The patient is side along the lingual cortical plate and
may be required for longer period. operated under general anesthesia, the drawn in the lingual vestibule. The wire
In case of condylar fractures, the im­ splint is adapted to the lower jaw thus, the is detached from the awl and the awl is
mobilization is done only during acute fracture gets automatically reduced as the withdrawn (Figs 20.29A to D). The same
phase of injury when pain is severe and splint is fabricated in reduced position and procedure is carried out on the opposite
the part requires rest for resolution of guides the fractured segments in same posi­ side also. The splint is placed in place and
acute symptoms. Hence, the IMF is kept for tion as established in the laboratory. The the buccal and lingual ends of the wire
416 Maxillofacial Trauma

halves in reduced position arbitrarily.


The shellac bases are prepared as in
case of complete denture, wax rims are
also prepared as for the jaw relation (JR).
The JR is recorded and the upper and
lower rims are sealed. The rims are made
discontinuous by removing block of wax
intermittently keeping only three blocks
of wax, i.e. two in the posterior areas and
A B
one anteriorly. The gaps in the rim are
useful for feeding the patient. Wire loops
or segment of arch bar are incorporated
in the splints in each block of wax. The
splint is acrylized, finished and sterilized
by chemical sterilization. The lower splint
is secured to the mandible with circum-
mandibular wiring and the upper one
is fixed to the maxilla by per alveolar
wiring. The IMF is done with the help of
wires passing through the loops of wire
C D incorporated in the upper and lower
Figs 20.29A to D: Steps in the circum-mandibular wiring splints during the fabrication (Fig. 20.30).

External Fixators
and tightened over it, securing the splint discomfort to the patient and the necrotic The fractures can also be treated by
to the mandible (see Figs 20.28A and B). tissue can serve as a nidus of infection. intro­
ducing the Steinman’s pins in the
The extraoral incision is closed with loose The wires are removed under aseptic bone percutaneously, on the either side
single suture. The splint is kept for 3 to 4 care. The oral cavity is disinfected with of fracture line. The projecting pins are
weeks and proper hygiene is maintained antiseptic solution. Like in suture removal, attached to each other with the help of
around it to prevent infection. the wire is gently pulled up after loosening, universal rod and joints, while the frac­tured
If the bone awl is not available then so that the portion of the wire, which fragments are reduced in proper app­r­oxi­
long (2”) hypodermic needle is used for this was buried in the tissue is drawn up and mation. The disadvantage of the external
procedure. Instead of bone awl the needle is the wire is cut at this point. The wire is fixator is that pins and the device project
passed through the submandibular incision pulled out catching the portion, which out through the skin for a long period
and drawn in the buccal vestibule. A piece is projecting in the oral cavity. Thus, the causing lot of morbidity and dis­com­fort
of 26 gauge stainless steel wire is taken and portion of the wire, which was projecting to the patient. They produce unes­thetic
passed through the lumen of the needle. the oral cavity never passes through the scars on the face. The chances of infection
The wire is drawn in the buccal vestibule tissue. The portion of the wire, which in the fracture line are more as the pins are
and the needle is withdrawn completely projects in the oral cavity is contaminated projecting out through the skin.
over the wire, leaving the wire in place. and if allowed to pass through the tissue
The needle is now passed in the lingual will carry the infection along with it in the Open Reduction
vestibule and passed along the bone, to deeper tissue planes. When the fracture line is exposed
draw it through the submandibular stab surgically and the fracture is reduced
incision. The wire end projecting extraorally Gunning Splint4
is passed through the lumen of the needle It is used for treating the edentulous
and is passed in the oral cavity and drawn in jaw fractures. If the patient is complete
the lingual vestibule and the needle is now denture wearer, the same denture can
withdrawn over the wire. The wire is thus be used as the splint, as it was fabricated
passed circumferentially to the mandible. when the jaw was intact. If the patient is
Rest of the procedure is same. It must be not denture wearer, an impression of the
remembered that the wire must be along the upper and lower fractured jaws are made.
bone and no soft tissue should be trapped The lower cast is split at the fracture
between the wire and the bone as such tissue site along the step in the ridge. The step Fig. 20.30: A gunning splint used to
can under go ischemic necrosis and cause is abolished by approximating the two achieve IMF in an edentulous jaw fracture
Fractures of Mandible 417

under direct visual supervision, it is called towards the bone to prevent soft-tissue Rigid internal fixation (RIF): The Swiss
as open reduction. The indications for the irritation (Fig. 20.31). organization Arbeitsgemeins­chaft für
open reduction are (Box 20.4): Krishner’s wire: The Krishner’s wire (K Oste­o­synthesefragen (AO) or Swiss Asso­
The modalities for open reduction are wire) was popu­larly used in the past not ciation for the Study of Internal Fixation
as follows: only for stabilization of the fractures, (AISF) noticed that when the fracture
• Intraosseous wiring—non-rigid fixation. but also for the reconstruction of the fragments are approximated and com­
• Krishener’s wire—non-rigid fixation mandible after segmental resection of the pressed together rigidly, with the help of
• Compression bone staples—rigid fixa­ mandible. It is introduced in the med­ an implant, the healing of the bone is faster
tion ullary portion of the bone on either side and without formation of the callus. The
• Lag screws—rigid fixation of the fracture line. It is used for fixing healing occurs by direct proliferation of the
• Champhy’s miniplates—semirigid fixa­ the subcondylar fractures. The main osteoblastic cells across the fracture line
tion. disadvantage of the K wire is loosening and they called it as primary bone healing.
Intraosseous wiring: It was the most of the wire and its dehiscence as the wire When the fragments are not com­pressed
common technique of open reduction comes out by perforating the skin. The K together rigidly, callus formation takes
practiced in the past, before the advent wire offers non-rigid fixation (Fig. 20.32). place, which gets ossified and the bone is
of the bone plates. In this method, the They are no longer used for treating fract­ formed. They designated it as secondary
fracture line is exposed surgically and the ures in maxillofacial surgery due to advent bone healing. Hence, in the former event
fracture segments were reduced with the of better modalities. there is osteosynthesis by way of almost
help of bone holding forceps and the bone
levers. The intervening granulation tissue,
clot, fibrous tissue, loose bone fragments
were removed and curetted.
The mandible is first immobilized
with intermaxillary fixation in occlusal
relationship because that is the primary
aim of the surgery. Once the occlusion
is established, i.e. the superior border
is aligned, then the inferior border is
reduced by proper approximation. Holes
are then drilled on either side of the
fracture line with the help of dental engine
and bur preventing damage to inferior
alveolar nerve and the roots of the teeth.
A 24 number stainless steel wire is passed
through the holes across the fracture line
and the wire ends are tightened together,
holding the fragments in a reduced posi­
tion. The wire is cut and the ends turned

Box 20.4: Indications for open reduction

1. Grossly displaced fractures with gross


displacement or over riding (tele­ sco­
ping) of the fractured segments.
Fig. 20.31: Various techniques for intraosseous wiring
2. Unfavorable fractures at the angle.
3. Old fractures which do not get reduced
due to the fibrous adhesions.
4. Malunited fractures at the condylar neck
where the proximal segment gets dis­
placed medially.
5. Fractures in epileptic patients where
inter­
maxillary fixation is contra-indi­
cated.
6. Where the morbidity to the patient due
to the intermaxillary fixation is to be avo­
i­ded. Fig. 20.32: Krishner’s wire (K wire)
418 Maxillofacial Trauma

a regenerative procedure and thus, the the plate, there will be relative motion bundle, it is not always possible to place
quality of healing is better than the latter. between the screw head and the plate until the plate along the alveolar border and
In order for this to occur, the stability of the the screws are fully tightened and the screw have to be placed along the inferior border
fixed fracture fragments must be enough heads sit flushed within the plate holes. (compression site). This violates the prin­
to neutralize all bending, torsional and This relative motion will force the screws ciple of compression plating. However, the
shearing forces to which the mandible is and therefore the bone fragments, to move application of the compression plate along
subjected to particularly during function. towards the fracture site. The fragments the inferior border of the mandi­ble would
Interfragmental compression increases are similarly forced to move towards not only be insufficient to stab­ ilize the
the friction between fragments and also the fracture site, thereby resulting in fragments, but also cause the flaring of the
increases the surface area of the fragments inter­frag­mentary compression. Additional alveolar side (Fig. 20.34). Function would
that are actually in contact. This study scr­­
ews are usually placed neutrally then cause movement of the fragments,
was first done on the long bones and then after the interfragmentary compression which would result in danger of infection,
applied to the flat bones like the mandible. (Fig. 20.33A). Rest of all additional screws pseudoarthrosis and malocclusion.
When the concept of interfragmentary are usually placed neutrally. A minimum In order to prevent this problem, a
compression was first developed, there of two screws are placed on each side of tension band or tension plate is applied to
was great concern that the pressure against the fracture line, mandatorily to prevent the alveolar side. The tension band means
the ends of the fragments would lead to rotational movement. Any movement the anatomic alignment of the tension
bony necrosis, however, it does not occur. between the fragments or gliding between site (alveolar) of the fracture via a device
In fact the compression fixation in good the metal implant and bone surface must that prevents distraction. If the patient has
alignment routinely leads to primary be prevented, because, infection will often sound teeth then tension band is applied
(direct) bone healing. For achieving the be the outcome when motion occurs. It on the teeth, which binds the alveolar
primary bone healing they recommended must be remembered that a plate and segment and prevents the distraction. The
the use of the compression bone plates, screw is only helpful when stability is alternative to this band is the application
the dynamic compression plates (DCP). ensured. If the motion is present the plate of tension plate, which neutralizes the
When used properly, it provides for rigid and screw behave as foreign bodies and tension forces and the compression
fixation and compression of the fractured source of infection and the stability is the plate at the inferior border is called the
fragments. The plate is designed so that best protection against infection. stabilizing plate (Figs 20.35A and B). The
interfragmentary compression can be Generally, the compression plate
achieved by the appropriate positioning is applied to the side of the bone that is
of the screws relative to the plate. To biomechanically the site (Tension site)
accomplish this, the fracture must be under tension during functional loading,
reduced. A special device, the mandibular i.e. the fracture border that tends to distract
reduction-compression pliers, has been owing to muscle pull and function. As the
designed to help reduce the fracture opposite or compression site of the fracture
and to obtain precompression prior to will tend to be compressed naturally A
the application of the compression. The during function, the placement of the
pliers screw into the inferior border of the compression plate on the tension side will
mandible, allowing easy manipulation of result in compression along the full length
the fragments and their fixation in pre­ of the fracture without distraction, thereby
compression. The plate must be accurately providing stability. For mandible the side
bent and seated over the fracture. The first under tension, which is determined by the
hole is drilled into the bone eccentrically in arrangement of the muscle and the forces
the plate hole so that the drill is positioned applied during function, is the alveolar
away from the fracture in the edge of the side, while the compression side is the
plate hole. After measuring the depth and inferior border (Fig. 20.33B). Therefore,
tapping the hole, the screw is inserted in order to achieve absolute stability, i.e.
only until the head of the screw reaches the fracture segments are kept in contact
the plate. The first hole in the opposing during the function without movement,
fragment is then drilled, again positioning a compression plate used for treating the B
the drill in the plate hole so that it is away mandibular fracture should be placed near
Figs 20.33A and B: (A) Dynamic compres­
from the fracture. After measuring and the alveolar border, if the biomechanical sion plate causing interfragmentary com­
tapping the hole the screw is now placed principles are observed. However, due to pression; (B) The alveolar border of the
and tightened alternately with the first the anatomical constrains like presence mandible tension site and the inferior bor­
screw. As the head of the screw encounters of roots of the teeth, the neurovascular der is the compression site
Fractures of Mandible 419

eccentric dynamic compression plates The disadvantage with the compres­ osteosynthetic lines to facilitate good and
(EDCP) overcome the above difficulty sion plate is that the plates are very bulky early healing. In this technique only one
and there is no need to use the tension and may be detectable subcutaneously cortex comes in full contact while the other
band or tension plate if the EDCP is used. in certain locations. The technique is opens up to a minor extent. The Champy’s
As the EDCP not only compresses the complicated and requires lot of precision. osteosynthetic lines are as shown in the
fracture fragments but also rotates the The stress shielding effect on the bone diagrams (Figs 20.36 to 20.39).
fracture fragments at the tension site in below the compression has also been In the interior region the line is double,
such a way that the fragments do not flare described. Stress shielding refers to the i.e. one at the inferior border and the
up at the tension site during the function reduction in bone density (osteopenia) as other below the apices of teeth. The line
(Fig. 20.35C). a result of removal of normal stress from gradually climbs upwards towards the
Before any internal fixation is applied the bone by an implant (for instance, external oblique ridge. The placement
it is mandatory to approximate the su­ the compression plates). This is because of the plates along this line on the buccal
perior border, i.e. the alveolar border by by Wolff’s law, bone in a healthy person cortical plate is recommended. The basic
achieving the intermaxillary fixation in the or animal will remodel in response to advantage of this technique is the plates
occlusal relationship. the loads it is placed under. Therefore, are less bulky and all the sites are readily
if the loading on a bone decreases, accessible intraorally, thus avoiding a scar
the bone will become less dense and on the face. In the mandibular anterior area
weaker because there is no stimulus for as the torsional forces are optimum two
continued remodeling that is required to plates are used, one along each Champhy’s
maintain bone mass. The osteoporotic lines. In the canine and premolar area
changes have been demonstrated under while placing the plates intraorally, care
the compression plate due to the stress should be taken to prevent damage to
shielding effect. the branches of the mental nerve. The
It was observed by Champy5 that the mandibular angle fractures are treated by
healing of the mandibular fractures is placing the plate along the external oblique
adequate even in absence of compression ridge through an intraoral incision. The
and with monocortical screws and non- subcondylar fractures are fixed through
compression plates also stabilize the preauricular or Risdon’s submandibular
fragments sufficiently. The need for incision with retromandibular extension
bulky plates is also not felt and thinner or by Hind’s post ramal approach. The low
plates as recommended by him offer subcondylar fractures are easy to plate,
reasonable stability. The kind of fixation but the high subcondylar fractures are
offered by the Champhy’s monocortical very difficult to manage as the proximal
plates is semirigid. Champy observed that fragment is usually displaced severely and
the osteosynthetic activity is optimum difficult to control.
Fig. 20.34: The compression plate fixed at along certain areas during the healing When the miniplates are used, they
compression site creating opening of the of the fracture and he recommend the should be properly adapted and contoured
alveolar border application of the plates along these to the buccal surface of the bone. The gap

A B C
Figs 20.35A to C: (A) DCP with tension band; (B) DCP with tension plate; (C) EDCP eccentric holes at 45 degree angle producing
compression and rotation
420 Maxillofacial Trauma

between the plate and the bone should be of the screw is possible with moderate force. tapping and non-self tapping. Self-tapping
minimal. The screws should be secured Excess of force may lead to micro-fractures is the ability of a screw to advance when
firmly and tightened until no more turning around the shaft of the screw leading to turned, while creating its own thread. Self-
loosening of the screw and micro-mobility, tapping screws come with a sharp, piercing
which may result into the failure of implant tip or a flat, blunt tip. The sharp-tipped
and increased chances of infection. As the screws are designed for drilling their own
Mini plates are applied onto the outer hole into bone and do not need a pilot hole.
cortex of the bone and the monocorti­ The pilot drill used for creating the tunnel
cal screws are used to fix them, a good for fixation of the screw should be smaller
contact between the buccal cortical plate in diameter than the screw shaft to have
is achieved. However, the lingual cortex better purchase of the screw onto the bone.
flares up slightly. To avoid the flaring of the In extremely thin layer of cortical
lingual cortex the slight over contouring of bone, such as facial bones, self tapping
the plate is recommended. screws appear to have better holding
The screws that are used for fixing the power than the non-self tapping screws of
Fig. 20.36: Champhy’s lines plate at the fracture site are of 2 types self, corresponding size.

A B C
Figs 20.37A to C: Champhy’s plates and screws and various locations on the mandible along the Champhy’s lines, where the plates can
be fixed

A B C

D E F
Figs 20.38A to F: Management of the comminuted fracture of the symphysis with a reconstruction plate and mini plate
Fractures of Mandible 421

A
A B
Fig. 20.40A: Lag screws
Figs 20.39A and B: Fixation of the Champhy’s miniplates at angle and subcondylar areas

sional forces during functional activities.7


Therefore, Champy who advo­cated only
one small bone plate in most of the regions
of the mandible always placed two bone
plates in the symphysis.
One bone screw may not provide
adequate stability, since the shear forces
may allow rotation of the mandibular
fragments around the screw.3 The only
B C resistance to rotation about one screw is
Figs 20.40B and C: Fixation of lag screw at the anterior mandible: (B) Sagittal fractures where the compaction of one fragment into other
two lag screws extending from one buccal plate to other buccal cortical plate are fixed; by virtue of compression imparted from
(C) Oblique fractures where two lag screws can be placed from the buccal to the lingual the lag screw. Application of an arch bar to
cortices the teeth may prohibit the rotational force;
however, application of a second lag screw
Lag Screws Anatomy and Biomechanics is the best insurance for providing rigidity.
A useful method of providing rigid of Anterior Mandible
fixation in the anterior mandible is by The anterior mandible from mental fora- Technique
using lag screws. The term lag screw men to mental foramen is uniquely suited Lag screw technique for anterior mandible
is used both, to describe a type of to application of lag screw fixations for can require 2.7 mm screws up to 15 to
screw as well as a technique of screw three reasons: 40 mm in length. Hence, every screw
placement. A true lag screw has threads 1. Curvature of the anterior mandible length up to 40 mm should be available
only on its terminal end. When used, allows the placement of lag screws before attempting. Following the ligation
the threads engage the far cortex, while across the symphysis from one side to of maxillary and mandibular arch bars,
the head seats against the near cortex, other, for sagittal fractures and from a vestibular incision are made from
providing compression upon tightening anterior to posterior for oblique frac­ just posterior to one mental foramen to
(Fig. 20.40A). A lag screw technique is tures and those of anterior body region other. The fracture site is exposed and
achieved with a cortical screw, which (Figs 20.40B and C). examined following slight distraction to
has threads along its entire length by 2. Thickness of bony cortices provide note the obliquity and the relationship of
over enlarging holes in the near cortex. extremely secure fixation when the the cortices. If there are extensive areas
This later procedure has been more screws are properly inserted. of communition, the lag screw technique
commonly used in maxillofacial surgery 3. There are no anatomic hazards below should be abandoned as it has little chance
than true lag screws. the apices of teeth until the mental of success in cases, where the continuity
Brons and Boering6 (1970) first intro­ foramina are encountered. This makes of the cortices is disturbed. The IMF is
duced the lag screw technique to maxil­ lag screw placement extremely simple. done while simultaneously reducing the
lofacial surgery who cautioned that at The directions of forces that are dis­ fracture. A small bur is used to drill holes
least two screws are necessary to prevent tributed through anterior mandible vary approximately 10 mm away from each
rotational movements of the fragments in with the activity of the mandible. The ante­ side of the fracture to provide a purchase
oblique fractures of the mandible. rior mandible undergoes shearing and tor­ for the modified towel clip, which is
422 Maxillofacial Trauma

engaged in these holes and tightened to extending beyond the countersinking the far segment. When tightened, the
firmly reduce the fracture fragments. It is flutes can be used. Countersinking screw will compress the two segments
helpful to dissect below the inferior border must be adequate to allow complete of bone together. Frequently the
of mandible in the area of the fracture to seating of screw head. One must avoid screw is over tigh­tened to the point of
directly expose the lingual cortex and countersinking deeper and deeper creating micro­ fractures around the
assure its proper reduction. into the bone to the point, where the screw head. This should be avoided
Selecting the point of entry into screw head rests on medullary instead if possible. It is essential that the
bone and alignment of the drill is crucial of cortical bone. screw exits the far cortex for maximal
since it will determine the success of the • Drilling through the second fragment strength (Figs 20.40D to F).
procedure and when improperly executed with 2 mm drill is next step. To ensure • The second screw is then inserted in the
may cause undesirable complications. Lag that 2 mm drill is perfectly centered same manner. To avoid damage to the
screw technique in other bones usually in the 2.7 mm hole previously drilled mental nerve while placing the second
involves drilling the screw hole at an angle through the near cortex, a special screw, a bone plate can be placed
that is the bisection of angle between line centering drill guide is used, which superior to the lag screw or maintenance
of fracture and outer cortex. Due to its has an outer diameter of 2.7 mm on of arch bar and compression wire and
curvature, the path of screw insertion in its working end, allowing a snug fit placement of patient on a soft diet.
anterior mandible traverses the fracture into the hole. During the drilling, it • The intraoral incision is closed in two
in as perpendicular manner as possible. is important to use slow speed under layers with resorbable sutures. The
This helps in enhancing the effectiveness copious irrigation to avoid clogging of MMF is then removed and the patient
of rigid stabilization of the fragments due flutes with debris. is maintained on soft diet.
to compressive force imparted by the • A depth gauge is inserted through
lag screws. Lag screws applied obliquely the drill hole and the screw length Advantages of Lag Screws Over
to fracture cause displacement of the is determined. The hole in the far Bone Plates
fracture. Bony cortex must be engaged segment is then tapped using a long • Lag screws can be applied more
with the terminal thread of the screws for tap. To prevent tissue engagement and rapidly since the time consuming task
anterior mandibular fractures. avoid wobble, the same drill guide, of adapting the bone plates is obviated
Selection of proper point of entry of which is used in drilling 2.7 mm hole and allows more anatomically accu­
the drill in buccal cortex is based on: should be used as a tap guide. The rate reduction.
• Placing it sufficiently away from hole should be thoroughly irrigated • Displacement of bone fragments is
fracture so that an ample amount of before placing the screws. much more common during placement
bone is present between the head of • Screw is inserted on a screwdriver of bone plates, which never occurs
the screws and the fracture after drilling into the screw hole. The outer hole is while applying lag screw fixation.
and countersinking. This is especially free of threads and screw should slip • Lag screw also permits the rapid appli­
important when drilling along the through until it contacts the thread in cation of fixation without decrease
curved surface of the anterior mandible.
• Providing sufficient space for second
screw, thus the first screw must be
placed just above the inferior border.
• The 2.7 mm drill is initially placed
perpendicular to the buccal cortex
at selected point of entry to prevent
skidding of drill bit and hole is begun
in cortex. The drill is then redirected
to previously selected angulation and
drilling completed till the medullary D E
bone of first fragment. The drill
and drill guide are withdrawn from
the hole and counter sinking tool
is used at slow speed to provide a
smooth platform for screw head
seating. While counter sinking the
hole, the same angulation should
be established by initial 2.7 mm drill F
hole for which an adjustable guide pin Figs 20.40D to F: Different diameter of drill used to secure the lag screw in the rigid manner
Fractures of Mandible 423

in rigidity of fracture reduction. The chances of fibrous and subsequently • The chances of injuries to the devel­
fracture gap frequently completely the bony ankylosis are high. This is oping teeth buds are high due to the
disappears from site due to the great partly due to the excellent reparative screws.
amount of compression that can be capacity in the childhood. As the healing • The implant may affect the growth of
imparted with the screw. potential is excellent in the children the the mandible or will be required to be
• Costs incurred are greatly diminished fractures heal faster and do not require removed by second surgery after the
because the screw cost much less than the immobilization for the period of 6 to fracture healing to prevent the growth
the bone plate. 8 weeks, but 3 to 4 weeks are enough for retardation.
Lag screws are however contrain­ the healing of pediatric fractures of the Thus, the most practical way of treating
dicated when there is a communition mandible. the pediatric mandibular fractures at the
and/or bone loss in the fracture gap. If The pediatric (deciduous) teeth in denture bearing area is by fabrication
the intervening bone is unstable, due the jaws are wider at the base (gingivally) and fixing of the cap splint with a circum-
to communition or is missing, com­ and thus, the gingival embrasures are mandibular wiring. The IMF is not required
pressing across this region will cause very narrow, the interdental wiring is not and thus the mobilization of the jaw
displacement of intervening bone possible. Secondly, the presence of the prevents the chances of fibrous adhesions
frag­
ment, over-riding of segments mixed dentition poses a great problem in the TMJ. Ideally the fractures need to be
and/or shortening of the fracture gap, in fixing the interdental wires or devices reduced accurately, however in pediatric
resulting in problems with the occlu­ as some teeth might have resorbed roots fractures minor discrepancies in alignment
sion. and are mobile and when the wiring is and occlusion are acceptable as the
attempted may get avulsed. The permanent erupting teeth compensate the same and
Special Considerations teeth, which are partially erupted, their the remodeling of the bone also overcomes
While treating the fractures of the man­ roots are not fully formed, there are wide these discrepancies. In case, the fracture in
dible certain special conditions warrant open primate spaces between them and the the body is grossly displaced and warrants
special attention and suitable alterations teeth may be in different stages of eruption management with the open reduction,
in the treatment. These areas are pediatric and at different occlusal levels. Due to in such cases the plates may be fixed at
fractures, condylar injuries and the geri­ all these factors the IMF using the wires the inferior border and small screws (4 to
atric fractures. may not be possible. In case of minimally 5 mm) may be used. Such plates should be
displaced fractures requiring short-term removed once the fracture heals.
immobilization for 3 weeks, bonding the The fractures of the condylar head,
PEDIATRIC FRACTURES
orthodontic brackets and using them for the subcondylar area can in most of the
The fractures of the pediatric mandible IMF may be a practical solution however it cases be treated conservatively. Short-
are usually undisplaced and although the cannot be useful in all the patients. term immobilization in the acute stage
classical green stick fractures like long The pediatric jaws are small in size and follo­wed by early mobilization is the key
bones are not seen, due to the elasticity at the age of 7 to 8 years may contain about in the treatment. Postoperative physio­
in the bone fragments are not grossly 42 teeth, including both the erupted and therapy may also be useful in preventing
displaced like the fractures in the older developing. Thus, a large area of the small the development of ankylosis. In case,
patients. The condyles are covered by bone is occupied by the developing teeth the fracture in the subcondylar area is
a fibrocartilaginous cap and have more buds (Figs 20.41A and B). Open reduction grossly displaced and is indicated for
vascularity and thus, eventhough there is and fixing the fracture with bone plates is the open reduction, it can be done with
no fracture the contusions of the condyle not practical as: bioresorbable plates and screws than the
leads to hemarthrosis and if the mandible • The space to fix the plate is not ad­ titanium or stainless steel implants as the
is immobilized for longer period, the equate as the jaw bones are small. later two may require their removal.

GERIATRIC FRACTURES
The fractures of the mandible in geriatric
age group are often difficult to treat.
In the elderly patients due to the loss
of teeth the alveolar process undergoes
severe resorption and the mandible
becomes atrophic and thin. The bones
A B become osteoporotic and fragile and frac­
Figs 20.41A and B: Pediatric mandibular fracture treated with cap splin and ture readily. In the younger individuals,
circumferential wiring the blood supply to the bone is said to be
424 Maxillofacial Trauma

centrifugal due to plenty of bone marrow, dissection should be chosen, i.e. lag – Cortical injuries/cortical chipp­
but in the older patients, it is centripetal, screws in place of bone plates. Some ing usually the medial portion
i.e. from periosteum to the center, due to authors have brought forwards a concept (Figs 20.42A and B).
the bone marrow undergoing myelofi­ of supraperiosteal plating to avoid the • Extracapsular fractures (condylar neck
brosis and the endosteal blood supply of periosteal dissection. fractures)
the mandible is diminished. The perio­ – High subcondylar (Fig. 20.43).
steum also undergoes fibrosis and thus, the – Low subcondylar (Figs 20.44A and
CONDYLAR FRACTURES
periosteal blood supply also gets reduced. B).
The osteoblastic and healing potential The condyles not only facilitate the man­ The subcondylar fractures can also be
of the bone goes down and the healing dibular excursions, but play a great role in classified as:
of the fracture is a slow process and the the mandibular growth. The condyle has a • Undisplaced
complications such as nonunion are more head, which rests in the glenoid fossa of the • Medially displaced (due to pull of
likely to occur. The dentition serves as a temporal bone. The neck, which is thin and lateral pterygoid)
good guide for the closed reduction of the slender connects the head to the rest of the • Laterally displaced (less common)
mandibular fracture and due to the loss of mandible. The glenoid fossa is located at • Fracture dislocation (the condyle gets
the teeth the accurate reduction cannot the base of the middle cranial fossa and to dislocated from the glenoid fossa and
be assessed, nor are the teeth available for avoid its fractures, which may have serious gets dislocated medially in the infra­
fixing interdental wires or devices for IMF implications, the nature has made the neck temporal fossa due to pull of lateral
in the geriatric patients. of the condyle thin and weak so that when­ pterygoid muscle) (Figs 20.45A to E).
The edentulous geriatric fractures can ever there is a force applied on the chin, it The intracapsular fractures are essen­
be treated by closed reduction using the gets transmitted along the condyles to the tially treated with closed reduction. There
gunning splints or if the patient is a denture glenoid fossa. The neck is weak and thus, are two schools of thought for the treat­
wearer, the dentures can be modified by it fractures absorbing the shock and pre­ ment of the high subcondylar fractures.
inserting hooks or arch bars in it for doing vent the more grievous injury. However, in Some people believe in closed reduction,
IMF, which can be used as a splint. The growing children, condylar neck is short, while others believe in the open reduction.
gunning splints can reduce the fractures of stout and broad. It is covered with thick cap The open reduction of the high subcondy­
the denture bearing area, but the fractures of fibrocartilage and the ratio of cancellous lar fracture, which is medially displaced
of the ramus, angle and the subconylar to cortical bone is high. Owing to these two or dislocated is often technically difficult.
area cannot be effectively managed factors when vertical forces act, the con­ The high subcondylar fractures are ap­
with the gunning splints as the proximal dyle fractures like cap of mushroom. This proached by the preauricular incision. The
fragment cannot be controlled, especially phenomenon is intracapsular and is the fixation is done using a miniplate or lag
if it is an unfavorable fracture. Secondly, if cause of post-traumatic ankylosis. screws. The use of the K wire for fixation
the fracture is not grossly displaced, minor The condylar fractures can be classi­ of the subcondylar fracture,8 as described
discrepancies can be subsequently taken fied as: in the literature is not commonly practiced
care of while fabricating the denture. But, • Intracapsular fractures (condylar head nowaday due to the availability of better
if the fracture is grossly displaced due fractures) modalities.
to the muscle pull the chances of non- – Undisplaced. The low subcondylar fractures are
healing are increased further. – Comminuted. easily treated with the open reduction. The
The open reduction of the geriatric
fractures is often associated with chances
of non-union. The bone is already
having diminished blood supply as
discussed earlier. The endosteal blood
supply is disrupted with the fracture. If
the open reduction is done by stripping
the periosteum excessively the chances
of avascular necrosis at the end of the
fractured fragments can occur leading
to non-union. Thus, the open reduction
of the geriatric mandibular fractures
should preferably avoided. If the situation
necessitates the open reduction, judicious
periosteal stripping should be done and A B
the modalities requiring lesser periosteal Figs 20.42A and B: Cortical chipping of the medial pole of the condyle
Fractures of Mandible 425

A B
Figs 20.46A and B: Postramal Hind’s approach for fixation of the fractures with
miniplates
Fig. 20.43: High subcondylar fracture

site is approached through transbuccal


approach or by Risdon’s or postramal
approach and can easily be fixed with
miniplates and screws (Figs 20.46A and B).
The problems with proper reduction
and fixation of condylar fractures using
a single mini plate have been evaluated
by Hammer et al. and they found that the
displacement of condylar segment due to
the adverse muscle pull of lateral pterygoid
muscle and the functional forces acting on
the proximal segment exceed the rigidity
A B
of one mini plate, plate failure and screw
Figs 20.44A and B: Low subcondylar fracture
loosening. Hence, they recommended
appli­cation of two mini plates, i.e. one at
the posterior border and one at the ant­
erior border and found the beneficial effect
of restoring tension and compression tra­
jec­tories and providing stability against the
muscle pull9 (Figs 20.47A and B).
The condylar fractures are always
asso­ ciated with injuries to the internal
soft tissues of the joint producing joint
effusions. If the condylar injuries are
A B C
treated with long-term immobilization of
the jaw, the chances of fibrous adhesions
and ankylosis are increased. Hence, while
treating them with closed reduction the
following protocol should be followed:
• Achieve the occlusion either by reduc­
tion manually or under general anes­
thesia after giving muscle relax­ants to
overcome the unfavorable muscle pull.
D E The fractures can also be reduced by
gradual traction using heavy intermax­
Figs 20.45A to E: (A) Minimally displaced/undisplaced; (B) Laterally displaced; (C and D)
Fracture dislocation; (E) Right side medially angulated left side fracture dislocation illary elastics. In case of telescoping of
426 Maxillofacial Trauma

the fracture fragments, radiographical ramus is also measured (A°). The the IMF for the fear of precipitating
assessment of the overlap of fracture loss of vertical height of the ramus ankylosis.
segments is ascertained and a bite (X’) due to telescoping is calcu­ • The patients are advised physiotherapy
block (fulcrum or hypomochlion10) is lated by the following formula: for long-term to prevent fibrous adhe­
placed between the posterior teeth, X’= X (1 – cos A°) sions and functional adaptation to the
which are gagging or meeting in pre­ • The hypomochlion works as a fulcrum new situation generated by this treat­
mature contact, creating anterior open and provides mechanical advantage ment modality, i.e. pseudarthrosis.
bite (Figs 20.48A to C). The height of of a class I lever. As the anterior
hypomochlion should be determined intermaxillary elastics are applied the
by any of the following two methods: unfavorable muscle pull is countered FRACTURE HEALING
– Clinical method: In which the and as the mandible rotates over the
amount of anterior open bite is fulcrum the anterior open bite reduces In general, fracture results in a well-defined
recorded (×) and 2 mm is added and proportional lengthening of the progression of tissue responses that are
to the value of anterior open bite ramus occurs due to its downward designed to remove tissue debris, to re-
(× + 2) + 2 mm signifies the normal displacement. The size of the hypo­ establish vascular supply and to produce
overbite value. mochlion is reduced gradually at the a new skeletal matrix. The processes that
– Radiographic method: The loss rate of 1 mm per week till satisfactory occur to accomplish healing are depen­
of mandibular ramal height is cal­ occlusal relationship of the molars is dent on the location of the injured bone
culated based upon the measure­ established, which suggests that the loss and on local and systemic factors.
ments taken on a standardized of ramal height is corrected. Like the soft tissue, bone can also heal
radiograph. The length of the frac­ • After the occlusal relationship is by primary or secondary intention. Spon­
tured condylar segment is mea­ established, the IMF for short-term taneous bone healing without surgical
sured on the X-ray (X). The angle (2–3 weeks) with heavy elastics may intervention and healing that occurs after
of the fractured condylar segment given to maintain and consolidate the semirigid fixation progress by secondary
with the distal segment of the established result and do not prefer intention. Healing by primary intention
occurs only when the following conditions
are met:
• Excellent anatomic reduction.
• Minimal or no mobility.
• Good vascular supply at the fracture
site.
• Rigid fixation and compression of the
fracture fragments to abolish micro­
movements.
Although similar terminology is also
applied to soft-tissue wounds, an analogy
between the two should be avoided. In
A B soft-tissue injury, healing by secondary
Figs 20.47A and B: Showing the distribution of the forces on the fractured segment intention involves the filling of a gap
and stabilization of the fracture segments using one miniplate (A) and two miniplates by granulation tissue with subsequent
(B) ( Courtesy: Meyer et al. Journal of Craniomaxillofacial Surgery 2006;34:173-181) replacement by a scar, which is less

A B C
Figs 20.48A to C: A case of subcondylar fracture causing open bite, treated with hypomochlion and anterior elastic traction
Fractures of Mandible 427

functional. Secondary bone healing is so from the dilated, damaged vessel, from Cartilaginous Callus (Soft Callus)
termed because initially an intermediate the endosteum, periosteum and Haversian Formation
fibrous tissue (callus) is formed within system leads to hematoma formation. Callus is derived from latin word callum or
the fracture gap and is only subsequently A great deal of emphasis has been placed callus means hard integument. It has been
replaced by bone, as opposed to primary on the importance of the hematoma in defined as collagenous, revascularizing,
bone healing, in which no intermediate healing. The clot is invaded by a variety osteogenic blastema, which unites the
fibrous tissue (callus) is formed and of blood-borne elements, which can bone fragments and from which the bone
the bone heals by direct proliferation contribute to healing. In addition to regenerates. The term soft callus appears
of the osteoprogenitor cells from either granul­ation tissue within the hematoma, to be contradictory in that the callus
side, which forms bone, osteosynthesis. frag­ments of bone and muscle may be implies hardness. Callus formation begins
However, unlike the scar formed by found. The small, non-vital muscle under­ externally and internally. Externally, nod­
secondary intention healing of the soft- goes autolysis within 5 to 10 days, and the ules of cartilage are separated by fibrous
tissue wounds, bones that have healed by pedicled, vascularized muscle undergoes septa. As the blood vessels within the
secondary intention continue, through fibrosis and does not interfere with septa increase, the tendency toward
adaptation and remodeling process, healing unless it is trapped between the hypoxemia is reversed and two changes
toward a form and function similar to what ends of the fractured bone. Small bone occur simultaneously. First, further
was present before the injury. fragments may undergo surface deposition calcification of the cartilage takes place,
of bone by migrating periosteal cells and with the trapping of chondroblasts and
Secondary Bone Repair associated devitalized marrow undergoes their conversion to chondrocytes. (Late
Fractures undergoing spontaneous heal­ fatty degeneration. Somewhat overlapping cartilaginous stage) (Fig. 20.50). Second,
ing and those treated with a majority of this inflammatory hematoma formation osteoblasts increase in number and
the currently used treatment modalities is the initiation of cellular proliferation. osteoclasts become apparent for the first
undergo secondary bone healing. Second­ Within 8 to 12 hours, DNA synthesis and time. As this external callus is forming, an
ary bone involves a well-defined sequence proliferation by the periosteal cells of the internal callus between the bone ends also
of steps:11 cambium layer (inner layer which is close forms. This area has a better blood supply
• Initial stage. to the bone) begin. This process initially and therefore less necrosis takes place.
• Cartilaginous callus. involves the periostium of the entire No intermediate fibrocartilage is formed
• Bony callus. injured bone, but decreases over a few days instead osteoblasts from the endosteum
• Remodeling. to remain only in the area of the fracture. form an internal bony callus directly.
During the initial stage, hematoma The basic work of Urist12 and others has When bone begins to heal after fracture,
formation occurs concurrent with an established that these cells are pluripotent a cuff or callus, forms around the fracture
inflammatory response, which brings and give rise to osteoblasts, fibroblasts site to stabilize the involved area. (Bony
new vascularity and the undifferentiated and cells with chondrogenic potential. As callus formation) (Fig. 20.49C and D and
mesenchymal cells differentiate to form these cells start to proliferate, capillary Fig. 20.51). The callus greatly increases
a fibrocartilaginous callus. This fibro­ in growth begins. The fibroblasts formed the area of inertia, thereby increasing
cartilage then ossifies to form the bony during the proliferative stage migrate into the strength and stiffness of the bone,
callus, which subsequently undergoes the wound and begin to lay down collagen. especially resistance against bending and
remodeling and functional adaptation in This combination of collagen and a rich torsion, during the healing period. If the
much same way as the preinjured bone. capillary network forms granulation tissue. fracture is not reduced properly during
In this stage, a low oxygen tension and a the healing then the hyperplastic callus
Initial Stage/Reaction low pH are noted in the early granulation is formed (callus adaptation), which
The disruption of blood vessels and tissue. It is thought that these conditions undergoes steady remodeling process
generation of heat from the energy neces­ of lower pH and relative hypoxia trigger until the functional adaption to the
sary for inducing fractures, lead to hypoxia a response within the hematoma toward stresses takes place (Fig 20.52).
and cellular death at the fracture site. This the formation of hyaline cartilage. In
situation produces necrosis at the bone addition to decreased oxygen tension Hard Callus (Bony Callus)
ends of the fracture for a variable distance. and decreased pH, it is thought that Formation
This aseptic (non-infected) necrosis the movement that occurs when bone In a fashion similar to the endochondral
leads to inflammation and edema. The fragments are not immobilized with formation of bone that occurs during growth
inflammatory response induces release rigid internal fixation causes continued and development, the cartilagenous callus
of numerous vasoactive angiogenic compression and tension at the site of the undergoes calcification into woven bone.
pyrogen, which produce vasodilation fracture and also directs cells toward the The spaces within the cartilaginous callus
within a few hour of injury. Hemorrhage formation of cartilage (Figs 20.49A and B). allow for further vascular ingrowth, which
428 Maxillofacial Trauma

brings with it a change in the environment.


The increase in oxygen tension, aided by
the transportation of nutrients to the site is
conducive to the formation of osteoblasts.
These osteoblasts pre-existed at the fracture
site and that there was some stimulus that
caused them to begin activity. McLean and
Urist believed that the cells were derived
from connective tissue precursors. Probably
both factors contribute somewhat because
abundant osteoblasts are present within
the endosteum and numerous precursors
are available within the conne­ctive tissue
surrounding the wound. It is well known
that these precursor cells can be induced
into bone-forming cells both in vivo and
in vitro. The osteoblasts deposit osteoid
A on the spicules of calcified cartilage and
the osteoid then undergoes a calcification
process, forming bone. The process begins
peripherally and progress as a homogeneous
B
calcification of the cartilaginous callus.
Figs 20.49A and B: Late fibroblastic stage. Osteoblast lay down new bone, in case of low Initially the bone that is formed is randomly
oxygen tension cartilage is laid down by chondroblast arranged (woven bone); it is then undergoes
organization and changes to lamellar bone
during the final stage of healing, which is the
remodeling stage.

Remodeling
The newly formed woven bone, which is
somewhat random in organization, under­
goes remodeling into the more familiar
pattern of lamellar bone. This slow process
progresses in accordance with Wolff’s
law,13 which states that a change in the
functional state of bone causes structural or
architectural changes in the tissue through
bioelectric field production. As osteoclasts
participate in remodeling by resorption of
bone, factors are released that help drive
and direct the remodeling process further.
The bone morphogenic protein (BMP)
is a collagenase-resistant glycoprotein,
isolated by Urist et al. and is one of these
factors. Acting as a mitogenic and tissue
growth factor (TGF), the BMP induces
differentiation of mesenchymal cells toward
C
bone formation. The preceding overview
applies to fractures for which the fixation
is such that the movement can occur at
the fracture site. Two other situations also
D exist. The first of these is that of linear
fractures of flat bones of the skull and some
Figs 20.49C and D: Calcification bone with formation of Haversian system facial bones. In this case, there is limited
Fractures of Mandible 429

stability afforded by a callus. Primary


healing probably occurs in cancellous
bone even without this rigid mechanical
stabilization if there is no gross mobility.
Osteogenic cells and capillaries proliferate
in the medullary bone on both sides of
the fracture, forming new bone along the
fracture site. In cortical bone, union without
callus formation was reported as early as
1949 when it was observed that radiographs
of long bone fractures that had been plated
Fig. 20.50: Late cartilaginous stage failed to show callus formation. Schenk
and Willenegger14 were the first to observe
the histologic features of primary bone
healing. The healing that occurs in cortical
bone frac­tures in which rigid fixation has
been acc­o­mplished occurs in two different
ways:
1. Gap healing
2. Contact healing.

Gap Healing
Even with rigid fixation by means of a
device that produces a stable relationship
between the fracture ends under the
deforming forces produced by muscle
Fig. 20.51: Bony callus formation pull and function, a perfect anatomic
reduction seldom exists. In some areas
of the fracture, small gaps occur between
the bone segments within a few days
after fracture gap healing begins at these
points. Blood vessels from the periosteum,
endosteum, or Haversian canals invade
the gaps, bringing mesenchymal osteo­
blastic precursors. Bone is deposited
directly on the surfaces of the fracture
fragments without resorption and without
intermediate cartilage formation. If the
gaps are less 0.3 mm, lamellar bone forms
directly. Gaps from 0.3 mm up to a critical
value, 0.5 to 1.0 mm, fill with woven bone
and lamellar bone is subsequently laid
down within the trabecular spaces.
The formation of lamellar bone occurs
Fig. 20.52: Bony callus stage, fracture with displacement illustrating callus adaptation
over 6 weeks. At the end of this time, the
lamellar bundles are oriented at right
movement and the surrounding tissue is is negated and nearly perfect anatomic angles to the longitudinal axis of the
very vascular. Periosteal osteo­progenitor reduction is achieved. In this instance remaining bone. Fractures repaired by
cells differentiate into osteo­ blasts and healing occurs primarily. healing have been shown to be consider­
bone is laid down directly without a ably stronger than similar fractures healed
cartilaginous phase. The second condition Primary Bone Healing by secondary repair in the same time,
is that which exists when rigid internal Primary bone healing occurs when enough despite the often large quantity periosteal
fixation is used, so that the effective strain rigidity and anatomic reduction exist to bone present within the bony callus of sec­
that normally induces callus formation preclude the necessity for the mechanical ondarily healing bone.
430 Maxillofacial Trauma

Contact Healing Stages of Fracture Healing unit based. Here the pocket of callus is
In areas in which contact is achieved, (Frost16: 1989) replaced by pocket of lamellar bone, it
the interfragmentary gap is essentially is slow process, takes from 1 to 2 years.
zero. Since vascular and cellular ingrowth • Stage of hematoma: This stage is from • Stage of modeling: Time: many years.
cannot proceed as it does in fractures in the day of fracture to 7th day. Due to Bone is gradually strengthened. The
which a gap exists, a special process of the stripping of local soft tissue and shaping of cortices occurs at the
bone formation occurs. This process has periosteum, ischemic necrosis of frac­ endo­ steal and periosteal surfaces.
been termed ‘contact healing’. Contact tured ends take place. Sensitization The major stimulus comes from local
healing occurs through the formation of precursors of osteoblast to form bone strain (weight-bearing stress and
of a bone metabolizing unit (BMU), a daughter cells begins due to decreased muscle force when person resumes
bone remodeling unit (BRU) or a bone blood supply. The undifferentiated the activity). This stage is more
repair unit (BRU), all synonyms for mesenchymal cells also differentiate conspicuous in children and limited
the newly forming (or regenerating) into the osteoclasts to resorb the over­ in adults.
osteon. Osteoblasts differentiate and hanging bone fragmants.
form new bone. The osteoclasts begin • Stage of granulation tissue: This stage Growth Factors in Bone
to cut away cones on either side of the last up to 2 to 3 weeks. The features are: Healing
fracture, progressing toward the fracture Various precursor cells produce The regulation of bone regeneration is a
site through necrotic bone and into the cells which differentiate and organize complex process that requires interplay
opposing bone end. The osteoclastic to provide blood vessels, fibroblast, by systemic hormones, e.g. calcitonin,17
cutting cone proceeds at a rate of 50 to osteoblast, etc. which collectively form parathyroid hormone18 and local bone gro­
80 µm per day.15 The resultant cone which the soft granulation tissue. The blood wth factors, which act on osteoblasts and
is 200 µm in diameter, provides a pathway clot gives rise to loose meshwork osteoclasts in an autocrine and paracrine
for vessel ingrowth and osteoblastic for in-growth of fibroblast and new manner and modulate proliferation and
proliferation, with formation of new capillaries. The clot is eventually cellular activity. Growth factors are recep­
bone. This process has been likened to a removed by macrophages, giant cells tor-specific polypeptides that bind to trans­
‘pegging together’ of the fracture ends by and other cells arising in granulation membrane cell surface receptors on their
newly formed bone. The osteon forms at a tissue. From this stage bone healing target cells. Extracellular recep­tor binding
rate of 1 to 2 µm per day. This lag between differs from soft healing in which is followed by intracell­ ular changes that
resorption and osteon ingrowth produces granulation tissue is replaced fibrous lead to activation of second messenger
a transient porosity in the compact bone tissue, in the former the granulation cascades, resulting in upregulation of
visible radiographically up to 3 months tissue further differentiates to create DNA transcription with translation into
after fracture in humans, with complete osteoblasts. Clinically the segments proteins. These proteins have a variety
reconstruction of the cortex requiring are still mobile. Radiographically no of roles including the induction of other
up to 6 months. During this period, the changes are seen. proteins and modulate chemotaxis, cell­
fixation device must maintain the stability • Stage of callus: Time: 4 to 12 weeks. ular proliferation, and differentiation. A
of the fractured segments. Features: Granulation tissue differ­ num­ber of growth factors are thought to
Direct fracture healing consists of entiate further and create osteoblasts. play a role in fracture repair including
direct bone formation with­out the classical These cells lay down an intercellular bone morphogenetic proteins (BMPs),19
multistage differentiation of connective matrix, which soon gets impregnated transforming growth factor (TGF),20 insulin-
tissue and cartilage (callus formation). with calcium salts. This results in like growth factor (IGF-I),21 IGF-II, platelet-
The direct union of the fragments in callus formation and is also called derived growth factor and acidic and basic
contact and under compression occurs woven bone. Callus is first sign of fibroblastic growth factor (aFGF and bFGF).
by the remod­eling of the Haversian canals union, which is visible usually after 3 Bone morphogenetic proteins belong
by cutting cones. These cutting cones weeks of fracture. Callus formation is to the TGF super family and bind to cell
contain osteoclasts and a conical surface slower in adults than in children and surface receptors that play a crucial role
of osteoblasts, which produce new osteons in cortical bone than in cancellous in osteoblast stimulation and recruitment,
with incorporated new living osteocytes. bone. resulting in bone formation. This group of
These osteocytes are connected among • Stage of remodeling: Time: 1 to 2 years. proteins were first isolated by Urist from
themselves and to the vascular supply This stage is also called the stage rabbit demineralized bone in 1979.22 With
in the Haversian canal by a network of of consolidation. Woven bone is the use of molecular genetics, a number
canaliculi. The contact in this type of re­placed by lamellar structure this of BMPs have been recombinantly pro­
healing is few micrometer. process of change is multicellular and duced and studied. In one of many similar
Fractures of Mandible 431

studies, Seto23 reported the use of BMP- fracture repair sites, where it is thought to • Loose implants
2 in conjunction with small amounts of play a role in both osteoblast and osteoclast • Immunocompromised patients, dia­
autologous bone in the reconstruction of induction. Although a number of clinical betics.
continuity defects of primates. In addit­ studies have demonstrated a role for PDGF The infection may resolve with the
ional research using immunolocalization in soft-tissue wound repair, but no defini­ medicinal treatment or get localized to form
has demonstrated BMP-2 and BMP-4 tive evidence exists in regard to fracture a localized abscess. The infection can also
in rat callus. In the future, this group of repair.24 The findings related to PDGF and spread to adjoining tissue planes. Severe
proteins may play a significant role in other growth factors released by platelets bone infections can lead to osteomyelitis.
the management of traumatic and non- have stimulated an interest in the role of The infection should be prevented by good
traumatic injuries of the facial skeleton. PRP in fracture repair and reconstruction. antibiotic prophylaxis, maintenance of
BMP 2-4 and BMP-7, also known At the present time, basic science in wound hygiene, adequate immobilization,
as osteogenic protein-1 (OP-1), are support of the effects of PRP is lacking. effective management of the teeth involved
expressed by osteoblasts, osteoclasts and Aghaloo et al.25 studied the effects of PRP in the fracture line and ensuring that the
other more primitive mesenchymal cells on non-critical cranial bone defects in implants are not loose. The infection will
within the fracture callus during the early 15 rabbits. The sites were then evaluated invariably interfere with the healing of the
stages of membranous fracture healing. with digital subtraction radiography, histo­ fracture.
These proteins continue to be expressed logically, and histomorphometry at 1, 2 and
during the process of bone remodeling, 4 months. Their results showed no notable Osteomyelitis
but less prominently. The return of BMP difference with the addition of PRP. Osteomyelitis is the complication second­
2-4 and OP-1 immunostaining to baseline ary to the infection. If the fracture is com­
intensity coincides with the histological Other Growth Factors minuted and small fragments of bone are
appearance of mature lamellar bone.3 A variety of other growth factors are under present, which are devoid of the soft tissue
Transforming growth factor-beta investigation in regard to their role in attachment, such fragments are likely to
(TGFs-b) induce normal cells to exhibit fracture repair (e.g. IGF-I26 and IGF-II and turn non-vital and serve as nidus for infec­
neoplastic characteristics through the acidic and basic aFGF and bFGF).27 It is tion. The fractures of mandible, which are
sti­mulation of transmembrane receptors likely that as technology advances many associated with soft tissue laceration, war­
and second messengers. A significant other similar factors will be identified rant an effective management of the soft
amount of data exists to support the role of and their roles delineated in the fracture tissue trauma. It is being said that the bone
TGF-b in bone formation and repair. The repair process. All of the growth factors is like a plant which has roots in the soft tis­
osteoinductive capacity of TGF-b alone is provide exciting possibilities for future sue. The bone derives its blood supply from
far less than that of BMP, but studies sug­ applications to traumatic repair of the oral endosteal and periosteal source. The for­
gest that this protein may in fact have a and maxillofacial complex. Recombinant mer is disrupted when the fracture occurs.
role in the potentiation of BMP. TGF-b is technology allows for the production of If the periosteum is also separated from it,
synthesized by a number of cells includ­ large quantities of these proteins, which the bone can undergo avascular necrosis. It
ing PMNs, mono­ cytes, platelets, T-lym­ could potentially be put to clinical use. is especially true in case of mandible, which
phocytes and macro­phages. It enhances is denser and has less collateral circulation
angiogenesis, stimu­lates collagen synthe­ than other facial bones. If injudicious strip­
sis and inhibits its degradation and is che­
Complications of Fracture ping of the periosteum is done, while doing
motactic for fibro­blasts and macrophages. Healing the open reduction and in cases of geriatric
Orthopedic animal models of fracture re­ The healing of the fracture is sometimes fractures, the chances of avascular necrosis
pair in associ­ation with exogenous TGF-b associated with complications like: of the bone are optimized.
have shown augmented healing. • Infection The teeth involved in the fracture line
Platelet-derived growth factors (PDGF) • Osteomyelitis always lead to compounding of the fracture
and platelet-rich plasma (PRP). PDGF is • Malunion intraorally and can lead to contamination
primarily stored in platelets and released • Delayed union and subsequently infection in the fracture
during the clotting cascade. It is angiogen­ • Non-union. line. It is not necessary to extract all the
ic, a mitogen for fibroblasts and smooth teeth that are involved in the fracture line
mus­ cle cells and a chemoattractant for Infection but there are distinct indications for doing
PMNs and macrophages. It is composed The fracture line can get infected due to so. The indications for extracting the teeth
of two polypeptide chains (A and B), which the following reasons: in the fracture line are:
have been synthesized using recombinant • Compound fractures with gross con­ • Grossly luxated teeth.
technology. Localization studies demon­ tamination • Teeth obstructing the reduction of the
strate increased concentrations of PDGF at • Inadequate immobilization fracture.
432 Maxillofacial Trauma

• Fractured teeth, which are beyond Local Factors freshening of the eburnated ends and
conservation. • Excessive gap or over-riding of the fixation of the fragments by rigid means.
• Carious teeth with infective patholo­ fracture segments. If the gap between the fragments is wide,
gies. • Entrapment of soft tissue between the to hasten the healing, cancellous bone
In case the teeth are firm and for fracture fragments. graft harvested from iliac crest should be
cosmetic consideration are decided to be • Infection. placed in the gap. The supportive systemic
retained, then conservative management • Inad­equate immobilization: The therapy, additional immobilization with
like endodontic therapy, splinting, proper move­ment across the fragments does IMF may be given as required in particular
local care should be taken to prevent not allow the callus to get stabilized case. The hyperbaric oxygen therapy
the infection. The teeth which are in the and pseudoarthrosis results rather facilitates the healing.
fracture line, but not erupted in oral cavity than bony union.
should not be removed as they do not • Irradiated jaw.
cause compounding of the fracture. • Sclerosed bone: Poor vascularity to REFERENCES
If the osteomyelitis sets in it should the bone delays healing.
be treated like any other osteomyelitis, 1. Fridrich KL, Pena-Velasco G, Olson
immobilization of the jaws with IMF RA. Changing trends with mandibular
Systemic Factors
is helpful in healing. During the acute fractures. A review of 1067 cases. J Oral
phase of osteomyelitis or when the • Poor general condition, malno­uri­ Maxillofac Surg. 1992; 50:586-9..
infection is present the placement of shment. 2. Teasdale G, Jennett B. Assessment of
implants like plates, screws should not • Diabetes—where the resistance of coma and impaired consciousness. A
be attempted. Similarly, the bone grafts the patient against infection is low practical scale. Lancet. 1974;2:81-4..
should not be used to mend the bony and the microangiopathy reduces the 3. Gilmer TL. A Case of Fracture of the
defects subsequent to osteomyelitis when vascularity. Lower Jaw With Remarks on Treatment,
infection is present. Rather it should be • Hyperparathyroidism. Arch. Dent. 1887;4:388..
done as a second stage surgery after the • Old age: The bones are osteoporotic, 4. Gunning TB. Treatment of fractures of the
infection is controlled and adequate soft vascularity is reduced and the healing lower jaw by interdental splints. Br J Dent
tissue cover is ensured. potential is low. Sci. 1866;9:481..
• Vitamin D and calcium deficiency. 5. Champy M, Lodde JP, Muster D, et al. Os­
Malunion • Immunosuppression. teosynthesis using miniaturized screwon
The healing of the fracture is an abnor­ The healing is delayed due to any of plates in facial and cranial surgery. Ann
mal position is called malunion. It can the above mentioned reasons, the immo­ Chir Plast Esthet. 1977;22:261-4..
occur as a result of inadequate reduc­ bilization period is increased to about 8 6. Brons R, Boering G. Fracture of the
tion, inadequate immobilization or if no weeks. If the fracture is treated with RIF, mandibular body treated by stable
treatment is done.28 The patient often additional IMF may be required to provide internal fixation. J Oral Surg. 1970;28:407.
presents with the complaints of inability rest to the part and avoid stresses on the 7. Ellis E III, Ghali GE. Lag screw fixation
to masticate, improper occlusion and healing bone. The cause whenever pos­ of anterior mandibular fractures. J Oral
sometimes poor esthetics. The clinical sible must be treated simu­ltaneously. If Maxillofac Surg. 1991;49:13-21.
findings are step deformity in the mandi­ the infection is present drainage, curet­ 8. Franc C, Braye F, Ngotene R, et al.
bular arch, extraoral deformity due to tage, extraction of the offending tooth, etc. Osteosynthesis using intrafocal nailing
hyperplastic callus and derangement of should be done. If the immobilization is of low subcondylar fractures in adults.
occlusion. The management comprises inadequate, it should be corrected. Nutri­ Surgical technics and initial results. Rev
of surgical exposure of the site, creating a tional defici­encies should be corrected. If Stomatol Chir Maxillofac. 1997;98(1):35-9.
refracture by osteotomising the mandible there is entrapment of the soft tissue then 9. Hammer et al. Osteosynthesis of condylar
at the previously fractured site, reduction surgical exploration and removal of inter­ neck fractures: Review of 30 patients.Br J
and recontouring the hyperplastic callus vening tissue may be required. Oral Maxillofac Surg. 1997;35:288.
and then reducing the fragments in such a In case of nonunion, the fragments 10. Ulrich Joos, Johannes Kleinheinz. Ther­
way that satisfactory occlusion is achieved. are united by fibrous tissue rather than apy of condylar neck fractures. Interna­
The fragments are then fixed with internal the bone and pseudarthrosis (false joint) tional Journal of Oral and Maxillofacial
fixation like miniplates and screws. results. The ends of the fragments get Surgery. 1998;27(4):247-54.
covered with cortical bone and the cortical 11. Schindeler A, McDonald MM, Bokko P,
Delayed Union and Nonunion barrier does not allow the fragments to et al. Bone remodeling during fracture
Both these conditions are considered unite. Such ends are called ‘eburnated repair: The cellular picture. Semin Cell
under the same heading because, their ends’. The treatment is essentially surgical Dev Biol. 2008;19(5):459-66.
etiology is similar. The healing may get comprising of surgical exploration of the 12. Urist MR. Bone: formation by auto­
delayed due to the following factors. site, excision of all the fibrous adhesions, induction. Science. 1965;150(698):893-9.
Fractures of Mandible 433

13. Wolff J, Das Gesetz der. Transformation bony defects. Trends Biotechnol. 1993; expression in normally healing human
der Knochen , Hirschwald, Berlin, 1892. 11(9):379-83. fractures. Bone. 1995;16(4):455-60.
14. Schenk R, Müller J, Willenegger H. Mor­ 20. Park SH. O’Connor K, Lin WS. Effect 25. Aghaloo TL, Moy PK, Freymiller EG.
phological findings in primary fracture of TGF-[beta]1 and active motion on Investigation of platelet-rich plasma in
healing. Symp Biol Hung. 1967;7:75. fracture healing. Journal of Orthopaedic rabbit cranial defects: A pilot study. J Oral
15. Bruce Doll, Matthew Aleef, Jeffrey O. Trauma. 1999;13(4):317. Maxillofac Surg. 2002;60(10):1176-81.
Hollinger. Overview of fracture repair. 21. Karachaliou FH, Stamogiannou L. Long 26. Schmidmaier G, Wildemann B, Gäbelein T,
Musculoskeletal tissue regeneration. bone fracture healing: IGF-I concentrations et al. Synergistic effect of IGF-I and TGF-be­
Humana Press. 2008:pp. 39-61. and specific binding to erythrocytes. J Pe­ ta1 on fracture healing in rats: single versus
16. Frost HM. The biology of fracture healing: diater Endocrinol Metab. 1996; 9(4):491-5. combined application of IGF-I and TGF-be­
an overview for clinicians. Part I. Clin 22. Urist MR, Mikulski A, Lietze A. Solubilized ta1. Acta Orthop Scand. 2003;74(5):604-10.
Orthop Relat Res. 1989;248:283-93. and insolubilized bone morphogenetic 27. Simpson AH, et al. The role of growth
17. Stanley Wallach. Effects of calcitonin protein. Proc Natl Acad Sci USA. 1979;76: factors and related agents in accelerating
on bone quality and osteoblastic func­ 1828-32. fracture healing. J Bone Joint Surg Br.
tion. Calcified Tissue International. 23. Seto I, Asabina I, Oda M, et al. Recons­ 2006; 88-B: 701-5.
1993;52(5):335-39. truction of the primate mandible with 28. Li Z, Zhang W, Li Z, Li J. Abnormal union
18. Michael J Gardner. Role of parathyroid a combination graft of recombinant of mandibular fractures: A Review of 84
hormone in the mechanosensitivity of human bone morphogenetic protein-2 Cases. Journal of Oral and Maxillofacial
fracture healing. Journal of Orthopaedic and bone marrow. J Oral Maxillofac Surg. Surgery. 2006;64(8):1225-31.
Research. 2007;25(11):1474-80. 2001;59(1):53-61; discussion 62-3.
19. Wang EA. Bone morphogenetic proteins 24. Andrew JG, Hoyland JA, Freemont AJ,
(BMPs): therapeutic potential in healing et al. Platelet-derived growth factor
21 Fractures of Middle Third
of Facial Skeleton
Borle Rajiv M, Arora Aakash, Bhola Nitin, Yadav Abhilasha

The middle third of the facial skeleton • Two lacrimal bones (Figs 21.3A and B). The bone grains are
is the area between the imaginary • A vomer oriented along these buttressing areas
lines passing superiorly through the • Paired palatine bones and thus, the facial skeleton withstands
supraorbital ridges and inferiorly • Sphenoid bone. force/trauma better from the inferior
through the tip of the maxill­ary alveolar These bones are further undermined direction than the horizontal direction.
bone, when the patient is edentulous due to presence of anatomical cavities
and through the incisal edges of the like the air sinuses nasal cavity and PATHOPHYSIOLOGY OF
teeth when the patient is dentulous orbital cavities. But, in certain areas like
MAXILLOFACIAL INJURIES
(Fig. 21.1). the orbital rims the bone is buttressed
The middle third of facial skeleton to protect the vital structure like eye. The fractures of this area are commonly
is formed by many small, fragile bones, The bones articulate at the base of the seen in clinical practice due to increasing
which articulate with each other in cranial cavity with the cranial bones
immobile sutural joints. The bones and thus, the cranial involvement
taking part in the formation of the commonly occurs when middle third
middle third of face are (Fig. 21.2): of facial skeleton fractures occur in
• Two maxillae severe facial injuries. The middle third
• Paired nasal bones of the facial skeleton articulates with
• Paired zygomatic bones the cranial base at three sites, i.e. the
• Two ethmoidal bones frontonasal buttress, the pterygoid
plates and the frontozygomatic suture/
buttress. These three buttresses are
designated as the pillars (like pillars
of a building) of the facial skeleton

B
Figs 21.3A and B: The frontonasal
Fig. 21.1: Division of facial skeleton in buttress, the pterygoid plates and the
three parts Fig. 21.2: Disarticulated facial bones frontozygomatic suture/buttress
Fractures of Middle Third of Facial Skeleton 435

A B C
Figs 21.4A to C: (A) Displacement of mid third of facial skeleton posteriorly and downwards, along the slope of the sphenoid;
(B) Leading to facial elongation and open bite due to gagging of molars; (C) Showing direction of the force

number of road traffic accidents (RTAs)


and interpersonal violence. The face is a
precious possession of every individual
and everybody cares for it and wants
to look good. Thus, inflicting damage
to it leaves a psychological dent on
the individual and this is the reason
that during the assault it becomes a
favorite and tempting site to be hit. If
the facial fractures are common then
the incidence of grievous head injuries
should also be high considering their Fig. 21.5: Fragile mid third facial skeleton Fig. 21.6: Dashboard injury causing impact
anatomical proximity. But, the nature compared with ‘Matchbox’ on the mid third of facial skeleton
has given us a protection against it by
way of making the facial skeleton weak person is traveling in a vehicle at a
and fragile. In the event of trauma, the high velocity and suddenly the vehicle INVOLVEMENT OF VARIOUS
fragile facial bones fracture and absorb comes to stand still, due to the gathered STRUCTURES DURING
the shock and prevent it from being momentum (inertia) the driver is MIDDLE THIRD FRACTURES
transmitted to the cranium and thus, thrown forward and his head strikes
prevent injury to it. Secondly, if a line against the dash board and the middle During the middle third facial fractures
is drawn from the nasion to the tip of third of the face gets traumatized. various anatomical structures in this area
the mastoid process, it forms an angle Similarly the chest gets traumatized are traumatized. They are as follows.
of 45 degree with the occlusal plane. against the steering wheel resulting in
It is called the slope of the sphenoid injuries to the rib cage (Fig. 21.6). This Involvement of the Nerves
(Figs 21.4A to C). When the facial bones is called coup-counter-coup injury or Various nerves pass through the facial
fracture and get displaced along this acceleration declaration injury. The bo­nes which are involved during the frac­
slope of the sphenoid, posteriorly and arrangement of the facial bones and the tures of the middle third of facial skeleton.
downward rather than only posteriorly. bone grains are such that the middle
Thus, the bones are displaced away from third of the face tolerates the forces Olfactory Nerve
the cranium and injury to the cranium better from the inferior direction than The olfactory nerves are multiple, small
and its contents is prevented. Due to its the anteroposterior direction. The nerves that pass through the cribriform
fragile character the facial skeleton is masticatory forces are transmitted along plate of the ethmoid bone and supply
compared with match box (Fig. 21.5). the bone grains around the anatomical the olfactory perception area situated
The maxillofacial injuries usually cavities to the base of the skull and are at the roof of the nasal cavity. They
result from what is conventionally disturbed over a large area, due to the are responsible for carrying the smell
called dash board injuries. When a peculiar orientation of the bone grains. sensation. The olfactory nerve is the
436 Maxillofacial Trauma

direct extension of the gray matter


of the olfactory area in the anterior
cranial fossa and as it lacks regenerative
potential, once the nerve is damaged,
it is irreversible. The blood clot in the
nasal cavity or the edema of the nasal
mucous membrane can also hamper
the function of this nerve temporarily.
The loss of the smell sensation is called
anosmia. It usually occurs when the
A B
cribriform plate gets fractured, during
the nasoethmoidal complex fractures or Figs 21.7A and B: Third cranial nerve (oculomotor nerve palsy) causing (A) Ptosis of
the Le Fort III fractures. upper eyelid; (B) Fixed dilated pupil nonresponsive to light

Infraorbital Nerve foramen and is not usually traumatized. orbital ecchymosis (Raccoon’s eye)
The infraorbital nerve is involved in the However, if there is retrobulbar bleed (Figs 21.9A and B). The fracture of the
Le Fort II fractures, zygomatic fractures or the fractured segments get displaced base of the skull produces bleeding per
and the orbital floor fractures. It is and impinge upon the nerve, the patient ear, hematotympanum (blood behind
mani­fested in the form of hypoesthesia can have diminished or loss of visual tympanic membrane), CSF otorrhea
or anesthesia in the distribution of its acuity. The optic nerve is also a direct and the Battle’s sign (ecchymosis over
terminal branches namely, the superior extension of the gray matter of brain and the mastoid process in absence of
labial, inferior palpebral and the lateral is very susceptible to pressure. Once the evidence of direct trauma to it). Battle’s
nasal branches. The branches given out nerve is damaged or gets compressed for sign, is also an indication of fracture of
in the infraorbital canal, i.e. the middle longer period its recovery is difficult and the base of the middle cranial fossa and
superior alveolar and the anterosuperior patient may loose vision permanently. It may suggest underlying brain trauma.
alveolar are also involved producing is therefore necessary to undertake optic Battle’s sign consists of bruising over
numbness in the maxillary anterior and nerve decompression within 6 hours to
pre­molar teeth and the gingiva. The prevent permanent damage to the optic
latter two nerves are also involved in nerve. Damage to the terminal branches
Le Fort I fracture. of the facial nerve can also occur in
compound zygomatic fractures.
The III (Oculomotor), IV (Trochlear),
VI (Abduscent) Cranial Nerves Cranial Involvement
These three nerves are collectively The involvement of the cranial cavity
called oculomotor nerves. These ner­ in the middle third fractures is not an
ves are involved when the fractures uncommon phenomenon. In severe
of the orbital walls take place and the mid facial trauma the fracture of the
nerves get compressed in the superior cribriform plate results in cerebrospinal
orbital fissure due to hematoma, bony fluid leakage in the nose producing
Fig. 21.8: Cerebrospinal fluid rhinorrhea.
fragments or as a result of direct injury CSF rhinorrhea (Fig. 21.8). The anterior Arrow showing clear CSF flowing out of the
to them. It produces paresis of the fossa injury produces bilateral circum- fracture site
extraocular muscles producing ‘external
ophthalmoplegia’ (loss of movements of
the eyeball) and diplopia. The blockade
of the parasympathetic supply to the eye,
which comes from the Edinger-Westphal
nucleus, via the IIIrd cranial nerve is
disrupted and results into a fixed dilated
pupil, not responding to light, ptosis of
upper eyelid (Figs 21.7A and B). The fixed
dilated pupil, not responding to light
leads to paralysis of accommodation
(internal ophthalmoplagia). The second
cranial nerve (optic nerve) is well guarded A B
by the thick cortication of the optic Figs 21.9A and B: Bilateral black eye (Raccoon’s eye)
Fractures of Middle Third of Facial Skeleton 437

Involvement of the Paranasal decreases and the eyeball is pushed out


Air Sinuses leading to proptosis. The entrapment of
the extraocular muscles in the fracture
The involvement of the maxillary si­ fragments hampers their action and
nus occurs in Le Fort I and II fractures, the eyeball fails to move in a particular
zygomatic fractures, blow out orbital direction depending on which muscle is
fractures, producing epistaxis due to involved. The eyeball on the unaffected
bleeding in the sinus, which escapes in side moves freely and the eyeball on the
the nose through the osteum maxillary. affected side fails to reciprocate leading
The surgical emphysema is produced to disruption of the focal axis, producing
due to leakage of the air in the soft tissue parallax between the images, resulting
planes. In case of Le Fort II, III fractures, in double image perception of the
Fig. 21.10: Ecchymosis over the mastoid
nasoethmoidal fractures, blow out frac­ single object (double vision or diplopia).
area (Battle’s sign)
tures of the orbit involving in the medial The binocular diplopia occurs due
the mastoid process, as a result of wall, ethmoidal air cells get exposed and to the vertical imbalance of the globe
extravasation of blood along the path the infection occur, which can extend whereas the monocular diplopia results
of the posterior auricular artery.1 The intracranially, through the emissary because of hemorrhage in the anterior
sign is named after William Henry Battle veins producing intracranial infections. chamber of the eye, mostly due to the
(Fig. 21.10). The danger associated with detachment of the lens which requires
such cranial involvement is spread of the immediate intervention unlike the bino­
infection in the cranial cavity, producing
Involvement of the Orbit cular diplopia, which results due to
meningitis to brain abscess. The other During the Le Fort II, III fractures, either muscle entrapment or retrobular
types of the head injuries like intercranial zygomatic fractures and the orbital hemorrhage, which resolves with time
bleeding, cerebral concussion, cerebral wall fractures, the orbit and its contents and the diplopia could be reversed.
contusion or laceration produces are involved. The bleeding that occurs A similar kind of phenomena occurs
cerebral edema and compression may due to the fractured bone travels in the when the III, IV or VI cranial nerves
be present, which deserves treatment on subperiosteal plane and escapes in the are involved. The paresis of the nerve
priority as they can be life-threatening. subconjuctival plane to manifest as leads to paralysis of the corresponding
In a polytrauma patient the treatment subconjuctival hemorrahage which is extraocular muscle and eyeball fails
needs to be prioritized. The life saving bright red in color and as the source of to move in that direction producing
treatment should be undertaken first bleeding is subperiosteal its posterior diplopia. The orbital walls, especially
and the management of facial fractures extent is not seen (Figs 21.11A and B). If the inferior and the medial, are thin and
can be delayed until the patient is stable. the blood escapes in the subcutaneous fragile. The eyeball is non-compressible
plane it produces circumorbital ecchy­ structure and thus, when the intraorbital
Involvement of the Blood mosis (Black eye) (Fig 21.12). When the pressure increases as a result of trauma,
Vessels orbital walls are displaced outwards, the these fragile walls give way and blow
The major blood vessels are not involved, orbital volume increases. The retracting out fracture of orbit results. As a result
but the branches of the internal maxillary action of the extraocular muscles draws of this fracture the orbital size increases
artery are involved producing hemor­ the eyeball inside and enophthalmos and the orbital contents herniate
rhage from the injury sites and the epi­ is produced. When the orbital walls outside, causing retraction of the eyeball
staxis. are displaced inward, the orbital size resulting in enophthalmos.

A B
Figs 21.11A and B: Subconjunctival hemorrhage, note the flame shape, posterior Fig. 21.12: Black eye (circumorbital
boundary not seen and bright-red color ecchymosis) blackish-red in color
438 Maxillofacial Trauma

A B
Figs 21.13A and B: (A) Suspensory ligament of lockwood; (B) Its displacement inferiorly produces hypoglobus and hooding of the globe

The eyeball is supported from the Table 21.1: Rowe and Williams’ • Traumatic exfoliation or avulsion
inferior side by the suspensory ligament classification of midface fractures (Fig. 21.14).
of Lockwood, which is attached medially 1. Central area fractures The fractures of the teeth can be
to the frontal process of maxillary bone A. Those involving occlusion: further classified as:
and laterally to the Whitnall’s tubercle i. Dentoalveolar fractures • Class I—those involving only enamel.
present on the orbital process of the ii. Le Fort I fracture • Class II—those involving the enamel
zygomatic bone. Whenever, the fracture iii. Le Fort II fracture and dentine.
iv. Le Fort III fracture
occurs superior to the Whitnall’s • Class III—those involving enamel,
B. Those not involving occlusion:
tube­rcle and the zygoma is displaced i. Fracture of the nasal bones dentine and pulp
infer­iorly, the eyeball also sinks down ii. Fracture of the frontal process of • Class IV—fracture at the cervical level.
pro­ducing alteration in the level of globe the maxilla • Class V—fracture of the root below
(hypoglobus). The lateral canthal liga­ iii. Fracture of the lacrimal bone the cervical level.
ment moves inferiorly along with the iv. Fracture of the ethmoidal bone The dentoalveolar injuries are caused
v. Combination of I, II, III, IV
fracture fragment and the upper lid also 2. Lateral area fractures by RTA, assault, fall, sports injuries
follows it and produces a characteristic A. Zygomatic bone fractures and are commonly seen in the clinical
‘Hooding of the globe’ (Figs 21.13A and B. Zygomatic arch fractures practice. In the anterior region these are
B), which becomes obvious after the C. Orbital fractures: caused by a hard and blunt object when
initial edema subsides. i. Blow out fractures—pure, impure
ii. Blow in fracture
More severe orbital injuries are
super­ ior orbital fissure syndrome
(invol­­
v­e­­
ment of III, IV, V, VI cranial DENTOALVEOLAR
nerves in the superior orbital fissure) FRACTURE
and orbital apex syndrome (all the
nerves in the superior orbital fissure The fracture of the alveolar bone along
syndrome plus the involvement of the with the injuries to the teeth is termed
optic nerve). as dentoalveolar fracture. There can be
a simple linear fracture of the alveolus
or a severe comminution of the alveolar
CLASSIFICATION OF
bone. The teeth are also injured leading
THE FRACTURES OF THE to their fracture, luxation, displacement
MIDDLE THIRD (ROWE AND or avulsion. The injuries to the teeth can
WILLIAMS2) be classified as:
• Luxation—instrusive, extrusive
The fractures are classified as given in • Proclination Fig. 21.14: Dentoalveolar fracture with
Table 21.1. • Retroclination traumatic avulsion of the incisors
Fractures of Middle Third of Facial Skeleton 439

it strikes the maxilla at lower level. In the has lacerated wound (LW) on the inner
posterior area they are caused by similar side of the lip, then before closing the
cause, but are rare. The posterior area laceration, the lip must be carefully
can also be traumatized by accidental inspected and palpated as the tooth
fracture of the dentoalveolar segment fragments may be embedded in the lip
during the extraction of the maxillary laceration. The lacerated gingiva should
posterior teeth. The clinical features are: be sutured. The teeth are splinted
• Bleeding per orally after reduction by any of the following
• The upper lip is traumatized bet­ methods:
ween the object and the teeth, alve­ • Figure of 8 wiring
olus and hence there is abra­sion/ • Essig’s wiring
contusion or laceration of the lip. The • Ligation of arch bar
lip is edematous and the mucosal • Using splints—lateral compression Fig. 21.15: Lower level of impact causing
aspect of the lip shows laceration or splint Le Fort I fracture line
ecchymosis. • Composite resin splints
• The gingivae are lacerated and • Lead foil splinting (not practical). fracture. As the fracture line runs below
bleed­­ing is seen from its margins. the zygomatic bone it is also called sub-
• The teeth are traumatized and may Conservation of the Fractured zygomatic fracture. This type of fracture
show fracture/displacement/mobil­ Teeth is produced due to the maxillary trauma
ity and the occlusion is deran­ged. The traumatized teeth are examined for at a lower level from the anterior or
• The luxated teeth come in the way of vitality as the nonvital teeth can serve as anterolateral direction (Fig. 21.15). The
occlusion, especially when they are nidus for infection, elective endod­ontic fracture could be unilateral or bilateral.
retroclined and the pati­ent is unable therapy should be undertaken. The res­ The bilateral Le Fort I fracture is also
to close the jaw. toration of the teeth is done subsequ­ called ‘Floating maxilla’.
• The intraoral periapical X-ray shows ently. The classical Le Fort I line starts
widening of the lamina dura and from the lateral margin of the pyriform
fracture line on the alveolar bone. aperture, at the junction of the supe­
FRACTURES OF MAXILLA
• In severe intrusive displacement, rior thin portion and the inferior thick
the root may perforate the nasal Rene Le Fort1 (1902), studied the portion, which forms the line of weak­
floor and is seen in the nasal cavity. fractures produced on the cadaver after ness. The fracture line then runs
• The patient complains of pain and hitting it with heavy stones and upon laterally on the anterior surface of the
sensitivity especially when the teeth autopsy that a typical pattern of injuries maxilla, above the apices of the teeth,
are fractured. were produced, depending upon the crosses the canine fossa superior to it to
• The teeth turn nonvital due to the level of the impact. He described three reach the zygomaticomaxillary buttress.
damage to the periapical vessels. types of fracture lines and they are The buttress is a thick, condensed area
eponymously named as Le Fort I, II or and thus, the fracture line curls around
Management III fracture lines. One must remember it and continues over the posterolateral
The management of the dentoalveolar that these fracture lines which are wall of the maxillary sinus, then it cros­
fracture comprises of two steps: described are standard patterns but, ses the pterygomaxillary fissure and
1. Reduction and splinting of the no injury is ideal, or no two injuries fractures the pterygoid plates at the
luxated teeth. are identical or no two individuals can junction of the lower one-third with
2. Conservation of the traumatized have similar bony configurations. The the upper two-third (Figs 21.16A to D).
teeth. severity of the trauma, strength of bone, This is the fracture line on the lateral
nature of object causing injury and its side. The fracture line also runs on the
Reduction and Splinting velocity vary and thus, in the clinical medial side, i.e. on the lateral nasal
of the Luxated Teeth practice some deviations from what is wall and runs posteriorly on it to reach
The teeth, which are displaced are classically described in the textbooks is the lateral fracture line at the pterygoid
reduced in their normal position and observed. However, for understanding plates. When a bilateral fracture line is
to facilitate the healing, they are spli­ the devia­ tions from the normal, the produced, the whole lower maxilla gets
nted till the healing takes place. The normal pattern must be known. detached from rest of the facial skeleton
soft tissue injuries are also managed and moves freely, thus the name, floating
simultaneously. The lacerations of the Le Fort I Fracture maxilla. It may be associated with the
lip are sutured. If the tooth is fractured The Le Fort I fracture is also called mid palatine split. The mid palatine split
and the fragment is lost and if the patient Guérin fracture or a low level horizontal cannot occur in an isolated way and
440 Maxillofacial Trauma

when it is seen it is always associated


with the lateral fracture of maxilla like
Le Fort I or II fracture.

Clinical Features
• The fracture is caused by a blunt
and hard object and the soft tissue
gets crushed between the bone and
the object producing contusion
and edema which can extend to
the upper lip. The ecchymosis and
degloving injuries can also be seen
in the gingivolabial sulcus.
• There is tenderness, step and crepi­ A B
tus in the gingivolabial sulcus on
lateral margin of the pyriform aper­
ture and anterior surface of maxilla.
• As the fracture line passes over the
walls of the maxillary sinus, there
is bleeding in the maxillary sinus,
which escapes in the nasal cavity
through the osteum maxillary, pro­
ducing epistaxis.
• The anterior and middle superior
alveolar nerves are traumatized,
which results in heaviness in the an­
terior teeth and gingiva.
• There is an ecchymosis on the zygo­
maticomaxillary buttress area, step
formation and tenderness. C D
• An ecchymosis over the junction Figs 21.16A to D: Le Fort I fracture line
of hard and soft palate may be
seen which is called Guérin sign3
(Alphonse François Marie Guérin)
(Figs 21.17A and B).
• The maxilla gets displaced post­
eriorly and downwards causing de­
rangement of occlusion.
• When the maxilla is palpated bima­
nually, keeping the thumb and index
finger of the left hand on the lower
one-third of the maxilla on either side
A B
and the anterior teeth and alveolus
Figs 21.17A and B: Ecchymosis at the junction of hard and soft palate ‘Guérin sign’
are grasped with the thumb and the
index finger of the right hand and
the jaw is moved anteroposteriorly, • When the maxillary teeth are per­ broken cortication in the zygomatic
the movements are felt by the fingers cussed a typical crack pot sound is buttress area. The fracture line over
of the left hand kept on the anterior produced. the anterior maxillary wall is not clearly
surface of the maxilla (Fig. 21.18). The Le Fort fractures are not properly seen due to super imposition of various
In cases of bilateral fracture the seen on the X-ray. The X-ray paranasal cranial and spinal shadows. The true
movements are felt bilaterally and sinus (PNS) shows break in continuity lateral view also shows the fracture line,
are free, giving the maxilla floating in the lateral wall of the nasal aperture, but again not very clearly. The CT scans
appearance. haziness in the maxillary sinus, step or in both, the axial and coronal sections
Fractures of Middle Third of Facial Skeleton 441

A B

Fig. 21.18: Bimanual palpation for Le Fort I


fracture, one hand grasps the maxilla and
elicits the mobility, while the fingers of
the other hand kept lateral to the pyriform
fossa feel the abnormal mobility

C D
are very helpful and show the fracture
lines clearly. The 3D reconstruction of Figs 21.19A to D: Application of the Rowe’s disimpaction forceps
the CT scans can be very informative.

Management of the Le Fort I


Fracture
The Le Fort I fractures are managed by:
• Closed reduction and immobiliza­
tion by:
– Internal suspension
– External suspension
• Open reduction and fixation with A B
plates and screws. Figs 21.20 A and B: (A) Application of the Hayton-William’s disimpaction forceps;
Proper disimpaction of the fracture (B) Application of the Hayton-William’s forceps
and its reduction is very important to
achieve proper occlusal relationship and then reduced by applying traction in the When there is unilateral Le Fort I
for restoring the facial symmetry, prior anterosuperior direction. The Hayton- fracture, the fractured maxilla is reduced
to fixation. The reduction is done using William’s maxilla holding forceps can and then sandwiched between the
a pair of Row’s maxillary disimpaction also be used for reduction of the fractured mandible and the contralateral intact
forceps (Figs 21.19A to D). The operator maxilla but, it can move the fractured maxi­lla with intermaxillary fixation
stands behind the head of the patient segment only in anteroposterior plane (IMF). The contralateral, intact maxilla
and the Row’s disimpaction forceps are and proper dis­ impaction cannot be prevents pulling down of the fractured
applied to hold the maxillae bilaterally achieved. It is not suitable in case of maxilla when the mandible is depressed.
by placing its beaks on the nasal floor maxillary fractures with mid palatine This is called ‘Sandwich technique’.
and the curved beak goes over the splits as the maxillae tend to get When the fracture is bilateral, only
maxillary anterior teeth and rests on collapsed due to the lateral pressure IMF is not adequate as the depression of
the hard palate. The beaks are padded applied by these forces (Figs 21.20A the mandible will pull dawn the fractured
to prevent trauma to the mucosa. The and B). The Hayton-William’s forceps maxilla. Hence, the fractured maxilla
maxillae are disimpacted by applying are more suitable for the manipulation of needs to be fixed against the intact facial
forceps which are directed backwards maxilla during the Le Fort osteotomies. bones superior to the fracture line. This
towards the operator, giving downwards The guidance for proper reduction is is achieved by either internal suspension
and side to side rocking movements and achievement of satisfactory occlusion. or external suspension.
442 Maxillofacial Trauma

Internal suspension • quate as the flat bone having good


Infraorbital rim suspension wiring:
•Pyriform fossa wiring: A degloving An incision is placed on the skin in vascularity heals faster.
incision is placed in the labial the infraorbital area. Layer by layer • Zygomatic suspension wiring: An
vestibule anteriorly and full thickness dissections are carried out to reach incision is placed in the buccal
mucoperiosteal flap is raised. The the infraorbital rim. The orbital vestibule in the molar area. A
anterior surface of the maxilla is periosteum is reflected with the subper­ iosteal dissection is carried
exposed and the lateral boundary of periosteal elevator. Keeping a guard out along the bone to expose the
the pyriform aperture is identified by in place to protect the eyeball, a zygomatic buttress. The maxillary
identifying the anterior nasal spine hole is drilled obliquely through process of zygoma is identified and
and then carrying the subperiosteal the infraorbital rim, from outside a through and through hole is drilled
dissection superolaterally along the to inside 5 to 6 mm away from the in it. A 24 number SS wire is passed
margins of the pyriform aperture. orbital margin. A wire is passed through the hole which is legated to
Care should be taken not to perforate through the hole and using the bone the maxillary arch bar or Ivy loops to
the nasal mucosa, while raising the awl, which is passed from the buccal achieve the zygomatic suspension.
mucoperiosteum from the nasal side vestibule, upward and drawn in the This suspension wiring is very useful
of the aperture. The nasal mucous infraorbital incision, both the wire in firmly stabilizing the maxilla along
membrane is reflected and the ends are drawn in oral cavity. The with the pyriform aperture wiring or
lateral wall of the pyriform aperture wire ends are legated to the arch plating, not only in cases of Le Fort I
is exposed. Keeping a guard medially bar or the Ivy loop after achieving fracture, but also in cases of Le Fort I
to protect the nasal mucosa a hole is the IMF (Fig. 21.22). The incision is osteotomies.
drilled from lateral side, 5 to 6 mm closed. The wires are removed after • Circumzygomatic wiring: The wire
apart from the lateral boundary of 3 to 4 weeks under aseptic care. is passed around the zygomatic arch
pyriform aperture to prevent fracture While removing the wire the oral to suspend the fractured maxilla. It is
of the bony margin. A piece of cavity is disinfected with antiseptic mandatory to rule out fracture of the
24 gauge stainless steel wire is passed solution and one end of the wire is zygomatic arch before the wiring is
through the hole and both the ends of cut very close to the mucosa through done, by good clinical examination
the wire are drawn in the oral cavity, which it is projecting out. The other and the submentovertex radio­
through the vestibular incision. The end is grasped and pulled out. graphs. The fracture of the arch is
wire ends are legated to the arch bar Thus, only that portion of the wire, contraindication for this wiring.
or Ivy loop in the maxillary arch, after which is embedded in the tissue In this technique a small 0.5 cm
the IMF is achieved in the desired travels through the tissue during incision is taken superior to the
position (Fig. 21.21). removal and the portion of the wire zygomatic arch and the tissues are
This suspension prevents the projecting in the oral cavity is not dissected up to the superior border
down­ ward displacement of the allowed to travel through the tissue of the arch. An Obwegeser bone awl
maxilla when the mandible is depre­ as it is contaminated and can carry is passed through the incision lateral
ssed. The incision is closed and the infection along it in the deeper tissue to the arch, directing it inferiorly and
wires project through the incision planes. In case of maxillary fractures slightly anteriorly until it is drawn
line in the oral cavity. three weeks immobilization is ade­ intraorally in the buccal vestibule.
A 24-gauge stainless steel wire is fed
in the eye of the awl and secured by
giving few twists. The awl is retracted
back slowly without withdrawing it
fully through incision. As the tip of
the awl reaches the superior border
of the arch, the awl is reinserted in
the same direction, medially to the
arch and drawn through the same
site intraorally. Both the ends of the
wire are ligated to the arch bar or
the Ivy loop in the maxillary arch
(Figs 21.23A to D). While doing the
circumferential wiring it must be
Fig. 21.21: Pyriform fossa wiring Fig. 21.22: Infraorbital rim suspension remembered that the wire must pass
wiring very closely to the bone and no soft
Fractures of Middle Third of Facial Skeleton 443

A B

Fig. 21.25: Impact at the level of base of


nose causing Le Fort II fracture

maxilla. The head frame can also be used


for anchoring the universal rods with the
help of the universal joints (Figs 21.26A
to E). A rod suspended from the frame
anteriorly can also be used for giving
anterior traction to the maxilla when it
is displaced posteriorly and is impacted.
The external suspension wirings are
C D basically indicated for the Le Fort III
Figs 21.23A to D: Circumzygomatic wiring using Obwegeser bone awl fractures or other Le Fort fractures
where there is poly trauma and facial
tissue should be trapped between skeleton is fractured at multiple sites
the wire and the bone, as the or when there is gross comminution,
pressure necrosis can occur and the which prevents/contradicts the internal
patient may experience pain. Proper suspension wirings.
hygiene must be maintained around
Open reduction
the wire to prevent infection and the
wires are removed under aseptic The Le Fort I fracture can be treated by
care after 3 to 4 weeks. open reduction. This is very effective
• Supraorbital rim suspension wir- modality and avoids morbidity to the
ing: In this technique a lateral eye­ patient, which occurs as a result of
brow incision is taken. The tissues the IMF and suspension wiring. The
are dissected layer by layer till the internal suspension is better tolerated
Fig. 21.24: Supraorbital rim wiring
bone is reached. The orbital peri­ than the external suspension as the
osteum is reflected and keeping projecting wires, POP head cap, head
a guard in place, a through and frames or hallows and cheek wiring. The frame are very uncomfortable to the
through hole is drilled in the supra­
prefabricated frames are fixed to the patient. The head frame and the POP
orbital rim. A wire is passed through
shaved head using a POP roll. The head head cap tend to get loose, impinge
the hole. A long bone awl is taken
frame has a cap like projection. A bone upon the skin, cause pressure sores
and passed percutaneously throughawl is passed from the buccal vestibule and do not allow the patient to sleep
the incision inferiorly and it is drawn
to the skin surface 1′ below the outer in lateral position. The open redu­ction
intraorally in the buccal vestibule.
canthus of the eye. A stainless steel wire ensures proper reduction and more
Rest of the procedure is same as in
(24–26 number) is passed in the oral rigid immobilization and faster healing.
case of any other suspension wiring
cavity, using the awl. The extraoral end In addition to this the miniplates can be
(Fig. 21.24). of the wire is legated to the head frame fixed transorally and thus, cosmetically
and the intraoral end is legated to the more acceptable to the patient. The
External suspension
arch bar or Ivy loop in the maxillary fracture line is accessible at lateral to
The external suspension wiring is done arch (Fig. 21.25). The wire is used to give pyriform fossa and the zygomatico-
by using the plaster of Paris (POP) head anterior and superior traction to the maxillary buttress area, intraorally.
444 Maxillofacial Trauma

that is fixed at the buttress is a four holed


straight plate without gap or a L shaped
plate, depending upon the anatomical
configuration of the bone, availability
of sound bone for anchoring the screws,
the direction of the fracture line and
presence of any comminution of bone
may warrant use of a particular form
B C
and size of bone plate. The plate is nicely
A
adapted to the bone and fixed across the
fracture line using 5 mm screws. The
2 mm plates are commonly used (Figs
21.27A to E).

Le Fort II Fracture
The Le Fort II fracture is also called
pyramidal fracture. The fracture line
originates at the nasal bones and ends
at the pterygoid plates. It is caused by
D E trauma at the higher level of the face, from
the anterior direction (See Fig. 21.25).
Figs 21.26A to E: Le Fort II fracture line The fracture can be unilateral or
bilateral. The nasal bones articulate
superiorly with the frontal bones at
frontonasal suture and with each other
in the midline at internasal suture. The
nasal bones are thicker at the frontonasal
suture and as the inferior border is
reached they become thin. The junction
between this thick and the thin part
of the nasal bone constitutes a line of
weaknesses. In the event of trauma the
Le Fort II fracture line originates at this
A B point and runs laterally on the frontal
process of maxilla and then extends on
to the lacrimal bone. Then it crosses the
inferior part of the lamina papyracea
of the ethmoidal bone, exposing the
ethmoidal air cells. The fracture line
runs on the floor of the orbit towards the
infraorbital rim and crosses the same at
C D E the level of zygomaticomaxillary suture.
Figs 21.27A to E: (A) Intraosseous wiring; (B) Various implants used for the RIF; It then runs on the anterior surface of
(C and D) Exposure of fracture line at the buttress through a degloving incision and plating; the maxilla, runs inferiorly towards the
(E) Plating at the buttress and lateral to pyriform fossa zygomatic buttress, during this course
it runs around the infraorbital foramen
A degloving incision is placed in the the pyriform aperture. The L shaped and does not involve the foramen as
buccal vestibule in the anterior and plate with 135 degree angulation is its walls are corticated. It then runs
the premolar-molar area to expose the better suited for application lateral to inferiorly around the buttress and runs
fracture line. The fracture is reduced the pyriform aperture than the regular on the posterolateral wall of the maxillary
by using a pair or Row’s maxillary L shaped plate with 90° angulation. The sinus, crosses the pterygomaxillary
disimpaction forceps, as described plate is adapted to the bone and fixed fissure to the fracture the pterygoid
previously. A 4 holed ‘L’ shaped plate across the fracture line with 5 mm long lamellae half way (See Figs 21.26A to E).
is used for fixing the fracture, lateral to screws as the bone is very thin. The plate The fracture also continues medially,
Fractures of Middle Third of Facial Skeleton 445

from its origin over the lateral nasal passing through the foramen as the of the mid third of facial skeleton
wall, runs posteriorly to meet the lateral line gets deflected around the fora­ resulting in classical ‘dish face defor­
fracture line behind the pterygoid plates. men due to its cortication. The later­ mity’ (Fig. 21.29A).
When the bilateral fracture occurs it al nasal, inferior palpebral, and su­ • In a classical Le Fort II fracture,
assumes the shape of a pyramid and thus perior labial branches are involved the injury to the cribriform plate
the name ‘pyramidal fracture’. along with the anterior and middle of ethmoid is not present and thus
superior alveolar branches. CSF rhinorrhea does not take place,
Clinical Features • There could be tenderness and step unless there is associated fracture of
The clinical features of the Le Fort II over the buttress intraorally. cribriform plate of ethmoid.
fracture are as follows: • The maxilla gets displaced posteri­ • As the walls of the maxillary sinus
• Due to the fracture of the nasal orly and downward resulting in get involved there could be leakage
bones there is edema over the nasal anterior cross bite, gagging of molars of the air in the soft tissue producing
bridge and epi­ staxis. Bilateral cir­ and anterior open bite. crepitus on palpation (surgical em­
cumorbital edema and/or ecchymo­ • On bimanual palpation, keeping physema) and the maxillary sinus
sis may be present. There is tender­ thumb and index finger of the left appears hazy on X-ray due to bleed­
ness over the nasal bridge. hand on the nasal bones and grasp­ ing in the sinus.
• As the fracture passes over the me­ ing the anterior maxillary teeth with
dial orbital wall, there may be sub­ the thumb and index fingers of the Investigations
conjunctival bleeding, which is more other hand if the maxilla is moved, The X-ray paranasal sinus (PNS) is
pronounced medially. The subcon­ the movements are felt at the nasal usually adequate. The maxillary sinus
junctival hemorrhage and then cir­ bone suggesting fracture at the site. appears hazy due to bleeding in it. Step
cumorbital ecchymosis are a result Similar bimanual palpation also elic­ deformity is also seen in the infraorbital
of the bleeding at the site of frac­ its the abnormal mobility over the rim (Figs 21.29B and C). The fracture line
ture, which through the subperios­ infraorbital rims (Figs 21.28A and B). is also seen at the level of the nasal bones.
teal plane escapes in different tissue • The face becomes flat or concave The Campbell-Trapnell lines are useful in
planes. If it goes in the subcutaneous due to the posterior displacement reading the X-ray properly (Fig. 21.30).
plane, it will present as a circumorbit­
al ecchymosis and if it goes in the sub­
conjunctival plane, subconjunctival
hemorrhage is the presentation.
• There is a step defect in the infra­
orbital rim. It also contributes
to the circumorbital edema and
ecchymosis.
• As the fracture line passes on the
floor of the orbit, the infraorbital
nerve gets traumatized in the in­
fraorbital canal and it results in
the neurological deficit in the area A B
of distribution of the infraorbital Figs 21.28A and B: Bimanual palpation in a case of Le Fort II fracture, one hand grasps
nerve. The infraorbital nerve seldom the maxilla and elicits the mobility, while the fingers of the other hand kept over the
gets traumatized due to the fracture infraorbital area feel the abnormal mobility

A B C
Figs 21.29A to C: (A) Dish face deformity; (B and C) X-ray and CT scan showing Le Fort II fracture
446 Maxillofacial Trauma

are the markers of proper reduction. usually not required and the nasal bone
Intermaxillary fix­ation is done and the fractures can be managed conservatively
fractured middle third is secured with by simple reduction and stabilization by
the intact superior skeleton with the nasal packing and external POP splints.
help of either: The two point fixation at the infraorbital
A. Internal suspension rim and the zygomatic buttress is usually
B. External suspension. adequate (Figs 21.31A to C). It is also
The internal suspension is similar observed that the infraorbital rim area is
to the Le Fort I fracture except, the pyri­ comminuted in high velocity trauma and
form fossa wiring suspension and infra­ sound bone for anchoring the screws is
orbital rim wirings are not used for treat­ not available, in such cases or in the cases
ing the Le Fort II fracture as the fracture where the fracture is minimally displaced
line passes above these points. The single point plating at the buttress area
circumzygomatic suspension wiring or may be opted. If the stability of the
supraorbital rim wiring can be done. Ex­ fracture fragments is doubtful with one
Fig. 21.30: Campbell-Trapnell lines ternal suspension with the help of POP point fixation then additional measures
head frame can be done. such as IMF for ten days may be resorted
to facilitate uneventful healing.
Open reduction
The fracture lines are appreciated on a
CT scans in a better way than the con­ The fracture line can be accessed at Le Fort III Fracture
ventional X-rays. the infraorbital rim and the zygomatic The Le Fort III fracture is also called
buttress area. Through the infraorbital or craniofacial disjunction, as the mid third
Management subcilliary incision; the infraorbital rim of facial skeleton gets disarticulated from
The management of the Le Fort II frac­ is exposed and after carefully reflecting the cranial base. This fracture is a supra­
ture is by: the orbital periosteum holes are drilled zy­gomatic fracture. It results from an
• Closed reduction on either side of the fracture line and impact that occurs at a high velocity at the
• Open reduction intraosseous wiring is done. If the plates level of frontonasal suture (Fig. 21.32).
are used, orbital plates with gap having The fracture line starts at the fron­
Closed reduction
4 to 6 holes is carefully adapted and tonasal suture, runs horizontally to
The fracture is reduced using a pair contoured to the bone and secured in separate the frontomaxillary suture, runs
of the Row’s maxillary disimpaction place using 5 mm screws. The zygomatic over the lacrimal bone, the lamina papy­
forceps as described earlier. The maxilla buttress area is accessible intraorally, racea of the ethomoid bone and runs
is disimpacted in the anterosuperior through an incision placed in buccal towards the optic foramen. As the optic
direction. When the fracture is old or vestibule in the molar area. The plates foramen is guarded by thick cortication,
the fracture segments are impacted, are fixed in a similar way as described to protect the optic nerve, the fracture
traction with the help of extraoral device in the Le Fort I fracture. The infraorbital line goes around it to reach the medial
using pulley and weights or elastics is rim is grossly comminuted sometimes boundary of the inferior orbital fissure,
done. Achieving satisfactory occlusion and bone is not available for fixing the which provides a readymade passage
and correction of facial deformity screws. The plating at the nasal bones is for the fracture line. At the medial

A B C
Figs 21.31A to C: Management of bilateral Le Fort II fracture by fixation at the buttress area
Fractures of Middle Third of Facial Skeleton 447

Fig. 21.32: High velocity impact at the A B


level of frontonasal suture Figs 21.34A and B: Clinical cases of Le Fort III fracture,
note gross edema of face in figure B

Fig. 21.33: Le Fort III fracture line

boundary of the inferior orbital fissure


the fracture line divides/bifurcates in
two lines. One line passes around the
frontozygomatic suture to separate the A B
zygomatic bone from the frontal bone.
Figs 21.35A and B: Clinical case of Le Fort III fracture showing elongation of the face
The other line passes posteriorly to
fracture the pterygoid plates at the root,
thus separating them from the cranial • There is flattening of the nasal bridge. which is called CSF rhinorrhea. If
base. Hence, in this fracture the facial • Profuse epistaxis is present. the patient is in upright position the
skeleton is separated from the cranium • As the facial bones are disarticulated CSF leads in the nasal cavity and
at frontonasal suture, frontozygomatic from the cranial base the elongation flows out. It appears as a glistening,
suture and the pterygoid plates thus, of the face takes place leading to clear fluid. It is often difficult to
total craniofacial disarticulation takes long face syndrome (Figs 21.35A detect the CSF as it is admixed with
place and hence the name, craniofacial and B). The facial bones not only the blood. The blood clots and dries
disjunction. The fracture line also runs get displaced inferiorly, but also earlier and the flowing CSF washes
medially from its point of origin runs posteriorly along the slope of the the dried blood on the face as it flows
over the lateral nasal wall to meet the sphenoid leading to concavity, which dawn producing classical rail tracts.
lateral fracture line behind the pterygoid gives a classical ‘dish face deformity’. It also forms classical ring around
plates (Fig. 21.33). • The posteroinferior displacement the clotted blood on the pillow. If
of the facial bones leads to derange­ the patient is in supine position it
Clinical Features ment of occlusion, anterior open passes in the pharynx giving salty
• There is massive edema of the face. bite and cross bite deformity. taste.
• Bilateral circumorbital edema/ecch­ • There may be fracture of the cribri­ • The damage to the branches of the
y­­­mosis is present (Figs 21.34A and B). form plate of the ethmoid, which may olfactory nerve or even edema or
• Subconjunctival hemorrhage is also lead to dural injury leading to the clot in the region of superior meatus
present. leakage of the CSF in the nasal cavity, leads to hampering of sense of smell
448 Maxillofacial Trauma

thus, causing anosmia. In case of • Step deformity is present at the Management


former it is irreversible but in case of frontonasal and frontozygomatic The fracture can be managed by closed
latter it is transient. sutures. and open reduction.
• The exposure of the ethmoidal air The Le Fort III fracture may be
Closed reduction
cells can lead to infection, which associ­ated with head injury more fre­
can pass intracranially and cause quently than any other facial fracture The closed reduction is done with Row’s
intracranial infections. due to the anatomical proximity of the maxi­ll­ary disimpaction forceps as descri­
• The size of the orbit increases and as fracture to the cranial base and the bed earlier. Achievement of the satis­
the fracture occurs at the frontozy­ higher level of the trauma that causes factory occlusion is the marker of the
gomatic suture area the Whitnall’s the fracture. fracture reduction in closed reduction.
tubercle along with the Lockwood’s The internal suspension is not effective
suspensary ligament attached to as the fracture line is very high and only
it migrates inferiorly to produce
Investigations supraorbital rim is available for internal
hypo­ globus and hooding of the The X-ray PNS, posteroanterior (PA) suspension (Table 21.2). The external
eye. view and the lateral radio­graphs are use­ suspension with POP head frame or halo
• Bimanual palpation as described ful in assessing the fracture. CT scans are frame is possible, through the cheek
earlier, depicts abnormal mobility the best method to visualize the fracture, wires with the anterior traction, through
at the fronto-nasal and frontozygo­ as in normal radio­graphs the superim­ the vertical suspended rods from the
matic sutures. position obscures the fracture line. head frame (Figs 21.36 and 21.37).

Table 21.2: Methods of closed reduction in mid-face fractures

Le Fort I fracture Le Fort II fracture Le Fort III fracture

Closed reduction Internal suspension Internal suspension Internal suspension


(for internal suspension, point Pyriform fossa Circumzygomatic Not desirable as the fracture
from which the suspension is Infraorbital rim Supraorbital rim is at a higher level and all the
done is superior Circumzygomatic External suspension suspension points are below
to the fracture line) Supraorbital rim Craniomaxillary suspension the fracture line
External suspension using halo frame and cheek
Craniomaxillary suspension wires or universal rods and
using halo frame and cheek joints External suspension
wires or universal rods and joints Craniomaxillary suspension
Sandwich technique using halo frame and cheek
In case of unilateral Le Fort I wires or universal rods and
fracture joints
Open reduction Plating at lateral margin Plating at the zygomatico- Plating at the frontozygomatic
of pyriform fossa and the maxillary buttress areas, if the sutures and if the fracture is
zygomaticomaxillary buttress fracture is unstable then plating still unstable then at the
area at infraorbital rim and at the frontonasal area
frontonasal area, which is seldom
required

A B Fig. 21.37: Management with


Figs 21.36A and B: Management with craniomaxillary suspension using POP head cap craniomaxillary halo frame
Fractures of Middle Third of Facial Skeleton 449

Open reduction be elaborated, which matter a lot in the clear fluid. This is the ring test. Similarly,
The open reduction is done with the management and the clinician must a drop of blood with CSF is taken on
help of intraosseous wires or bone plates be aware of. The CSF rhinorrhea is one the blotting paper the blood clots and
placed at the frontozygomatic suture and such condition. forms the central area around which
frontonasal sutures. In case of pan facial clear CSF forms a ring. The CSF must
trauma when there are multiple facial CSF Rhinorrhea be differentiated from the serum which
fractures, the outer most fractures are first The leakage of the CSF through the nose is expressed out when the blood clots
reduced and the inner fractures are treat­ following the fracture of the cribriform and from the mucous secreted by the
ed later, i.e. the fracture at the zygoma plate of the ethmoid bone results in CSF nasal mucous membrane. Both of them
and mandible will be reduced first and rhinorrhea as the dural attachment at have lower glucose content than the
the nasal bone fracture at the end to avoid this site gets torn and the leak results. CSF (Identification of CSF rhinorrhea:
facial widening (Fig. 21.38). The advan­ This can occur commonly in Le Fort III clear CSF should be collec­ted in a vial
tage of open reduction in the treatment fracture and the nasoethmoidal fracture and a glucose level of 45 mg/dL or
of mid third fractures is that it causes least and occasionally Le Fort II fracture, if more confirms its presence, as does the
morbidity to the patient and not only the the associated injury to the ethmoid is absence of it’s sedimentation. CSF will
occlusion, but the facial deformities are present. The CSF leaks in the nasal cavity not stiffen the handkerchief, whereas
also corrected more accurately. and trickles out through the nose. It is nasal secretions will. CSF also produces
If the Le Fort III fracture is associ­ated glistening, clear fluid. When the patient concentric rings when poured on linen).
with the head injury then the manage­ is in supine position, the CSF instead The leakage of the CSF can lead to
ment of the fracture is always the sec­ of flowing out, trickles in the throat, progress of retrograde infection in the
ond priority. The head injury and other giving salty taste in a conscious patient. cranial cavity which can result in menin­
life threatening, grievous injuries must Immediately following the trauma the gitis, venous thrombosis to more severe
be attended to first. If the CSF leakage CSF is mixed with blood and is difficult intracranial sepsis, which could prove
is present then neurosurgical opinion to detect. The blood flows dawn the fatal. Thus, every attempt must be made
must be sought, antibiotics that cross face and clots and dries but the CSF to prevent the infection, the antibiotics
the blood brain-barrier (BBB) like chlo­ does not clot and flows dawn the face that cross the BBB should be prescribed.
romycetin, third generation celephalo­ washing out the dried blood on the face The minor CSF leakage is managed con­
sporins should be started to prevent the along the path of its flow and creates servatively with antibiotic prophylaxis,
intracranial infections. The ethmoidal classical rail tracks. The blood mixed propped-up position formation of blood
air cell exposure must also be covered with the CSF collects on the pillow of clot and organization of the same may
with the similar antibiotic therapy. the patient. The blood clots earlier and lead to spontaneous arrest of the CSF
While studying the mid facial frac­ forms the central area of clotted blood leak. Nasal packing, nasotracheal intu­
tures certain associated conditions must around which the CSF forms a ring of bation, passing of the nasogastric tube
(Ryle’s tube) is strictly contraindicated
in presence of the CSF rhinorrhea. If the
leak is profuse and does not get arrested
spontaneously, then the neurosurgical
intervention is required and cranioplas­
ty is done to repair the dural tear.

FRACTURES OF THE
ZYGOMATIC BONE
The zygomatic bone is also called ma­
lar bone; it forms the prominence of the
cheek and thus, also referred as cheek
bone. It is a flat bone and has four pro­
cesses, the frontal process which articu­
lates with the frontal bone, superiorly at
the frontozygomatic (F-Z) suture. The
maxillary process arti­ culates with the
zygomatic process of the maxillary bone
to form the zygo­maticomaxillary suture,
Fig. 21.38: Various sites on facial skeleton where plates can be fixed during internal fixation near the zygo­maticomaxillary buttress.
450 Maxillofacial Trauma

The temporal process articulates with the


zygomatic process of temporal bone to
form the zygomaticotemporal suture and
both these processes form the zygo­matic
arch. The orbital processes of the zygoma
forms the lateral orbital wall. Because of
the three processes of the zygomatic bone
are involved in the fracture these fractures
are often described as tripoid fractures.
As the forth process, the orbital process is
also involved some clinicians describe it
as quadripoid fracture. All the joints with
adjacent bones are sutural joints.4 Below
the F-Z suture, on the lateral orbital mar­
A B
gin a small bony projection is seen, which
is called Whitnall’s tubercle which gives Figs 21.39A and B: Fracture of the zygomaticomaxillary complex
attachment to the suspensary ligament
of Lockwood, which is a Hammock like – 3 o’clock position follo­wing the trauma and later it is
ligament and supports the eyeball.5 The – 6 o’clock position masked by the edema. It can be seen
masseter muscle originates from the in­ – 9 o’clock position again when the edema subsides. In
ferior border of the zygomatic arch and – 12 o’clock position case of outward displacement the
the deep temporal fascia is attached to it • According to the displacement along malar prominence is accentuated
superiorly. Due to these attachments the the vertical and the horizontal axis (Fig. 21.41).
displacement of the zygoma is prevented (Figs 21.40A to E): • Circumorbital edema is present. Blee­
in superoinferior direction in the event of – Undisplaced fractures—only the ding below the periosteum esca­pes
the fracture.6 The sutural joints existing sutures are widened without below the subcutaneous plane to
between the zygoma and adjacent bone gross displacement of the bone produce circumorbital ecc­h­y­mosis
leads to separation of these sutures and – Upward and inward displacement (Fig. 21.42A).
if reduced properly the interlocking —the zygoma encroaches upon • Subconjunctival hemorrhage is pre­
of the sutures makes the fracture self- the orbital cavity sent laterally. As it is produced as a
retai­ning. – Downward and outward displa­ result of bleeding in the subperiosteal
The fractures of the zygoma are divi­ ce­ment—size of the orbit gets plane due to fracture which escapes in
ded into two categories, which produce expan­ded the subconjunctival plane, its posterior
distinct clinical signs and symptoms. – Comminuted fracture—multi­ple boundary is not seen when the patient
They are: fragments are present. is asked to look medially, rotating the
• Fractures of the body of zygoma Further the zygomatic fractures have eyeballs medially. It is bright red in
(malar bone fractures). also been classified on the basis of pre­ color, unlike the circumorbital ecchy­
• Fractures of the zygomatic arch. sence of comminution at the sutures. If mosis, as the conjunctiva are paper
The fractures of the zygoma the comminution is present it is referred thin and allow the oxygenation of
were previ­ously called as the zygo­ as a high velocity fracture and if minimal the extravasated RBCs. The shape
maticomaxillary complex fractures as the or no comminution is present it is called of the subconjunctival hemorrhage
zygomaticomaxillary suture is involved. low velocity fracture. Most of the times is often described as flame shaped
However, presently they are referred to it is noticed on surgical exposure of (Fig. 21.42B).
as zygomatico-orbital complex fractures these fractures that the infraorbital area • Unilateral epistaxis is present due
as the involvement of the orbital rim is and the buttress area are communited, to bleeding in the maxillary sinus,
inevitable (Figs 21.39A and B). while as the frontozygomatic suture which escapes in the nose through
Many authors have devised classifi­ is by and large not comminuted and the osteum maxillary.
cation schemes for zygomaticomaxil­ provides firm anchorage for the screws • The infraorbital nerve often gets
lary complex (ZMC) fractures (Ellis,7 used for fixing the plates, while treating traumatized in the infraorbital canal
1985; Yanagesawa,8 1973; Knight,1961).9 these fractures. producing numbness in the area of
Zingg10 (1992), Yamashiro M11, 1983. its distribution.
The zygomatic fractures can be clas­ Clinical Features • On palpation there is tenderness,
sified as:9 • Flattening of the malar prominence, crepitus and step deformity over the
• As per the conspicuous presentation in case of the depressed fractures. frontozygomatic suture. Similar
of step: The depression is seen immediately findings are also present over the
Fractures of Middle Third of Facial Skeleton 451

A B C

D E
Figs 21.40A to E: Classification of ZMC according to the displacement along the vertical and the horizontal axis
(Adopted from Rowe and William’s maxillofacial injuries. Churchill Livingstone 1994)

A B
Fig. 21.41: Flattening of malar prominence Figs 21.42A and B: (A) Circumorbital ecchymosis; (B) Subconjunctival hemorrhage
(note the bright-red color)

zygomatic arch, infraorbital rim and comminuted and offers a stable When the fracture is displaced out­
the zygomaticomaxillary buttress point for internal fixation during the wards the orbital size increases and
area. In high velocity accidents the management. the retracting action of the extraocular
infraorbital area is usually com­ m­ • When the fracture is inwardly dis­ muscles pull the eyeball in, causing
inuted and so is the area of zygo­ placed, i.e. depressed fracture, the enophthalmos.
maticomaxillary buttress. The fro­n- orbital size gets reduced and the eye­ • When the fracture is severely dis­
­to­zygomatic suture is usually not ball is pushed out causing proptosis. placed downwards, the support of
452 Maxillofacial Trauma

the suspensory ligament of Lock­


wood is lost and the alteration in the
level of globe takes place, which pro­
duces enophthalmos, hypoglobus
and the lowering of the lateral can­
thus is called as hooding of the eye.
• The entrapment of the extraocular
muscles in the fracture segments or
the compression of the III, IV or VI
cranial nerves in the superior orbital
fissure, due to intraorbital hematoma
or displaced fracture segments,
leads to compromised action of the
Fig. 21.43: Strabismus
extraocular muscles. When the patient
looks side wards the normal eyeball Fig. 21.44: Forced duction test
moves, but the affected eyeball fails to is restricted due to muscle
reciprocate, which presents clinically entrapment and not due to
as a pseudosquint (Strabismus (Fig. muscle paresis. Some times
21.43) and the focal axis gets alte­ the orbital wall may not show
red and two images of one object defect on the X-ray but still
are perceived. It is called diplopia. there is dilopia due to muscle
Normally the two eyes work like two entrapment. This occurs due
different cameras and produce two to trap door phenomenon. A
images but due to adaptation over linear fracture occurs in the
the years, the parallax between the orbital wall, which during the
two images is removed and only one truma widens, the muscle gets
image is perceived. The extraocular entrapped in the widened defect
muscles have pully like action, i.e. and the widening closes after the
if the superior rectus contracts the traumatic episode. The trapped Fig. 21.45: X-ray showing fracture of
inferior rectus relaxes and thus, muscle needs to be released to zygoma
the eyeball moves upwards. If any of correct the diplopia.
the extraocular muscles is entrapped
or is paralyzed, it fails to complement Investigations open reduction. All the fractures do not
the action of its antagonist muscle X-ray PNS shows the zygomatic bone and require treatment, but there are distinct
and the movements of the eyeball are all its sutures very well. This X-ray is not
indications where the fractures are
hampered producing diplopia. The good to visualize the arch. The undis­ treated surgically. The indications are:
Hess chart shows directions or gazes placed fracture is seen as widening of the
• For cosmetic consideration—where
of the diplopia which is produced due sutures.12 The displaced fractures result the displacement causes facial disfig­
to involvement of the particular extra- in break in continuity of the orbital rims. urement.
ocular muscle. The maxillary sinus appears hazy due to • For considerations of function—the
• The soft tissue around the eye ball bleeding in the sinus (Fig. 21.45). Due to mandibular movements are rest­
is anesthetized using 4 to 5 percent superimpositions of adjacent anatomical ricted due to impingement of the
sterile ledocaine solution and for­ structures the visualization of the frac­ coronoid process and the orbi­ tal
cibly moved with forceps as indi­ ture line and the displacement therfeof constriction or expansion is produ­
cated in Fig. 21.44. is not properly visualized. However, the ced as a result of outward or inward
– If the eye moves freely to forced CT scan often provide more precise in­ displacement of the fractured seg­
movement, then this indicates formation about the fracture line and the ment. The orbital size changes pro­
that any restriction in eye move­ displacement (Figs 21.46A to C). duce inophthalmos or proptosis. The
ment in that direction is caused entrapment of the muscles causes
by a muscle paresis. Management of the Zygomatic diplopia. In such cases the fracture
– If the eye cannot be moved, even needs to be treated.
with this forced duction in a
Bone Fracture The undisplaced fractures without
particular gaze direction, then it The zygomatic bone fractures can be any cosmetic or functional problems
suggests that the eye movement managed by either closed reduction or by may be treated conservatively.
Fractures of Middle Third of Facial Skeleton 453

A B C
Figs 21.46A to C: CT scans showing fracture of zygomatic bone and bleeding in the sinus

Fig. 21.47: Girard-Carroll screw Fig. 21.48: Poswillow’s hook Fig. 21.49: Bristow’s elevator through the
modified Keen’s approach

the sutural border and rounding of the • Other approaches mentioned in the
Closed Reduction
sutures, which makes the fracture less literature like transnasal approach,17
The closed reduction of the fracture is self-retaining. Hence, older fractures direct approach are impractical and
based on the assumption of the self- are treated with the open reduction. are seldom practiced.
retaining nature of the fracture. The As the time lapses the adhesions may
Keen’s intraoral approach
zygomatic fractures are self-retaining develop around the fracture ends
due to its sutural joints with the adjacent which also prevents the reduction of Keen in 193214 described this method of
bones and as the fractures results in the the fracture. The comminuted fractures reducing the fractured zygomatic bone
separation of the sutures and when the are treated with open reduction as the (Fig. 21.49). In this approach an incision
fracture is reduced properly there is self-retaining phenomenon is absent is placed in the buccal vestibule, over
interlocking of the sutures, which makes due to multiple fragments.13 the zygomaticomaxillary buttress area.
the fracture self-retaining. However, In the past, the concept of the percu­ The tissues are dissected carefully by
most of the fractures show communition taneous elevation of the zygomatic sharp and blunt dissection and along
of edges and this philosophy does not fracture was in place which was the medical surface of the zygomatic
work. Secondly, the masseter is attached accomplished using either the Girard- bone. A bone lever or the periosteal
to the inferior border of the zygomatic Carroll screw or Poswillow’s hook, but it elevator is passed behind the body
arch and the deep temporal fascia is did not last longer as it lacked precision of the zygoma. The key is to stay in
attached to its superior border, both and was not esthetically viable as it the subperiosteal plane and dissect
these anatomical structures splint the involved scar on face due to small access along the bone as one may enter in
bone and prevent its superoinferior incision (Figs 21.47 and 21.48). the infratemporal fossa if this plane is
movement. For doing the closed For doing the closed reduction the missed and encounter bleeding due
reduction the fracture should be tre­ approaches are: to the damage to the pterygoid plexus
ated within 72 hours as more the time • Keen’s intraoral approach14 of the veins. Using the buccal alveolar
lapse more are the chances of the • Gillies temporal approach15 bone as fulcrum the zygoma is gently
resorptive and remodeling activity at • Transantral approach16 elevated. Simultaneously, the orbital
454 Maxillofacial Trauma

rims are palated with the finger of the


other hand at the frontozygomatic
suture and over the infraorbital rim
to feel the step deformity, which gets
abolished as the fracture is elevated
and reduced. The comparison of the
malar prominence on both the sides
is also done to assess the correction
of the malar prominence flattening.
When the edema is cons­picuous, the
malar prominence is masked and it is
not possible to assess, it and one has to
rely on the palpation of the orbital rims
A B
only.18 When there is step at the buttress
the abolition of the step there is also Figs 21.50A and B: Bristow’s zygoma elevator. The elevator is passed between the deep
taken as the marker of the reduction. temporal fascia and temporalis muscle to engage the medial surface of the zygoma. Note:
The fulcrum, while using the Bristow’s elevator comes on the temporal bone
While doing the closed reduction if
the fracture is not self-retaining, the
moment of the leverage is released, the fracture as most of the fractures of the proper precautions like avoiding exces­
zygoma sinks back. This happens in zygoma are depressed fractures due to sive pressure over the temporal bone or
the old fractures or fractures which are the inward displacement. This is a good keeping a rolled gauze at the fulcrum
comminuted. As such if the fracture is technique for elevating the fractures point to avoid direct pressure over the
not self-retaining, the result of closed of the zygoma and the arch as well. In temporal bone are not taken the temporal
reduction is unlikely to stay and in such this procedure, an incision is placed bone can fracture. The Rowe’s zygoma
cases and open reduction is indicated. in the hair line over the temporal area, elevator is considered to be better than
In the literature it is mentioned that 45 degree to the vertical line in preauri­ the Bristow’s elevator as it avoids the
the Bristow’s zygoma elevator is used cular fold. This incision goes between the fulcrum point on the temporal bone and
to elevate the fractured zygoma, but bifurcation of the superficial temporal the fulcrum lies at the junction of the two
it is too bulky to be used intraorally.19 vessels and avoids trauma to them and blades of the elevator. The position of the
The Keen’s approach is suited for the the scar is also hidden in the hair line. handle (outer blade) corresponds to the
reduction of the zygomatic bone, but it is The skin, superfacial facia are dissected position of the inner (lever) blade as their
cumbersome for reducing the fractures in layers to expose the deep temporal length is same and gives the operator an
of the arch. The wound is closed pri­ fascia, which looks as a white tenacious idea regarding the position of the lever
marily. During the postoperative peri­ structure. The deep temporal facia is blade, which goes in the tissue plane and
od the assistants are instructed not divided and plane is created between it elevates the zygoma (Figs 21.51A to D).
to handle the area of the fracture as and the temporalis muscle. The Bristow’s
Transantral approach11
the fracture may sink back due to the zygoma elevator is passed between these
pressure. The zygomatic area is marked two structures to engage the medial The apex of the maxillary sinus extends
with red ink cross indicating that the area surface of the zygoma (Figs 21.50A into the zygoma and the later also
should not be handled, while turning and B). The leverage is given to elevate constitutes a part of the anterolateral
the head of the patient or while shifting the zygoma in its proper reduced wall of the maxillary sinus. Thus, the
the patient. The patient is not allowed to position. The marker of the reduction is sinus gets involved in the fractures of
sleep on that side and sand bag support the correction of malar flattening and the the zygoma. The inwardly displaced
is given to prevent so. The supportive abolition of the step in the orbital rim. fractures encroach upon the maxillary
treatment in form of anti-inflammatory/ The postoperative check X-rays help in sinus and hence for reducing (elevating)
analgesics is prescribed. Antibiotics are ascertaining the adequacy of reduction such fractures transantral approach is
also prescribed as prophylaxis. of the fracture. Rest of the postoperative useful. In this technique a Caldwell-LuC
precautions and management is similar opening is created and the antrum is
Gillies temporal approach15 to that described in the Keen’s approach. opened the fracture is manipulated by
Gillies temporal approach is a popular The disadvantage with the Bristow’s inserting a finger in the sinus. After the
approach for elevating the fractures of the elevator is that the fulcrum point comes in fracture is reduced satisfactorily, the
zygoma. The word elevation is commonly the region of the squama of the temporal sinus is packed with a roll guaze soaked
used to describe the reduction of the bone, which is thin and delicate. If in White head’s varnish or petroleum
Fractures of Middle Third of Facial Skeleton 455

sions are present due to displacement


of the fracture.
The open reduction is followed by
fixation of the fracture segments with
the help of either intraosseous wires21,22
or miniplates.23 The wires or plates can
be fixed at frontozygomatic suture, in­
fraorbital rim, the buttress and rarely
at the zygomaticotemporal suture. The
fractures should be fixed at minimum
two points. For exposing the fracture
line at frontozygomatic suture, a lateral
eyebrow incision is taken. While taking
the incision precaution must be taken
A B that the direction of the blade is paral­
lel to the hair follicles and not through
them, as it leaves unsightly alopecia in
the region of the eyebrow. The incision
is masked in the hair as they grow. The
orbital rim is exposed and the orbital
periosteum is reflected carefully taking
care not to injure the eyeball or other
intraorbital structures. A malleable cop­
per retractor is kept as a guard and af­
C D ter reducing the fracture, through and
Figs 21.51A to D: Application of Row’s zygoma elevator, note the similar lengths of both through holes is drilled on the either
the blades and avoiding the fulcrum on the temporal bone side of the fracture line on the lateral or­
bital rim. A piece of 26 number stainless
steel wire is passed and intraosseous
wire is tied across the fracture line.
The infraorbital rim is exposed
through inferior palpebral, subcilliary
or infraorbital incisions (Figs 21.52A
and B).24 All the incisi­ons are intended to
be cosmetically acc­eptable. Through the
layer by layer dissection the infraorbital
rim is exposed and the orbital periosteum
is reflected. If the orbital contents are
herniated through the fracture they are
carefully separated and the fracture is
A B reduced by elevation. Two holes are
Figs 21.52A and B: (A) 1–Inferior palpebral, 2–Subcilliary, 3–Infraorbital incisions; drilled on either side of the fracture
(B) Lateral eyebrow incision line, keeping a guard for protecting the
eyeball, using a 26 number stainless
gelly created separately in the inferior • Severely displaced and impacted, steel wire, intraossesous wiring is
meatus.20 The pack supports the fracture fractures which do not yield to the done. The zygomaticotemporal suture
from within. The intraoral incision, closed reduction is exposed by placing a direct incision
which is taken for Caldwell–Luc’s opera­ • Old fractures, which are not self- on the arch. But this incision is not
tion is closed primarily. The pack is left retaining cosmetically acceptable and the chances
in situ and removed after 3 to 4 days. • Malunited fractures of injuring the branches of facial nerve
• Comminuted fractures are optimum.
Open Reduction • Fractures where functional loss is like The best incision of approaching
The open reduction of the fracture of the diplopia, inophthalmos, proptosis, the frontozygomatic suture and the
zygoma is indicated in: restriction of the mandibular excur­ zygomaticotemporal sutures is the
456 Maxillofacial Trauma

unicoronal incision (Figs 21.53A and


B).25,26 The in­fraorbital/subcillary/infer­
ior palpebral in­cision may be taken along
with unico­ ronal incision to expose all
the three fracture lines, the infraorbital
incision is placed in the infraorbital
groove to hide the scar. If rigid internal
fixation (RIF) is planned then 1.5 mm
miniplates are used as the thicker plates
may show below the skin as the plates
are on the areas, which are almost
A B subperiosteal. The orbital plates with 4 to
Figs 21.53A and B: Bicoronal incision 6 holes are best for plating the orbital rim
as they get adapted well to the curvature
of the orbit. The temporozygomatic
suture is plated using straight 4 to 6 holed
plate. The screws used at these locations
are 4 to 5 mm long as the bone­­s are thin.
Although all the four areas, i.e.
the frontozygomatic, temporozygomatic
(arch), infraorbital and the buttress
areas can be used for the fixation of the
zygomatic bone fractures, it is not always
necessary to fix all the four points. The
two point fixation, one point each along
the vertical axis, i.e. frontozygomatic
A B suture and the horizontal axis, i.e. at
Figs 21.54A and B: Comminuted infraorbital rim plated with orbital plate the buttress area, is usually adequate to
give adequate fixation and the stability
to the fracture. More over many times
due to the high velocity accidents there
is gross comminution at the infraorbital,
arch and buttress area in such cases the
technique needs to be suitably modified
as per the presentation and requirements
in each case (Figs 21.54 to 21.59).
The fractures of the zygomatic bone
with involvement of orbital floor (Impure
blow-out fractures of orbit) often require
A B the reconstruction of the orbital wall using
either allogenic material like titanium
mesh, silastic, etc. or autogenous grafts
like iliac crest or calvarial grafts, along with
the fixation of the fracture of the zygomatic
bone (Figs 21.60A to F).

Complications
• Infection
• Osteomyelitis
• Dehiscence of the plates
C D • Damage to the branches of the facial
Figs 21.55A to D: Plating at zygomatic buttress nerve
Fractures of Middle Third of Facial Skeleton 457

rectus and inferior oblicus muscles of


the eye. The lateral rectus is supplied
by the 6th (abduscent) nerve. The 4th
(trochlear) nerve supplies the superior
oblicus muscle of the eye. Due to the
involvement of the nerves all these
extraocular muscles undergo paralysis
and the eyeball fails to move, which is
called ‘external ophthalmoplegia’. As
A B
the affected eye does not move while
the contralateral normal eyeball moves
Figs 21.56A and B: Plating at the infraorbital area
the focal axis gets distributed and two
images of one object are per­ cei­ved
producing diplopia. The IIIrd cranial
nerve relays the preganglionic para­
sympathetic fibers from the Edinger-
Westphal nucleus in the mid brain,
which are relayed in the ciliary ganglion
situated on the lateral rectus muscle. The
postganglionic fibers are distributed the
papillary and ciliary muscles of the pupil
through the short ciliary nerve. Normally
A B the parasympathetic stimulation leads
Figs 21.57A and B: Plating at the frontozygomatic suture to constriction of the pupil. As the
IIIrd carnial nerve gets paralyzed, the
parasympathetic supply is cut off and it
results in sympathetic predominance,
leading to fixed dilated pupil not
respon­ding to light. This is called
‘internal ophthalmoplegia’ (Figs 21.62A
and B). The parasympathetic fibers
also go to the upper eyelid and they
help in maintaining the tonus of the
upper lid. Due to the interruption of
the parasympathetic supply to the lid
A B it drops dawn like a curtain and it is
Figs 21.58A and B: Plating of the zygomatic arch through coronal exposure called ptosis of the eye, characterized
by obliteration of the supratarsal fold.
The optic nerve is not involved in this
• Ophthalmic complications like dip­ of the contents of the superior orbital syndrome. But when in addition to this
lopia, proptosis, inophthalmos, supe­ fissure as a result of raised intraor­ if the optic nerve is also involved it is
rior orbital fissure syndrome, orbital bital pressure due to hermatoma or called the ‘orbital apex syndrome’.
apex syndrome. the displaced fracture segments.29 The
• Showing of the plates below the skin. structures that pass through the supe­ Management
rior orbital fissure are the 3rd, 4th, 6th The management comprises of conser­
SUPERIOR ORBITAL cranial nerve, the ophthalmic division vative and surgical. The conservative
of the 5th cranial nerve, ophthalmic management is resorted to when the
FISSURE SYNDROME artery, and ophthalmic vein (Fig. 21.61). symptoms are mild. The CT scan or MRI
Superior orbital fissure syndrome, also Owing to the raised intraorbital pressure of the orbit is done to find the cause. If a
known as Rochon-Duvigneaud syn­ these structures are compressed resul­ large hematoma is present retrobulbar or
drome.27 Hirschfeld28 first described ting in the paresis of the nerves and in the muscle cone or a fracture is severe­
superior orbital fissure syndrome in neurological deficit in their distribution. ly displaced or some fragment is imping­
1858. The superior orbital syndrome The 3rd (oculomotor) nerve supplies the ing upon the superior orbital fissure then
results secondary to the compression superior rectus, medial rectus, inferior surgical decompression is indicated.
458 Maxillofacial Trauma

A B C D

E F G
Figs 21.59A to G: Management of zygomatic fracture by two point fixation at the frontozygomatic suture and buttress

A B C

D E F
Figs 21.60A to F: Impure blow out fracture treated with reduction of zygomatic fracture and reconstruction of orbital floor with
a calvarial graft
Fractures of Middle Third of Facial Skeleton 459

Fig. 21.63: Diagrammatic representation


of V in zygomatic arch fracture
Fig. 21.61: Structures involved in superior orbital fissure syndrome

A B
Figs 21.62A and B: Superior orbital fissure syndrome note the ptosis of eyelid, fixed Fig. 21.64: Submentovertex view showing
dilated pupil and lack of extraocular movements (external ophthalmoplegia) V in type of zygomatic arch fracture

Supportive treatment in the form of corti­ of the fracture the coronoid process • Edema over the temporal and the
costeroid therapy, ocular physiotherapy gets obstructed mechanically and the preauricular area. The edema may
should be prescribed to the patient. mandibular movements are restricted. extend to the adjacent structures.
The fractures of the arch can be • Trismus and restricted mandibular
FRACTURES OF THE classified as: excursions. When the fracture is a
• Undisplaced fractures V-in type in trismus can be produced
ZYGOMATIC ARCH • ‘V’ in type of the fractures (Figs 21.63 due to the spasm of the masseter
Although the arch is anatomically very and 21.64) and the mechanical obstruction of
close to the zygoma, the isolated fracture • A ‘V’ in fracture results when the the coronoid process.
of the arch can take place and they zygomatic arch fractures at 3 points, • Pain or mastication as a result of
produce distinct clinical features. The thus, there are more than two fracture contraction of the masseter during
arch is formed by the temporal process fragments and the V in fracture function, which brings about the
of the zygoma and the zygomatic process in true sense is a comminuted movement across the fragments and
of the temporal bone. The masseter fracture. produces pain.
originates from the inferomedial border • Tenderness, crepitus and step defor­
of the arch and the deep temporal fascia Clinical Features mity over the arch.
is attached to it superiorly. Both these • Dimpling over the arch—the dimp­
structures prevent the superoinferior ling is seen immediately follo­wing Investigations
displacement of the arch in the event of trauma (Fig. 21.65) and it is masked The submentovertex view of the skull
the fracture. The coronoid process of the by the edema in short period of time. (Jug handle view) is taken to visualize the
mandible lies deep to the arch and when It is seen cases of depressed (V-in) arch. The medicolateral displacement
there is severe medial displacement fractures. is better assessed on the X-ray. The
460 Maxillofacial Trauma

Fig. 21.65: Zygomatic arch fracture


leading to dimpling
A B
X-ray PNS also shows the arch, but not Figs 21.66A and B: Submentovertex view and CT scan of zygomatic arch fracture
very clearly. The submentovertex view
of skull is often adequate to properly
visualize the zygomatic arch fracture the soft tissue care must be taken not to wall is formed by lamina papyracea of
but the CT scan provides better details dissect the periosteum injudiciously as the ethmoidal bone and the lacrimal
(Figs 21.66A and B). there can be a vascular necrosis due to bones, which themselves are thin and
excessive periosteal stripping. The dis­ fragile (Fig. 21.67).30 The vital content
Management advantages of the direct approach are of the orbit is the eyeball and it is non­
The management comprises of closed poor esthetic results due to scar, chances compressible structure. The eye has
and open reduction. The closed reduc­ of damage to the zygomatico- temporal six extraocular muscles, which control
tion is done by the intraoral Keen’s branch of the facial nerve. To avoid such the movements of the eyeball, which
approach14 or by extraoral Gillies tem­ complications hemicoronal exposure is originate from the common tendinous
poral approach.15 The Bristow’s zygoma preferred (Figs 21.58A and B). fibrous ring. The Annulus of Zinn is a
elevator is used for the same. The fibrous ring formed by the common
procedure is the same as described for Complications origin of the four rectus muscles. The
the zygomatic bone reduction, only • Osteomyelitis eyeball and the muscles are cushioned
difference being the direction of the • Malunion in the orbit with the periorbital fat. The
elevator is little posteriorly towards • Fusion of the arch with the coronoid optic foramen is guarded by thick, cor­
the arch. The indicator of the adequate process leading to false ankylosis. ticated rim, which protects the optic
reduction is correction of the dimpling nerve. The optic nerve is a direct exten­
and abolition of the step over the arch. sion of the gray matter. It is very sensi­
ORBITAL FRACTURES
To prevent the collapse of the reduced tive to compression and once damaged
arch, an external splint is applied on the The orbit is conical cavity with its base fails to regenerate. The superior orbital
reduced arch and is secured in place anteriorly and the apex directed at the fissure transmits the 3rd, 4th, 6th oph­
with the help of thick suture thread optic foramen. It has four walls com­ thalmic division of the 5th cranial nerve
passed circumferential to the arch and posed of seven bones; ethmoid, frontal, in addition to the ophthalmic vein and
tying a knot above the splint. Post­ lacrimal, maxillary, palatine, sphenoid the artery. These cranial nerves inner­
operative radiographs are often helpful and zygomatic. The walls (roof, lateral, vate the extraocular muscles and the
in ascertaining the proper reduction. medial, floor) taper posteriorly to the 3rd cranial nerve also relays the pre­
The comminuted old fractures are apex and optic canal. The medial orbital ganglionic parasympathetic fibers. The
treated by open reduction as they are walls are approximately 1 cm apart and eyelids contain cartilaginous plates
not self-retaining and tend to collapse parallel and the adult orbit volume is called tarsal plates. In the event of the
after elevation. The open reduction of 30 cc. The orbital boundries are called trauma the thick rims protect the eye­
the arch is done either through direct the rims of the orbit, which are dense, balls and absorb shock by way of frac­
approach, taking incision over the arch corticated to protect the eyeball. The turing themselves. The orbital walls
and exposing the arch by layer by layer medial wall and the floor of the orbital especially the medial and the floor can
dissection, the fracture is reduced using are thin and fragile, while the roof and also fracture in an isolated way and get
a bone lever and intraosseous wiring the lateral walls are stronger. The floor the displaced inwards or outwards and
or miniplates can be used to plate to is weakened due to the infraorbital ca­ such fractures are called blow in and
stabilize the segments. While dissecting nal passing through it and the medial blow out fractures, respectively. When
Fractures of Middle Third of Facial Skeleton 461

Fig. 21.68: Pathophysiology of blow out


fracture of the orbit

Fig. 21.67: Anatomy of the bony orbit

the orbital walls fracture in isolation intraorbital pressure is compensated.


they are called pure blow out or blow in This fragility of walls prevents the
fractures. When the walls fracture along rupture of the eyeball which is vital. Fig. 21.69: Enophthalmos following the
with the rim it is called impure blow out The blowing out of the walls results blow out fracture
or blow in fracture depending upon the in herniation of the periorbital fat
direction of the displacement of the wall. and thus, the orbital contents are also
reduced and due to the retracting action • If the floor is fractured the periorbital
Blow Out Fracture of Orbit of the extraocular muscles the eyeball fat herniates in the maxillary sinus
The term ‘blow out fracture’ was sinks in, resulting in inophthalmos. and on X-ray PNS produces a classi­
coined in 1957 by Smith and Regan31 The extraocular muscles especially the cal ‘hanging drop’ appearance.
who were investigating injuries to inferior rectus and the inferior oblicus • The fracture and herination of the
the orbit by placing a hurling ball on get entrapped in the fracture fragments orbital contents also leads to bleed­­
cadaverous orbits and striking it with a and diplopia results in vertical gage. ing in the antrum producing unil­
mallet. According to Ng P et al., orbital ateral epistaxis.
floor fractures first were described Clinical Features • The infraorbital nerve gets trau­
by MacKenzie in Paris in 1844.32 The • Due to the trauma there is circum matized producing numbness in its
pathophysiology of the blow out fracture orbital edema, which sometimes is area of distribution.
is that the eyeball is a noncompressible so severe that the examination of • The inferior rectus and the inferior
structure. When an object which is the eye may not be possible until it oblicus get entrapped in the fracture
larger in size than the orbit strikes the recedes. producing inability of the eyeball to
orbit, the eyeball is compressed, but • Due to the fracture of the wall there move in vertical direction producing
as it is incompressible the intraorbital is subperiosteal bleeding, which es­ diplopia on vertical gage.
pressure increases and the pressure is capes in the subconjunctival plane to • When the medial wall is blown out in
exerted indirectly on the walls of the produce subconjunctival bleeding. addition to inophthalmos, epistaxis,
orbit. As the walls are thin and fragile • As the walls are blown out the the diplopia will be produced on
they give way and fracture and are blown orbital size expands and the eyeball medial gage.
outward, this produces the blow out sinks in resulting in inophthalmos
fracture (Fig. 21.68) thus, the thin and (Figs 21.69 and 21.70A). Management
fragile nature of the medial wall and the • Due to the fracture of the wall the The orbital fractures are assessed by
floor is a natural protection offered by peri­or­bital fat herinates through it X-ray PNS, which shows haziness of the
the nature. As they fracture readily and produ­ cing further increase in the maxillary sinus and a classical hanging
the orbital size expands and the raised size of the orbit (Fig. 21.70C). drop appearance. In case the medial
462 Maxillofacial Trauma

A B C D

E F G
Figs 21.70A to G: A case of blow out fracture managed by bone graft, (A and B) Change in the level of the globe (enophthalmos);
(C) Fracture of the floor of the orbit; (D) Exposure of the floor of the orbit through infraorbital incision and lateral wall of orbit through
eyebrow approach; (E and F) Harvesting of bone graft from iliac crest; (G) Placement of iliac crest bone graft to reconstruct the floor of the
orbit

wall fracture the nasal passage locks and cannula. A balloon catheter
obliterated on the affected side. The (Foley’s catheter) is passed through
better evaluation is by the CT scan33 the antrostomy site in the maxillary
(Fig. 21.70B) and the assessment of the antrum and the ballon is inflated
periorbital structures is done with MRI, (Fig. 21.71). As the balloon gets
which gives fair idea of the injury to the inflated the herniated orbital
extraocular muscles. contents get lifted. The catheter is
The floor of the orbit fractures can left in situ in inflated condition for
be managed by closed reduction or by support 5 to 6 days.
open reduction.34 Disadvantage: The disadvantage of the
closed reduction is that the reduction is
Closed Reduction arbitrary. The sharp bony fragments may
The closed reduction is done by: injure the eyeball and the entrapped Fig. 21.71: Impure blow out fracture, the
herniated floor of orbit elevated by a Foley’s
• Transantrally: Caldwell-Luc oper­ muscle is not released and thus the
catheter introduced in the sinus through
ation is performed and the herniated diplopia may persist. transnasal antrostomy and the infraorbital
orbital contents are carefully elevated rim exposed for plating
with digital pressure then the maxil­ Open Reduction
lary sinus is packed with a guaze The open reduction is the more accurate
soaked in petro­leum jelly to support method of reducing the blow out rim is exposed through the infraorbital/
the fractured floor and the end of the fracture as this is not only reduces the subcilliary/inferior pal­pe­­bral incision.
roll guaze is drawn out through the fracture, but also released the entrapped The orbital periosteum is identified
nasal antrostomy opening in the cav­ muscles and the help in correcting the and carefully raised by subperiosteal
ity. The intraoral incision is closed diplopia. The orbital floor invariably dissection. The entrapped muscles
primarily. The pack is removed on fractures in small fragments and often are released. The herniated structures
5th to 6th postoperative day. needs reconstruction and thus, the are present above the periosteum and
• Transnasally:35 A nasal antrostomy open reduction is not only reduction hence, if the periosteum is lifted the
is performed through the inferior but processes of the reconstruction of herination is automatically corrected.
turbinate approach, using a trochar the fractured floor. The inferior orbital Sometimes, the wall is severely damaged
Fractures of Middle Third of Facial Skeleton 463

and the periosteum is also lacerated in


such cases the herniated contents are
lifted and the eyeball is retracted upward
using an eyeball retractor. The fractured
floor is examined and the modality of
reconstruction is decided. The average
depth of the orbit is 40 to 45 mm and the
graft/implant/mesh should cover 2/3rd
the depth of the orbit (25 mm) for proper
and adequate reconstruction of the floor
of orbit defects during the management
of the blow out fractures of the orbit. The
extension of the dissection should not
be extended beyond the 25 mm as the A B
anterior ethmoid artery or optic nerve
can be injured.
The orbital floor can be recon­stru­c­
ted with36
• Alloplastic material37-39 like pro­
line mesh, titanium mesh,40 silas­
tic, stainless steel (SS) mesh, etc.
(Figs 21.72 and 21.73).
• Autogenous material41 like cartilage,
iliac crest cortico cancellous bone
graft (See Figs 21.70A to G) (See Figs
21.65 and 21.74), Calvarial bone
graft (See Fig. 21.60 A to F), split
rib graft, nasal septal cartilage, etc. C D
The calvarial graft are best suited Figs 21.72A to D: (A and B) Clinical and CT scan view showing comminuted fracture of
for this purpose as they are thin, the orbit; (C and D) Exposure of the fracture through pre-existing laceration/scar
provide natural favorable curvature
and most importantly show least
resorption. After the surgery ocular
physiotherapy is prescribed to
correct the diplopia.

NASAL BONE FRACTURES


The nasal bone is the most commonly
fractured bone due to its prominent
position on the face, little protection and
A B
support and minimal force required for it
to fracture. It most commonly occurs in Figs 21.73A and B: Reconstruction of the orbit and its floor using the titanium mesh and
fixation of the fracture using miniplates
males than females. Highest incidence is
between ages of 15 to 25 years in males
and more than 60 years old females. with the frontal bone at the frontonasal frontal process of maxilla, the ethmoid
The most common causes are road suture and laterally they articulate with bone and the lacrimal bone can also
traffic accident in 70 percent of cases the frontal process of the maxilla while occur and in such cases the fractures
other causes are assault, sports injuries,
they articulate with each other in the are termed the nasoethmoidal complex
industrial injuries. midline at the internasal suture. The fracture. The nasal bone fractures lead
perpendicular plate of the ethmoid to the deformities of the nasal bridge
Applied Anatomy lies below the internasal suture. The and are comparatively easier to treat,
The nasal bones are small, paired bones, nasal bones can fracture in isolated way, but the nasoethmoidal fractures are
which constitute the nasal bridge. but with a trauma of greater velocity, complica­ ted and may have anterior
Superi­orly the nasal bones articulate the fractures of adjacent bones like the cranial fossa involvement and are
464 Maxillofacial Trauma

A B C

D E
Figs 21.74A to E: A case of blow out fracture managed by bone graft

difficult to treat. The nasoethmoidal


complex fracture may be associated
with the detachment of the medial
canthal ligament and injury to the na­
solacrimal duct.
Kiesselbach’s plexus or Little’s
area: It is the important area of arterial
anastomosis present at anterior nasal
septum, linking branches of greater
Fig. 21.75: Mechanism of fracture of nasal bone due to
palatine, superior labial, sphenopalatine injury from lateral aspect
and anterior ethmoid arteries. This area
is most common source of epistaxis
when fracture line or trauma effects • Laterally displaced Injuries from lateral aspect
• 
this area. The nasal mucosa is highly • Comminuted. (Fig. 21.75):
vascular and is lined by pseudostratified – Moderate force result in depre­
columnar ciliated epithelium. Rowe and Killey Classification ssion of nasal bones and associ­
(1968) ated anterior edge of the frontal
Classification process of maxillary bone and
The isolated nasal bone fractures can be Described lateral and anterior nasal buckling of nasal septum.
classified as: injur­
ies resulting from impact either – Severe force results in dis­place­
• Undisplaced from lateral or anterior direction. ment of nasal pyramid to opposite
Fractures of Middle Third of Facial Skeleton 465

Clinical Features
The clinical features of the isolated nasal
bone fractures are:
• Edema over the nasal bridge.
• Bilateral circumorbital edema and
ecchymosis.
• Depression/flattening of the nasal
bridge in the cases of anterior
im­pact leading to open book defor­
Fig. 21.76: Mechanism of fracture of nasal bone due to mity and deviation of the nasal
injury from anterior aspect bridge due to lateral impact leading
to lateral displacement of the nasal
bones.
• Epistaxis due to injury to nasal
mucosa and the Little’s zone.
• Septal dislocation from the groove of
the vomer and deviation or buckling
on one side (traumatic DNS). The
presence of blood clot, edema of
nasal mucous membrane and the
deviated nasal septum (DNS) leads
to nasal stuffiness or obstruction.
A B • Fracture and disruption of the nasal
cartilage leads to deformities of the
cartilaginous part of the nose.

Treatment of Nasal Injuries


• Careful preoperative clinical and
radiological diagnosis is made.
• Radiographs are taken in two
directions, PA and lateral.
• Nasal bone fractures are usually vis­
ualized on soft tissue radiographs of
nose, lateral nasal radiograph and
CT scans.
• The septal deviations are visualized
C D on the X-ray PA Water’s view (PNS).
Figs 21.77A to D: (A) Stranc and Robertson classification (plane 1, 2 and 3); (B) Stranc Soft tissue injuries of the distal por­
and Robertson classification (plane 2); (C) Stranc and Robertson classification (plane 2); tion of the nose or injuries overlying
(D) Stranc and Robertson classification (plane 3) the cartilaginous portion supported in­
ternally with packing or internal stabi­
lization for 24 to 48 hours.
Stranc and Robertson
side and fracture of nasal sep­
tum. Classification (1979) (Fig. 21.77A) Closed Reduction
• Nasal injuries from anterior impact Plane 1: Injuries do not extend beyond a
Timing of treatment
(Fig. 21.76): line joining the lower end of nasal bones
– Moderate force frequently results to anterior nasal spine (Fig. 21.77B). • Isolated nasal fracture can be re­
in fracture of nasal pyramid. Plane 2: Injuries are limited to the duced in first 24 hours.
– Severe impact results in fracture external nose and do not transgress the • Treatment can be delayed until the
of the septum and comminution orbital rims (Fig. 21.77C). 10th to 12th day.
of nasal pyramid resulting in Plane 3: Injuries are more serious • Nasal fractures associated with
so called ‘open book’ nasal and they involve orbital and possibly other fractures should be treated at
fracture. intracranial structures (Fig. 21.77D). the same time.
466 Maxillofacial Trauma

Fig. 21.78: Instruments—Walsham’s A


forceps and Asch septum forceps

B
Figs 21.80A and B: Asch forcep application Fig. 21.81: Ribbon gauze pack

prevent aspira­ tion, as the bleeding is ffin paste (BIPP) is gently packed
anticipated while reducing the nasal in the nasal cavity to impart sup­
bone fracture. The beaks of the forceps port and for achieving hemostasis
are padded with red rubber catheter to (Fig. 21.81). The disadvantages of
avoid trauma to the nasal mucosa. The packing are that it obstruct airway,
thinner beak of the Walsham’s forceps is acts as a source of potent infection
introduced in the nasal cavity, while as and the intranasal support is often
the thicker beak stays out side (Fig. 21.79). inadequate. If over packing is done
The nasal bone is grasped firmly with it leads to postoperative widening of
the forceps, supporting the nasal bones the nares. Hence, it is used for only
with thumb and the index finger of other hemostatic purpose.
hand the nasal bones are slowly rotated • S-S intranasal splint: The SS splints
and reduced in the desired position. were described by Sear in 1977.
Fig. 21.79: Application of Walsham’s Once the nasal bones are reduced, the They provide better support when
forceps
septal dislocation is corrected using the anteroposterior collapse is present.
Asch’s septal forceps (Figs 21.80A and They are fixed using a transnasal
B). The padded beaks of the forceps are wiring. Instead of the SS splints,
The closed reduction comprises introduced in the nasal cavity on either custom made acrylic splints can be
of reducing the nasal bone fractures side of the septum and the septum is fabricated and used as per the need
using the Walsham’s nasal bone for­ grasped firmly and repositioned in the of the case. The splints are useful
ceps and reducing the dislocated groove of the vomer in the midline, and rapid method when treating
septum using Asch septum forceps abolishing the septal deviation. The patients of multiple trauma.
(Fig. 21.78). The patient is operated achieved result needs to be maintained • POP splint: The ‘Butterfly shaped’
preferably under general anesthesia. by using the following methods: are prepared by cutting 4 to 5 layers of
As the nasal bones are required to 10 cm POP bandage and is moistened
Methods of immobilization
be handled nasal intubation is not in water. The splint is applied to the
done, but oral intubation is preferred • Ribbon gauze packs: A 2.5 cm rib­ nasal bone contour and held in place
with a cuffed endotracheal tube and bon gauze in paraffin/flavine emul­ till the plaster of Paris sets. The set
meticulous pha­ ryngeal packing to sion or bismuth iodoform para­ splint is lined by thin layer of cotton
Fractures of Middle Third of Facial Skeleton 467

Complications
Hemorrhage—the posterior nasal bleed
can be controlled by pressure applied
through the postnasal packing.
Anterior nasal bleeding can be
effectively controlled by pressure
applied through the anterior packing
using the ribbon gauze soaked in
petroleum gelly or by cauterizing the
A B bleeding points.
• Scarring or mucosal adhesions.
• Septal hematoma.
• Incomplete reduction leads to air­
way (nasal) obstruction.
• Traumatic deviated nasal septum
(DNS).

NASOETHMOIDAL
FRACTURES
Nasoethmoid fractures typically result
from a forceful blow to the central area of
the midface.42 The fractures of the nasal
bones can occur in isolation or they
C D may be accompanied with the fractures
of the ethmoidal bone, frontal process
Figs 21.82A to D: POP splint and nasal packing for splinting the nasal bone fracture
of the maxilla and the lacrimal bone
(Figs 21.83A to C). The complex injuries
wool to prevent pressure injuries to Open Reduction involving these bones are often termed
skin. Care should be taken to ensure The indications for the open reduction nasoethmoidal complex injuries.
that the splint margins are medial to of the nasal bone fractures are: The ethmoidal bone has various
the inner canthus of each eye. The • Malunited Nasal bone fractures. processes. The lamina papyracea forms
splint is fixed in place using adhesive • The grossly displaced fragments the medial wall of the orbit and behind
plaster strips (Figs 21.82A to D). where stable reduction is not possible it the ethmoidal air cells are present.
• Collodion gauze and soft metal without opening. The cribriform plate forms the floor
sheet (Asch soft-metal sheet—tin/ • Comminuted fractures. of the anterior cranial fossa and the
lead alloy): Several layers of cotton • Visibly displaced nasal bone and perpendicular plate forms the superior
gauze are cut to size and soaked in disruption of septal cartilage. part of the nasal septum and superiorly
collodion solution. A piece of soft- (details of the procedure are given projects in the anterior cranial fossa
metal sheet is cut to shape, applied under the nasoethmoidal complex (crista galli) to which the dura is attached.
and contoured. fractures). The cribriform plate transmits the

A B C
Figs 21.83A to C: Anatomy of the nasoethmoidal region
468 Maxillofacial Trauma

A B C
Figs 21.84A to C: (A) Type I fracture of NOE; (B) Type II fracture of NOE; (C) Type III fracture of NOE

emissary veins and the olfactory nerves. Classification of occur in isolation or may be associated
The ethmoidal air cells are normally not Nasoethmoidal Complex with Le Fort II or III fractures.
exposed to the external environments The clinical fractures of the nasal bone
Fractures43
and in the event of the fracture they get fracture are:45-49
exposed and infected and the infection Comminution and the status of the medial • Flattening of the nasal bridge pro­
can pass in a retrograde manner in canthal tendon (MCT) separate NOE ducing open book deformity.
the cranial cavity through the veins fractures into the following three groups:44 • Epistaxis—Hemorrhage due to rup­
resulting in the intracranial infections 1. Type I: Fractures involve a single, ture of anterior and posterior branch­
like meningitis. The olfactory nerves non-comminuted, central fragment es of ethmoidal artery.
are in the direct extension of the gray without medial canthal tendon dis­ • Due to the loose areolar tissue
matter and lacks regenerative potential, ruption (left-unilateral, right-bilat­ around the eye there is bilateral cir­
which results in permanent loss of the eral) (Fig. 21.84A). cumorbital ecchymosis/edema.
smell sensation (anosmia) once it is 2. Type II: Fractures involve comminu­ • There is tenderness, crepitus over the
traumatized. The crista galli provides tion of the central fragment without nasal bones.
attachment to the dura in the anterior medial canthal tendon disruption • Subconjunctival hemorrhage medially.
cranial fossa, in the event of fracture of (Fig. 21.84B). • The nasal septum gets dislocated
the cribriform plate the dural attachment 3. Type III: Fractures result in severe from the groove of the vomer and may
may get torn and result in CSF rhinorrhea. central fragment comminution with lead to deviated nasal septum (DNS).
The nasal bones are paired and medial canthal tendon disruption • The fracture of the frontal processes
articulate with each other in the midline (Fig. 21.84C). of maxilla can result in the detach­
at the internasal suture. Laterally they The nasal bones are articulate with ment of the medial canthal ligament
articulate with the frontal process of each other at an angle of about 45 de­ and the canthal angle becomes
the maxilla and superiorly with the grees and form the nasal bridge. The rounded. This apparently increases
frontal bone by frontonasal suture. The septum is formed by the vomer, septal the dis­ tance between the medial
medial canthal ligament is attached processes of the palatine bone and the canthi of both the eyes. The normal
to the frontal process of the maxilla perpendicular plate of the ethmoid su­ distance is about 36 mm and this
and is responsible for the shape of the periorly. The vomer has a groove anteri­ increases beyond the normal
medial canthus of the eye. The fracture orly in which the septal cartilage articu­ value and the condition is called
of the frontal process of the maxillary lates. The septum is located behind the telecanthus. Thus, the traumatic
bone leads to detachment of the medial internasal suture and is traumatized telecanthus results.50
canthal ligament leading to rounding during the nasal bone injuries and gets • Almond shaped palpabral fissure
of the medial cantus (Almond shaped disloc­ated from the groove of the vomer. due to roundening of the medial
palpabral fissure) and the intercanthal The dislocated septum buckles/deviates canthus of the eye (Fig. 21.85).
distance gets widened, it is called on one side producing traumatic devi­ • Diplopia may result due to involve­
traumatic telecanthus or pseudo- ated nasal sebtum (DNS), resulting in ment of medial rectus or inferior
hypertelorism. The term hypertelorism nasal obstruction. obliques muscle.
implies when the distance between When associated with the fractures • The damage to the cribriform plate
the two bony orbits is widened as seen of the frontal process of maxilla of ethmoid results in damage to the
in in various deformities involving the and ethmoid bone they are termed branches of the olfactory nerve and
craniofacial skeleton (e.g. Treacher nasoethmoidal complex injuries. The leads to loss of smell sensation, i.e.
Collin’s syndrome). nasoethmoidal complex injuries can anosmia.
Fractures of Middle Third of Facial Skeleton 469

Fig. 21.87: Lateral tension test

is frequently visible clinically in


cases where the canthal ligament is
disrupted.
• Examination of the nasal cavity: A
complete intranasal examination for
nasal septum deviation, bleeding,
Fig. 21.85: Almond shaped palpebral fiss­ Fig. 21.86: Normal and abnormal intercan­
ure on left side due to detachment of medial concha, nasal mucosa, position of os­
thal distance and interpupillary distance seous structures and the presence of
canthal ligament
the CSF rhinorrhea (Figs 21.88A to C).

• The fracture of the cribriform plate 34 mm in males. The intercanthal Investigations


of ethmoid also results in detach­ distance of more than 35 mm is The nasal bone fractures are seen on
ment and tear of the dura and CSF indicative of canthal spread (tele­ the true lateral view of the skull. The
rhinorrhea results. canthus) (Fig. 21.86). X-ray PNS shows the nasal septum and
• The ethmoidal air cells get exposed • Palpabral fissure: It becomes nar­ its deviation. Proper assessment of the
due to the fracture of the lamina ro­
wed and almond shaped. The nasoethmoidal complex is possible CT
papyracea of the ethmoid. Both the medial canthal angle becomes scan (Fig. 21.89).
later condition facilitate the spread blunted with obliteration of caruncle
of infection in the cranial cavity and may be displaced down and Management51-55
resulting in meningitis. laterally, due to the disruption of The management of the nasoethmoidal
the medial canthal ligament tendon. complex fractures is more complex as
Criteria for Making Diagnosis • Eyelids: Becomes lax and epicanthal compared to the isolated nasal bone
• High index of suspicion and possi­ fold becomes prominent fractures. Due to the involvement of many
bility of canthal spread should be • Canthal ligament: The medial can­ tiny bones, presence of comminution,
considered with all severe nasal and thal ligament is assessed by lateral gross displacement, detachment of the
midfacial injuries. tension test (Fig. 21.87). On palpation canthal ligaments and severe defor­mity,
• Measurement: Normal intercanthal there is diminished tension of the most of the nasoethmoidal comp­lex frac­
distance—the intercanthal distance canthal ligament, which normally tures are treated with open reduction.
is 32 to 33 mm in females and 33 to is firm and tensed and this sign The presence of cranial invo­lvement in

A B C
Figs 21.88A to C: Severe nasoethmoidal injury
470 Maxillofacial Trauma

the form of presence of CSF rhinorrhea are present the fracture site can be
further complicates the management. exposed through the same lacera­
In the presence of severe nasoethmo­ tion or scar (Figs 21.92A and B). The
idal injuries the nasotracheal intubation disadvantage of this access is that,
is contraindicated as the handling of the as the lacerations are unplanned
area may lead to CSF leak in borderline they invariably provide inadequate
cases. In the presence of active CSF leak access.
the nasal intubation must not be done as • H-shaped incision: This incision
it can widen the dural defect and can lead provides an excellent exposure of
to infection and meningitis. In such cases nasal bridge and the medial can­
the oral intubation is best suited as the thal ligament (Figs 21.93 and 21.94).
nasoethmoidal complex fractures do not However, in extensive nasoeth­
involve occlusion and IMF is not required. moidal injuries the access is ina­
However, in polytrauma patients when dequate. The other disadvantage is
the nasoe­thmoidal fracture is associated that it provides an inadequate expo­ Fig. 21.89: CT scan of NOE fracture
with a Le Fort II or III fracture and if the sure of frontal bone to allow fixation
IMF is required during the reduction of the bone plating and direct tran­
and the fixation of these fractures then sosseous wiring of fractures.
oral intubation is not suitable and either • Bilateral Z approach described by
a transmyelohyoid (Fig. 21.90) or if that Digman et al. the two Z incisions can
is not possible tracheostomy should be joined by a horizontal incision at
be done. The airway must be guarded base of nose to enhance the exposure
using cuffed endotracheal tubes of by of the fracture site (Fig. 21.95). This
meticulous pharyngeal packing to pre­ access also has the same merits and
vent aspiration of the blood in the lower demerit as the ‘H’ incision.
respiratory passage, as the bleeding is • Midline vertical approach: It
anticipated during the management of was described by Stranc. In this
Fig. 21.90: Transmyelohyoid intubation
nasoethmoidal frac­ tures. The packing technique a 2 to 3 mm incision
of the nasal cavity is contraindicated in
presence of CSF rhinorrhea as it increases
chances of the intracranial infections.
For accomplishing the open reduc­tion
of the nasoethmoidal fractures different
surgical approaches are described.
• Bicoronal approach is commonly
used. It provides excellent exposure
of the nasoethmoidal area and the
glabella. It is useful if the frontal sinus
fractures or frontal bone fractures
are also present and facilitates the
fixation of the plates. In case of A B
anterior cranial fossa involvement
Figs 21.91A and B: Bicoronal incision
and CSF leakage if the dural repair is
also planned simultaneously, using
a galial flap, the bicoronal incision
provides opportunity to accomplish
both the surgeries. The bicoronal
flap also facilitates the harvesting
of the calvarial grafts, if required
for reconstructing the nasal defects
in the event of severe comminution
and bone loss (Figs 21.91A and B).
A B
• Through exsisting laceration: If the
compound nasoethmoidal injuries Figs 21.92A and B: Exposure of NOE fracture through existing laceration
Fractures of Middle Third of Facial Skeleton 471

A B

Fig. 21.93: H-shaped incision

C D
made from forehead to base of nose
(Fig. 21.96). Although it gives an
excellent visibility, but difficulty in
wiring or plate fixation. The ensuing
scar is unesthetic and unacceptable
hence not commonly practiced.
• W-shaped approach described by
Bowseman: The incision is made
across: the base of nose within the
skin crease (Fig. 21.97). Provides
E F
excellent access and visibility, but
produces an unacceptable scar on
the base of nose.
Edward Ellis in 1993 suggested a
8-step protocol for the management
of Nasoethmoidal complex fract­
ures, which gives priorities in the
management (Table 21.3).

CANTHOPLASTY
G H
Medial Canthal Anatomy Figs 21.94A to H: Management of NOE fracture with bone graft: (A) Clinical; (B) Radiological
presentation of NOE fracture; (C and D) Exposure of the fracture through pre-exisiting
Medial canthus is formed by medial
laceration; (E) Bone graft harvested from anterior wall of maxillary sinus; (F) Fixation of the
aspect of upper and lower eyelid, which
bone graft to reconstruct the base of the nose; (G) Fixation at infraorbital rim with miniplate
converges into an acute angle. It has two based on Champy’s principle; (H) Closure of the incision with prolene sutures
limbs. Between anterior and posterior
limb lies the lacrimal punctum, superior Most important part of medial Method of Securing Tendon
and inferior canaliculi and superior 1/3 canthal ligament to be secured at the (Figs 21.98A and B)
of lacrimal sac. repair is the anterior limb. When it is
As the tendon serves as the insertion correctly and securely repositioned, Direct suturing of the tendon to the
for orbicularis occuli muscle, loss of fixed and splinted the complications like loop of the wire with a braided non-
anchorage allows the muscle to contract dacryocystitis, post-traumatic hyper­ resorbable suture.
unopposed, producing a rounded cant­ telorisim, epiphoria and widening of Passing the free end of the wire
hal ligament. nasal bridge are uncomm­on. through the tendon in a continous fashion
472 Maxillofacial Trauma

Fig. 21.95: Bilateral Z approach Fig. 21.96: Midline vertical approach Fig. 21.97: W-shaped approach

Table 21.3: Sequencing naso-orbito-


ethmoidal frac­tures Edward Ellis 1993

Eight steps in treatment:


Step I—exposure through existing lacer­
ation, open sky and/or W incision, coronal +
lower eyelid.
Step II—identify the medial canthal tendon/
tendon bearing bone
Step III- reduce/reconstruct the medial orbital
rim. Atleast one hole is drilled posterior to
lacri­mal fossa to prevent lateral splaying of
posterior portion of bonefragment, which
can result in telecanthus. Other wire sup­
erior to lacrimal fossa. 2–4 mm diameter
hole so that ligament is pulled in the hole
canthal bear­ing bone fixed first.
Step IV—reconstruction of medial orbital A
wall with bone graft (rib, cranial bone)
Step V—transnasal canthopexy
Step VI—reduce septal fracture/displace­
ment (upwards, anteriorly)
Step VII—nasal dorsum reconstruction/aug­
mentation
Step VIII—soft tissue readaptation, nasal split,
transnasal bistress silicone sheeting

before directing the wire through the


second transnasal channel. If both canthal
tendons are detached and separated wire
loop is used for each attachment.
When contralateral stabilization of
wire is compromised by insufficiency of
bone a ‘toggle bone’ graft may be used to B
anchor the wire or a screw can be placed Figs 21.98A and B: Method of securing medial canthal tendon
into solid bone and the wire secured to
the screw.
Fractures of Middle Third of Facial Skeleton 473

Table 21.4: Complications of the NOE Box 21.1: Priorities in the management of polytrauma patient
fractures
1. Lifesaving treatment first
Complications of NOE fractures 2. Management of fractures later
a. Airway/breathing
Immediate Delayed b. Shock/circulation
Anosmia Meningitis, epiphorea c. Head injury
Enophthalmos, Uncorrected deformity, d. Cervical spine fracture
Diplopia soft tissue thickening a. Air way
and contracture • Clean the oral cavity of blood, clot, secretions, foreign bodies
Prominent plate and • Prevent tongue fall-air way, tongue stitch, oropharyngeal or nasopharyngeal
Nasal obstruction sc­r­­e­ws. airway
• Intubate
The complications of the nasoeth­ • Tracheostomy
• Cricothyroidectomy
moidal complex fractures can be either
• Assisted ventilation if indi­c­ated
of immediate or delayed nature and are b. Circulation/Hemorrhagic shock
summarized in the Table 21.4. • Fluid resuscitation—crystall­oids, colloids
• Control bleeding
• Vasopressors, steroids, O2, cor­r­ection of acidosis
PRIORITIES IN THE • Blood transfusion.
MANAGEMENT OF A c. Head injury
• History of unconciousness, con­­vu­lsions, vomiting
POLYTRAUMA PATIENT • Orientation
(BOX 21.1) • Amnesia
• Level of consciousness
Most of the maxillofacial injuries are • ENT bleeding
• Posture
as a part of poly trauma. The high
• Neurological examination.
velocity RTA results in the injuries Establish the Glasgow coma scale score and necessary neu­ rosurgical
at multiple areas of the body and intervention to be done immediately.
some of them are more critical and d. Cervical spine fracture
warrant urgent attention due to their • Tenderness
fatal consequences. The maxillofacial • Splinting
• Neurological deficit
injuries may be associated with the
• Careful shifting
head injury, spinal injuries, fractures of • Avoid ET intubation/trach­eos­tomy, cricothy­roidectomy best suited.
the long bones, injuries to the ribs, flail
chest, blunt injuries to the abdomen with
visceral lacerations/ruptures. Thus, the blood loss and the patient may land in could be present in patients with head
management is usually a teamwork and a state of hypovolmic shock and thus, injury. The Glasgow coma scale score
priority wise that means the lifesaving restoration of the circulatory efficiency should be recorded and should be
treatment must be done first and then must be the priority by appropriate periodically monitored as a prognostic
the management of the fractures. The measures. The traumatized brain has index in the patients with head injury.
patient who has head injury must diminished tolerance to hypoxia and The presence of rigidity/flaccidity, ten­
be evaluated and get neurosurgical thus it becomes imperative to restore don reflex, planter reflex should be done.
attention first. In view of cervical spine circulatory efficiency and maintain The papillary signs such as size, light
injuries, need to be handled carefully, adequate perfusion of vital organs. reflex (3rd cranial nerve evaluation) is
while shifting the patient. The neck Careful neurological examination an important examination in presence of
should be supported with sand bags, comprising history of the event, un­ raised intracranial pressure and coning
rigid collar or pneumatic splints as the consciousness, convulsions, vomiting of the brain (transtentorial herniation).
movements may aggravate the spinal should be obtained as these signs may The evaluation of individual cranial
damage. The endotracheal intubation suggest cerebral concussion. The level nerve examinations should be done to
and tracheo­stomy is contraindicated in of consciousness should be ascer­tained complete the neurological examination.
the patients with cervical spine fractures periodically and presence of any amnesia The cases with head injury be further
as it requires extension of the neck. should be noted. The retrograde amnesia evaluated by CT scans or MRI scans and
A cricothyroidotomy should be resorted is more significant finding than the appropriate neurosurgical interventions
to in case access to the air way is required. anterograde amnesia. The posture of the should be undertaken along with attem­
The other injuries like rupture viscera, patient should be observed as abnormal pts to reduce raised intracranial therapy
fractures of long bones lead to massive posturing like decerebrate or decorticate like use of steroids, mannitol, etc. The
474 Maxillofacial Trauma

use of sedatives and narcotic analgesics


should be avoided in patients with head
injury as they may interfere with level of
consciousness, pupillary signs and the
subsequent neurological evaluation may
be difficult.
The circulatory efficiency should
be monitored by detecting the signs of
hypovolumia such as thready pulse,
hypo­tension, oliguria, collapsed periph­
eral veins, pallor, tachypnea, cyanosis,
etc. the blood loss should be ascertained
and signs of intraperitoneal bleed should
be elicited. The fracture of the femur Fig. 21.99: CT scan with 3D reconstr­uction
can sequestrate about 750 mL of blood for a facial polytrauma patient
in the muscle compartment and the
intraperitoneal bleed can loose about
1,500 to 2,000 mL blood. The signs of
intraperitoneal bleed such as guarding, happens to be the first person to handle
rigidity, distension, Turner’s hematoma the case. The patients with grievous
should be elicited. Some of these signs injuries are monitored critically and Fig. 21.100: Golden rule to fix the fractures,
may be masked in a patient with head or should be provided critical care. i.e. fixation of outer ring first and the central
spinal cord injuries especially in presence The patients are given good pro­ area fractures at the end
of generalized rigidity and flaccidity. The phylaxis against the infections with
scalp lacerations may appear small, but appropriate antibiotics and immuni­
are known to bleed disproportionately, zation against tetanus. In the patients passive immunity provides immediate
as the open blood vessels fail to colla­ with clean contaminated wounds rou­ cover against the tetanus and lasts
pse due to the presence of dense apone­ tine antibiotics with immunization for 8 to 10 days only. By the time the
urosis. The replacement of the lost blood with tetanus toxoid will be enough, but passive immunity wanes the active
volume with crystalloids, colloids or in cases where the wounds are badly immunity develops and provides longer
blood transfusion be undertaken along contaminated, soiled, plenty of crushed, protection against the tetanus. In the
with the measures to arrest the bleeding. devitalized tissue is present then the past antitetanic serum (ATS), which was
The chest should be evaluated for antibiotics should be broad spectrum. the horse’s serum was used in place of
the presence of contusions, fractures of In the presence of cranial involvement human diploid cell vaccines. As it was a
the ribs, presence of flail chest (fracture such as CSF rhinorrhea the antibiotics foreign protein there was a risk of severe
of more than 2 ribs at more than one that can cross BBB should be opted allergic reactions, which is minimized
point), presence of pnemothorax, hemo­ to prevent the intracranial sepsis. The largely due to the advent of diploid cell
thorax and necessary drainage using the prophylaxis against tetanus should vaccine. The ATS was administered
intercostals drain should be undertaken. be with injection of tetanus toxoid in a dose of 1,500 to 3,000 IU, after the
All such injuries may lead to compromised 1 mL, intramuscularly, if the patient is intradermal test dose of 200 IU to avoid
chest expansion, collapse of lung and previously immunized against tetanus. severe allergic reactions.
compromise respiratory efficiency. The The tetanus toxoid is an antigen and it Once the condition of the patient
patients who have compromised respi­ evokes active immunity which takes is stabilized, the treatments of the
ratory efficiency due to either central or about 3 weeks to be fully established. fractures of the facial skeleton may be
peripheral cause may be provided with However, if the wound is badly soiled undertaken. If the patient has multiple
assisted ventilation, nasal O2 suppliments and there is crushed, devitalized facial fractures (Fig. 21.99) then the
as indicated in a given case. tissue, which enhances the chances of golden rule is that treat the injuries or fix
An oral and maxillofacial surgeon contracting tetanus, the patient requires the fractures in the outer ring first and
is expected to consider all these things, immediate protection in such cases the central area fractures are treated at
be able to provide basic lifesaving and passive immunity in the form of human the end, i.e. the zygomatic fracture is
supportive treatment and summon help diploid cell vaccines (antibodies) can be treated first then the nasal bone fracture
in time from concerned specialists, if he given along with the tetanus toxoid. The (Figs 21.100 and 21.101).
Fractures of Middle Third of Facial Skeleton 475

computed tomography. J Oral Maxil­


lofac Surg. 1983;41(9):562-7.
12. Ardekian L, Kaffe I, Taicher S. Com­
parative evaluation of different radio­
graphic projections of zygomatic com­
plex fractures. J Craniomaxillofac Surg.
1993;21:120-8.
13. Perino KE, Zide MF, Kinnebrew MC.
Late treatment of malunited malar
fractures. J Oral Maxillofac Surg.
1984;42(1):20-34.
14. Keen WW. Surgery, its principles and
A B practice. Saunders (Ed). Philadelphia;
1909.
15. Gillies HD, Kilmer TP, Stone D.
Fractures of the malar-zygomatic
com­ pound with a description of a
new X-ray position. Br J Surg. 1927;14:
651.
16. Lothrop HA. Fractures of the superior
maxillary bone caused by directs blows
over the malar bone. Boston Med Surg
J. 1906;154:8.
17. Shea JJ. The management of fractures
involving the paranasal sinuses. JAMA.
1931;96:418.
18. Fryer MP. A simple direct method of re­
C D
ducing a fracture-dislocation of zygo­
Figs 21.101A to D: Sequence of fixations of fracture in panfacial trauma case lower to ma. Surg Clin North Am. 1950; 30:1361.
upper and outer to inner 19. Balasubramanian S. Intraoral approach
for reduction of malar fractures. Br J
Oral Surg. 1967;4:189-91.
6. Frank Dal Santo, Edward Ellis III, 20. Wavak P, Zook EG. Immobilization of
REFERENCES
Gaylord S Throckmorton. The effects fractures of the zygomatic bone with
1. Lefort R. Etude experimentale Sur les of zygomatic complex fracture on an antral pack. Surg Gynecol Obstet.
fractures de le menchoire superieure, masseteric muscle force. J Oral Maxil­ 1979;149(4):587-89.
Rev Chir. 1901;20:8. lofac Surg. 1992;50:791-99. 21. Adams WM. Internal wiring fixation of
2. Row NL (Ed). William maxillofacial in­ 7. Ellis E 3rd, el-Attar A, Moos KF. An facial fractures. Surgery. 1942;12:523.
juries. New York: Churchill Livingston, analysis of 2,067 cases of zygomatico- 22. Dingman RO, Alling CC. Open redu­
1985.pp.538-58. orbital fracture. J Oral Maxillofac Surg. ction and internal wire fixation of
3. Guérin AF. Des fractures des maxil­ 1985;43(6):417-28. maxillofacial fractures. J Oral Surg.
laires supérieurs. Nouveu moyen de 8. Yanagisawa E. Symposium on maxil­ 1954;12:40.
les reconnaitre dans les cas fréquents lofacial trauma. 3. Pitfalls in the 23. Michelet FX, Deymes J, Dessus B.
ou elles ne s’accompagnement pas de management of zygomatic fractures. Osteosynthesis with miniaturized scre­
déplacement Archives générales de Laryngoscope. 1973;83(4):527-46. wed plates in maxillofacial surgery.
médecine, Paris. 1866; 2:5-13. 9. Knight JS, North JF. The classification J Maxillofac Surg. 1973; 1: 79-92
4. Strong EB, Sykes JM. Zygoma com­plex of malar fractures: an analysis of 24. Holtmann B, Wray CR. Little AG.
frac­tures. Facial Plast Surg. 1998;14(1): displacement as a guide to treatment. A randomized comparison of four
105-15. Br J Plast Surg.1961;13:325-32. incisions for orbital fractures. Plast
5. Manson PN, et al. Mechanisms of global 10. Zingg M, Laedrach K, Chen J, et al. Reconstr Surg. 1981;67:731-7.
support in post-traumatic enoph­ th­ Classi­fication and treatment of zygo­ 25. Abubaker AO, Sotereamos G, Patterson
almos: the anatomy of the ligament matic fractures: a review of 1,025 cases. J GT, Use of the coronal surgical inci­sion
sling and its relation to intramuscular Oral Maxillofac Surg. 1992;50(8):778-90. for reconstruction of severe cranio­
cone orbit fat. Plastic Reconstr Surg. 11. Fujii N, Yamashiro M. Classification maxillofacial injuries. J Oral Maxillofac
1986;77:193-8. of malar complex fractures using Surg. 1990; 48: 579-86.
476 Maxillofacial Trauma

26. Frodel JL, Marentette LJ. The coronal endonasal-transantral approach in 45. Sargent LA, Rogers GF. Nasoethmoid
approach. Anatomic and technical the repair of blowout fractures involv­ orbital fractures: diagnosis and man­
considerations and morbidity. Arch ing the orbital floor. Br J Plast Surg. agement. J Craniomaxillofac Trauma.
Otolaryngol Head Neck Surgery. 1993; 2004;57(1):37-44. 1999;5(1):19-27.
119: 201-7. 36. Selection of Materials for Orbital 46. Leipziger LS, Manson PN. Nasoeth­
27. Rochon-Duvigneaud. Quelques cas de Floor Reconstruction Chowdhury and moid orbital fractures. Current con­
paralysie de tous les nerfs orbitaires Krause Arch Otolaryngol Head Neck cepts and management principles. Clin
(ophthalmoplegie totale avec amau­ Surg. 1998;124:1398-401. Plast Surg. 1992;19(1):167-93.
rosse en anesthésie dans le domaine de 37. Baumann A, et al. Orbital floor recons­ 47. Holt GR, Holt JE. Nasoethmoid com­
l’ophthalmique d’origine syphilitique). truction with an alloplastic resorbable plex injuries. Otolaryngol Clin North
Archives d’ophthalmologie, Paris, polydioxanone sheet International Am. 1985;18(1):87-98.
1896; 16:746-60. Journal of Oral and Maxillofacial Sur­ 48. Heine RD, Catone GA, Bavitz JB, et al.
28. Zachariades N, Vairaktaris E, Papavas­ gery. 2002;31(4):367-73. Nasoorbital-ethmoid injury: report
siliou D, Papademetriou I, Mezitis M, 38. Dougherty WR, et al The natural history of a case and review of the literature.
Triantafyllou D. The superior orbital of alloplastic implants in orbital floor re­ Oral Surg Oral Med Oral Pathol. 1990;
fissure syndrome. J Maxillofacial Surg construction: an animal model. J Cranio­ 69(5):542-9.
1985; 13:125-8. fac Surg. 1994;5(1):26-32; discussion 33. 49. Cruse CW, Blevins PK, Luce EA. Naso-
29. Bun RJ, Vissink A, Bos RRM. Traumatic 39. Buchel P, Rahal A, Seto I. Recon­ ethmoid-orbital fractures. J Trauma.
superior orbital fissure syndrome: struction of orbital floor fracture with 1980;20(7):551-6.
report of two cases. J Oral Maxillofacial polyglactin 910/polydioxanon patch 50. Mathog RH. Posttraumatic telecanthus.
Surg 1996; 54:758-61 (ethisorb): a retrospective study. J Oral In: Mathog RH (Ed). Maxillofacial
30. Burm JS, Chung CH, Oh SJ. Pure orbit­ Maxillofac Surg. 2005;63(5):646-50. Trauma. Baltimore, Md: Williams &
al blowout fracture: new concepts and 40. Metzger MC, Schon R, Weyer N. Ana­ Wilkins; 1984: pp.303-17.
importance of medial orbital blow­out tomical 3-dimensional Pre-bent Tita­ 51. Potter JK, Muzaffar AR, Ellis E, et al.
fracture. Plast Reconstr Surg. 1999; nium Implant for Orbital Floor Frac­ Aesthetic management of the nasal
103(7):1839-49. tures. Ophthalmology 2006. component of naso-orbital ethmoid
31. Blowout fracture of the orbit: mecha­ 41. Lew D. Orbital floor reconstruction fractures. Plast Reconstr Surg. 2006;
nism and correction of internal orbital with autogenous mandibular symphy­ 117(1):10e-18e
fracture. By Byron Smith and William seal bone grafts. J Oral Maxillofac Surg. 52. Crockett DM, Funk GF. Management
F. Regan, Jr”. Adv Ophthalmic Plast 1977;55(4):330-32. of complicated fractures involving the
Reconstr Surg 1987;6:197-205. 42. Sargent LA. Nasoethmoid orbital orbits and nasoethmoid complex in
32. Ng P, Chu C, Young N, Soo M. Imaging frac­
tures: diagnosis and treatment. young children. Otolaryngol Clin North
of orbital floor fractures. Australas Plast Reconstr Surg. 2007;120(7 Suppl Am. 1991;24(1):119-37.
Radiol. Aug 1996;40(3):264-8 2):16S-31S. 53. Ellis E. 3rd Sequencing treatment for
33. Gilbard SM, Mafee MF, Lagouros PA, et al. 43. Morgan RF, et al. Management of naso- naso-orbito-ethmoid fractures. J Oral
Orbital blowout fractures. The prognostic ethmoid-orbital fractures. Am Surg. Maxillofac Surg. 1993;51(5):543-58.
significance of computed tomography. 1982;48:447. 54. Fedok FG. Comprehensive management
Ophthalmology. 1985;92 (11):1523-8. 44. Markowitz BL, Manson PN, Sargent of nasoethmoid-orbital injuries. J Cra­
34. Hawes MJ, Dortzbach RK. Surgery L, et al. Management of the medial niomaxillofac Trauma. 1995;1(4):36-48.
on orbital floor fractures. Influence canthal tendon in nasoethmoid orbi­ 55. Sargent LA, Rogers GF. Nasoethmoid
of time of repair and fracture size. tal fractures: the importance of the orbital fractures: diagnosis and man­
Ophthalmology. 2183;90(9):1066-70. central fragment in classification and agement. J Craniomaxillofac Trauma.
35. Kackibushi M, Fukazawa K, Fukada K. treatment. Plast Reconstr Surg. 1991; 1999;5(1):19-27.
Combination of transconjunctival and 87(5):843-53.
22 Facial Burns
Jajoo Suhas N, Yadav Abhilasha, Garg Rajat

inflicted by someone. The facial burns partial and full thickness dermal burn
INTRODUCTION
can be isolated or they may be part of injuries are included. Erythema (super­
A very few areas of medicine are as the whole body burn. The burn injuries ficial burn involving epidermis only) is
challenging medically or surgically as can be caused due to suicidal, homicidal not included.2
the burn care. It affects mainly young intent or could be accidental. Wallace’s rule of nine (Fig. 22.1) is
and children and in both sexes equally. good for adults for assessing the burn
It may vary from small minor burn percentage, but proportion of surface
EVALUATION
injuries, which can be managed as area in infants and children are differ­
outpatient to more extensive injuries Airway, breathing and circulation are ent.1 Patient’s palm approximately is
resulting in multiorgan system failure assessed immediately. Associated life- 1 percent TBSA. Lund and Browder charts
and subsequent mortality. threatening injuries should be excluded. are more accurate method of assessing
Improvement in resuscitation faci­ Vital signs like pulse, blood pressure the extent of burn injury3 (Fig. 22.2).
lities, use of topical antimicrobials and along with the level of consciousness
practice of early burn wound excision has should also be assessed and basic life
contributed to the improved outcome of support be initiated.
Depth of the Burn Injury
treatment with probably lesser morbidity. Thorough history is mandatory as The depth of burn injury is very impor­
The facial burns are most challenging it affects the management. Location tant from the management and prog­
to manage, as the esthetic and functional of injury (indoor/outdoor), history of nostic point.1 It is dependent upon:
outcome is critical and is intimately standing or running with flames (respi­ • Initial temperature of object causing
related to feelings of self-esteem and ratory burn due to fumes) type of liquid the injury.
social acceptance. involved in the scald or chemical burn, • Duration of contact.
duration required to extract the patient • Viscosity of liquid causing injury.
out of heat or dilution of chemicals are Facial burns are usually associated
ETIOLOGY
all important. with inhalational respiratory injury
Burn injuries could be caused due to: Admission is required for large burns, due to inhalation of smoke, gases and
• Dry heat- flame burns which require resuscitation or full thick­ irritant chemical fumes. Thus, the most
• Moist heat ness burns, which needs an early surgical critical issue is airway especially, when it
• Electrical intervention. The patients are also suscep­ is a closed space fire.
• Radiation tible to infection and need to be kept under Assessment of depth of injury is
• Flash friction controlled, aseptic environments. Minor important as it is an important marker
• Blast or frost bite burns can be treated on outpatient basis, if for the wound management.1 There are
• Contact burns due to direct contact the proper care from the family mem­bers four degrees of burn2 as given below:
of hot object, which are localized but is assured. First degree: Erythema (Figs 22.3A
deep.1 and B).
Moist heat-scald, steam are the Second degree: Superficial partial
Determination of the Extent
most common causes of the burn and thickness (Figs 22.4 and 22.5). Epidermis
the scald being the most common of Burn and superficial dermis is damaged. Gen­
in children. Chemical burn of face is When calculating the TBSA (Total Body erally this condition does not advance to
usually which can be accidental or Surface Area), only those areas having full thickness if proper care is constituted.
478 Maxillofacial Trauma

will be the healing along with bad scars.


The degree of burn and its correlation
with the involvement of epithelial ele­
ments is given in Table 22.1.
Accurate determination of depth of
the burn injuries and their healing po­
tential is challenging. The depth changes
with time as there is gradual proximal ex­
tension of the vascular thrombosis at the
burn site. The assessment of burn which
is done initially may not be accurate as
it changes according to the duration
due to the loss of tissue due to dryness,
infection, chemical insult and progres­
sive vascular thrombosis. The wound,
which is anticipated to take more than
3 weeks for healing should be managed
by excision and skin grafting because it
will heal slowly by granulation tissue for­
mation ultimately leading to scarring and
increased morbidity.3 Also the chances of
infection to occur will be more in an open
wound for such a long period.
Burn depth can be assessed by fluo­
rescein dyes, ultrasound, LASER Doppler
and magnetic resonance imaging (MRI),
but they are no better than a clinical acu­
men of experienced burn surgeon.3

Classification of Burn Severity


This simplified classification helps the
Fig. 22.1: Wallace’s rule of nine clini­
cian in prioritizing the treatment
and thereby rendering the necessary
a. Superficial Partial Thickness (sec­ Burnt tissue shows three different treatment according to the need.
ond degree A) zones, zone of necrosis, zone of stasis The burn severity can be classified
b. Deep Partial Thickness (second and zone of hyperemia (Fig. 22.13). The as under (Box 22.1).
degree B) (Figs 22.6 to 22.8): Re­ zone of stasis is the area, which needs
generation progresses very slow­ to be protected, otherwise depth of the First-aid Treatment
ly and conversion to full thick­ burn increases, i.e. conversion of partial Needs to be initiated at the scene of
ness burns is high. These burns thickness into full thickness burn. The accident to minimize extent of injury
are best treated conservatively most important part of the management and the ensuing complications.
and sequelae are rare. is to prevent deep partial thickness burn • Try to extinguish the fire.
Third degree (Full thickness): These getting converted into a full thickness • Prevent the patient from running as
injuries cannot heal spontaneously and burn owing to dryness of tissue due to running may flare up the fire.
treatment involves excision of injured exposure, secondary infection and use of – Place the patient in a supine posi­
tissue followed by skin grafting/Flap antiseptic solutions in an inappropriate tion to avoid inhalation injury.
(Figs 22.9A and B). concentration, thus reducing the mor­ – Pour cold water to dissipate the
Fourth degree (Full thickness bidity and mortality. heat and prevent the deeper
involving deep struc­tures): Thrombosis Three epithelial elements, i.e. seba­ penetration of the heat to cause
of subcutaneous venous plexus occurs. ceous gland, hair follicle and sweat more complicated deep burns.
Pain involved in these injuries is low gland help in healing of the wound, – Wash/irrigate the chemical burn
as all sensory terminations to skin are being helped by basal layer of epidermis copiously with water to dilute the
destroyed. Potential for infection is high, from periphery. After burn, if more the chemical to reduce the extent of
if not excised (Figs 22.10 to 22.12). epithelial elements are damaged, poorer the injury.
Facial Burns 479

Fig. 22.2: The Lund and Browder chart. It provides more accurate estimate of burns TBSA for each body part based on the
patient’s age (Source: Advanced Life Support Burn Manual Chicago, American Burn Association, 2005)
480 Maxillofacial Trauma

A B
Figs 22.3A and B: First degree burn. Only the epidermis has been damaged Fig. 22.4: Epidermis and superficial dermis

Fig. 22.5: Superficial second-degree burns Fig. 26.6: Deep second-degree burn (deep
damaging dorsa of fingers partial thickness burn). Epidermis, papillary Fig. 22.8: Sutured lacerated wound. Deep
dermis, and various depths of reticular partial thickness burn due to steam following
(deep) dermis have been damaged pressure cooker blast

A B C
Figs 22.7A to C: Deep partial thickness burn
Facial Burns 481

Acute Complications of Burn


The acute complications of burn are as
follows:
• Carbon monoxide poisoning due to
inhalation of the smoke and fumes
is treated with administration of
oxygen through a mask.
• Ventricular fibrillation—the patient
needs to be defibrillated.
• Neurogenic shock—the patient is to
be treated with necessary resu­sci­
tation and basic life support (BLS).

A B Management of Burns
Figs 22.9A and B: Third degree burn (full thickness burn). Epidermis, papillary and on Outdoor Basis
reticular dermis, and different depths of subcutaneous tissue have been damaged The following precautions can be taken
for burns on outdoor basis4:
• Wound protection—topical antibacte­
rial and dressing
• Analgesics
• Antibiotics
• Tetanus prophylaxis
• Scar care and physiotherapy to pre­
vent scar contracture and sub­seq­
uent mor­bidity.

Management of Burns in the


Inpatient Department
The BLS comprising of airway, breath­
Fig. 22.12: Closure done using scalp ing, circulation (ABC) should be started
Fig. 22.10: Fourth-degree burns (full thick­
rotation flap immediately.
ness burns with involvement of deep struc­
tures, like muscle and bone, is present)
Airway
Methods of securing the airway like
oropharyngeal, nasopharyngeal airway
or endotracheal intubation should be
carried out to maintain patency. Tra­
cheostomy is done as a last resort and
is needed especially, when inhalational
injury has occurred.

Breathing
Oxygenation of the patient is carried
out through the mask or airway, if the
patient’s own respiratory effort is ad­
Fig. 22.13: Zones of necrosis, stasis and equate, but in the unconscious patients
Fig. 22.11: Fourth-degree electrical injury hyperemia corresponding to a partial
with diminished respiratory drive or
following contact with a high power wire thickness burn5
effort, assisted venti­lation or positive
pressure ventilation using a ventilator is
– In case of electrical burns switch • No household medicament should provided to prevent hypoxia.
off the electrical supply before be applied as they may lead to con­
you touch the patient. tamination of the wound. Circulation
• Cover the area of burn injury with • Oral feeds are withheld, if the burn Significant burn injury, not only result
clean sheet to prevent contamination injuries are more than 30 percent of in local tissue injury, but initiates a gen­
and dehydration. surface area. eralized inflammatory response that
482 Maxillofacial Trauma

Table 22.1: Correlation of degree of burn, structures involved, clinical appearance and management

Degree of burn Involves Appearance Treatment Heals Result

• Superficial (Erythema) Only epidermis Erythematous, painful Dressings 3–5 days No scar
• S uperficial partial Superficial dermis, hair Pink, moist, painful Dressings 2 weeks No scar,
thickness follicle, sweat glands not pigmentation +
destroyed
• Deep partial thickness Reticular dermis–hair Dry, mottled, pink, white Early surgery 3–8 weeks Contraction +
follicle destroyed. Sweat variable sensation Scar +
gland not destroyed
• Full thickness Full dermis reaching fat, Brown black, leathery, Early surgery 8 weeks–6 months Contraction+
hair follicle, sweat gland insensate, dry, depressed Scar +
destroyed thrombosed veins seen

Box 22.1: Classification of burn severity Box 22.2: Parkland formula for estimation
of fluid required for 24 hours
Minor burn
• 15% TBSA or less in adults Parkland formula
• 10% TBSA or less in children and the elderly • 4 mL/kg/% TBSA = total fluid for first
• 2% TBSA or less full thickness burn in children or adults without cosmetic or functional 24 hours—all ringer lactate
risk to eyes, ear, face, hands, feet, or perineum • 50% fluid should be given in first
Moderate burn 8 hours post burn (not post admission)
• 15–25% TBSA in adults with less than 10% full-thickness burn • Rest 50% in 16 hours.
• 10–20% TBSA partial-thickness burn in children under 10 and adults over 40 years of
age with less than 10% full thickness burn
• 10% TBSA or less full-thickness burn in children or adults without cosmetic or Thus, newer formula came in vogue,
functional risk to eyes, ears, face, hands, feet, or perineum
described by Baxter, i.e. Parkland formu­
Major burn la, which provides an estimation of fluid
• 25% TBSA or greater
• 20% TBSA or greater in children under 10 and adults over 40 years of age
required for 24 hours4 shown in Box 22.2.
• 10% TBSA or greater full-thickness burn The Parkland formula quantifies the
• All burns involving eyes, ears, face, hands, feet, or perineum that are likely to result in burn trauma and is a guideline only.
cosmetic or functional impairment Monitoring and urine output 50 to 70 mL
• All high-voltage electrical burns per hour is maintained, which decides the
• All burn injury complicated by major trauma or inhalational injury
fluid administration. Fluid administration
• All poor-risk patients with burn injury
• TBSA, Total Body Surface Area in children is different.

Monitoring
can affect nearly every organ system. The first formula of fluid resusci­ Urine output is the best monitoring
The release of inflammatory mediators tation was developed by Evans and criteria. Good bouncing pulse, good
[histamine, kinins, prostaglandins, cyto­ was used in 1950 to 60.4 The capillary capillary circulation, clear sensorium is
kines, interleukins, tumor necrosis factor permeability is increased not only in the best criteria. Drop in pulse and blood
(TNF)-alpha] can lead to decreased car­ burnt tissue, but as well as in normal pressure (BP) is late manifestations and
diac output, increased vascular perme­ tissue, so the capillary leakage is throug­ aim of fluid replacement is to preserve
ability and alteration in cell membrane hout the body. The fluid losses are end organ perfusion and prevent the
potential (sick cell syndrome) and a state still greater, if the inhalation injury is shock rather than treating it. Hematuria
of oligemic shock. Decrease in cardiac present. According to Evan’s 1.0 mL/kg/ suggest acute tubular necrosis and myo­
function is due to myocardial depressant percent of burn of crystalloid and equal globinurea is seen with extensive burn
factor (it is claimed, but not yet identi­ amount of colloid should be given in injury.
fied) and the effect of cytokines. first 24 hours, but permeable capillaries
The purpose of fluid resuscitation are unable to hold colloids as the space Invasive hemodynamic monitoring
is to provide adequate replacement between endothelial cells increases. Invasive hemodynamic monitoring is
for fluid lost in skin and interstitium to Thus, there is no logic to use colloids in especially useful when associated pre­
maintain organ perfusion. first 24 hours. morbid conditions, i.e. when cardiac or
Facial Burns 483

pulmonary diseases are present. Pulmo­ nebu­lization, chest phy­­sio­therapy are ness wounds need dressings for the same
nary artery catheters pulmonary wedge supportive measures. Blood gas analysis purpose till the wound starts epithelial­
pressure monitoring help to avoid over helps deciding treatment. Tracheostomy izing. The dressings are changed, which
infusion. can also be done as a last resort. Hyper­ help the epithelium to grow. Full thick­
baric oxygen therapy can be tried. The ness burn needs cover of topical agents
Analgesics role of surfactant is doubtful in the over­ to avoid infection until burn excision is
Analgesics should always be given intra­ all management of respiratory complica­ contemplated.5 One percent silver sul­
venous (IV) and never intramuscular tions. fadiazine is the most commonly used
(IM) as the patient is in circulatory shock topical antibacterial agent6 with excellent
and absorption of the drug from muscles Wound Management streptococcal and staphylococcal cover­
would be reduced because of decreased Aim of the treatment is prevention of age. Principal drawbacks of silver sulfa­
circulation and patient may not get relief. infection, reducing the morbidity and diazine therapy are:
Later when circulation is re-established avoiding the complications. Gentle • Leucopenia, which is self-limiting.
all this drug in muscles will be absorbed cleansing with antiseptic solution like • It does not penetrate eschar, thus
which can lead to increased toxicity of the 0.5 percent savlon is done. Loose burnt less useful in infected burn wounds.
drug if multiple doses have been given. tissues are debrided. Blisters should not • It may evoke allergic reactions.
be broken unless they are more than 6 It impedes epithelization, hence it
Tetanus Prophylaxis cm in size. They get absorbed avoiding should not be used once the necrotic
Discussed else­where under Chapter 19, protein loss, infection and pain. tissue is debrided. It should not be used
Management of Soft Tissue Injuries. Escharotomy is indicated for full in pregnant women, nursing mothers
thickness circumferential burns of ex­ and infants less than 2 months of age.
Inhalation Injury Management tremities or chest wall to improve the Mafenide7 (sulfamylon) readily pen­
Inhalation of products of combustion can vascular supply and overcoming the etrates burn eschar and is an excellent
lead to devastating pulmonary injury and breathing difficulty. drug for burn wound infection. It pro­
increases burn mortality significantly. Fasciotomy is indicated only when tects against suppurative chondritis,
Three clinical aspects are seen: the electrical burns are causing com­ thus used on nose and ear (as good as
1. Carbon Monoxide (CO) poisoning. partment syndrome. silver sulfadiazine).
2. Thermal airway injury. Drawbacks are:
3. Smoke inhalation. Topical wound agents • It is a potent carbonic anhydrase
Diagnosis is based on circumstances The wound should be cleaned with inhibitor. This can cause metabolic
surrounding the burn injury and find­ 0.5 percent savlon and all the loose tissue acidosis.
ings on physical examination. History is to be debrided. The blisters need not • Application is painful.
of burns in an enclosed space, while be opened as keratin layer of blister Other topical agents are:
on run, neurologic impairment should works as biological dressing and avoids – Silver nitrate
suggest it. CO poisoning interferes with pain and infection of raw surfaces. No – Bacitracin
oxygen delivery and is toxic to muscles forceful rubbing should be done, while – Neomycin
so also causes demyelination of central doing the dressing. Exposure therapy – Polymyxin B.
nervous system (CNS). is used only on face and perineum, Bacitracin, neomycin and polymyxin
Thermal airway injury causes muco­ whereas all other areas should be B accelerate epithelialization, commonly
sal edema, ulceration and hemorrhage covered with dressing. Dressings are used for superficial facial burns. Mupi­
of upper airway. Steam and exploding needed to avoid loss of epithelial cells rocin is used only when cultured proven
gases cause lower respiratory injury from drying and dying. It protects from MRSA (Methycillin Resistant Staphylo­
leading to untractable asphyxiation. infection, reduces evaporative loss and coccus aureus) is present.
Smoke inhalation cause chemical ir­ reduces pain. Prophylactic use of systemic antibiotic
ritation of respiratory tract through 280 Choice of topical wound agents de­ has no role because they increase the
carbonaceous toxic products identified. pends on depth of injury and goals of chances of oppor­tunistic infection. Burn
It leads to stridor, wheeze, ronchi and management. eschar has no microcirculation, thus,
carbonaceous sputum comes out. Loss Superficial burn wounds (erythema) the systemic antibiotics do not penetrate
of alveolar surfactant leads to atelecta­ requires soothing lotions such as alo­ it. Thus, topical antibacterial agents
sis, hypoventilation, hypoxia and acute evera that can expedite epithelialization and subeschar deli­ very of antibiotics
respiratory distress syndrome (ARDS). pro­cess. Superficial partial thickness (Subeschar clysis) is useful. Once there
Treatment: Endotracheal intubation is burn wound need coverage that keeps is healthy granulation tissue is present,
done and oxygen therapy insti­­ tuted the wound moist and provide antimi­ it should be grafted with split thickness
with assisted ventilation. Bron­­cho­dilators, crobial protection. Deep partial thick­ graft.
484 Maxillofacial Trauma

Biologic wound dressings The resultant raw areas are covered These patients are also functionally
with a skin graft. Adequate hemostasis is imm­ unocompromised as cellular and
Allogeneic amnion
critical to minimize hematoma to avoid humoral responses are compromised. All
Innermost layer of fetal membrane is graft loss. Epinephrine, topical pressure, these risk factors are further compli­men­
used as protective dressing on partial cauterization and use of tissue sealants ted by the risk of cross infection from self,
thickness burn wound. However, with are the various methods used. attending personnel and atmo­sphere.
this the risk of biologic transmission can Skin graft used can be either as a Colonization of eschar, spreading
never be eliminated completely, e.g. sheet or meshed. Sheet graft placed to normal tissues and then to the blood
Hepatitis, HIV. as per esthetic zones of face give best stream, i.e. burn wound sepsis to septic
Synthetic tissue engineered dress- results. In larger burns, there is inade­ shock follows.
ings: The advantages of these dressings quate skin available thus, grafts are mes­ Best treatment is prevention of burn
are less pain, shorter wound healing hed 3 to 6 times, but mostly 2 : 1 is used. wound sepsis for which early burn wound
time, better scar, e.g. Biobrane, Hydro­ Grafts can be stapled or sutures are excision is propagated.
colloid dressings, Transcyte. placed to fix it to the bed. Hypafix is a Diagnosis of infection can be done
Human cadaveric allografts and pig elastic adhesive dressing, which can be by regular and repeated culture studies
xenografts can be used in extensive burns. used with mastisol as adhesive.8 Vaccum of wound surface, blood, urine and
A variety of proteolytic enzymatic agents assisted closer device is used along with stool. These are evidences, but may not
have been used to debride the wound, but graft to help closure of wound. be available at the time of sepsis barring
it causes bacteremia in extensive wounds. trend of hospital is understood. Surface
Advances in wound closure culture may not match the bacteria
Surgical management Dermal replacement material such as causing sepsis.
Traditionally burn eschar was allowed Integra,9 Terudermis10 can be used to Best modalities are:
to separate by proteolytic enzymes. The reduce chances of contracture. Use of • Burn wound biopsy with more than
underlying granulation tissue was then cultured skin (cultured epithelial auto­ 105 organism/gram of tissue and/or
skin grafted. In extensive burn injury grafts) although promising have prob­ histologic evidence of viable tissue
this delay in covering the wound leads lems of shearing and blistering. invasion
to burn wound sepsis due to extensive Tissue engineering technology provi­­ • Positive burn wound biopsy and
bacterial colonization, catabolic state, ding skin is expected to deliver spectacu­ blood culture.
multiorgan failure and death. lar results. Stem cell culture technology • Urinary tract infection (UTI) with
The practice of early burn wound is also in offing. more than 105 organism/mL of urine
excision has significantly decreased the • Pulmonary infection.
incidence of burn wound sepsis and Infections Extremely virulent organisms are
improved survival. Infection is a significant risk following Pseudomonas, Fusarium and Candida
This should be done between 3rd burn injury. Colonization of burn es­ can be isolated from burn wounds.
to 5th post burn days in staged manner char, prolon­ged periods of intubation Nonbacteriologic causes of infection
spaced 2 to 3 days apart. This spacing and mechanical ventilation, respira­ are viruses, e.g. Cytomegalovirus, herpes,
helps stabilization and resuscitation tory, urinary tract infection and throm­ chicken pox and fungi. Fungi commonly
of burns. Excised wounds are covered bophlebitis also contribute to develop­ are Candida, Aspergillus, Fusarium and
with auto or homografts or synthetic ment of infection (Fig. 22.14). anaerobes (Bacteroides and Fusobacte­
biological dressings. rium species).
• Tangential excision—sequential re­ Burn associated infections are chon­
moval of eschar till viable tissue ap­ dritis, pneumonia, UTI, throm­bophlebitis
pears. It leads to substantial blood and venous abscesses and suppurative
loss. sinusitis. ‘Ghosting’ of grafts, i.e. disap­
• Fascia excision—excision down to pearance of graft which was already taken
the layer of muscle fascia. Although up is a clinical problem with obscure
blood loss is less, one removes viable etiology.
tissue also leading to unsightly con­ Clinically fever and leukocytosis
tour deformity and lymphedema. may be due to systemic inflammatory
Newer device is water jet powered res­ponse syndrome (SIRS) rather than
versajet, which is very good for concave infection. Periodic culture after 72 hours
surface of hand and feet and for excision is useful in making diagnosis of infec­tion.
at eyelids, ears and nose. Fig. 22.14: Infection at burn site (Urine, sputum, blood, central lines).
Facial Burns 485

In addition to identification of septic Table 22.2: Harris-Benedict’s formula and Curreri formula
source following criteria should be wat­
ched for: Harris- Benedict’s formula Basal energy expenditure:
Men: 66.5 + (13.8)W + (5)H – (6.76)A
• Tachypnea
Women: 655 + (9.6)W + (1.85)H – (4.68)A
• Paralytic ileus Adjust for stress by multiplying BEE by a
• Hyperthermia or hypothermia factor of 1.2 – 2.0.
• Altered mental status Curreri formula Age 16–59: (25)W + (40)TBSA
• Thrombocytopenia Age ≥ 60: (20)W + (65)TBSA
• Leucopenia or leukocytosis
W­­–weight in kg, H–height in cm, A–age in years.
• Metabolic acidosis
• Hyperglycemia.
Local evidence of invasive wound
infection includes black or brown patches Long’s modification of Harris-Bene­ In periorbital burns, look for injury to
of wound discoloration, rapid eschar dict’s formula11 and Curreri formula12 as eyeball, which is more common with acid
separation, wound conversion to full shown in Table 22.2. splash. Exposure keratitis needs to be
thickness and ecthyma gangrenosum. Nutritional expert should be available cared for, especially with lid contracture.
When patient exhibits signs and symp­ to support and look after supervision and In such cases tarsorrhaphy may be need­
toms of sepsis, immediate institution or persuasion in TEN as well as ileus and in­ ed. Traditional method was to perform
broadening of coverage antibiotics is man­ tubated states compelling TPN needs are daily wound care until the facial wound
datory, while awaiting confirmatory cul­ helped by them. Immunological support has either healed or the eschar got sepa­
tures depending on routine hospital flora is needed, but still is in research phase. rated so that the raw can be grafted. It is
and its resistance pattern. In addition there Psychological support is mandatory now clear that better outcomes can be
should also be a rapid aggressive surgical keep­­ing in mind the etiology of burn, its achieved if the nonhealing areas are ex­
intervention for the control of infection. In scar deformities and disabilities. cised (likely to take 3 weeks or more) and
presence of human immune deficiency vi­ then skin grafted. The donor skin needs
rus (HIV) (CD4 and CD8) immunosuppres­ Rehabilitation to be taken from area above the nipple
sion adds to the problem and graft survival
It includes: for the best color match. Many surgeons
is compromised. • Splinting in acute burns. favor the scalp skin but, alopecia and hair
Antibacterial agents include cover­ • Splinting after wound has healed. growth from transplanted skin is of con­
age against gram-positive (streptococci, • Compression by elastic garments for cern whereas the upper part of back has
staphylococci and enterococci), gram- hypertropic scar and keloid. thick skin.
negative (Pseudomonas aeruginosa, • Physiotherapy—active and passive Facial excision is carried out using
Esch­eri­chia coli and Klebsiella) and for joint mobilization. Goulian knives or versajet water dissec­
yeast and fungal infections. • Pigmentation—hypo- and hyper- tor. Exposed cartilage needs excision
pig­­m­en­tation needs dermatologist’s with closure of skin.
Nutritional Support advice. Sheet of autografts are used as the
Less nutritional intake, hypermetabo­ • Operative correction and recon­ meshed grafts are cosmetically unac­
lism and hypercatabolism persists until struction after scar has matured. ceptable. Epinephrine clysis is essential
complete wound coverage is achieved. to limit hemorrhage. A face mask should
Supporting the increased nutritional be placed to help immobilization of skin
FACIAL BURN
needs is a cornerstone of burn patient graft. Graft should be placed in such a
management. If not done, it results in Facial burns are most challenging as fashion as to mimic the esthetic units.
severe weight loss, debility, anemia, hy­ esthetic and functional outcomes is Fibrin glue can be used to enhance
poproteinemia, immunocompromised critical to the daily life of the patient and the graft adherence. Post-operative fa­
state, sepsis and death.11 is intimately related to feeling of self- cial elastic mask compression helps in
Burns up to 20 percent burn can be esteem. Many patients with facial burns avoiding hypertrophic scar.
managed by total oral and or enteral sustain inha­ lation injury and need In the cold cases of burn, the burn
(TEN) route alone. But more than 20 per­ intubation. Endotracheal tube should contractures are common which lead to
cent may need total parenteral support be secured in such a way as to minimize significant morbidity. In presence of the
(TPN). pressure necrosis of lip. Same is true neck contractions, administer­ing Gen­
There are several equations for esti­ with naso­gastric tube, which can cause eral anesthesia for release of contraction
mation of nutritional requirements, i.e. pressure necrosis of ala and columella. with multiple Z plasties and subsequent
486 Maxillofacial Trauma

A B
Figs 22.15A and B: Burn contracture of the neck preventing extension of the neck

A B C
Figs 22.16A to C: (A) Burn contracture of the neck; (B) Contracture released and skin graft placed; (C) Postoperative view

A B

C D
Figs 22.17A to D: (A) Burn contracture of face; (B) Contracture released;
(C) Skin graft placed; (D) Elastic bandage applied for better graft uptake
Facial Burns 487

skin grafting is very difficult and some­ ution after excision and graft­ing of burns.
REFERENCES
times, not possible as laryngoscopy can­ J Burn Care Rehabil. 1988;9:602-5.
not be done and neck angulation is not 1. David Herndon. Total burn care third 8. Cassey JG, Davey RB, Wallis KA.
favorable for intubation (Figs 22.15A edition page no 78-9. Hypafix—a new technique of skin graft
and B). In such cases fiber optic guided 2. Juan P. Barret. Colour atlas of burn fix­ation. Aust NZJ Surg. 59:479.
intubation can be done or else the pa­ care, page 2-7. 9. Jeng JC, Fidler PE, Sokolich JC, et al.
tient is given keta­mine and local anes­ 3. A. Forage. The history of the classifi­ Seven years experience with Inte­gra as
thesia and the contracture is released. cation of burns (diagnosis of depth). a reconstructive tool. J Burn Care Res.
After the release of the contracture, the British Journal of Plastic Surgery, Vol­ 2007;28(1):120-6.
patient can be safely intubated and ad­ ume 16, Issue null, Pages 239-42. 10. Terashi Hiroto. Successful Application
ministered general anesthesia and split 4. Mertens DM, Jenkins ME, Warden GD. of Artificial Dermis (Terudermis)
thickness skin grafting can be done. “Outpatient burn mana­gement”. Nurs for Deep Burn on Big Toe with Bone
Grafts on the neck should be carefully Clin North Am. 1997;32(2): 343-64. Necro­sis. Nishinihon Journal of Der­
harvested as long sheets and the de­ 5. Orgill DP. Excision and skin grafting ma­tology. 2001;63(5):557-60.
fect is covered with skin graft, while the of thermal burns. N Engl J Med. 2009; 11. Long CL, Schaffel N, Geiger JW, et al.
neck is in hyperextension (Figs 22.16A 360(9):893-901. Metabolic response to injury and illness:
to C). The postoperative spint should be 6. Charles L. Fox, jun. Silver sulpha­dia­ esti­mation of energy and protein needs
given to keep the neck extended to pre­ zine-poly hydroxyethyl­meth­acrylate from indirect calorimetry and nitrogen
vent graft contracture and relapse. Long (PHEMA) dressing. Burns. 1981;7(4). balance. JPEN J Parenter Enteral Nutr.
term physiotherapy with neck extension pp. 295-7. 1979;3(6):452-6.
exercises are advocated to get opti­­mum 7. Lee JJ, Marvin JA, Heimbach DM, et al. 12. Curreri PW, Luterman A.: Nutritional
results and to prevent contractures Use of 5% Sulfamylon (mafe­nide) sol­­ support of burned patients. Surg Clin
(Figs 22.17A to D). North Am. 1978;58:1151-6.
23 Medicolegal
Aspects of Injury
Anjankar AJ, Borle Rajiv M, Garg Rajat

Today is a world of the fast and the furious. Injuries caused by


Types of Injuries
On one hand newer technological inno­
v­ations have proved to be a boon for Before proceeding to details of types of
Mechanical Violence
the upliftment of mankind, however, injuries we will discuss about the nature of For medicolegal purposes, injuries caused
on the other hand they have also led to injuries (Table 23.1). It can be as follows:1 by mechanical violence are divided into:
an increase in the number of accidents • Abrasion
and associated injuries. These days due • Contusion
Grievous Injuries
to increased interpersonal violence and • Incised wound
the increasing hatred amongst mankind, These are the injuries as described • Laceration
it is absolutely necessary to rule out any under section 320 of the Indian Penal • Stab (penetrating, punctured)
foul play in case of any injury, whether Code (IPC), refers to the following:2 • Ballistic injuries.
major or trivial. Also, these injuries • Emasculation—it is castration or loss
may be associated with lawsuits and of power of erection (spinal injury). Abrasion
insurance claims. Hence, it becomes • Permanent privation of the sight of Abrasions are injuries involving loss of
mandatory to record the injuries when either eye. the superficial epithelial layer of the skin
they are first reported. As a doctor is the • Permanent privation of the hearing and they do not leave a scar on healing
first one to see such patients, he is under of either ear. (Fig. 23.1). These blunt impact injuries
legal obligation to correctly report them • Privation of any member or joint. (usually friction against the hard blunt
to the concerned police station and • Destruction or permanent impairing surface or object) are hardly of any
is also an important witness in such of the powers of any member or joint. significance from the point of view of
cases. He might even be one of the first • Permanent disfiguration of the head loss of life, but medicolegally they are of
persons to report the incident to the law or face. great importance. Abrasions may also be
enforcing authorities. In this chapter we • Fracture or dislocation of a bone or covered with mud and straw and their
will discuss about the various duties of tooth. shape and pattern may indicate the type
doctor on duty, preparation of injury • Any hurt, which endangers life or of surface on which the victim may have
report and record keeping. Injury report which causes the sufferer to be,
form must be filled for every patient who during the space of 20 days, in severe
is seen in casualty by medical officer on bodily pain or unable to follow his
duty to report that case in a police station ordinary pur­suits.
for medicolegal purpose. To fill up this
Table 23.1: Types of injuries
form (Annexure-I, page 493) doctor
should examine the patient carefully • Simple: A simple or slight injury is nei­ther
and should record all the injuries nature, extensive nor severe and heals rapidly
type, number, depth, size, site, edges without leaving permanent defor­mity or
disfigurement.
and line of direction. For all this he/she • Grievous: These injuries are serious,
must have a thorough basic knowledge severe, deforming and heal slowly.
how various injuries are classified and • Dangerous: Grievous injury, which end­
Fig. 23.1: Grazing type of abrasion due
characteristics of various injuries. an­gers life immediately.
to RTA
Medicolegal Aspects of Injury 489

been impacted or dragged. The direction sloughing and gangrene of the parts.
of the abrasion may be made out by the However, several bruise, though trivial
heaped surface layer (epidermis) or tags individually, may cause death from shock.
at one end. Abrasions caused by finger Postmortem bruise do not show any
nails indicate a struggle and an assault color changes, but if the red blood cells
are usually seen on the exposed parts of have not hemolyzed, and the blood is in
the body. a liquid state, then severe trauma, like
a forcible blow drive the blood into the
Types of Abrasions2 Fig. 23.2: Contusion over right side of chest issues through ruptured blood vessels
• Scratch: Cause by sharp pointed and produce a bruise similar to an ante-
object. They are linear in shape. Its mortem bruise.4 However, it is mostly
beginning is clean and end is heaped subcutaneous tissues without solution restricted to bony prominences, while
indicating direction of injury. of continuity of the skin. The swelling antemortem can be anywhere.
• Grazing/Sliding/Gliding: As the is due to rupture of small subcutaneous
name suggests it occurs due to slid­ blood vessels producing in the cellular Incised Wound
ing between an object and skin. It tissues, extravasation of blood, known Incised wounds are sharp with clear cut
occurs in road traffic accidents. They as ecchymosis. Hematomas are formed margins by a sharp object drawn across
are present as multiple, parallel and when large blood vessels are injured. the skin. Sharp instruments may be
longitudinal lines. They appear after sustaining the injury. like knife, razor, scissors or sword, axe,
• Patterned or imprint or impact: It Sometimes it is delayed by 1 or 2 days. hatchet. Incised wound is always broader
is caused by tyre marks and radiator Contusion can be divided as2: than the edge of the weapon causing it
grill. • Intradermal owing to the retraction of the divided
• Crushing or Pressure: It occurs in • Subcutaneous tissues (Fig. 23.3). It is somewhat spindle
ligature strangulation of hanging and • Deep (may be associated with abra­ is shaped; its length greater than depth
strangulation. Pressure is sustained.3 sion) and width. The direction of the injury
• Collection may be distant to the can be decided as these injuries have
Age of an Abrasive Wound site of injury. Blood may gravitate deep beginning and superficial end or
It can be judged by inspecting the injury. to some other place in the same tails off towards the end called ‘tailing’.
It is also a very important finding in anatomical plane—‘black eye’. When a curved weapon is used it always
medicolegal cases (Table 23.2). The age of a bruise may be ascer­ produces a stab or punctures and than an
Postmortem abrasions are pale white tained from the color changes, which its incised wound.
in color and usually caused by ant bites ecchymosis undergoes. These changes Age of the wound can be decided by
and no changes can be seen with days in commence from 18 to 24 hours after inspecting Table 23.4.
abrasions as in antemortem abrasion. its infliction and pass through various The differences between antemor­
stages (Table 23.3). tem and postmortem incised wounds
Contusion are as that of laceration. The only
Hemorrhage into skin, subcutaneous Color Changes seen in Contusion
tissue or deep without break in Bruises are as a rule, simple injuries. They
continuity of skin (Fig. 23.2). These are are seldom fatal unless accompanied
the injuries, which are caused by a blow by the rupture of an internal organ or
from a hard and blunt weapon such as by extensive crushing of the tissues and
lathi, iron bar, stone, fist, boots or by a large extravasation of blood, producing
fall. These are accompanied by a painful
swelling and crushing or tearing of the
Table 23.3: Color changes in contusion
Table 23.2: Age of an abrasive wound Fresh Reddish in color
(Hemoglobin)
Fresh No scab or red in color
24 hours Bluish in color (reduced
12–24 hours Dark red scab he­m­­o­globin)
1–2 days Brownish red scab 2–4 days Bluish-black to brownish
3–5 days Dark brownish red scab (he­m­osiderin)
5–7 days Peripheral healing with 5–7 days Greenish – hematoidin
shrin­kage of the scab 7–12 days Yellowish (bilirubin)
Fig. 23.3: An incised wound over upper
and falling off 12–14 days Fades to normal
eyelid
490 Maxillofacial Trauma

Table 23.4: Age of an incised and lacerated


stab wounds

Age of the wound—lacerated or


incised stab wounds
Unsutured
Inflamed skin edges 12–24 hours
Appearance of infection 36–48 hours
Sutured
Inflamed edges 12–24 hours
Edges can be easily separated 1–3 days
Firm union—edges are 3–5 days Fig. 23.4: Tear type of laceration over the
difficult to separate face Fig. 23.7: Degloving laceration in lower
Red, linear, tender scar 7–10 days labial vestibule
Pale, firm, nontender scar > weeks

difference is that when incised wound is


made, no gaping (due to loss of elasticity
of skin) is formed and it is straight.

Beveling Cuts
When sharp weapon struck obliquely
will cause beveling of one edge of the
wound and also indicate the direction Fig. 23.8: Crush injury of hand
of the blow, while if the sharp edge
struck almost horizontally, it produces a
wound with a flap. Fig. 23.5: Split laceration over the
forehead
Hesitation Cuts
They are usually suicidal or self-infli­cted.
It is formed when the blade moves in saw
like fashion. These are small, multiple,
superficial cuts usually parallel.

Laceration
Laceration means the edges are irre­gular
with surrounding abrasion or bruises and
the deeper tissues are torn irregularly. Fig. 23.9: Contused lacerated wound on
Fig 23.6: Laceration over left thigh with a upper lip
Types of Laceration hanging skin flap
• Tears: Caused due to projecting Punctured or Stab Wounds
object (Fig. 23.4). affected limb is separated from the Punctured or stab wounds are also
• Split: Incision like wounds occur underlying tissues and hangs loosely called penetrating injuries when passing
when the skin is closely adherent (Fig. 23.7). through the tissues, they enter a cavity of
the bone—iliac crest, scalp due to a • Crushing: Compression of the skin, the body. It is due to pointed sharp object
per­pendicular impact (Fig. 23.5). To crushing of the underlying tissues with greatest dimension at depth. For
differ­entiate it from incised wound, and bones (Figs 23.8 and 23.9). example, dagger, needle, spear, arrow,
exam­i­nation with hand lens is a must. scissor, ice pick. The length of stab wound
• Stretch: caused in a run over by a is equal to the breadth of the blade at the
Differences between
motor vehicle. Hanging skin is an point of entry wound. The deeper point
indication of a run over producing Antemortem and of the wound is tapering if tapering knife
flap. For example, scalp laceration Postmortem Lacerations is used. If the ends are sharp that means
(Fig. 23.6). The difference between antemortem knife having both edges sharp where as
• Avulsion: It is otherwise known as and postmortem lacerations is described with one-sided blunt knife wound have
degloving of the skin. The skin of the in Table 23.5. ragged margins on blunt side of the knife.2
Medicolegal Aspects of Injury 491

Table 23.5: Differences between antemortem and postmortem laceration • Caliber of the weapon. For example,
a wound from a small diameter
Antemortem Postmortem
bullet is generally less severe than a
Extravasated blood cannot be wiped out Extravasated blood can be wiped out wound inflicted by a larger diameter
Coagulated blood is seen Coagulated blood is absent at the same velocity.
• Design of the bullet and its velocity;
Increased enzyme activity is seen at the No enzyme activity
periphery of the wound
expan­ding bullets are more dama­
ging than nonexpanding. Of the non-
Signs of healing present No signs of healing
expanding bullets, flat or very blunt-
nosed bullets are more damaging
than more pointed bullets, as the
In case of a punctured wound per­ Table 23.6: Factors determining severity of more pointed bullet may push some
forating a part of the body, there are two bullet injury tissue aside. Heavier bullets will
wounds, one of entry and the other of exit. penetrate more deeply than lighter
The wound entry is usually larger with Bullet Tissue bullets at the same velocity.
characteristics characteristics
inver­ted edges and the wound of exit is • Range at which the victim was shot;
smaller and has everted edges. The site Velocity Distance and path within i.e. wounds inflicted from a distance
body
of wound indicates whether it is suicidal of 5 meters, invariably are more severe
Mass Biological characteristics
or homicidal. A careful examination of of tissues than those fired from 500 meters, if all
the clothes for cuts may reveal valuable Shape Mechanism of tissue other factors are equal.
information. dis­r­up­tion • Path of the wound—initial entry is
Design and a poor guide, as it is only a single
Ballistic Injuries composition point where as the exit point is more
Range
Ballistic injuries it is essential for a severe in expanding type of bullets.
medical person to have some basic
know­ ledge of the common firearms and there is no doubt that bullet velocity Bomb Blast Injuries
and physical aspects of firearms injuries is an important determinant of wound Civilian bomb blast injuries are often
(for­e­nsic ballistics). The term ballistic severity. The kinetic energy transferred indus­trial and occur in mining, chemical
trauma (generally refer­red to by the type to the target is defined as mass multi­ storage facilities, explosive and fireworks
of weapon, such as gunshot wound, plied by velocity to the second power manufacturing plants and stone-crushing
etc.) refers to a form of physical trauma (KE = MV2). A number of factors deter­ industries. Explosions are classi­fied into
sustained from the various weapons.5 mine the severity of injury (Table 23.6). atomic, mechanical and chemical explo­
Gunshot injuries are an increasing The mass, velocity, shape and com­ sions.
pro­ blem in many countries, with the positions of the bullet all help determine The principal chemical explosives are
continuation of warfare in many parts the degree of injury. Larger bullets trave­ black powder, nitroglycerine, dynamite
of the world, together with a very large ling at lower velocities may cause more and trinitrotoluene (TNT). TNT is a most
number of guns in circulation, there damage than smaller high-velocity common conventional military explosive.
has been an increase in the number bullets. Tissue characteristics are also Chemical explosives can be gaseous,
of gunshot injuries and fatalities since impor­tant. As a bullet passes through liquid or solid. Chemical explosives are
the 1970s. The most common forms of the tissues, they offer resistance, which also classified as:
ballistic trauma is from small arms fire, depends on their elasticity, cohesiveness • Low explosives or deflagrating explo­
namely semiautomatic pistols, machine and density. Thus, although liver and sives
guns, submachine guns, and assault muscle absorb about the same amount • High explosives.
rifles used in armed conflicts, civilian of energy per centimeter of tissue, their Royal demolition explosive (RDX)
sporting and recreational pursuits, and different structural charac­teristics mean or cyclotrimethylene trinitramine is a
criminal activity.5 that the liver is more severely traum­ most powerful explosive used in mili­
Gunshot injuries are classified as low atized by bullet wounds. tary. When an explosion occurs, the
velocity if the bullets traveled at less than When assessing the likely severity explosive material is suddenly conver­
1,000 feet per second and high velocity of gunshot wounds, the numerous vari­ ted into a large volume of gas with the
if the bullets traveled at more than ables include the following, considered release of a tremendous amount of
2,000 feet per second. This is an arbitrary singly or in concert: energy. Pres­sures of up to 1,000 tons
definition and varies among different • The particular type of weapon used; per square inch (psi) can be generated.
authorities. Clearly the inference is that rifles are generally more destructive The temperature of explosive can rise to
high-velocity wounds are more serious than handguns. 3,000°C.
492 Maxillofacial Trauma

A person can be injured by explosive • In the fracture of a bone following


Differences between
in many ways: data can provide us the approximate
• If he is near the seat of the explosion, suicidal wounds and age of the fracture (Table 23.8).
he can be blown to pieces and scatt­ homicidal wounds • In the dislocation of joint the time
ered by the force of the explosion can be judged from the color chan­
gases. The difference between suicidal and ho­ ges of a bruise, when caused by
• If he is near enough for the skin to be micidal injuries are given in Table 23.7. violence.
in contact with the explosion flame, Note: Homicidal wounds are usually pro­ • When a tooth has been knocked
he can sustain the usual kind of flame duced to support a false charge of assault out, bleeding from its socket stops
burn. This type of burn is also caused or attempted murder against an oppo­ in about 24 hours. The cavity of the
by contact with clothing or other nent, which one has already received socket usually fills up in 7 to 10 days
material ignited by the explosion. during a quarrel, to prove self-defense. and the alveolar process becomes
• The person can be struck by flying quite smooth after 14 days.
missiles propelled by the explosion.
Age of Injury
• He can be injured or crushed by
Types of Weapon
debris usually of building demo­lished It is not possible for a doctor to give
by explosion. exact time of infliction of any injury, but Kind of weapon used can be inferred
• The person can be injured by the an approximate time can be given with by examining the edges, margins, ends,
wave of pressure, which spreads following data: width and shape in case of a wound.
concentrically from the blast center. • The age of a bruise may be ascer­tai­ Width of the wound is important as by
This air blast can: ned from the color changes, which examining width, we can judge actual
– Damage the ear by hyperemia or its ecchymosis undergoes. These penetration of knife in wound as width
punctate bruising or rupture of changes commence from 18 to varies of knife from tip onwards. When
the tympanic membrane. Even it 24 hours after its infliction and pass there is any doubt whether the wound is
can lead to damage to the cochlea. through various stages. lacerated by a weapon or contusion by
– The lung lesion takes the form • The age of wound may be ascertained a fall, it is always better to mention both
of alveolar hemorrhage, its seve­ from observing the stages of healing possibility and probability.
rity varying directly with the process.
size of the explosion charge and
becoming greater, the nearer the
victim is to the explosion. Table 23.7: Differences between suicidal and homicidal injuries
Clinical effects after air blast injuries
Suicidal or self-inflicted Homicidal
can be:
• Pulmonary hemorrhage Accessible and elective anatomical sites Anywhere in the body
like wrist or neck
• Pulmonary edema
Multiple, linear, parallel cuts Their position and shape vary
• Circulatory failure Usually incised stab wound Usually chop wounds. Stabs and lacerations
• Systemic air embolism may also be present
• When it is extensive, copious bloody They are superficial at the commencement They are deeper at the commencement and
froth in the air passage, the victim and end is deeper end is superficial
may suffocate. In right handed persons from left to right Any direction
and from above downwards
• Obstruction of respiratory passages
Defense or protection cuts absent Defense or protection cuts present usually
or pulmonary circulation and lethal over the ulnar border of forearm
reflexes initiated in the vagus nerve Hesitation cuts usually present Hesitation cuts usually absent
lead to profound circulatory changes. Weapons are usually found grasped due to Weapons are usually missing
The following samples should be cadaveric spasm or found near body
collected after blast injuries for forensic Scene of crime is usually closed room. There Scene of crime is disturbed and signs of
examination: are no disturbances of surroundings struggle may present
Clothes not damaged Clothes may be damaged
• For toxicology: blood; urine; liver
and stomach and their contents if
required. Table 23.8: Criteria for determination of age of fractures
• For tissue matching: hair and blood. 1–3 days Signs of inflammation and exudation of blood (hematoma)
• Other trace evidence: powder traces; around fracture ends in soft part
paint fragments; oil or grease stains 3–14 days Soft provisional callus formation
and any foreign material. 14th day – 5 weeks Ossification of callus
• Clothing and footwear. 6–8 weeks Fracture ends united entirely by bone
Medicolegal Aspects of Injury 493

Annexure I: Proforma for Injury report Form


Place: ___________________________________ Date: ___________________________ Time:
1. Full Name: ___________________________ Age: ____________________________ Sex: ____________________________________
2. Address: Village/Town: ________________ PS: _____________________________________________________________________
Tah. _____________________________________________ Dist. _______________________________________________________
3. Brought by: PC _______________________ Buccal No. ______________________ Police Station (PS): ______________________
4. Consent : I am willing to be examined by Dr. _____________________________________________________________________
Signature or thumb impression_________________________________________________________________________________
5. Marks of Identification: a. ___________________________________________________________________________________
b. ___________________________________________________________________________________
6. Brief history: _________________________________________________________________________________________________
_____________________________________________________________________________________________________________
7. General examination: _________________________________________________________________________________________
_____________________________________________________________________________________________________________
8. Local examination of injuries:

S. No. of injury Type of injury Size and shape Situation on Simple or Approx. age of Kind of weapon
body grievous injury used
1.
2.
3.

N. B. Separate paper may be used if injuries are much more in number.


9. Healing period required: ______________________________________________________________________________________
10. Exfoliated/extracted teeth; weapon inspected and handed over to PC after sealing: Yes/No
Signature of PC: ______________________ Signature of MO: ________________________________________________________
Name of PC: _________________________ Name of Dr: ____________________________________________________________
No:__________________________________ PS: _____________________________ Designation:_____________________________
Date: ________________________________ Seal if any:

Left thumb
impression of the
patient

2. Mathiharan K, Patnaik AK. Modi’s 4. Bernard Knight, Simpson’s Forensic


References
Medical Jurisprudence and Toxicology. Medicine CRC Press; 11 edition, 1996.
1. Parikh CK. Textbook of Medical Eastern book co. Calcutta, 23rd edition, 5. Kumar K. Forensic Ballistics in Criminal
Jurisprudence, Forensic Medicine and 4th reprint 2005. Justice. Eastern Book Company, 1987.
Toxicology. New Delhi. CBS Publishers 3. Keith Mant A. Taylor’s Principles and
and Distributors; 6th Ed. 2005. Practice of Medical Jurisprudence.
Churchill Livingstone, UK 13th Ed 1984.
Section 8
Facial Deformities

n Introduction to Cleft Lip and Palate


n Orthognathic Surgery
24 Introduction to Cleft Lip
and Palate
Jajoo Suhas N, Yadav Abhilasha, Garg Rajat

Introduction Historical Aspect Mirault3 introduced the modern cross


flap technique of lip closure in 1844
Cleft lip is the second most common In ancient times many congenital defor­ and Hagedorn4 in 1884 modified this
embryological (Congenital) deformity, mities, including cleft lip and palate, technique by rectangular flap technique
after the clubfoot (Figs 24.1A to D). were considered to be evidence of an to prevent linear contracture. Then
Although it is localized to a small ana­ evil spirit in an afflicted child. These period of Z-plasties came, which led
tomic area, but being on face it requires children were often removed from the Tennison5 (1952) to introduce low
more attention and priorities. It is a tribe or cultural unit and left to die in the triangular flap technique and the high
three-dimensional anomaly involving surrounding wilderness. Z-plasty rotation flap of Millard6 (1958).
soft and skeletal tissue that changes in Boo-Chai1 (1966) reported a case However, it was as late as the 16th
the fourth dimension with growth and of successful closure of a cleft lip in century that Franco7 (1561) noted “pati­
function. Successful treatment of these approximately 390 AD in China. Yper­ ents having cleft palate are more diffi­
children requires a multidisciplinary man (1295–1351) was a Flemish surgeon cult to cure”. In ancient times around
team approach including pediatrician, who appears to have written the first 2,500 BC use of dental prosthesis was
oral and maxillofacial surgeon, plastic fully documented description of cleft introduced for cleft palate mostly made
surgeon, craniofacial surgeon, ortho­ lip and its surgical repair.2 Treatment of gold or silver.
dontist, pedodontist, ent surgeon, of protruding premaxilla using a head Von Graefe8 in 1816 and Roux9
anesthetist, prosthodontist, speech the­ bandage to achieve external com­ in 1819 were the first to perform the
rapist and psychiatrist with technical pression of the pre­maxillary segment, success­ful surgery of soft palate and later
skill, in-depth knowledge of the abnor­ thereby bringing it to more favorable Dieffenbach10 recommended separation
mal anatomy and appreciation of three- position was introduced by Desault of the hard palate mucosa from the bone
dimensional facial esthetics. and Bichat (1798) (Figs 24.2A to F). as a mean of closing the cleft of palate.

A B C D
Figs 24.1A to D: Different craniofacial cleft deformities seen among children: (A) Oro-occular cleft; (B) Unilateral cleft; (C) Bilateral cleft;
(D) Midline cleft
498 Facial Deformities

A B C

D E F
Figs 24.2A to F: Protruding premaxilla treated with external band compression in bilateral cleft lip and palate: (A) Frontal view;
(B) Lateral view; (C) Protruding premaxilla-pretreatment; (D) Adhesive tape in place to retract the premaxilla; (E) Pretreatment worms view;
(F) Posttreatment worms view

Von Langenbeck11,12 collaborated 33 percent, followed by isolated cleft


Development during this period entails
these concepts and emphasized on lip at 21 percent. migration and fusion of mesenchymal
subperiosteal undermining and use of • The majority of bilateral cleft lips
cells with facial structures. If this migra­
mucoperiosteal flap, which was a major (86%) and unilateral cleft lips (68%)
tion and fusion is interrupted, a cleft can
factor in healing of wound. are associated with a cleft palate.develop along the lip and palate. The
• Unilateral clefts are nine times astype of cleft varies with the embryonic
common as bilateral clefts and occur
stages of development. Important thing
Epidemiology
twice as after frequently on the left
to remember is basically abnormality
Cleft lip occurs in approximately 1 in side than on the right. of mesoderm for a cleft to occur, either
750 to 1,000 live births.13 The highest • Males are predominant in the cleft mesoderm is less or mesoderm does not
incidence exists in North Americans, lip and palate population, the after
reach for fusion, if at all it reaches then it
Indians and Japanese (approximately whereas isolated cleft palate occurs
may be late.
1 in 350 births). African Americans and more commonly in females. There are several types of cleft lip,
Africans represent the lowest incidence • This racial heterogeneity is not ranging from a small groove on the
of cleft lip deformity (approximately obser­ ved for isolated cleft palate,
border of the lip to a larger deformity
1 in 1,500 births). There is a higher which has an overall incidence of that extends into the floor of the nostril
incidence of cleft in certain populations 0.5 per 1,000 live births. and part of the maxilla.
of Scandinavia and Middle European Unilateral cleft lip results from
countries. Applied Surgical failure of the maxillary process on the
Among the cleft lip and palate popu­ affected side to fuse with median nasal
lation, the most common diagnosis is:
Anatomy prominences (Fig. 24.3). The result is
• Cleft lip and palate at 46 percent, Important structures of the embryo’s called as persistent labial groove. The
followed by isolated cleft palate at mouth form at 4 to 7 weeks of gestation. cells of the lip become stretched and the
Introduction to Cleft Lip and Palate 499

Fig. 24.3: A developing embryo showing


fusion of both the maxillary processes on
either side with median nasal process in
center. Any abnormality in fusion leads to
cleft Fig. 24.5: Depiction of the abnormal musculature surrounding a cleft lip

prominences on both sides. All these


three elements are initially widely sepa­
rated because of the presence of tongue.14
During 8th week, the orientation of the
lateral palatine processes alters from
vertical to horizontal to initiate their
fusion. During this process the mandi­
ble becomes more prognathic, thereby
allowing the tongue to move downwards
to avoid any interference for fusion to
occur.
Fusion then occurs between the
Fig. 24.4: Simonart band joining lip on Fig. 24.6: Development of palate
secondary palate and primary palate as
both the sides of cleft
shown in Figure 24.6.
Ossification occurs in the primary
tissues in the persistent groove break degrees of deformity on each side of palate and the anterior portion of the
down, resulting in a lip that is divided the defect. An anatomical structure secondary palate to form the hard pal­
into medial and lateral portions. In prolabium projects to the front and ate, while the posterior portion of the
some cases, a bridge of tissue (Simo­nart hangs unattached. Defects associated secondary palate does not undergo ossi­
band) joins together, the two incom­ with bilateral cleft lip are particularly fication and remains as the soft palate.
plete lip portions shown in Figure 24.4. problematic due to disconti­nuity of the The embryologic basis of cleft palate
The orbicularis oris muscle anatomy muscle fibers of the orbicularis oris. is failure of the fusion of these pro­
is abnormal in the cleft lip patients. cesses with each other. Cleft of either
The orbicularis muscle fibers do not the primary or secondary palate can be
Formation of Palate
decussate transversely across the mid­ complete or incomplete, depending on
line over the maxilla but tend to run-up The palate is formed with the fusion the degree of fusion that occurred dur­
parallel to the cleft edges toward the of primary palate (median palatine ing embryonic development.
base of the nose (Fig. 24.5). process), which is derived from the A cleft of the lip and palate is the
Bilateral cleft lip occurs in a fashion frontonasal process and the secon­ result of the failure of lip elements, and
similar to the unilateral cleft. Patients dary palate (lateral palatine processes), right and left palatal segment, to come
with bilateral cleft lip may have varying which are derived from the maxillary together within the first 9 weeks of fetal
500 Facial Deformities

external aberrant lip-cheek muscular


forces, as well as spread apart by the
tongue pushing into the cleft space.
Because clefts differ in their location and
extent, lip and palate clefts can vary in the
degree of geometric distortion, as well as
in the size and shape of the cleft palatal
segments. The muscular forces that act
on the bony scaffolding of the palate and
pharynx begins to develop very early in
intrauterine life; therefore, the palatal
and facial configuration at birth has been
formed over the major portion of the
Fig. 24.7: Abnormal forces acting on cleft and normal side leading to variations in size of infant’s existence prior to birth.
the cleft In complete unilateral clefts of the
lip and palate, the premaxillary portion
of the non-cleft segment is pulled
anterolaterally. In addition to the lateral
displacement of the lateral palatal seg­
ments, the pre­maxilla in the larger seg­
ment is carried forward in the facial
skeleton. Alveolar bone deficiencies
can be seen in related abnormal tooth
development or absence, as growth
of alveolar bone is based on tooth
development. Nose is also deviated to
the normal side because of muscle pull
except the alar base of cleft side, because
of which nose appears to be depressed
A B as shown in Figures 24.8A and B. If a soft
Figs 24.8A and B: Wide unilateral cleft lip with depressed nose tissue, which collectively form Simonart
band, bridges the alveolar cleft, the
attached palatal segments are limited in
their degree of geometric displacement
(Figs 24.9A and B).
In complete bilateral cleft lip and
palate, there is excessive growth in the
premaxillary-vomerine suture is caused
by increased tension at this site, precipi­
tated by mechanical force stresses dur­
ing periods of rapid growth (Figs 24.10A
and B). This growth is continuous dur­
ing early postnatal years and provides
a fourth dimension to the deformity,
which can alter the cleft palatal seg­
A B ments and their associated parts and
Figs 24.9A and B: Minimally displaced cleft margins due to Simonart band either simplify or complicate treatment.
In complete cleft palate cases, there
is abnormal muscle attachment seen at
life. The loss of muscular continuity of forces act to displace tissue masses the junction of hard palate and soft pal­
the orbicularis oris-buccinator-superior (Fig. 24.7). In complete clefts of the lip ate. In the normal palate, complete ring
constrictor ring in complete unilateral and palate, if the lateral palatal cleft of muscles (tensor veli palatini and leva­
and bilateral clefts changes the normal segments are detached from the vomer, tor veli palatini) can be seen, where as
muscular force. The aberrant muscular they will be pulled laterally by the in cleft there are abnormal attachment
Introduction to Cleft Lip and Palate 501

of these muscles on the posterior border


of hard palate, instead of intermingling
with each other in center as seen in nor­
mal palate. This abnormal attachment
restricts the normal movement of soft
palate, while performing various func­
tions (Figs 24.11A and B).
Maxillary growth occurs on pos­
terior surface of maxilla with the for­
ward push of maxilla against basal
bone and deposition of bone at the tub­
erosity region. In the cleft palate surgery
mucoperiosteal flap is raised and sutu­
red leaving denuded bone area on both A B
sides, which heals with scar tissue. This Figs 24.10A and B: Displaced unsupported premaxilla and palate
tissue contracts, while healing helps in
reducing width of the maxillary arch
form although this effect is minimal. At
the same time if hamulus is fractured
in pterygopalatomaxillary junction scar
tissue may form across this sensitive area
of growth and inhibits forward move­
ment of maxilla. It also affects eruption
of teeth, teeth erupts more palatally
than its normal eruption pathway.
In infants with cleft lip and palate,
feeding is a major problem as child
cannot suck, because of inability to
create negative pressure in mouth.
Poor feeding also leads to improper
growth of the child. Otitis media is also
a common problem with cleft palate
patients, as ventilation of ear is affected
A
due to abnormal muscle attachment,
blockage of eustachian tube and its pull,
which leads to accumulation of fluid
in ear and leading to inflammation.15
Children have speech related difficulties
as there is no closure of nasopharynx
(velopharyngeal incompetence), hence
a nasal twang is present, which makes
words incomprehensible.

Etiology
Both environmental and genetic factors
are implicated in the genesis of cleft lip
and palate. Facial clefts can occur as
part of a syndrome or an isolated clefts.
Factors most commonly causing cleft
are as follows: B
• Genetic factors Figs 24.11A and B: Abnormal attachment of palatal musculature in cleft palate (Courtesy:
• Environmental factors Salyer and Bardach’s Atlas of Craniofacial and Cleft Surgery: Craniofacial Surgery, Vol. 1 by
• Syndromic clefts. Kenneth E Salyer, Janusz Bardach)
502 Facial Deformities

Genetic Factors and viral infections also predisposes to palate with congenital heart diseases,
Parents with a non-syndromic child cleft lip and palate. Mechanical factors hypernasal speech and learning dis­
having cleft, often have a query whether are like attempt to abort the baby by abilities. Syndromes associated with
their subsequent child will also have uterine manipulation and hormonal cleft are many. Some of them commonly
CLP deformity. However, it should therapy. seen as given in Box 24.2.
be explained to such parents that the Intrauterine exposure to the anti­
relative risk of having CLP deformity in convulsant phenytoin,20 valproic acid,
Classification
subsequent offsprings depends upon oxazolidine is associated with a 10 fold
the type of CLP the previous child had, increase in the incidence of cleft lip. The Many different classification systems of
i.e. cleft lip alone (CL), cleft lip with cleft drug methotrexate which is used as a varying complexity have been proposed
palate (CLP) or a cleft palate alone (CP) chemotherapeutic agent is also said to for cleft lip and palate, but few have
(Box 24.1). be associated with increase in the risk found wide clinical acceptance and
• If the family has one affected child or of clefts.21 Deficiency of folic acid also application.
parent with CLP, the risk of the child causes cleft in human beings but the In 1922, Davis and Ritchie,23 classi­
of the next pregnancy having CLP is exact etiopathogenesis for this is still fied congenital clefts in three groups
4 percent.16 unclear, most accepted being the role according to the position of the cleft
• If two previous children have CLP, of folate in nucleic acids synthesis and in relation to the alveolar process
the risk increases to 9 percent. methylation cycle.22 Any deficiency of (Box 24.3).
• If one parent and one child were folic acid leads to genetic abnormality. In 1931, Veau24 suggested a classifi­
previously affected, the risk to child­ Continuing advances in this field of re­ cat­ ion, which has four categories
ren of subsequent pregnancies is search will have obvious implications (Box 24.4).
17 percent. for global prevention programs. However, this classification is inco­
• For families with a history of CP, the m­­­plete because it makes no pro­vision for
risk of CP to children of subsequent Syndromic Clefts isolated cleft lip and cleft alveolus. Fogh-
pregnancies is 34 percent. Genetic abnormalities can result in Andersen25 intro­ duced embryological
syndromes that include clefts of the concepts into his simple classification,
Environmental Factors primary or secondary palate among which he used to describe the epide­
A relation between some environmental the developmental fields affected as miology of cleft lip and palate in Denmark
factors (smoking, alcohol, anticonvul­ shown in Box 24.2 and Figures 24.12A in 1942. Kernahan and Stark26 further
sants, steroids, radiation, viral infections to F. More than 40 percent of isolated developed this concept in 1958 and
and mechanical factors) during preg­ cleft palates are part of malformation Kernahan27 represented symbolically
nancy and risk of having baby with syndromes, compared to less than as a ‘striped Y’ in 1971 (Fig. 24.13). The
an orofacial cleft is well established. 15 percent of cleft lip and palate cases. involved area is filled in by pen and
Maternal smoking during pregnancy The most common syndrome associ­ provides rapid graphic presentation of
doubles the incidence of cleft lip. In ated with cleft lip and palate is van der the site and extent of cleft involvement.
literature it is summarized that risk of Woude syndrome with or without lower However, it has got few limitations
cleft with maternal smoking is 1:29 for lip pits or blind sinuses. Microdeletions like no differentiation of cleft lip with
CLP and 1:32 for CP.17 There is increased of chromosome 22q resulting in velocar­ and without involving nose and clefts
risk of both syndromic and non-syn­ diofacial syndrome is the most common of secondary palate cannot be classified
dromic cleft with higher quantities of diagnoses associated with isolated cleft into right or left sides. Kernahan later on
alcohol consumption.18 Role of steroid
as a risk factor is well demonstrated. Box 24.2: Various syndromes associated with cleft
Therapeutic doses of prednisone do
increase the risk of cleft by 3 to 4 times.19 1. Chromosomal a. Trisomy 13 and 18
Radiation exposure during pregnancy b. Velocardiofacial syndrome
2. Non-mendelian a. Pierre Robin’s syndrome
b. Goldenhar syndrome
Box 24.1: Genetic risk of cleft to children
3. Mendelian disorders a. Van der Woude syndrome
2% If one previously affected child b. Gorlin syndrome
c. Stickler’s syndrome
1% If two children were previously
d. Treacher-Collin’s syndrome
affected
e. Ectrodactyly-ectoderm
6% If one parent has CP
15% If one parent and one previous 4. Unknown a. Kabuki syndrome
child have CP. b. de Lange syndrome
Introduction to Cleft Lip and Palate 503

A B C

D E F
Figs 24.12A to F: (A) Van der Woude syndrome; (B) Down syndrome; (C) Pierre Robin sequence; (D and E) Binder, syndrome;
(F) Goldenhar syndrome

Box 24.3: Davis and Ritchie’s classification of clefts

Group 1 Prealveolar clefts, unilateral, median or bilateral.


Group 2 Postalveolar clefts involving the soft palate only, the soft and hard palates or a
submucous cleft.
Group 3 Alveolar clefts, unilateral, bilateral or median.

Box 24.4: Veau’s classification

Group 1 Cleft of soft palate only.


Group 2 Cleft of hard and soft palate
not extending further incisive
foramen, involving secondary
palate alone.
Group 3 Complete unilateral cleft,
extending from uvula to the
1 2
incisive foramen in midline,
than deviating to one side and Fig. 24.13: Kernahan’s stripped Y-symbol
usually extending through the
to classify various clefts. The upper limbs
alveolus at the position of the
represent the right (1, 2, 3) and left sides
future lateral incisor tooth.
(4, 5, 6) lip (1 and 4), alveolus (2 and 5),
Group 4 Complete bilateral cleft, same as hard palate anterior to the incisive foramen
group 3 with two clefts extend- (3 and 6). The lower limb represents the hard
ing forward from the incisive palate posterior to the incisive foramen
foramen through the alveolus. 3 4 (7 and 8) and soft palate (9)
504 Facial Deformities

Fig. 24.14: Modified Kernahan classification


Fig. 24.15: Partial cleft lip

modified his stripped Y to involve nose


and nasal floor as shown in Figure 24.14.
Various types of clefts and how to
classify according to Kernahan classifi­
cation is given in Figures 24.15 to 24.21.
A new classification, Nagpur classifi­
cation has also been suggested as shown
in Box 24.5.
Still remaining is a group of rare
craniofacial clefts that lie outside the
classification systems of the clefts of the
lip and palate deformities, described
pre­viously.
Tessier29 described an anatomical
system of classification for craniofacial
clefts that depended on the site and Fig. 24.16: Partial cleft lip and alveolus
relationship of the cleft to the midline
sagittal plane (Fig. 24.22). The classi­
fication describes 14 different types of
clefting according to, whether clefts are
cranial or facial and their relation to the
midsagittal line. Clefts of lip and alveolus
are numbered 1, 2 and 3 (Tables 24.1
and 24.2).

Prenatal Diagnosis and


Counseling of Parents
Intrauterine diagnosis of orofacial clefts
is possible by ultrasonography. Com­
plete clefts are easily seen at 16 weeks
gesta­tion, however incomplete clefts
are seen more readily at 27 weeks.30 Fig. 24.17: Complete unilateral cleft lip and alveolus
Palatal clefts are difficult to visualize by
prenatal ultra­sono­graphy (Figs 24.23A of the parents is very impor­tant part of the parents should be psychologically
to I). Prenatal diagnosis can be done the treatment for cleft patient as they prepared to be the part of the team for the
during routine screening and with high have to learn various feeding methods manage­ment of the child. Counseling is
resolu­tion ultrasonography. Counseling to feed the child during infancy, also also important as sometimes parents
Introduction to Cleft Lip and Palate 505

termination of pregnancy. Intrauterine


foetal surgeries are the upcoming
modalities to avoid such terminations.

Management Protocols
for the Patients with
Cleft Lip and Palate
Many treatment protocols have been
given in the literature for the manage­
ment of cleft deformities however, only
standardized and widely acclaimed and
practiced treatment modalities are dis­
cussed in the present chapter. The com­
Fig. 24.18: Partial bilateral cleft lip and alveolus
prehensive treat­ ment of cleft lip and
palate deformities requ­ires thoughtful
consideration of the ana­ tomic com­
plexities of the deformity and the deli­
cate balance between inter­vention and
growth. There are many modalities, but
all have same aims and objectives to
achieve:
• Normal dentofacial growth and
deve­­lopment.
• Normalized esthetic appearance of
face.
• Intact primary and secondary palate.
• Normal speech, language and hea­ring.
• Nasal airway patency.
• Class I occlusion with normal masti­
catory function.
Fig. 24.19: Complete unilateral cleft lip, alveolus and palate
• Good dental and periodontal health.
• Normal psychosocial development.
To achieve all these goals only sur­
gical procedure is not sufficient enough.
The line of treatment for the child is as
follows:
• Preoperative management.
• Primary operative management.
• Secondary management.

Preoperative Management
During the first day of life the most
critical aspect is feeding, as child can­
not generate negative intraoral pres­sure
having cleft palate, parents have to feed
the child. Otherwise caloric require­
ments of the child will not be met. There
Fig. 24.20: Complete bilateral cleft lip, alveolus and palate
are various devices available to aid in
feeding (Figs 24.24 to 24.27).
may want to terminate pregnancy, but patients, but if the child is syn­dromic The child must be fed in sitting
pare­nts must be explained about the and having other congenital anomalies, up position and frequent burping is
treatment options available for cleft then it may be an indi­ cation for required as child ingests air along with
506 Facial Deformities

the food (aerophagia), because of this


cleft children get fatigue early and
they require frequent small quantity
of feeds, other­wise child will be under­
nourished. If the child cannot be fed
with this method, a palatal prosthesis,
which spans the defect may be required.
The prosthesis helps in feeding as
well as nasoalveolar moulding (NAM)
preoperatively to decrease the width of
the cleft. Despite these attempts, more
than 25 percent of CLAP children have
feeding difficulties with poor weight
gain until palatal repair.
Respiratory infections is also com­
Fig. 24.21: Cleft soft palate and uvula
mon in children with cleft lip and
palate, hence, they require extra care
Box 24.5: Nagpur classification
by the parents to prevent any infection
Nagpur classification for cleft lip and palate28: It is a simplified classification and does and avoid people having respiratory
not tell whether cleft is complete or incomplete. infection coming close to the child.
Group 1—cleft lip. Parents need to spend more time with
Group 1A—cleft lip and alveolus. the child and need to be counseled
Group 2—cleft palate. properly about the importance of regular
Group 3—cleft lip and palate. follow-up for hemoglobin estimation,
It could be unilateral or bilateral. management of recurrent diarrhea,
needful interventions to prevent weight
loss, as all these factors delay the surgery
and compromise the surgical outcomes.

Presurgical Orthodontics
The goal of presurgical orthodontics
is to move the abnormally positioned
maxillary arches into a normal relation­
ship prior to the surgery. The soft tissues
follow the bony foundation and cleft
lip elements move closer to each other
narrowing the cleft. There are many
devices used for this, such as:
• Extraoral devices
– Simple surgical tape on lip from
cheek to cheek.
– Head bonnet with elastic strap.
• Intraoral devices
– Passive devices (palatal obtura­
tors).
– Active devices (pin retained
devices ‘Latham appliance’)
(Figs 24.28A and B).
Extraoral devices are economical
and simple to apply, but they require
cooperation from parents for application
of new tapes and adjustment of straps
at periodic intervals. The appliance is
Fig. 24.22: Tessier classification of craniofacial clefts. Right side depicts the osseous clefts visible externally and can damage the
while the left side shows soft tissue clefts (Numbers 0 and 30 represent midline clefts) tender skin of the child.
Introduction to Cleft Lip and Palate 507

Table 24.1: Tessier’s classification showing bony clefts Intraoral devices aid in feeding and
presurgical orthodontics. Latham appli­
Bony or skeletal Extent
clefts
ance is used most commonly in bilateral
cleft patients to expand the dental arch,
#14 Midline Cleft so that displaced premaxilla can be retro­
#13 On the cranium comes through frontal bone through olfactory groove positioned. This device is given at 6 weeks
between nasal bone and frontal process of maxilla of age and removed by 2 to 3 months of
#12 Through lateral mass of ethmoid age for definitive lip repair. Their major
#11 Upper medial orbital cleft, cranial counterpart of #3 disadvantage is that they require special­
#10 It is a central orbit cleft, extends to roof of eye socket and forehead, the ized orthodontic care, they are expensive
cranial extension of #4 and frequently need short anesthesia for
#9 Upper lateral orbital cleft, seems to correspond with #5 making necessary adjustments.
#8 Frontozygomatic cleft which appears to be the cranial counterpart
of #6 Nasoalveolar Molding31
#7 Temporozygomatic cleft with absence of zygomatic arch, deformities Nasoalveolar Molding (NAM) is a non­
of mandibular ramus, condyle and coronoid process surgical method of reshaping the alve­olar
#6 Maxillary zygomatic cleft opens into infraorbital fissure travels through processes, lip and moulding the nasal
back of upper jaw with high palate and choanal atresia (absence of cartilages in favorable position before the
inner ear structure) cleft lip and palate surgery, to facilitate the
#5 It runs through infraorbital rim, orbital floor and maxilla lateral to the surgical procedure and enhance the out­
infraorbital nerve and maxillary ainus, proceeds to alveolus behind comes. It is used mainly in children with
canine tooth in premolar region
wide clefts (Figs 24.29 and 24.30). NAM is
#4 It is a central orbito–maxillary cleft through infraorbital rim, orbital floor employed in early mana­­gement of both
and medial to infraorbital nerve through maxillary sinus or alveolus
unilateral and bilateral cleft anomalies in
#3 Runs from inside (medial) lower edge of orbit through lacrimal bone,
newborns. The therapy is started as early as
across maxilla and alveolus to lateral incisor
2 weeks postnatally, as the cartilage and
#2 Across premaxilla, 2 appears to split the tooth
the ridges have high elasticity and can be
#1 From between central and lateral incisor to floor of nasal cavity easily molded in the desired way. The de­
lay in initiating the therapy by few months
fails to produce the desired results. It
gives excellent early results, but, the long-
Table 24.2: Tessier’s classification showing soft tissue clefts term results are questionable. Surgery is
performed after the molding is complete,
Soft tissue Extent
approxi­mately 3 to 6 mon­ths after birth.
clefts
Purpose of NAM:
#14 Midline facial cleft • Minimal tension in soft tissue during
#13 Cranial Counterpart of #1, medial to the eyebrow surgical repair.
#12 Cranial cleft between nasal bridge and inner corner of eye, coloboma of • Preoperative NAM aid in obtaining
the root of the eyebrow optimal scar.
#11 Notch of upper lid and eyebrow • Increases symmetry of nose.
#10 Notch of the upper lid and divides the eyebrow • Reduction in number of revision
#9 Upper lateral orbital cleft in the outer third of upper eyelid surgeries.
#8 True cleft of lateral canthus associated with Goldenhar syndrome • Reduction in overall cost of therapy.
#7 Presents as macrostomia and preauricular tags
#6 Lower lid coloboma with a marked furrow across cheek Primary Operative
#5 Lateral orbito–maxillary cleft through the outer third of lower lid Management
through cheek to lip near outer corner of mouth
#4 Lateral to the tear duct, across the cheek, skirting the nose, to the lip Treatment Planning and Timing
between the cuspid’s bow and corner of mouth of Surgery
#3 Through the lacrimal punctum around the nostril and into the lip at the
cuspid’s bow
The timing of cleft lip and palate rep­air
is controversial. Despite several mean­
#2 Slightly to the outer curve of the nostril and into the lip
ingful advancements in the care of
#1 Through the dome of the nostril cartilage, occasionally through the lip
patients with cleft lip and palate, a lack
508 Facial Deformities

A B C D Fig. 24.24: Soft bottle with a large hole,


as this fills the palatal defect and requires
minimal sucking by the neonate

E F G

H I

Figs 24.23A to I: Various transvaginal ultrasound images of the fetus with normal lip Fig. 24.25: Haberman nipple—it delivers
and cleft lip (Source: Cleft Lip and Palate Editor Samuel Berkowitz 2nd Edition, Chapter 2 milk under slight pressure, more posteriorly
Prenatal Diagnosis of Oral Clefts pages 23 and 14) in the oropharynx

A B
Figs 24.26A and B: (A) Bowl and spoon; (B) Dropper if these nipples are not available Fig. 24.27: Feeding tube secured to feed
the cleft child

of consensus exists regarding the timing the timing of treatment interventions Cleft lip repair is generally under­
and specific techniques used during is considerably variable amongst cleft taken at some point after 10 weeks of age
each stage of cleft reconstruction. centers. Therefore, it is difficult to pro­ because:
Timing of surgery depends on the duce a timing regimen that everyone • It allows a complete medical evalu­
bal­­
ance between functional needs, agrees upon. ation of the patient so that any as­
aes­th­
etic concerns, and the issue of The staged reconstruction of cleft sociated congenital defects affecting
ongo­ ing growth of the child. Due to lip and palate deformities are shown in other organ systems (e.g. cardiac or
many different treatment philosophies, Table 24.3. renal anomalies) may be detected.
Introduction to Cleft Lip and Palate 509

A B
Figs 24.28A and B: Latham’s appliance (Source: Clefts of the Lip and Palate—Tennessee Craniofacial Center 1(800) 418-3223)

A B C

D E F
Figs 24.29A to F: Nasoalveolar moulding: (A) Child with a wide unilateral complete cleft lip, alveolus and palate; (B) Custom made tray;
(C) Wire, elastics and bandage used to secure the custom made tray; (D) Appliance in situ; (E) Reduced size of the defect post therapy;
(F) Surgical result post NAM
510 Facial Deformities

• The surgical procedure itself may


be easier when the child is slightly
older, and the anatomic landmarks
more prominent and well defined.
• The anesthetic risk-related data,
histo­ri­cally suggested that the safest
time period for surgery in this popu­
lation of infants could be outlined
simply by using the ‘rule of 10.’
Rule of 10:
• 10 weeks old
A B
• 10 pounds in weight
• With a minimum hemoglobin value
of 10 dL/mg.32
Note: When anesthetic facilities were not
adequate the rule of ten was followed, but
now barring hemoglobin other criteria
can be relaxed to certain extent and the
surgeries can be performed safely.
Presurgical evaluation: Before the
patient undergoes surgical intervention
a presurgical evaluation of the patient
is mandatory regarding fitness for sur­­
gery by pediatrician/physician (as
applicable) and the anesthetist. Rout­
ine hematological investigations are
required including (complete blood
C D count, serum profiles, sickling, blood
Figs 24.30A to D: Nasoalveolar moulding—Child with bilateral cleft lip, alveolus and grouping, hepatitis B). According to
palate. To correct the protruding premaxilla a custom made tray is prepared which is ‘rule of ten’, patient must have at least
secured in mouth using elastic bandages. Retrusion can be seen in pre therapy and post 10 gm percent of hemoglobin, blood
therapy pictures: (A) NAM appliance in situ; (B) Retrusion of premaxilla after NAM; (C) Frontal grouping is must if any transfusion is
view after NAM; (D) Postsurgical result of the child treated with NAM planned during surgery or immediately
after surgery for which compatible
blood should be ready before surgery.
Table 24.3: Timing for staged reconstruction of cleft deformities All patients should be evaluated by the
anesthesiologist the day before surgery.
Sr. Procedure Timing mentioned in the literature
No. Patients requiring general anesthesia
should receive maintenance fluids at
1. Cleft lip repair After 10 weeks least 12 hours before surgery, with strict
2. Cleft palate repair 9–18 months attention paid to urinary output and
3. Pharyngeal flap/pharyngoplasty 3–5 years or later based on speech weight. Preoperative assessment of the
development patient should include checking for signs
4. Alveolar reconstruction with bone graft 6–9 years based on dental development of vaso-occlusion, fever, respiratory
5. Cleft orthognathic surgery 14–16 years in girls, 16–18 years in boys tract infection and dehydration. The
laboratory and physical examination
6. Cleft rhinoplasty After age 5 years, but preferably at skeletal
maturity; after orthognathic surgery when
results should be reviewed to identify
possible. Nowadays the concept is primary abnormalities in the heart, liver,
rhinoplasty at the time of lip correction, kidneys, brain and lungs. through
preschool rhinoplasty and final procedure the clinical examination and relevant
at 15–18 years is practiced. investigations must be done in all cases
7. Cleft lip revision Anytime once initial remodeling and scar as the patients may have associated
maturation is complete. Best done after congenital anomalies like VSD, ASD,
5 years. PDA, Dextrocardia. It is preferable to
Introduction to Cleft Lip and Palate 511

ascertain the ASA grading. Normally Postoperatively, oxygen should be Surgical Procedures
patients beyond ASA grade II require administered until the effects of anes­
high degree of care and monitoring thesia have worn off. In cleft patients,
for Cleft Lip Repair
and relative operative risk is high. The surgical wounds interfere with the Various procedures have evolved over
parents must be taken in confidence respiration and hence requires an the period of time. The first procedure
and explained about the same. In high extended administrator of oxygen. Con­ to be based on sound surgical principles
risk group, if the underlying anomaly tinued monitoring is recommended in was the straight line repair of Rose and
is treatable, it should be treated first the intensive care unit. Postoperative Thompson.33,34 Other commonly used
and then the definitive cleft repair can parenteral hydration should keep the tech­niques are:
be undertaken to minimize the risk of patient at 1 to 1½ times maintenance. • Straight line repair (when it was
surgery, e.g. repair of ASD/VSD/PDA Aggressive respiratory care is necessary noticed that scar on lip contracts
should be undertaken prior to the cleft in sickle cell disease to minimize and notching is produced, the other
repair if it is significant. pulmonary complications. After the techniques came in existence)
After ascertaining the fitness for repair of the palate the wide open airway • Quadrangular flap technique.35
surgery, the patient preparation is gets narrowed and the child takes time • Triangular flap technique (Ten­
under­­
taken. The counseling of the to get accustomed to the new situation. nison36 and Randall37 triangular flap
parents or the patient himself in cases The air way patency should be ensured. repair) (see Figs 24.27 and 24.28)
of adults is done. Patient is kept nil by Placing a tongue stitch to prevent tongue • Rotation flap technique (Millard38
mouth (NBM) for at least 4 hours before fall is recommended. Similarly, vigorous rotation and advancement repair)
surgery in case of children and at least suction directly over the repaired palate (see Figs 24.29 and 24.30)
6 hours in case of adults. should be avoided as the fragile mucosa • Delaire technique.39
can get avulsed and bleeding can occur.
Blunt tipped catheters should be used Straight Line Repair
Intra- and Postoperative
and direct suction over the suture line Straight line repair is not a commonly
Monitoring should be avoided. The children are also practiced technique for the unilateral
Surgical procedures that have an increa­ prone to develop the broncospasm as cleft lip deformities as the scar con­
sed probability of ischemia or hypoxia, the airway is hyper reactive and minor tractures invariably results in the
hypo­tension and hypothermia deserve aspiration can lead to broncospasm, notching of the lip. As in case of the
special attention. hence this should be prevented. Use of bilateral cleft lip deformity in prolabium
All patients should be monitored safer anesthetic drugs like sevofluorane, segment has inadequate tissue and the
with at least an ECG and have a intravenous inducing agents like pro­ mobilization or advancement/rotation
deter­mination of inspired oxygen con­ pofol/ketamine and muscle rela­ xants is not possible, generally it is resorted
centra­tion by pulse oximetry or blood like veccuronium/atracurium should to straight line repair and the bilateral
gas testing. A warm temperature should be used in place of conventional drugs, scars produced thereof are considered
be maintained in the operating room. in spite of their higher cost to ensure as philtral columns (Figs 24.31A and B).
General anesthesia should aim for a mild smooth induction, uneventful recovery
respiratory alkalosis (pH about 7.45) and and preventing complications like ma­-­ Tennison and Randall Triangular
a normothermic, well-hydrated patient. li­gnant hyperthermia.
The patient should receive a minimum of
Flap Repair
50 percent oxygen in combination with Surgical Procedures The repair of cleft lip deformity by ten­
the anesthetic agent. Blood replacement nison and Randall Triangular flap tech­
for significant intraoperative blood loss
for Cleft Lip and Palate nique is shown in Figures 24.32A and B.
is recommended. The children are very • Primary • Preoperative picture with marking
susceptible for fluid and electrolyte – Closure of the lip/anterior palate • Intraoperative with both side flap
imbal­ance as the regulatory functions repair. raised
are not well established. Hence, calcul­a- – Closure of the palate. • Final closure.
tion of fluid requirement should be • Secondary
­
done meticulously. The pediatric influ­ – Rhinoplasty and scar revision of Advantages
s­ion pumps are very useful during the the lip. • Lengthens both the lip segments of
administration of IV fluids at appro­priate – Closure of the palatal fistulae. cleft as well as non-cleft sides
rate and in desired quantity. The selection – Pharyngoplasty. • It results in final symmetric, balan­ced
of appropriate fluid like Ringer’s lactate – Alveolar bone grafting. lip with a well defined Cupid bow
and isolyte-P should be done, unless – Orthodontic treatment. • Only a small amount of tissue is
other fluids are specifically indicated. – Orthognathic procedures. discarded
512 Facial Deformities

• It also contributes to correction of • All layers to be sutured on the basis ment repair is shown in Figs 24.33A
nasal deformity of triangular flap. If any mistake and B.
• This technique is comparatively eas­ done in marking or incision it cannot
ier for inexperienced surgeons. be recorrected Advantages
• Procedure is difficult for revision dur­ • This procedure allows adjustments
Disadvantages ing secondary surgical proced­ures. at the time of surgery (cut as you go)
• It results in a final horizontal scar on • Minimal amount of tissue is discar­
the lip
Millard Rotation Advancement ded
• Precise matching of the incisions on Repair • Places scar in anatomically correct
both the sides are essential for both The markings and technique of cleft lip position, i.e. scar line forms philtral
muscle and mucosa closure by Millard rotational advance­ ridge on cleft side
• Nostril sill is reinforced and built up
with this procedure
• Revision is easy at time of secondary
surgeries.

Disadvantages
• This technique is difficult to master,
especially in wide clefts
• Major bulk of lip segments is in center
and not on lower free border giving
pouting appearance in wide clefts
• Difficulty in obtaining adequate lip
length
A B • It has got a tendency toward vertical
Figs 24.31A and B: (A) Preoperative photograph for straight line repair of bilateral partial scar contracture
cleft lip; (B) Final closure photograph • It forms constricted nostril toward
the cleft side.

Delaire’s Philosophy to Repair


Cleft Lip and Palate
This philosophy given by Professor Jean
Delaire, who has developed philo­sophy
concerning the significance, rela­ tion­
ships and interactions of various struc­
tures from which he derived a rationale
for treatment of cleft lip and palate defor­
mities (Fig. 24.34). Accor­ding to him:
I II • Careful muscular reconstruction and
 Fig 24.32A: Marking for incisions and final suture line of a triangular flap alignment is key to good esthetics

I II III
Fig. 24.32B: Triangular flap technique
Introduction to Cleft Lip and Palate 513

I II III
Fig. 24.33A: Marking for incisions and final suture line of a Millard rotational flap technique (1. Deepest point of Cupid’s bow; 2. Highest
point of Cupid’s bow on noncleft side; 3 and 3′ High points of Cupid’s bow of cleft; 4 and 6′ Located at base of columella; x-Midpoint of
columella; 5 and 5′ Represents the alar base, 8 and 8′ Represents the corner of lip)

and function of the soft palate, lip


and nose.
• The concept of primary functional
cheilorhinoplasty is launched.
• Subperiosteal undermining of the
cleft-sided cheek is considered a pre­
requisite for tension free suturing of
the nasolabial musculature with the
extended subperiosteal undermining
I II of anterior maxilla, the nasal pyramid
and the lower orbital border.
• Hard palate closure is performed with
bipedicled flaps of only fibro­mucosa
of the palatal shelves, leaving the
maxillary fibromucosa untouched.
When the cleft is narrow, undermining
of the palatal fibro­mucosa and paring
of the edges is sufficient.
• The two stage closure of all wide
palatal flaps (soft palate first) and
III IV
the one stage closure of narrow
 Fig. 24.33B: Millard rotational flap technique

Fig. 24.34: Marking of Delaire technique for cleft lip (A. Upper corner of the noncleft
nostril; A′ Upper corner of the cleft nostril; B. Base of columella at the noncleft side;
C. Center line of the philtrum and of the future Cupid’s bow; D. peak of cupid’s bow at
the noncleft side; E. end of the mucocutaneous rim (white roll) on the lateral lip segment;
1. Landmark on the base of the columella on the cleft side, at a distance from the midline
that is equal to the distance from the midline to B (the line B-1 will be parallel to the line
A-A’); 2. landmark at which the continuation of the line; B-1 intersects the mucocutaneous
rim; 3. landmark on the mucocutaneous rim the distance of which from the midline of
the philtrum is just a little than that of the distance C-D (in fact, account must be taken
of the transverse retraction of the skin); 4. landmark on border between vermillion and the
wet mucosa, the distance of which to the median frenum is equal to the distance C-3; 5. base
of the nasal ala on the cleft side; 6. intersection of the mucocutaneous rim by a perpendicular
to it originating from landmark 5; 7. landmark of greatest vermillion height on the cleft
side, where the mucocutaneous rim begins to diminish (future lateral peak of cupid’s bow);
8. Landmark on the wet line, marked by the perpendicular to the muco­cutaneous rim
originating in landmark 7)
514 Facial Deformities

A B C

D E
Figs 24.35A to E: Push-back technique: (A) Preoperative photograph; (B) Freshening of edges and palatal incision; (C) Mobilization of
flap and closure of nasal layer; (D) Closure of palatal layer; (E) Healed palate

palatal clefts using the fibromucosa repositioning the levator muscle in a single nasal mucosa layer anteri­
of the palate shelves. a more favorable position. However, orly.
Closure of the soft palate at 7 months this modification involves extensive • von Langenbeck40 (Figs 24.36A
and the hard palate at 16 to 18 months. dissection. The superior pedicle is and B)
Hard palate repair can be postponed till divided leaving the mucoperiosteal • Two-flap palatoplasty (Bardach
the age of 3 years, if closure necessitates flap on either side of the cleft based and Salyers41) (Figs 24.37A to
the transposition of maxillary fibromu­ on the greater palatine pedicle pos­ D): Janusz Bardach in Poland first
cosa. teriorly. At the free anterior end, the described the two-flap palatoplasty
mucoperiosteal flaps can then be in 1967. The design of this flap is
Surgical Procedures of Cleft approximated directly or in a V-Y entirely dependent on the greater
Palate Repair closure to lengthen the soft palate. palatine neurovascular pedicle and
This modification allows more flap it provides greater versatility to cover
Hard Palate and Soft Palate advancement than the von Langen­ the cleft. In a complete unilateral
• Veau-Wardill-Kilner or VY push­ beck technique and enables poste­ cleft, the mucoperiosteal flap from
back palatoplasty (Figs 24.35A to E): rior lengthening of the palate, thus the medial segment can be shifted
Veau-Wardill-Kilner or V-Y push­ improving velopharyngeal com­ across the cleft and closed directly
back palatoplasty is derived from a petence. The Wardill-Kilner push­ behind the alveolar margin. The
modification of the von Langen­beck back palato­plasty offers significant fistula in the anterior hard palate
technique. It can be used to increase longterm improvement in speech can be virtually eliminated by this
the palatal length. The Veau-War­ in terms of nasality and nasalance technique. Two-flap palatoplasty
dill-Kilner pushback pala­to­plasty score. The pushback palatoplasty also has a minimal effect on sub­
can be suitably used for incomplete has several disadvantages. The de­ sequent maxillofacial growth due to
clefts of the hard palate. The flap nuded palatal bone from which the the limited area of bone denudation
design is similar to the von Langen­ mucoperiosteal flaps are raised ad­ on the hard palate when the muco­
beck palatoplasty. The essence of versely affects midfacial growth in periosteal flaps are elevated. The
this technique is the V to Y incision cleft palate patients. This technique limitation of this technique is that it
and closure on the hard palate. The also has a higher rate of fistula in does not provide additional length to
pushback technique has the advan­ complete cleft palate than other the repaired palate to allow normal
tage of lengthening the palate and techniques because it provides only speech production. A variation from
Introduction to Cleft Lip and Palate 515

I II III IV
Figs 24.36(A) I to IV: Technique of von Langenbeck procedure: (I) Marking of incision; (II) Flap raised; (III) Nasal layer closure; (IV) Oral
layer closure

I II III IV
Figs 24.36(B) I and IV: von Langenbeck procedure: (I) Cleft soft palate; (II) Incision; (III) Closure; (IV) Postoperative view

insu­­fficiency include retropositioning


and reor­ien­tation of the velar muscles
by performing either an intravelar
velopasty or Furlow double oppos­ing
Z palatoplasty.
• Vomer flaps: In 1926, Pichler intro­
duced the use of a vomer muco­ ­
peri­osteal flap for palatal clo­
sure. The original vomer flap was
A B inferiorly based. It was raised by
an incision made high on the nasal
septum and reflected downward
to provide a single-layer closure on
the oral side. This flap has a high
incidence of maxillary retrusion,
presumably from injury from
vomer-premaxillary sutures, and a
high fistula rate. However, similar
problems have not been commonly
found in a superiorly based vomer
C D flap. This technique involves reflect­
Figs 24.37A to D: Two-flap palatoplasty technique: (A) Preoperative; (B and C) Mobilization ing the mucosa from the septum
of flap; (D) Closure of nasal and oral layers close to the cleft margin with limited
dissection to allow adequate closure
the standard technique of two flap series to ascertain its applications. of the nasal mucosa on the opposite
palatoplasty has been reported using Nevertheless, the goal of palatal site. In a bilateral complete cleft
supraperiosteal flaps instead of the lengthen­ing in palatoplasty is still palate, a midline incision along the
mucoperiosteal technique for palatal con­sidered essential to reduce the free margin of vomer is required to
closure. Although this new approach space in the posterior pharyngeal create two septal-mucosal flaps in
improves speech outcome, it still wall. Presently, widely accepted opposite directions. These two flaps
requires further evaluation in a larger methods to reduce velopharyngeal are used to bridge the gap between
516 Facial Deformities

the free edges of the nasal mucosa.


The two-flap palatoplasty combined
with a vomer flap results in a four-
flap palatoplasty that can be applied
for simultaneous closure of the nasal
and oral defects in the cleft palate.
This technique results in a two layer
closure with a low fistula rate and less
maxillary growth retardation. The
long-term effect of this technique on
facial growth is minimal.
A

von Langenbeck Procedure


A simple palatal closure introduced by
von Langenbeck in 1859 is possibly the
oldest palatoplasty still widely used to­
day. The von Langenbeck palatoplasty is
commonly used for an incomplete cleft
of the secondary palate without the pres­
ence of a cleft lip and alveolus. This tech­
nique closes the incomplete cleft of the
hard and soft palates without lengthen­
ing the palate by mobilizing bipedicled
mucoperiosteal flaps medially. The cleft B
margins can be approximated with a lat­
eral relaxing incision that begins poste­
rior to the maxillary tuberosity and fol­
lows the posterior portion of the alveolar
ridge. Modifications of the von Langen­
beck technique include repair of the le­
vator palatini muscle and intravelar ve­
loplasty to reproduce the normal muscle
sling. von Langenbeck repair can also be
used in combination with a Furlow dou­
ble opposing Z-palatoplasty to increase
palatal length with minimal mucoperi­ C
osteal undermining. Advantage with this
technique is it does not leave any scar­
ring in the anterior palate region, which
Bardach’s method leaves, but disadvan­
tage with these techniques is they leave
denuded areas of palatal bone at the
lateral releasing incisions, midline longi­
tudinal scar with risk of contracture, ten­
dency towards anterior fistula formation
and little palatal lenghthening.

Two Flap Palatoplasty


Two flap palatoplasty technique is
D
shown in Figures 24.37A to D.
Figs 24.38A to D: Furlow’s technique: (A) Marking and incision; (B) Flap raised on one side;
Soft Palate Repair (C) Both sides flap raised; (D) Nasal layer closure and then final closure; (Source: Salyer and
• Double opposing Z-plasty (Furlow42) Bardach’s Atlas of Craniofacial and Cleft Surgery: Craniofacial Surgery, Vol. 1 by Kenneth E
(Figs 24.38 and 24.39) Salyer, Janusz Bardach)
Introduction to Cleft Lip and Palate 517

uvula muscle, but overall speech results Despite the extensive training pro­
are comparable to or better than those vided, up to 20 percent of patients still
with other techniques. Problems may be require pharyngoplasty to reduce VPI.
encountered when this technique is used
to close a very wide cleft palate, in which
the distance traversed by the Z-plasty
Orthodontic Treatment
may be excessive. Modification of this Presurgical orthodontics is done in
technique to overcome excessive tension cases, which has alveolar asymmetry
during closure involves extension of the especially in very wide cleft. Orthodontic
A
relaxing incisions anteriorly to the cleft treatment begins at the age of eruption
margin to create an island flap based of the permanent teeth. The final stage
on the palatine vessels. This maneuver of orthodontic treatment includes the
provides greater mobility and shifts the use of fixed appliances, which consist
closure to the side of the posteriorly of bonded brackets and full banded
based flap. Other ancillary procedures molars.
for tension free closure in a wide cleft
palate include a combination of Furlow Goals of Orthodontic Treatment
Z-palatoplasty with any of the following Stage
maneuvers: hard palate mucoperiosteal • To obtain an adequate arch form
undermining, careful dissection into the and alignment
B space of Ernst, infracture of the hamulus • To achieve the best occlusion and
Figs 24.39A and B: (A) Unilateral cleft or stretching of the greater palatine neuro­ function
palate; (B) Repair by Furlow’s technique vascular bundles. • To maintain or to improve the sag­
ittal and transverse relationship
• Intravelar veloplasty (Sommerland43) between arches
• Microscopic repair of cleft palate • To avoid or to correct cross-bites
Secondary Procedures
(Som­m­erland44) • To prepare for orthognathic surgery
if needed or receive a prosthetic res­
Speech Therapy toration.
Furlow Double Opposing
Adequate speech usually requires spe­
Z-palatoplasty
ech therapy and the speech patho­logist Prosthetic Considerations
Furlow technique is shown in Figures sees the child frequently until age seven. • Absence of lateral incisor in the cleft
24.38A to D. In 1978, Leonard T. Furlow area is common, prosthetic restor­
Jr. unofficially introduced the double Factors Addressed by the ation of the tooth in the treatment
opposing Z-palatoplasty and much of Speech-Language Pathologist plan should be included.
his work was later published in 1986. • Feeding • Transpalatal retainer with an acry­
This technique involves alternating the • Hearing lic tooth can be used to aid in
reversing Z-plasties of the nasal and oral • Cognitive ability maintaining the surgical result and
flaps and repositioning the levator veli • Development provide a better dental appearance.
palatini muscle within the posteriorly • Language • If desired, fixed prosthetic appliance
mobilized flaps. With this technique, there • Articulation can be used 6 months after surgery
is no need to raise large mucoperiosteal • Velopharyngeal function. (Figs 24.40A and B).
flaps from the hard palate. At the same • A four-unit fixed bridge can be used,
time, the soft palate can be lengthened Factors Affecting Speech but an implant-borne prosthesis
within the substance of the soft palate Impairment in Patients with in a bone grafted alveolus gives
together with palatal muscle reorientation. Cleft Lip and Palate the best result. Bone grafting of the
This technique has shown early success • Articulation errors alveolar cleft in cases in which the
in both speech outcomes and midfacial • Velopharyngeal insufficiency (VPI) lateral incisor is missing should be
skeletal growth. Furlow Z-palatoplasty leading to: performed with the aim of providing
is effective for primary closure of a – Resonance enough bone for a dental implant.
submucous cleft palate and secondary – Nasal air emission
correction of marginal velopharyngeal – Low oral pressure
insufficiency. Palatal closure in Furlow • Hearing loss
Alveolar Bone Grafting
Z-palatoplasty is not anatomic and • Malocclusion Alveolar bone grafting is to reconstruct
completely ignores the small longitudinal • Nasal obstruction. cleft alveolus with bone grafts. This
518 Facial Deformities

• Poor speech
• Missing or extra teeth in cleft area
• Lack of support for alar base, colu­
mella and lip.

Aims of Alveolar Bone Grafting


• To restore physiological continuity
of dental arch to enable oral and
dental health to be maintained
• To provide bone for stability of
dental arch, to allow eruption of
unerupted teeth or placement of
implant
• To allow orthodontic alignment of
teeth
• To provide support for lip and nose
and to close persistent oronasal fis­
A B
tula.
Figs 24.40A and B: Fixed prosthetic appliance for the missing lateral incisor: (A) Pre-
treatment: (B) Post-treatment Procedure (Figs 24.41A to F)
Before bone grafting, radiographs
method popularized by Abyholm45 in Problems Faced by Patients should be taken to evaluate the status of
1981. In literature bone grafting was Having Cleft Alveolus the canine and lateral incisor, if present.
done in 1901 by Von Eiselberg46 who This is well visualized using a panoramic
used pedicled bone to fill the alveolus, Problems faced by patients having cleft tomogram, periapical radiographs of
in 1908 Lexer47 tried using free bone alveolus are as follows: the cleft side and a occlusal view of
grafts. By 1950’s bone grafting was well • Patient may complain of food/fluid anterior maxilla. Bone grafting is mostly
accepted was performed routinely regurgitation from nose performed at approximately one-half
before patient’s first birthday. Rib grafts • An inability to blow balloon or suck to two-thirds root development of the
were used to fill the defects. But by 1960’s a straw tooth about to erupt into the cleft side.
there was evidence that primary bone • A persistent smell and discharge Mostly iliac crest grfats are used
grafting is hampering facial growth due from their nose as adequate cancellous bone can be
to dissection around vomeromaxillary
suture, which is pri­ marly midfacial
growth center. Then it was cosidered
that secondary bone-grafting during
mixed dentition period is preferable and
prefered sites for bone-grafting are iliac
crest and tibia as rib grafts were too dense
hence erruption of tooth was delayed.
In wide clefts corticocancellous bone
grafts are preferred. Overcorrection A B C
with cancellous bone graft is done since
25 percent of bone graft gets resorbed
after surgery. Calvarial grafts has been
recommended by some as an alternative
to iliac crest grafting. However success
rate of calvarial graft is not better than
iliac crest graft, as bone grafts consisting
of diploic bone have shown to be more D E F
successful, than those grafts harvested Figs 24.41A to F: Alveolar bone grafting: (A) Preoperative photograph; (B) Nasal layer
using a high speed rotary device to closed and recipient site for graft prepared; (C) Exposure illiac crest; (D) Bone graft
shave off primarily cortical bone from placement into the alveolar defect; (E) Closure of surgical site after graft placement;
the surface of the calvaria. (F) Erruption of canine through the grafted bone
Introduction to Cleft Lip and Palate 519

harvested from this site. In children • Limping, while walking due to injury proximation of tissues. The oral layer of
under the age of 9 to 10, cancellous to lateral cutaneous nerve of thigh soft palate is closed, resulting in large
bone is not as much in quantity as in and improper closure of scarpa’s portion of coverage of soft palate. This
adults since apophysis of iliac crest is fascia can occur. will prevent shrinkage of pharyngeal
still largely cartilagenous. The first step • Hematoma formation if inner corti­ flap and change in size of lateral ports
requires development of full thickness cal table perforates during harvest­ (Figs 24.42 and 24.43).
muco­periosteal buccal flaps. After the ing. Patient may present later with
soft tissue flaps are developed by giving comp­ laints like inability to stand Distraction Osteogenesis
incisions on alveolus and palatal and and walk, pain at donor site and on Distraction osteogenesis (DO) (Figs
nasal linings are mobilized. The nasal examination patient may have per­ 24.44A to D) was propagated by llizarov
lining is sutured to provide base for the sistent tachy­cardia with features of for orthopedic surgeries and populari­
graft. Then bone graft is harvested from anemia. zed for correction of the craniofacial
iliac crest site by giving either a medial • There can be unsightly scar and con­ ske­ leton in the early 1990s. McCar­
or an incision just lateral to the anterior tour abnormalities. thy et al. reported using distraction to
iliac crest spine, as it cannot be given on All these complications can be re­ leng­then the mandible in patients with
bony prominence of iliac crest spine, duced by practicing meticulous surgical hemifacial microsomia.49 Figueroa and
keeping in mind that lateral cutaneous technique. Polley50 reported success with no signi­
nerve is present 1 cm lateral to the iliac ficant complications when DO was used
crest spine. If any damage to the nerve, Pharyngoplasty to advance the maxilla in children with
it can lead to complications in future. The success of palatoplasty is measured cleft lip and palate. Recently, DO was
The graft is harvested from the iliac primarily by quality of speech. Nasality used to advance the maxilla in patients
crest donor site by trap door technique of voice requires further surgical inter­ with cleft palate. A well-known modal­
in which both cortical plates are kept vention to improve the function of velo­ ity is surgically assisted maxillary expan­
intact. If any perforation of inner cortical pharyngeal sphincter, which is formed sion in adults that transversely distracts
plate occurs it leads to hematoma by muscles of soft palate and by supe­ the hard palate through the midpalatal
formation. The cancellous bone is rior constrictor muscle of pharynx. The suture. This technique reduces the com­
harvested using bone gouge. After inability of velopharyngeal sphincter plications of rapid maxillary expansion,
achieving the hemostasis, the donor site to separate the oropharynx from naso­ which relies on tooth abutments alone
is sutured in layers. During donor site pharynx results in hypernasality and with­out surgical assistance and can re­
closure scarpa’s fascia (deep thick fascia nasal air emission. Speech assessment sult in gingival recession, ankylosis, and
at iliac crest) should be closed carefully by speech pathologist, nasal endoscopy root resorption. The scarred tissue in
as it provides airtight closure, better and air flow studies are used to deter­ repaired palate limits the advancement
protection and aids in preventing pain mine the necessity of performing pha­ of the osteotomized maxilla and tends
and limping. The cancellous bone graft ryngoplasty. The main aim of pharyngo­ to pull them pack after the advance­
is packed in the cleft alveolus defect and plasty is speech improvement. ment leading to relapse. With the use
the palatal layer is also closed. The most commonly practiced tech­ of distraction osteogenesis in such, this
nique for pharyngoplasty is Hogan’s48 problem is avoided. The distractors can
Complications (1973). The soft palate is split in the be either extraoral or intraoral distr­actor
Complications, which can occur after midline. A suture is inserted for better (Figs 24.45 and 24.46).
surgery at the cleft site are: visualization of posterior pharyngeal
• There can be persistent bleeding wall. The incision is carried on posterior Orthognathic Surgery
and pain. wall of pharynx to create a superiorly The correction of maxillary hypoplasia
• Low-grade infections, which can based flap. The flap is raised over nasal is achieved by the orthognathic surgery.
leads to wound breakage or bone loss. surface of soft palate and it is dissected Indications for the orthognathic surgery
• Any injury to adjacent teeth. and turned upwards. Pharyngeal flap in the cleft patients are:
The donor site complications after is sutured to the edges of soft palate on • Concave profile after repair of a cleft
surgery are: nasal side. Mucosal flap is raised on na­ lip and palate.
• There can be persistent pain at the site. sal surface of soft palate is used to close • Disproportion between middle and
• Any neurological complications can raw surface at its base. Superiorly based lower thirds of the face.
occur such as loss of cutaneous pharyngeal flap is closed at nasal surface • Underdevelopment of the maxilla
sensations due to injury to lateral of soft palate, mucosal flap raised on na­ and relatively greater growth of the
cutaneous nerve. It also can leads sal side of soft palate is used to close the mandible.
to neuroma formation at the site of defect at its base. Defect on posterior • It has been estimated that 25 to
nerve injury and painful scar. pharyngeal wall is closed by simple ap­ 60 percent of all patients born with
520 Facial Deformities

A B C D

E F G H
Figs 24.42A to H: Pharyngoplasty technique: (A) Incision on posterior wall of pharynx; (B and C) Soft palate flaps raised; (D) Pharyngeal
flap sutured at nasal layer of soft palate; (E) Pharyngeal defect is closed; (F to H) Closure of soft palate (Source: Salyer and Bardach’s Atlas
of Craniofacial and Cleft Surgery: Craniofacial Surgery, Vol. 1 by Kenneth E Salyer, Janusz Bardach)

A B C
Figs 24.43A to C: Pharyngoplasty technique: (A) Preoperative; (B) Intraoperative; (C) Postoperative views

complete unilateral cleft lip and pal­ osteotomy is seldom needed, However, alveolar bone grafting before planning
ate require maxillary advancement to in cases of significant deformity, high for ortho­gnathic surgery. If for some
correct the maxillary hypoplasia and Le-Fort I osteotomy could be required reason, alveolar bone grafting was not
improve esthetic facial proportions. to correct concave facial deformity. done, then it can be done in the same
• Genial osteotomies surgery when orthognathic surgery is
Timing of Surgery planned, but this should be avoided.
It is prudent to delay surgery until com­ Osteotomies for cleft patients
(Figs 24.47 and 24.48) Use of Bone Grafts in Midface
plete maturation is achieved. Delaying
surgery until the canine and second Because the skeleton is always asymme­ Advancement
molars have erupted minimizes the risk trical in cleft patients, osteotomy design • The bone graft can be wedged into
of injury to the teeth during osteotomy.
is important for maximum improvement the defects in the lateral maxil­lary
of esthetics. The osteotomy cuts may walls after the maxillary advance­
Procedures require modifications and may not be ment, which helps maintain the
Maxillary osteotomy at Le-Fort I level symmetrical and are based on the need posi­
tion of the maxilla during
is usually adequate and the Le-Fort II of individual case. It is advisable to do heal­­ing.
Introduction to Cleft Lip and Palate 521

A B

C D
Figs 24.44A to D: (A) Preoperative frontal and profile views; (B) Osteotomy cut; (C) Postoperative frontal and profile views;
(D) Prelateral and postlateral ceph X-rays

A B C D
Figs 24.45A to D: Extraoral distractor components

• The bone graft also encourages bone the treatment if needed should be
healing and reduces the risks of the given. Palatal fistula if present should
fibrous union. be repaired as per the demand and
• The third use of bone grafts in requirement of the patient. The patient
midface advancement is to contour should not be encouraged to undergo
the middle face. surgery for fistula unless the patient is
having problem like nasal regurgitation,
speech problems, etc.
Palatal Fistula
The operated cases of palate should Techniques of Fistula Repair
be examined after 1 year of surgery for • Local tissue flaps (Figs 24.49A to D)
presence of any palatal fistula due to • Tongue flaps (Figs 24.50A and B)
break down of the palatal repair and • Extraoral flaps.
Fig. 24.46: Intraoral distractors
522 Facial Deformities

A B C
Figs 24.47A to C: Osteotomies for cleft palate

• Interpositional grafts.
• Buccal fat pad (Figs 24.51A to C)
• Local tissue flap from the adjacent
site of the palate can be used to close
the fistula.
• The pedicled tongue flap is widely
used to close the palatal fistula.
After the closure of the fistula the
division of the tongue flap is done on
postoperative 21st day.
• Buccal fat pad can also used intraop­
eratively by placing the buccal fat pad
in between the deficient nasal layer
and the oral layer in cases of wide cleft
to avoid fistula formation in future.
A B
Figs 24.48A and B: Lateral cephalometric X-ray: (A) Preoperative; (B) 6 months postoperative Scar Revision of the
Cleft Lip
Surgical intervention to revise scar in CL
must be based on complete analysis of
the problem. Evaluating lip deformities
should take into account ethnic varia­
tions, original deformity and previous
surgical method of primary repair.

Evaluation of Postsurgical Lip


A B Deformities
Wilson51 (1985) looked at six different
aspects of the lip:
• Amount of lip tissue present post
surgically.
• Freedom of movement of upper lip.
• Equality of bulk over complete len­
gth of lip.
• Cupid’s bow position and presence
of all components.
C D • Width of philtrum, direction of scars,
Figs 24.49A to D: (A) Preoperative photograph of fistula; (B) Palatal flap raised; (C) Palatal and relocation of philtral ridges.
flap rotated and sutured to close the fistula; (D) Postoperative photograph • Alignment of circumoral muscles.
Introduction to Cleft Lip and Palate 523

Figs 24.50A and B: (A) Anterior palatal


A B fistula; (B) Tongue flap to close the fistula

A B C
Figs 24.51A to C: (A) Buccal fat pad to close palatal fistula; (B) Harvesting of the BFP; (C) BFP used to close the fistula

Then in 2002, and Doonquah and


Ogle52 evaluated various deformities of
lip present postsurgically under follow­
ing categories:
• Lip volume defects
• Mobility defects
A
• Lip architectural deficiencies.
B

Procedures for Lip Scar Revision


Various procedures commonly prac­
ticed for scar revision are:
• V-Y advancement flap: This tech­
nique is routinely practiced for C D
correc­ting vermillion deficiencies or Figs 24.52A to D: V-Y advancement to recruit tissue into the areas of vermilion
defo­rmities. The deformity can be a deficiency (Source: TB of Plastic Surgery Vol. 4 by Joseph G McCarthy)
mis­match of the vermillion margins,
vertical notching deformity or ab­ • Z-plasty: The Z plasty technique is flap (Figs 24.56A and B). The cross
sent vermillion ridge. In cases of usually carried out for correction of flap was initially described by Sab­
bilateral cleft lip, the classic ‘whistle minor misalignment of the vermi­ batini (1838) and was subsequently
deformity’ or central notching defect lion border or step deformities of modified by Estlander (1872) and
of vermilion is common (Figs 24.52 vermilion (Figs 24.55A to C). Abbe (1898). The flap is basically a
and 24.53). This technique can also • Abbe flap: Correction of marked composite transfer of skin, muscle
be used for lengthening of the short horizontal deficiencies with gross lip and mucosa based on a pedicle con­
bilateral lip (Figs 24.54A to C). disproportion may require an Abbe taining the labial vessels. There is
524 Facial Deformities

A B C
Figs 24.53A to C: (A) Marking for V-Y advancement; (B) Mucosal flap raised; (C) Closure done recruit tissue into the areas of
vermilion deficiency

A B C
Figs 24.54A to C: Lengthening of the short bilateral lip with a V-Y procedure: (A) The design of the incisions enables lengthening of the
midportion of the lip and narrowing of the alar bases; (B) Incisions are carried through all lip layers and a hook is inserted at the midline
to pull the lip inferiorly, lengthening the midportion and approximating the lateral lip elements; (C) Completed procedure

A B C
Figs 24.55A to C: (A) Z-plasty for correction of step deformity of vermilion border; (B) Preoperative; (C) Postoperative views
(Source: L Doonquah, OE Ogle/Oral Maxillofacial Surg Clin N Am 2002;14:425-37)

180° rotation of flap and always bet­ there is gross deficiency of the tissue
ter to make a triangular flap, as it has for undertaking repair. Rhinoplasty
a advantage of closer apposition to • Kapetansky-Juri advancement flaps:
the upper lip orbicularis oris mus­ This technique is used to create a For many cosmetic surgeons rhinoplasty
cle superiorly. It is more commonly central lip tubercle by over-rotation is one of the most challenging surgical
practiced in the management of bi­ of the pendulum flaps on both sides procedures. A clear understanding of
lateral cleft lip deformities, where in the midline (Figs 24.57A and B). nasal anatomy is critical in order to
Introduction to Cleft Lip and Palate 525

A B(i)

Figs 24.56A and B: (A) Abbe flap is used


for lip volume defects in which cross-lip
transfer is done. Flap is divided after 3
weeks postoperative approximately; (B)
Abbe flap is used for replacement of the
midline vermilion defect. Flap is divided
B(ii) B(iii) after approximately 3 weeks postoperative

Fig. 24.57A: Kapetansky-Juri advancement


flap (design and suturing) for cupid’s bow
A(i) A(ii) correction

provide an esthetic result that does not growth of septal and nasal cartilage
Objectives Of
compromise nasal function. Numerous is over. In this procedure septal
rhinoplasty techniques have been des­ cartilage is repaired. Corrective Surgery
cr­ibed. Rhino­plasty can be: The various nasal deformities, • To restore the symmetry of alar
• Primary rhinoplasty: It is done at which can be seen in cleft patients cartilages.
the time of lip repair in this lower are: • To produce a cosmetically accept­
lateral cartilage is repaired. • Slumping of lower lateral cartilage able nose and a harmonious rela­
• Secondary rhinoplasty: It is done • Lateral vestibular webbing tionship between the repaired lip
after age of 15 years till that time • Laterally displayed alar base. and the nose.
526 Facial Deformities

• To create a nasal sill, nasal floor and


columella of equal size on both sides.
• To produce an ala without flare and
a vestibule without webbing.

Procedures
The various procedures, which can be
performed for above listed deformities
are as follows:
• Correction of narrow nostril floor:
B(i) B(ii)
Narrow nostril floor is commonly
seen in operated cleft lip patients
which can be corrected as shown by
Figures 24.58A and B.
• Correction of wide flaring nostril:
Similarly wide flaring nostrils also is
a common finding in operated cleft
lip patients when primary rhino­
plasty is not done at the time of
cleft lip surgery, it can be corrected
B(iii) B(iv) using technique as shown by Figures
Fig. 24.57B: (i) Preoperative view with midline vermilion defect; (ii) Design for the 24.59A and B.
Kapetansky-Juri advancement flap; (iii) Closure; (iv) Postoperative view • Correction of webbing: Webbing
is projection of fold that can either
be skin or mucosa, which causes
obstruction of the opening. It can
be corrected using techniques as
shown by Figures 24.60A to C.
• Columella lengthening: The colu­
mella may need lengthening using
one of the many methods described
in Figures 24.61 to 24.63.
Composite grafts are also used for
correction of nasal deformities. These
A B
composite grafts are combination
of skin and cartilage taken from ear
(Figs 24.64A and B). This graft is then
Figs 24.58A and B: Design of flap taken from the area lateral to the ala and transposed
into floor of the vestibule of nose added to the inside of nose to help
correct retracted or notched ala. In
simpler terms, the nostrils may pull up
following rhinoplasty surgery, which
will reveal the nostril openings and
show too much of the columella. This
is a common finding in revision or
secondary rhinoplasty surgery. Once
the graft is taken from the ear, either
the defect (area where the skin/cartilage
has been removed) is stitched together
(Fig. 24.64C) or in some cases a piece
of skin (full thickness skin graft) is
taken from behind the ear and then
A B
placed in the defect (Fig. 24.64D) where
Figs 24.59A and B: Correction of the wide flaring nostrils: (A) Flap is raised from the floor composite graft was removed. This
of the nasal vestibule. An incision frees the alar base; (B) The alar base flap is rotated and usually heals with minimal to no visible
sutured at floor of the nasal vestibule
Introduction to Cleft Lip and Palate 527

A B C
Figs 24.60A to C: (A) Z-plasty; (B) V-Y advancement; (C) Medial advancement.
A full-thickness skin graft is placed in the resulting lateral defect

C
Figs 24.61A to C: Various methods for columella lengthening: (A) Diamond-sha­ped excision;
(B) V-Y advancement of the tip; (C) Bilateral alar wing flap
528 Facial Deformities

A B C

Figs 24.62A to E: Correction of depressed


nose: (A and B) Preoperative photograph;
(C) Intraoperative photograph showing cartil­
D E age repair; (D and E) Postoperative photograph

A B

C D
Figs 24.63A to D: (A) Preoperative frontal photograph; (B) Postoperative frontal photograph;
(C) Preoperative worms view; (D) Postoperative worms view
Introduction to Cleft Lip and Palate 529

A B C

D E
Figs 24.64A to E: (A) Composite graft taken from left ear; (B) Composite grafts; (C) Graft site stitched together; (D) Full thickness skin
graft inserted into defect; (E) Behind ear where full thickness skin graft is harvested (Source: www.rhinoplasty specialist.com)

scar (Fig. 24.64E). The graft is inserted 2. Carolus JMF. La chirurgie de Maitre talen Gaumenüberzuges. Arch Klin
into the nostril and with time, will Jean Yperman. F and E. Gyselynck, Chir. 1861;2:205.
heal and becomes part of ala/nostril. Gand; 1954. 13. Stanier P, Moore GE. Genetics of cleft
Occasionally, the graft can become 3. Blair VP, Brown JB. Mirault operation lip and palate: syndromic genes con­
swollen up to approximately 3 months for single harelip. Surg Gynec Obstet. tribute to the incidence of non-syn­
and there is a small risk that the graft will 1930;51:81-98. dromic clefts. Hum Mol Genet 13. (Re­
not survive. 4. Hagedorn, M. Uber eine Modification view Issue Number 1): R73-R81.2004
der Hasen schartenoperation. Zhl Chir. 14. Ferguson MW. The mechanism of pala­
1884;11.756. tal shelf elevation and the pathogenesis
Conclusion
5. Tennison CW. The repair of unilateral of cleft palate. Virchows Arch A Pathol
Cleft lip and palate is not a cosmetic cleft lip by stencil method. Plast Anat Histol. 1977; 375(2):97-113.
surgery and it is moreover a functional Reconstr Surg. 1952;9:115-120. 15. Zingade ND. The prevalence of oto­
repair. Religious counseling of parents 6. Millard DR Jr. A radical rotation in logical manifestations in children with
for regular follow-up, good relation single harelip. Am J Surg. 1958;95:318. cleft palate. Indian Journal of Otolar­
between surgeon and parent, timing of 7. Franco P. Traite des Hernies. Lyon, yngology and Head and Neck Surgery.
surgery and support from other faculty Thibauld Payan; 1561. 2009;61(3):218-22.
is very important for a team approach 8. von Graefe CF, Bericht über die erste 16. Bonaiti-Pellié C, Smith C. Risk tables
for better life of the child. Basically now Staphyloplastik, Hufeland’s Journal 44 for genetic counselling in some com­
it is an era when we can have isolated (1817), p. 116. mon congenital malformations. J Med
clinics for cleft lip and palate because it 9. Stephenson J. Repair of cleft palate by Genet. 1974;11:374-7. PMID:4613831.
is one deformity, which can be corrected Philibert Roux in 1819. Plast Reconstr 17. Lammer EJ, Shaw GM, Iovannisci DM, et
to a level so that there is no postsurgical Surg. 1971 Mar;47(3):277-83. al. Maternal smoking and the risk of oro­
morbidity and deficiency. 10. Dieffenbach, J. F. Uber das Gaumensegel facial clefts: Susceptibility with NAT1 and
des Menschen und der Saeugethiere. NAT2 polymorphisms. Epi­de­­miology.
Litt Ann d ges Heilk. 1826. 2004; 15(2):150-156. Ref ID: 263.
References
11. von Langenbeck B. Beitraege zur 18. Shaw GM, Lammer EJ. Maternal peri­
1. Boo-Chai K. An ancient Chinese text Osteoplastic. Deutsch Klin. 1859;2:471. conceptional alcohol consumption
on a cleft lip. Plast Reconstr Surg. 12. Von Langenbeck B. Die Uranoplastik and risk for orofacial clefts. Journal of
1966;38(2):89-91. Mittels Abl�sung des Mukös-perios­ Pediatrics. 1999;134(3):298-303.
530 Facial Deformities

19. Park-Wyllie L, Mazzotta P, Pastuszak 31. Grayson BH, Santiago PE, Brecht LE. 44. Sommerlad BC. The use of the opera­
A, et al. Birth defects after maternal Presurgical nasoalveolar molding in ting microscope for cleft palate repair
exposure to corticosteroids. Teratology. infants with cleft lip and palate. Cleft and pharyngoplasty. Plast Reconstr
2000;62:385-92. Palate Craniofac J. 1999;36(6):486-98. Surg. 2003;112(6):1540-1.
20. Puhó EH. Drug treatment during pre­ 32. Gillies H, Millard DR. The Principles 45. Åbyholm F, Bergland O, Semb G. Sec­
gnancy and isolated orofacial clefts and Art of Plastic Surgery. Vol. 1. ondary bone grafting of alveolar clefts.
in hungary. Cleft Palate Cran­iofac J. Boston:Little, Brown and Co.; 1957. Scandinavian Journal of Plastic and Re­
2007;44(2):194-202. PMID: 17328645. 33. Rose W. On Harelip and Cleft Palate. constructive Surgery. 1981;15:127–40.
21. Darab DJ. Pathogenesis of median fa­ London: HK Lewis, 1891. 46. von Eiselberg F. Zur Technic der Urano­
cial clefts in mice treated with metho­ 34. Thompson JE. An artistic and math­ plastik. Archiv Klin Chir. 1901;64: 509-29.
trexate. Teratology. 1987:36:77-86. ematically accurate method of repair­ 47. Lexer E. Die Verwendung der frien
22. Hernández-Díaz S. Folic acid anta­go­ ing the defect incases of harelip. Surg knochenplastic nebst versuchen uber
nists during pregnancy and the risk Gynecol. Obstet. 1912;14:498. gelenkversteifung and gelenktransplan­
of birth defects. N Engl J Med. 2000; 35. Le Mesurier AB. A Quadrilateral Mi­ tation. Arch Klin Chir. 1908;86:939-43.
343(22):1608-14. PMID: 11096168. rault flap operation for harelip. Plast 48. Hogan VM. A clarification of the
23. Davis JS, Ritchie HP. Classification of and Reconstruct Surg. 1955;16:422. surgical goals in cleft palate speech
congenital clefts of the lip and palate. 36. Tennison CW, The repair of unilateral and the introduction of the lateral port
Journal of the American Medical cleft lip by the stencil method. Plast control (LPC) pharyngeal flap. Cleft
Association. 1922;79:1324. Reconstr Surg. 1952;9:115. Palate J. 1973;10:331.
24. Veau V, Borei S. Division Palatine, Ana­ 37. Randall P. A triangular flap operation 49. Hollier LH, Kim JH, Grayson B, et al.
tomie, Chi rurgie, Phonétique. Paris: for primary repair of unilateral clefts Mandibular growth after distraction in
Masson; 1931. of the lip. Plast Reconstr Surg. 1959; patients under 48 months of age. Plast
25. Fogh-Andersen P. Inheritance of 24:331-47. Reconstr Surg. 1999;103:1361-70.
Harelip and Cleft Palate. Copenhagen: 38. Millard DR. A radical rotation in single 50. Figueroa AA, Polley JW, Ko EW. Maxil­
Arnold Busck; 1942. harelip. Am J Surg. 1958;95:318. lary distraction for the management of
26. Kernahan DA, Stark RB. A New Classi­ 39. Markus AF, Delaire J. Functional pri­ cleft maxillary hypoplasia with a rigid
fication for Cleft Lip and Palate. Plast mary closure of cleft lip. Br J Oral Maxi­ external distraction system. Seminars
reconstr Surg. 1958;22:435. llo­fac Surg. 1993;31:281. in Orthodontics. Distraction Osteogen­
27. Kernahan DA. The striped Y: A symbolic 40. Von Langenbeck B. Die uranoplastik esis. 1999;5(1):46-51.
classification of cleft lips and palates. mittels ablosung des mukos-perio­ 51. Wilson LF. Correction of residual de­
Plast Reconstr Surg. 1971;47:469. stalen Gaumenuberzuges. Arch Klin formities of the lip and nose in repaired
28. Balakrishnan C. Indian classification Chir. 1861;2:205. clefts of the primary palate (lip and
of cleft lip and palate. Ind J Plast Surg. 41. Bardach J, Salyer KE (Eds). Surgical alveolus). Clin Plast Surg. 1985;12(4):
1975;8:23-4. techniques in cleft lip and palate. 2nd 719-33.
29. Tessier P. Anatomical classification of edn. St Louis, Mosby Year Book, 1991. 52. Doonquah L, Ogle OE. Scar revision of
facial, cranio-facial and latero-facial 42. Furlow LT. Cleft palate repair by double the cleft lip. Oral Maxillofac Surg Clin
clefts. J Maxillo-Facial Surg. 1976;4:69. opposing Z-plasty. Plast Reconstr Surg. North Am. 2002;14(4):425-37.
30. Benacerraf BRMD. Fetal cleft lip and 1986;78:724–36.
palate: sonographic diagnosis and 43. Sommerlad BC. A technique for cleft
post­natal outcome. Plast Reconstr palate repair. Plast Reconstr Surg.
Surg. 1993;92:1045-51. 2003;112(6):1542-8.
25 Orthognathic Surgery
Borle Rajiv M, Bhola Nitin, Vibhute Pawan J

tissue deformities of the jaws and asso­ did it for the removal of nasopharyngeal
INTRODUCTION ciated structures. polyps. Cheever3 in 1867 did first
The word orthognathic comes from maxillary osteotomy for correc­ tion of
The facial deformity caused by asym­ the Greek word ‘Ortho’ meaning to com­plete nasal obstru­ction secondary
metry has long been of great mutual straighten and ‘Gnathia’, meaning jaw. to recurrent epistaxis for which right
interest to the orthodontist and the Orthognathic surgery thus, means to hemi­­maxillary down fracture was used,
oral and maxillofacial surgeon. The straighten a jaw. this was the first maxillary osteotomy
deformities of maxillofacial region are reported in America. In 1897, Blair
readily expressed as a profile disfig­ perfor­med ost­e­o­­­­tomy of the mandibular
urement, since the soft tissues of the face HISTORICAL ASPECTS body (St. Louis operation). In 1907, he
depend on the jaws for their contour. described several operative techniques
The selection of the proper type and site Hullihen1 in 1849 performed the first for the corr­ ection of maxillofacial
of osteotomies in orth­­o­gnathic surgery anterior mandibular osteotomy in USA defor­mities.4 Wass­mund5 in 1927 first
is based on the extent of the dentofacial for the patient of distortion of face due described LeFort I osteotomy for the
deformity, the degree of the desirable to severe burns. The first description of correction of midface deformities. How­
jaw movement and the anticipated Orthognathic surgery (Box 25.1) of the ever, total mobilization of the maxilla
soft tissue changes following surgical maxilla documented in the liter­ature in with imme­diate repositioning was per­
inter­ vention. Clinically, deformities 1859 is credited to Von Lan­genbeck.2 He formed in 1934 by Axhausen.6
of the middle and lower third of face
range from simple dentoalveolar dis­
cre­­
pancy (malocclusion) to severe Box 25.1: History of orthognathic surgery
facial asymmetry and disfigurement.
1921 : Cohn Stock7 : Anterior maxillary osteotomies (Two stage)
Facial disfigurement causes social em­
1935 : Wassmund : One stage anterior maxillary osteotomy.
b­ar­r­­assment and often results in com­
promised masticatory and speech fun­c­ 1952 : Converse8 : Step osteotomy of the mandibular body for the correction of mandi­
bular prognathism.
tion. Furthermore, it often has a severe
1954 : Caldwell- Letterman9 : Vertical subsigmoid osteotomy of ramus.
impact on the patient’s self-esteem and
1955 : Schuchhardt10 : Developed posterior maxillary osteotomy.
jeopardizes his or her quality of life.
1955 : Obwegeser11 : Intraoral sagittal split of the mandible.
1958 : Dalpont12 : Modified intraoral sagittal split technique.
DEFINITION 1959 : Kole13 : First to describe bimaxillary surgery for the correction of bimaxillary protr­
usion. Proposed surgeries for open bite closure and for genioplasty procedures.
Orthognathic surgery is the art and sci­
1968 : Hunsuck14 : Further modified sagittal split osteotomy.
ence of diagnosis, treatment plann­
1969 : Obwegeser : Presented a large series of Le Fort I osteotomy.
ing and execution of treatment by
1970 : Obwegeser : Two jaw surgery.
combining orthodontics and oral and
1974 : Spiessl : First to apply rigid fixation in orthognathic surgery.
maxillofacial surgery to correct mus­
1979 : Luhr : Introduced the miniplate fixation in orthognathic surgery.
culoskeletal, den­to-osseous and soft
532 Facial Deformities

may not be present depending on • Hemifacial hypertrophy


CLASSIFICATION OF FACIAL
any compensatory growth in the • Neurofibromatosis (von Reckling­
DEFORMITIES maxilla which may or may not have hausen’s disease).
occurred.
Maxillary Deformities • Chin deformities: The deformities Midface deficiencies
• Maxillary anteroposterior (AP) of the chin are often associated with • Craniosynostoses
excess: Protrusive maxilla where other mandibular deformities. • Apert’s syndrome
there is an overgrowth in an anterior • Macrogenia: Overgrowth of chin in • Crouzon’s syndrome
horizontal direction. There is often vertical or anterior direction. • Pfeifer syndrome
a class II molar relationship, some­ • Microgenia: Chin deficiency in ver­ • Binder’s syndrome
times combined with mandi­ bular ti­cal and/or anterior direction. • Achondroplasia dwarf
protrusion (bimaxillary pro­tru­sion). • Cleidocranial dysplasia.
• Maxillary AP deficiency: Inad­ Short Face Syndrome
equate growth of the maxilla in an • Brachy facial: It is a deficient lo­wer Mandibular deficiencies
anterior direction with a class III facial growth in the vertical dim­ • Pierre Robin sequence
malocclusion. ension. It is often associated with low • Treacher-Collins syndrome (oto­
• Vertical maxillary excess: Over­ mandibular and occlusal plane angles. mandibulofacial dysostosis)
growth of the maxillary alveolus in Usually there is Class II malocclusion • Hemifacial microsomia (Goldenhar
the inferior direction, creating excess with mandibular AP deficiency, but it syndrome).
teeth and gingival display and often is sometimes combined with vertical
associated with an incompetent lip maxillary defi­ci­ency. Mandibular prognathism
seal, without mentalis muscle strain. • Long face syndrome: Dolicofacial— • Gorlin-Goltz syndrome
• Vertical maxillary deficiency: Ede­ there is excess of lower facial height • Osteogenesis imperfacta
n­tulous appearance showing no usually associated with increased • Marfan syndrome
teeth, often combined with a deep occlusal and mandibular plane an­ • Klinefelter syndrome.
bite in the mandible and prominent gles. There is often a combination of
‘chin button’ and a short lower face. vertical maxillary excess and man­ PATIENT EVALUATION
• Alveolar clefts: The alveolar defects dibular hypoplasia.
usu­ally present with maxillary • Apertognathia: It is characterized
AND PLANNING
con­­
striction in AP and transverse by anterior open bite. It is associated
dim­ensions. The defects are more with long face syndrome or simply General Patient Evaluation
pronounced in the patient with cleft increased posterior facial height. The following evaluation criteria should
palate deformity and in the cases of • Lower facial asymmetry: It is usually be thoroughly implemented while plan­
ankylosis. caused by unbalanced aberrant gro­ ning an orthognathic surgery:
wth in the mandible, e.g. condylar • Medical history: Some of the defor­
Mandibular Deformities hyperplasia/hypoplasia. mities are associated with syndromic
• Mandibular AP excess (hyperpla- con­ditions and often have other
sia): It is characterized by mandibu­ Uncommon Dentofacial asso­ciated congenital anomalies
lar Prognathism with class III maloc­ Deformities which need to be corrected or
clusion. These are often associated with rare may com­ promise the treatment
• Mandibular AP deficiency (hypo­ craniofacial syndromes. Some of the plan. Such conditions must be
plasia): This is characterized by de­ conditions wherein the facial deformities identified prior to the planning
ficient anterior growth of mandible are commonly seen are as follows: of the ortognathic surgery. Facial
(retrognathia) with class II maloc­ deformities are also associated with
clusion. Cleft Lip and Palate the endocrinal distur­ bances (e.g.
• Mandibular asymmetry: It is as a • Pierre Robin sequence Acromegaly) and unless the un­ d­
result of lack of growth on one side • Treacher-Collins syndrome erlying disorders are not brought
of the mandible, often the condylar • Apert’s syndrome. under control the relapse can occur
process, but sometimes ramus and and thus they must be treated prior
body may be involved. It is seen in Facial Asymmetry to the ortho­gnathic surgery.
Temporomandibular joint ankylosis, • Hemifacial atrophy (Parry-Romberg • Dental evaluation and dental
condylar hypolasia/hyperplasia, he­ syndrome) health: The facial esthetics is in­
mi­facial microsomia or tumors of • Hemifacial microsomia (Goldenhar com­ pletely addressed unless the
the condyle. Malocclusion may or syndrome) osseous and the dental components
Orthognathic Surgery 533

are considered intandem. Mobiliz­ equili­­brium which might lead to relapse patient should be done as the patient
ation of the jaw bones often alter or mal­function. Similarly the TMJ is also should be fit to undergo the procedure
the dental relationship and may subjected to stress and malfunction ow­ under suitable anesthesia.
result in unsatisfactory occlusion, ing to abnormal maxillomandibular re­ After medical history, consideration is
mal­fun­ ction and secondary TMJ lationship. Surgical repositioning will given to dental history, dental health, and
com­plications. Teeth also serves as further alter the muscle balance, posi­ periodontal status of the patient. Before
an excellent guide in planning the tion, alter the condylar position which the surgery, restorative orthodontic, peri­
orthognathic surgery and for reten­ may lead to malfunction of the mastica­ o­dontal and facial pain control therapy
tion and fixation of various appli­ tory apparatus or would lead to relapse should be done. Before the surgical
ances for stabilizing of the osteo­ following surgical correction and hence, procedure is undertaken, healthy denti­
tomized jaw segments and thus, it is necessary to evaluate the muscular tion should be established by dental pro­
thorough dental evaluation and activity, TMJ functioning prior to sur­ phylaxis and proper home care.
necessary orthodontic interventions gery and also the likely alterations in Inadequate attached gingival and
are mandatory while planning an them following the surgery so as to make acute periodontal disease must be ma­
orthognathic surgery. proper planning. na­ged before surgery.
• Radiological evaluation: Panoram­
ic or full-mouth periapical radio­ Psychological Evaluation
PROFILE ASSESSMENT
graphic evaluation for studying the In the psychological evaluation, pati­ent’s
jaw bones and dentoalveolar seg­ Apart from the routine profile photo­ expectation about the surgery should be
ment. graphs additional photographs like evaluated and it is the duty of the sur­
• Social and psychological evaluation. Symmetry view, Submental view; super­ geon to give the brief idea of the outcome
• Esthetic facial evaluation. ior view and three-quarter view are of the surgery to the patients. Patients
• Frontal facial analysis. useful in ascertaining the facial pro­file, who come for orthognathic surgery are
• Profile analysis. its descripancies and the need for the mainly of two types. The first group in­
• Cephalometric analysis. correction. Computer assisted analy­ cludes patients who want to improve
• Soft tissue profile analysis. sis and video manipulation are use­ their facial appearance for esthetic rea­
• Skeletal relations. ful in comprehensive evaluation and sons. These patients are self-motivated
• Dental relations. pre­dicting the surgical out come. The and are more reliable. The other group
photo­graphs can be used as a record to includes patients who attribute their so­
OCCLUSAL EVALUATION facili­tate comparison of results. cial and personal pro­blems to their facial
Additional evaluation comprising of appearance, so esth­etic correction alone
AND MODEL ANALYSIS the following may be done as indicated does not correct their personality prob­
A satisfactory and functional occlusal in each case: lem. These patients remain un­ happy
relationship is necessary for the suc­ • Three dimentional CT scan recons- even after the good surgical re­sults. The
cessful completion of the orthognathic truction patients at times have a very high expec­
surgery apart from the facial esthetic • Diagnostic occlusal splint tations about the results of the orthogna­
corrections. Hence, it is necessary to • Velopharyngeal evaluation thic surgery. The surgeon must counsel
study the occlusion, existing descripan­ • Speech evaluation the patients and explain him/her the re­
cies, and compensatory changes as a • Nasoendoscopy alistic outcome of the surgery.
result of the deformity. The need for the • Clinical evaluation of tongue and its
pre- and postsurgical orthodontic inter­ posture and also the radiographic Esthetic Facial Evaluation
ventions required to achieve an accept­ evaluation of tongue posture. The patient is asked to sit or stand in up­
able, fun­ctional occlusion and esthetic • Final treatment plan right position at the eye level of clini­cian
alignment of the dental arches and teeth • Presurgical orthodontics during complete evaluation. At the time
must be planned. • Surgical plan of examination the Frankfort horizontal
• Dental occlusion • Postsurgical orthodontics and main- plane and interpupillary lines should be
• Dental arch form/length tenance. parallel to the floor. Teeth should be in
• Dental alignment/symmetry centric position and the lips reposed.
• Tooth mass relation. General Evaluation All the photographs are taken with
The muscle imbalance is often as­ Frankfort horizontal plane and inter­
sociated with the dentofacial deformi­ Medical and Dental Evaluation pupillary lines parallel to the floor for
ties as a compensatory mechanism. Orthognathic surgery is mostly an ele­ records and photographic analysis. The
The repositioning of the jaw bones in ctive procedure hence, a thorough eval­ frontal analysis and profile analysis are
the desired position alters the muscle uation of the medical condition of the the most useful facial analysis.
534 Facial Deformities

Frontal Face Analysis • The facial midline, nasal midline, lip facial third, i.e. lower lip stomion to
The face is divided into three equal parts midlines, dental midlines, and chin soft tissue menton should be twice
for vertical facial analysis. Upper third midline all should be con­gruent, and the vertical dimension of the upper
extends from the hairline to the glabella, the face should be reason­ably sym­ lip, provided that the upper lip is
middle third extends from glabella to metric, vertically and trans­ver­sely. normal in length.
subnasale and the lower third extends • A normal upper tooth-to-lip rela­
from subnasale to soft tissue menton tion­ship exposes 2.5 + 1.5 mm of Lateral or Profile View
(Figs 25.1A and B). incisal edge with the lips in repose Vertical and anteroposterior plane pro­
The frontal view evaluation should • If the lips of the patient are over­ blems of the jaws can be determined by
include 14 anatomic relationships which closed, the jaws should be opened evaluating the lateral plane.
are as follows: until the lips just begin to separate. The facial profile can be classified
• The forehead, eyes, orbits and nose The condyles should remain seated into convex, concave or straight (Fig.
are evaluated for symmetry, size and in the centric relation. The true lip 25.1C). The various parameter that are
deformity. length and tooth-to-lip relationship taken into account are:
• Normal intercanthal distance is then may be evaluated. • The distance from the glabella to
32 + 3 mm. • Smile line: During smiling, the ver­ sub-nasale and from subnasale to
• Normal interpupillary distance is milion of the upper lip should fall at soft tissue menton should be in a 1:1
65 + 3 mm. the cervicogingival margin with no ratio if the upper lip length is normal.
• The intercanthal distance, alar base more than 1 to 2 mm of exposed gin­ • With the maxilla in normal AP
width and palpebral fissure width gival. Patient should be asked to give position and the upper lip of normal
should be equal. full smile to detect ‘gummy smile’. thickness, ideal chin projection is
• The width of the nasal dorsum • The lower eyelid should be level 3 ± 3 mm posterior to a line through
should be one-half the intercanthal with or slightly above the most subnasale that is perpendicular to
distance and width of the nasal inferior aspect of the iris. Sclera bet­ clinical Frankfort horizontal plane.
lobule should be two-thirds the ween the inferior aspect of the iris • The morphologic characteristics
inter­canthal dis­tance. and lower lid (scleral show) may and relationships of the nose, lips,
• A vertical line through the medial indicate infraorbital hypoplasia or cheeks and chin are evaluated.
canthus and perpendicular to the exophthalmos. • The cervicomandibular angle is eva­
papillary plane should fall on the • The distance from glabella to sub­ lu­ated in reference to chin position
alar bases + 2 mm. nasale and subnasale to menton • The length of the upper lip should
• The upper lip length is measured should be approximately in a 1:1 be one third the length of the lower
from subnasale to upper lip stomion. ratio, providing that the upper lip facial third, i.e. lower lip stomion to
The normal upper lip length is length is normal. soft tissue menton should be twice
22 + 2 mm for males and 20 + 2 mm • The length of the upper lip should the vertical dimension of the upper
for females. be one-third the length of the lower lip if the upper lip is normal in length

A B C
Figs 25.1A to C: Normal facial proportions in: (A) Frontal view; (B) Frontal view analysis: The transverse facial balance; A—The normal
intercanthal distance—32 mm ± 3 mm; B—Normal interpupillary distance—65 mm ± 3 mm; C—The width of the palpebral fissures should
be equal to the intercanthal distance; (C) Profile view
Orthognathic Surgery 535

• Upper lip supralabrale should be • Acute gonial angle • Deep mentolabial fold ‘Knobby’
1 to 3 mm anterior to subnasale. • The lip strain will be evident on app­ea­ rance of the chin (prominent
• A line perpendicular to Frankfort clo­
sure with hyperactive mentalis chin button)
horizontal and tangent to the globe muscle. • Overclosure of lips.
should fall on the infraorbital soft
tissue ±2 mm. Dental Features Dental Features
• Angle’s Class II molar relationship • Angle’s Class I or Class II molar rel­
• Increased overjet ation
CLINICAL FEATURES
• Accentuated curve of spee of lower • Deep over bite
Mandibular Excess— anteriors • Mandibular incisor frequently occl­
• Lower anterior teeth may be tipped ude with the palatal gingival
Prognathic Mandible anteriorly (fanning) or crowded • Severe attrition of the teeth may be
Facial Features • Skeletal deep bite may be present. seen.
• Prominent chin is a dominant fea­
ture (prominent lower third of face) Maxillary Excess (Long Face Skeletal Bimaxillary
• A concave profile Syndrome): Vertical Maxillary Protrusion with or without
• Severe cases show lip incompetence Excess Anterior Open Bite
• Steep mandibular plane which may
be parallel to high mandibular plane Facial Features Facial Features
(angle over 35o normal is 25o) • Increased height of lower third of the • Convex profile
• Obtuse gonial angle face • Extreme protrusion of maxillary and
• Middle third of the face appears • Recessive paranasal areas mandibular teeth
relatively deficient • Narrow alar base • Anterior teeth prominent and visible
• Labiomental fold may be diminished • Prominence of infraorbital rim, in the frontal and profile views
or absent cheek bones, prominent nose • Lip strain is evident, if the mouth is
• Nasolabial angle may be acute • Large interlabial gaps (more then closed
• Anterior facial height may be incre­ 4 mm) incompetent lips • Lip incompetence
ased. • Excessive incisor display—typical • Thick looking lips, with an everted
‘Gum­my Smile’ vermilion border and rolled appear­
Dental Features • Retroposition or recessive chin ance
• Angle’s Class III malocclusion is • Steep mandibular plane. • Apparent chin deficiency.
present
• Reverse horizontal overjet in the Dental Features Dental Features
inci­­sor region • An Angle’s class II molar occlusion • Anterior open bite or edge to edge
• Anterior cross bite • A high arched palate bite may be present.
• Mandibular anterior teeth may be • ‘V’ shaped maxillary dental arch • Mild to severe crowding or spacing
in­cl­i­ned lingually or may be up­right • Accentuated curve of spee. may be seen.
• Maxillary anterior teeth may be Further, there are two variants: • May be associated with severe ton­
protrusive 1. With anterior open bite—excessive gue thrust habit.
• An anterior open bite may be pre­sent. posterior maxillary growth. A short • When severe protusion of maxillary
or normal ramus. Two-third of the incisors is seen, accentuated curve
Mandibular Deficiency/ patients have anterior open bite. of spee with mandibular incisors
Mandibular Retrognathism/ 2. Without anterior open bite—dental cro­wding and deep bite may follow.
Micrognathism compensation with over eruption of
incisor (an increased ramus hei­ght). Nasomaxillary Hypoplasia
Facial Features Associated with a Prognathic
• A convex profile Maxillary Deficiency/Vertical Mandible
• Retruded chin Maxillary Deficiency (VMD)
• “Bird Face Deformity” in very severe Facial Features
cases Facial Features • Flatening of face
• Short upper lip, curled or protrusive • A short square shaped face with • Sunken appearance of face
at rest edentulous appearance • Prognathic mandible
• An everted lower lip, curled under • Decreased lower facial height • Upper lip is flat and relatively short
the protrusive upper incisors with • The mandible appears square and • No display of upper incisors
deep mentolabial fold prominent due to overclosure • Deepened nasolabial fold
536 Facial Deformities

Dental Features • Curve of Wilson relationships in the anteroposterior


• Anterior and posterior cross bite • Curve of Spee (AP), transverse, and vertical dimen­
• Maxillary incisors tend to be protru­ • Dental crowding or spacing sions. Panoramic and periapical radio­
sive in relation to hypoplastic max­ • Missing, decayed, retained primary, graphs can be helpful to determine
illa nonsalvageable teeth tooth alignment, root angul­ation and
• Mandibular incisors upright to the • Discrepancies between centric occ­ existing pathology.
mandibular basal bone lusion and centric relation
• Mandibular posterior teeth have an • Periodontal evaluation
CEPHALOMETRIC ANALYSIS
exaggerated lingual inclination • Transverse, anteroposterior or ver­
• Maxillary posterior teeth tend to tical asymmetries
lean outward. • Anatomic or functional tongue ab­ Hard Tissue Analysis
normalities The hard tissue analysis helps in:
Nasomaxillary Hypoplasia • Recording of any masticatory diffi­ • Establishing two-dimensional rela­
Associated with Cleft Lip- culties tionships of craniofacial components.
palate Deformities • Any other pathologic processes. • Classifying skeletal and dental
abnor­malities with respect to cranial
Facial Features Temporomandibular Joint base, skeletal pattern, inter- and
• Severe mid face hypoplasia Any signs of TMJ dysfunction or patho­ intr­a-arch dental relationships and
• Short, distorted upper lip sis, in the form of hypermobility, hypo­ soft tissue profile.
• Asymmetry of nose (typical speech mobility, subluxation, propping, click­ • Analyzing growth and development
‘nasal twang’) ing, pain, etc. should be detected prior responsible for dentofacial pattern,
• Mandible appears relatively progna­ to surgery. whether for cranial base configura­
thic (pseudoprognathism). tion, congenital abnormalities,
Nasal and Pharyngeal Evaluation patho­ logic conditions, or facial
Dental Features Any nasal trauma, nasal airway obstruc­ asymmetry.
• Angle’s Class III molar relation tion, allergies, sinus pathologies, pre­ • Planning treatment for orthodontic
• Constricted maxillary arch dominant mouth breathing, etc. are and/or surgical procedures.
• Anterior cross bite eva­luated. Similarly in the cases of man­ • Analyzing changes after treatment
• Crowding of maxillary teeth. dibular or maxillary hypoplasia the pha­ effe­ct­iveness of different treatment
ryngeal airway is compromised. It may moda­ lities and effectiveness of
Conditions with Facial be associated with snoring and sleep reten­tion.
Asymmetry pathologies such as sleep apnoea syn­ • Determining dentofacial growth
drome. In severe cases the sleep stud­ changes after treatment.
Features ies and through eva­­l­u­­ation of air way • Predicting hard and soft tissue con­
• Asymmetrical mandibular progna­ should be done. McNa­mara analysis is tours before initiation of treatment.
thism useful in assessing the pharygngeal air­
• With or without anterior open bite way. Hard Tissue Landmarks
• Unilateral condylar hypoplasia Similarly, after a major setback sur­ (Fig. 25.2)
• Hemimandibular elongation gery the pharyngeal space may get com­ • Sella (S): The center of pituitary
• Hemimandibular hyperplasia promised, leading to sleep apnea. Thus fossa.
• Hemifacial hypertrophy (rare). preoperative assessment should be • Nasion (N): The most anterior point
done and the problems must be antici­ of the nasofrontal suture in the
Oral Examination pated and addressed. midsagittal plane.
The following parameters must be as­ • Articulare (Ar): It is a point at the
certained during the comprehensive Radiographic Evaluation junction of the posterior border of
evaluation of the oral structures. The The radiographs used in the diagnosis of ramus and inferior border of basilar
evaluation comprises of: dentofacial deformities are: part of the occipital bone.
• Occlusal relationship (Class I, Class • The lateral and PA cephalometric • Anterior nasal spine (ANS): The
II, Class III) radi­o­­graphs anterior most midsagittal point
• Anterior openbite or posterior Open • The panoramic radiograph on the tip of sharp bony process of
bite • The periapical radiograph. maxilla.
• Anterior overjet and any crossbites Lateral and PA cephalometric • Prosthion (Pr): The lowest and
• Health of the dentition radio­graphs are used to analyze ske­ most anterior point on the alveolar
• Tooth size discrepancies letal, dentoalveolar and soft tissue bone in the middle between the
Orthognathic Surgery 537

• Posterior nasal spine (PNS): The Lower Incisor Inclination


most posterior point on the contour Normally, the angle between the long
of the palate. axis of the lower incisor and N-Po line is
• Gonion (Go): The most inferior, 22 + 4 degrees. The angulation gives the
post­erior, and lateral point on the amount of tipping of the lower incisors
external angle of the mandible. (Fig. 25.3C).

Interincisal Angle
DENTAL RELATIONS
This is the angle formed by the long
There are four measurements for dental axis of the upper and lower central inci­
analysis relationships (Table 25.1). sors. Normal value: 130 + 6 degrees.
Low angle indicates protrusion of the
Position of Upper Molar inci­­­
sors and high angle is associated
Fig. 25.2: Hard tissue landmarks
A vertical line perpendicular to the with retroclination with deep bite
Frankfort plane and passing through (Fig. 25.3D).
upper central incisors. It is also the posterior aspect of the pterygoid
called sup­ra­d­entale. plate is drawn and the horizontal dis­ Skeletal Analysis
• Subspinale (A): The deepest midsag­ tance from the pterygoid vertical to Following skeletal measurements for
ittal point on the concavity between the most distal aspect of the first molar the skeletal analysis are commonly used
Anterior Nasal Spine and Prosthion. crown is measured. This measurement (Table 25.1 and Fig. 25.4).
• Supramentale (B): The deepest helps to determine the maxillary molar
point in mid sagittal plane on the position and to relate this position to the Facial Axis Angle
con­cavity between infradentale and malocclusion. The value is misleading A line is drawn from the basion to the
pogo­nion. when maxillary teeth have been extra­ nas­ion. Another line is drawn from the
• Pogonion (Pg): Most anterior mid cted (Fig. 25.3A). gnathion to the posterosuperior point of
sagittal point on the contour of the Normal value: the pterygomaxillary fissure (facial axis).
chin. • Age of the patient in years + 3 mm The inferior angle formed when these
• Gnathion (Gn): Constructed by • Adult women: 18 + 3 mm two lines intersect is called the facial
bisecting the Facial plane and tan­ • Adult man: 21 + 3 mm. axis angle. The normal value is 90 + 3
gent to lower border of mandible. deg­rees.
• Menton (Me): Most inferior point Lower Incisor Protrusion Decreased value:
on the inferior contour of the chin. The normal distance from the tip of • Recessive chin, or
• Pterygomaxillary fissure (Ptm): the lower incisor to the A-Po line in • Vertically excessive face.
The most posterior point on the perpendicular is 1 + 2 mm. This value Increased value:
anter­ior contour of the maxillary tu­ helps to determine the protrusion of the • Prominent chin
berosity. lower arch (Fig. 25.3B). • Vertically deficient face.

A B C D

Figs 25.3A to D: Dental relations: (A) Relation of molar to the malocclusion; (B) Lower incisor protrusion; (C) Lower incisor inclination;
(D) Interincisal angle
538 Facial Deformities

Table 25.1: Skeletal parameters along with their normal values and conditions altering them

Sr. No. Parameter Normal value Increased Decreased

1. Facial-axis angle 90° ± 3.5° Mandible rotated forward and upward Mandible rotated downward and backward
Ba.Na-Ptm.Gn
2. Facial depth 87° ± 3° Prognathic mandible Retrognathic mandible
N.Pog-Fh
3. Mandibular plane angle 25° Long face/vertical growth pattern Short face/horizontal growth pattern
4. Maxillary depth angle 90°
5. Facial convexity 0 ± 8.5 Mandibular prognathism Mandibular retrognathism
Na.A- A.Pog
6. Maxillary length 100 mm Prognathic maxilla Retrognathic maxilla
Co-Point A
7. Mandibular length 131 mm Mandibular prognathism Mandibular retrognathism
Co-Gn
8. N perp to A point 0 ± 8.7 Prognathic maxilla Retrognathic maxilla
9. Jarabaks ratio (62%–65%) Short face/horizontal growth pattern Long face/vertical growth pattern
S.G0/N.Me

plane (A line tangent to the symphysis Maxillary Length: Mandibular


and the gonial portion of the mandible). Length
This angle relates the posterior facial
height to the anterior facial height. The ratio, measured from the condylion
• Normal value: At 9 years: 26 + 4 de­ to point A (maxillary length) and from
grees (It decreases by 1 degree every the condylion to gnathion (mandibular
3 years) length) is 1:1.3.
• Adult: 24 + 4 degrees This helps in finding out the relative
High angle: Weak musculature and length of each jaw, independent of any
open bite vertical discrepancy.
Low angle: Strong musculature and
deep bite. POSTEROANTERIOR
Maxillary Depth Angle CEPHALOMETRIC ANALYSIS
Fig. 25.4: Hard tissue cephalometric
analysis for orthognathic surgery It is the angle formed by the anatomic The main indication of Posteroanterior
Frankfurt plane and the line from nasion (PA) analysis is asymmetry and deviation.
to point A (Na-A). This angle gives an First vertical line is drawn joining the
Facial Depth Angle idea of the anteroposterior position of midline of the nose and chin and the
It is the posteroinferior angle formed by the maxilla. dental arch—midsagittal line, second
the intersection of the anatomic Frank­ • Normal value: 90 + 3 degrees passing through the zygomatic arch on
furt plane and the facial plane (line con­ Reduced angle: Retrusion of the maxilla either side of midsagittal line, third on
necting nasion to pogonion). Increased angle: Protrusion of the maxilla. either side of midsagittal line passing
Normal value: through the angle of the mandible. From
• At 9 years : 87 + 3 degrees (It increases Facial Convexity these lines comparison can be made
1 degree every 3 years) This is the distance between point A from the normal side. Horizontal lines
• Adult: 89 + 3 degrees and the facial plane (Na-Po). If point A are drawn along the zygomatic plane,
Decreased value: Recessive chin is more anteriorly placed, the maxilla occlusal plane, infraorbital plane, plane
Increased value: Prominent chin. is anterior in relation to the mandible of the lower border of the mandible, to
(Class II), and vice versa (Class III). This assess deviation in relation to horizontal
Mandibular Plane Angle measurement, however, does not help plane. The commonly done analyses
It is the angle formed by the anatomic in finding out which jaw is defective. are Rickett’s analysis and Grummon’s
Frankfurt plane and the mandibular • Normal value: 1 + 2 mm. analysis.
Orthognathic Surgery 539

Important Planes in A is measured from this perpendi­cular facial divergence with respect to the
Cephalometric Analysis line. This measurement describes the anterior facial height.
apical base of the maxilla in relation Vertical skeletal measurements help
Cranial Base to N, and enables to determine if the in the diagnosis of inferior posterior and
The base line for comparison of most of anterior part of the maxilla is protrusive total maxillary hyperplasia or hypoplasia
the data in this cephalometric analysis or retrusive. Similarly position of point and also clockwise or counterclockwise
is a constructed plane called hor­izontal B from this perpendicular line des­­cri­ rotation of the maxilla and mandible.
plane (HP). It is constructed by drawing bes the horizontal position of the apical Surgical correction of these prob­
a line 7° from the line SN (Burstone’s base of the mandible in relation to N. lems includes total maxillary verti­
cephalometric analysis for orthognathic When inferior anatom­ical landmark is cal advan­ cement or reduction, ante­
surgery). It is a substitute to Frankfurt measured in relation to the superior rior maxi­llary vertical augmentation or
plane. Most of the measurements are structure, positive sign (+) denotes an­ redu­ ction, post­
erior maxillary vertical
made from projections either parallel or ter­ior and negative sign (–) posterior. augmentation or reduction, combina­
perpendicular to horizontal plane. The Thus, these measurements are use­ tion of anterior and posterior maxillary
length of the cranial base is measured ful in the planning of treatment of maxi­ vertical augmentation or reduction, and
from Ar to N and parallel to HP. This llary or mandibular advancement or mandibular ramus rotation and ramus
mea­surement is not an absolute value, red­u­­ction. height reduction.
but a skeletal baseline to be correlated to N-Pog is measured in the same
other measurements such as maxillary manner as NA and NB and indicates the
or mandibular length. For example, a prominence of the chin. These measure­ SOFT TISSUE
pati­ent with cephalometrically large ments determine if there is horizontal
maxi­­­
lla and mandible should have a genial hyperplasia or hypoplasia and
CEPHALOMETRIC ANALYSIS
normal appearance because of large useful in the planning of treatment of
cranial base. augmentation and reduction genio­ pl­ Soft Tissue Landmarks
asty, of anterior mandibular horizontal (Fig. 25.5 and Table 25.2)
Horizontal Skeletal Profile advancement or reduc­ tion, and total
Analysis mandibular horizon­tal advancement or • Glabella (G): The most prominent
Horizontal skeletal profile analyses are reduction. point in the midsagittal plane of the
made parallel to HP. These are very forehead.
impor­­­tant because most surgical cor­r­e­ Vertical Skeletal Profile • Soft tissue nasion (N’): The point
ctions are primarily made in the anter­ Analysis of greatest concavity in the midline
opo­­­­sterior direction. The McNamara an­ Vertical skeletal discrepancy may reflect between the forehead and nose.
a­ly­­­­sis, Tweed analysis, Bustone analy­sis, anterior, posteri­or or complex dys­plasia • Columella point (Cm): The most
Down’s analysis and Steiner analysis are of the face. Therefore, vertical skeletal anterior point on the columella of
commonly done which include both the cephalometric measurements are divi­ded the nose.
horizontal and vertical skeletal profile into anterior and posterior com­po­nents. • Subnasale (Sn): The point at which
analy­sis, based on skeletal proportions • Anterior component: The anterior the columella merges with the upper
and linear measurements. com­ po­nent is subdivided into lip in the midsagittal plane.
measurements of: (i) the middle • Labiale superius (Ls): A point indi­
Degree of Skeletal Convexity third facial height (dis­tance from N cating the mucocutaneous border of
The angle of facial convexity is measured to ANS) that is mea­sured perpendi­ the upper lip.
by the angle formed by the line NA and cular to HP, and (ii) the lower third • Labiale inferius (Li): A point indi­
the line from A to PoG. The N-A-PoG facial height which is the mea­ cating the mucocutaneous border of
angle gives an indication of the overall surement from ANS to Gn and is the lower lip.
facial convexity, but does not specify the measured per­pendicular to HP. • Soft tissue pogonion (Pg’): The for­
diagnosis that whether the maxilla or • Posterior component: Posterior e­­­most point on the soft tissue chin in
the mandible is at fault. maxillary height is the length of a the midsagittal plane.
A positive angle of convexity denotes perpendicular line dropped from HP • Soft tissue menton (Me’): The low­
convex face and a negative angle deno­ intersecting the PNS. The divergence er­most point on the soft tissue chin
tes concave face. A clockwise angle is of the mandible posteriorly is shown in the sagittal plane.
positive (+ve), a counterclockwise angle by the mandibular plane angle (MP- • Angle of throat (C): The intersection
is negative (–ve). HP), which is the angle formed of the horizontal and vertical tang­
A line perpendicular from HP is dro­ between Go and Gn and HP. This ents to the profile of the soft tissue
pped through N. Horizontal position of angle helps in relating the posterior throat.
540 Facial Deformities

be approximately 20° to the NB line,


with the labial face of the incisors
4 mm anterior to that line
• To align and level the teeth
• To adjust for tooth discrepancies
• To relieve arch crowding
• Closure of diastemas
• To correct rotated teeth
• To correct divergence of roots adja­
cent to surgical sites
• To achieve root paralleling to create
space for segmental osteotomies
• To eliminate gross dental interfer­
ences
• Co-ordination of upper and lower
arch width and to correct the tran­
Fig. 25.5: Soft tissue landmarks s­verse discrepancies without com­
pro­mising stability and dental
Presurgical Orthodontics red anterior teeth would cause a health.
interference. Hence, by doing pre­
Goals of Presurgical Orthodontics surgical orthodontics we would Advantages of Presurgical
• The basic goal is to position the like to upright the teeth so as to Orthodontics
teeth upright over basal bone while achi­ eve a normal tooth to basal • Relapse tendencies are controlled.
satisfying the spatial requirements. bone relationship and then go for a Most oftenly sugical relapse and
In simple words it is decompensation surgical correction ortho­dontic relapse are compen­
of nature’s compensation, e.g. when • To position of the teeth over their satory to each other, since dentition
a patient has a retrognathic mandible respective basal bones is decompensated before surgery
the anterior teeth tend to procline • To position the long axis of the maxi­ • Total treatment time is reduced
which is a nature’s compensatory llary central incisors so that the final • Results in proper intraoperative in­
mechanism to maintain a normal position would be appro­xi­mately 22° terdigitation (occlusion)
dental relationship on an abnormal to the NA line, with the labial face of • Allows quick and easy postsurgical
basal bone framework. In such situ­ the incisors 4 mm anterior to that orthodontic correc­tion
ation without presurgical ortho­ line • Allows effective surgical correction
dontics if the surgery is attempted • Position the mandibular central • Improves results in terms of stability
to advance the mandible, these fla­ inci­sors so that final position will and occlusion.

Table 25.2: Soft tissue cephalometric parameters, standard values and conditions altering them

Sr. No. Parameter Normal value Increased Decreased

1. Nasolabial angle 102° ± 4° Lips retrusive Protruded lips


2. Nasomental angle 120° to 132° Protrusive chin and retrusive nose Retrusive chin and prominent nose
3. Chin prominance –1 to –4 mm Prominent chin Retrusive chin
4. E Line: Upper lip –4 mm Prominent lips Retrusive lips
   Lower lip –2 mm Retrusive lips Prominent lips
5. S Line: Upper lip 0 mm Prominent lips Retrusive lips
   Lower lip 0 mm Retrusive lips Prominent lips
6. Facial symmetry: Equal three parts in vertical
Upper 1/3 proportion
Middle 1/3 Maxillary excess Maxillary deficiency
Lower 1/3: Maxillary excess Maxillary deficiency
Orthognathic Surgery 541

Presurgical Aids in Orthodontics


While performing orthognathic surgery,
if any surgical procedure is considered
to help the treatment, it is known as
surgical aid to orthodontics. Following
are some of the common surgical aids to
orthodontic treatment:
• Serial extractions A B
• Therapeutic extractions
Figs 25.6A and B: Cut for correcting anterior open bite
• Surgical removal or surgical expo­ on cast for mock surgery
sure of unerupted teeth
• Extraction of submerged deciduous
molars, removal of odontomes • To determine the direction in which • There can be errors related to the
• Correction of diastema dento-osseous segment moves actual model orienta­tion itself
• Corticotomy. • To obtain measurements of osteo­ • There can be measurement errors
tomies related to instruments and pers­
Postsurgical Orthodontics • To get postoperative relationship of pective.
Four-to-six weeks after the surgery, the jaws, dentition and occlusion
when the surgeon confirms the satisfac­ • To decide about postsurgical ortho­ Technique
t­ory bony healing, the stabilizing arch dontic treatment First the models are positioned in the
wires are replaced by light arch wir­es • Fabrication of splints for stabilization required jaw relationship using semi­
and occlusion is allowed to settle. after surgery. ad­justible articulators. The models
are cut exactly similar to the planned
Goals of Postsurgical Indications surgery, avoiding root apices. Detect
Orthodontics Model surgery is used in double jaw sur­ the problem areas like proximity
• Closure of residual spaces gery, as well as in single jaw surgery where of roots, bony inter­ ference, etc.
• Root paralleling at the extraction unoperated jaw will act as a template. Observe rotation and expan­ sion of
sites the dento-osseous segment. Achi­ eve
• Maximum interdigitation Advantages maximum interdigitation and measure
• Finer tooth alignment • The simulation of the patient’s facial anteroposterior (AP), trans­ verse and
• Retention of the reoriented oral mu­ structure functionally and spatially inter­ dental chan­ ges and re-evaluate
s­culature to prevent relapse in three dimensions and compare with prediction tracing
• To establish ideal overbite and over­ • The surgeon can correlate the rele­vant mea­s­urements.
jet information and arrive at the surgical
• To stabilize the results obtained prediction in three dimen­sions Surgical Splints
through the surgery. • Model surgery gives an accurate Surgical splints are also known as occ­
1:1 replica of the patient’s dentition lusal wafer splints. They are utilized
Dental Model Surgery— allowing an increased accuracy of in the operating room to position the
(Mock Surgery) prediction when compared to the 10 teeth and add to stabilization. They are
Mock surgery gives three dimensional percent discrepancy seen in ceph­ used during the surgery as well as post­
understanding of the postoperative rela­ alometric distortion surgically.
tionship of the jaws (Figs 25.6A and B). • Model platform and block is capable
Cep­h­a­lometric analysis cannot repro- of accurately measuring articulator Advantages
duce three-dimensional view of the mounted models in three planes of • Provide a clearly visualized goal for
pati­ent’s dental arch. space allowing the surgeon to carry the surgeon at the operating table
out accurate model surgery move­ • Aids in positioning bone fragments
Aims of Model Surgery ments on a full sized anatomic arti­ correctly to aid healing
• To determine the feasible surgical culator. • Possible to put teeth in a planned
plane, extent of bone/arch advance­ position at surgery, even if they do
ment or reduction required in the Disadvantages not interdigitate perfectly without a
surgery Condyles are never perfectly symmet­ splint.
• To determine vertical change that rical therefore: Surgical splints are utilized in the follow­
will be achieved at the time of sur­ • Model surgery performed on the ing procedures:
gery in such a way that it can be ac­ mou­nt­ ed casts gives slightly inaccu­ • Maxillary surgery
curately duplicated intraoperatively rate reading • Mandibular ramus surgery
542 Facial Deformities

• Segmental jaw surgery Various surgical procedures done for


OPERATIVE PROCEDURES
• Dual jaw surgery. the correction of the jaw deformities are
shown in Box 25.2.
Maxillary Osteotomies
Construction of Splints The Le Fort I osteotomy, anterior subap­
The splint is made on the casts as they
Principles of Surgical Treatment ical osteotomies, and posterior subapical
have been related by mock surgery on • Psychological preparation of the osteotomies are commonly performed
models. After they have been checked patient. in maxilla and Le Fort II and Le Fort III
by the surgeon and orthodontist, the • Maintenance of blood supply thro­ osteotomies are done in cases with severe
following steps are under­taken: ugh the appropriate pedicle. mid facial hypoplasia. According to the
• Stabilize cast with plaster or stone, • Care of nerves, vessels, teeth and bone. clinical situ­
ation modifications can be
so that no shift occurs as splint is • Minimum periosteal stripping. done in these procedures and these can
fabricated • Rotary instruments or saws should be combined with other procedures also.
• Articulator is opened to allow for be used under copious saline irrig­
enough thickness of splint material ation to prevent thermal damage of Le Fort I Osteotomy
• Self-curing acrylic is formed into the bone. This is the most versatile procedure used
the desired U-shaped configuration. • Osteotomy cuts should be 3 to 5 mm to correct the deformities of maxilla in
Care is taken to avoid rolling the away from the apices of the teeth. all planes and with low complication
acrylic excessively, as this causes • Osteotomized fragments should be rate. The maxilla may be mobilized and
cra­cks and bub­bles approximated in class I canine and repositioned and its survival continues
• Lay the U-shaped roll of uncured molar relation (ideal). as long as the mobilized maxilla rema­
acrylic on the lower occlusal surface. • Bone grafts should be used if bone ins attached to a broad soft tissue pedi­
The casts are then closed onto defect is created. cle. Even if the maxilla is segmented in
it, when the acrylic is still soft. At • Short term immobilization to pre­ several pieces, healing will occur as long
this point, the casts must be firmly vent movement of osteotomy site. as the vascular pedicle is maintained.
secured to the articulator. If the casts • Postsurgical care includes balance The nec­rosis occurs when the vascular
shift, splint dictates wrong position of fluid intake and output, control of pedicles are damaged or compromised
at surgery infection, edema and pain. (Figs 25.7 and 25.8).
• While the acrylic is still soft, scissors/ • Maintenance of oral hygiene.
scalpel is used to trim the excess on • Regular follow-up. Indications
the labial aspect. Ensure that it does • It is used most commonly in such
not tear away while carrying out this deformities coexist in multiple planes.
procedure Box 25.2: Surgical procedures • Shortening of maxilla, especially at
• After the acrylic has cured, a semi- premolar extraction sites, is possible
Maxillary procedures
trimmed splint with occlusal inden­ and was commonly performed until
Subapical osteotomies
tations is obtained awareness of the tendency to flatten
• Anterior
• Trim away excessive bulk of acrylic, the upper lip was recognized.
• Posterior
labially and lingually with burs. • Superior repositioning of the maxilla
Le Fort I osteotomy with modifications
Buccal as­pect of splint must be con­ Le Fort II osteotomy
was noted to increase the stability of
toured to avoid interference with Le Fort III osteotomy anterior open bite and offered signi­
orthodontic appli­ances and to allow Mandibular procedures fi­cant cosmetic benefits, especially
visual deter­ mination of proper • Body procedures in long faced patients.
seating during surgery. The acrylic – Body osteotomy • Inferior repositioning and widening
should be reli­eved on lingual aspect – Genioplasty of maxilla are also possible.
of anterior teeth and dis­tal aspect of – Inferior border osteotomy • Three dimensional repositioning of
buccal segment cusp tip to allow a • Ramus procedures the maxilla is possible, but this req­
smooth arc of closure – Sagittal split osteotomy uires that the maxilla be segmen­ted.
• Trim occlusal surfaces so that only – Intra oral vertical ramal osteotomy • In all cases of apertognathia, Le Fort I
shallow occlusal indentations remain (IVRO) osteotomy should be given consi­
• Finally, place bur holes along labial – C osteotomy deration because of stability issues.
and buccal sur­ face for attaching – Subsigmoid osteotomy
splint to the arch wires – Condylectomy Surgical Procedure
• Routine finishing and polishing must • New techniques Before the surgical procedure the head
be carried out for patient’s comfort Mid facial and mandibular distraction of the patient is elevated approximately
osteosynthesis using Ilizarov’s technique.
and maintenance of oral hygiene. 10 degrees. Hypotensive anesthesia
Orthognathic Surgery 543

A B C

D E F
Figs 25.7A to F: Le Fort I osteotomy

A B C
Figs 25.8A to C: Preoperative, intraoperative and postoperative photographs of a case treated with Le Fort I osteotomy

technique is preferred (systol­ ic blood Incision is placed high in the to maintain additional vascular pedicle
pressure of 90 mm of Hg), to reduce the mucobuccal fold of the upper lip, ext­e­ to maxilla. The maxilla is exposed by
blood loss during the surgery. A diluted nds from the zygomatic buttress regi­on reflecting the tissue subperiosteally
solution of 2 percent lignocanine hydro­ above the first molar to the midline. The from the buttress region to the ant­erior
chloride with 1:100,000 epinephrine is incision is carried through the mucosa, nasal spine. The subperiosteal diss­
infiltrated into the buccal vestibule of the muscle, and periosteum of the bone. ection carried upto the infraorbital rim
maxilla on either sides. Palatal infiltration Some surgeons do not take a continuous taking care not to damage the infra­
is not adviced since it can compromise the incision but, leave a band of tissue in the orbital nerve. The ant­er­ior nasal spine
palatel perfusion of blood to the maxilla. region of nasal aperture in the midline and piriform rim are identified and
544 Facial Deformities

septopremaxillary ligament is detached the nasal mucosa during sectioning. portion of the septum is also removed
from the anterior nasal spine. The nasal The guarded osteotome should be otherwise while positioning the maxilla
muc­osa is then dissected from the lateral placed at the piriform rim region and superiorly, the buckling of septum can
nasal wall and floor. The dissection is directed inferiorly along the lateral occur. Any bony interference should be
carried out posteriorly, strictly adhering nasal wall toward the perpendicular removed using rongeur. Inter­maxillary
to the bone (subperiosteally) towards plate of the palatine bone. Complete fixation is done using 26-gauge wire
the maxillary tuberosity and inferiorly to sectioning of the palatine bone should after plac­ ing prefabricated occlusal
the pterygomaxillary junction. be accomplished, even if it results in splint, taking care that condyle should
Horizontal reference points are pla­ damage to the descending pa­ l­
atine not be displaced inferiorly. During the
ced at piriform aperture region and at vessel and if damage occurs packing procedure care should be taken not to
the zygomaticomaxillary buttress area. should be done. Incomplete sec­tioning damage the greater palatine vessels as
The osteotomy initiates at the zygomati­ of the palatine bone can result in they are major vascular pedicle for the
comaxillary buttress region. A recipro­ inadvertent fracture, which may extend ost­eo­to­mized maxilla. However, minor
cating saw or fissure bur and micromo­ to the orbit. Similarly the opposite nasal vas­­
cularity is also derived from the
tor is used and proceeds anteriorly to wall is sectioned. The nasal septum is phar­yn ­ geal arteries but its not reliable.
the nose. The nasal mucosa is protected also sectioned after stripping out the Simil­arly mucoperiosteal dissection
by using a periosteal elevator or copper muco­periosteum on either side, using over the palate should be avoided
malleable retractor while cutting the pir­ double guarded osteotomes. (Figs 25.9 and 25.10). After the maxilla
iform rim. The cut should be made about The final step in Le Fort I osteotomy is brought in the desired position, it
3 to 5 mm above the apex of the root to is separation of maxilla from pterygoid is fixed with suitable mini plates and
preserve blood supply of the teeth. plates. Pterygoid chisel or curved osteo­ screws.
The posterolateral wall of the maxilla is tome is used to separate the maxilla, During the closure of any maxillary
sectioned under the mucosal tunnels with which is directed anteromedially and degloving incision crossing the midline
direct visualization. A reverse L retractor inferiorly at the lowest part of the taken for Le Fort I or subapical osteo­
is placed subperiosteally extending to the junction of the maxilla and the pterygoid tomies, care must be taken to place
pterygomaxillary junction. The osteo­ plate, to prevent damage to the internal alar cinch sutures as the alar cartilages
tomy cut decends inferiorly as it proceeds maxillary artery or its branches. Index get detached during dissection and if
posteriorly from the buttress region to finger is placed at the hamular notch the alar cinching is not done flaring
the junction of the maxilla and the ptery­ on the palate which helps to direct and of the nose can result. Secondly, lip
goid plate. This minimizes the risk of orient the cut. The osteotome is malleted lengthening can also be done while
damaging the internal maxillary artery to achieve bony separation which can closing these incisions by doing simple
or any of its terminal branches as they be felt by placing the index finger in V-Y closure in the midline.
descend from the pterygopalatine fossa, the palatal region. On the opposite
after the posterior wall is cut, saw is side same step is repeated. Nowadays,
reversed so that the blade is placed into the classical disjunction of maxilla and
High Le Fort I Osteotomy
the maxillary sinus and osteotomy is pterygoid plates is not done. The cut The high Le Fort I osteotomy is indicated
completed from the sinus to the outside. is place vertically in the region of the for correction of the maxillary deficiency
If the impacted third molar is pre­sent, maxillary tuberosity and the disjuction along with paranasal hypoplasia. The
the osteotomy is not altered and third is done at the tuberosity, i.e. anterior osteotomy cut starts at the upper level at
molar is removed after maxilla is down to the pterygomaxillary junction. It is the lateral rim of pyriform aperture and
fractured. Ideally the third mol­ars are ex­ considered safe and as effective as the then in a step like manner descends to
tracted 2 to 3 months prior to the surgery classical pterygoid disjuction. Maxilla the zygomaticomaxillary buttress area
so that the cuts can be taken more pre­ is down fractured after all the bony over the anterior surface of the maxilla.
cisely. When the bone cuts are complete cuts are over. The maxilla is gently Rest of the procedure remains same as
the region is packed with moistened depressed at the anterior aspect with the classical Le Fort I osteotomy.
gauze, soaked in the solution of saline hand pressure. As the maxilla moved
and adrenaline in a dilution of 1:200000. downwards and if any attachment
The same steps are repeated on the op­ of nasal soft tissues are present, they
Le Fort II Osteotomy
posite side from the incision onwards. should be dissected free. Excess bone Severe paranasal hypoplasia extending
The lateral wall of the nasal cavity is to from the nasal crest, vomer, medial to the infraorbital rims necessitates a
be sectioned next. A periosteal elevator wall of maxillary sinus, etc. is removed Le Fort II osteotomy as described: Hen­
or copper malleable retractor is placed by using rongeur forceps and burs. If derson and Jackson (1973), but it should
sub­­periosteally on the medial aspect of superior repositioning is planned an­ be under­stood that this is not a common
the lateral wall of the nose. This protects ter­
ior nasal spine is removed. The occurrence.
Orthognathic Surgery 545

A B C
Figs 25.9A to C: Case of maxillary retrusion treated with Le Fort I advancement: (A) Preoperative photograph; (B) Intraoperative
photograph; (C) Postoperative photograph

A B C

D E F
Figs 25.10A to F: Case of maxillary hypoplasia with mandibular prognathism treated with mandibular set back by BSSO and maxillary
advancement by Le Fort I osteotomy. (Bijaw surgery) (A and B) Preoperative photographs; (C and D) Osteotomy cuts; (E and F)
Postoperative photographs

Exposure is gained through a bico­ exter­


nal scar. Intraoral access was Medial canthal tendons are left undi­
ronal incision or bilateral paranasal also described for Le Fort II osteotomy sturbed. An osteotomy is made with a
incisions (Figs 25.11A and B). The former (Figs 25.12A and B). side-cutting bur down the medial orbi­
is a more extensive procedure, possibly The medial orbital floor, infraorbital tal wall behind the lacrimal groove. It
ent­ailing medial canthal disruption; rim, medial orbital wall, and lacrimal is extended medially to the infraorbital
the latter results in potentially visible sac are exposed in a subperiosteal plane. nerve area through the orbital floor, over
546 Facial Deformities

A B
Figs 25.12A and B: Le Fort II osteotomy cuts

Pellett and Smith, 1983). Wire or multi­ osteotomies that separated the nasal
ple screws and miniplates pla­ced from bones from the frontal bones. Oste­
B
the frontal bone to the nasal skeleton otomy of the orbital floor was placed
Figs 25.11A and B: (A) Paranasal access provide secure fixation of the central immediately within the infraor­bital mar­
incision; (B) Bicoronal incision
maxilla to the skull. If nasal height is gin and extended across the floor of the
lacking, a split cra­nial bone graft can orbit to the lateral orbital wall anterior
be placed beneath the dorsal nasal skin to the lacrimal groove. Osteotomies
the anterior maxilla, and caudally as far and secured with two screws or wire were also performed through frontal
as possible. Aufricht retractor is inserted to provide a cantilever type of dorsal process­es of the maxilla to diminish the
from one paranasal incision to the other graft. width of the nose. Temporal process of
to retract the dorsal nasal skin, and the the zygoma was divided on each side.
osteotomies are connected to the nasal Le Fort III Advancement An osteotome was then introduced into
dorsum using a reciprocating saw. Any Osteotomy (Figs 25.13A and B) the pterygomaxillary junction. Anter­
unconnected areas are cut with a fine ior to the greater palatine fora­men, an
osteotome; exposure for the osteotomies Gillies and Harrison (1950–51) reported incision was made transversely across
is improved with the bicoronal approach. the first high maxillary (a modified Le the mucoperiosteum of the hard palate,
Through a posterior buccal sulcus inci­ Fort III) osteotomy in a patient with extending laterally and post­ erior to
sion, osteotomy cuts are located and are craniofacial dysostosis. Through exter­ the alveolar ridge. The hard palate was
extended across the maxillary tuber­ nal incisions they performed tran­sve­rse divi­­ded and the line of osteotomy was
osities till the pterygomaxillary fissures.
Maxillary tuberosities are separated
from the pterygoid plates with a curved
osteo­tome. To complete the osteotomy,
a cur­ ved osteotome is placed in
transverse cut across the nasofrontal
junction and is driven posteriorly and
inferiorly to separate the vomer from
the anterior skull base. Mobilization of
the maxilla is achieved as in the Le Fort I
procedure.
The infraorbital rim defects are
accurately bone grafted through the
paranasal incisions. Anter­ ior osteo­
tomy sites are filled with inlay and
onlay bone grafts using the buc­ cal
sulcus approach. Split cranial bone
grafts are readily avai­ l­
able when a A B
coronal approach is used (Jackson, Figs 25.13A and B: Le Fort III osteotomy cuts for total advancement of zygomatic complex
Orthognathic Surgery 547

rejoined at the pterygomaxillary junct­ Surgical Procedure


ion. In this way, spatial relation­ships of
A horizontal incision is given in the
the soft palate were undisturbed. The vestibule and a mucoperiosteal flap is
operation was completed by severing reflected upto the attached gingival to
the septum with a pair of large scissorspreserve the blood supply. The anterior
introduced through the osteotomy line nasal spine and pyriform rim/aperture
at the root of the nose. Intermaxillary of the nose are to be exposed.
fixation was established. If the diastema is present at more
than one place then multiple vertical
Segmental Maxillary interdental incision can be taken.
Osteotomy Osteotomy cut is then made with the
bur in the vertical direction in the labial
Indications cortex from the nasal floor to the level of
Fig. 25.14: Segmental osteotomy cut
• Transverse discrepancies between the attached gingival. 5 mm above the
the dental arches apices of the teeth, so that the vitality of
• Vertical steps in the maxillary occl­ the pulp is maintained. Then cut extend­ Other indications include:
usal plane ed up to the palatal cortex. Then with the • For correction of marked protrusion
• Space remaining in the maxillary help of the fine osteotome alveolar crest of maxillary teeth
arch. bone is sectioned. Separate horizon­ • Correction of anterior open bite
tal cut can be made if sufficient bone is • To correct anterior teeth proclination
Single Tooth Osteotomy present in between the nasal floor and • When tooth movement with ortho-
the root apex. The segment is then mo­ dontic therapy is not indicated.
Indications bilized into the correct position and then In 1921 Cohn-Stock first reported
• Tooth malposition splint is placed and closure done. segmental maxillary osteotomy proce­
• Dental ankylosis dure. Wassmund in 1935 and Wund­erer
• For closure of diastema. Anterior Maxillary Osteotomy in 1962 modified the procedure which
were widely accepted and used till today.
Advantages Indications
• Treatment time is reduced Excess in vertical and/or anteroposterior Wassmund Technique
• Dental relapse is less. dimension of maxillary alveolar process After infiltration with lignocaine
in patients with acceptable posterior 1:100,000 epinephrine, a vertical inci­
Disadvantages occlusion (Figs 25.14 and 25.15). sion is given between canine and first
• Chances of injury to adjacent teeth The most common indication is pre­molar exten­ding to the nasal floor
• Periodontal compromise of treated correction of bimaxillary protrusion and the muco­ perio­ steum is reflected.
tooth when it is combined with mandibular The first premolar is extracted if required
• Chances of devitalization of the teeth. subapical osteotomy. and the palatal muc­osa is reflected by

A B C D
Figs 25.15A to D: A case of anterior maxillary osteotomy showing anterior osteotomy cuts with postoperative results: (A) preoperative
photograph; (B) Intraoperative photograph showing down fracture of the osteotomized segment; (C) Osteotomy segment fixed in
superior and posterior position; (D) Postoperative photograph
548 Facial Deformities

A B C
Figs 25.16A to C: (A) Midpalatine split; (B) Buccal cut through canine and premolar; (C) Vertical incision given at anterior nasal spine

tunneling past mid­line. Now with the gingiva over the premolar can be tunnelled it provides good access to the palate
help of the bur or reci­procating saw and inferiorly both, labially and palatally. The region. This osteotomy technique relies
under copious saline irrigation buccal premolar is extracted and then the vertical on the intact buccal pedicle for its blood
cut is made in the vertical direction osteotomy cuts can be placed below the supply (Figs 25.17A to C).
5 mm above the apex of the canine and tunnelled gingiva. The operator keeps After the buccal surgical procedure
turned medially at the level of pyriform a finger palatally while taking vertical the palatal surgical procedure is started
rim region. Then through the mid and horizontal cuts and feels the bur or by giving the transverse incision at the
palatine incision in the antero­posterior osteotome movement. This avoids injury planned osteotomy site. The soft tissue
direction (Figs 25.16A to C), the palatal to the palatal pedicle. This technique reflection is done posteriorly behind the
bone is removed from the alveolus to the provides additional blood supply to the planned osteotomy site. The osteotomy
midline taking care not to damage the osteotomized maxillary segment through procedure is then performed with the
palatine soft tissues. Similar procedure is the labial pedicle (see Fig. 25.14). help of the saw or bur under copious
repeated on the opposite side. A vertical After completion of all the oste­ saline irrigation. After the completion of
incision is then given over the anterior otomies, the anterior maxillary dento­ the osteotomy cuts, osteotomy seg­ment
nasal spine and the mucoperiosteum osseous segment can be repositioned is mobilized and separated from the nasal
is reflected, then with the help of nasal and the prefabricated occlusal splint is septum. The segment is then positioned
osteotome septum is separated from the fitted to the dental component. Closure after placing the prefa­bri­cated occlusal
anterior maxillary seg­ment. done with 3-0 vicryl. splint and closure done with 3-0 vicryl.
This procedure can be completed
without taking the vertical labial incision Wunderer Technique Posterior Maxillary
and palatal incision, as described in the The labial osteotomy procedure is sim­ Osteotomy
original technique. A degloving incision ilar to the Wassmund technique. The Schuchardt in 1959 described this pro­
is taken in the labial vestibule and the advantage of this technique is that cedure for the correction of open-bite

A B C
Figs 25.17A to C: (A) Buccal osteotomy cut; (B) Transverse palatal cut; (C) Down fracture with separation at nasal septum
Orthognathic Surgery 549

de­for­­mities. Bilateral osteotomies can • Infection out laterally anterior to the proposed
be performed at a time to correct the de­ • Wound dehiscence osteotomy site (Figs 25.21A to C).
formities. • Necrosis of segment
• Relapse. Sagittal Split Osteotomy
Indications The sagittal split osteotomy (SSO) of the
• Posterior maxillary alveolar hyper­pl­
Variations of Posterior ra­mus of the mandible was described
asia Segmental Maxillary by Obwegessor. Later the technique
• Total maxillary hyperplasia (when Osteotomy was modified by his student Dal Pont to
combined with AMO) In 1970, Kufner made only a horizontal make it more versatile. The SSO is one of
• Posterior open bite incision above the apices of the involved the most commonly practiced surgical
• Transverse excess or deficiency teeth, gaining access to the palatal procedures to correct the mandibular
• Distal repositioning of the posterior aspect (Figs 25.20A and B). deformities due to its versatility.
maxillary alveolar fragment Perko in 1972 and later Bell in 1975
• Spacing in the dentition. made a hockey stick incision along the Bilateral Sagittal Split
midline of the palate as far forward as Osteotomy (BSSO)
Surgical Technique the incisive papilla and then carried it It is the surgical procedure for the corre­
The buccal vestibular incision is given ction of lower jaw deformities. This is
from canine to the second molar region
below the zygomatic buttress. The muc­­
o­periosteal flap tunneling is done superi­
orly and inferiorly. The lateral maxillary
wall and region posterior to the ptery­
goid plates is exposed (Fig. 25.18).
The horizontal osteotomy cut is star­
ted 5 mm above apices of the post­erior
teeth using bur or saw from the location
of the anterior vertical osteotomy to the
maxillary tuberosity. The vertical cut is
done either between the adjoining teeth
(interdentally) or if preplanned then in
the extraction socket region. About 1 mm Fig. 25.18: Limited buccal incision with Fig. 25.19: Coronal view indicating bone
of bone support is kept along the root combined horizontal and anterior vertical and cuts
surfaces of the adjacent teeth in order to osteotomies
prevent the formation of a periodontal
defect. Vertical and horizontal cuts are
completed through the palatal cortex by
keeping the index finger on the palate to
prevent the soft tissue damage. A small
curved osteotome is used to sepa­ rate
the entire posterior segment from the
pte­ry­gomaxillary junction and down­fra­
ctured it, which is pedicled on the pal­
atal mucosa. Now under the direct visi­on
palatal bone can be removed (Fig. 25.19).
After completion of all the osteotomy
the segment is well mobilized, the pre­
fabricated splint is fitted and wired to the
teeth. If large gap is to be created at the
osteotomy site, then bone grafts are used.

Complications
• Loss of vitality of teeth A B
• Periodontal defect of teeth adjacent Figs 25.20A and B: (A) Coronal view—Transantral palatal osteotomy via chisel following
to vertical osteotomy site lateral sinus wall osteotomy; (B) Transantral palatal osteotomy trimming of bone segment
550 Facial Deformities

A B C
Figs 25.21A to C: (A) Limited buccal incision with combined horizontal and vertical osteotomies; (B) Palatal incision located medial to
planned lateral palatal osteotomy; (C) Coronal view: bone cuts with transantral medial nasal wall osteotomy

acc­
o­mplished through transoral inci­ electrocautery. The incision is car­ ried first molar or premolar region to ensure
sion. The osteotomy splits the ramus inferiorly, lateral to the exter­nal oblique good overlap during advancement and
and the posterior body of the mandible ridge into the area of the sec­ond molar, for setback procedures, the vertical
sag­
ittally, which allow either setback, where the incision is made more lateral osteotomy cut is placed lateral to second
advancement or rotation. into the vestibule to the distal of first molar. The vertical cut is completed
molar. The soft tissue dis­section is started through the lateral cortex only. The cut
Indications subperiosteally with the help of periosteal extends thro­ugh both the cortical plates
• Horizontal mandibular excess, defi­ elevator, al­­ong the anterior border up­ at the inferior border of the mandible.
ciency and asymmetry ward, towar­ ds the coronoid process. (Taken cir­ cum­ ferentially around the
• Correction of open bite Medi­ally the soft tissue is reflected, until inferior border keeping the channel
• Correction of the cross bite the lingula and the inferior alveolar ner­ retractor at the inferior border to retract
• It is the procedure of choice for man­ ve bundle and mandibular foramen the soft tissue and facial artery away from
di­bular advancement (10 to 12 mm) is identified (to prevent excessive diss­ the bone). The bony cuts are checked
• Excellent operation for a mandibular ec­ tion and easy identification of the for completeness with osteotome, the
setback of small to moderate mag­ foramen, a blunt nerver hook can be segments are separ­ ated with Smith’s
nitude (7 to 8 mm) passed along the bone and hooked bone spreader. The two beaks of the
• Procedure of choice for minor asym­ around the neuro­ vascular bundle and spreader are on the buccal side and
metries. the sphenomandibular ligament attached single third beak is on the lingual side to
• Mandibular advancement for corr­ to the lingula of the mandible, to locate prevent the fracture of the thinner buccal
ection of sleep apnea. the level of the mandibular foramen. The cortex due to pressure. While using the
boney cut on the medial cortex is taken 3 to spreader controlled force should be used
Surgical Procedure 4 mm above the handle of the probe while to gradually spread the bone. In case of
The procedure is performed under it is kept parallel to the madibular occlusal excessive resistance the cortical cuts
gen­­­­eral anesthesia through nasoen­do­ plane to avoid injury to the neurovascular should be rechecked for completeness.
tra­­ch­eal intubation. Bilateral inferior bundle) (Figs 25.22A to D). A spatula osteotome can be used which
alve­olar nerve blocks with a long acting Once the lingula has been visualized, is gently tapped in the cancellous bone
lo­cal anesthetic (Bupivacaine) and vas­ the medial bone cut is made through the and intermittently rotated to separate
o­constrictor are given. A bite block is lingual cortex about 3 to 4 mm above the buccal and lingual cortices. The
placed on the contralateral side between neurovascular bundle and extending osteotome can be used in tandem with
upper and lower molars for easy access posterior to lingula. After completion of the spreader. Some surgeons do not
and projecting the ramus anteriorly. horizontal medial osteotomy, cut is then prefer to use the osteotome as it may
The landmarks for the intraoral incision carried down the lateral most aspect traumatize the inferior alveolar nerve.
include the anterior border of the ramus of the anterior border of the ascending The bone is spread gentally and the
and the external oblique ridge. ramus to the region of the second molar. neurovascular bundle is visualized as
The incision starts superiorly, two Then the bite block is removed and the bone is spreading. This is the best
thirds up the anterior border of the ram­ dissection is carried along the ascending method of avoiding trauma it. Usually
us over the bone, an incision is made ramus, inferiorly and laterally. For after the proper cut the neurovascular
through mucosa with a sharp scal­pel or advan­cement vertical cut is placed in the bundle lies in the distal segment but
Orthognathic Surgery 551

A B C D
Figs 25.22A to D: Sagittal split osteotomy

occasionally it may be seen clinging to It is therefore recommended that if the • Relapse following surgery. The cha­
the proximal segment, in such cases it tongue is large and is not properly ac­ n­­ces are more if the amount of aug­
should be carefully separated from the commodated in the reduced mandibu­ m­­en­tation or set back is exces­sive
bone. The same procedure is repeated lar tray, a reduc­tion glossectomy should or the surgery is attempted in the
on other side (Figs 25.23 and 25.24). be done (Figs 25.25A to C). grow­ing age before growth matu­
After the bone is spread, the im­ rity.
pacted third molars, if present, should Advantages • Injury to the inferior alveolar nerve
be removed. It is preferable that the im­ • Transoral procedure well accepted (most common), rarely injury to the
pacted third molars should be electively by the patients. lin­­gual nerve.
removed 3 to 4 months before the sur­ • Mandibular augmentation in excess • TMJ dysfunction and hypomobility
gery to ensure proper bony healing so of 10 mm possible. • Hemorrhage/hematoma
that the osteotomy cuts are placed prop­ • Correction of obtuse gonial angle is
erly and there is no hindrance due to the possible during correction of skel­
impacted third molars. etal class III deformities.
Modification of Sagittal Split
For the setback procedure, the dis­ Osteotomy
tal fragment is pushed back, there will Complications Trauner and Obwegeser (1957) made
be overlap of the buccal cortex of proxi­ • Malpositioning of condyle leading to horizontal cut just above the mandibu­
mal fragment in the molar region. The TMJ pain syndrome. lar fora­men on the mesial side of ramus.
excess bone on the proximal fragment • Malocclusion, open bite The vertical cut was taken down the an­
is cut off by taking another vertical cut • Lateral shift terior border of ramus of the mandible.
on the buccal cortex, distal to previous • Unfavorable splits (Bad split) An oblique cut was made through the
cut. The fragments should be checked • Proximal segment fracture late­ral cortex towards angle of the jaw.
for proper approximation and fixation • Distal fragment fracture It is a good technique for mandibu­
of fragments done by intraosseous wir­ • Excessive inflammatory edema which lar set­back but had poor bone contact
ing or lag screws or by bone plates. Care may extend to the larynx and cause with mandibular advancement. Avas­
should be taken not to cause too much respiratory embarrassment cular nec­­r­osis of angle due to extensive
rotation of mandibular condyles as it
may cause joint pain later. In case of ad­
vancement distal fragment is advanced
and fixed into desired position and fixa­
tion is carried out using mini plate and
screws. When the mandibular setback is
done the mandibular tray gets reduced
and the tongue is not accommodated.
In such cases there is a possibility of
the tongue getting pushed backwards
causing enchroachment on the pharyn­
geal space and obstructing the air way
or there can be tongue bite and due to A B C
the pressure there can be more relaspse. Figs 25.23A to C: Osteotomy cuts for SSO on mandible
552 Facial Deformities

A B C D

E F G H
Figs 25.24A to H: Clinical case of BSSO for mandibular set back and midline correction: (A and B) Preoperative photographs;
(C and D) Intraoperative photographs showing split; (E and F) Pre- and postoperative occlusion; (G and H) Postoperative photographs

A B C
Figs 25.25A to C: Reduction glossectomy: (A) Marking of the incision; (B) Excision of the myomucosal tissue in an elliptical manner;
(C) Closure of the defect with absorbable suture by placing inverted sutures

stripping of the pterygomasseteric sling by taking it only as far as the mandibular cle and limited medial dissection. These
may occur. foramen which prevented occasional modifications decreased postoperative
Dalpont (1961) modified the sagit­ shattering of the ramus in mandibular swelling, hemorrhage, and manipula­
tal split by advanc­ing the oblique cut to­ setbacks. tion of the neuro­vascular bundle. Blood
wards the molar region and mak­ing the Bell and Schendel (1977) and supply to the ramus is preserved as the
vertical cut through the lateral cortex. Epker (1978) made an anterior verti­ need to strip the pterygomasseteric sling
The main problem with setbacks was cal cut, through which whole of the is eliminated and intraosseous ischemia
interference between main retroposi­ lower border is sectioned through and and necrosis of the proximal segment
tioned proximal fragment and the mas­ through. The split is kept more later­ were significantly reduced.
toid process where occasional pressure ally by directing fine osteotomes down Spiessel (1976) advocated rigid
on the facial nerve may occur as well. the inner surface of the lateral cortex to inter­nal fixation of the BSSO to pro­
Hunsuck (1968) shortened the cut produce easier splitting. Epker included mote healing, restore early function and
through the medial cortex of the ramus minimal stripping of the masseter mus­ attenu­ate relapse.
Orthognathic Surgery 553

Inverted ‘L’ Osteotomy Indications • To correct minor occlusal discre­


It is described by Trauner and Obwe­ The C osteotomy is preffered for treat­ panies resulting after isolated Le
geser in 1957 as an intraoral procedure, ment of horizontal mandibular deficien­ Fort I osteotomy.
but it can also be accomplished through cies and to correct anterior open bite. • In patients with significant tempo­
subman­dibular incision. It is a versatile romandibular joint (TMJ) complaints.
procedure to treat severe mandibular Surgical Procedure
deformities. The inverted- L osteotomy is Except the inferior horizontal cut in the Contraindications
particularly well suited to secondary cor­ C osteotomy as shown in Figures 25.27A • Advancement of the distal, tooth-
rection of proximal segment malrotation and B, the surgical procedure for in­ bearing mandibular segment.
following sagittal split ramus osteotomy verted L and C osteotomy is almost the • Recent condylar fractures.
(SSRO), as well as simultaneous ad­ same. Both the procedures are primarily
vancement and lengthening of the ramus indicated for mandibular advancement. Surgical Procedure
in cases of severe ramus under develop­ This is the technique indicated for corre­
ment (e.g. Treacher Collins syndrome, ction of the mandibular progna­ thism
Goldenhar’s syndrome). It is best suited
Intraoral Vertical Ramus (Class III) the procedure can be done
method for mandibular advancement. Osteotomy intr­­ao
­ rally by taking an incision along the
anter­ior border of the coronoid process
Surgical Procedure Indications extending from the tip to the molar area.
The ramus is approached by submandib­ • In patients with horizontal mandib­ The lateral side of the ramus is degloved
ular incision. The approximate length of ular excess in whom a good profile, completely by the sub periosteal dissec­
the incision is 6 cm. The inferior border arch and dental relationship can tion, detaching the masseter completely.
of the mandible is rea­ched, care is taken be obtained by retruding the intact The posterior border of the ramus and
to avoid damage to the marginal man­ mandibular arch. the sigmoid notch are identified. The soft
dibular nerve. The dissection is further • Mandibular asymmetry which req­ tissue is retracted using channel ret­ra­ ­
continued to expose the sigmoid notch uires largely rotational movement ctors placed over the posterior border and
by reflecting the masseter muscle. The of one or both mandibular rami to the sigmoid notch. For performing this
vertical cut is made at least 7 mm ante­ achieve correction of deformity. osteo­ tomy procedure intraorally osci­
rior to posterior border of ramus upto • To achieve vertical correction in the ll­ating saw is mandatory. The ramus is
the inferior border of angle of mandible man­dibular arch. osteo­tomised roughly 7 to 8 mm ant­er­ior
to ensure that the cut is posterior to the
mandibular foramen and to avoid cutting
through it. Horizontal cut is made above
the anti­cipated position of the inferior al­
veolar foramen. Once cuts are completed
me­dial periosteum may have to be ele­
vated from some of the distal fragment
to allow its advancement. Similar pro­
cedure is repeated on other side and IMF
A B
is done. Next step depends on the type of
mandibular movement. If the distal seg­ Figs 25.26A and B: Inverted L osteotomy
ment is set back, then proximal seg­ment
has to be overlapped laterally. If the man­
dibular advancement is done cancellous
bone graft is packed in the gap between
the proximal segment and the advanced
distal segment (Fig. 25.26B). Fragments
are secured with mini plates or lag screws
and closure done in layers. Extraoral pre­
ssure dressing is maintained for 24 to
48 hours (Figs 25.26A and B).

C–Ramus Osteotomy A B
This technique was first described by Figs 25.27A and B: Caldwell, Hayward and Lister (1968) presented ‘vertical L osteotomy’
Caldwell and colleagues in 1968. which was later modified to conform to a ‘C osteotomy’
554 Facial Deformities

to the posterior border of the ramus, to en­ If the vertical osteotomy cut is pro­ closed in two layers, i.e. the muscle and
sure that it is posterior to the mandi­bular ximal to the mental foramen, it will be a mucosal layer and a pressure dressing
foramen to avoid injury to the neuro­ necessary to reposition and retract the is given externally.
vas­cular bundle and extends verti­ cally mental nerve (Figs 25.28A to D). The
from the sigmoid notch to the inferior oste­ot­omy is accomplished with rotary Complications
bord­er. After the osteotomy, the distal instrument or with microsaws. After • Loss of bone and/or teeth in the ost­
mandibular segment is placed backward com­pleting the vertical osteotomy cut, eotomized segment
and medially while the proximal segment a horizontal cut is made, connecting • Root damage and devitalization of
lies laterally. The dis­ tal and proximal the vertical cuts at their inferior extent. the teeth if bone cuts are too close to
segments need not be fixed rigidly but Hori­zontal osteotomy cut should be roots
only IMF in desired posi­tion as guided by made atleast 5 mm below the apices of • Mental nerve damage
guiding splints for four weeks is enough. teeth to prevent devitalization. • Nonunion or malunion if segments
If the oscillating saw is not available, The segment is mobilized by using an are not properly fixed.
this procedure can be done extraorally osteotome. A preformed surgical splint
through small extra­oral Risdon’s incision. should be used to guide the segment
into its predetermined position. All
Total Mandibular
Complications bony interferences should be removed. Subapical Osteotomy
• Bleeding The segment is secured by transosseous Hullihen in 1849, described a procedure
• Inferior alveolar nerve injury wires or with miniplates. The incision is similar to subapical osteotomy who
• Unfavorable osteotomy.

Anterior Mandibular
Subapical Osteotomy
Indications
• Correction of mild anterior open bite.
• Correction of mandibular dento­alv­
e­olar proclination and dental arch
asymmetry.
• Leveling an accentuated curve of spee.

Surgical Procedure
A degloving incision is given in the la­
bial vestibule after infiltration with vas­
o­constrictor to achieve hemostasis. A
No. 15 scalpel or an electrucautery is A B
used to make an incision in the lower lip
approximately 1.5 mm labially from the
vestibule. The incision extends from first
premolar to the first premolar of other
side and is initially carried only through
the mucosa, then it extends upto the
periosteum through the mentalis mus­
cle. The periosteum is incised and diss­
ection is done up to the lower border
of mandible and continued posteriorly
along the inferior border until the mental
neurovascular bundle is visualized.
Once the nerve is visible and protected,
the mucosal incision can be extended
post­eriorly as dictated by the proposed C D
osteo­tomy site. If extraction is planned, Figs 25.28A to D: (A) Anterior maxillary subapical ostetomy; (B and C) Anterior mandibular
it can be performed at this time. subapical osteotomy with genioplasty and (D) Final positioning of the osteotomized segments
Orthognathic Surgery 555

used it to treat “elongation of the under­ buccal cut is then completed through The osteotomy cut is started from
jaw”. Hofer and Kole described the only outer cortex and remainder of the the sigmoid notch above the level of
modi­fications of the procedure. This is lingual cortex adjacent to and below the mandibular foramen through both the
not per­formed routinely. bundle, is fractured with the osteotome. cortices. Then the cut is started from
inferior border going up to the level of
Indications Vertical Subsigmoid mandibular foramen, both the cuts then
• Malocclusion caused by a mandi­ Osteotomy (VSO) joined together. Care is taken to protect
bular dentoalveolar deformity with Caldwell–Letterman in 1954 first pro­ the medial tiss­ues. Similar procedure is
app­ropriately positioned maxi­llary posed this procedure through extra­oral carried out on the opposite side. After
and mandibular skeletal bases. approach. that proxi­mal fragments pla­ced over dis­
• It is used to reposition entire mandi­ tal frag­ments and tempory IMF is done.
bular dentoalveolar segment anteri­ Indications Decorti­cation of the dis­tal segment is
orly, posteriorly or superiorly. • It is limited to deformities requiring carried out on the lateral aspect of the
mandible to be setback for mandi­ overlap area and the proxi­mal segment
Surgical Procedure bular horizontal excess or to be rot­ on the medial aspect. The proximal seg­
A circumvestibular incision is made ated for mandibular asymmetry. ment is fixed laterally to the distal seg­
from retromolar area of one side of man­ • Large mandibular setbacks of gre­ ment overlapping it with intraosseous
dible to other side; care is taken to incise ater than 10 mm. wiring, lag screws or bone plates.
mucosa and submucosa only. The men­
tal neurovascular bundle is iden­tified Surgical Procedure Mandibular Body Osteotomy
and skeletonized with blunt dissection Extraoral approach is used for VSO; Blair in 1907 first described body
to avoid damage. Anterior to neurovas­ however the procedure can also be ac­ osteo­tomy as an extraoral procedure.
cular bundle, the incision is carried out complished intraorally. Submandibular Later Ding­­man used a combination
into the anterior vestibule (as for a ge­ or postramal incision is given; sharp and of intraoral and extraoral access with
nioplasty). Dissection is then completed blunt dissection is used to reach the low­ preservation of the inferior alveolar
in the subperiosteal plane while protect­ er border of the mandible. Care is taken neurovascular and bone graft­ ing to
ing the mental neuro­ vascular bundle to avoid damage the marginal mandibu­ assist bony union. This was one of the
(Figs 25.29A and B). lar branch of the facial nerve. With the earliest procedures used for mandibular
The buccal cortical bone above and help of periosteal elevator periosteum prognathism. Since the advent of the
below the neurovascular canal is cut is reflected and the ascending ramus, ramus procedures the body osteotomy
with fissure bur, then removed with an sigmoid notch and coronoid process has lost popularity (Figs 25.31A to D).
osteotome. This cortical bone can be are exposed. Mandible is pulled down­
morselized and replaced in strategic lo­ wards with the help of the bone forceps Indications
cations later. Before beginning horizon­ applied at the angle of the mandible • Mandibular setback
tal osteotomy, vertical reference marks (Figs 25.30A and B). • Progenia correction
are made anteriorly and posteriorly.
The actual osteotomy site is marked by
taking direct measurement from the oc­
clusal plane. The horizontal osteotomy
started from symphysis region and con­
tinued posterior to the last molar. Care
must be taken when completing the
horizontal osteotomy to prevent dam­
age to the lingual vascular pedicle; this
is acc­omplished by placing the guiding
finger on the lingual side. The horizontal
osteo­tomy is completed 0.5 cm or more
from the apices of the teeth in order to
preserve pulpal circulation.
A vertical osteotomy is performed A B
through an extraction socket or between Figs 25.29A and B: Osteotomy cut for total mandibular subapical ostetomy. Prior to this
the adjacent teeth using bur, saw or ostetomy cut buccal cortical plate graft is harvested and then osteotomy cut is completed
osteotome. Care must be taken to above neurovascular bundle but below apices of tooth and then buccal graft is placed
prevent damage to lingual nerve. The back in position
556 Facial Deformities

move the anterior segment of the man­


dible posteriorly, or alter the vertical and
transverse position (Figs 25.33A and B).
The main disadvantage of this technique
is less bone contacts and in the past ow­
ing to lack of the rigid fixation the results
were unstable. The chances of damage to
the neurovascular bundle are high.

Genioplasty
A B
It is the surgical procedure done for corr­
Figs 25.30A and B: Vertical subsigmoid osteotomy e­ct­ ing the deformities of the chin. The de­
formities of the chin like chin excess, chin
• Mandibular advancement that involves a step-cut made anterior retrusion and chin deviation can be cor­
• Anterior open bite closure and curve to the mental foramen. It is indicated for rected with this procedure and the genio­
of spee reduction. correction of mandibular prognathism plasty is typed accordingly. It is also indi­
by either using the space from extraction cated for the correction of chin asymmetry
Surgical Technique of a posterior tooth or by closing an ex­ following the TMJ ankylosis and case of
isting edentulous space (Figs 25.32A and condylar hyperplasia or hypoplasia.
Mandibular Step Osteotomy B). MSO is different from ramus osteoto­ • Augmentation genioplasty—the
Von Eiselburg first described the mandib­ my in that it allows further modification augmentation could be either verti­
ular step osteotomy (MSO) technique for of the dental arch form vertically for clo­ cal or horizontal. This technique is
correction of mandibular retrognathia in sure of anterior open bite or correction used for the correc­tion of the hypo­
1906. Shortly after, Pichler (in 1918) de­ of reverse curve of spee and transversely plastic or retruded chin. (bil­ateral
scribed the use of MSO for correction of for arch constriction. The stability of the TMJ ankylosis, micrognathia) as
mandibular pro­­gnathism. They both per­ osteo­ tomy is enhanced mechanically shown in Figures 25.34A and B.
formed the technique through an extra­ by the step-cut design, which provides • Reduction genioplasty—for the
oral route with no intention of preserving a favorable fracture pattern as well as correction of excess in the vertical
the mental nerve. In 1948, Dingman com­ maximal bony approximation. Fixation or horizontal directions. (Skeletal
bined the intraoral and extraoral appro­ can be easily achieved by single miniplate class III or prognathism) as shown in
aches for correction of mandibular retru­ on each side. The basic disadvantage with Figures 25.35 and 25.36B.
sion. Converse and Shapiro were the first this technique is chances of damage to • Sliding genioplasty—it is indicated
to perform MSO using a pure intraoral the neurovascular bundle and necessity for the correction of the asymmetry of
approach. They recommended different for extraction of the functioning pre­mo­ lower jaw due to deviation of the chin
step designs for the correction of a variety lars. on one side (unilateral TMJ ankylo­
of mandibular deformities; this included sis, unilateral condylar hyperplasia,
the conventional step-cut for correction Vertical Body Osteotomy etc.) (Figs 25.37, 25.38 and 25.36C)
of mandibular advancement. MSO is a The vertical body osteotomies can be • Flip genioplasty—it is the pro­
mandibular body osteotomy tech­nique performed in any area of the mandible to cess which is generally done for the

A B C D

Figs 25.31A to D: Body osteotomy: (A) Preoperative photograph; (B) Postoperative photograph; (C) Preoperative radiograph showing
Class III malocclusion; (D) Postoperative radiograph showing surgical correction and bone plates in place
Orthognathic Surgery 557

co­rr­ection of the deformity of the the acute twisting of the pedicle may chin is moved in multiple segments
chin following the TMJ ankylosis. lead to avulsion of the segment or in a stepwise manner rather than
The genioplasty cut is taken and avasular necrosis if the vascularity is moving it forward in one block. The
based on the geniohyoid pedicle compromised (Fig. 25.36D). advantage is that there is gradual
the osteotomized segment is twist­ • Double sliding genioplasty­—it is incremental augmentation of the
ed 360° and flipped to other side. It used to treat severe deficiency of the chin which gives good profile. But,
produces good cosmetic results but chin, when occlusion is stable. The the disadvantage being that there
can be loss of vascularity of smaller
fragments (Fig. 25.37).
• Sandwitch genioplasty­—when the
gap between the fragments is more
and bone contact is less, to facilitate
the bone healing cancellous bone
graft is placed between the two
fragments (Fig. 25.38).
• Alloplastic augmentation genio­
plasty—it is a simple procedure
which is dien transorally. A vestibu­
lar incision is placed in the anterior
A region, protecting the mental nerves.
An implant biopore, silicone, silastic
is placed over the bone as an overlay,
after carving it to the desired shape
and secured in place with screws. The
basic disadvantage is rejection of the
implant. This technique is not very
popular as most of the chin deformi­
ties can be corrected with augmenta­
tion, reduction or sliding genioplasty,
without any need for the alloplastic
implants (Fig. 25.39A and B).

Procedure
B The procedure is essentially done intra-
Figs 25.32A and B: Mandibular step osteotomy orally through a degloving incision in

A B

Figs 25.33A and B: Vertical body osteotomy


558 Facial Deformities

the labial vestibule of the lower jaw, dissection is carried out to expose the the chin retractor. The dissection is
extending from the premolar to pre­ symphyseal area from mental foramen carried out up to the inferior border
molar (Figs 25.36A to N). Care should be to mental foramen on either side. The to expose it. A chin retractor is used to
taken to avoid damage to the branches mental nerve is carefully retracted. retract the soft tissue and the lower lip.
of the mental nerve. The sharp and blunt The labial soft tisse is retracted using The genioplasty cut is marked using the
recroprocting saw or a fine bur. The cut
extends from mental foramen to mental
foramen without damaging the mental
nerve and goes below the apices of
the teeth. The cut is deepened and the
osteotomy is completed. Care should
be taken not to damage the lingual soft
tiss­ue and the osteotomised chin seg­
ment should be handled carefully to
avoid avulsion of the attachments of
A B
geni­­oglossus and geniohyoid muscles
which serve as a vascular pedicle to
Figs 25.34A and B: Horizontal genioplasty with advancement
the osteotomised segment. If the aug­
men­tation genio­plasty is planned then
the osteotomised segment is held with
a to­ wel clip and slided anteriorly up
to the desired position. The soft tissue
contour is checked. The segment is fixed
rigidly, using a mini plate and screws.
As far as the bone contact bet­­ ween
the superior and the inferior (osteo­ ­
A B tomized) segments is good the heal­ing
will take place satisfactorily, but if the
Figs 25.35A and B: Vertical reduction genioplasty
augmentation is excessive and the bone
contact is not adequate, then cancellous
bone graft harvested from the iliac crest
should be packed in the gap between the
upper and lower fragments (Fig. 25.38).
The augmentation genio­plasty can also
be done by giving overlay graft (Figs
25.39A and B) or implants (medpore
implants) to improve the chin contour
(Figs 25.40A to E).
The reduction genioplasty is done
to correct the genial excess. To correct
the vertical excess similar type of osteo­
A B
tomy is done and the intervening bone
is removed to correct the excess. It is
not good idea to grind and reduce the
chin as the corticated margin of the
symphysis gives good contour.
In case of the horizontal excess, the
osteotomised segment is pushed back
and secured in the retruded position
with the help of lag screw or properly
contoured and adapted plate.
C D E In sliding genioplasty the osteoto­
Figs 25.36A to E: Surgical procedure for horizontal augmentation genioplasty: mised segment is slid to the deficient
(A to C) Intraoperative photographs; (D) Preoperative photagraph; (E) Postoperative result side to correct the asymmetry.
Orthognathic Surgery 559

COMPLICATIONS OF
ORTHOGNATHIC SURGERY
The immediate complications are:
• Vascular complications: Hemorrha­
ge occurs due to damage to regional
vess­sels like inferior alveolar artery,
posterior superior alveolar artery,
pte­ rigoid plexus of veins, greater
palatine artery or branches of
internal maxillary artery. Care should
be taken to do the dissection in a
subperiosteal plane and the soft
tissue should be properly guarded
and retracted duri­ng the surgery.
F G • Edema, hematoma, airway edema:
The edema is the common complic­
Figs 25.36F and G: Surgical procedure for vertical reduction genioplasty:
(F) Preoperative; (G) Postoperative photographs ation following the sagittal split
osteo­tomy and Le Fort osteotomies.
It is due to the fact that the surgeries
are performed transorally and the
wounds are closed primarily. The
osteo­tomy site lies in the closed com­
part­ ment and there is no nat­ ural
deco­mpression/drainage. Thus, the
edema accumulates and distends the
tissue. Minor oozing of the blood at
the surgical site leads to hematoma
formation. The edema can spread
to the adjacent areas like pharynx
and larynx causing respiratory obstr­
uction. To avoid excess of edema
peri­surgical steroid therapy with hy­
drocortisone or dexamethasone is
helpful. The incision is closed with
loose sutures so that it works as natural
H I
drainage site. The judicious use of the
vacuum drains also helps in reducing
the edema and hematoma. The
hemostasis should be meticulous.
Periodic evaluation of the airway for
patency and airway edema should
be done especially in the initial 24 to
48 hours. In case the excessive edema
is anticipated the nasal endotracheal
tube may be left indwelling for
24 hours to ensure respiratory
passage patency.
• Dental and periodontal injuries are
more common in cases of subapical
osteotomies and body osteotomies.
J K
• Sensory and motor nerve inju-
Figs 25.36H to K: Sliding genioplasty: (H) Preoperative photograph; (I) Postoperative photo­ ries: Inj­ury to inferior alveolar dur­
graph; (J) Osteotomy cut; (K) Sliding genioplasty, segment fixed with screw and plates ing the sagittal split osteotomy or
560 Facial Deformities

M N

Figs 25.36L to N: Case of flip genioplasty: (L) Diagrammatic representation of the flip genioplasty;
(M) Osteotomy cut; (N) Flipped segment secured in place

Le Fort osteotomies of maxilla the created in the maxilla (floor of pyri­


septal osteo­tomy is done and after form fossa) to reposition the septum.
placing the maxilla in the desired The alar cartilages are detached
position the septum is repositioned. during the degloving incision taken
If care is not taken the septal de­ for the Le Fort osteotomy. During the
viation and obstruction/narrowing closure alar cinch is done by placing a
the nasal p­as­ sage
­­ may result creat­ non absorbable suture engaging bases
ing subs­ eq­
uent nasal obstruction. of both the alar cartilages to prevent
Fig. 25.37: Double sliding horizontal During the superior positioning of flaring and distortion of the nose.
genioplasty the maxilla a wedge of septal bone/ • Proximal segment fracture: The
cartilage is removed (septoplasty) proximal fragment during the
to prevent buckling of the septum. sagittal split osteotomy are often
distr­
acti­
on, ramal osteotomies and Alternatively a deep groove may be thinner and weak as the vertical cut
mental nerve during genioplasty
or anterior segmental osteotomy of
mandible are possible. Even after ad­
equate pre­­cau­tions minor neurologi­
cal dis­
tur­bances may occur which
usually recover within few weeks.
The chances of inferior alveolar nerve
injuries are more during the man­
dibular body osteotomies, but, these
procedures are seldom performed. A B
• Alteration in nasal septum, na- Figs 25.38A and B: Sandwitch genioplasty. (A) Vertical as well horizontal augmentation;
sal valve, alar base: Following the (B) Verticle augmentation, by sandwiching the cancellous bone graft
Orthognathic Surgery 561

A B
Figs 25.39A and B: Overlay grafting for augmentation genioplasty: (A) Exposure of surgical site; (B) Overlay iliac crest graft,
fixed with screws

A B C

Figs 25.40A to E: Alloplastic augmentation genioplasty using


biopore implant: (A and B) Preoperative photographs; (C) Biopore
implant carved as per the need of the patient; (D and E) Postoperative
D E photographs. (Source: Dr Sanjay Deshpande, MS, MCh, Mumbai)

is taken more buccally to prevent n­ing and patient approach during excess of the overlapping bone on
injury to the inferior alveolar nerve. the split without using undue force the buccal cortex of the proximal
Injudicious application of the force can avoid such complications. segment should be trimmed to en­
with bone spreader may lead to • Excessive lateral displacement or sure that the displacement is not in
fracture of pro­ximal segment. rotation of the proximal segment excess of 10 degrees.
• Lingual segment fracture: A bad may occur during the sagittal split
Delayed Complications are:
split due to the inadequate cortical osteotomy or VRO and mandibular
cuts, excessive force or anatomical set back. It leads to abnormal con­ • Loss of vascularity: Loss of vascu­
variations such as thin ramus may dylar position and subsequent TMJ lar pedicle due to injudicious han­
occur. Meticulous evaluation, plan­ complications. To avoid the same dling leads to such complications
562 Facial Deformities

especially in maxillary segmental os­ corrected by postsurgical orthodon­ Curr­ently, both extraoral and intraoral
teotomies, Le Fort osteotomies and tics. The occlusal discrepancies are devices may be used depending on the
the genioplasty. more severe if the orthodontic eval­ condition to be treated (Goldwaser et al.,
• Necrosis of hard and soft tissues: uations, planning and interventions 2011).15 Commonly treated conditions
Due to excessive trauma, loss of vas­ are not done in presurgical period. include craniofacial deficiencies, syn­
cular pedicle and excessive edema, dro­mic craniosynostosis, Pierre Robin
Miscellaneous complications could be:
hematoma formation and infection Sequence, post-traumatic deformities,
of surgical site, the soft tissue or bony • Epiphora in cases of Le Fort II osteo­ and sleep-related breathing disorders
fragments may undergo necrosis. tomy due to injury to nasola­cry­mal (Vander Kolk et al. 2001).15
• Nonunion or delayed union: duct. The concepts of distraction osteo­
Improper immobilization/fixation, • Auriculotemporal syndrome: Frey’s genesis in the maxillofacial region are
infec­tion and avascular necrosis of syndrome is rare complication asso­ similar in many respects to those used for
the osteotomised bone ends can lead ciated with the ramal osteotomies. long bones, yet differences in the shape,
to healing complications like delayed • Facial scars: Le Fort II and III osteo­ development and configuration of the
union, fibrous union, or non union. tomy necessitates incisions on skin bones of the face make its use more chal­
• Fistulas: Oronasal and oroantral fist­ and can leave behind scars. Most of lenging than traditional ost­ eo­
tomies.
ulas could be the commonest fistulas other procedures are done tran­sorally. Dis­trac­tion osteogenesis (DO), a useful
following maxillary osteo­tomies. The • Salivary injuries: It is rare compli­ tech­nique to generate bone and soft tis­
salivary fistula is rare complication. cation associated with ramal or sue, can be applied to cra­nio­facial recon­
• Infection: Surgical site complication maxi­ll­ary osteotomies. struction, including ort­hognathic surgery,
is a common complication follow­ cleft lip and palate reconstruction, a new
ing any surgical procedure. It can be DISTRACTION mandibular con­dyle regeneration, a den­
prevented by meticulous planning, toalveolar unit reconstruction for dental
OSTEOGENESIS
aspetic precautions, judicious tissue implants and transport DO for disconti­
handling and prophylactic antibiotics. Introduction nuity defects.
• TMJ dysfunction: Due to repositi­ The principles of distraction as refi­ned
oning of the osteotomized bone, Historical Background by Ilizarov and other orthopedic surgeons
altered muscle position and orien­ Codivilla from Italy is credited for and they continue to be refined when
tation and change of the codyle having performed the first lengthening used by orthopedic and maxillofacial
position, the TMJ dysfunction can be procedure by applying skeletal traction surgeons. An almost bewildering array
precipitated. Care should be taken through a calcaneal pin, following oste­ of appliances is available to distract the
not to grossly alter the condylar otomy of the femur.15 bones of the face, including intraoral
position and gradual muscle toning However, it was a Russian surgeon, and extraoral appliances, univectors and
with physiotherapy. Occasionally Gavril Ilizarov, who pioneered the multivectors, and tooth-borne and bone-
myotomies may be performed to biological principles of bone and soft borne appliances.
minimize this complication in rare tissue regeneration and popularized the
cases warranting gross change of technique of distraction osteogenesis, Concept of Distraction
muscle positions due to gross alter­ when he discovered that under slow and Osteogenesis
ation of bone position. gradual distraction, the callous will be Regardless of the surgical site, adherence
• Relapse: Adverse muscle pull is one gradually stretched and new bone will to the following basic Ilizarov principles
of the major factor in inducing re­ regenerate in the distracted gap.15 is the key to surgical success:
lapse. Certain degree of relapse is Starting in the early 1950s, he worked • Osteotomy of the bone site with
unavoidable. The relapse is more in a village in Siberia, Kurgan, unknown minimal periosteal stripping
significant when the advancement or to the rest of the world. Subsequently, in • Latency period: 3, 5, or 7 days, dep­
setbacks are significantly high. Selec­ 1982, he successfully treated a famous ending on the surgical site
tive myotomy (muscle stripping) may Italian explorer “Carlo Mauri” for a • Distraction rate: 1.0 mm per day
avoid the relapse. However, if the resistant nonunion of his tibia and it (0.5–2.0 mm)
augmentation is more, distraction was only then when his principles were • Distraction rhythm: Continuous
should be preferred over osteotomy made known to the Western World. force application is best, yet device
to get more lasting and stable results. Mandibular distraction was first activation twice a day is more prac­
• Occlusal discrepancies: Even after performed in 1973 in a canine model tical and allows for better patient
meticulous planning and presurgi­ (Snyder et al., 1973). However, it was compliance
cal orthodontics minor occlusal dis­ only in 1992 when it was first reported • Consolidation: Until a cortical out­
harmony may remain which can be in humans (Mccarthy et al., 1992). line can be seen radiographically
Orthognathic Surgery 563

across the distraction gap, usually Variables in Distraction Vector


6 weeks. Vector is the direction that the segment
Using distraction rates of 0.5, 1, or Rate and Rhythm is moved. Extrinsic and intrinsic vectors
2 mm/day and different distraction In practice, most surgeons use a 3 to must be considered when planning a
frequencies with both osteotomies 5 days latency period followed by a rate case. In the case of a single vector ra­mus
and closed techniques, Ilizarov found of 1 mm/day with a twice-a-day rhythm distractor, the primary vector is the di­
that a distraction rate of 1 mm/day in the mandible. A shorter latency is rection that the tram is pointed. Intrinsic
led to the best results for bone, fascia, used in the maxilla.16,17 vectors (the masseter and medial ptery­
skeletal muscles, smooth muscle, blood goid muscles) are more resistant to ver­
vessels, nerves and skin regeneration Age of the Patient tical movement of the segment than the
(lengthening). He observed that the In a pediatric population, Hollier and suprahyoid musculature is to anterior
greater the distraction frequency, the coll­ea­gues were able to eliminate the movement of the mandible.18
better is the outcome. He concluded that latency period and successfully distra­ In contrast to vertical distraction of
the best results were obtained with pre­ cted the mandibles of 22 patients at a the ramus with mandibular advance­
ser­vation of periosseous tissues, bone rate of 2 mm/day. Most surgeons use a ment the suprahyoid musculature ex­
marrow and blood supply at the time shorter latency in pediatric patients and erts a vertical pull on the distal segment
of osteotomy, stability of the distractor a more rapid rate of expansion.16 One as the mandible is advanced. To coun­
(external) and a rate of 1 mm/day with a of the complications of a long latency teract these intrinsic vectors, the dis­
rhythm of four turns per day.16 or a slow distraction rate in a pediatric tracters should be directed in a slightly
population is premature consolidation. upward direction toward the maxillary
Histology dentition.
From a histologic evaluation, when dis­ Systemic Factors
traction is completed, new bone forms The ideal management of patients with Treatment Planning
in parallel columns that extend in both history of smoking and alcohol use As with orthognathic surgery, treatment
directions from the osteotomy. The dis­ involves eliminating or markedly redu­ planning for distraction osteogenesis
traction process can be divided into cing their use before surgery. includes predicting the amount and traj­
three phases. During the latency period ectory of the planned bone movement.
(first phase), histologic and molecular Indications Although the DO device may be
events are similar to those seen during • Severe deficiency of maxilla and acti­vated 1.0 mm per day, this does not
fracture healing, with the osteotomy mandible (bilateral or unilateral) translate to 1.0 mm of bone advance­
site surrounded by a hyaline cartilage • Jaw bone deficiency related to syn­ ment per day. The amount of actual
external callus. In the distraction phase dro­mes bone movement is always less than the
(second phase), chondrocytes are stre­ • Cases in which large amount of distance that is indicated on the dis­
tched along the tension vector and advancement is required which can­ tra­ction device, therefore the clinician
become fibroblast-like in shape. not be corrected by orthognathic mon­i­tors the patient’s progress closely,
As distraction is advanced (third surgery.17 including radiographs. The surgical
phase), the cartilaginous callus is pro­ approach and technique are similar to
gre­s­sively replaced by a bone callus Contraindications orthognathic surgery. When locating
first by endochrondral ossification; later As a method of new bone formation in and positioning the bone cut, also
new bone is directly formed by intra­ patients with osseous dysplasia.17 consider the placement and orientation
membranous ossification. of the distraction devi­ ce. Mark the
During distraction, several mole­ Type of Distractors planned osteotomy. Then create a
cules of the bone morphogenic protein Fundamentally, external distractors are corticotomy, verifying the ability to
super family have been noted. Several less stable than internal ones. Under place the distractor in the pro­ per
studies have noted increased blood flow bio­mechanical testing that external dis­ orientation. Make the screw fixation
and vessel formation within the zone actors failed with permanent defor­ holes for the distraction device, and
tr­
of distraction. Pacicca and colleagues mation of the pins rather than fracture of remove the device. The corticotomy
showed two different angiogenic the model, as seen in the ones with inter­ is then converted atraumatically to an
factors localized at the leading edge nal distractors. The situation beco­mes osteotomy and the distraction device is
of the distraction gap where new bone more complex when soft tissue consid­ refixed in place. The device is activated
was forming.17 They also found these erations are made. The position in which to ensure impedance-free advancement
factors to be maximal during active the distractor is placed to simulate soft of the distraction segments. Remove
distraction. tissues affects the distraction vector. any bony interferences and return the
564 Facial Deformities

device to its closed neutral position. – The vector can be made to pass anteroposterior deficiency with some
Prior to initial device orientation and through or above the center of patients presenting with a component
placement, activate the distractor 1.0 resistance of maxilla. of both deficiencies.
to 2.0 mm. Thus, after the osteotomy – It is not necessary to wait until Submerged distractors can be acce­
and the device are secured into place, skeletal maturity to treat severe ssed by a transcutaneous or intra­oral
the DO device can be “closed” 1.0 to midface hypoplasia. approach. The ramus may be ver­ti­cally
2.0 mm, reducing and minimizing the – Patient tolerance to the device is lengthened, the body can be horizontally
initially created distraction gap.16 less. lengthened, or both.
Transcutaneous distractor for vertical
Technique lengthening of the ramus can be manipu­
DISTRACTION DEVICES A complete Le Fort I osteotomy is per­ lated extraorally to achieve an ideal posi­
AND OPTIONS formed with pterygomaxillary and septal tion. They usually come in a right and left
disjunction followed by mobilization. side. Distractors for the body come in dif­
Midface and Maxilla Once the maxillary osteotomy is com­ ferent designs and can be adapted to the
plete the halo portion of the device is ad­ body or ramus depending on the desired
Submerged Versus Nonsubmerged justed to the width of the neurocranium access and surgeons pre­ference.19
The basic distractor is a tram that allows and is rigidly fixed around the head with • Submerged device: It is a device that
expansion in one or more directions two or three scalp screws per side. The can be attached to the mandible with
that has some sort of attachment to the screws must be over solid bone about 2 to 1.9 or 2.3 mm self-tapping monocor­
bone, teeth, or both. 4 cm above helix of the ear. Vertical bar of tical or bicortical screws. The bone
• Submerged device: The submerged the device should be centered with mid plate component of the device can
device is designed to be internal, sagittal plane, parallel to the facial plane be contoured or shortened intraop­
self-retaining and remains fully bur­ and sufficiently anterior to allow desired eratively to accommodate the local
ied in the tissue after the distraction amount of distraction. After the halo is anatomy. The important design fea­
is complete and thus, can be used as secured, the vertical facial bar is removed tures that improve the performance
retentive device as well during the since distraction is not begun 3 to 5 days and ease of use include:
consolidation phase (Figs 25.41 and after surgery. Once the latent phase is – Antiback activation screw pro­
25.42). The important design fea­ over, the vertical rod is replaced and the vides excellent stability and offers
tures that improve the performance tooth borne appliance is attached to it adjustment of mediolateral vector
and ease of use include: and is activated periodically to distract of distraction during unilateral or
– Internal, submergible design to the maxilla at the rate of 1 mm per day. bilateral mandibular lengthening.
allow prolonged fixation period. – Device is suitable for children,
– Self-retention to eliminate prob­ Bone-borne Versus Tooth-borne adolescents and the adults with
lems with fixation screw loosening. Appliances that are applied to the teeth hemifacial microsomia.
– Bilateral, parallel distraction usually create a moment arm resulting – After consolidation approximately
vector to decrease unfavorable in uneven distraction because they are 3 months later a second surgery
forces at anchorage sites. not at the center point of segment to is required for device removal
– It is torque calibrated to allow be distracted. Tooth-borne appliances (Figs 25.43A to E).
control of distraction forces. in the maxilla usually are custom made • Nonsubmerged device: The device
– Permanently implantable or and cemented to teeth before surgery. essentially consists of an angulation
readily removable. The most common use is to widen the joint and two geared rods of variable
• Nonsubmerged device: The device maxilla by surgically assisted rapid pala­ lengths. It can be a hinge joint or a
utilizes a skeletally (cranial) fixed tal exp­an­sion. Anteroposterior intra- double ball joint (Figs 25.44A to E).
distraction device that is fully adjust­ arch dis­traction, however, can be done The important design features that
able and offers the ability to change for arch length discrepancies in the improve the performance and ease
the vertical and horizontal vectors of maxilla with and without crowding. of use include:
distraction at any time without pa­ – The pin holders facilitate move­
tient discomfort during the distrac­ Mandible ment of the riders in different
tion process. The important design direction.
features that improve the perfor­ Submerged Versus Nonsubmerged – The device can be adapted ac­
mance and ease of use include: Like the maxilla, the desired move­ cording to individual anatomic
– It controls the vector of distrac­ ment of the mandible seldom is in situation.
tion relative to the maxillary cen­ one direction. Deficiencies may be – Bony segments can be moved in
ter of resistance. in vertical ramus length and sagittal almost any direction.
Orthognathic Surgery 565

A B C

D E F
Figs 25.41A to F: A case of maxillary hypoplasia secondary to cleft lip and palate treated with maxillary distraction: (A) Preoperative
photograph showing midface deficiency (frontal view); (B) Postdistraction advancement of maxilla (frontal view); (C) Preoperative
photograph (three quarter view); (D) Postdistraction advancement of maxilla (three quarter view); (E) Preoperative lateral cephalogram;
(F) Postoperative lateral cephalogram with maxillary advancement

Bone-borne Versus Tooth-borne be placed. Other indications include more asymmetric segment continues to
patients with mixed dentition stage. be advanced at the planned rate until it
Several of the tooth-borne distracters catches up with the contralateral side.
are for intra-arch dis­ traction of the Dancing Distraction Carry out any final adjustments to the
mandible. The most pop­ ular type of Perform “dancing” of the distraction seg­­­ mandibular positioning when the asym­
intra-arch distraction is at the sym­ ment if a discrepancy occurs in pla­n­ned metry has been corrected by advancing
physis to increase arch len­ gth while distraction, such as bil­ateral mandibular or dancing of the two sides as needed.16
simul­taneously resolving crow­ding. advancement for asy­mm ­ etries.
They produce symmetric distraction of Initially, both segments are advan­ Mandibular Distraction
both the alveolar crest and the inferior ced at the planned distraction rate. For patients with craniofacial micro­
border. They can be used when the teeth When the larger, less asymmetric side somia, mandibular distraction of the
are healthy and the crown to root ratio reaches its final position, this segment affected side is a useful technique for
is adequate. Bone borne distraction becomes the dancing side, i.e. advancing generating both bone and soft tissue.
devices should be considered when the larger segment in the morning and The surgical approach is similar to a
there is poor bony support to the teeth then turning it back the same amount in sagittal osteotomy. Intraoral distracters
on which the distraction device would the evening. In the meantime, the lesser (Figs 25.43 and 25.45) are preferred to
566 Facial Deformities

A B C

Figs 25.42A to E: Case of maxillary


hypoplasia secondary to cleft lip and
palate treated with maxillary distractor.
(A) Preoperative e photograph; (B) Le Fort I
osteotomy cut; (C and D); Preoperative
and postoperative lateral cephalograms;
D E (E) Postoperative photograph.

external devices (see Figs 25.44A to E) cro­wding, it is often combined with • Most applicable when chin appears
to decrease scarring. Compared with a maxillary transverse widening and narrow clinically.
completely submerged device, DO devices surgically assisted palatal expansion. • Arch length inadequacy.
in which the distraction mecha­ nism is Distraction is a treatment alternative • Crowded anterior teeth.
intraoral yet extramucosal, allow the when transverse mandibular deficiency • Absolute bone deficiency.
clinician to monitor the distractor directly is too large for conventional orthodon­ A horizontal vestibular incision
without the need for radiographs. The tic or surgical procedure. The goal of is made like for the genioplasty from
vector of distraction is calculated based on symphyseal osteodistraction is to create canine to canine. The dissection is
the trajectory of the bone segment and on new bone and soft tissue. Distraction directed obliquely through the men­
the local anatomy, including bone stock, may avoid inherent limitations of bone talis muscle to reach the bone. A
tooth buds and/or roots, and position graft and permit a better adaptation of subperiosteal dissection is then per­
of the inferior alveolar nerve. The chin surrounding soft tissue in the area, thus formed until the inferior border of the
point correction is achieved by vertical avoiding the soft tissue flap. Since distrac­ mandible is exposed, taking care not to
distraction of the ramus. The distraction tion is a slower procedure, less trauma is damage the mental nerves. Tooth root
process con­tinues 1.0 mm per day until caused to the TMJ when compared to the prominences are either visualized or
the mandibular asymmetry is corrected.16 conventional orthognathic surgery. palpated in order to mark the location of
the vertical interdental osteotomy. This
Indications is often between the central incisor or
EXTRAORAL DISTRACTOR
• When it is necessary to significantly sometimes between roots of the canine
after the mandibular arch form and and lateral incisors, depending upon the
Mandibular Widening treatment requirements exceeds amount and location of crowding and
Distraction osteogenesis is a useful tool the limits of conventional surgery the site with the maximum interdental
to create space for severe mandibular (> 4 mm). bone. Midline osteotomy is preferred.
Orthognathic Surgery 567

A B C

D E
Figs 25.43A to E: Case of TMJ ankylosis, residual deformity treated by mandibular distraction: (A) Preoperative photograph; (B) Osteotomy
cut; (C) Distractor placement; (D) Preoperative (E) Postoperative profile photograph

A complete osteotomy is performed


below the level of the roots of the incisors
with a reciprocating saw blade. The la­
bial alveolar bone cortex is then sectioned
with a Lindemann bur, while the superior
flap is reflected with a hook. An osteotomy
is used to complete the lingual osteotomy
of the alveolus, taking care not to injure
the tooth roots and the gingival tissue.
A B
When the roots are too close to the
superior aspect of the osteotomy, the
remainder of the upper osteotomy is
completed by using an expansion forceps
(spreader) inserted at the inferior aspect
of the symphysis, immediate expansion
without tearing the gingival tissue is
performed to ensure that the vertical
interdental osteotomy is complete. The
mini plates incorporated in the device are
C D E
then adapted to the symphysis. Screws
Figs 25.44A to E: A case of unilateral TMJ ankylosis with deviation of chin treated with near the midline transmit the most
extraoral mandibular distraction device: (A) Preoperative profile photograph; (B) Osteotomy amount of force. The mucosa is closed by
cut; (C) Distractor placement; (D) Extraoral distraction device in place; (E) Postoperative interrupted 3-0 vicryl sutures, leaving the
profile photograph upper part of the device uncovered.
568 Facial Deformities

A B C

Figs 25.45A to E: A case of mandibular


distraction using intra oral, bone borne
distractor: (A) Deviation of the chin secondary
to ankylosis; (B) Osteotomy cut; (C) Intraoral
distractor in place; (D) Postoperative radiograph
showing distractor in place, (E) Radiograph
D E showing distraction of about 10 mm

Most distractors are tooth and bone ress region is a good point for device veolar unit for implant reconstruction
borne. Distractors that are solely bone fixation. Ideal trajectory would locate or for final periosteoplasty and smaller
borne tend to produce a V-shaped the two distractors that are parallel to bone graft, if indicated. This segmental
regenerate chamber, with more widen­ each other and the midsagittal plane. distraction is a form of transport DO.16
ing at the level of the alveolus and less Ensure that the resultant movement arm The premaxillary distraction is done
widening at the level of the inferior of the two distractors will not counter in case of severe maxillary hypoplasia
border. After DO, the surgeon may place each other as the distractors reach their secondary to the cleft palate. The anterior
a plastic pontic tooth in the gap between maximal length. Use anterior traction segmental osteotomy is performed
the central incisors to stabilize the teeth elastics to guide the maxilla to its proper and a custom made distractor devise is
and to prevent their central migration. position (Figs 25.45A to F). fabricated using the Hyrax screw placed
To prevent migration of the teeth into in anteroposterior orientation rather
the DO gap, include these teeth in the than the lateral orientation as it is placed
Maxillary Segmental
orthodontic arch wire, with the possible for the arch expansion. It is a type of tooth
placement of a light spring. Remove the Distraction borne distractor and is more effective as
distractor once a cortical outline can be In patients who have a wide alveolar compared to conventional osteotomy
seen on the radiograph. Place a lingual cleft, perform a segmental osteotomy as the scarred palatal tissue restricts the
arch to help stabilize the new transverse in the lesser segment, advancing it via maxillary advancement after the cleft
dimension.16 distraction to close the alveolar defect. palate surgery. It causes reasonable and
The bone cut is usually located between stable distraction of the anterior maxilla
Maxillary Distraction the bicuspid and the molar teeth of the and the regenerated bone is used for
lesser segment. Use of orthodontic ap­ the prosthodontic rehabilitation of the
This technique is especially useful for pliances and the arch wire allows the patient with implant supported pro­
pati­ents with large advancements or distraction segment to follow the curva­ sthesis (Figs 25.46A to F).
in patients postpalatoplasty for cleft ture of the maxillary arch (Figs 25.46A to
lip and palate whose scarring causes F). During post­distraction phase place
COMPLICATIONS
inadequate tissue or difficulty in moving an orthodontic spring on the arch wire,
the maxilla. The surgical approach is paralleling the regenerate chamber to The complications that arise from DO
similar to conventional orthognathic help hold the segment in proper orien­ should not be viewed as expected or
sur­­­
gery, with the osteotomy at the tation. Within 1 to 2 weeks after distra­ acceptable side effects of the technique.
Le Fort I level. The maxilla is freed but ction ossification, move the bicuspid Ilizarov has pointed out that ‘there are
not completely down-fractured. The and cuspid teeth orthodontically back no complications with the technique,
dis­tr­­­actors are precontoured to facilitate to their correct position into the ossified there are only inexperienced surgeons
dev­ice placement. The zygomatic butt­ DO bone, leaving the anterior dentoal­ causing problems for their patients.’19
Orthognathic Surgery 569

A B C

D E F

Figs 25.46A to F: A case of maxillary hypoplasia secondary to cleft lip and palate treated with tooth-borne intraoral distraction device:
(A) Preoperative photograph; (B) Preoperative lateral cephalogram; (C) Occlusal radiograph of tooth-borne distractor; (D) Lateral
cephalogram showing advancement of maxilla; (E and F) Preoperative and postoperative profile photographs

Cherkashin and Samchukov have a regular basis during the distraction the magnitude of bone lengthening re­
defined a complication of DO as ‘an un­ phase. quired.
expected deviation from the treatment
plan that, without appropriate correc­ Distraction Vector Operative (Distractor
tion, will lead to worsening of the exist­ Malocclusion that results from an in­ Placement) Phase
ing, development of a new, or recurrence correct vector of distraction is a com­
of the initial pathologic process.’19 mon complication. As with other tech­ Anatomic Complications
niques in orthognathic surgery, success Intraoperative surgical complications
Preoperative (Planning) Phase or failure of DO is often determined by are similar to those seen with traditional
the accuracy of the preoperative plan­ mandibular procedures, including ble­
Patient Selection ning. Clinical examination and analysis edi­ng, injury to inferior alveolar or lin­
The surgeon must select patients who of photographs, radiographs (lateral gual nerves, damage to teeth or tooth
are willing and psychologically and and anteroposterior cephalograms, buds, improper position of corticotomy
physically capable of activating the dis­ orthopantomogram, and three-dimen­ or osteotomy, or incomplete corticotomy
traction device on a daily basis. The sur­ sional CT images) and dental casts are or osteotomy.
geon must be prepared to counsel and currently used to determine the desired If the device placement, execution
encourage the patient (and family) on vector of distraction and approximate of proper vector, the orientation and
570 Facial Deformities

Table 25.3: Distraction osteogenesis versus orthognathic surgery20

Feature Distraction osteogenesis Orthognathic surgery

Stability More stable outcome Relatively less stable


Effect on tissue Bone and soft tissue advancement possible Only hard tissue advancement
• Better adaptability of soft tissues • Acute changes lead to stretching of tissues
Relapse Less common (up to 15 mm advancement More common (Maximum 10 mm advancement
can be done) can be done)
Operative procedure Technique sensitive and tedious Less cumbersome
(parallelism of vectors)
Patient compliance Of utmost importance for success of therapy Better compliance as correction is done in single step

location of the osteotomy and place­ orthopedic literature, the infection rate of tensional stress and a typical bony re­
ment of the device are incorrect, the in the craniomaxillofacial region seems generate is formed between the residual
resultant distraction vector produces a to be much lower. host bone segment and the trailing end
new malocclusion or makes the existing of the transport segment. After the trans­
occlusion worse. Inadequate Regenerate port bone segment reaches the opposite
Inadequate bone formation is a risk in or residual target bone segment, com­
Postoperative older patients, smokers, irradi­ated jaws pression forces are applied at the dock­
(Postdistraction) Phase and persons with poor oral hygiene. Even ing site until the bony margins of the
under these circum­stances, if the device transport and target segments are fused.
Device Failure is left in place for a prolonged period the Several bone transport techniques have
Hardware breakage and device failures bone regeneration is often poor.20 been developed and are included in
can occur, although these events are rare­ The distraction osteogenesis has Ilizarov’s classification of distraction—
ly reported. This complication often re­ certain advantages over the conventional compression osteosynthesis and related
quires a secondary surgical procedure to orthognathic surgeries at the same time osteogenesis method.
replace the nonfunctional device. External it also has few disadvantages which are According to Ilizarov, the technique
pins may fracture or become mobile. Bur­ summerized in Table 25.3. are divided into three groups based on
ied or semiburied screw-fixated devices Distraction osteogenesis is an exci­ the number of distraction/compression
rarely become loose if applied incorrectly. ting and promising technique for skeletal sites:
Once the regenerate has consolidated, it is expansion. It is technically demanding, • Monofocal
common to have loosening of the device however and requires precise planning • Bifocal
with no adverse consequences.19 and a significant commitment on the part • Trifocal.
of the surgeon, patient and family. Most Monofocal osteosynthesis is used
Inadequate Distraction complications arise from poor pati­ ent primarily in cases with small osseous
preparation and compliance, ina­de­ quate defects of up to several millimeters,
Anatomic Factors preoperative planning and inaccurate where healing of the two bone ends is
The movement of the proximal and dis­ surgical execution. In the future, technical abnormal, resulting in nonunion. In
tal fragments during mandibular DO, complications will be minimized by more cases not requiring an increase in limb
especially in patients with abnormal accurate three-dimensional planning length, compression forces are applied
morphology of the ramus/condyle unit sys­­tems and surgical navigation during and the pathologic tissue undergoes
(e.g. hemifacial microsomia), can be the distra­ction phase. reparative remodelling, which results in
complex. Accurate visualization of the reparative callus formation and fusion
proximal and distal fragments or pre­ Transport Bone Distraction of both the bone ends. This is termed
diction of their movements is not always Osteogenesis monofocal compression osteosynthesis.
appreciated on plain radiographs. Pain Conversely an increase in limb length,
may result when the coronoid process This technique was first introduced by distraction forces are applied to sepa­
collides with the skull base, for example. Ilizarov for treating long bone defects rate the bone ends. As distraction
resulting from trauma, oncological re­ continues, the pathologic tissues are
Infection section, and other severe congenital or gradually transformed into regenerate
Although reported rates of infection acquired deformities. The distraction bone. This is termed ‘monofocal distrac­
range between 5 and 30 percent in the osteogenesis occurs under the influence tion osteosynthesis.
Orthognathic Surgery 571

Bifocal bone transport is used used in maxillofacial surgery to The transport device is then applied
for larger bone defects having one reconstruct moderate sized defects of the using bicortical screw fixation. To avoid
distraction and one compression site. mandible secondary to tumor resection. a significant scar on the facial skin, the
During bifocal osteosynthesis, a free Trifocal distraction is used in very pins are placed through individual
bone segment (TS) (transport segment) large bony defects, the two transport stab incisions rather than through the
is created by performing an osteotomy, segments are created from both residual submandibular incision. In an effort to
from one of the residual segments, i.e bone segments and simultaneously minimize the visibility and magnitude
the host bone segment (RHBS). This moved centripetally toward each of the screw-tract scars, the external
transport disk is then moved from the other so that they meet in the center screw should be introduced through the
residual host segment (from which the of the defect. It is characterized by two skin low in the neck while pinching the
transport disk is created) to the residual simultaneously formed distraction skin between the screw site and lifting
target bone segment (RTBS) (the end regenerates at the docking site in the the skin superiorly. The device is then
towards the transport segment is center of the defect (Fig. 25.48). attached to the screw, verifying the vector
distracted). This technique involves the and trajectory of the planned transport
gradual movement of a free segment also Surgical Technique segment. The device is adjusted to fit
known as the transport segment of bone The surgical procedure is minimally passively onto the fixation screws and
across the osseous defect. The transport invasive and can be performed in an locked so that further adjustment is
segment has two ends the leading end outpatient setting. A small standard not possible and then removed. The
and the trailing end. The leading end of submandibular incision is placed to corticotomy is then gently converted
the transport segment faces the residual create an access to the bone. Using to an osteotomy using a chisel placed
target segment and forms part of the tunnelling technique, the lateral border at the inferior mandibular border. The
docking site. During movement of the of the mandible is exposed with mini­ distraction device is reattached to the
transport segment, new bone is formed mal periosteal stripping on the buccal screws in the same orientation and
between the residual host bone segment cortex and no periosteal stripping is activated to verify that the transport
and the transport segment (Fig. 25.47). done on the lingual cortex as it serves disk is mobile. The device is then closed
Once the transport segment reaches as the vascular pedicle. Using a fissure until the bone edges touch, following by
the residual target bone segment, bur or a reciprocating saw, a corticoto­ closure of the surgical site in layers.
compressive forces are applied at the my is created through the lateral cortex Normally, a 5-day latency period is
docking site (final destination point). and inferior border of the mandible, observed for bone transport. Since the
At the docking site, the compressive approximately 15 mm from the distal purpose of the latency period is to allow
forces stimulate gradual fusion of the end of the proximal bone stump. Care the formation of the reparative callus
contacting bony margins into solid bone is taken to avoid violating the inferior and to allow the wound to enter into the
regenerate. This technique is commonly alveolar neurovascular bundle. next phase of healing. After latency, the
transport disk is distracted at a rate of
0.5 mm twice per day. In cases of
vascularity compromised tissues, a rate of
0.25 twice per day is indicated. If blanching
is noticed during distraction then rate
should be changed to 0.25 mm four
times per day. The consolidation period
may range from 4 months to 6 months
depending on the size of the defect.
Fig. 25.47: Bifocal transport distraction The reconstruction of the mandible
is often challenging. The transport
distraction is good modality of bone
regeneration for reconstructing small
to moderate mandibular defects along
with regeneration of the soft tissues.
The reconstruction of the mandibular
defects spanning across the midline is far
more challenging with the conventional
Fig. 25.48: Trifocal transport distraction modalities like reconstruction plate and
572 Facial Deformities

Correction of Prognathism. J Oral Surg.


1954;12:p.185.
10. Schuchardt K. Experiences with the
surgical treatment of deformities of the
jaws: prognathia, micrognathia, and
open bite. In: Wallace AG, ed. Second.
Con­ gress of International Society of
Plastic Surgeons. London: E and S
Livingstone, 1959.
11. Obwegeser H. In: Zur Operationstech­
nik bei der Progenie und anderen
Unterkieferanomalien. (In Germany)
Dtsch. Z. Mund Kiefer. Gesichtschir.
1955;23:1.
12. Dal Pont G. Retromolar osteotomy for the
Fig. 25.49: Plate guided, intraoral mandibular transport distractor correction of prognathism. J Oral Surg
Anesth Hosp Dent Serv. 1961;19: 42-7.
13. Kole H. Surgical operations on the
bone grafts due to typical stress pattern alveolar ridge to correct occlusal ab­
in this region. The transport distraction REFERENCES nor­malities. Oral Surgery, Oral Med
is a good modality to reconstruct such and Oral Pathology 1959;12:515-29.
bony defects along with the regeneration 1 Hullihen SP. Case of elongation of the 14. Hunsuck EE. A modified intra-oral
of the soft tissues. underjaw and distortion of the face and sagittal splitting technique for correc­
neck by burn, successfully treated. Am tion of mandibular prognathism. J Oral
Intraoral Transport J Dent Sac. 1849;9:157.. Surg. 1968,26;pp.250-3.
2. Von Langenbeck, B. Die Uranoplastik. 15. Reggie C. Hamdy, Juan S Rendon,
Distraction Device Arch Klin Chir. 1861;2:252.. Maryam Tabrizian. Distraction Os­
The first intraoral distraction device for 3. Cheever DW. Nasopharyngeal polypus teogenesis and Its Challenges in Bone
mandibular bone transport was devel­ attached to the basilar process of Regeneration “Bone Regeneration”
oped in 1987 by Wolfson. The device occipital and body of sphenoid bone edited by Haim Tal, ISBN 978-953-51-
consisted of a slotted reconstruction successfully removed by a section, 0487-2, InTech, 2012.
plate attached to the residual bone seg­ displace­ment and subsequent replace­ 16. Distraction Osteogenesis: Advance­
ments by screws. The treaded distrac­ ment and reunion of superior maxillary ments in the Last 10 Years Joseph E.
tion rod rotated inside the plates slot bone. Bost Med and Surg J. 1867;8:162.. Van Sickels, DDS Oral Maxillofacial
thereby translating the sliding clamp 4. Blair VP. Operations on the jaw-bone Surg Clin N Am. 2007;19:565-574.
attached to the transport bone segment and face. Dental Era. 1907;6:169.. 17. Suzanne U. Stucki-McCormick, Dis­
(Fig. 25.49). 5. Wassmund M. Textbook of the practical traction Osteogenesis Chapter 62 Pe­
More recently, different intraoral surgery of the mouth and the pine [Leh­ terson’s Principles of Oral and Maxil­
devices were developed for correction rbuch der praktischen Chirurgie des lofacial Surgery Vol II. 2nd edn. Publ
of large mandibular continuity defects, Mundes und der Kiefer], Hermann Me­ by BC Decker, Hamilton Ontario.
reconstruction of neocondyles and cleft usser, Vol. 1, in German, Leipzig, 1935.. 2004;pp.1277-95.
palates. 6. Axhausen G. Uber die korrigierende 18. Van E. Sickels Likith Reddy V. Distrac­
The advantange of intraoral trans­ Os­teo­
tomie am Oberkiefer. Dtsch Z tor Design and OptionsJoseph, Atlas
port bone distracters includes mini­ Chir. 1936;248:515. Oral Maxillofacial Surg Clin N Am.
mal patient discomfort although the 7. Cohn Stock H. Die chirurgische Imm­ 2008;6:159-67.
regeneration of large defects takes a ediatregulierung der Kiefer, speziell 19. Complications of mandibular distrac­
long time. The placement of the device der chirurgischen Behandlung der tion osteogenesis Maria J. Troulis,
is barely noticeable. The surgery is less Pro­gnathie, Vjschr Zahnheilkd. 1921; Leonard B. Kaban, Oral Maxillofacial
complicated and leaves no facial scars 37.p.320. Surg Clin N Am. 2003;251-64.
and can be performed in an ambula­ 8. Converse JM, Shapiro HH. Treatment 20. Adi Rachmeil. Treatment of maxillary
tory setting. of developmental malformations of the cleft palate: Distraction osteogenesis
The transport devices can be custom jaws. Plast Reconstr Surg. 1952;10:473. vs Orthognathic surgery. Annals of Oral
made using the stereolithographic mod­ 9. Caldwell JB, Letterman GS, Vertical and Maxillofacial Surgery. 2012;2(2):
els. Osteotomy in the Mandibular Rami for 127-30.
Section 9
Temporomandibular Joint

n Temporomandibular Joint Disorders


26 Temporomandibular
Joint Disorders
Borle Rajiv M, Arora Aakash, Singh Divya

The temporomandibular joint (TMJ) is nerve crosses the zygomatic arch and
complex articulation between condylar runs in between the two layers of the
head of the mandible and glenoid deep temporal fascia in the fat lobules,
fossa of the temporal bone. Over the near their attachment to the zygomatic
course of evolution it has evolved to a arch. Fat lobules are present between
more complex structure. This joint is these two layers of the fascia, which
not only involved in the inflammatory give valuable indication of proper plane
pathologies, but also involved secondary of dissection during the TMJ surgery
to the stress and the psychological (Figs 26.2A and B). The cartilaginous
disorders due to the mandibular para­ external auditory canal lies posterior to
Fig. 26.1: Cadaveric specimen of TMJ
functions. In the present chapter the the joint and if proper care is not taken
ankylosis, notice the hypertrophy of the
common pathologies involving the TMJ coronoid process (Courtesy: Kurt H Thoma,
during the dissection it may get damaged
are discussed. TB of Oral surgery) and result into its stenosis or painful
perichondritis. The auriculotemporal
TEMPOROMANDIBULAR tissue, which is traversed by numerous, nerve fibers are present anterosuperiorly
tiny capillaries. In the event of trauma to the joint in the preauricular area
JOINT ANKYLOSIS these capillaries rupture and effu­ and may get damaged if the incision is
Ankylosis is defined as ‘a pathological sion of blood takes place in the joint taken anterior to the preauricular fold,
fusion between two articulating sur­ (hemarthrosis) and if not treated producing num­ bness of skin of the
faces of a joint’. The TMJ ankylosis is properly, it results in fibrous adhesions, preauricular area. The internal maxillary
‘the pathological fusion between the leading to fibrous ankylosis, which in artery, one of the terminal branches of
glenoid fossa of the temporal bone and due course of time gets ossified and the external carotid artery, originates in
the condylar process of the mandible’ changes into bony ankylosis. the substance of par­ot­ id gland and passes
(Fig. 26.1). It is more commonly seen in The superficial temporal artery and deep to the neck of the condyle (Figs 26.2A
developing countries like India, but its vein is present deep to the superficial and B). It also gives the inferior alveolar
incidence is less in Western countries. temporal fascia. The artery bifurcates branch which descends inferiorly to
into temporal and transverse facial the mandibular foramen and enters the
Applied Surgical Anatomy branches. The incisions for exposing inferior alveolar canal. This artery also lies
The temporomandibular joint (TMJ) this joint are placed in such way that medial to the condylar neck and is likely to
is a synovial joint and is described as they lie in the bifurcation and do not be damaged if a guard is not kept medially,
ginglymodiarthroidial type of joint, due damage these vessels. The facial nerve during the release of ankylosis. In the
to two different types of movements that emerges from the anterior border of the chronic, severe cases of ankylosis the
occur in it, i.e. translatory and rota­tory. superficial lobe of parotid gland and ramus is so short that while releasing the
The injuries of the chin due to fall are lies below the lobule of ear inferior to ankylosis the inferior cut in the bone may
common during the childhood, which its attachment to the facial skin. If the damage the inferior alveolar artery and
cause indirect injuries to the man­ di­ incision is extended beyond this point, cause profuse bleeding. The coronoid
bular condyle. The condylar head in the the nerve is likely to be damaged. The process becomes elongated in ankylosis
children is covered by fibrocartilaginous zygomaticotemporal branch of the facial and the temporalis muscle becomes
576 Temporomandibular Joint

A B
Figs 26.2A and B: Branches of: (A) Facial nerve; (B) External carotid artery (superficial temporal and internal maxillary)
in relation to TMJ

atro­phic. It restricts the mandibular adhesions and subsequently the ankylo­ the forceps beaks can lead to damage to
excur­­sions even after adequate release sis. The condylar fractures/injuries are the tender, fibrocartilagenous condylar
of ankylosis and the coronoid process of­ten treated inadequately and lead to heads, leading to ankylosis. Although
is required to be excised for achieving subsequent anky­ losis. The hemarthr­ this problem was more common in
free and passive movements of the osis makes the environments in the joint the past, but in recent times as the
mandible and get good postoperative space hypoxic, which facilitates calcifi­ procedure of labor has refined and as
mouth open­­­ing. cation and may result in ankylosis. majority of pregnancies are precious and
The second most common cause of the facilities of caesarian sections are
Etiopathogenesis (Box 26.1) the TMJ ankylosis is chronic suppurative available even at smaller towns, majority
The trauma or infection in the joint otitis media (CSOM). The middle ear in­ of deliveries are carried out by caesarian
tends to heal by fibrosis if not treat­ fections are rampant in India. Apart from section, to ensure the safety in difficult
ed pro­ perly. The childhood falls on poor personal hygiene in rural popula­ cases, the incidence of forceps assisted
chin lead to indirect TMJ injuries and tion, the social customs like putt­ing medi­ deliveries has drastically redu­ ced and
joint effusions, which lead to fibrous cated oil in the external auditory meatus so has the incidence of TMJ ankylosis
of newborn and child­ren is a common secondary to this cause.
Box 26.1: Etiology of ankylosis
practice not only in rural area, but also
in the urban areas of India. This practice Classification (Box 26.2 and
1. Trauma
a. Fall on the chin leading to indirect
predisposes the middle ear infections. 26.3)
injuries to TMJ like hemarthrosis, The middle ear infections are not always • True ankylosis or intra-articular
contusion. attended by speci­alists and are often inad­ ankylosis.
b. Intracapsular and extracapsular equately treated leading to chronic course – Fibrous
fractures of condyle. of the infection and its spread to adjacent – Bony.
c. Birth trauma—application of forceps
TMJ leading to infective damage to the • False or extra-articular ankylosis
during labor.
2. Infections growing condylar head and healing by fi­ – Fusion of coronoid process with
a. Middle ear infections—CSOM brosis, which results in ankylosis. the zygomatic arch.
b. Septic fractures of condyle, During the labor, when the fetus
zygomatic arch has vertex presentation and the labor is Box 26.2: Topazian’s classification
c. Osteomyelitis of condyle obstructed, the vaginal delivery is facilit­
d. Mastoiditis
ated by application of delivery forceps. Stage-1: Ankylotic bone limited to condylar
e. Hematogenous infections
f. Specific infections—tuberculosis, The beaks of the forceps are often applied process.
syphilis, actinomycosis, etc. over the preauricular region and not on Stage-2 : Ankylotic bone extending to sig-
3. Inflammatory joint pathologies— the head as the skull bones are not fully moid notch.
Osteoarthritis, rheumatoid arthritis, ossified and can get damaged leading Stage-3 : Ankylotic bone extending to coro­
rheumatic arthritis. to gravious injury. The application of noid process.
Temporomandibular Joint Disorders 577

Box 26.3: Approaches to the TMJ

• Preauricular
– Hockey stick
– Angulated vertical
– Al-Kayat Bramley’s.
• Postauricular.
• Endaural.
• Submandibular.
• Retromandibular (Hind’s).
• Uni and bicoronal.

– Muscle fibrosis
– Myositis ossificans
– Oral submucous fibrosis
– Trismus hystericus
– Neurogenic—tetanus, tetany, me­­ Fig. 26.4: Prominent gonial angle and Fig. 26.5: Deviation of the chin to the
n­­­ingitis, bulbar paralysis, etc. accentuated antegonial notch affected side (right)
– Congenital—Pierrie-Robins syn­
drome
– Miscellaneous—pericoronitis, de­
pre­ssed zygomatic fractures, oral
– Malignancy with retromolar ext­
en­sion or infratemporal exten­
sion, etc.

Clinical Features
• Trismus—the mouth opening is
gradually decreased. It is severely
restricted in bony ankylosis as com­
pared to fibrous ankylosis (Fig. 26.3).
• The TMJ movements are severely
restricted in all excursions, i.e. pro­
trusion, lateral excursion, including
the opening. The joint movements
are poorly palpable. In case of fibrous A B
Figs 26.6A and B: Unilateral TMJ ankylosis of left side

ankylosis, the joint movements are gro­wing normally (Figs 26.5 and 26.6).
better felt as compared to bony anky­ • ‘Bird face deformity’ in case of bil­
losis. In children the false joint move­ ateral ankylosis (Figs 26.7A and B).
ments are palpable due to stretching • Fullness of face on the affected side,
in the cranial sutures during forced while the normal side is flattened.
opening. • Convex facial profile.
• Restricted vertical growth of ramus. • Poor oral hygiene.
• Prominent gonial angle with accen­ • Rampant caries and periodontal pro­­
tuated antigonial angle, due to pull blems.
from supra hyoid group of muscles • The coronoid process gets elongated
(Fig. 26.4). due to atrophy of the temporalis
• Deviation of chin to the affected side, mus­cle and the chronic pull exerted
in case of unilateral ankylosis due to on it. The anatomy of the ramus,
restricted vertical and horizontal gro­ cond­yle and the coronoid process
wth of the mandible on the affected is distorted and the distortion
Fig. 26.3: Severe trismus, deep bite and side, while as the other side keeps on becomes more conspicuous with the
loss of anterior teeth due to caries
578 Temporomandibular Joint

Fig. 26.8: Panoramic radiograph showing


severe bony ankylosis with coronoid elong­
ation

A B
Figs 26.7A and B: Severe bird face deformity due to bilateral TMJ ankylosis

Table 26.1: Sawhney’s grading

Sawhneys (1986) grading of TMJ ankylosis

Type-1: Condylar head is present without much distortion, fibrous adhesions make
movement impossible.
Type-2: Bony fusion of misshaped head of condyle and articular surface. No
involvement of sigmoid notch and coronoid process.
Type-3: A bony block bridging across the zygomatic arch and the ramus. Medially
an atrophic, dislocated fragment of former head of condyle. Elongation of
coronoid process seen.
Type-4: Normal anatomy of TMJ is totally destroyed by complete bony block between
ramus and skull base. Fig. 26.9: CT scan showing deformed
con­dyle and ankylosis

chronicity of the ankylosis. In long pharyngeal space ular joint graft is planned.
standing ankylosis the boney morph­ • The patient suffers from psychologi­ • Proper preoperative assessment of
ology is totally lost and replaced by cal problems due to the facial disfig­ respiratory passage is required pre­
a block of bone at the base of the urement. operatively as the intubation is often
skull. Depending on the radiological difficult due to trismus.
picture of the lesion, Sawhney (1986) Investigations • Routine preoperative investigations
has proposed the grading of the TMJ are done to rule out any medical
ankylosis as shown in Table 26.1. • X-rays—PA view of mandible, compromise, which may adversely
• Crowding of teeth, the lower inci­ pan­oramic view of the mandible affect the outcome of the surgery.
sors often exhibit supraeruption and (Fig. 26.8), lateral oblique view of the
fanning and often tend to touch the man­ dible, transcranial and trans­ Anesthesia
palatal mucosa, especially in long pha­ryn­geal views of the TMJ. As these patients have trismus laryngo­
standing cases. It is the compensa­ • CT scan, 2D or 3D reconstruction are scopy is not possible, hence the endotra­
tory phe­nomenon as the mandible very useful as they show the medial cheal intubation is extremely difficult.
is too far posteriorly placed as com­ extent of the ankylosis properly, Thus, the patient is intubated either by
pared to the maxilla. which is not otherwise visualized on blind nasal intu­bation or by retrograde
• The over all physical growth of the conventional radiographs (Figs 26.9 intubation or by using fiberoptic intuba­
child is restricted due to malnour­ and 26.10). ting bronchoscope/laryngoscope (Fig.
ishment. • X-ray chest to rule out pulmonary 26.11). When such skill or facilities are
• Snoring in case of bilateral ankylosis pathology and study the ribs in case not avail­able, elective tracheostomy may
cases due to decrease in posterior costochondral graft or sternoclavic­ be done to intubate the patient for safe
Temporomandibular Joint Disorders 579

• Unicoronal or bicoronal incisions­—


give good exposure and facilitate
cor­o­noidectomy and temporal mus­
cle interposition.
• Endaural incision—the incision is cu­
r­led in the external ear to hide the scar.
• Postauricular incision—not comm­
only practiced.
• Submandibular incision (Risdon’s)—
this incision is (discussed in Chapter
3—Incisions in Maxillofacial Surgery).
• Retro-mandibular extension (Hind’s)
This incision is (discussed in Chapter
A B 3—Incisions in Maxillofacial Surgery).
The last two incisions are seldom used
Figs 26.10A and B: (A) Coronal section showing severe bony ankylosis on left side;
for the management of ankylosis, but
(B) Axial section showing large bony mass replacing condyle in a severe case of ankylosis
the ankylosis is almost extending to the sphenoid bone are commonly used for fixation of
subcondylar fractures of other ramal
• It should give good, passive access to surgeries (Figs 26.12A to D).
the surgical site.
• The scar should be hidden in the Management of TMJ Ankylosis
skin folds or hair line to get good Various treatment modalities have been
cosmetic results. proposed for the management of the
• It should avoid damage to the im­ TMJ ankylosis as shown in the Box 26.4.
por­tant structures like superficial The treatment should be com­prehensive
tem­poral vessels and facial nerve. ensuring long-term, recurrence free
The following incisions are recom­ mana­­­­gement with adequate, sustainable
mended for the TMJ surgery. mouth opening and correction of the fac­
• Preauricular incisions ial deformities for improving esthetics and
– Angulated vertical incision1—the social acceptance. The aims of the TMJ
vertical limb lies in the preauricu­ ankylosis are summarized in Box 26.5.
lar fold and is angulated 45° to the
vertical incision in the hairline, Kaban’s Protocol
which goes in the bifurcation of Kaban5 proposed (Box 26.6) a com­
superficial temporal vessels. The pre­­
hensive protocol for the effective
expo­ sure is often inadequate mana­gement of TMJ ankylosis, which is
with this incision. popularly known as Kaban’s protocol.
– Hockey stick incision2,3—the
verti­cal limb lies in the preauri­ Brisement Force
cular fo­ld and bends on the zygo­ Brisement force is the forceful mouth
Fig. 26.11: Endotracheal intubation using matic arch. The incision is too open­­­ing, under general anesthesia, us­ing
a fiberoptic bronchoscope inadequate, leaves an unsightly heavy mouth gags. It is a treat­ment moda­
scar in the zygomatic arch and lity for treating the fibrous ankylosis. The
the chances of damage to zygo­ assessment of the con­dylar head and the
admini­stration of general anesthesia. If maticotemporal branch of the joint space is very critical before opting
the tracheostomy is done the cuffed PVC facial nerve are very high. for this treatment modality. When the
tracheostomy tube is used to admi­nister – Al-Kayat Bramley’s incision4 (re­ condylar head is not deformed and
the anesthesia through it, as it seals the verse question mark incision)—it joint space is not severely narrowed,
trachea. The cuff makes the tube self- is one of the most commonly prac­ this method may be used. But, when
retaining and prevents aspiration. ticed incisions as it gives an excel­ the condyle is deformed and the joint
lent access without damaging the space is severely narrowed it should be
Surgical Access to the TMJ important anatomical structures considered as transition from fibrous
The surgical access is created by giving and is cosmetically acceptable to bony ankylosis and condylectomy
various incisions. The ideal require­ (details of this incision are given in should be performed as the chances
ments of the incision are: Chapter 3). of recurrence are very high. However,
580 Temporomandibular Joint

A B
Fig. 26.14: Exposure of ankylosed joint
and insertion of the condylar retractor as
a guard to prevent injury to blood vessels
present medially

of glenoid fossa and the condyle is


resected by completing the osteotomy
by taking the inferior cut at the neck.
This procedure is done in early cases
of bony ankylosis and cases of fibrous
C D ankylosis where the condyle is deformed
Figs 26.12A to D: Various approaches for TMJ: (A) Al-Kayat Bramley incision; (Fig. 26.14).
(B) Preauricular incision; (C) Postauricular incision; (D) Unicoronal incision
Gap Arthroplasty
The joint is exposed surgically using
Box 26.4: Treatment modalities any of the above approaches. The joint
morphology is invariably disturbed and
• Brisement force
the joint is replaced by an irregular bony
• Condylectomy
• Gap arthroplasty mass. Usually the bony mass is more on
• Interpositional arthroplasty with the medial aspect than the lateral. The
reconstruction of the joint. root of the zygomatic arch is identified;
the superior osteotomy cut is placed
Box 26.5: Aims of treatment just below it to ensure that accidental
• Release of ankylosis perforation into the middle cranial
• Prevention of re-ankylosis fossa. After marking the superior cut
• To restore vertical height of mandible the inferior cut is marked about 1 to 1.5
• To facilitate growth cm inferiorly to get a good clearance.
• Correction of residual facial deformities. The intervening bone is removed, and
the gap is created. It is desirable to
Box 26.6: Kaban’s protocol create a gap of 1.5 cm. However, due
• Aggressive surgical resection creating to long standing, severe ankylosis as
gap of minimum 1.5 cm
seen in India, the height of the ramus
• Ipsilateral coronoidectomy
• Contralateral coronoidectomy (mini­ is so short that the inferior cut lies near
mum mouth opening of 35 mm) the inferior border of the mandible or
• Interpositioning Fig. 26.13: Fibrous ankylosis with distortion one is likely cut through the impacted
• Aggressive postoperative of the condylar head, an indication for third molar present in the ramus, thus,
physiotherapy condylectomy a gap of 1 cm should be regarded as
• Regular follow-up
adequate (Figs 26.15A to C). While
• Rehabilitation.
doing the osteotomy with a bur or saw
Condylectomy care should be taken to prevent damage
such assessment is not often possible on When the outline of the glenoid fossa to the internal maxillary artery and its
routine radiographs and CT scans are and condyle is identifiable, the superior descending bra­nch, the inferior alveolar
more suitable investigation (Fig. 26.13). osteotomy cut is placed at this level artery, which lies medial to the condylar
Temporomandibular Joint Disorders 581

A B C
Figs 26.15A to C: Marking superior and inferior cuts for gap arthroplasty and final gap arthroplasty with interposition

long-term, aggressive physiotherapy, to


prevent re-ankylosis.

Interpositional Arthroplasty
After the drawbacks of gap arthroplasty
became evident, efforts were made to
pre­vent the reankylosis by interposing
a barrier between the two osteotomized
bony ends to prevent the bony growth
and reunion. According to Verneuil, the
first arthroplasty was made by Percy and
A B Barton in 1826. In 1860 Verneuil was the
Figs 26.16A and B: Open bite deformity due to shortening of ramus after bilateral gap first to suggest the interpositional art­
arthroplasty hr­o­plasty.6 Many materials were tried
for the interposition with varied degree
of success and the choice of the inter­
neck, by keeping a guard (condylar coronoidectomy is indicated. The wou­ positional material varies from surgeon
retractor). After the complete release nd is closed in layers, keeping a drain to surgeon. The interpositional materials
of the anky­losis, the mouth opening is in place. The main disadvantage with can be classified as:
veri­fied on the table by forceful opening gap arthroplasty is recurrence. The gap
with the help of a mouth gag. The tends to get narrowed due to upward Alloplastic Material
mouth opening of minimum 35 mm pull­­ing of the mandible due to muscle Titanium, teflon, silastic, stainless steel,
is considered to be adequate, which pull and fibrosis during the healing acrylic, silicon, etc.7-9
grad­ ually improves with postoperative phase. It is more conspicuous in cases of The use of silastic10 was very popular
physiotherapy. The raw edges of the bone bilateral ankylosis where shortening of in the mid seventies, but due to its high
are smoothened and the posterosuperior ramus following creation of the gaps and failure rate it lost its popularity. The
edge of the os­t­e­­to­mized ramus should upward pull of mandible leads to anterior acrylic, teflon and titanium have been
be rou­ n­
ded off to prevent obstruction open bite deformity (aper­t­ognathia). The used with varied degree of success. The
dur­ing the man­ dibular opening. Free, mechanics of the man­dible get altered use of metallic condyle for reconstruction
uno­bstr­u­cted move­ments of the mandi­ and changes from a class I lever to the of joint was recommended. However,
ble should be eli­ cited by man­ ually class III lever. This can be prevented the metallic condyle tends to erode
mov­ ing the mandible. If the mouth to certain extent by giving the patient the roof of the glenoid fossa and cause
open­ing is not adequate and the mandi­ a hypomochlion and anterior inter perforation into the middle cranial
bular movements appear to be obstru­ maxillary guiding elastics (Figs 26.16A fossa.11 The total joint replacement with
cted when the mandible is moved in and B). All the cases of TMJ ankylosis are met­allic glenoid fossa and the condyle is
different excursions by the operator, the essentially followed up postoperatively by also recommended.
582 Temporomandibular Joint

Autogenous Material or with temporal muscle and fascia. The the 5th or 6th costochondral junction
Full thickness skin, cartilage, , fascia
12 13,
cranial surface of the osteomized bone is harvested from the right side. In case
lata,14 temporal muscle-fascia,15 costo­ is lined by a pedicled temporal muscle- of females the 6th or 7th CC junction
chondral joint (CCG), sternoclavicular fascia–pericranium flap, keep­ ing the is harvested to ensure that the incision
joint,16 meta­carpal joint, etc. have been pericranium facing cranially and then is placed in the inframammary fold to
used as interpositional material. a costochondral junction is harvested prevent deformity of the breast. During
The surgical procedure remains from 5th or 6th rib on the right side. The the harvesting of the CCG, care should
simi­lar to that of gap arthroplasty, except cartilaginous cap over the rib is trimmed be taken not to injure the parietal pleura
that the interpositional material is inter­ and contoured and not more than 3 to as it leads to pneumothorax (Figs 26.17A
posed in the gap. When the ankylosis is 4 mm of cartilage is kept, (2 mm according to D). An intercostal drain should always
released by performing an osteotomy to new protocol by Kaban) because the be kept as a standby in case the pleura
both the superior and inferior ends costochondral junction is fragile and is perforated. Before closing the chest
of the bone are raw and are likely to tends to fracture under stress if kept incision, saline should be sprayed at the
reunite due to bone formation as it is longer. Some surgeons prefer to preserve surgical site and the anesthetist should
seen during the healing of the fracture. a strip of periosteum and perichondrium be asked to inflate the chest, presence of
The interpositional mat­ erial prevents over the costochondral junction to impart air bubbles suggests pleural puncture.
the proliferation of bone and subsequent it strength. The CCG is interposed either All the cases where the CCG is harvested
reankylosis by serving as a subsequent through the same incision or is tunneled should be evaluated postoperatively for
materials like CCG, sternoclavicular joint, in proper position through separate detecting the signs of pneumothorax if
metacarpal joint, help in restoration of Risdon’s submandibular incision, below the small perforation is missed on table
vertical hei­ght of ramus and prevent the the masseter muscle. The graft is fixed to or the eroded pleura gets perforated
open bite deformity. The CCG is a pop­ the ramus with the help of SS or titanium later due to positive pressure ventilation
ular interpositional material, either alone screws. For harvesting the CCG usually during the anesthesia. The clinical signs
like diminished chest movements and
air entry, surgical emphysema, hyper-
resonant percussion note should be
noted and in suspected cases PA view
of the chest should be done to rule
out pneumothorax (Fig. 26.18). If the
pneumothorax is present then the air
in the pleural space should be drained
by inserting an intercostal drain (under
water seal) and advising blowing exer­
cises to the patient.

Advantages of CCG
• Restores the vertical height of man­
A B dible.

C D
Figs 26.17A to D: (A) Incision and exposure of the 6th rib and CC junction; (B) Harvested Fig. 26.18: X-ray chest showing pneumo­
CC graft; (C) Reduction of the cartilage cap to 3 to 4 mm to prevent fracture; (D) Fixation of thorax (absence of lung shadow on the
CCG with screws to the lateral aspect of the ramus right side)
Temporomandibular Joint Disorders 583

A B C
Figs 26.19A to C: Ipsilateral coronoidectomy through the same incision and contralateral coronoidectomy by transoral approach

• Facilitates the growth of mandible thinning out of the muscle. In order to the coronoid process (coronoidotomy)
by growing like a natural condyle. achieve the satisfactory mouth opening is ade­quate to overcome the restraining
of minimum 35 mm following the release effect of the atrophic temporalis muscle.
Disadvantages of CCG of ankylosis, it becomes imperative to The moment the coronoid process is
• Infection excise the ipsilateral coronoid process resected the strong pull of the atrophic
• Fracture of CC junction and evaluate the mouth opening. If the temporalis muscle retracts it superiorly
• Rejection mouth opening and the jaw excursions in the infra­ temporal fossa. Although
• Over growth especially in growth spurs are still inadequate then the contral­ there is no fixed criterion to decide when
and during pregnancy in females. ateral coronoid process should also be the coro­noidectomy should be done, but
• Pleural puncture while harvesting excised. The ipsilateral coronoid process it becomes necessary if the duration of
the graft may lead to pneumothorax. can be excised through the same incision ankylosis is more than 2 years as this time
taken for the release of ankylosis and the is adequate to induce atrophic changes
Role of Coronoidectomy contralateral coron­ oid process can be in the temporalis muscle. The most
The coronoid process often gets elon­ easily excised through a transoral incision appro­priate decision is taken on table by
gated and deformed in cases of long taken over the anterior border of the assessing the interincisal opening and
standing TMJ ankylosis. The temporalis coronoid process (Figs 26.19A to C). After passive mandibular excursions, following
muscle inserted onto the coronoid excision of the coronoid processes not release of ankylosis.
process is also severely atrophic and only the interincisal opening is assessed,
restricts the mandibular opening even but the passive mandibular excursions Role of Physiotherapy
after the ankylosis is adequately released. sho­uld also be demonstrable. It is not The postoperative physiotherapy is
During the surgery the wasting of the always necessary to remove the resected of vital importance to improve and
temporalis is evident in the form of coronoid process and only release of maintain the results achieved by the
surgery. Most of the failures following
the surgery are due to inadequate efforts
taken by the surgeon to highlight the
importance of physiotherapy to the
patient or due to noncompliance of
the patient. The physiotherapy should
be started after 7 to 10 days of latency
period postoperatively and should
be continued for a period of 2 years
following the surgery. During the initial
phase the physiotherapy is started with
ice cream sticks and later the Heister’s
jaw exerciser is a good instrument to
A A impart physiotherapy. Periodic follow
Figs 26.20A and B: (A) Passive jaw exercises using ice cream sticks; up and supervision of the physiotherapy
(B) Heister’s jaw exercises is mandatory (Figs 26.20A and B).
584 Temporomandibular Joint

Apart from the forceful jaw opening


exercises, physiotherapy in form of
TENS is indicated to treat the accidental
damage to the facial nerve (neuropraxia)
during the TMJ surgery.

Surgical Photos of Cases


Case 1: Figures 26.21A to H
Case 2: Figures 26.22A to I
Case 3: Figures 26.23A to J
Case 4: Figures 26.24A to E

Complications A B

The complications associated with TMJ


surgery are:
• Infection.
• Hemorrhage—due to damage to
super­ficial temporal vessels, inter­
nal maxillary artery, inferior alveolar
artery, internal jugular vein.
• Reankylosis.
• Open bite deformity.
• Damage to the facial nerve and
auriculotemporal nerve (Figs 26.25A C D
and B).
• Stenosis of external auditory canal.
• Perforation in middle cranial fossa.

Management of Mandibular
Deformities
The mandibular growth is severely res­
tri­­cted in ankylosis, which results in sev­
ere deformities like retrusion of chin,
deviation of chin, reduced vertical height,
crowding, malocclusion, etc. These F
deformities can be corrected by ortho­
gnathic surgical procedures like geni­
oplasty, sagittal split osteotomy, distrac­
E
tion osteogenesis, orthodontic therapy,
etc. depending the merit of each case. The
details of these procedures are discussed
in the Chapter 25 (Orthognathic Surgery).
The distraction osteogenesis is
more commonly practiced modality for
correc­ ting the mandibular deformity
following the TMJ ankylosis. The dis­
traction can be done preoperatively or
postoperatively. The advantage of pre­
G H
operative distraction is that the distrac­
tion vector is more controlled. In case Figs 26.21A to H: (A) Mouth opening restricted in a case of bilateral TMJ ankylosis;
of postoperative distraction the proxy­ (B) CT scan showing bony ankylosis on left side and early fibrous union on right side in
coronal cuts; (C) Osteotomy cuts for gap arthroplasty; (D) Ankylotic bony mass removed;
mal fragments tends to move cranially,
(E) Mouth opening achieved after gap arthroplasty; (F) Temporalis muscle harvested
reducing the gap created during the for interpositional arthroplasty; (G) Temporalis muscle sutured over the zygomatic arch;
release of ankylosis, thus enhancing the (H) Final closure with activated drain
Temporomandibular Joint Disorders 585

A B C

D E F

G H I
Figs 26.22A to I: A case of bilateral TMJ ankylosis with surgical photos: (A) Bilateral ankylosis; (B) Al-Kayat Bramley’s incision; (C) and
(D) Splitting the layers of deep temporal fascia to prevent damage to the facial nerve and exposure of ankylotic area; (E and F) Osteotomy
cut below the root of the zygomatic arch and creation of gap and release of ankylosis; (G and H) Coronoidectomy through the same
incision and harvested temporal muscle-fascia-pericranium flap; (I) Interpositioning of temporal muscle fascia pericranium flap in the
gap

chances of reankylosis. The other prob­ the mandible backward and upward
lem with the postoperative distraction is
OTHER and the intervening soft tissues like
that once the mouth opening is achieved TEMPOROMANDIBULAR the capsule, meniscus and synovial
by release of ankylosis, the patients do JOINT DISORDERS mem­brane get contused and undergo
not report for the correction of deformity infla­
mm­ation. The inflammatory rea­
in the Indian circumstances. The dis­ Arthritis c­­
tion makes the joint painful and
traction can be two dimentional, i.e. the hypomobile. The effusion of the joint
verical ramal height can be increased
Traumatic Arthritis, Hemarthrosis space by the inflammatory exudates and
along with the horizontal elongation of The TMJ is often subjected to indirect or blood takes place, because of which
the atrophic mandible. trauma. The fall on the chin thrusts the condyle gets pushed downwards
586 Temporomandibular Joint

A B C D

E F G

H I J
Figs 26.23A to J: Surgical management of ankylosis with interpositional arthroplasty: (A and B) Preoperative photographs;
(C) Exposure of deep temporal fascia; (D) Exposure of ankylotic mass; (E) Release of ankylosis; (F) Harvesting temporal muscle fascia flap;
(G) Interpositioning temporal muscle fascia flap; (H) Ipsilateral coronoidectomy; (I) Interincisal opening; (J) Improved interincisal opening
after contralateral coronoidectomy

and pro­duces open bite on the involved Management Exercises are contraindicated in acute
side. In the acute phase of inflammation the phase and physiotherapy in the form
The clinical features of the traumatic inflamed joint needs rest and thus, the of diathermy may be prescribed. The
arthritis are: jaw movements should be restricted heat induces vasodilatation and helps
• Positive history of trauma. by placing inter maxillary elastics or by in clearing the inflammatory reaction.
• Pain tenderness and swelling over placing temporary IMF for a period of a Once the acute phase subsides, the
the TMJ. week. Supportive treatment in the form patient is advised active physiotherapy
• Trismus and restricted excursions. of prescription of anti-inflammatory to prevent adhesions and ankylosis.
• There is open bite on the involved drugs is started. If there is hemarthrosis,
side due to effusion of exudates or then drugs like trypsin, chymotrypsin, Osteoarthritis (Degenerative Joint
blood (hemarthrosis) in the joint serratio­peptidase may be helpful. Pro­ Disorder)
space. phylactic antibiotics to prevent secon­ Osteoarthritis is a noninflammatory dis­­
• X-ray shows widening of the joint dary infection can be considered. The order characterized by joint deterio­rat­
space. patient is prescribed liquid and soft diet. ion and proliferation. It is also thought
Temporomandibular Joint Disorders 587

to be the most common type of arthritis.


Although the etiology is unknown it is a
disease associated with aging process.
Clinical signs and symptoms are
remarkably absent even in the phase of
histological changes in the joint. Since
the TMJ is not a weight-bearing joint,
changes here are insignificant even
though arthro­ pathy may be present
in other joints. Patient may complain
of pain on palpation and movements,
A B which is associated with muscle spasm.
The onset of these symptoms may be
sudden or gradual and symptoms may
disappear spontaneously, only to return
in recurring cycles.

Radiographic features
When the patient is in maximum inter­
cuspation, the joint space may be nar­
row or absent. Flattening of condylar
head may be evident. Loss of cortex or
erosion of the articulating surfaces of
the condyle or temporal component are
characteristic of this disease. ‘Ely cysts’,
small round radiolucent areas with
C D
irregular margins surrounded by incre­
ased density, are visible. In the advanced
stage of the disease bony proliferation
occurs at the periphery of the articulating
surface area. This new bone, which is
formed is known as osteo­ phyte. The
Figs 26.24A to E: Management of ankylosis in
broken osteophytes lie within the joint
a child with temporal muscle fascia and CCG
interposition: (A) Preoperative photograph; space, known as ‘joint mice’.
(B) Release of ankylosis; (C) Harvesting CCG;
(D) Preparation of the tunnel through the Treatment
separate submandibular incision; (E) Fixing Treatment is directed towards relieving
E the CCG to the ramus with screws joint stress-splint therapy, relieving
secondary inflammation with anti-
inflammatory drugs and physiotherapy.
Arthro­centesis has been effective in
wash­ing out noxious metabolites and
‘bone sand’ that are present in the joint
and can produce symptomatic relief
from pain. Intra-arti­ cular injections
of corticosteroids also produce symp­
tomatic relief. In severe cases high
conylotomy (condylar shave) or
excision of the affected condyle and join
replacement can be done.

Rheumatoid Arthritis
A B Rheumatoid arthritis is an autoimm­
Figs 26.25A and B: Damage to the zygomaticotemporal branch of facial nerve leading une infla­ mmatory condition in which
to loss of wrinkling over forehead and incomplete closure of upper eyelid the infl­a­med and hypertrophic synovial
588 Temporomandibular Joint

me­m­­­brane grows onto the articulating more than the normal. The pos­ terior condition is described as dislocation.
sur­faces. atta­chment of the meniscus, the fibers of The clinical features of the dislocation
The TM joint is frequently involved the bilamellar zone, gets stret­ched and are as follows:
in rheumatoid arthritis. Ganik and become inflamed, which pro­duces pain • Inability to close the jaw.
Willi­ams reported 65 percent patients in the joint. The chronic stretching in • The jaw deviates to the normal side
with juve­nile arthritis have TM disorder. the fibers makes them lax and meniscus in case of unilateral dislocation and
Haa­ndes et al reported that more than condylar disharmony may be precipitated, in case of the bilateral dislocation
half of the cases involved TM joints. leading to clicking, painful joint. the chin is in midline, but the lower
It is more common in females The management of hypermobility third of the face becomes elongated
and may occur at any age, but there is consists of restraining the excessive jaw due to open bite. The lips remain
increase in the incidence with increasing movements by advising the patient not parted (Fig. 26.26A).
age. Usually small joints of the hands, to open the mouth wide or support the • The saliva dribbles as the patient is
wrist, knees and feet are affected in a lower jaw at the chin, while yawning. In unable to swallow.
bilateral, symmetric fashion, similarly severe cases the jaw movements can be • The patient complains of pain over
TM joint involvement usually occurs restrained by placing the intermaxillary the joint. The pain produces spasm
bil­ater­ally and symmetrically. Patients elastics. of the periarticular muscles and the
with TM joint involvement complain of A step ahead of the hypermobility is spastic muscles prevent the reduc­
swell­­ing, pain, tenderness, stiffness on the subluxation or dislocation. In this tion of the dislocated jaw.
opening, limited range of motion and condi­ tion the condylar head travels • The glenoid fossae appear empty
crepitus. Bilateral destruction of joint ant­er­ior to the eminence articularis on inspection and palpation (Figs
may lead to anterosuperior positioning and gets dislocated. The failure of the 26.26B and C).
of condyles, which may further lead to con­­dylar head to travel back in the • Occlusal derangement—in case of
anterior open bite. fossa, leads to inability to close the jaw. unilateral dislocation the teeth on the
When the patient is able to reduce the involved side are in open bite and on
Radiographic features condyle in its normal position in the the contralateral side there is cross
Diminished width of a joint space due glenoid fossa of his own, it is called bite. In case of bilateral dislocation
to destruction of disk may be visible. subluxation. When the patient is unable there is gagging of the molars and
bony erosion of the condylar anterior to reduce the dislocated jaw himself the anterior open bite (Fig. 26.26D).
or posterior surfaces may occur giving
a ‘sharpened pencil’ appearance of the
con­­dyle. Erosive changes sometimes are
so severe that entire condyle is des­troyed.

Treatment
Treatment is directed towards pain relief-
analgesics, reduction or suppression of
inflammation-NSAID or corticosteroids
and physiotherapy. High condylotomy
or joint replacement in the patients with
severe joint destruction may be required. A B

Hypermobility, Subluxation
and Dislocation
The inherent weakness in the joint cap­
sule, the laxity anteromedially, makes it
susceptible to hypermobility and related
disorders. Normally during the opening
of the jaw, the condyle trans­lates up to
the posterior slope of articular eminence.
When the capsule is lax, the restraining
action on the condyle is lost and the con­ C D
dyle moves ahead of the articular emi­ Figs 26.26A to D: A case of bilateral TMJ dislocation showing inability to close the jaw,
nence. This condition is clinically mani­ elongation of the face, open bite with gagging of the posterior teeth, hollowing in the
fested as hypermobility. The jaw opens TMJ region
Temporomandibular Joint Disorders 589

fibrosis in the capsule and make it


stiff. The intra-articular injections
with sclerosing agents like sodium
mor­r­­huate are also indicated. Surgi­
cal exploration of the joint and
pla­ce­ment of plicating stitch with
nonabsorbable material is also ad­
vo­cated.17,18
A B • Removal of barrier: The articular
emi­ nence serves as a barrier and
Figs 26.27A and B: The X-rays show the condyle anterior to the articular eminence
prevents the reduction of the con­
dylar head in the glenoid fossa. If
which prevents the reduction or where this barrier is removed then the
the dislocation is relatively old or if the condyle will not get locked and
patient is apprehensive the reduction will travel freely to and fro and
may be attempted under GA with full the subluxation or dislocation will
muscle relaxation. Once the reduction is not take place. This is achieved by
achieved, to prevent the recurrence, the reducing the height of the articular
lower jaw is supported by giving ext­ra­oral eminence by exposing it surgically
barrel or four tailed bandage or inter­maxi­ through a preauricular incision and
llary elastics are given in pati­ents with reducing it with a bur. This pro­
recurrent dislocation. The patient is edu­ cedure is called as ‘eminectomy’
cated and instructed to support the jaw, (Figs 26.29A and B).
while yawning and prevent wide open­ing. The alternative to eminectomy is
In cases with chronic dislocation reducing the height of the condyle.
fibrous adhesions develop, which pre­ This is done by entering the joint
vent the reduction of the dislocated jaw space and shaving off the superior
Fig. 26.28: Reduction of the dislocation in spite of attempts under GA. In such condylar surface. This is called con­
cases surgical treatment like eminec­ dyloplasty or high condylectomy or
• X-ray shows empty glenoid fossae tomy or condylectomy may be required. condylar shave procedure.19
and condyle lies ahead of articular The preventive treatment in cases • Creating a barrier: The dislocation
eminence (Figs 26.27A and B). of recurrent subluxation or dislocation or subluxation results due to too
comprises of: far anterior translation of the con­
Management • Capsule plication procedures: The dyle during opening. If this anter­
In acute condition the dislocation can plication (tightening) is achieved by ior translation is prevented mech­
be reduced by manipulation of the lower injecting corticosteroids in the joint anically by creating a barrier, the
jaw. The patient is made to sit in the space. The steroids not only reduce dislocation can be prevented. This
dental chair with the occiputes supported the inflammation, but also induce barrier is created by:
by head rest. The operator stands in
front at 7 o’clock position and holds the
mandible by keeping the thumbs on the
molars and the index and middle fingers
on the inferior border. The mandible
is then drawn slightly anterior, down
wards and then pushed backwards
and upwards to reduce the dislocated
condyles back in the fossae (Fig. 26.28).
This maneuver helps in negotiating
the articular eminence. This procedure
is usually done without anesthesia.
When the muscle spasm or pain is
present administration of the sedatives,
analgesics and muscle relaxants may be
required. In the cases where the acute A B
pain and severe muscle spasm is present, Figs 26.29A and B: Eminectomy to remove the barrier
590 Temporomandibular Joint

was called Coston’s syndrome. He restricted movement, unilaterally or


correlated bite over closure (due to loss bilaterally.
of posterior teeth), as well as ear and In summary the clinical signs can be
sinus problems including diminished listed as:
hearing, tinnitus, dizziness, burning and • Pain
occipito vertex headache to it. Although, • Muscle tenderness
proved inaccurate it acknowledged • Alteration of limitation of motion.
the fact that the TMJ symptoms and Besides having one or more of the
occlusion often seem intimately related. four cardinal symptoms the patient con­
The relationship was referred to as the sidered to have the syndrome must also
‘TMJ syndrome’. Later Schawrtz 1952, have these negative characteristics.
drew attention to the fact that the suf­ • Absence of clinical, radiological or
ferers of the TMJ syndrome were sym­ bio­chemical evidence of organic
ptomatic because of the masticatory chan­ges in TMJ.
Fig. 26.30: Dautry’s procedure to create a and perimasticatory muscle spasm. He • Lack of tenderness in the TMJ when
barrier expanded the syndrome to the ‘TMJ pain- palpated via the external auditory
dysfunction syndrome’ and perceptively meatus.
noted that many sufferers had an altered The significance of these negative
or unusual psychological make up as characteristics in establishing the diag­
well. This represents a transition from nosis lies in their indication that the pri­
the age of strict occlusal etiology to the mary site of problem is in the mus­culature
age in which occlusion plus the entire rather than the structure of the joint.
suspensory jaw apparatus and the pati­ There are many synonymous termi­
ent’s psychological make up are seen as nologies used to designate the TMJ pain
causative. Travell21, 1960 showed how associated with spasm of the surround­
pain could be referred from one area ing muscles of mastication and they
of head and neck to another, through are Coston’s syndrome, myofacial pain
the use of injections of isotonic saline dysfunction syndrome, myelogelosen
solutions, intramuscularly. He described interstitial myofibrosities, non-articular
sore points in the periarticular muscles rheumatism, TMJ dysfunction, myalgia,
as ‘Trigger points’. He also noted that etc. However, myofacial pain dysfunc­
whenever the pain is associated with tion is the most accepted terminology.
Fig. 26.31: Overlay graft to create a barrier skeletal muscle spasm, it almost always The condition is characterized by uni­
gets referred a distance from the muscle, lateral facial pain secondary to the TMJ
i.e. its source, trigger areas are often disorder, which is often associated with
– Implanting titanium pins in the easily located by palpation. Since there periarticular muscle spasm and pain
articular eminence is lowered pain threshold deep pressure with dysfunction of the spastic muscles.
– Down fracturing of the zygomatic on the trigger zone leads to referred
arch as its root and fixing it at pain. Etiological Factors
lower level (Dautry’s procedure) Laskin22 (1969) summarized the cha­ The etiological factors for the MPDs are:
(Fig. 26.30). ra­cteristics and significance of TMJ pain • Intracapsular causes—internal de­
– Overlay bone grafts to augment dysfunction theory. The characteristics rangements like:
the height of the articular emi­ of pain according to him are: – Anterior disc dislocation with
nence (Fig. 26.31). • Unilateral pain reduction and without reduction
• Located in preauricular region – Disc perforation
• May be referred in all directions – Disc adhesions.
MYOFACIAL PAIN • Often described as dull and constant • Extracapsular causes
DYSFUNCTION SYNDROME • Mostly associated with muscle ten­ – Occlusal disharmony
derness, which could be demonstrat­ – Psychosis
This entity has been identified in the ed clinically by careful palpation. – Muscular imbalance
clinical practice since a long. It was • Clicking or popping sound over the – Hypermobility, subluxation
described by Coston20 in 1934 as the affected TMJ (66%) – Whiplash injury
pain in TMJ associated with ankylosing • Alteration or limitation of jaw fun­ – Muscle over extension due to
spondilitis, occlusal disharmony and ction seen as opening deviation or restorations or prosthesis, which
Temporomandibular Joint Disorders 591

Flow chart 26.1: Etiopathogenesis of The occlusal disharmony due to this malocclusion. But, when the spasm
MPDS malocclusion, malunited fractures, post- is relieved the patients develop another
ortho­ gnathic surgery, alters the man­ occlusal imbalance. The initial muscle
dibular posture, which leads to abnormal spasm indicates homeostatic protection
resting position of the jaw and the TMJ, against injury. This protective splinting
muscle over activity. The para functions of myospasm, however, tends to get more
like tongue thrusting, lip biting, excursive momentum so that increasing number of
movements, bruxism, etc. lead to muscle related muscle groups develop spasm and
over activity. The fatigued muscle is de­ the pathways of pain-spasm-pain chain
pleted of ATP. The muscle metabolism rea­ction becomes extensively facilitated.
becomes anerobic due to relative hypoxic Apart from these two organic changes,
environment as the O2 consumption is degenerative arthritis and fibrosis of prea­
increased and it is not readily available. uricular tissue are seen.
Thus, the noxious metabolic end products
like lactic acid accumulate in the muscle Clinical Features
and the muscle become spastic, sore and • Pain, which is usually unilateral and is
stiff. It leads to further altered posture, aggravated on chewing, yawning and
further stretch­ing, fatigue and the vicious opening. The pain and the restricted
cycle of pain-spasm is created. jaw movements are some times more
The internal derangements in the pronounced in the mor­ ning and
joint like meniscus dislocation, menis­ wanes off as the day progresses. This
cus perforations, meniscus adhesions is often designated as morning stiff­
and degenerative changes in the joint, ness.
produce pain in the joint. Secondary to • Pain in temples, vertex, occipital ar­
the pain, a protective myospasm sets in, eas, headaches, neck and shoulder
encroach on the intermaxillary which leads to altered posture, fatigue, aches are common.
space (high points) soreness and all the events are repeated • Restricted joint excursions—there is
– Muscle overcontraction–loss of in a cyclic manner. not only trismus, but the other joint
posterior teeth. The development of muscle spasm, exc­ur­sions like protrusion and lateral
– Parafunctions–bruxism, clench­ pain, limitation of motion results in minor excursions are painful and restricted.
ing, grinding, etc. shift in the rest position of the jaw so that The jaw movements are not steady
The etiopathogenesis is shown in the teeth do not occlude properly. The and there may be deviation due to
(Flow chart 26.1). teeth may gradually shift to accommodate muscle spasm and imbalance during

A B
Figs 26.32A and B: (A) Normal condyle meniscus complex movements during open­ing; (B) Tension is generated in the bila­mellar zone
while opening due to stret­ching and it also balances the pull of lateral pterygoid contraction while closing
592 Temporomandibular Joint

the opening. The meniscus dislocation


produces jerky jaw movements often
termed as ‘propping of the jaw’.
• Pathological joint sounds—Usually
the meniscus glides smoothly in
the joint space during the opening
and the closing of the jaw (Figs
26.32A and B). Due to the laxity of
the fibers of the bilamellar zone
A B (Figs 26.33A and B) or the loosening
of the attachment of the meniscus on
Figs 26.33A and B: Laxity of bilamellar zone
the mediolateral poles of the condyle,
the movements of the meniscus
become jerky due to meniscus-
condyle disharmony and the jerky
movement produces a snapping
sound which is called click. When
the meniscus condyle disharmony
(anter­ior dislocation of the meniscus
with reduction) exists (Figs 26.34A
and B), during the jaw opening
the clicking sound is produced
due to snapping movements of the
meniscus. This clicking sound is
also heard on closing and when it
is present on both the opening and
A B closing it is called reciprocal clicking
Figs 26.34A and B: Anterior lock with reduction: (A) Anteriorly dislocated menis­cus; (Fig. 26.35). Then the bilamellar
(B) Reduction of the dislocated meni­scus during opening zone is severely damaged and the
meniscus gets dislocated anteriorly,
without reduction, it creates an
anterior lock. In such cases the
previously noisy joints become silent
but the restricted mouth opening
is present due to the obstruction to
the forward translation of condyle
due to dislocated meniscus (Figs
26.36A and B). When there are severe
degenerative changes, dryness of the
joint, roughening of the joint surfaces
and meniscus perforations, during
the joint movement there is frictional
sound. This sound is often described
as crepitus or velcro like sound. The
clicks are usually loud and are easily
audible. However, other adventitious
sound like crepitus are better heard
through the bell of a stethoscope.
• Muscle tenderness (trigger zones)—
the fatigued muscle becomes spastic
and sore due to accumulation of no­
Fig. 26.35: Reciprocal click due to snapping of the meniscus during opening and closing due xious metabolic end products. Such
to laxity of bilamellar zone fibers, resulting into anterior dislocation of meniscus with reduction muscle becomes painful and tender.
Temporomandibular Joint Disorders 593

• Occlusal discrepancies—the occlusal


discrepancies in the form of crowding,
premature contacts, attrition, deep
bite, loss of teeth leading to over clo­
sure and straining of the joint may
be present. These discrepancies may
be developmental or acquired as a
result of malunited fracture, postor­
thognathic surgery.

Clinical Examination
• Palpation of TMJ.
A B • Palpation of muscle of mastication
Fig. 26.36A and B: Anterior dislocation of meniscus without reduction: (A) Anteriorly and neck muscles for detecting the
dislocated meniscus; (B) During opening it does not get reduced but forms a mass of sore points (Trigger areas) in the
dislocated meniscus, obstructing the forward translation of the condyle, resulting in spastic muscles (Figs 26.37A to F).
restricted mouth opening • Assessment of range of movement,
deviation of mandible and smooth­
On palpation definite tender points • Altered psychosis—the patients with ness or jerky movements (popping).
are elicited over these periarticular psychosis commonly have the habit • Assessment of clicking/grating/syn­
muscles like masseter (70%), tempo­ of parafunctions like lip biting, bru­ chrony of joint movements.
ralis (49%), medial (35%) and lateral xism and mandibular para­functions. • Intraoral examination of deflective
pterygoid (84%) cervical, scalp and fa­ It leads to strain in the muscle, spasm occlusal contacts, occlusal discrep­
cial muscles (43%). Tenderness is also and soreness. Other findings of stress ancies, prematurities, interferences,
elicited on the condylar neck above like acid peptic disorders, migraine, attrition, wear facets, missing/mo­
maxillary tuberosity, at angle of the headache, dermatitis, significant bile teeth, anterior open bite, cross
mandible and at the temporal crest. elevation of urinary steroid levels bite, reduced vertical dimension.
• Otologic symptoms like ringing in and catecholamines may be present.
ear, heaviness in the ear. Hence, psychological evaluation Investigations
• Referred dental pain. and management of the patient with The radiographic evaluation is needed
• Subluxation or dislocation (17%). MPDS is also very important aspect to rule out associated pathologies of
• Vertigo (7%). of the management. TMJ:

A B C D

Figs 26.37A to F: Palpation of the mus­­


cles of mastication to detect sore points
(trigger areas): (A) Masseter; (B) Tempor­­alis;
(C) Medial pterygoid; (D) Lateral ptery­
E F goid; (E) Ster­no­ma­stoid; (F) Trapezius
594 Temporomandibular Joint

Antidepressant agents
• Monoamine oxidase inhibitor
• Tricyclic antidepressant.

Local anesthetics
• Auriculotemporal nerve block
• Injection at the trigger points located
in the muscles
• Local anesthetic spray provides tem­
po­rary pain relief.
A B
Intra-articular Injections
Figs 26.38A and B: MRI showing normal disc position and disc dislocation
of Corticosteroids
The injection of corticosteroids (hydro­
• OPG with caratodynia. The elongated sty­ cort) in upper joint space with local
• Transpharyngeal view loid process can be felt on transoral anesthetics should be given under
• Transcranial view palpation in the retromolar area strict aseptic precautions. The intra-
• MRI is the most appropriate inves­ medial to the ramus and can also be articular steroids help in reducing the
tigation to asses the internal soft visualized on X-rays. inflammation within the joint and bring
tis­
sue pathologies of the joint down the pain. The codylar irregularities
(Figs 26.38A and B). are also remodelled to certain extent and
Management thus, it is also called ‘chemical condylo­
Differential Diagnosis of the • Pharmacological modalities. tomy’. Steroids should not be injected
• Intra-articular injections. very frequently and there should be a
Myofacial Pain Dysfunction • Occlusal splints. gap of about 5 to 6 months between the
Syndrome • Physiotherapeutic modalities. two injections.
Various conditions associated with the • Stress management.
head and neck region may mimic the pain • Biofeedback and relaxation therapy. Occlusal Splints
secondary to myofacial pain dysfunction • Psychologic modalities. The occlusal splints are given to serve
syndrome (MPDS) and thus, they warrant • Surgical management. the following purpose:
consideration for ruling them out. • To create balanced joint-tooth rela­
• Migraine—more commonly seen in Pharmacological Modalities tion­­ship.
females, pain is severe in the morning, Anti-inflammatory drugs • To reduce spasm, contracture, hyp­
associated with nausea, vomiting and er­­activity of musculature.
visual abrasions. It is precipitated by The analgesic anti-inflammatory drugs • To improve vertical dimension and
stress, gastrointestinal upsets, oral like ibuprofen, diclofenac sodium and prevent the over rotation of the
contraceptives, menses, consump­ salicylates provide relief from the pain condyle during the closure so as to
tion of alcohol, candies, chocolates. and reduce the inflammation. prevent stretching of the fibers of
• Otitis media—chronic condition, ass­ bilamellar zone.
o­ciated with purulent ear dis­charge, Muscle relaxants • As the mandible is pushed down
predominantly ear pain, hear­ing imp­ Centrally acting muscle relaxants like by the splint, the condyle also gets
airment. Baclofen 10 to 25 mg, Chlorzoxazone pushed inferiorly increasing the space
• Mastoiditis—pain, tenderness, swell­ 500 mg, Metaxalone, Methocarbamol within the joint, which facili­tates the
ing over the mastoid process. 500 mg, etc. can be prescribed to relive free movement of the inflamed and
• Temporal arthritis—typical pain and the muscle spasm. These drugs reduce edematous meniscus without getting
tenderness along the course of tem­ skeletal muscle tone by selective action traumatized and helps in reducing its
poral arteries. on the cerebrospinal axis without alter­ inflammation (Figs 26.39A and B).
• Vascular headaches, cluster head­ ing consciousness. • Anterior repositioning splint:
ache. When the meniscus is anteriorly
• Eagle’s syndrome—pain due to elo­ Stress reduction with anxiolytic dislocated, the anterior reposi­
n­gation of the styloid process or agents tioning splints are indicated. The
calcification of the stylomandibular • Alprazolam: 0.25 and 0.5 mg HS lingual ramp glides the mandible
ligament. It is felt during opening of • Diazepam: 2 to 5 mg HS. It also works anteriorly and the condyle glides
the jaws, deglutition and associated as a skeletal muscle relaxant. over the dislocated meniscus
Temporomandibular Joint Disorders 595

A B
Figs 26.39A and B: Occlusal splint

A B C
Figs 26.40A to C: Anterior repositioning splint: (A) Anteriorly displaced disc; (B) Spl­int in place and teeth are occluded;
(C) The mandible is pushed anteriorly and the con­dyle glides anteroinferiorly

heat and provide deeper penetra­


tion of the heat.
– Short wave diathermy: It is a high
frequency alternating current
and the heat energy is obtained
from the wave. The frequency is
27,120,000 cycles per second and
the wavelength is 11 meter and
provides deeper penetration of
A B
heat in the periarticular muscles.
– Ultrasonic therapy: These elec­
Figs 26.41A and B: Anterior repositioning splint with lingual ramp for positioning the
tromagnetic waves are different
mandible anteriorly
from sound waves. The frequen­
cies of waves are between 500,000
anteroinferiorly. This prevents Physiotherapeutic Modalities and 3,000,000 cycles/sec.
abnormal posturing of the man­ • Acute stage—no active physio­ther­ – Microwave diathermy: They are
dible, muscle imbalance and pain apy is advisable in an acute stage, but the electromagnetic waves with a
due to muscle fatigue. It also helps the joint should be provided rest. wavelength between infrared rays
in reduction of the meniscus in its • Chronic stage. and short wave diathermy waves,
normal position (Figs 26.40 and – Infrared diathermy: The electro­ and the wavelength is 12.25 cm
26.41). magnetic waves that generate with frequency of 2,450 cycles/sec.
596 Temporomandibular Joint

During the conventional hot fomen­ dig­astric and stylohyoid), there­by inacti­ ment in these exer­cises while the depres­
tations, the heat does not penetrate vat­ing the elevators of the jaw (medial sor muscles are activated, allow­ing for
the deeper structures like muscles and pt­e­r­­ygoid, masseter, tem­poralis). This relaxation of the opposite elevator mus­
the joint. The shorter the wavelength, may allow relaxation of the hyper­active cles (medial pterygoid, mass­eter, tempo­
deeper is the heat penetration. Hence, mus­ cles of mastication and assist in ralis). These exercises are performed by
microwave diathermy produces deeper achi­eving maximal inter­incisal opening. holding the mandible station­ary, while
heat penetration than the short wave In the active stretch phase patient is the muscles are acti­vated isometrically.
diathermy. asked to open the mouth for several For isometric exercises, patient is as­
seconds and relax. They are advised to ked to visualize the jaw as working in four
Exercises open the mouth till they perceive pain separate directions—open-closed and
Exercises of the TMJ can be divided into: and keep the mouth open for several right-left. Isometric exercises are then
• Loading exercises. second and to repeat this exercise several accomplished as the patient attempts
– Active jaw exercises. times in a day. In the active protrusion, to move the jaw in all these directions
– Passive jaw exercises. patient stands in front of the mirror against the resistance. Iso­metric exer­
• Isometric exercises. and protrudes the mandible forward cise, to be effective, should be done with
stretching lateral pterygoid bila­terally. great effort and be sustained for short
Loading exercises period of time. Generally, exercise is
Loading exercises are used to stretch Passive jaw exercises started with three sustained seconds in
and increase the strength and bulk of It allow the patient to manually increase each direction, three to four times a day.
the muscle mass. Loading exercises can interincisal opening. Passive jaw exercises The exercise is increased to six to eight
be used in certain TMJ dysfunctions are effective in patients with muscular sustained seconds in each direction four
like fibrous ankylosis but they are not trismus and MPDS. It is contraindicated times a day over a period of few weeks
recommended for relief of acute myo­ in patients with severely displaced disk, (Figs 26.42A and B).
spasm as increasing the load on already due to possibility of damage to disk or
spastic muscle worsens the problem. retrodiskal tissue. Surgical Management
Muscle spasticity once initiated can The surgeries on TMJ could be either
be self-perpetuating because of the Isometric exercises open surgeries or the arthroscopic sur­
accumulation of the ADP and other cell­ Isometric exercises are recommended for geries. Various procedures that are done
ular metabolites. Loading exercises tend patients with pain and tris­mus. Isometric can be enumerated as:
to increase ADP and other anaerobic exercises work on the principle of reflex- • Arthrocentesis.
meta­bolites, thus increasing myospasm. relaxation, as one group of the muscle is • Capsule tightening procedures.
in total contrac­ture, the other group of the • Creating mechanical obstacle (des­
Active jaw exercise/kinetic exercises muscle in total relaxation, allowing vaso­ cri­bed above).
Using patient’s musculature allow the dilation and increased blood flow and the • Removal of mechanical obstacle
patient to activate for example, their sup­ elimination of the micro­ana­erobic mus­ (des­­cribed above).
r­a­­­hyoid muscle (geniohyoid, myl­o­­­h­­yoid, cle environment, e.g. there is no move­ • Creation of new muscle balance.

A B
Figs 26.42A and B: Isometric jaw exercises: (A) Opening the jaw against resistance, (B) Lateral excursion against resistance
applied by clenched fist
Temporomandibular Joint Disorders 597

TMJ arthrocentesis mmatory disease and is essential for into the synovial fluid. A 19-gauge ne­
Arthrocentesis is traditionally defined as judging therapeutic success. The pres­ e­dle connected to a syringe filled with
a procedure in which the fluid in a joint ence of succinic acid and to a lesser lactated Ringer’s solution is then inser­
cavity is aspirated with a needle and a extent lactic acid or depressed glucose ted into the superior compartment at the
therapeutic substance is injected. The concentrations in synovial fluid is a useful articular fossa (posterior point) aided
procedure is generally performed under marker in diagnosing septic arthritis. by palpation. The solution is injected
local anesthesia and strictly sterile Measuring total protein, albumin and and immediately aspirated. The fluid
conditions. Because of its simplicity, it individual immunoglobulins permits in the syringe is often sucked into the
may be performed repeatedly if neces­ mechanical, acute inflammatory and joint space, which normally has negative
sary. Alarcón-Segovia23 reported how chronic inflammatory processes to be pressure. Then 2 to 3 mL lactated Ringer’s
Mexican prehispanic physicians used distinguished, especially when com­ solution or bupivacaine, 0.5 percent, are
therapeutic arthrocentesis in swollen pared with serum values. However, the injected to distend the upper joint space
unwounded knees. Swollen knees were value of biochemical studies of synovial and anesthetize the adjacent tissues. A
punctured with a thorn to relieve pain fluid has often been challenged. second 19-gauge needle is then inserted
and restore function.24 Fray Bernardino into the distended compartment in the
de Sahagún gathered this information Indications for TMJ arthrocentesis area of the articular eminence to en­able
through direct interviews with the • Diagnostic: Biochemical and micro­ free flow of Ringer’s solution through the
surviving Aztec nobility in México city bial analysis of synovial fliuid. superior compartment. Due to lavage,
in the 16th century and realized that an • Toileting of the joint space to flush the pain mediators pro­staglandin E2 and
inflamed joint was potentially harmful away the accumulated chemical leukotriene get wa­shed out, reducing the
and were the first to perform therapeutic mediators of inflammation, thus inflammation and pain. The inability
arthrocentesis using an unspecified reducing pain and inflammation. of disc to slide can readily be reversed
thorn. They also described the nature of • Instillation or administration of by lavage. The injec­ ted fluid distends
the aspirated fluid, which they compared drugs (hyalauronic acid, Steroids) hydraulically, the joint space and enables
with the viscid fluid from the leaves of Murakami and colleagues25 offered the disc to slide. During the lavage, the
the nopal cactus. Numerous studies the first systematic description of TMJ mandible is moved through opening,
have shown the exceptional diagnostic arthrocentesis, which they termed mani­ excursive and protrusive movements to
and therapeutic value of arthrocentesis, pulation technique after pumping and facilitate lysis of adhesions. At the end
while emphasizing the low incidence of hydraulic pressure. Arthrocentesis of the of the pro­­cedure and after one needle
associated complications, including joint TMJ is a modification of the traditional is removed, medication can be injected
contamination and local irrit­ation caused method, whereby two needles instead into the joint space. Temporary facial
by introduction of for­ eign materials. of one are introduced into the upper paresis or paralysis caused by the use
Most studies on TMJ arthrocentesis joint space. This adaptation permits of a local anesthetic or swelling of the
refer to temporo­ mandibular disorder massive lavage of the joint, in addition neighboring tissues caused by perfusion
(TMD), which comprises a wide variety to aspiration and injection. of Ringer’s solution may occur during
of disorders of the TMJ, the mas­ti­catory The patient is seated at a 45­ degree arth­rocentesis. However, these effects
mus­­cles, or both. Pain and dysfunction angle, with the head turned to the un­ are transient and disappear within a few
of the TMJ itself acco­unts for a small affected side to provide an easy app­ hours (Figs 26.43A and B).
proportion of TMD condi­tions, and are roach to the affected joint. After proper
often insufficiently diag­nosed. The prime preparation of the target site, the external Advantages of Arthrocentesis
suspects in sym­pto­matic synovial joint auditory meatus is blocked with cotton • Simple and less invasive technique.
are intra- and extra-articular overloading soaked in mineral oil. A line is drawn • Minimum armamentarium and less
and immo­bilization. Microscopic ana­ from the middle of the tragus to the outer expensive.
l­y­sis of the synovial fluid is also a valu­ canthus. The posterior entrance point • Therapeutic advantage.
able diagnostic tool. Identification of is located along the canthotragal line,
crystals allows innocuous effusion cau­ 10 mm from the middle of the tragus and Capsule tightening procedures
sed by osteoarthritis to be differen­tiated 2 mm below the line. The anterior point Placation stitch, intracapsular injection
from that which is caused by crystal- of entry is placed 10 mm farther along the of steroids, sodium morrhuate.
indu­ ced inflammation and the vastly line and 10 mm below it. These markings
more dangerous septic arthritis. Deter­ over the skin indicate the location of the Disc plication
mining total white blood cell count and articular fossa and the eminence of the • Full thickness excision of wedge
the percentage of polymor­ phonuclear TMJ. A local anaesthetic is injected at shaped tissue of poste­rior portion.
cells in synovial fluid may distinguish the planned entrance points, avoiding • Partial thickness excision of supe­
bet­ ween inflammatory and noninfla­ penetration into the joint and injection rior retrodiskal lamina—in this
598 Temporomandibular Joint

mandibular Joint Ankylosis. J Oral


Maxfac Surg. 1990;48:1145-51.
6. Orhan Güven. A clinical study on tem­
poromandibular joint ankylosis. Auris
Nasus Larynx. 2000;27(1):27-33.
7. Güven, Orhan. A Clinical Study on
Temporomandibular Joint Ankylosis in
Children. Journal of Craniofacial Sur­
gery. 2008;19(5):1263-9.
8. Ahmad QG. Interposition arthro­
plasty in temporomandibular joint
A B ankylosis. Indian Journal of Otolaryn­
gology and Head and Neck Surgery.
Figs 26.43A and B: (A) Markings for insertion of the needles during arthrocentesis;
2004;54(1):5-8.
(B) Arth­rocentesis in process
9. Spiessl B, Schmoker R, Mathys R.
Treatment of ankylosis by a condylar
prosthesis of the mandible. New
Concepts in Maxillofacial Bone Surgery
(1976) Springer, Berlin.
10. Richard W DeChamplain. Autopoly­
merizing silastic for interpositional ar­
throplasty. JOMS. 1988;46(6):522-5.
11. Westermark A. Condylar replacement
alone is not sufficient for prosthetic
A B
recon­struction of the temporomandibu­
Figs 26.44A and B: Full thickness excision of superior retrodiskal lamina
lar joint. International Journal of Oral and
Maxillofacial Surgery. 2006; 35(6):488-92.
12. Chossegros C, Guyot L, Cheynet F, et al.
Full-thickness skin graft interposition
after temporomandibular joint anky­
losis surgery. A study of 31 cases. Int. J
Oral Maxillofac Surg. 1999;28:330-4.
13. Lei Z. Auricular cartilage graft interpo­
sition after temporomandibular joint
ankylosis surgery in children. J Oral
A B Maxillofac Surg. 2002;60:985-7.
14. Paterson AW, Shepherd JP. Fascia
Figs 26.45A and B: A full thickness wedge shaped portion of posterior attachment is
removed and lateroposterior tissues are approximated lata interpositional arthroplasty in the
treatment of temporomandibular joint
ankylosis caused by psoriatic arthri­
procedure, a partial thickness exci­ cases. American Journal of Orthodontics tis. Int J Oral Maxillofac Surg. 1992;
sion of superior lamina of retrodiskal and Oral Surgery. 1945;31(10):597-607. 21(3):137-9.
tissue is done and its posterior attach­ 2. Blair VP. Operative Treatment of Anky­ 15. Kim Su-Gwan. Treatment of temporo­
ments are remo­ved. The lateroposte­ losis of the Mandible With a History mandibular joint ankylosis with tem­
rior tissues are approximated (Figs of the Operation and Ankylosis of 212 poralis muscle and fascia flap. Int J Oral
26.44 and 26.45). Cases. Surg Gynecol Obstet. 1914;19: Maxillofac Surg. 2001;30(3):189-93.
• The disk repositioning is achieved 436-51. 16. Wolford LM, Cottrell DA, Henry C.
by plication of posterior attachment 3. Blair, Ivy, Brown. Essential of Oral Sternoclavicular grafts for temporo­
or disk is sutured to lateral capsular Surgery. CV Mosbv Co., 2nd edn. 1936. mandibular joint reconstruction. J Oral
ligament. 4. Al-Kayat A, Bramley P. A modified pre- Maxillofac Surg. 1994;52(2):119-28;
auricular approach to the temporo­ discussion 128-9.
mandibular joint and malar arch. Br J 17. Bruce Sanders. Surgical treatment for
REFERENCES
Oral Surg. 1979;17:91-103. recurrent dislocation or chronic sub­
1. Kurt H Thoma. Hyperostosis of the 5. Kaban LB, Perott DH, Fisher K. A Pro­ luxation of the temporomandibular
man­di­bular condyle: with report of two tocol for Management of Temporo­ joint. Int J Oral Surg. 1975;4(5):179-83.
Temporomandibular Joint Disorders 599

18. Raja Kummoona. Surgical reconstruc­ 21. Travell JG, Simons DG. Myofascial 24. Sahagún B. Historia General de las
tion of the temporomandibular joint for pain and dysfunction: The trigger point Cosas de Nueva España (3 volumes).
chronic subluxation and disloca­tion. Int manual. Baltimore: William Wilkins, Intro­duction, paleography, glossary and
J Oral Maxillofac Surg. 2001; 30(4):344-8. 1983;4(544):103-64. notes by López Austin A, García Quin­
19. Robert D Marciani. Healing following 22. Laskin DM. Etiology of the pain-dys­ tana. J Mexico: Conaculta, 2000.
condylar shave in the monkey tem­ function syndrome. J Am Dent Assoc. 25. Murakami K, Hosaka H, Moriya Y, et al.
poromandibular joint. JOMS. 1988; 1969;79(1):147-53. Short-term treatment outcome study
46(12):1071-6. 23. Alarcón-Segovia D. Descriptions of for the management of temporoman­
20. Costen JB. A Syndrome of Ear and Sinus therapeutic arthrocentesis and of syno­ dibular joint closed lock. A comparison
Symptoms Dependent upon Disturbed vial fluid in a Nahuatl text from prehis­ of arthrocentesis to non-surgical ther­
Function of the Temporo­mandibular panic Mexico. Ann Rheum Dis. 1980; apy and arthroscopic lysis and lavage.
Joint. Ann Otol Rhinol. 1934;43:1. 39:291-3. Oral Surg Oral Med Oral Pathol Oral
Radiol Endodontics. 1995; 80(3):253-7.
Section 10
Neoplastic Conditions of
Head, Neck and Face

n Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region


n Odontogenic Tumors
n Potentially Malignant Disorders of the Oral Cavity
n Oral Cancer
Odontogenic and

27 Nonodontogenic Cysts
of the Maxillofacial Region
Borle Rajiv M, Gadbail Amol, Singh Divya

‘A surgeon should be a pathologist who does operations’.


—Eric Carlson

odontogenic in origin and are centrally developmental epithelial cells leading


Odontogenic Cysts
located within the bone. The non- to proliferation, but not invasion of the
odontogenic cysts of the oral cavity are adjacent tissues (Table 27.1).
Definitions seen both centrally (fissural cysts like
A cyst is defined as ‘a pathological globulomaxillary cysts, median pala­ Classification of the
cavity, which may or may not be lined tine cyst) or peripherally in the oral
by epithelium, and contains liquid, semi­ tissues (mucocele, ranula, thyroglossal,
Cyst of Oral Cavity
solid or gaseous contents’. sublingual dermoid, etc). Although in the past many researchers
All odontogenic cysts arise from tried to classify the cysts of the orofacial
remnants related to embryonic deve­ region (Robinson1 1945, Gorlin2 1964,
Development of a Cyst
lopment and therefore termed as (Box 27.1) Pindborg and Karmer3 1992)
developmental cysts. The etiology of The common behavioral feature of in an attempt to categorize the cystic
the cyst ranges from the embryonic all cysts is the stimulation of residual lesions, the recent being the WHO
remnants to the parasitic infections. For
example, the thyroglossal cyst or the
branchial cleft cyst originates from the Table 27.1: Development of cyst in relation to stage of development of tooth
embryonic remnants, while the hydatid
cyst is formed secondary to the parasitic Stage of tooth Defect Pathology
infection. The traumatic bone cyst is an Initiation Failure of initiation Primordial
empty cavity, while the dermoid cyst Basal cell offshoots Midpalatal cyst
may contain the hard tissues like teeth. Gingival cyst of newborn
The sebaceous cyst and the mucocele are Bud stage Failure of layer formation Primordial cyst, OKC
types of retention cyst. The sebaceous Cap stage Degeneration of stellate reticulum Primordial cyst, OKC
cyst has semisolid contents while the Bell stage Degeneration of stellate reticulum Primordial cyst, OKC
mucocele contains mucoid contents. Apposition Failure of apposition Primordial cyst
The aneurismal bone cyst contains frank Cell rests of HERS Lat periodontal cyst
blood while most of the odontogenic Maturation Hypoplasia of enamel Dentigerous cyst
cysts contain straw or amber colored Lat periodontal cyst
fluid. Eruption After eruption from epithelial rests Eruption cyst
A majority of cysts which are Gingival cyst of adult ? OKC,
Dentigerous cyst
seen commonly in the oral cavity are
604 Neoplastic Conditions of Head, Neck and Face

Box 27.1: Classifications of cyst—Gorlin Box 27.2: Classifications of cysts expansion is more commonly seen
(1964) (WHO 2005) at the buccal cortex; however in
very large cysts both the buccal and
A. Odontogenic cysts Developmental odontogenic cysts
lingual cortices may get expanded.
• Dentigerous cyst a. Primordial
• Eruption cyst b. Gingival cyst of infants This could be a differentiating
• Gingival cyst of newborn infants c. Eruption cyst feature between the ameloblastoma
• Lateral periodontal and gingival d. Dentigerous cyst (folicular) and a cyst, as in the former expan­
cyst e. Gingival cyst of adults sion of all the four cortices is seen,
• Keratinizing and calcifying cyst f. Lateral periodontal cyst i.e. buccal, lingual inferior border
• Radicular cyst g. Glandular odontogenic cyst,
and alveolar bone. The odon­
• Primordial cyst sialo-odontogenic cyst
• Multiple cysts of jaws and multiple togenic keratocyst also causes bony
cutaneous nevoid basal cell expansion, but the expansion is
carcinoma and skeletal anomalies not as conspicuous as the other
B. Nonodontogenic and fissural cysts cyst. If the cystic changes occur after varieties of the odon­togenic cysts.
• Globulomaxillary cyst (premaxilla the completion of the crown then a It is common to see an odontogenic
maxillary cyst)
• Nasoalveolar (Nasolabial Klestadt’s
dentigerous cyst will occur. The other cyst infiltrating a large area of the
cyst) odontogenic cysts originate from the bone without any significant facial
• Nasopalatine (median anterior remnants of the odontogenic epithelium asymmetry or bone expansion. This
maxillary) cyst in the jaws. is due to the infiltrative nature of the
• Median mandibular cyst OKC (Fig. 27.1).
• Anterior lingual cyst
• The overlying bone is thinned out
• Dermoid and epidermoid cyst
• Palatal cyst of newborn infants General Clinical and becomes paper thin and on
C. Cysts of neck and oral floor and salivary Features of palpation crackles under pres­ sure
gland Odontogenic Cysts producing classical “egg shell crack­
• Thyroglossal duct cyst ling”. When the cortex is completely
• Lymphoepithelial (bronchial cleft) Before the individual cysts are dis­ perforated then the fluctu­ations can
cyst
cussed, their general features like beha­ be elicited.
• Oral cysts with gastric or intestinal
epithelium vior, presentation in oral cavity and • The teeth in the involved area are
• Salivary gland cyst management, are discussed. usually displaced and may become
• Mucocele and ranula • The cysts are slow growing, pain­less mobile at a later stage due to resorp­
D. Pseudocyst and asymptomatic, unless secon­ tion of the roots.
• Aneurysmal bone cyst darily infected or are very large in • The X-ray shows a classical radio­
• Static (developmental latent) bone
cyst
size and cause pressure signs. lucent lesion, surrounded by well
• Traumatic (hemorrhagic solitary) • They usually cause expansion of sclerotic/corticated borders, due
bone cyst the bone. As they grow slowly, the to bone apposition at the edges
pressure due to growth will cause (Fig. 27.1). The radiolucency could
resorption of the adjacent bone from be uniloculated or multiloculated.
classification4 2005, (Box 27.2) which is inside and as reparative pheno­ In the latter case fine bony septa
widely accepted. mena, bone apposition will occur can be seen in the lesion, which
simultaneously at the periphery, divide the cystic cavity in different
causing expansion of the bone. The compartments (locula). The inferior
etiopathogenesis
The odontogenic cysts originate from the
Table 27.2: Stages of cyst formation and type of cyst formed
odontogenic epithelium. The etiopath­
ogenesis of the odontogenic cysts is
Stage of development Tissue Type of cyst formed
related closely to the development of
of tooth
the tooth (Tables 27.1 and 27.2). The
stage at which the pathological changes Bud stage, cap stage, Odontogenic epithelium Primordial cyst, OKC
are initiated leads to formation of a bell stage
particular type of cyst, i.e. if the cystic Formation of crown Reduced enamel epithelium Dentigerous cyst,
changes occur at the bud or cap stage eruption cyst
the further development of the tooth After root formation Cell rests of Malasez Periapical cyst, residual cyst
does not take place and in its place a Odontogenic remnants of Cell rests of Malasez, the OKC, CEOC
dental lamina remnants of dental lamina
cyst is formed which is called primordial
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 605

processes by which the surface area


of the sac increases. This is achieved
by either peripheral cell division or
accumulation of cellular contents.

Peripheral Cell Division


Proliferation of local groups of epithelial
cells brings about multicentric growth
pattern, e.g. keratocyst. High mitotic
rates of certain epithelial linings result­ Fig. 27.2: Growth of the cyst
ing in unremitting growth and cystic
Fig. 27.1: Cystic lesions in mandible
enlargement, e.g. Keratocyst. Accumu­ further from blood supply at periphery
showing a radiolucent lesion with well-
corticated borders, displacement of the
lation of cellular content occurs by col­ of the mass (Fig. 27.2).
teeth and resorption of the roots legenase activity (increased collagenoly­ As the distance increases (usually
sis) could also result in cyst expansion, 0.18 to 0.2 mm), the cells at center get
e.g. primordial cyst and radicular cyst. too far shifted from nearest blood vessel
alveolar canal is displaced due to the Low-grade infection stimulates cells to survive by nutritional diffusion. They
pressure created by cysts within the such as cell rests of Malassez to prolifer­ degenerate, thus creating a lumen in the
mandible. ate and form arcades, e.g. radicular cyst. center. Their intracellular products make
• The aspiration of the cystic lesion is lumen hypertonic, which transudates
important aid in the diagnosis of the Hydrostatic Cyst Enlargement fluid into the lumen (Fig. 27.2). This
cyst. The color of the aspirate can Certain cysts have lining which secrete creates hydrostatic pressure, producing
give idea regarding the nature of the mucin. Accu­mulation of mucus incre­ bone resorption, clinical expansion and
cyst, e.g. the dentigerous cyst con­ ases the cyst volume and hence the sometimes mild paresthesia or pain. As
tains the straw-colored fluid, while enlargement, e.g. mucus secreting cyst. additional cells die, their slough per­
the OKC contains cheesy material petuates the hypertonic state and the
and the ABC con­tains frank blood. Transudation and Exudation hydrostatic pressure. The cell mem­
Further the aspi­rated material can Inflammatory cells (which are present in branes and nuclear membranes are
be subjected for cytological exami­ cases of infection) release cofactors, lym­ high in cholesterol, hence presence of
nation or bio­chemical examination phocytes release lymphokines, osteoclast cholesterol clefts in cyst lumen or wall.2
(protein contents) for reaching a di­ activating factor (OAF), and monocytes
agnosis. The OKC has more protein release IL-1. All these factors stimulate
Diagnosis of the Cyst
content than the other odontogenic fibroblast to release prostaglandin (Pg).
cysts.1 However, histopathology is This produces a hyperosmolar cyst fluid. The cystic lesion in the jaw may simulate
the most appropriate and confirma­ Increased hyperosmolarity draws fluid the tumors like ameloblastoma and
tory diag­nostic aid. from surrounding. This increases hydro­ other cystic neoplasms. Sometimes,
static pressure leading to cyst enlarge­ the presen­tation is so similar that on
ment, e.g. inflammatory cysts like radicu­ clinical findings alone the diagnosis
Theories of Cyst lar cyst, residual cyst, paradental cyst. may be difficult. Other nonodonto­
Enlargement genic conditions, aneurysmal bone cyst
Bone Resorption (ABC), osteoclastoma and cherubism
Harris5 in 1974 classified cyst theories:
Enlarging cysts often release bone re­ may produce expansion of the bone and
• Mural Growth sorbing factors from cyst capsule which a radiological picture similar to that of a
– Peripheral cell division. stimulate osteoclastic, e.g. prostanoids cyst and need to be differentiated from
– Accumulation of cellular con­ PGE2 and PGI2, leucotrienes. Differenc­ the cyst. Accidental opening into an ABC
tent. es in size of various cystic lesions could may lead to a catastrophic hemorrhage.
• Hydrostatic enlargement possibly be dependent on the quantity Thus, a definitive methodology needs to
– Secretion. of these osteoclastic factors. be followed while diagnosing a cyst.
– Transudation and exudation. To summarize the growth of • Clinical examination: A cyst will be
• Bone resorbing factor. cyst, there is proliferation of residual slowly growing, painless, expansile
developmental epithelial cells leading lesion. The expansion of buccal
Mural Growth Theory to formation of solid mass of epithelial cortex is commonly seen in small to
Mural growth in the form of epithelial cells. As the mass enlarges, the epithelial moderate sized cystic lesions, unlike
proliferation is one of the essential cells in the center become positioned the amelo­ blastoma where all the
606 Neoplastic Conditions of Head, Neck and Face

and aspiration to establish a correct show a cavity in bone devoid of any soft
diagnosis can be achieved by inci­ tissue lining. In OKC the nature of the
sional biopsy. Such a difficulty is cyst is infiltrative and thus the cavity may
often encountered while dealing with not appear smooth after the enucleation
large multiloculated lesions where of the lining and thus may need further
it is difficult to differentiate between curettage or carbolization of the base.
OKC and an ameloblastoma. The The advantage of the enucleation
ameloblastic changes in the lining is that the whole pathological lining is
of the cyst cannot be diagnosed on removed completely, thus the chances
clinical grounds alone and the biopsy of recurrence and neoplastic transfor­
Fig. 27.3: Radicular cyst associated with is of critical value as the treatment mation are minimal. The disadvantage
nonvital tooth modalities for the cyst and the amelo­ is that in large cystic lesions when it is in
blastoma are different.1 close proximity with the vital structures,
cortices are expanded. The teeth The incisional biopsy is not required these structures may get traumatized.
are displaced due to the pressure for smaller lesions as the treatment is The enucleation produces big defect
and sometimes fail to erupt in the otherwise also going to be same, i.e. which heals slowly by secondary inten­
oral cavity due to the pressure. enucleation, irrespective of the type of tion and needs to be packed open and
The neurovascular bundle is also the cyst. maintenance of good local hygiene.
displaced and in spite of the large
size the neurological deficit is seldom Treatment Surgical Procedure
present. The overlying bone is paper The procedure of enucleation comprises
thin and produces egg shell crackling
Modalities of the Cyst6 of reflection of mucoperiosteal flap,
on palpation. When the bone is The cyst can be treated by following removal of overlying bone to create an
perforated, fluctuations may be pre­ mod­alities: access (corticotomy) the lining is then
sent. The radicular/periapical cyst is • Enucleation carefully separated from the bone and
usually associated with the nonvital • Marsupialization (Partsch operation) removed with the help of the sharp
tooth (Fig. 27.3). • Combination of marsupialization and curette. The cavity is carefully inspected
• Radiologically the cyst presents as a enucleation (Waldron operation) and any remnants are enucleated easily
well corticated, uniloculated or multi­ • Enucleation with chemical cauter­ and the lining is removed in toto. But,
loculated, redioluscent lesion. The ization of the base the cysts which have thin, friable lining
bone is expanded. The teeth in the • Enblock excision (e.g. OKC) or where the lining becomes
region are displaced and resor­ption • Segmental resection. friable due to secondary infection, is
of the roots may be seen (Fig. 27.4). The later two are rarely practiced in removed in piecemeal. The residual
• The aspiration of the cyst yields the large lesions where the bone is severely bony defect is packed with gauze soaked
yellowish fluid, which shows pre­ undermined, if there is pathological in iodoform or white­ head varnish.
sence of cholesterol crystals. The fracture or suspicion of ameloblastic This procedure is called “packing the
OKC has protein content (<4 mg/dL). transformation. cavity open”. The pack initially helps in
Cytology is usually non-conclusive. hemostasis and also protects the wound
• When it is difficult to make a defini­ Enucleation from con­tami­nation. Primary closure of
tive diagnosis on clinical, radiological Separation of a lesion from bone, with the wound is often unsuccessful as the
preservation of bone continuity, by mucoperiosteal flap often lies on the
virtue of the lesion’s containment within bony defect and is unsupported and
an encapsulating or circumscribing invariably leads to dehiscence (gaping)
con­­n­ective tissue envelope derived of the suture line. Rather than keeping the
from the lesion or surrounding bone whole cavity open, the defect should be
(Figs 27.5A to F). packed with roll gauze and the flap is then
It is the most commonly practiced sutured keeping an area open, through
modality where the whole cystic lining which the end of the pack is drawn out.
is removed from the bony cavity, either The pack is changed daily after gently
in toto or in piecemeal. Most of the irrigating the wound and also reduced
cystic lesions are slowly growing and progressively in size to facilitate healing.
Fig 27.4: Multiloculated cystic lesion with the bony cavity has smooth cortication The packing may be discontinued after
displacement and resorption of the roots all around. A complete enucleation will 8 to 10 days as during this period the
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 607

A B C

D E F
Figs 27.5A to F: (A) Radiograph showing cystic lesions; (B) Cortical expansion; (C) Buccal decortications; (D) Enucleation cystic lining;
(E) Cystic cavity after enucleation; (F) Specimen of enucleated lining

base of the cavity gets granulated and Table 27.3: Time dependent depth penetra­ • Immunohistochemical fixation and
subsequently, epithelized and does not tion in different tissues on application of detection of NMDA receptors within
require further protection. Only the Carnoy’s solution for 5 minutes the murine hippocampus.
local hygiene needs to be maintained. To • In some cases direct application follo­
prevent the food particles from entering Tissue Depth of penetration (mm) wing enucleation for certain kinds
in the cavity an acrylic obturator may be Nerve 0.15 of unicystic ameloblastomas. This
fabricated and placed. Mucosa 0.51 appears to decrease the likelihood of
In case of OKC, the cystic lining is Bone 1.54 recurrence over enucleation alone.
fragile and thus the chances of incom­ Protein coagulation is thought to
plete removal of lining are high. Secon­ limit uptake of these toxic materials
dly, the cyst has a high recurrence rate Carnoy’s solution for 5 minutes as by surrounding tissues, however it is
and being infiltrative in nature infil­ shown in Table 27.3. this fact that limits its usefulness as a
trates in the medullary bone. To avoid treatment agent in general.
the recurrence and to eliminate the re­ Uses • As a fixative for pap smear samples.
sidual lining, after the enucleation the Some of the uses of Carnoy’s solution • As a fixative agent for both nuclear
adjoining bone is thoroughly cur­etted are: and mitochondrial DNA in various
and the base of the cavity is cauterized • Applied directly following enuclea­ tissues.
using 1 percent carbolic acid solution or tion for the treatment of keratocystic Carnoy’s solution penetrates to a pre­
using a Carnoy’s solution.7 odon­togenic tumors. dictable, time-dependent depth without
Time dependent depth penetration • Enhancing lymph node detection injuring the neurovascular structures.
in different tissues on application of during dissection of cadavers. Five minute application penetrates bone
608 Neoplastic Conditions of Head, Neck and Face

to a depth of 1.54 mm, nerve to a depth • Cysts with very thin and friable lining
of 0.15 mm and mucosa to a depth of which is difficult to be removed
0.51 mm.8 completely, e.g. sublingual ranula.
Primary bone grafting in the defect • Medically compromised patients
following the surgical removal is debat­ where the major surgical procedure
able topic. Some surgeons may recom­ or expo­sure to general anesthesia is
mend it, but the risk involved is that the con­traindicated.
chances of graft infection and rejection • As a combination with the enucle­
are optimum as the watertight closure of ation in cases of large lesions. Ini­
the defect is not always possible which Fig. 27.6: Diagrammatic representation of tially, the marsupialization is done
marsupialization
may lead to oral contamination and in­ and the cystic size is allowed to
fection which may subsequently result shrink and subsequently the enucle­
in graft rejection. Secondly in case of ation is done which avoids injury to
cysts like OKC there is a high recurrence the lesion (deroofing) bordering that the vital structures in the vicinity and
potential and unless the recurrence is surface or cavity. It is the procedure in the ensuing surgical defect is also
not ruled out by reasonable length of which the cystic lining is not removed smaller and manageable. This also
follow-up, primary grafting may not be fully, but instead a small portion of the prevents the weakening and frac­
a good idea. Instead secondary bone cystic lining along with the overlying ture of the bone. This procedure also
grafting is considered to be safe. The oral epithelium is excised, the contents called Waldron operation.
enucleated cystic lining must be sent are evacuated and the cystic lining is
for the histopathological examination sutured to the oral mucosa (Fig. 27.6). Advantages of Marsupialization
and the entire lining must be screened The cavity is packed gently with a guaze • It is technically simple
thoroughly by histo­logical examination soaked in the antiseptic solution and • Spares vital structures
to rule out any ameloblastic changes, so the pack is changed daily with reducing • Allows eruption of teeth
that in case of positive histopathological size. Alternatively, an impression of • Prevents oronasal, oroantral fistula
findings an appropriate follow-up pro­ the defect is made after the base has • Prevents pathologic fracture
tocol can be advised to the patient and granulated and an acrylic obturator with • Reduces operating time
remedial steps can be taken earlier in a bulb is fabricated. The bulb projects • Helps shrinkage of cystic cavity and
case of any recurrence. in the lumen and the size of the bulb is allows for endosteal bone formation.
gradually reduced by trimming as the
Advantages of Enucleation cyst heals. As the cyst is deroofed, the Disadvantages of Marsupialization
• Primary closure of the wound is pressure in the cystic cavity drops and • The demerit of this procedure is that
possible the further growth of the cyst is arrested the pathological tissue, i.e. the cystic
• Healing is rapid and the cyst begins to shrink with lining is left behind, which can lead
• Postoperative care is reduced simultaneous healing at the periphery. to the recurrence and neoplastic
• Thorough examination of whole After few months the cyst heals com­ trans­formations.
cystic lining is possible. pletely and the cystic lining merges with • Histologic examination of entire cys­
the oral mucosa. This procedure is also tic lining not possible.
Disadvantages of Enucleation called as a Partsch’s operation. • Postoperative care is required for
• Unerupted teeth in dentigerous cyst The indications of marsupialization long time.
will be removed with the lesion are: • Prolonged follow-up is required to
• Large cyst removal will make the • Large cystic lesions where enuc­ maintain larger opening than under­
jaws prone to fracture leation may cause weakening or lying cavity (formation of slit like
• Damage to adjacent vital structures pathological fracture of the bone. pocket that may harbor foodstuffs).
• Pulp necrosis and nonvitality of the • Cystic lesions in close proxim­ • Secondary surgery may be required
adjacent teeth. ity with the vital structures, where with risk of invagination and new
enucleation may damage the vital cyst formation.2
Marsupialization structures.
The word marsupial is derived from • Dentigerous cysts associated with Waldron’s Method9 (1941)
the Greek for “pouch”. It is the surgical tooth which is required to be pre­ In this technique the cyst is first marsupi­
exteriorization of a lesion by removal served or the tooth is in such a alized and then enucleated subse­quently.
of overlying tissue to expose its internal position that their eruption in the Due to deroofing of the cyst there is
surface to the oral cavity or another oral cavity can be facilitated, e.g. decrease in the osmotic pressure which
body cavity, by excision of a portion of maxillary canine. in return decreases the osteoclastic
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 609

activity around the cyst resulting in the is also quite early in the life, i.e. the late
gradual decrease in the size of the cyst first or second decade of life. Clinically
due to healing at the periphery. it may vary widely in size. This cyst is
• Large cysts contain multiple septae relatively docile in nature and seldom
so during marsupialization the cav­ recurs after adequate surgical removal.
ity is converted into single one. This The cyst produces a well circumscribed,
causes ease in the complete enucle­ radiolucent lesion and often does not
ation process. grown to a large size. The management
• Vital structures in approximation comprises of enucleation.
with the cysts are protected. Histopathologically, most of the
cases of primordial cysts, diagnosed on
Advantages Fig. 27.7: Specimen of resected mandible,
the basis of clinical features, turned out
severely undermined by OKC showing
• Development of thickened cystic lin­ multiple pathological fractures
to be odontogenic keratocysts (Para or
ing which makes enucleation easy Orthokeratinized). In view of the same
• Spares adjacent vital structures the terminology “primordial cyst” is not
• Combined approach reduces mor­ the surrounding tissue adjunctively in used for histopathogical diagnosis if the
bidity effort to eradicate residual disease and evidence of keratinization is present. In
• Accelerated healing process minimize recurrence. Chemical cauter­ such cases it will be reported as odon­
• Allows histopathological examina­ ization followed by enucleation serves togenic cyst and on clinical correlation
tion of residual tissue. the purpose. Carnoy’s solution is a pop­ it will be primordial cyst formed at the
ular chemical tissue fixative. initiation stage of tooth development.
Disadvantages
It requires secondary surgery for remo­ Cryosurgery
10
Dentigerous Cyst
val of residual pathological lining. Cryosurgery is an adjunct to the surgi­ A dentigerous cyst is the cyst which
cal treatment of benign cyst and tumors encircles the crown of an unerupted
Other Modalities of jaw. Similar to cryotherapy it allows tooth. At least two types of dentigerous
for removal of cyst by enucleation and cyst. Dentigerous cyst arising due to
Segmental Resection curettage followed by treatment of the degeneration of stellate reticulum in
Segmental resection is done when the surrounding structures. Cryosurgery for early stages of tooth development, ena­
bone is severely thinned out and multi­ osseous lesions produce cellular necro­ mel hypoplasia is a ensuing feature.
ple perforations are present, in cases of sis in bone, while maintaining the inor­ Dentigerous cyst also can arise after
pathological fractures and ameloblastic ganic osseous frame work. Predictable tooth formation by accumulation of fluid
trans­formation within the cyst. In such cell lysis occur at the temperature below within the reduced enamel epithelium or
advanced cases, the cyst extends to 20°C and is caused by: just below it; enamel hypoplasia may not
adjoining soft tissue and attempts for its • Direct damage to the intracellular and be a feature. Other theories of dentigerous
enucleation are usually inadequate lead­ extracellular ice crystal forma­tion cyst include enamel hypoplasia which
ing to the recurrence in the soft tissue. • Osmotic disturbance diminishes the adherence of reduced
This is more relevant and applicable to • Electrolyte imbalance. enamel epithelium to crown and
the OKCs as compared to the other odon­ provides starting point for development
togenic cysts as the former behave more of cyst. Crown of a permanent tooth
aggressively. In cases where the lesions are Developmental Cysts of sometimes erupts into a radicular cyst of
extensive, the bone is so severely thinned Odontogenic Origin its deciduous predecessor. This is rare as
out that it becomes virtually impossible cystic condition in primary dentition is
to preserve it and during the surgery itself Primordial Cyst seldom seen.
multiple patholo­ gical fractures occur The primordial cyst is formed as a result Shibata et al.11 (2004) conducted a
warranting the segmental resection of the of the cystic degeneration in the tooth retrospective study on 70 patients, who
thinned out bone (Fig. 27.7). bud of a developing tooth as early as had histologically confirmed denti­
the bud, cap or early bell stage. Thus, gerous cyst in anterior region. They
Chemical Cauterization the involved tooth fails to develop concluded that inflammatory changes
Enucleation followed by chemical cau­ and is missing. It can originate from at the apex of a deciduous tooth may be
terization—the presence of epithelial the tooth of the normal series or from responsible for initiating a dentigerous
islands within mucosa overlying the cyst the bud of the supernumerary tooth. cyst of the permanent successor. It is
and the bony cavity have prompted the As it originates quite early state of the cyst that surrounds the crown of an
use of various surgical strategies to treat odontogenesis, the age of occurrence unerupted tooth. It is formed as a result
610 Neoplastic Conditions of Head, Neck and Face

of accumulation of the fluid between bone and the involved tooth is often
the reduced enamel epithelium and the missing as it is displaced away from the
crown of the tooth. alveolar bone due to pressure exerted
by the cyst. The adjacent teeth may also a b c
Clinical Features be displaced due to the pressure. The
Figs 27.9A to C: Varieties of dentigerous
Dentigerous cysts is commonly seen overlying cortical bone is thinned and
cyst. (A) Central; (B) Lateral; (C) Circum­fe­
in early part of life, i.e. second decade. cortex is expanded more often.
rential type
It is most commonly seen in maxillary Three varieties of the dentigerous
canine and mandibular third molar cyst have been described namely cen­
area, but can occur with any tooth tral, lateral and circumferential. The • Central
inclu­ ing the supernumerary tooth ameloblastic transformations are more
d­ • Lateral
may be displaced as low as the inferior common in a dentigerous cyst. The rap­ • Circumferential types of dentigerous
border. Dentigerous cysts associated id growth, expansion of other cortices, Cysts (Figs 27.9A to C).
with supernumerary teeth are rare and multilocular appearance may suggest
estimated to constitute 5 to 6 percent ameloblastic transformation. Malignant Aspiration
of all dentigerous cysts. They resemble transformation is comparatively less Aspiration is done using a wide bore
the usual dentigerous cysts in terms of common than the ameloblastic trans­ (18 gauge) needle. The dentigerous cyst
sex predilection and age distribution. formation. The malignancy associated usually contains a straw colored fluid.
The vast majority, about 90 percent, are with the dentigerous cyst is squamous The cystic fluid contains cholesterol
associated with a maxillary mesiodens.6 cell carcinoma and possibly the muco­ crystals and is rich in protein on bio­
The incidence of association dentige­rous epidermoid carcinoma than the amelo­ chemical investigation.
cyst with an impacted tooth increases blastic carcinoma. Incisional biopsy is indicated only
with age. It is characterized by missing in large cysts to rule out ameloblastic
tooth with hard swelling. It is usually Radiograghic Features chan­ges in the cystic lining. However,
painless unless and until secondarily Dertigerous cysts presents as smooth the preoperative incisional biopsy in
infected or very large. It may lead to well-corticated radiolucency, common­ small and moderate cases is usually
failure of eruption of adjacent tooth due ly unilocular or multilocular if infected. unn­ece­ssary.
to pressure. There is no neurologic deficit It is associated with unerupted tooth
even though the neurovascular bundle is attached at cemento enamel junction Differential Diagnosis
grossly displaced. Expansion of cortices (Fig. 27.8C). It mostly causes displace­ • Ameloblastoma and ameloblastic
especially buccal cortex (Fig. 27.8B). ment of roots, but if lesion is fast grow­ fib­roma
Sometimes in case of lower molars ing or is of long, standing duration it • Adenomatoid odontogenic tumor
lingual cortex and if the cyst is very large may lead to resorbtion of roots and may occ­urs in maxilla.
both the cortices get expanded. If cyst also cause displacement of the neuro­
is rapid growing cortices become paper vascular bundle. The involved tooth gets Management
thin and on palpation there is egg shell severely displaced due to pressure from The treatment of choice is enucleation
crackling. Fluctuation can be elicited on the growing cyst and may be present at along with removal of the involved tooth.
palpation when the bone is perforated. the inferior border of the mandible or The lining is thick and has nice capsule
The maxillary canines can also be seve­ very high in the orbital floor in maxillary which facilitates the removal of the cyst
rely displaced up to the infraorbital cysts (Figs 27.8A and C). in Toto. When the tooth is not severely
margin due to the pressure from the Dental follicle may expand to pro­duce displaced and can erupt in its normal
cyst. The cyst causes expansion of the radiographic appearance of following: position and needs conservation, in such

a b c
Figs 27.8A to C: Dentigerous cyst with severely displaced unerupted molars
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 611

cases marsupialization can be done. 27.12). The cyst does not recur after in young patients during the eruption
The eruption of the tooth can be assisted adequate surgical procedure. According period and the radiographic and clinical
orthodontically. The lining must be sent to most authors, the common treatment features are suggestive of dentigerous
for histopathological examination to for the dentigerous cysts has been total cysts an alternative treatment is the
rule out ameloblastic changes, especi­ elimination of the cyst including the tooth main­tenance of the permanent tooth and
ally in large cysts (Figs 27.10, 27.11 and involved; however if the lesion is present enucleation of the lesion alone, stating

A B c
Figs 27.10A to C: Dentigerous cyst with maxillary premolar managed by enucleation

A B

C D E
Figs 27.11A to E: Dentigerous cyst with maxillary canine treated with enucleation
612 Neoplastic Conditions of Head, Neck and Face

A B
Fig. 27.12: Enucleation of dentigerous cyst in the mandibular body and ramus with preservation of neurovascular bundle

dontic assistance may be required in such keratocyst was used to describe any jaw
cases to facilitate the eruption of the tooth cyst in which keratin was formed to a
in its desired position. large extent.
The odontogenic keratocyst (OKC)
Histopathological Findings is the term coined by Phillipsen (1956)
The lesions consist of a fibrous connec­ to describe a class of odontogenic cyst
tive tissue wall which is loosely arranged. where the lining epithelium proliferates
The epithelium lining consist of two to and differentiates to the extent of for­
three layers of cuboidal epithelial cell. mation of keratin.
In infected dentigerous cyst due to
infection the fibrous wall become more Etiology and Pathogenesis
Fig. 27.13: Dentigerous cyst undergoing collagenized, with a variable infiltration Paul Stoelinga16 stated in the past that
ameloblastic changes of chronic inflammatory cell along with OKC was considered to originate from
some areas of hyperplastic squamous epi­ primordium of tooth before mineraliza­
that amelo­blastomatous changes or other thelial lining was seen (Figs 27.14A to C). tion has taken place, remnants of dental
odonto­ genic lesions (Fig. 27.13) have lamina or basal cell hamartias. It may
been ruled out after histopathological Odontogenic Keratocyst (OKC) arise from the cell rests of Malassez,
ana­ly­sis and a diagnosis of dentigerous remnants of dental lamina or in the
cysts is confirmed.12 Alternatively if Historical Aspect lining of other odontogenic cysts.
the involved tooth is noticed to be in Mikulicz13 (1876), described the OKC as a
favorable position for its eruption in dermoid cyst. Hauer (1926) and Kos­tecka Enlargement of Keratocyst
the oral cavity in a young individual the (1929) described keratocyst as a choles­ Scharfetter et al.17 (1989) found that inva­
marsupialization of the cyst may be done. teatoma.14 The term odontogenic kerato­ sive growth of keratocyst was likely to be
As the pressure from the growing cyst cyst was introduced by Phili­psen15 (1956) a result of active growth of the connec­
drops the tooth starts erupting. Ortho­ and is now widely used. The desig­nation tive tissue wall. Toller18 (1970) suggested

A B C
Figs 27.14A to C: Photomicrograph showing the lining of a dentigerous cyst
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 613

that osmolality plays an important role in • When cyst occurs entirely on gin­
expansive growth of OKC. Main19 (1970) giva it is known as peripheral odon­
suggested that mural growth in the form togenic keratocyst.
of epithelial proliferation causes expan­ • In 60 percent of cases there is bony
sion of OKC. The rate of growth of kera­ expansion, more on buccal than lin­
tocyst varies from 2 to 14 mm a year, with gual side. In 39 percent perforation
average of about 7 mm2. Browne20 (1970) of bone is also noted. However it
and Kramer21 (1974) proposed that mul­ is observed that the OKC usually
tilocular outlines is due to proliferation attains a large size without causing a
of local groups of epithelial cells against conspicuous bony expansion.
the semisolid cyst content. Fenestrated • The cyst may even extend from maxi­
capillaries in OKC cause expansion. lla to base of skull behaving like a
low-grade squamous cell car­cinoma.
Clinical Features Neurological symptoms occ­asi­­onally
• It occurs as early as 1st decade and noted.
as late as 9th decade, with pro­ • The cyst has high rate of recurrence
nounced peak frequency in 2nd and after incomplete inucleation and
3rd decade of life. There Bimodal the patients are required to be
age distribution with 2nd peak in 5th kept under long term postoperative
decade or later. follow-up.
• There is a male predilection. • Multiple OKC are seen in case of
• Whites races are more affected than “Jaw cyst—Basal cell nervus – Bifid Fig. 27.16: Types of keratocyst
blacks. rib syndrome” and the Gorlin – Goltz
• Mandible is commonly involved syndrome. beha­­vior, the expression of various
than maxilla. Approximately half of The recurrence rate is very high in pro­liferation markers in the epithelial
all keratocysts occur in angle and OKC due to: lining and over expression of p53
extends to varying distances into the • Thin and fragile lining. protein and mutations in p53 and PTCH
ascending ramus and forward into • Infiltrative nature. genes (tumor suppressor genes) have
body. Pain, swelling and discharge • Incomplete removal of cyst lining. led several investigators to consider
may present with paraesthesia of • Retention of daughter cysts/micro­ odo­ nt­
ogenic keratocyst as a benign
­
lower lip. The cyst can attain large cyst or epithelial islands in the wall cystic neoplasm. The components of
size involving maxillary sinus, entire of original cyst. the connective tissue in KCOT revealed
ascending ramus including condylar • There is development of new kera­ some res­ emblance with the stromal
and coronoid process (Fig. 27.15). tocysts from epithelial offshoots of com­­­ponents of aggressive tumors such
• There may be displacement and/or the basal layer of oral epithelium as ameloblastoma: high frequency of
resorption of teeth. and infiltrative nature of the cyst. stromal myofibroblasts, differences in
• When maxillary sinus is involved the collagen fibers of the extracellular
there can be displacement and Types of Keratocyst (Fig. 27.16) matrix, high enzymatic activity with
destruction of floor of orbit and • Replacement increased matrix metalloproteinases
proptosis of eyeball. • Envelopmental (MMPs) and mast cell tryptase, and in­
• Extraneous cre­ased expression of receptor acti­vator
• Collateral. of nuclear factor-kB (RANK), RANK lig­
and (RANKL), osteoprotegerin (OPG)
Odontogenic Keratocysts and tumor angiogenesis. Focusing on
the importance of the epithelial-mes­en­­
Reclassified as Keratocystic
chymal interactions in odontoge­ nic
Odontogenic Tumor tumors, previous studies supported that
The odontogenic keratocyst is regarded the stroma of keratocysts should not
as a developmental abnormality and is be regarded just a structural support of
generally known for its aggressive nature the cyst wall, but rather as portraying
and high recurrence rate, especially in the features of a “tumoral stroma”.
comparison with other developmental However, its growing potential to a large
Fig. 27.15: Site predilection for occurrence odontogenic cysts. In addition to a dis­ size before manifesting clinically and
of OKC tinctive clinical aggressive biological the tendency to recur following surgical
614 Neoplastic Conditions of Head, Neck and Face

treatment, gave rise to a discussion as to and predominantly parakeratotic; and a bifid rib syndrome’ and the ‘Gorlin-
its true pathological nature and termi­ fibrous connective tissue cyst wall that Goltz syndrome’.
nology. Hence, in 2005 World Health is thin and usually uninflamed. Additi­ Radiologically the cyst has a cla­ss­ical
Organization, based on behavior, histo­ onally, satellite cysts, solid epi­thelialmultiloculated appearance with sclerotic
logy and genetics, reclassified the tradi­ pro­liferations, odontogenic rests, and borders. The classical scallop­ing of the
tional designation, stressing the benign basal layer budding have been described borders is seen in this cyst and the loculi
behaviour of this lesion was sub­stituted in association with the odon­ togenic are separated by fine bony septae. The
by a term that would better reflect its keratocyst (OKC). loculi are variable in size and the cyst
neoplastic nature—keratocystic odon­ The histologic variants of the odon­ extends between the roots of the teeth
togenic tumor (KCOT)—and the lesion togenic keratocyst (OKC) are: (1) para­ (Figs 27.18A to D). The CT scans provide
was thus described as a benign uni or keratinized (2) orthokeratinized, and (3) more accurate information regarding the
multicystic, intraosseous tumor arising combined. The recurrence rate is much perforation of cortex and extraosseous
from the dental lamina or its remnants. higher in the parakeratinized variant spread of the lesion. This information
The orthokeratinized variant of the than that the orthokeratinized variant is more vital as the extraosseous spread
odontogenic keratocyst is not currently (Figs 27.17A and B). warrants more comprehensive surgical
included as being part of the spectrum management to prevent soft tissue
of keratocystic odontogenic tumor.22 Contents of Cyst recurrence (Figs 27.19 and 27.20). The
The main histopathological features Heparin sulfate, Chondroitin 4 sulphate, cyst initially contains a straw-colored
defined in 2005 enable to differentiate Hyaluronic acid, GAG. On aspiration
KCOTs from jaw cysts with keratinization. there it is whitish, cheesy material with
• Well defined, often palisaded, basal Keratin flecks. There is low protein
layer of columnar or cuboidal cells content (< 4 mg/dL), with specific
• Intense basophilic nuclei of the gravity 1.018. Histologic differential
columnar basal cells oriented away diagnosis from cystic ameloblastoma,
from the basement membrane dentigerous cyst, glandular odontogenic
• Parakeratotic layers with an often cyst, lateral periodontal cyst. The OKC
corrugated surface is also known to undergo ameloblastic
• Mitotic figures frequently present in transformations. Multiple OKC are seen
the suprabasal layers. in case of ‘Jaw cyst-basal cell nervus- Fig. 27.17A: Orthokeratinized OKC

Histopathological findings
The epithelial lining and connective tis­
sue wall of the odontogenic keratocyst
(OKC) is characteristically thin and
fri­able, thus causing the specimen to
frag­ment when treated. Grossly, the
lesion often has a bosselated, gray, cystic
appe­arance mimicking the appearance
of a glove.
In 1962, Pindborg and Phillipsen
and Henriksen established strict histo­
logic criteria for the diagnosis of an
odontogenic keratocyst (OKC). These
criteria include an epithelial lining that
is usually thin and uniform in thickness,
with little or no evidence of rete ridges; a
well-defined basal cell layer, the compo­
nent cells of which are cuboidal or
columnar in shape and often fashioned
in a palisaded arrangement; a thin,
spinous cell layer which often shows a
direct transition from the basal cell layer;
spinous-cell layer intracellular edema; Fig. 27.17B: Photomicrograph of Parakeratinized OKC
surface keratinization that is corrugated (Keratocystic odontogenic tumor)
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 615

• Segmental resection in case of mul­


tiple perforations of the cortex,
path­ ological fracture, where the
bone so severely thinned out that
it is difficult to conserve it. The
spillage of the cyst in the soft tissue
also requires attention as the cyst is
a b known to recur in the soft tissue as
well. If the perforation in the soft
tissue is encountered, excision of
soft tissue upto the next anatomical
boundary is recommended and the
excised tissue be subjected for frozen
sections to determine adequacy of
surgical margins.
c d • Marsupialization is mentioned in the
Figs 27.18A to D: Keratocyst showing multiloculated radiluscent appearance literature as the treatment modality,
but it is a poor choice of therapy as
the cyst is aggressive and it is danger­
ous to leave behind the pathological
difficulty is that during the marsupi­
alization all the loculi, especially the
smaller ones may not be opened and
the cyst will start growing again. The
daughter cysts may proliferate and
cause recurrence. The risk of amelo­
blastic changes is always there. Mar­
supialization followed by enucleation
is also recommended in the literature
in the management of the large lesions
however it is not a popular treatment
Fig. 27.19: Multiloculated lesion, with bony Fig. 27.20: 3-D CT scan showing multiple modality for the obvious reasons.
septae CT scan showing perforation of lin­ cortical perforations Decompression of cyst involves any
gual and scalooping of the border cortex
technique that relieves the pressure
within the cyst that causes it to grow.
fluid, which changes into cheesy material The selection of the appropriate Growth of cysts is believed to occur
due to accumulation of the exfoliated treatment modality is based on various by a combination of osmotic pres­
keratin in its lumen. This may be differ­ factors like age of the patient, location sure and pressure resorption, cou­
entiating feature of the OKC from the of the lesion, extent of the lesion and pled with release of prostaglandins
ame­ lo­
blastoma, as both may appear presence of cortical perforation and and gro­w­th factors. Decompression,
similar radiographically. extension of the cyst in the adjacent soft by any means, appears to change
tissue. to environment and decreases the
Management The OKC is treated with more agg­ amount of interleukin-α which is
The different modalities that are pro­ ressive way due to its high rate of recu­ released. Decompression can be per­
posed for the management are: rrence. The treatment modalities are: formed by making a small opening
• Enucleation and curettage • Enucleation with vigorous curettage in the cyst and keeping it open with a
• Enucleation and peripheral ostec­ of the adjacent bone. drain. Marsupialization, on the other
tomy • Enucleation with chemical caute­ hand, involves converting the cyst
• Marsupialization riza­
tion of the base of the bony into a pouch. By converting the cyst to
• Osseous resection cavity. Many authors recommend a pouch, the lesion is decompressed,
• Cryotherapy the use of Carnoy’s solution, a tissue but this is a more definitive treatment
• Excision of overlying mucosa in fixative that is applied to the bone for the cavity and exposes the cyst lin­
conjunction with cyst enucleation cavity following the enucleation and ing to the oral environment. Mandib­
and treatment of bony defect with curettage of the cyst lining and bone ular cysts are normally marsupiali­zed
Carnoy’s solution. cavity. into the oral cavity, although maxillary
616 Neoplastic Conditions of Head, Neck and Face

cysts can also be marsupialized into


epon­y­­mously named as Gorlin’s cyst. keratinization (Figs 27.22A to C). The
the maxillary sinus or nasal cavity,
The cyst is commonly seen in the mandi­ other lesion which also shows presence
as well as the oral cavity.8 The basic
ble (Fig. 27.21A). The central CEOCs are of the ghost cells is craniopharyngeoma.
more common than peri­pheral lesions
limitation of the mar­supialization is The ghost cells are degenerating epi­
that the cyst is multi­ (3:1) and they are usually diagnosed in
loculated and thelial cells. The presence of patchy
has many loculi and even daughter the second decade of life, whereas the foci of calcification within the lesion is
peripheral ones are usually noted after
cysts in the lining. The marsupializa­ another peculiarity of this cyst. It war­
tion may lead to decompression of the age of 50. The CEOC may associated rants differentiation from the CEOT,
with odontoms.9 The age incidence is
the major locule, but other loculi may which has different age incidence,
remain unaddressed and thus the 2nd and 3rd decades of life with equal clinical behavior and histopathological
treatment with this modality may not
predelection to males and females. features. The radiological picture is a
be adequate to treat the large lesions.
There are two variants of CEOC, a cystic well-corticated radiolucent lesion with
• Long-term follow-up is mandatory and neo­plastic variant. It is considered to patchy foci of dystrophic calcification in
after any treatment to detect the be the oral counterpart of the cutaneous it (Fig. 27.21B). The diagnostic incisional
recurrence early. calcifying epitelioma of Malherbe. Both biopsy may be conclusive in establishing
The enucleated lining should be the lesions are characte­ rized by the the preoperative diagnosis in case of
submitted for the histopathlogcial ex­ presence of “ghost cells” histologically. large lesions. The treatment of choice
amination to confirm the diagnosis and The main histopathologic criteria for the for the CEOC comprises of enucleation
to rule out other changes. diagnosis of the calcifying odontogenic (Fig. 27.21C). The recurrence rate after
cyst are well-established. The cyst lining adequate enucleation is low.
Calcifying Epithelial should show proliferation to the point
that it resembles ameloblastoma, (i.e.
Gingival Cyst and Midpalatal
Odon­togenic Cyst columnar cells over which are stellate Raphae Cyst of Infants
(Gorlin’s Cyst) and spindled cells in an arrangement It was first described by Moscow and
Calcifying epithelial odontogenic cyst that suggest stellate reticulum). Within Bloom24 1983. During the morpho­
(CEOC) was first described by Gor­ this proliferation of epithelium, cells differentiation (late bell stage), disinte­
lin and associates23 in 1962 and thus undergo the characteristic ‘ghost cell’ gration of the dental lamina begins to

a b c
Figs 27.21A to C: CEOC: (A) Clinical appearance; (B) Radiographic appearance; (C) Treatment with enucleation

a B C
Figs 27.22A to C: Photomicrograph showing the proliferation of the lining epithelium with palisaded,
hyperchromatic columnar nuclei, stellate reticulum—like area and sheets of ghost cells (H and E stain)
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 617

nounced plaquelike thickenings, mural cells secrete lymphokines to neutr­alize,


protrusions, and a multilocular pattern immobilize and degrade bacteria.
histologically. The thickened areas are These cells are thought to elaborate
usually separated by thin, fibrous septa. many other factors that either directly
Microscopic assess­ment is necessary to or indirectly act as epithelial growth
distinguish lateral periodontal cyst from factors, stimulating the proliferation of
other odontogenic cysts and pathologic rests of Malassez.
processes. A radicular cyst is an inflammatory
cyst which is usually associated with
Eruption Cyst a non-vital tooth. The tooth is either
Eruption cyst is essentially a dentige­ carious, fractured or attrided, causing
rous cyst occurring in the soft tissues. exposure of the pulp. The pulp becomes
Crown of the tooth associated with an inflamed, necrotic and the tooth becomes
eruption cyst usually projects into cyst non-vital. The repeated infection leads
lumen, derived from reduced enamel to chronic periapical infection. The
Fig. 27.23: lateral periodontal cyst epithelium. remnants of the root sheath of Hertwig
get irritated and they proliferate to give
occur and numerous islands and strands rise to a radicular cyst. The cyst seldom
of odontogenic epithe­lium are seen in Odontogenic Cyst of more than 1 cm in diameter. But larger
the corium between the tooth germ and Inflammatory Origin lesions are also seen in some patients. The
the oral epithelium, remote from the cyst causes expansion of the bone and
alveolar process. Those dental lamina Radicular Cyst the overlying cortex becomes thin and
remnants which had already evolved The origin of cyst epithelium lies in cell eroded to produce egg shell crackling in
into small cysts, expanded rapidly at rests of malassez. The products of pulpal cases of larger cysts (Figs 27.24 and 27.25).
this stage (15–20 weeks) and there was infection and necrosis spill out into the As the cyst is inflammatory in origin, dull
thinning of overlying oral epithelium. periapical tissues, initiating an infla­ pain is associated with this cyst. Long
m­matory response. The inflam­matory standing periapical cysts may present as a
Lateral Periodontal Cyst
Lateral periodontal cyst is uncommon,
but well-recognized type of develop­
mental odontogenic cyst. It arises from
odonto­ genic epithelial cell rests, trau­
matic implantation of surface epithelium
or cystic degeneration of deep projec­
tions of surface epithelium (Fig. 27.23).

Histopathological features
The lateral periodontal cyst is compo­
sed of a cystic cavity with a connective
tissue wall. The cyst lining of the lateral
a b
periodontal cyst is generally compo­sed of
1 to 5 cell layers of cuboidal to stratified,
nonkeratinized, squamous epithelium,
with focal plaque like thickenings that
appear as whorls and mural protrusions.
Shear and Pindborg suggested that these
thickenings represented an example of
the odontogenic epithelium establishing
original morphology under pathologic
conditions, akin to the thickening of stom­
atodeal ectoderm in the formation of den­
tal lamina during early odontogenesis.
The Botryoid odontogenic cyst has c d
a similar histology to that of the lateral Figs 27.24A to D: Radicular cyst: (A and B) Clinical presentation; (C) Radiographic
periodontal cyst, except for more pro­ appearance; (D) Surgically exposed lesion
618 Neoplastic Conditions of Head, Neck and Face

gingival sinus, drai­ning pus intermittently and the clinical picture could be similar Radiologically, this cyst produces a
(Fig. 27.27A). Acute exacerbation of the to a periapical abscess. well-circumscribed, radio­lucent lesion
infection may produce throbbing pain around the root apex of the involved
tooth. The cortication of the cystic lining
is continuous with the lamina dura of
the tooth (Figs 27.24C, 27.26A and B,
27.27B). Radiologically, this condition
looks similar to a peri­apical granuloma.
The cyst has a thick lining (fig. 27.24
D) and can be effectively treated with
enucleation along with the extraction
or endodontic therapy of the offending
tooth (Figs 27.26A and B). It is not known
to recur after complete enuc­leation.

Macroscopic findings
The gross specimen may be spherical or
a b ovoid intact cystic masses, but often they
Figs 27.25A and B: Radicular cyst with nonvital maxillary incisors, a common clinical entity are irregular and collapsed. The walls
vary from extremely thin to a thickness
of about 5 mm. The inner surface may
be smooth or corrugated.

Histopatholgical findings
The histopathological studies shows
following features:
Epithelial lining: Almost all radicular
cysts are lined by stratified Squamous
Epithelium and range in thickness from
1 to 50 cell layers. The only exception to
this is in those rare cases of periapical
lesions of Maxillary Sinus. In such cases,
cyst is then lined with a pseudo strati­
a b fied cilliated columnar epithelium or
Figs 27.26A and B: Management of a large radicular cyst with enucleation respiratory type of epithelium. Rush­ton’s

a b
Figs 27.27A and B: Radicular cyst with incisors presenting as a palatal sinus
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 619

a b c
Figs 27.28A to C: Photomicrograph of radicular cyst, note chronic inflammatory cell infilteration in the lining

Hyaline bodies are found in epi­thelial ceptualized as resulting from tooth lucent lesion causing the divergence of
linings. Very rarely they are found in extraction that did not include removal the adjacent teeth.
Fibrous capsule. of an associated radicular cyst. But more The globulomaxillary cyst forms at
Fibrous capsule: Fibrous capsule of commonly it occurs due to failure of the junction of the globular process of the
radi­cular cyst is composed of mainly endodontic treatment or misdiagnosed medial nasal process and the maxillary
condensed parallel bundles of collagen accessory canal. process. The globulomaxillary fissure is
fibres peripherally and a loose connective present between the lateral incisor and
tissue adjacent to epithelial lining. Depo­ the canine teeth (Fig. 27.31). It is often
Non-Odontogenic CYSTS
sition of cholesterol crystals are found in asymptomatic clinically and is detected
many radicular cysts, slow but consider­ on routine radiographs or during the
able amount of cholesterol accu­mulation Inclusion Cysts orthodontic treatment. The treatment
could occur through dege­neration and comprises of surgical removal, sparing
disintegation of lymphocytes, plasma Midpalatal Cysts the adjacent teeth.
cells and macrophages taking part in They arise from epithelial inclusions
inflammatory process, with consequent at the line of fusion of palatal folds Traumatic Bone Cyst
release of cholesterol from their walls. and nasal processes. After birth these (Synonyms—Traumatic, simple, hemor­
Acute inflammatory cells are present epithelial inclusions usually atrophy and hagic, solitary, simple, idiopathic bone
when epithelium is proliferating. Chron­ are absorbed. Some however produce cyst, extravasation cyst, unicaramel cyst).
ic inflammatory cells are present in con­ keratin containing keratocyst which The traumatic cyst is an unusual lesion
nective tissue immediately adjacent to extend onto the surface. Burke et al.25 which occurs with considerable frequency
epithelium (Figs 27.28A to C). 1966 suggested possibility of abortive in jaws as well as in other bones.
glandular differentiation leading to
Residual Cyst cyst formation. The exact cause of the Traumatic Theory
Residual cyst refers to an inflammatory epithelial pro­ liferation and the cyst After trauma to an area of spongy
cyst of the jaws that fails to involute formation is not known. bone containing hemopoietic marrow
after root canal therapy or tooth re­ The median palatal cyst is located in enclosed by a layer of dense cortical
moval (Fig. 27.29). Although, it is con­ the midline of the hard palate between bone there is a failure of organization of
the lateral palatal processes. The cyst the blood clot and for some unexplained
may become large to be visible clinically reason, subsequent degeneration of the
as a midline palatal swelling. It produces clot occurs that eventually produces
a well-circumscribed radiolucent lesion an empty cavity within the bone. In
on the palatal radiograph (Figs 27.30A the deve­ lopment of the lesion, the
and B). trabe­culae of bone in the involed area
becomes necrotic after degeneration of
Globulomaxillary Cyst the clot and the bone marrow, although
The globullomaxillary cyst has been some viable tissue must persist to initiate
described as an intrabony fissural cyst the resorbtion of the involved trabe­
between the maxillary lateral incisor culae. The expansion tends to cease
Fig. 27.29: X-ray showing residual cyst in and the canine teeth. Radiologically, it when the cyst reaches the cortical bone,
lower left second molar region is a well corticated, heart shaped radio­ thus there is no cortical expansion.
620 Neoplastic Conditions of Head, Neck and Face

A B
Figs 27.30A and B: Median palatal cyst

Other Theories of Origin presence of hematopoietic marrow


• (Figs 27.32A to C). The traumatic bone
Origin from bone tumors that have
undergone cystic degeneration cyst occurs in mandible and very seldom Fig. 27.31: Globulomaxillary cyst between
• A result of calcium metabolism in maxilla. the lateral incisor and canine producing
such as that induced by parathyroidThe teeth in the involved region pear shaped shadow
disease are generally vital. When the cavity is
• surgically opened, it is found to be an
Necrosis of fatty marrow due to isch­ enough to involves the whole of body
emia empty which may contain either small or ramus. The cavity may be lobulated
• Low grade chronic infection amount of straw-colored fluid, shreds or scalloped if it involves root apices.
• of necrotic blood clots, fragments of
Trauma creating unequal balance of The cyst in the molar region should
osteoclasis and repair of bone.connective tissue or nothing. be differentiated from lingual salivary
The hydrostatic pressure in cystic gland depression which is located below
Clinical Features lumen is exceptionally low as compared mandibular canal where as solitary cyst is
The traumatic bone cyst usually occurs to other cysts. present above it.
in young patients. Males are more fre­ The histopathologic features are a
quently affected than females probably Radiographic Features thin connective tissue membrane lining
because they are more exposed to It reveals a rather smoothly outlined the cavity.
trauma. Mandibular molars are more radiolucent area of variable size which
common site although cases with may be lined by sclerotic bone depending Treatment
anterior mandible have also been re­ on the duration of the lesion. The size may Since the definitive diagnosis of the
ported which may be probably due to be small in centimeter or may be large solitary bone cyst cannot be established

a b c
Figs 27.32A to C: (A and B) A case of traumatic bone cyst in a young girl of 15 years age watch the bony expansion;
(C) Empty cavity without lining
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 621

without surgical exploration. So attempts venous pressure leading to development


to enucleate the lining and in course of of dilated engorged veins. It has also
manipulation reestablish bleeding into been explained as exuberant attempt to
the lesion should be attempted. If the repair hema­toma of bone similar to cen­
cavity is then closed, it has been found tral giant cell granuloma. But in cases
that healing and filling of the space by of aneurysmal bone cyst it is postulated
bone occur in 6 to 12 months. If the that the hematoma maintains circula­tory
space is large, cancellous bone chips and Fig. 27.33: A case of aneurismal bone cyst connection with damaged blood vessels.
hydroxyl appetite crystals can be used to (ABC) showing Honey comb appearance on The slow flow of blood thought the lesion
fill the defect. The platelet rich plasma radiograph leading welling of the lesion when entered.
when added with the cancellous bone It has been associated with solitary cyst,
chips facilitiates the faster healing of the and trabaculae that produce the giant cell tumors or osteosarcomas.
bony defect. classic soap bubble appearance.
• Healing phase, with progressive cal­ Treatment
Aneurysmal Bone Cyst cification (  formation of the phlebo­ Surgical curettage of the lesion is ad­
The aneurysmal bone cyst is an interes­ liths) and ossification of the cyst and its vised. The flow pattern is evaluated and
ting entity described by Jaffe and Lich­ eventual transformation into a dense if possible the feeding vessels are ligat­
ten­stein26 (1942), they coined the term bony mass with a irregular structure. ed. High flow lesions may require inter­
anuerysmal bone cyst to describe the Thus, the lesion is known to regress ventional radiological support by way
characteristic blow out of the bone seen spontaneously after incomplete removal. of embolization of the feeding vessels
in the radiograph. using enbutyl cinoacrylate or polyvinyl
Radiographic Features alcohol particles or micro coils to reduce
Clinical Features The radiological picture is a radiolucent vascularity and then the lesion is treated
The cyst is rarely found in jaws. It is area which produces ovoid or cru­ciform by surgical curettage within 24 hours.
generally fond in 1st and 2nd decade expansion of the bone. It is gen­erally uni­ Low-dose radiation has also been used.
with female predilection. The common locular or may be multilocular or have But, the possibility of radiation sarcoma
sites of involvement are mandibular honey comb appearance (Fig. 27.33). is always a hazard.
and maxillary molar region and also
invol­ve angle and ascending ramus Histopathological Features
region. Aneurysmal cysts of jaws produce Aneurysmal bone cysts’ histopathologi­ Cyst of Soft Tissue of
firm swelling which may be associ­ated cal features show mixture of benign stro­ Head, Neck and Face
with tenderness. Swelling may be asso­ mal tissue consisting of large vascular
ciated with malocclusion and displace­ lacunae separated by septa in which nu­
Sebaceous Cyst
ment of teeth. It may enlarge to perforate merous giant cells are found and filled
the cortex being covered by periosteum with clotted blood (blood-filled spaces A sebaceous cyst is a closed sac or cyst
or thin shell of bone and may be with bland fibrous connective tissue below the surface of the skin that has
associated with egg shell crackling. The septa) that resembles cranberry sauce; a lining that resembles the uppermost
intraoperative findings are characteris­ cavernous spaces vessel lack walls and part (infundibulum) of a hair follicle
tic in a way that typical welling of the normal features of blood vessels; stroma and fills with a fatty white, semisolid
blood from the tissue is encountered has histiocytes, fibroblasts, scattered gi­
material called sebum.
on entering the lesion. The involved ant cells, hemosiderin and occasional If the duct or mouth of the seba­
tissue is often described as ‘blood soaked inflammatory cells; giant cells; ABC may ceous gland becomes blocked, the
sponge’ with large pores representing the be difficult to distinguish from that of gland becomes distended with its own
cavernous spaces of the lesion. giant cell tumor of bone; large amounts secretions and forms sebaceous cyst.
Four phases of the pathogenesis of hemosiderin. It is retention cyst and is also called
have been identified as follows: Secondary aneurysmal bone cysts epidermoid cyst as it is lined by superficial
• initial osteolytic phase. occur in conjunction with other lesions squamous cells. It contains sebum which
• Active growth phase, characterized (e.g., chondroblastoma, osteoblastoma, is yellowish pultaceous material with
by rapid destruction of the bone and osteosarcoma, nonossifying fibroma). unpleasant smell. Such material contains
a subperiosteal blow out pattern. sebum, fat and des­quamated epithelial
• Mature stage, also known as stage of Pathogenesis cells. It may be seen anywhere in the
stabilization, which is manifested by Various reasons have been postulated. In body, but is commonly seen in parts of
the formation of a distinct peripheral may be due to persistent local change in body with plenty of sebaceous glands like
bony shell and internal bony septae the hemodynamics, leading to increase the face and the scalp.
622 Neoplastic Conditions of Head, Neck and Face

It presents as typical cystic swelling dissected from the surrounding cleft in embryonic development. At the
which is spherical in shape and varies skin till the entire cyst can be rem­o­ 4th week of embryonic life, the develop­
in shape from few millimeters to 5 cm ved intact as it may recur if removed ment of four branchial (or pharyngeal)
in size. It has smooth surface and there incompletely. This meth­od is suitable clefts results in five ridges known as the
is bluish spot or punctum which indi­­­- when the cyst is infec­ted previously branchial (or pharyngeal) arches, which
cated the blocked opening of the duct as this makes the cyst wall thick and contribute to the formation of various
(Figs 27.34A to C). Sebaceous cyst is well defined (Figs 27.35A to D). structures of the head, the neck and the
always fixed to the skin and is cystic in 2. Incision avulsion technique: Under thorax. The second arch or the hyoid
consistency. It indents to finger due to local anesthesia, incision is made arch grows caudally as well as ventrally
the presence of sebum. In large cyst, through the skin into the cyst and and at greater pace than the third and
fluctuation is positive. This cyst is freely some contents of the cyst are squeezed fourth arch at the end of the 5th week.
mobile over the underlying structures. It is out. The cyst wall is then held with pair The ridge produced by this arch grows
non-tender till it gets secondarily infected. of disseting forceps and cyst is avulsed downward and meets caudally a small
Total excision is the treatment of out. bridge termed as the epipericardial ridge
choice. If infected, antibiotic should be just above the pericardium. According to
given and excision should be performed Branchial Cyst some, it meets the fifth arch and the two
only when the infection subsides. fuse. A small depression is formed which
Two types of surgical methods for Development lies superficial to the 3rd and 4th arch and
excision are recommended: Branchial cleft cysts are congenital epi­ deep to the second arch. This depression
1. Dissection method: elliptical incis­ thelial cysts, which arise on the late­ is called precervical sinus. Ultimately this
ion is made on the skin including ral part of the neck from a failure of sinus disappears, but if it persists, it forms
the punctum. The cyst is gradually obli­
teration of the second branchial a cystic swelling in the upper part of the

A B C

Figs 27.34A to C: Sebaceous cyst, note the classical black punctum

A B C D
Figs 27.35A to D: Excision of the sebaceous cyst
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 623

neck, which is called brachial cyst. If the symptom. If manifested the swelling not palpable, unless the cyst is not
second arch fails to fuse with the 5th arch may be painful and it becomes difficult to infected. The cyst cannot be redu­
or epipericardial ridge, a fistula develops differentiate from acute lymphadenitis, ced or compressed. On aspiration
and it connects the precervical sinus and chronic lymphadenitis or tuberculosis cholesterol crystals can be demons­
is called the brachial sinus or fistula. lymphadenitis and cold abscess. trated in the aspirated fluid. Cysts
According to Illingworth theory it containing cholesterol crystals are
develops from inclusion of the parotid Physical Examination branchial cyst, dental cyst, denti­
epithelium in the upper deep cervical • Site: Branchial cyst occupies upper gerous cyst, cystic hygroma, old hyd­
lymph node. and lateral part of the neck deep to rocele, thyroglossal cyst.
the upper third of the sternomastoid
Pathology muscle. It protrudes from beneath the Treatment
The cyst is usually lined by stratified anterior border of the sternomastoid. Excision is the treatment of choice,
squa­mous epithelium. If it arises from the The ster­nomastoid muscle develops incision is made parallel to the skin
internal branchial furrow the epithelium from the migrated myotome in the crease, one must be particular not to
may be columnar and ciliated. The strik­ ridge of the second branchial arch leave behind a portion of the cyst wall,
ing feature of this cyst is that its wall which covers the precervical sinus. to ensure this, dissection must be made
contains large amount of lymphoid The branchial cyst develops from the carefully (Figs 27.36B and C). Some
tissue. For this, the cyst is prone to precervical sinus. So it will always be amount of the content may be aspirated
infection and this has laid to Illingworth’s deep to the sternomastoid muscle. before the dissection so that the wall of
theory of inclusion of ectopic epithelium It may be round, but is usually oval cyst may be grasped with forceps without
in upper deep cervical lymph nodes. in shape with its long axis running injuring it. Sometimes, it extends between
The contents are viscid, mucoid, cheesy forwards and downwards. It is of the origins of the internal and external
material and cholesterol crystals in large variable sizes and may attain size of an carotid arteries upto the pharyngeal wall.
numbers. orange, majority are of sizes between Hypoglos­sal and glossopharengeal nerves
5 to 10 cm in diameter (Fig. 27.36A). lie deep into the cyst and they should be
Clinical Features • Surface: It is smooth and edge protected. The cyst usually lies deep to the
is distinct, but yields under the posterior belly of daigas­tric. The spinal
Age incidence palpating fingers. The overlying skin accessory nerve also lies deep to the cyst
though congenital, yet it does not looks normal, though its infected, and should be protected.
manifest itself before puberty. Majority may be red and angry looking. Sclerotherapy with OK-432 (pici­
of the patients are between 20 to • Consistency: It is soft, when the banil) has been reported to be an
25 years or even later. This is because the content is under tension, feel may effective alternative to surgical excision
fluid which it contains takes this time to be firm or even hard, fluctuation test of branchial cleft cysts by some groups.27
accumulate. There is equal distribution will be positive. Transillumination
of sex is noticed. test is usually negative, but may be Thyroglossal Tract Cyst
positive if the content is clear fluid. Thyroglossal tract cyst is a swelling
Symptoms The lump is not freely movable as it is in the remnants of thyroglossal tract
Painless swelling in the upper and particularly deep to sternomastoid. (Fig. 27.37A). The development is from
the lateral part of the neck is the main Regional lymph nodes are usually the ventral portion of the entoderm

a b c
Figs 27.36A to C: Excision of branchical cleft cyst
624 Neoplastic Conditions of Head, Neck and Face

Systemic symptoms are never seen in this


condition.

Examination
Position: A thyroglossal cyst may deve­
lop anywhere along the thyroglossal
tract, starting from the Foramen Caecum
to the isthmus of the thyroid gland, but
according to frequency its position may
be as follows subhyoid position, in the
a b region of thyroid cartilage, suprahyoid
position, at the level of carotid cartilage,
in the floor of the mouth; beneath the
foramen caceum. Thyroglossal cyst is
spherical or oval with the long axis along
the thyroglossal tract. The cyst may
become tender if it is infected. Though it
is a cystic swelling, yet it’s consistency is
often firm or hard depending upon the
tension of fluid within the cyst. Paget’s
test should be done. It may occasionally
c d
be positive, when a cyst is a small
one, but due to the thick content with
Figs 27.37A to D: (A and B) Thyroglossal cyst; (C and D) CT scan showing
epithelial debris it is usually negative
thyroglossal cyst
(Paget’s test—A solid tumor is hardest
in the center, whereas the cyst is least
between the first and second branchial Pathology hard in the center). The cyst can be
arch, a divercation is made which extends The thyroglossal cyst is lined by pseudo­ moved sideways, but not vertically, the
downwards and forms the median stratified ciliated columnar epithelium, cyst moves with deglutition, it moves
thyroid diverticulum. The diverticulum there may be squamous lining and mu­ with protrusion of the tongue. Regional
moves downward and comes infront of cous glands. There may be some lym­ lymph nodes are usually not enlarged
the thyroid cartilage to form the isthmus phoid tissue outside the epithelial lin­ unless they are infected. The cyst can
and the pyramidal lobe of thyroid gland. ing, for which the cyst is prone to get be best visualized on MRI scan as it is a
This tract is known as thyroglossal tract. infected. It may contain thyroid tissue. soft tissue pathology. The MRI also gives
The hyoid bone which is developed information regarding the relation of
from the second and the third branchial Clinical Features the cyst to the adjacent vital structures
arches comes in very close relation with • Age: Thyroglossal cyst may appear at (Figs 27.37C and D).
this tract. The entoderm from where the any age, but majority of the patients It should be excised routinely, as due
tract or the thyroglossal duct has started are between 15 to 30 years of age. to the presence of the lymphatic tissue
ultimately forms the foramen ceacum of • Sex: The cyst is more commonly in the wall infection is inevitable, an
the tongue. seen in women. infected cyst often looks like an abscess
The course of the thyroglossal tract and a incision will lead to the formation
or duct—the thyroglossal duct passes Symptoms of a sinus, excision of the cyst should
down from the foramen caecum of the The commonest symptom is the pain­ also include any persistent portion of
tongue between the genoglossus mus­ less swelling in the neck; it is usually a the track (Fig. 27.37B).
cles, then it passes along the midline midline swelling except when the midline
downwards, it descends either infront of is below the thyroid cartilage (Figs 27.37A
Dermoid Cyst
the hyoid bone or it hooks below and be­ and B). where it may shift to one side,
hind the hyoid bone and then descends more commonly to the left. The lump Epidermoid and dermoid cysts repre­
downwards along the midline to the may be present for many years before the sent less than 0.01 percent of all oral
upper border of the thyroid cartilage. It patient comes to the doctor, it is actually cavity cysts. The cysts can be defined
then moves slightly to the left and ulti­ the swelling which gets the patient to the as epidermoid when the lining presents
mately ends in the pyramidal lobe of the clinician. Pain in the cyst is almost always only epithelium, dermoid cysts when
thyroid gland. assosciated with infection of the cyst. skin adnexa are found and teratoid cysts
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 625

when other tissue such as muscle, carti­ There may be bony indentations, if the contain different amounts of fatty masses;
lage and bone are present. bone lies exactly deep to the cyst which occasionally, they contain horny mas­ses
A dermoid cyst can be described as a may be palpated. Transillumination test and hairs.
sac-like growth that is present at birth. is always negative. Surgical excision is the
A dermoid cyst is a cystic teratoma treatment of choice. Pathophysiology
that contains developmentally mature The pathogenesis of midline cysts of the
skin complete with hair follicles and Implantation Dermoid floor of the mouth is not well established
sweat glands, sometimes luxuriant clu­ Implantation dermoid is a acquired and dysontogenetic, traumatic and thy­
mps of long hair and often pockets of se­ dermoid and arises from the indriven roglossal anomaly theories have been
bum, blood, fat, bone, nails, teeth, eyes, epithelium beneath the skin due to the suggested. Histologically, Meyer divided
cartilage and thyroid tissue. Beca­use it puncture injury, e.g. needle prick or the cysts of the floor of the mouth into
contains mature tissue, a dermoid cyst thorn prick. It is lined by stratified squa­ three groups: Epidermoid, dermoid and
is almost always benign. mous epithelium and contains white teratoid. Although dermoid cysts rep­
There are four types of dermoid cyst: cheesy material formed by desquamat­ resent a separate entity, the term “der­
1. Sequestration dermoid. ed epi­thelial cells and sebum. Hair is moid” is typically used to indicate all
2. Implantation dermoid—acquired usually absent. It usually painful. three categories. In fact, dermoid cysts
variety. occur primarily in the testes and ovaries
3. Tubulodermoid. Tubulodermoid and the most common location in the
4. Teratomatous dermoid. Tubulodermoid is epidermal cyst, but head and neck is the external third of
develop from the unobliterated por­ the eyebrows.
Sequestration Dermoid tion of congenital ectodermal duct or
Sequestration dermoid is congenital va­ tube. It is usually formed by the accu­ Race
riety of dermoid cyst, which is formed by mulation of secretion of the lining No racial predilection is apparent;
inclusion of the epithelium buried in the ectodermal cells of the unobliterated however, most cases of dermoid cysts
line of the embryonic fusion. It contains por­ tion of the embryonic duct, e.g. in the literature are described in white
white pultaceous desquamated material thy­­ro­glossal cyst which develops from persons.
with or without hairs. It is mixture of se­ thyroglossal duct.
bum, sweat and desquamated epithelial Sex
cells. It is commonly seen in midline of Teratomatous Dermoid Cyst Dermoid cysts of the ovary or omentum
the body particularly in the neck, above Teratomatous dermoid is a cystic swell­ are sex restricted, i.e. they occur only in
the angle of the eye at the line of fusion ing which develop from the totipotent the female population. In other dermoid
of frontonasal and maxillary processes, cells with ectodermal predominance. It cysts, no sex predilection has been
postauricular and at the midline of the usually contains mesodermal elements found.
face particularly at the root of the nose. like bone, cartilage, etc. hairs are always
At the line of the embryonic fusion, present in such cyst. Age
a few ectodermal cells are sequestrated Dermoid cysts grow slowly and are Dermoid cysts generally present with
into the deeper layer which proliferate not tender unless ruptured. They usually slow and progressive growth and even if
and form sequestration dermoid cyst. It occur on the face, inside the skull, on the they are congenital, the diagnosis is usu­
lies near the mesoderm from where the lower back, and in the ovaries. It present ally possible in the 2nd or 3rd decade of
bones develop. as a solitary or occasionally multiple, life. Dermoid cysts are described in per­
It may be noticed at birth, but is usu­ hamartomatous tumor. The tumor is sons of all ages.
ally seen sometimes afterwards as it takes covered by a thick dermis like wall that Dermoid cysts on the face, neck or
sometime to form the cyst. It presents as contains multiple sebaceous glands and scalp are subcutaneous cysts that are
painless swelling which is slow growing almost all skin adnexa. Hair and large usually present at birth. Intracranial or
and is present at the areas of the embry­ amounts of fatty masses cover poorly perispinal dermoid cysts are most of­
onic fusion. They remain small in size, i.e. to fully differentiated structures derived ten found in infants, children or young
around 2 cm in diameter and are usually from the ectoderm. adolescents. Intra-abdominal dermoid
ovoid or spherical in shape with smooth Depending on the location of the le­ cysts are described in females aged 15
surface and soft in consistency. It may in­ sion, dermoid cysts may contain subs­ to 40 years. Most dermoid cysts on the
dent with pressure as the content is thick tances such as nails and teeth, cartilage floor of the mouth occur in individuals
pultaceous material. It is non-compress­ and bone like structures. If limited to aged 10 to 30 years. Only a few cases de­
ible, non-reducible and is not attached to the skin or subcutaneous tissue, der­ scribe oral dermoid cysts in newborns or
the skin as well as underlying structures. moid cysts are thin-walled tumors that children.
626 Neoplastic Conditions of Head, Neck and Face

History
Dermoid cysts that are congenital and
localized on the neck, head or trunk are
usually visible at birth. The intracranial,
intraspinal, or intra-abdominal dermoid
cysts may be suspected after specific or
non-specific neurologic or gynecologic
symptoms occur. In these instances,
imaging studies may help in distinguish­
ing dermoid cysts from other tumors
or organ malformations. A congenital a b
intracranial frontotemporal dermoid
cyst may be first evident as a cutaneous
fistula, although intracranial extension
and cutaneous sinus tract formation are
rarely seen with these dermoid cysts.
Unilateral upper eyelid swelling may
be the first sign, with imaging studies
demonstrating a soft tissue orbital der­
moid cyst arising from the lacrimal
gland.

Physical Examination c d
Dermoid cysts can appear as cutaneous Figs 27.38A to D: Dermoid cysts of the head neck area
cysts on the head, as cysts on the floor
of the mouth or elsewhere in the head
(Figs 27.38A to D and 27.39A).15
Cutaneous cysts most commonly
occur on the head, mainly around the
eyes. Occasionally, they occur on the
neck or in a midline region. When on
the head, dermoid cysts are often
adh­er­ent to the periosteum. The usual
dia­meter of the lesions is 1 to 4 cm.
Dermoid cysts on the forehead and
brow are known to cause pressure-
related erosion of the underlying bony
tissue, and surgical intervention may be a b
helpful. Occasionally, skin-related der­ Figs 27.39A and B: (A) Dermoid cyst near the medial canthus of eye; (B) Excision of a
moid cysts are multiple and develop over dermoid cyst
periods as long as 20 years. In many pa­
tients, dermoid cysts occur on the floor
of the mouth or elsewhere in the mouth. magnetic reso­ nance imaging together Epidermoid cysts may be classi­
The differential diagnosis of sub­ with cytologic examination by fine- fied as congenital or acquired, even if
lingual lesions includes: Infectious pro­­ nee­dle aspiration biopsy. there is no difference between the two
cess, ranula, lymphatic malformation, on presentation or histologically. Many
dermoid cyst, epidermoid cyst, het­ero­­­ Causes etiopathogenetical theories have been
topic gastrointestinal cyst and dupli­ Dermoid cysts are true hamartomas. proposed. Congenital cysts are dys­
cation foregut cyst. For this reason, Dermoid cysts occur when skin and skin embryogenetic lesions that arise from
bima­ nual palpation and conventional structures get entrapped during fetal ectodermic elements entrapped dur­
radiography are not always sufficient development. Histogenetically, dermoid ing the midline fusion of the first and
in making differential diagnoses. In cysts are a result of the sequestration of second branchial arches between the
these cases, it is necessary to use ultra­ skin along the lines of embryonic clo­ 3rd and 4th weeks of intrauterine life.
sonography, computed tomography or sure. Alternatively, they may arise from the
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 627

‘tuberculum impar of His’ which, with Treatment visible scarring is an additional advan­
each mandibular arch, forms the floor of The treatment of dermoid cysts of maxil­ tage of endoscopy-assisted sur­gery.13,14
the mouth and the body of the tongue. lofacial region is surgical and can be
Acquired cysts derive from traumatic or by an intraoral or extraoral approach
iatrogenic inclusion of epithelial cells or (Fig. 27.39B), according to the localiza­ Hydatid Cyst
from the occlusion of a sebaceous gland tion and the size of the mass. There are
duct. Moreover, other authors proposed no rules regarding the timing for opera­ Hydatid disease of the head and neck
that midline cysts may represent a vari­ tion; because dermoid cysts are mainly is rare. It accounts for only two out of
ant form of thyroglossal duct cyst. congenital, they can appear in every age every thousand cases of hydatid disease.
Congenital cysts of ectodermal ori­ of life, so the time when they appear Most hydatid cysts are “silent,” but be­
gin are uncommon in the oral cavity (generally with dysphagia, dysphonia come clinically apparent because of
(1.6%), with epidermoid cysts occurring and dyspnea) is generally the right time their mass effects, when they rupture
rarely. to operate on them. Also, in very young or if they become super infected. Hyda­
Radiography, CT scanning and MRI patients, a problem can arise from the tid disease is a worldwide parasitic
are helpful in making the correct differ­ anesthesiologic risk, which is gener­ disease, particularly in areas where
ential diagnosis of dermoid cysts. Ultra­ ally quite low in patients weighing more livestock and subsistence farming
sonography represents the first choice than 20 kg. are practiced. Echinococcus infection
of imaging technique because it is reli­ The extraoral approach is generally may cause serious morbidity and even
able, economical and without X-ray preferred in the case of median geni­ death in the intermediate host. It is an
exposure, thus, it is easily suitable for ohyoid or very large sublingual cysts, endemic disease in many parts of the
young patients also. Computed tomog­ whereas the intraoral approach is typi­ world including the Mediterranean, the
raphy and magnetic resonance imaging cally used for smaller sublingual cysts. Middle East, South America, Australasia
allow more precise localization of the In some patients, surgery should and is highly endemic in sub-Saharan
lesion in relationship to geniohyoid and be performed even more carefully than Africa. Of the three forms of hydatid
mylohyoid muscles and they also enable usual because the fatty content of the cyst disease, Echinococcus granulosis is most
the surgeon to choose the most appro­ may spread to the surrounding tissues common and gives rise to cystic hydatid
priate surgical approach, especially for or anatomic structures, especially if the disease. Echinococcus granulosis is a
very large lesions. cyst is infected with bacteria. The spread small tapeworm, 3 to 5 mm in length,
of these contents can cause foreign body comprising three to four segments. It
Histologic Findings reactions and severe complications. lives in the small intestine of the definitive
Dermoid cysts are a result of the seques­ Recently, minimally invasive surgi­ host, the dog. The oldest segments at the
tration of the skin along the lines of cal techniques have been successful in end of the worms produce eggs, which
embryonic closure. In contrast to epider­ removing dermoid cysts from difficult are excreted in feces. Intermediate hosts
mal cysts, dermoid cysts in the skin are locations, such as those on the tongue or ingest contaminated feces. Humans are
lined by an epidermis that possesses the floor of the mouth. Intralingual der­ accidental intermediate hosts. The eggs
various epidermal appendages. As a rule, moid cysts lead to lingual motility de­ hatch in the intestine of the intermediate
these appendages are fully mature. Hair fects and speech problems. These cysts hosts, cattle, sheep and pigs. Humans
follicles containing hairs that project into should be surgically removed to restore are also a susceptible intermediate
the lumen of the cyst are often present. The normal lingual function and to correct hosts and as dogs are common house
dermis of dermoid cysts usually contains speech problems. hold pets, may accidently ingest the ova
sebaceous glands; eccrine glands and, Intracranial, intramedullary and and the embryo migrates through the
in many patients, apocrine glands. Occ­ ovarian dermoid cysts are difficult to intestinal wall into the portal system.
a­sionally, the lining epithelium may treat and sophisticated neurosurgical Most embryos (65%) lodge in the liver.
proli­ferate as papillary boundaries or gynecologic surgical techniques are Some (25%) escape this first filter and
extend externally or inward toward the often needed to remove the lesion and lodge in the lung. A small percentage
lumen of the cyst. This proliferation may prevent possible complications. escape to the systemic circulation where
have some superficial resemblance to In some patients with dermoid cysts they may lodge in any organ, most co­
epidermal carcinomatous proliferation on the forehead and brow, successful mmonly the spleen, kidneys, heart,
and the growth may be misclassified as excision with endoscopy-assisted sur­ bone, muscle or central nervous system.
a cancer. A congenital dermoid together gery has been described.
with a bronchogenic cyst of the tongue is In the reported cases, no compli­ Clinical Features
extremely rare, but has been described in cations (e.g. paresthesia or numbness Hydatid cyst is more common in liver,
a few patients. on the scalp) occurred. The absence of but also reported in lung, bones and
628 Neoplastic Conditions of Head, Neck and Face

brain. Liver involvement causes hepa­ inner nucleated germinal layer. The Treatment
tomegaly and jaundice. Pulmonary cyst fluid is relatively clear, albumin Treatment is primarily surgical (exci­
involvement may cause shortness of free and contains the so called “hydatid sion). Excision of the hydatid cyst using
breath and hemoptysis. Hydatid cysts sand” consisting of brood capsules the natural cleavage plane which exists
have been reported in a variety of sites in and scolices. These brood capsules or between germinative layer and the surr­
the head and neck region including sali­ daughter cysts develop originally as ounding tissue. Care should be taken to
vary glands (most commonly subman­ minute projections of the germinative avoid accidental rupture and spillage
dibular gland and parotid), orbit, thyroid layer which develop central vesicles and of the contents of the cystic cavity. Fatal
gland, superficial temporal muscles, become minute cysts. Scolices of the anaphylaxis on spilling the contents of
paraspinal muscles, cervical soft tis­ head of the worm develop in the inner the cyst has been reported. The surgical
sues, sternocleidomastoid muscle, ret­ aspects of the brood capsules. It is when strategy varies widely between radical
ropharyngeal tissues, tongue, mastoid, they separate from the germinative layer clearance followed by lavage and simple
infratemporal fossa, pterygopalatine that they form of the “Hydatid sand”. instillation of scolicide. Chlorhexidine,
fossa, and posterior cranial fossa. They The hydatid cyst of the maxillofacial 80 percent alcohol and 0.5 percent
do not appear to have a predilection for area are the rare entity occasional cases cetrimide solution may be instilled into
any particular site. Only 2 percent of the have been reported in the literature. the cystic cavity which destroys 80 to
hydatid cysts are located in the skeleton 90 percent of scolices. Supplementary
and of these only 3 to 4 percent are in Diagnosis chemotherapy, such as mebendazole or
the skull. Oral hydatid cysts presents as Radiographically calcification of cysts albendazole, can also be used.
painless, progressively increasing, soft wall may be visualised in 50 percent of If the cyst gets infected secondarily,
elastic and well-circumscribed fluctu­ cases. USG may reveal daughter cysts all the parasites die and the treatment
ant swelling. They may pose speech and and hydatid sand. CT scan furnishes use­ becomes much easier and needs to be
mastication problems. ful information, investigations include treated like an abscess by incision and
blood examination, which will reveal eo­ drainage. The whitish lining sloughs
Histological Features sinophilia in 20 to 25 percent cases. out and should be curetted (Figs 27.40A
The hydatid cysts are initially of Of the serological tests, the indirect and B).
microscopic dimensions, but enlarge hemagglutination test, Casoni’s test and
progressively. The natural cyst consists complement fixation would be positive.
of three layers; an outer layer of host Casoni’s test includes intradermal injec­ References
origin and two inner layers of parasitic tion of 0.2 mL of fresh sterile aspirated
origin. The host layer consists of fibrous cystic fluid which produces a wheel of 1. Robinson HBG. Classification of Cysts
tissue in which there is an infiltrate of 5 cm in diameter within 30 minutes. of the Jaws. Am J Orthodontics and Oral
chronic inflammatory cells, eosinophils Problems with Casoni’s test are that Surg. (Oral Surg Sect). 1945;31:370.
and giant cells. The intermediate layer it may cause false positive result and 2. Gorlin RJ, Pindborg JJ, Redman RS,
is white, non-nucleated and consists produce anaphylaxis. This stands to et al. The calcifying odontogenic cyst:
of numerous delicate laminations. It reason as to aspiration is usually avoided A new entity and possible analogue of
usually shrinks away from the outer in these cases as it may result in spillage the cutaneous calcifying epithelioma of
fibrous layer when the tension within of the cystic content and result in fatal Malherbe. Cancer. 1964;17:723-9.
the cyst is relieved. Finally, there is the anaphylaxis. 3. Karmer IRH, Pindborg JJ, Shear M.
Histological typing of odontogenic
tumours: WHO International Histo­
logical Classification of Tumours (ed 2).
Springer. 1992.
4. The new WHO classification of tumors of
the head and neck. What has chan­ged? J
Oral Pathol Med. 2005;34(9): 558-64.
5. Harris M, Toller P. The pathogenesis
of dental cysts. Br Med Bull. 1975;31:
159-63.
6. Gold L, Upton G, Marx R. Standardized
surgical terminology for the excision
of lesions in bone: An argument for
a b accuracy in reporting. J Oral Maxillofac
Figs 27.40A and B: Whitish lining of the hydatid cyst Surg. 1991;49(11):1214-7.
Odontogenic and Nonodontogenic Cysts of the Maxillofacial Region 629

7. Morgan TA, Burton CC, Qian F. A 14. Kostecka F. Ein Cholesteatom im Unter­ 22. Barnes L, Eveson JW, Reichart P, et al.
retrospective review of treatment of kiefer Ztschr f Stomatol. 1929;27:1102. World Health Organization Classifica­
the odontogenic keratocyst. J Oral 15. Philipsen HP. Om keratocyster (koles­ tion of Tumors. WHO Histological clas­
Maxillofac Surg. 2005;63(5):635-9. teatomer) I kaeberne. Tandlaegebladet. sification of odontogenic tumors. Lyon:
8. Bell R, Dierks E. Treatment options for 1956; 60.pp.693-7. IARC Press; 2005.pp.306-7.
the recurrent odontogenic keratocyst. 16. Stoelinga PJW. Long-term follow-up 23. Gorlin RJ, Pindborg JJ, Clausen FP,
Oral and Maxillofacial Surgery Clinics on keratocysts treated according to a et al. The calcifying odontogenic cyst—
of North America. 2003;15(3):429-46. defined protocol. Int J Oral Maxillofac a possible analogue of the cutaneous
9. Waldron CW. Tumors of the Upper Surg. 2001;30:p.14. calcifying epithelioma of Malherbe.
Jaw. Surg Gynec and Obst. 1971;72:503. 17. Scharfetter, Balz-Hermann C, Lagrange 1963; pp.249-51.
10. Dr Makoto Toida. A simple cryosurgical W, et al. Proliferation kinetics—study 24 Moscow BS, Siegel K, Zegarelli EV, et al.
method for treatment of oral mucous of the growth of keratocysts. J Cran- Gingival and lateral periodontal cysts.
cysts. Int J Oral Maxillofac Surg. 1993;22 Max-Fac Surg. 1989;17:226-33. Periodontol. 1970;41:249-60.
(6):353-5. 18. Toller PA. Protein substances in odon­ 25. Burke GW, Feagans Jr. WM, Elzay RP,
11. Shibata Y, Asaumi J, Yanagi Y, et al. togenic cyst fluids. Br Dent J. 1970; et al. Some aspects of the origin and fate
Radiographic examination of denti­ 128(7):317-22. of midpalatal cysts in human fetuses.
gerous cysts in the transitional denti­ 19. Main, DMG. The enlargement of epi­ J Dent Res. 1966;45:159-64.
tion Dentomaxillofaial Radio­logy. 2004; thelial jaw cysts. Odontologisk Revy. 26. Lichtenstein L. Aneurysmal Bone Cyst.
33:17. 1970; 21:29-49. J. Bone and Joint Surg. 1956;38-B:310-1.
12. Anthony Pogrel M. Treatment of Kera­ 20. Browne RM. The odontogenic keratocyst: 27. Kim MG, Kim SG, Lee JH, et al. The
tocysts: The Case for Decompression Clinical aspects. Br Dent J. 1970;128:225. therapeutic effect of OK-432 (picibanil)
and Marsupialization. J Oral Maxillo 21. Kramer IR, Toller PA. The use of exfoli­ sclerotherapy for benign neck cysts.
Surg. 2005;63(11):1667-73. ative cytology and protein estimations Laryngoscope. 2008;118(12): 2177-81.
13. Mikulicz J, Beitrag zur Genese der in preoperative diagnosis of odon­
Dermoide am Kopfe, Wien Med Woch­ togenic keratocysts. Int J Oral Surg.
enschr. 1876;26:pp. 953-6. 1973;2(4):143-51.
28 Odontogenic Tumors
Borle Rajiv M, Singh Divya

sequential changes in odonto­ genesis


Introduction According to WHO
with tumor formation.
Odontogenic tumors comprise a group “Odontogenic tumors and tumor-like It was in 1971, when a five-year
of lesions of the jaw derived from lesions constitute a group of hetero­collaborated effort organized by World
the primordial tooth forming tissues Health Organization resulted in the first
geneous diseases that range from hamar­
(odontogenic epithelium) and presenting consensus on taxonomy of odontogenic
tomatous or non-neoplastic tissue proli­
a large number of histologic patterns. tumors. The appearance of this first
ferations to benign malignant tumors with
Some of these lesions, particularly authoritative guide to the classification
metastatic potential. They are derived
the odontomas are now interpreted of odontogenic tumor marked the start
from epithelial, ecto­mesenchymal and/
as developmental malformations or or mesenchymal elements of the tooth of an era of quite intensive interest for
hamartomatous lesions rather than forming apparatus. Odontogenic tumorsstudying this particular field of tumors.
true neoplasms. Other lesions such as In 1971, WHO gave histological typing of
are rare, some even extremely rare, but
ameloblastoma are accepted as true can pose a significant diagnostic andodontogenic tumors,8 jaw cysts and allied
neoplasms and must be diagnosed and therapeutic challenge.” lesions which was based on the concept
treated as such. Odontogenic tumors suggested by Pindbord and Clausen that
Broca,3 a French physician, first
share two major characteristics, namely described an odontogenic neoplasm the characteristic interaction between
they arise from the tissues with the in 1868 and since then various aut- epithelium and mesenchymal tissue
potential for differentiation into tooth or elements occurring during normal
hors have proposed classifications for
periodontal structures and are therefore such neoplasms based on different tooth development to a certain extent
found exclusively in the mandible criterias. also operates in pathogenesis and histo­
and maxilla and, on rare occasions, differentiation of odontogenic tumors.
Malassez4 (1885) and Sutton5 (1888)
the gingiva. Another variable, but dis­ included numerous odontogenic neo­ A wealth of new information which
tinctive feature includes formation of plasms within their all encompassing provided new variants and entities, led
tooth related extracellular substances term odontome. In 1946, Thoma and to the proposal of second edition of
some of which may calcify and be visible Goldman6 introduced a classification histological typing of odontogenic tum­
on radiographs; they are products of ors by WHO in 1992,9 which pro­vided an
based on the germ cell layer of origin and
epithelial-mesen­chymal interaction. they classified tumor in three categories,
updated classification. The WHO classi­
The most common sites for these i.e. epithelial, mesenchymal and mixed.
fication was further updated in 2004 and
tumors are mandibular molar region Spouge7 (1968) tried to correlate tumor
the latest edition being in 2005.10
and the maxillary cuspid region. They histogenesis with odontogenesis and
are usually slow growing and asymp­ suggested that odontogenic tumors who Classification of
tomatic. Certain odontogenic tumors arise from various components of the
have a predilection for particular age, odontogenic apparatus at one phase
Odontogenic Tumors10
gender, geographic location and race. or stage of odontogenesis. Since then, Tumors (neoplasms) and tumor-like
(Sawyer et al.1 1985; Assael.2 1992). many authors have tried to correlate lesions in the jaws.
Odontogenic Tumors 631

(Including non-neoplastic, non- Other Jaw Tumors (Neoplasias) as a benign, but locally invasive epithelial
infla­mmatory jaw lesions) • Benign odontogenic neoplasm, which has a
Odontogenic tumors (modified 2005 – Ossifying fibroma (cemento- strong tendency to recur. According
WHO classification). ossifying fibroma) to Robinson,11 “it is usually unicentric,
– Osteoma non-functional, intermittent in growth,
Benign – Osteoblastoma/osteoid osteoma anatomically benign and clinically
• Odontogenic epithelium with ma­ – Chondroma persistent” type of tumor. Churchill12
ture, fibrous stroma without odon­­ – Chondromyxoid fibroma suggested the term ameloblastoma in
togenic ectomesenchyme – Desmoplastic fibroma (intraos­ 1934 to replace the term adamantinoma
– Ameloblastoma (solid/multicy­ seous non-odontogenic fibroma) coined by Malassez4 in 1885, since the
stic, extraosseous/peripheral, – Melanotic neuroectodermal tu­ latter term implies the formation of
desmoplastic, unicystic) m­or of infancy hard tissue and such material is not
– Squamous odontogenic tumor – Others (neurofibroma, neuril­ necessarily present in this lesion.
– Calcifying epithelial odontogenic emmoma, hemangioma (angio),
tumor (Pindborg’s tumor) leiomyoma, etc.) Pathogenesis
– Adenomatoid odontogenic tumor • Malignant The resemblance between the odonto­
– Keratocystic odontogenic tumor*. – Osteosarcoma genic apparatus and the ameloblastoma
• Odontogenic epithelium with odon­ – Chondrosarcoma is well documented. The ameloblastoma
to­ genic ectomesenchyme with or – Metastatic tumors to the jaws has a varied origin; however the stimulus
without hard tissue formation – Others (Ewing’s sarcoma, mye­loid for ameloblastic transformation in the
– Ameloblastic fibroma and lymphoid neopl­asias, etc.) odontogenic epithelium is not under­
– Ameloblastic fibrodentinoma stood. Thus, the tumor is thought to
– Ameloblastic fibro-odontoma Non-neoplastic Jaw Lesions develop from:
– Odontoma • Fibro-osseous dysplasias • Residual epithelium of the tooth for­
a. Complex type – Fibrous dysplasia ming apparatus such as the cell rests
b. Compound type – Focal osseous dysplasia (focal of enamel, remnants of the Hertwig’s
– Odontoameloblastoma ceme­nto-osseous dysplasia) root sheath and the remnants of
– Calcifying cystic odontogenic – Florid osseous dysplasia (inclu­ dental lamina.
tumor ding familial gigantiform cemen­ • Epithelium of odontogenic cysts,
– Dentinogenic ghost cell tumor toma) particularly the dentigerous cyst and
• Mesenchyme and/or odontogenic – Periapical cemental dysplasia the odontomas. In different studies,
ecto­ me­ senchyme with or without (periapical fibrous dysplasia) it has been reported that the inci­
odonto­genic epithelium • Others dence of ameloblastoma developing
– Odontogenic fibroma – Cherubism from a follicular (denti­gerous) cyst
– Odontogenic myxoma (myxofi­ – Central giant cell lesion (granulo­ associated with the impacted tooth
bro­ma) ma) (incl. hyperparathyroidism) is approximately 17 percent.
– Cementoblastoma – Aneurismal bone cyst • Basal cells of the surface epithelium.
– Simple bone cyst (traumatic bone • Disturbances of the enamel organ.
Malignant (Examples) cyst, hemorrhagic bone cyst, soli­ • Heterotropic epithelium from extra­
• Odontogenic carcinomas tary bone cyst) oral sites such as the pituitary gland.
– Malignant ameloblastoma – Tori and exostoses
– Ameloblastic carcinoma – Langerhans cell histiocytosis. Incidence
– Primary intraosseous carcinoma It accounts for 1 percent of all oral
– Clear cell odontogenic carcin­oma tumors and for 9 to 11 percent of all
Ameloblastoma
– Ghost cell odontogenic carcin­ odontogenic tumors. It occurs over a
oma broad range of age; cases have been
• Odontogenic sarcomas Introduction reported in children younger than 10
– Ameloblastic fibrosarcoma The ameloblastoma is the most common years to adults and older persons than
– Ameloblastic fibrodentino­sar­ neoplasm arising from odontogenic 90 years of age.13 The occurrence in
coma epithelium. According to WHO, “it is the mandible is 4 times higher than in
– Ameloblastic fibro-odontosar­ a true neoplasm of enamel organ type maxilla. Within the mandible, the molar
coma tissue, which does not undergo differenti­ angle ramus14 area is involved 3 times
*This is the odontogenic keratocyst. You will ation to the point of enamel formation”. more commonly than are the premolar
find it in the classification of odontogenic cysts. In 1992, WHO classified ameloblastoma and anterior regions combined.
632 Neoplastic Conditions of Head, Neck and Face

In the literature, the average age


of occ­urrence is in the third or fourth
decade (Joseph and Savage,15 1992),
both men and women being afflicted
equally (Robinson,11 1937; Burkhard,
1991: Ric­ hert and Philipson 1999).
However, some Nigerian and one Indian
study showed a male preponderance
with a male:female ratio of 1.7:1.
Small and Waldron16 (1955) showed
that 47 percent of maxillary ameloblasto­
mas occur in the molar region, 33 percent A B
in the antrum and floor of the nose, 9 per­
cent both in premolar region and in the
canine region and 2 percent in the palate.
Ameloblastomas also have been reported
to arise primarily in the sinonasal region
without overt evidence of origin from
the tooth bearing alveolar bone.17 When
comparing large studies, it appears that
maxillary tumors tend to occur in slightly
older patients than do mandibular le­
sions. Asians seem to have fewer tumors
involving the ramus than do whites or
blacks, whereas blacks have an increased C D
frequency of tumors in the anterior man­
dible compared with other 2 groups.18
The ameloblastoma is notorious
for its slow growth, the histological
benign appearance, local invasiveness
and a high incidence (50–72%) of local
recurrence (Infante-Cossio et al.19 1998).
Malignant features and metastasis
are rare, exhibiting various kinds of
histology and clinical behavior.
• Slowly growing painless swelling
(Figs 28.1A to G).
• All the cortices expand, viz. E F
buccal, lingual, inferior cortex
(Fig. 28.2A).
• Thinning of the bone with egg shell
crackling (Fig. 28.2C). If the tumor
perforates the cortex the cystic
variants show fluctuations while the
solid variant is firm in consistency
(Fig. 28.2B).
• Displacement and resorption of the
roots of the teeth involved in the
region of the tumor.
• Aspiration yields straw colored fluid G
in cases of cystic variants and is
negative in solid tumors. Figs 28.1A to G: Different clinical presentations of the ameloblastoma
Odontogenic Tumors 633

A B C
Figs 28.2A to C: (A) Ameloblastoma showing severe thinning of the cortex; (B and C) Cortical expansion due to ameloblastoma and
paper thin cortices

Radiological Features ired to make an accurate diagnosis as bone (which nicks the microtome blade
Radiologically, ameloblastoma exhi­ sometimes the clinical picture may and disrupts the tissue section).
bits a multiloculated radiolucent lesion mimic the odontogenic keratocyst, giant The biopsy is an important pro­
with expansion of the bone. The loculi cell granuloma, dentigerous cyst and cedure and must be planned and con­
are of variable size (Soap bubble appea­ other slow growing, multiloculated, ducted carefully. Because of its key role
rance).20 In case of unicystic lesions, a expansile lesions. The treatment for in the diagnotic process and later in the
large uniloculated radiolucent lesion ameloblastoma is more radical as com­ surgical procedure, some aspects of the
is seen with bony expansion and well pared to the lesions mentioned in the biopsy are discussed here:
corticated borders (Figs 28.3A to I). differential diagnosis and the radical • The lesion is approached, with
If the ameloblastoma has deve­ loped treatment needs to be justified. radio­graphic guidance, by incision
secondary to a dentigerous cyst, a dis­ The definitive diagnosis is establi­ through intact crestal mucosa over
placed tooth is often seen asso­ ciated shed only after incision, excision or bone, in order to preserve ‘non­
with the lesion. A mixed lucent-opaque intraoperative frozen section biopsy and contaminated’ mucosal soft tissue
radiographic appearance in a lesion histopathologic analysis. The specific that may be used for wound closure
histopathologically diagnosed as ame­ biopsy technique is selected after careful after a postbiopsy surgical procedure.
loblastoma signals the presence of assessment of the patient (age, physical • The lesion is aspirated through the
desmoplastic type of ameloblastoma. health, emotional status) and of the use intact bone to rule out a vascular les­
This variant was first described in 1984 of local sedation or general anesthesia ion masquerading as an odontogenic
by Eversole et al.21 The unicystic amelo­ to ensure patient cooperation, gain tumor (other poten­tial radiographic
blastoma mimics the cystic lesion. access to the lesion, and obtain suffi­ imitators of odontogenic tumor inclu­
According to WHO, ameloblastoma cient tissue for study. Intraoperative des aneury­smal bone cyst, giant cell
can be divided clinically as: frozen section should be used to study lesion and fibro-osseous disease).
• Solid or multicystic questionable soft tissue encountered in • Aspiration of the cystic fluid neither
• Unicystic areas not sampled by incisional biopsy confirms nor disproves the presence
• Peripheral (extraosseous) and to examine the adequacy of the of a cystic odontogenic tumor; the
• Desmoplastic. boundary between lesion and host bone fluid may or may not be retained for
The distinction between these vari­ and/or soft tissue in instances in which a cell block preparation.
ants of ameloblastoma is important extensive resection is not planned. The • Entrance through the bone to the
clinically. frozen sections are useful in ascertaining lesion should be selected and ob­
adequate peripheral clearance especially tained without injury to nerve or
Diagnosis when the tumor has perforated the teeth, if possible.
The diagnosis is based on the clinical cortical bone and spilled in the adjacent • If the radiographs indicate variations
and radiological presentation. However, soft tissues. The preparation of a good in the lesion (solid, cystic or calcified
the diagnosis is confirmed on histo­ frozen section is technique sensitive and areas), a sufficient number of tissue
pathological examination of the biopsied requires proper specimen orientation samples should be removed for
specimen. An incisional biopsy is requ­ and avoidance of incorporated dense thorough histologic study, including
634 Neoplastic Conditions of Head, Neck and Face

A B C

D E F

G H I
Figs 28.3A to I: Radiological pictures of ameloblastoma: (A) CT scan showing multiloculated lesion; (B and C) Radiograph showing the
multiloculated lesion; (D) CT scan showing the multiloculated ameloblastoma in the ramus; (E) Expansion of the bone with bony septae
in the lesion; (F) Multiloculated radiolucency; (G and H) Soap bubble appearance; (I) CT scan of ameloblastoma involving entire mandible

tissue bordering the lesion-host Ameloblastoma: a benign of establishing pulmonary metastases, a


bone interface. The specimens are possible, though infrequent, occurrence.
incised for removal and not crushed
or malignant tumor? These characteristics of the amelo­
with forceps or hemostats. Ameloblastoma is justly considered blastoma simulate the basal-cell carci­
• Before suture closure of the biopsy the most unexplainable of odontogenic noma, a known malignant neoplasm.
incision, if desired, a non-resorbable tumors, because of its clinical and histo­ The similarities between the ameloblas­
tissue barrier can be placed over logical features, intriguingly contradic­ toma and the basal cell carcinoma are
the bone entrance to the lesion, to tory, paradoxical and incongruent, if its that both are locally invasive, seldom
prevent fluid or lesional cell escape benign histological aspect and its inva­ metastasize, radioresistant and exhibit
into non-involved periosteum or sive and destructive clinical behavior are similar histopathological characteris­
mucosa. considered, besides the reported capacity tics in some cases. Amelo­blastoma is
Odontogenic Tumors 635

known to be benign by its histological The reason for the neoplastic change mended for the central tumors. The tu­
aspect, nevertheless, presents a highly in the epithelium from which the amelo­ mor is known to recur after incomplete
aggressive behavior and, despite its blastoma develops is not known. It has excision. Fonseca24 has emphasized the
slow growth, it is extremely invasive, been suggested that, trauma, infection role of radical treatment for the am­
as are malignant tumors and produces or the tissue changes associated with the eloblastoma and went on to state that
occasional meta­stases. The final result, tooth eruption may be involved. How­ “anything short of radical resection for
in both cases, is exactly the same. ever, these factors are so often present, the management of ameloblastoma
Basal cell carcinoma is a neoplasm, whether or not a turn over develops, it amounts to the planned recurrence”.
which develops exclusively in the skin, is difficult to show that there is anythingHowever, in spite of the fact that amelo­
from the epidermal basal layer or root more than the random association. The blastoma needs to be treated radically,
sheaths of hair follicles, never occurring similar tumors arising in the parapitu­ in the clinical practice occasionally con­
in the mucosa (Shafer et al. 1983). itary epithelium (Craniopharyngioma of servative treatment is opted in the inter­
As the basal layer of the epidermis is Rathke’s pouch) residues are not associ­ est of the patient with a calculated risk
composed of cells potentially capable ated with these factors. of recurrence (e.g. very young patients,
of differentiating into tiny of the skin unicystic nature and medically compro­
appendages, aborted attempts to pro­ Tumor Spread mised patients). The various surgical
duce these types of structures are at Ameloblastoma spreads slowly by infil­ modalities for the management of the
times seen in basal cell carcinomas. tration through the medullary spaces ameloblastoma are:
Ameloblastoma is equally a tumor and may erode the cortical bone.
derived indirectly from the epithelial Eventually, it will resorb the cortical Enucleation and Curettage
basal layer, however from the covering plate and may extend into the adjacent It is usually an inadequate treatment
of the gingival mucosa, perhaps from soft tissues. Tumors of the posterior and has high incidence of recurrence,
embryonic remnants of that which maxilla tend to obliterate the maxillary primarily due to the infilterative nature
could be considered grossly as gingivo­ sinus, extend to ethmoidal air cells, of the tumor. The tumor invades the
maxillary appendages; the teeth. infratemporal fossa and subsequently adjoining cancellous bone and thus
The histology of a typical basal cell extend intracranially. enucleation and curettage is inadequate.
carcinoma is very similar to that of pri­ In exceptional cases where the lesion is
mordial or basaloid type of ameloblas­ Histopathological Types very large and encroaching upon the
toma. The follicular aspect obs­erved in The ameloblastoma has 6 histopath­olo­ vital structures, medically compromised
many of the cellular islets of the tumor gical subtypes namely:13,18,23 patients, extreme ages, i.e. very old or
represents only an aborted attempt of 1. Follicular very young patient who are not willing
the neoplastic tissue to form teeth, in 2. Acanthomatous to undergo segmental resection of the
the same manner in which the basal- 3. Granular cell bone, the enucleation may be done along
cell carcinoma also attempts to form 4. Plexiform with the cauterization of the base with
hair follicles. Both the tumors are locally 5. Basal cell Cornoy’s solution. Such patients requ­
invasive and capable of inflicting dam­ 6. Desmoplastic. ire long-term, periodic postoperative
age to the local hard and soft tissues, do Reichart et al. have shown that follow-up to detect any recurrence.
not metastasize and are radioresistant. these histological subtypes have differ­ While opting for such treatment, the
This analogy of clinical behavior as ent clinical behavior and have bearing clinician must remember that this is
well as the histological picture between on the treatment and prognosis. The not what is ideally required and the
the two tumors was what led Willis22 follicular ameloblastoma shows high­ tumor could recur and it has been done
(1948) to categorically affirm that “at­ est recurrence rate (29.5%) while the due to compelling circumstances and
tempts to distinguish benign and ma­ acanthomatus has 4.5 percent re­ cur­ not by choice. The patient needs to be
lignant adamantinomas are futile; they rence rate. The plexiform variety shows counseled for regular follow-up.
are all malignant in that they are locally 16.7 percent recurrence rate and the The unicystic ameloblastomas, which
invasive and prone to recur”. desmoplastic ameloblastoma has recur­ mimic the cyst in its clinical presentation
In a small number of cases, a tumor rence rate in the range of the other his­ are intentionally or unin­tentionally trea­
of ameloblastoma type forms outside tological subtypes of amelo­blastoma.13 ted with enucleation (see Figs 28.12D and
the bone presumably from some of E). When the lesion is diagnosed as a cyst
the numerous epithelial residues lying Management and no preoperative biopsy is done, the
between the periosteum and the oral The basic modality of the management natural treatment choice becomes enu­
epithelium. Such tumors may show no of the ameloblastoma is surgery. Wide cleation. Even if the preoperative biopsy
fusion with the epithelium of the oral local excisions with at least 1 to 1.5 cm is done and if the representing area is not
mucosa. margins of normal bone are recom­ included in biopsy, the lesion is diagnosed
636 Neoplastic Conditions of Head, Neck and Face

as a cyst and treated conservatively by Resection of the Mandible • Hemimandibulectomy: A classical


enucleation. It must be remembered • Resection with continuity: Mar­ hemimandibulectomy comprises
that in cases of mural ameloblastoma ginal mandibulectomy or wedge of resection of half of the mandible
the ameloblastic changes may not be mandibulectomy is the method of along with the disarticulation of the
present throughout its lining and thus, maintaining the continuity of the condyle. When an ameloblastoma
the preoperative diagnosis of amelo­ bone at the same time excising the involves the ramus extensively and
blastoma is not always possible unless lesion. The ameloblastoma tends to surgical clearance is doubtful then
the biopsy includes the representative infilterate the cancellous bone and the classical hemimandibulectomy
area. Moreover in younger patients where the thick cortical plates are eroded with disarticlation of the conyle is
the segmental resection is more morbid, but not invaded. The mandibular undertaken (Figs 28.5A to D). Pre­
most of the surgeons prefer to treat the anterior has plenty of cortical bone serving the condyle by resecting the
unicystic ameloblastomas conservatively and the ameloblastomas, which are tumor at subsigmoid level helps in
and keep the patients under long-term relatively small and have not eroded better reconstruction as the implant
follow-up to rule out recurrence. The the cortical bone significantly can can be secured to the resected proxi­
enucleation and cauterization of the base be treated with marginal mandibu­ mal fragment. However, it should
is often an adequate treatment for the lectomy. The large lesions which not be the only consideration while
unicystic ameloblastomas. have severely undermined the cor­ treating the patient and attempt
tex and are likely to sustain a patho­ must be made to get an adequate
Irradiation logical fracture require segmental clearance as the recurrence at this
There is a lack of well-documented evi­ resection. site is often very difficult to treat.
dence in the literature concerning the • Resection without continuity: Seg­ • Although the treatment is often dis­
relative radioresponsiveness or radio­ mental resection—when the tumor cussed in terms of the bony clearance,
resistance of ameloblastomas, although has grown sizably and the inferior it is equally important to address the
they are generally considered radiore­ border of the mandible is severely soft tissue clearance. When the tumor
sistant. It has been recommended as undermined the segmental resec­ is central in location and the bony
one of the modalities of the treatment of tion is recommended (Figs 28.4A cortex is not perforated, one can easily
ameloblastoma in the older literature.25 and B). The attempts to preserve the dissect in the subperiosteal plane
Although radiotherapy can reduce the inferior border may compromise the around the involved bone and remove
size of an ameloblastoma, primarily that surgical clearance and the chances the tumor adequately. But, When the
part of the tumor which has expanded of recurrence are very high. The tumor perforates through the cortex
the jaw or broken into the soft tissues, thinned out inferior border does not and extends in the soft tissue the plain
it does not appear to be an appropriate serve any purpose as the chances of dissection needs to be changed
treatment for an operable ameloblas­ of pathological fracture can occur. and safe resection margins must be
toma. Its main use is in inoperable cases, Moreover, it is better to treat the pri­ established by excising the adjoining
primarily in the posterior maxilla. In the mary tumor radically than treating soft tissue. The frozen section biopsies
recent times, this treatment modality for a nasty recurrence, especially in the may be very useful in such cases to
ameloblastoma has become obsolete. ramal area. ascertain adequate surgical clearance.

Maxillary Tumors
• Subtotal/partial maxillectomy
• Total maxillectomy
• Extended maxillectomy.
The treatment in the maxillary tumors
is more radical as the tumor invades the
bone more commonly due to its spongy
nature and the recur­rence is more likely
if the excision is inadequate. The pro­
ximity with air sinuses and subsequently
A B through them to the cranial cavity makes
Figs 28.4A and B: Specimen of resected plexiform ameloblastoma the surgical defect the resection of the tumor more difficult
reconstructed with reconstructed plate and iliac crest corticocancellous graft if these structures are involved. Similarly,
Odontogenic Tumors 637

the perforation of the thin posterior wall


of the maxilla facilitates the spread of the
tumor in the infratemporal fossa where
the proximity with the vital structures
makes the tumor resection difficult. The
recurrence in the maxilla could be very
difficult to treat due to the proximity to
the vital structures, especially to the skull
base.

Specimen Radiography
A B
It is generally accepted that the central
ameloblastomas should be excised along
with 1 to 1.5 cm margins of healthy bone
to achieve adequate surgical clearance,
as the tumor invades in the cancellous
bone. Studies have shown that the tumor
extends microscopically 5 to 6 mm
beyond the radiological and 3 to 4 mm
beyond the CT margins of the tumor.
Thus, minimum 1 cm clearance in the
normal bone is recommended. When
the radiographs are taken in a patient C D
there is certain amount of distortion and
Figs 28.5A to D: Solid variant of ameloblastoma in ramus perforating the cortex and
the tumor margins may not be accurate.
fungating through the mucosa. Treated with hemimandibulectomy and reconstruction
Thus, after excision the specimen is with titanium plate
radiographed to confirm minimum 1 cm
margin beyond the radiological extent
of the tumor (Figs 28.6A and B). If the
margins are found to be inadequate then
still the surgeon has the chance to resect
additi­onal small segment of the bone.
Reconstruction of the surgical defect
is mandatory to prevent postoperative
morbidity. As the majority of the
patients are young, the reconstruction
should fulfill following goals:
• Restoration of movements and
equilibrium of mandible
• Maintenance of normal occlusal
plane, floor of the mouth and ton­
gue’s anatomical position A B
• Restoration of near normal feed­ing Figs 28.6A and B: Specimen radiographs showing adequate surgical margins of 1 cm
• Acceptable esthetics and func­tion
• More favorable social accep­tance
The reconstruction should ideally be The various modalities for recons­ secured to the distal and proximal
done primarily to prevent deformity and tructing the surgical defect in the man­ bony fragments with the help of the
collapse of the resected segments due dible are: screws (Figs 28.7 and 28.8). A variety
to fibrosis. However, in certain cases • Reconstruction plates: The metallic of reconstruction plates are available
where the primary reconstruction is reconstruction plates made up of tita­ which are suitable in different situa­
not advisable due to uncertainty of the nium or stainless steel are commonly tions. The reconstruction plates with
resection margins and higher chances used. The plates effectively bridge condyle are also available for recon­
of recurrence, the reconstruction can be the bony defect. The plates are con­ structing the defect following hemi­
done as a secondary procedure. toured to match the facial profile and mandibulectomy with disarticulation
638 Neoplastic Conditions of Head, Neck and Face

A B

C D E
Figs 28.7A to E: Ameloblastoma of mandible treated with segmental resection and reconstruction with reconstruction plate:
(A) Preoperative picture; (B) Preoperative OPG; (C) Fixation of recostruction plate; (D) Postoperative OPG; (E) Postoperative result

re­construct the mandible. The bone


grafts can get rejected due to the
infection and can undergo variable
degree of resorption and thus are
unpredictable. The free grafts can
get infected and rejected.
• Free microvascular fibular grafts:
Anastamosed to regional artery
and vein, they are the best option
to reconstruct the mandible and
Fig. 28.8: Reconstruction plate with Fig. 28.9: Fractured reconstruction plate in selected cases maxillary defects
condylar prosthesis (Figs 28.10 and 28.11). The graft
provides adequate bone to restore
of the condyle. The disadvantages of – The midline reconstruction with the contour and in cases of deficient
the reconstruction plate are: the plates is often problematic cover due to excision of the mucosa,
– They help only in establishing and dehiscence of plate is a the skin pedal can be harvested and
the contour, but the masticatory common complication. used to bridge the soft tissue defect
function cannot be restored as – The plates can fracture due to provide adequate cover for the
the fabrication of the denture is to trauma or extreme stress bone graft. Subsequently, dental
not possible. (Fig. 28.9). rehabilitation can also be done by
– The plates are liable to get • Bone grafts: Corticocancellous insertion of implants. However,
loosened, infected and can evoke bone grafts harvested from the the facilities for the (microvascular
tissue reaction and need to be anterior iliac crest (See Fig. 28.4B) anastomosis) free tissue transfer are
removed. or the rib grafts can also be used to not universally available.
Odontogenic Tumors 639

• Bone transport: The transport tech­


nique using the Elizarow technique
by means of distraction devices can be
used to bridge smaller bony defects.

Reconstruction of the
Maxillary Defects
The reconstruction of the maxillary
defects is always challenging. The defects
are large and complex. The common
A B modalities for maxillary reconstruction
after the maxillectomy are:
• Use of temporalis muscle fascia flaps
• Use of nasal septum to reconstruct
the orbital floor.
Free vascularized flaps like fibula
are not ideal as the vascular pedicle is
short. However, with the insertion of
implants in the fibular graft the dental
rehabilitation is possible. For maxillary
reconstruction, free scapular flaps are
C D preferred because of the long vascular
pedicle and good bone quality.

Obturators
The ensuing surgical defect following the
maxillectomy performed for exci­sing the
ameloblastoma can be plugged using
prosthesis in the form of an obturator.

Extraosseous/Peripheral
E F
Ameloblastoma
History
The peripheral ameloblastoma was first
reported by Stanley and Krogh26 in 1959
and has a histopathological appearance
similar to the solid ameloblastoma. It is an
uncommon lesion usually presenting as a
painless, nonulcerated sessile or pedun­
culated gingival or alveolar lesion. The
lesion shows an innocuous clinical behav­
G H ior and is treated with local excision.
Figs 28.10A to H: Case of ameloblastoma of mandible treated with segmental resection The tumor was first described by
and reconstruction of the defect with free fibular graft: (A) Preoperative photograph; Kuru27 (1911). In a review by Mintz
(B) Preoperative radiograph; (C) Exposed tumor; (D) Resected specimen; (E) Marking et al.28 (1999) covering the period be­
of fibular graft and skin pedal; (F) Harvesting fibular graft on peroneal vessels pedicle; tween 1959 and 1989, only 33 cases
(G) Microvascular anastomosis of graft; (H) Postoperative radiograph showing graft in place were documented, while Redman et al.29
(1994) found 55 cases in the Anglo-Sax­
• Custom made implants: Using defe­
cts. It provides better results on literature. Reichart et al.13 (1995), in a
the stereolithography and rapid as compared to the reconstruction review of 3677 cases of ameloblastoma,
prototyping the custom made im­ plate. However the other short com­ found only 2 percent to possess periph­
plants can be fabricated and used ings are similar to the reconstruction eral ameloblastomas. Likewise, Gurol
to recons­truct the surgical bony plates. and Burkes (Gardner 1996) reviewed
640 Neoplastic Conditions of Head, Neck and Face

A B C
Figs 28.11A to C: Case of ameloblastoma of mandible in the anterior area treated with segmental resection and reconstruction of the
defect with free fibular graft and reconstructed plate

205 ameloblastomas in the period from Synonyms tive tissue of the gingiva, show­ing no
1956 to 1994 and found only eight cases Soft tissue ameloblastoma, ameloblas­ continuity with the surface epithelium,
to correspond to peripheral ameloblas­ toma of the mucosal origin, amelo­ whereas others seem to fuse with or
toma. In a 2002 review conducted by blastoma of the gingiva. originate from the mucosal epithe­
Philipsen et al. peripheral amelo­ lium. It is generally believed that basal
blastoma was seen to account for 2 to Epidemiology cell carcinoma of the gingiva and pe­
10 percent of all ameloblastomas. All Peripheral ameloblastoma is a very ripheral ameloblastoma represents the
these studies document the rarity of this rare odontogenic tumor, representing same neoplasm. Squa­mous cells in the
variant of the ameloblastoma. approximately 1 to 5 percent of all acanthomatous areas of peripheral am­
One of the main uncertainties re­ amelo­blastomas (El-Mofty et al. 1991, eloblastomas may show ghost cell for­
garding the origin of this tumor, is that Gardner 199635). The lesion is exclusively mation and in some parts of the tumor
it is believed to be derived directly from located in the gingiva or oral mucosa islands,39 vacuolated or clear cells occur
the lining epithelium or from remains of (Guralnick et al.37 1983, Buchner and in discrete clusters. The stroma is that of
the dental lamina located in non-bony Sciuba34 1987). Age range varies from 9 a mature fibrous connective tissue.
soft tissues (Moskow and Baden30 1982, and 92 years with 64 percent of all cases
Kaneko and Ueno31 1986, Horowitz occurring in the 5th to 7th decade. Differential Diagnosis
et al.32 1987, Gurol and Burkes33 1995, Peripheral ameloblastomas are loca­ • Peripheral odontogenic fibroma
Ide et al. 2002). ted in the tooth bearing areas (gingiva) • Peripheral variant squamous odon­
Histologically, peripheral ameloblas­ or alveolar mucosa in eden­tulous areas. to­genic tumor
toma is similar to central ameloblastoma, Mandible: Maxilla ratio of 2.4:1 is noted. • Odontogenic gingival epithelial ham­
although the former is less aggressive artoma.
(Buchner and Sciuba34 1987). Clinical Features/Imaging
The maximum incidence is ob­ The peripheral ameloblastoma is a Treatment and Prognosis
served between the fifth and sixth de­ painless, firm and exophytic growth with It does not show invasive behavior and
cades of life, with an average patient age a smooth, pebbly or papillary surface. conservative excision is a treatment of
at initial appearance of the lesion to be Rarely, intraosseous ameloblastomas choice. Although the recurrence rate
50 years. A slight male predominance may extend to the gingival tissues and is low, long-term follow-up is recom­
has been reported (Gardner 199635). In merge with the gingival epithelium, mended.
most cases (65%), the lesion is located in creating an exophytic peripheral amelo­
the mandible, particularly on the lingual blastoma like lesions.38 Pituitary Ameloblastoma
aspect of the premolar zone (represent­
Histopathology (Craniopharyngioma, Rathke’s
ing 32.6% of all locations) (Philipsen
et al. 200136). In the upper maxilla the The peripheral ameloblastoma con­ pouch tumor)
most frequent location corresponds to sists of odontogenic epithelium with This is the tumor involving the central
the anterior zone for Japanese patients, the same histomorphic cell types and nervous system, which grows as a pseu­
while in Caucasians it corresponds to patterns as seen in central solid vari­ doencapsulated mass. It is usu­ally seen
the region of the tuberosity (Shiba et al. ant of ameloblastoma. Some les­ ions as suprasellar mass, but occasionally
1983, Orsini et al. 2000). are located entirely within the connec­ present as an intrasellar mass destroying
Odontogenic Tumors 641

the pituitary gland. The peak incidence mimic a dentigerous cyst. Ackermann diagnosis is frequently a dentiger­
is reported between 13 and 23 years of et al.41 (1988) described three distinct ous cyst (Fig. 28.12C). The differences
age. It is generally thought to originate histological types as: between conventional and unicystic
from the unobliterated por­tion of the • Cyst lined by variable epithelium ameloblastoma are shown in Box 28.1.
fetal craniopharyngeal duct, which itself with no infiltration into the fibrous The lesions vary in size and when
originates from the Rathke’s pouch. The cyst wall. removed intact, are typically cystic and
epithelial remnants of cra­niopharyngeal • Cyst showing intraluminal plexiform generally attached to an unerupted
duct are common in adults. These cells epithelial proliferation with no infil­ tooth at the cementoenamel junction
are pleuripotent and can give rise to tration. (Figs 28.13A and B). The cyst wall may
histologically similar tumor-like amelo­ • Cyst with invasion of epithelium into contain one or more tumor proliferations
blastoma of the jaws. the cyst wall in either a follicular or a extending into the lumen. These prolif­
The microscopic features of cranio­ plexiform pattern. erations and other thickened areas must
pharyngioma differ from ameloblastoma Microscopically, it was demonstra­ be selected for microscopic examination.
due to the almost universal presence of ted that in all types there is a basal layer
calcified foci and neoplastic bone or car­ of columnar preameloblasts with hyper­ Histopathology
tilage. It has histological similarity with chromatic nuclei polarized away from The unicystic ameloblastoma has two
the calcifying epithelial odontogenic the basement membrane, with a clear histopathological variants (Fig. 28.14).41
cyst (CEOC) due to the presence of ghost basal cytoplasm and a more superficial 1. The luminal variant is a cystic lesion
cells. Tooth formation in a craniopha­ loose stellate reticulum-like epithelium lined by ameloblastomatous epi­
ryngioma has also been reported. (Leider et al.43 1985, Li et al.44 2000, thelium. In addition, intraluminal
The rate of growth of this tumor is Philipsen and Reichart.45 1998, Neville extensions may occur. These exten­
different from the ameloblastoma and et al.14 2002). Due to its clinical behavior, sions usually exhibit plexiform epi­
often presents with endocrine dysfun­ this lesion is commonly seen as an thelial pattern. There is no tumor
ctions, drowsiness and toxic symptoms. incidental finding on radiographs taken infiltration into the fibrous wall.
for other purposes. In these circums­ 2. The mural variant, the cyst wall is
tances, some lesions could remain infiltrated by ameloblastomatous
Unicystic Type (Synonym - undiagnosed in the early stages of their epithelium that exhibits either a fol­
Cytogenic ameloblastoma) development (Eversole et al.46 1984). licular or plexiform pattern. Some­
times, both variants may occur in
History Epidemiology the same lesion. The mural variant
The unicystic ameloblastoma represents The cases associated with unerupted of unicystic ameloblastoma may be
an ameloblastoma variant, presenting tooth show a mean age of 16 years as confused with either dentigerous cyst
as a cyst (WHO). The unicystic amelo­ opposed to 35 years in the absence of or dental follicles containing a lot of
blastoma was first described in 1977 by an unerupted tooth.45 The mean age odontogenic epithelial remnants.
Robinson and Martinez.40 This variant is significantly lower than that of solid These epithelial nests, however, do
has a large cystic cavity with either lumi­ ameloblastoma. There is no gender not show the typical histologic fea­
nal or mural proliferation of ameloblas­ predilection. About 5 to 15 percent of all tures of ameloblastoma, peripheral
tic cells. It has been shown that this type ameloblastomas are unicystic type. More palisading and nuclear polarization.
of ameloblastoma has a low recurrence than 90 percent cases involve mandible, The ameloblastic changes in the
rate. Ackermann41 advocated simple usually the posterior region. lining may be focal and not general­
enucleation for cystic ameloblastoma, ized throughout the lining. In such
with more aggressive surgery if the con­ Clinical Features/Imaging cases even if the biopsy is done, it
nective tissue of the wall was shown to Some cases are asymptomatic and may not be from the representing
have invasive islands of ameloblastoma­ some present as a swelling of the pos­ site and the histopathological report
tous epithelium. terior mandible (Fig. 28.12A). About may be a cyst. In such cases it is
The unicystic ameloblastoma tends 80 percent cases are associated with essentially treated by conservative
to occur at an earlier age than the sol­ unerupted mandibular third molars. approach, i.e. enucleation, rather
id or multicystic forms (Gardner and The lesion presents radiographi­ than resection (Figs 28.15A to D).
Corio42 1984). It frequently presents as cally as a well corticated, unilocu­
a unilocular well-defined radiolucency lar, often pericoronal radiolucency Prognosis
surrounding the crown of an unerupted (Fig. 28.12B).46 Root resorption may Most unicystic ameloblastomas are
mandibular third molar and may also occur.47 The clinical radiographic enucleated with the preoperative clinical
642 Neoplastic Conditions of Head, Neck and Face

diagnosis of dentigerous cyst and it is


only on pathologic examination of the
enucleated lining that their true nature
is determined. The luminal variant does
not infiltrate the surrounding bone
and as a result no further treatment is
required for those lesions. Long-term
follow-up is recommended to detect
recurrence, if any (Figs 28.12 and 28.14).

Desmoplastic Ameloblastoma
Desmoplastic ameloblastoma is a vari­
A B ant of ameloblastoma with specific clini­
cal, imaging and histological features
(WHO). Desmoplasia is the term which
refers to the presence of excessive
connective tissue stroma.
Eversole was the first to describe
it in English literature. Desmoplastic
ameloblastoma has also been reviewed
by Waldron CA et al.48 in 1987 in his
histopathological study of 116 ame­
loblastomas with special reference to the
desmoplastic variant.
Desmoplastic ameloblastoma has
also been reviewed by Ashman et al.49
C
(1993) and in more detail by Philipsen
et al. (1992) who analyzed the findings
in 29 reported cases.
Desmoplastic ameloblastoma variant
accounted for 1.4 percent of 1593 amelo­
blastomas reviewed by Reichart et al.13
(1995).

Epidemiology
Desmoplastic ameloblastoma exhib­
its no gender predilection and occurs
over a wide range. Most of the cases are
diagnosed between 30 and 60 years of
D E age. The maxilla: mandible ratio is 1:1
Figs 28.12A to E: A clinical case of unicystic ameloblastoma in the ramus managed by (Fig. 28.16A). The desmoplastic amelo­
enucleation the cavity packed open for healing by secondary intention blastomas are found predominantly in
the anterior mandibular region.

Clinical Features
Box 28.1: Differences between conventional and unicystic ameloblastomas
A painless swelling of the jaw bone
Conventional Unicystic represents the chief initial complaint.
Grows in its typical island, strand and cord- Cystic areas nearly always noted, grows The size of the tumor varies between
like patterns, but presents surgically as a predominantly as a cystic lesion 1.0 and 8.5 cm in diameter. An extra­
largely solid tumor mass within the bone osseous variant of desmoplastic amelo­
More than 90% of all ameloblastomas 6–10% of all ameloblastomas blastoma has not been reported. The
100% recurrence rate for that treated only by Better prognosis, lesser recurrence (10.7–25%) lesional tissue has a gritty consistency
curettage, however most studies report lower (Philipsen and Reichart)
and the cut surface is solid in most of
rates, ranging from 50% to greater than 90%
the cases.
Odontogenic Tumors 643

A B
Figs 28.13A and B: Unicystic ameloblastoma involving the anterior mandible in a Fig. 28.14: Histological aspects of the
16-year-old boy treated by enucleation unicystic ameloblastoma. Note that epi­
thelial lining presents the overlying epi­
thelial cells loosely disposed resembling
stellate reticulum. In the insert a basal layer
can be seen showing a hyperchromatic and
polarized basal cells

Radiographically, about 50 percent


A B C D of the desmoplastic ameloblastomas
Figs 28.15A to D: Diagrammatic representation of various situations that may be show a mottled mixed radiolucency/
found in unicystic ameloblastoma on histologic examination: (A) The lining epithelium radio­pacity with diffuse margins, sugges­
is ameloblastomatous; (B) A nodule of ameloblastoma projects in the lumen; (C) The ting a fibro-osseous lesion. Resorp­tion
ameloblastoma has proliferated from the cystic lining into the connective tissue wall of the of tooth roots may occur (Fig. 28.16B).
cyst; (D) islands of ameloblastoma are present in connective tissue wall of an apparently
The ill-defined borders of desmoplastic
non-neoplastic cyst
ameloblastomas make high resolution
CT and MRI helpful in treatment
planning.50

Histopathology (Fig. 28.17)


In desmoplastic ameloblastoma, the
stromal component dominates com­
pressing the odontogenic epithelial
components. The epithelial tumor
islands are very irregular or bizarre in
shape with a pointed stellate appear­
ance. The epithelial cells at the periph­
A B
ery of the islands are cuboidal with
occasional hyperchromatic nuclei. Col­
umnar cells with nuclear polarity are
rarely conspicuous. The islands have
a swirled, hypercellular center with
spindle shaped or squamous epithelial
cells. Microcytes may occur centrally.
Myxoid changes in the juxtaepithelial
stroma are often found. Formation of
metastatic osteoid trabaculae (osteo­
plasia) may be present. A fibrous cap­
sule is not present corresponding to
the radiographically poorly defined
C D tumor margin. A combination desmo­
Figs 28.16A to D: Desmoplastic ameloblastoma involving the maxilla plastic ameloblastoma with A-S/M is
644 Neoplastic Conditions of Head, Neck and Face

The radical approach includes, plates often erode the overlying


resection and the excision of a lesion skin in due course of time and
that includes a measurable perimeter dehi­scence takes place. However,
of investing bone. In the mandible this in the large lesions where the con­
could be done with (segmental) or servative excision is not possible,
without (marginal) continuity defect segmental resection is required with
or extend to disarticulation if the TMJ reconstruction of the defect using
is involved. In the maxilla, it would be the free fibular graft.
defined by the anatomic extension of • Posterior mandible (bicuspid or
the excision in subtotal (partial) or total condyle): Gardner and Pecak55 indi­
Fig. 28.17: Desmoplastic ameloblastoma. maxillectomy. cated that ‘small lesions of the poste­
Irregularly shaped epithelial island sur- rior mandible’ should be treated by
rounded by narrow zone of loose structures Surgical Management of marginal resection leav­ing the poste­
embedded in desmoblastic stroma
Ameloblastoma According to rior border intact, where­as more ex­
Anatomic Location of the Lesion52 tensive lesions should be treated by
known and has been termed as hybrid segmental resection. They also sug­
lesion.51 • Anterior mandible (cuspid to gested that curettage alone should
cuspid): Radical resection with con­ not be done because of the close rela­
Management tinuity defects of the anterior man­ tionship of the margins of the tumor
Present knowledge leads to recommen­ dible are complex reconstructive to vital structures that could result in
dation to apply same treatment moda­ cases. If at all possible, attempts a recurrence rate of 55 to 90 percent.
lity as for multicystic ameloblastoma should be made to maintain the Cryotherapy increased the chance of
(Figs 28.16C and D). Treatment deci­ infe­
rior border of the symphyseal success by causing devitalization of
sions for ameloblastoma are based on region. The use of a marginal the bone to a depth of 1 to 3 cm. Even
the individual patient situation and resection is made possible because though the follow-up period was
the best judgment of the surgeons. The the thickness of cortical bone in short (10 years is the ‘gold standard’)
surgical plan should be influenced by the symphyseal region is more they suggested that radical treatment
whether the lesion involves maxilla or resistant to infiltration by tumor. should be preserved for treatment
mandible. Maxillary lesions behave Mehlisch et al.53 suggested that failure. Ueno et al.56 reviewed 91 cas­
distinctly different from mandibular small lesions (less than 3 cm in es of ameloblastomas with follow-
lesions. The higher cancellous bone diameter) located in the anterior ups from 1 to 15 years and suggested
per­centage in the maxilla facilitates part of the jaws could be treated by that extensive resectioning of the
the spread of ameloblastoma, whereas excision with cautery whereas larger mandible was over treatment. This
the density of the cortical plates in the lesions required ‘segmental or en philosophy may be particularly true
mandible tends to limit the spread of bloc resection’. Gardner reported in young patients where interrup­tion
neoplasm. The location of the maxilla that treatment of ameloblastoma in in growth and development may in­
in the center of the maxillofacial com­ the anterior body of the mandible terfere with future function and es­
plex allows greater ease of extension of could be approached conservatively thetics. Kahn found that 68.6 percent
the ameloblastoma into vital structures, because of the distance from ma­ of amelo­blastomas in young people
sinus, orbit and skull base, resulting in jor anatomic structures. However, were associated with impacted teeth
increased morbidity and mortality rates. if curettage is used, recur­ rence and 72.2 percent of these were uni­
Successful treatment is the treatment should be anticipated. Holland locular. The majority of these tumors
that renders an acceptable prognosis, and Mellor54 suggested that cautery were treated conservatively with
complete eradication of the lesion, recon­ could be considered in conservative enucle­ation or curettage and result­
struction of the resultant defect, causes management even though scientific ed in a 6.9 percent recurrence rate
minimal disfigurement and is based on evidence to support its use is lacking. over an average of 5.2 years it was
the behavior and potential of the tumor, In summary, ameloblastoma of the suggested that this type of manage­
the growth patterns of the various physi­ anterior mandible at times can be ment is appropriate in children, es­
cal forms, duration, the anatomic site of treated by a marginal resection. pecially in unicystic ameloblastomas
the occurrence, the clinical extent and Moreover, the reconstruction of the with­out tumor cell extension beyond
size of the tumor and histological assess­ anterior mandibular defect, sprea­ the margins of the cyst wall. Stephen
ment. The treatment modality is also de­ ding across the midline is often E Feinberg57 believes on the basis of
termined considering the general health unsatisfactory if the conventional their clinical experience and the lit­
and age of the patient. reconstruction plates are used. The erature review, that treatment of solid
Odontogenic Tumors 645

or multilocular ameloblastomas of be easily separated from the bone makes definitive treatment difficult.
the body and posterior mandible and can be removed completely. The Bredenkamp et al.58 described maxi­
requires radical therapy. Marginal authors strongly recommend and llary ameloblastomas as being lo­
resection without continuity defect practice the conservative treatment cally aggressive, incurable and le­thal,
with 1 to 2 cm margins (maintenance for the unicystic ameloblatomas with they found a 5-year survival rate of
of the inferior or posterior border reasonable success which comprises 16 percent when initial treatment
when possible) should be the treat­ of enucleation of the lining, vigorous consisted of a limited resectioning as
ment of choice for solid multilocu­ curettage of the adjoining cancel­ their recurrences were treated with a
lar lesions. Patients who undergo lous bone followed by application maxillectomy or debulking procedure
marginal resection with continuity of Cornoy's solution to the base (see if total remo­val is impossible, it is
defects might requ­ire maxilloman­ Figs 28.12A to E and Figs 28.13A and clear that there is little support for
dibular fixation if pathologic fracture B). The patients should be kept un­ conser­ vative management of solid
is a possibility. Reconstruction plates der long term follow-up and failures or multicystic ameloblastomas of the
should be adapted before segmental of conservative treatment should be posterior maxilla. Initial treatment
resection without continuity defect in treated with radical treatment like should include surgical margins of
order to maintain a normal anatomic segmental madibulectomy and ap­ 1 to 2 cm. The surgical approach to
rela­tionship between the remain­ propriate reconstruction. obtain these margins, depending on
ing distal and proximal segments. In • Anterior maxilla (cuspid to cus­ the location and size of the tumor,
contrast, unicystic ameloblastoma pid): Ameloblastomas of anterior may require a transoral resection
of the posterior mandible can be maxilla represents approximately or a maxillectomy could be done
treated conservatively with curettage 2 percent of all documented oc­ via a Weber-Fergusson incision to
or peripheral ostectomy if adequate currences. Gardner suggested that gain adequate exposure for tumor
follow-up is possible. Most of the ameloblastoma of the anterior max­ resection. Tumors of the infratem­
unicystic ameloblastomas are seen at illa could be treated less aggressively poral fossa and pterygo­ maxillary
an early age and are often associated than those of the posterior maxilla as region would need combined surgical
with impacted teeth. They clinically sufficient distances from vital struc­ approach necessitating intraoral and
adjoining cancellous bone and often tures allow for less radical treatment. bicoronal or hemi coronal incis­ion.
diagnosed as the same and treated Data suggests that conservative The maxillary amelo­ bla­stomas by
with enucleation and curettage. Only treatment has the risk of occurrence and large require more aggressive
upon postsurgical histopathology of with potential extension to the or­ treatment as the tumor infilterates
the specimen, diagnosis of unicystic bits, nasal cavity, and ethmoid cells. the spongy maxillary bone and
ameloblastoma is arrived at adjoin­ On the other hand, radical treatment the attempts towards conserv­
ing cancellous bone is done preop­ (partial or total maxillectomy) may ative excision invariably fail and
eratively, considering the fact that the result in a significant deformity re­ recurrence is more common. The
ameloblastic changes in the lining of quiring complex reconstruction. recurrence may be at a site, which
the cyst may not be generalized, the • Posterior maxilla (bicuspid to pte­ is more difficult to excise surgi­cally
biopsy need not be from this repre­ rygoid plates): Approximately 47 making it unresectable. Thus, the first
senting site and the histopathological to 50 percent of maxillary amelo­ attempt for the complete removal
diagnosis may come as dentigerous blastomas are found in the molar should be well planned and radical.
cyst. Under these circumstances the region and 15 to 30 percent in the
lesion is treated conservatively. In ei­ maxillary sinus region and the Use of Carnoy’s Solution
ther cases the long term follow-up to floor of the nose, it is generally felt
detect recurrence is the only solution. that maxillary ameloblastomas are
after Enucleation of Unicystic
As the unicystic ameloblastomas oc­ more dangerous than mandibular Ameloblastoma
cur at an early age and are extensive ameloblastomas because of a lack • Carnoy’s solution59 was described
at the time of the first diagnosis, a of maxillary cortical bone to contain in 1933 as a sclerozing agent for the
radical treatment comprising the the tumor and their difficulty in treatment of cysts and fistulae and
segmental resection is too morbid early detection in conjugation with remains in use today as a fixative.
for the patient. It does not only cause their intimate relationship with • The use of carnoy’s solution for
functional and cosmetic morbidity complex regional anatomy, poste­ this specific purpose in relation
but also leads to retarded growth and rior maxillary tumors are not well to unicystic ameloblastoma was
also psycological problems to the af­ confined by the thin maxillary cor­ initially suggested by Stoelinga and
fected child. The unicystic amelo­ tical bone and can easily spread Bronkhorst60 in 1988 and recently
blastomas have thick lining and it can outside maxillary boundaries, which proposed again as a possible means
646 Neoplastic Conditions of Head, Neck and Face

to diminish the recurrence risk after controlling ameloblastomas there are • Adenoid adamantoblastoma
conservative treatment. two other reasons why this modality • Cystic complex odontoma
• Carnoy’s solution is probably able should not be used other than in • As a variant of the simple amelo­
to fix residual ameloblastoma tis­ exceptional cases: First, the danger of blastoma.
sue after enucleation of unicystic osteoradionecrosis and second the risk The Pindborg’s tumor is classified
amelo­blastoma with mural invasion inducing a malignant transformation. as an uncommon, benign, odontogenic
and diminish the risk of recurrence, Radiation and chemotherapy have neoplasm that is exclusively epithelial in
but based on the two studies this is been used for primary and recurrent its tissue of origin.
unlike­ly to be effective for conven­ tumors. Atkinson et al. did a retrospective
tional multi­cystic amelobl­astoma study of 10 cases of ameloblastoma Epidemiology63,64
and some of the unicystic lesions with in which 7 were primarily treated The calcifying epithelial odontogenic
mural invasion. It was surprising to with radiation alone and 3 patients tumor is generally considered a rare
find the patients treated by enuclea­ had combined radiation and surgery; odontogenic neoplasm. The age range
tion, but without the application of 9 patients treated initially with mega of all patients with CEOT varies between
carnoy’s solution experienced recur­ voltage radiation alone or radiotherapy 8 and 92 years at the time of diagnosis
rence (100% recurrence). Carnoy’s surgery had successful treatment with with a mean of 36.9 years. However, if
solution is effective in diminishing only one recurrence noted. Based on the tumor is divided according to the
expected recurrence. their data, they suggested that radiation two topographical variants, the age
• Carnoy’s solution was applied to therapy could be used in cases when ranges and means are as follows:
the bony cavity for 3 minutes using surgical treatment would be technically • Intraosseous type (range 8–92, mean
cotton applicators or ribbon gauze complex because of tumor bulk, loc­ 38.9 years)
soaked with carnoy’s solution. ation or medical status of the patient. • Extraosseous type (range 12–64, mean
When mandibular nerve was visible Gardner felt that radiation therapy was 34.4 years).
in the bony cavity, contact with unsuccessful for intraosseous amelo­ Almost two-thirds (64%) of the intra­
carnoy’s solution was avoided as blastomas, but may be more beneficial o­sseous variants are found in the third,
far possible. This was followed by in assisting in inoperable cases. fourth and fifth decades of life. The
copious irrigation with normal sali­ male : female ratio is almost same and
ne. Bismuth iodoform paraffin paste there is no gender predilection. There is
(BIPP) impregnated gauze was then Calcifying epithelial predilection for the premolar/molar re­
inserted into the bony defect and odontogenic tumor gion, although any site may be involved.
the wound kept open over the gauze Peripheral lesions usually occur in the an­
pack. Introduction61 terior gingiva. Most cases are intraosseous
The calcifying epithelial odontogenic and approximately 6 percent arise in ex­
tumor (CEOT) is a locally invasive epith­ traosseous locations. Intrao­sseous lesions
Radiosensitivity of elial odontogenic neoplasm, character­ affect the mandible more often than the
Ameloblastomas ized by the presence of amy­loid material maxilla with a ratio of 2 : 1.
It is usually accepted that ameloblas­tomas that may become calcified (WHO).
are radioresistant but this is incorrect. The calcifying epithelial odontogenic Clinical Features65,66
As they are well-differentiated epithelial tumor was first introduced into the Pindborg tumor begins asymptomati­
tumors, they are quite radio­ sensitive, scientific literature almost 50 years ago cally and consequently may be discov­
this is illustrated by the way therapeutic by JJ Pindborg,61 the term Pindborg’s ered only through routine radio­graphic
irradiation can reduce the extraosseous tumor, is now a universally recognized examinations by the dentist. It is a slow-
components of large amelo­ blastomas. synonym for this neoplasm. The CEOT growing, painless, expansile, hard, bony
However, tumors that are radiosensitive is a benign, though occasionally locally swelling causing cortical bone to be­
may not beds controlled by therapeutic invasive, slow-growing, odontogenic come egg-shell thin before perforation
irradiation; this is true of ameloblastomas neoplasm that is exclusively epithelial in and subsequent soft tissue infiltration
that are basically infrabony tumors. its tissue of origin. takes place.
Their intraosseous location makes them The tumor had, however, been re­ Pindborg tumor may potentially
resistant to radio­therapy in the same way ported prior to 1955 under different cause associated tooth tipping, rota­
those squamous cell carcinomas are names such as:62 tion, migration and/or mobility sec­
resistant to this modality once they have • Ameloblastoma of unusual type with ondary to root resorption. Just as there
invaded bone. calcification is an uncommon peripheral variant of
Tumors, apart from therapeutic irra­ • Calcifying ameloblastoma ameloblastoma, so there is also a dis­
diation not being reliably effective in • Malignant odontoma tinctly uncommon peripheral variant
Odontogenic Tumors 647

of Pindborg tumor, limited to soft tissue


only that presents clinically as a nodu­
lar mass on gingival mucosa, frequently
in the anterior region.

Radiographic Features67
The Pindborg tumor displays a range of
radiographic features with regards to le­
sion size and bone pattern. On examina­
tion of routine dental radio­graphic im­
ages (periapical, occlu­sal, panoral and
plain film skull), Pindborg tumor may
be completely radiolucent in character
or in the case of more mature lesions,
exhibit a mixed radiolucent and radi­
opaque appearance (Figs 28.18A to C). A
When present, the radiopacities
from the calcifications in this tumor
are said to resemble ‘wind driven
snow’ (Figs 28.19A and B), according to
Pindborg.
Pindborg’s tumor may be unilocular
and cystic in appearance (Fig. 28.18B),
often associated with an unerupted tooth
or more characteristically demonstrate
a mixture of small and large multilocular
spaces described respectively as ‘honey­ B C
comb’ or ‘soap bubble’ in appearance Figs 28.18A to C: Segment of panoramic radiograph showing mixed radiolucent and
(Figs 28.18A and B). In almost all cases, radiopaque lesion of the posterior body of the mandible
the radiographic border between tumor
and surrounding bone appears to be
well defined and circumscribed. this cytological similarity, the calci­
On CT examination, calcifying epi­ fying epithelial odontogenic tumor is
thelial odontogenic tumor has been supposed to arise from stratum inter­
reported in the mandible as demon­ medium cells. Furthermore, some oral
strating expansion and thinning of and maxillofacial pathologists have sug­
buccal and lingual cortical plates by a gested that amyloid deposi­tion within
well-defined mass containing scattered A B
Pindborg tumors is an immu­ nologic
radiopaque areas of varying size and response to these stratum intermedium Figs 28.19A and B: Extraosseous CEOT
involving anterior maxilla in 45-year-old
signal intensity. cells that have been pre­viously seque­
female
When Pindborg tumor is analyzed stered from exposure, which as neo­
by MRI, it reveals predominantly a plastic cells are now expo­sed and un­ In order to conceptualize a uni­fied
hypo- intense lesion on T1-weighted recognized as host tissue. source of origin for the diverse locations
images and a mixed hyperintense lesion With the appearance of reported of CEOT, one has to look for odonto­
on T2-weighted images. cases of intraosseous CEOT without an genic epithelium with a widespread oc­
associated unerupted tooth and cases of currence. Of all the possible candidates
Pathogenesis68 the peripheral variant, it became evident only one matches the requirements of
The tumor develops from the reduced that sources other than reduced enamel widespread distri­ bution, namely, the
enamel organ. Some have suggested that epithelium should be considered while dental lamina complex or its remnants.
the epithelial cells of the Pindborg tumor discussing the histogenesis of CEOT. Disintegration of the complex system
are reminiscent of the sequestered cells The peripheral location strongly sug­ of dental lamina gives rise to a countless
in the stratum intermedium layer of the gests the possibility that the tumor arises number of epithelial remnants persisting
enamel organ in tooth development or from remnents of the dental lamina or in the jawbones and gingiva after the
odontogenesis. Therefore, based on from the basal cells of the oral epithelium. completion of odontogenesis. The latter
648 Neoplastic Conditions of Head, Neck and Face

argument concerning the histogenesis could be expected for a similar procedure affected jaw portion and any associated
seems relevant for several odontogenic performed in treatment of a solid variant soft tissues with no less than 1 cm in
tumors and hamartomatous lesions. or multilocular ameloblastoma (10–15% every direction, as might be performed
versus 35–40%). Small maxillary lesions for any other variant of odontogenic
Gross Pathology may be surgically excised by either thor­ carcinoma (carcinoma arising in a long
The intraosseously located CEOT is often ough intrabony curettage or conservative standing odontogenic cyst, ameloblas­
easily enucleated and the tumor volume en-bloc resection sacrificing a thinner tic carcinoma or clear cell odontogenic
varies from 1 to 4 cm. The mass varies margin of healthy adjacent bone than carcinoma). Adjunctive external beam
in color from grayish-white or yellow would normally be required for resection radiation therapy is advocated following
to tan pink. Bisecting the specimen of ameloblastoma. Lesions designated determination of local spread to cervical
reveals most often calcified particles recurrences following conservative ap­ lymph nodes and adjunctive chemo­
giving a crunching sound while cutting. proaches like intrabony curettage may therapy may play some role in control
The tumor may be all solid or minute in fact represent persistence of disease. of distant organ metastasis in some pa­
cystic spaces may be encountered. If Like ameloblastoma, small infiltrative tients. Radiotherapy in lieu of surgical
associated with an unerupted tooth, the foci of Pindborg tumor may insinuate resection is contraindicated as a recom­
crown (or hard dental structures of an along bony trabeculae and appear as mended treatment for Pindborg tumor,
odontoma) can be found embedded in uninvolved bone radiographically. Some because osteoradionecrosis, xerosto­
the tumor mass. oral and maxillofacial pathologists have mia and radiation-induced malignancy
suggested that even with an expected low present as serious complications of this
Microscopic Features rate of local recurrence compared with therapy.
The calcifying epithelial odontogenic solid ameloblastoma, maxillary tumors Treatment of peripheral Pindborg
tumor consists of polyhedral epithelial can be treated more aggressively than a tumors as advocated by Houston and
cells, in either compact sheets or scat­ similar-sized lesion in the mandible, with Fowler71 is simple local excision based
tered small islands, in a fibrous con­ an opportunity to confirm histopatho­ on their review of pertinent literature.
nective tissue stroma. The cells have logically tumor-free bone margins. Obvi­
eosinophilic granular cytoplasm and ously, recurrent or persistent disease and Prognosis
prominent intercellular bridges. The tumors diagnosed late in the duration Most studies of Pindborg tumor report
nuclei are often hyperchromatic with of their clinical course, which over an a local recurrence rate of between 10
pleomorphism. The giant nuclei and extended time have become larger and and 20 percent following conservative,
multinucleation is common but mitotic more extensive (greater than 4 cm), may but complete removal of the lesion. Like
figures are rare. The tumor has homo­ not be curable by conservative surgical ameloblastoma, the time interval bet­
geneous, eosinophilic material often measures such as en-bloc resection only. ween initial and recurrent tumor may be
described as amyloid, comparable gly­ Consequently, segmental resections measured in years or decades, making
coprotein, basal lamina, keratin and such as partial or hemimandibulectomy rou­tine annual follow-up examination
enamel matrix. The calcification in or hemimaxillectomy—which leave a with radiographic survey a prudent
Liesegang fashion is present. significant bone discontinuity requiring measure.
either distraction osteogenesis or, more Bouckaert MMR, Raubenheimer EJ,
Treatment69 likely, graft and reconstruction proce­ Jacobs FJ72 (2000) reported one case of
There are a variety of alternative surgical dures may be required. advanced disease in the patient’s max­
treatment methods to successfully man­ Treatment of histopathologically illa resulted in local extension to the
age Pindborg tumors. Treatment is atypical or frankly malignant calcifying brain.
dependent on the size and location of the epithelial odontogenic tumors is limited The incidence of malignant trans­
neoplasm, the patient’s overall medical by the paucity of cases reported. Rob­ formation to odontogenic carcinoma
condition or tolerance to withstand ert K Goode70 advocates early interven­ ex-Pindborg tumor is extremely low and
the surgical procedure and the skill or tion before such a lesion could escape should be considered distinctly rare. To
experience level of the operator. the confines of the involved mandible date, only three such cases that either
Small, intrabony mandibular lesions or maxilla (stage 1 and 2 disease). The suggested this outcome or definitely
with well-defined borders may possibly size and extent of tumor determine the rendered such a diagnosis have been
be cured by simple complete, but con­ appropriate surgical operation needed reported in the literature. No follow-up
servative tumor enucleation or curet­ to achieve complete assured removal information is available.
tage followed by judicious removal of a of all neoplastic tissue with a generous With regard to peripheral Pindborg
thin layer of bone adjacent to the tumor. histopathologically confirmed tumor- tumors, no recurrence has been repor­
This operation characteristically enjoys a free margin in all directions. This gen­ ted in the 11 cases known to have been
significantly lower recurrence rate than erally requires radical resection of the treated with simple local excision.
Odontogenic Tumors 649

Squamous Odontogenic is a hamartomatous epi­thelial prolifer­ angular or semicircular radiolucency


ation, probably arising from cell rests located in the alveolar bone along the
Tumors of Malassez. Recurrences have been lateral surface of the roots with the nar­
recorded by Pullon et al.73 but they row portion (apex) towards the alveolar
Introduction seem to be extremely rare and are crest. In some instances this suggests
The squamous odontogenic tumor is most likely results of insufficient initial vertical bone loss. The radiolucent area is
“A benign, but locally infiltrative neo­ removal. somewhat ill defined or may show well-
plasm consisting of islands of well-dif­ defined sclerotic margins. They are mostly
ferentiated squamous epithelium in a Histogenesis small lesions, up to 1.5 cm in diameter.
fibrous stroma. The epithelial islands The histogenesis of the squamous odon­ The tooth mobility may be a presen­
occasionally show foci of central cystic to­genic tumor may be multifactorial. ting symptom. If crestal bone has been
degeneration” (WHO). It was first de­ destroyed, the lesion may mimic alveo­
scribed by Pullon et al.73 in 1975. Intraosseous lar bone loss seen in chronic periodon­
Before 1975, the squamous odonto­ • The lesions associated with the titis. Other documented cases presented
genic tumor was reported under a vari­ alveolar process adjacent to the lat­ as pericoronal radiolucency associated
ety of names such as: eral root surface of the teeth: Rests of with an impacted or uneru­pted tooth.
• Benign epithelial odontogenic tumor Malassez is the source of epithelial Peripheral lesions may cause saucer­
• Acanthomatous ameloblastoma proliferation. ization of underlying bone, which is like­
• Hyperplasia and squamous metapl­ • The lesions developed in association ly to be a pressure phenomenon rather
asia of residual with the crowns of unerupted or than the result of true tumor infiltration.
• Odontogenic epithelium acantho­ impacted teeth: dental lamina may No periodontal ligament can be
matous ameloblastic fibroma be the source. visualized between the lesion and the
• Benign odontogenic tumor, unclass­ root of the tooth, suggesting that lesion
i­fied. Extraosseous arises from cell rests of Malassez in the
These names were given due to Surface stratified squamous epithelium periodontal ligament or closely adjacent
the presence of islands of squamous (dropping off effect) and from the Rests mucous membrane.
epithelium, which have a morphologic of Serres.75 Some of the rare extensive lesions
similarity to that seen in the follicular may have a multilocular appearance
pattern of ameloblastoma. Its inclusion Features involving the body of the mandible or
as a separate entity in a classification pushing aside the maxillary sinus.
of odontogenic tumors is based on its Clinical Features
characteristic histologic features and The reported incidence peaks in third Differential Diagnosis
distinct biologic entity. decade of life however; wide age range Squamous odontogenic tumor may be
It is a rare, sometimes multifocal, (8–74 years) is reported. It is more com­ overdiagnosed as:
benign epithelial odontogenic tumor, mon in males than the females. It occurs • Ameloblastoma particularly acan­
consisting of islands of stratified squa­ throughout the alveolar processes of the thomatous and the desmoplastic
mous epithelium that commonly contain maxilla and man­dible with no site of variant
microcysts and calcifications in a dense predilection. A few patients have been • Well-differentiated squamous cell
fibrous background. reported to have multiple squamous carcinoma.
odontogenic tumor that involved sev­
History eral quadrants of the mouth. It involves Acanthomatous and the
Pullon et al.73 (1975) called attention the maxilla and mandible with equal Desmoplastic Variant
to the possible hamartomatous nature frequency. In maxilla incisor-cuspid Both exhibit squamous differentiation
of the squamous odontogenic tumor area and in mandible bicuspid-molar within the tumor islands, but there is
because of multiple site involvement in area are more commonly involved. It demonstrable ameloblastic change of
one of their cases. presents as a painless or mildly painful the peripheral cells, including:
The multicentric lesions have ty­ gingival swelling associated with mobil­ • Columnar shape
pically exhibited a less aggressive ity of associated teeth as the most com­ • Polarization of elongated nuclei
biological behavior. Unal et al.74 (1987) mon complaint. away from the basement membrane
suggested using the term ‘squamous • Vacuolated or clear cytoplasm.
odontogenic hamartomatoid lesion’, Radiographic Features These changes are less evident in
for squamous odontogenic tumor-like No radiographic features are sufficiently squamous odontogenic tumor. In which
islands in the walls of the odontogenic characteristic to suggest the diagnosis. the peripheral cell layer is composed of
cyst. Most investigators believe that it The reported cases have exhibited a tri­ flat to cuboidal cells.
650 Neoplastic Conditions of Head, Neck and Face

The islands and strands of desmo­ cally, aggressive lesions have been ma’, ‘ameloblastic adenomatoid tumor’,
plastic ameloblastoma often are thin treated by en bloc excision. Ide has ‘odontogenic adenomatoid tumor’.
and compressed rather than rounded reported a case in which a squamous
and broad shaped as seen in squamous cell carcinoma was associated with a Hamartoma Versus Neoplasm
odontogenic tumor. The squamoid areas squamous odontogenic tumor78 and Previously, the AOT was considered
in desmoplastic ameloblastoma often Norris79 reported a case of bilateral to be a hamartoma because of its lim­
exhibit swirls of squamous cells, which maxillary squamous odontogenic ited size in most cases (attributed to its
are not seen in squamous odontogenic tum­or in a patient with a mandibular minimal growth potential) and lack of
tumor. intraosseous carcinoma. It could not recurrence (even following definitely
be confirmed that the mandibular incomplete removal). AOT is consid­
Well Differentiated Squamous squa­mous cell carcinoma developed ered to be a non-invasive benign neo­
Cell Carcinoma within a squamous odontogenic tumor. plasm presumably because the limited
• The islands in squamous odonto­ In their review of literature, Baden size in most of the cases is due to the
genic tumor are well defined and the et al.80 noted two recurrences. fact that they are detected early (often,
cells lack variation in cell size, shape on a routine dental radiograph) and re­
and nuclear staining characteristics Adenomatoid moved before the slow-growing tumor
that are seen in squamous cell carci­ reaches a clinically noticeable size. They
noma.
Odontogenic Tumor also point to the considerable size of
• Mitotic figures are rare to non- some reported cases that had gone un­
exis­tent in squamous odontogenic Introduction detected or untreated for many years.
tumor and atypical, mitotic figures The adenomatoid odontogenic tumor Additional support comes from the mi­
or chromatin abnormalities are not (AOT) is included in classifications of croscopic features of the lesional tissue
seen. odontogenic tumors because it occurs that show greater departure from the
• Significant keratin formation also is only in the tooth-bearing area of the arrangement of the normal odontogenic
not typical. jaws and because of its histomorpho­ apparatus than should be expected in a
• Occasionally dentigerous, apical logic resemblance to components of the developmental anomaly. AOT is “most
periodontal (radicular) cysts and dental organ (tooth germ). The AOT is a appropriately considered a benign em­
periodontal granulomatous tissue locally invasive neoplasm characte­rized bryonal neoplasm.”82
exhibit foci of squamous odonto­ by ameloblastoma like islands of epithe­
genic tumor-like proliferation. These lial cells in a mature connective tissue Epidemiology
charac­teristics have been interpreted stroma. Abberant keratinization may The incidence and prevalence of odon­
as a neoplastic, reactive process that be found in the form of ghost cells in as­ togenic tumors is unknown, largely
is secondary to cyst formation or sociation with varying amounts of dys­ because most of them are benign and
inflam­mation.74, 76 plastic dentin (WHO). AOT gene­rally is are not reported to local, regional or
• Definitive criteria differentiating considered to be an uncommon tumor. national tumor registries that compile
this reactive proliferation from the Its distinctive, although not pathog­ and track malignant tumors. AOT
neoplastic process have not been nomonic, clinicopathologic profile is accounts for approximately 3 to 7 per­
established but Melrose77 (1999) unique among odontogenic tumors be­ cent83,84 of odontogenic tumors that are
indicates that, the reactive islands cause most lesions occur in association acces­sioned by a variety of institutions
seldom form microcysts or contain with an unerupted maxillary cuspid in around the world, which makes it the 4th
intraepithelial calcifications. teenage girls. The so-called ‘duct-like or 5th among the odontogenic tumors,
• Reactive foci of squamous odonto­ structures’ are a unique (although not only surpassed by odontomas, myxomas,
genic tumor within the connective always present) micro­scopic feature of ameloblastomas and cemento-osseous
tissue wall of odontogenic cysts do AOT. No unequivocal recur­rences have tumors.
not appear to cause any alteration been reported despite known incom­
in the usual biologic behavior of the plete removal of some tumors. Demographic Features
cyst and do not appear to develop Philipsen and Birn81 in 1969 gave the
into the tumor. name ‘Adenomatoid Odontogenic Tu­ Age83,84
mor’ to this condition and previously it Although AOT has been reported in
Treatment and Prognosis was described by variety of names such as patients from 3 to 82 years of age, its
Enucleation, curettage and local exci­ adamantoma, ‘adenoadamantoblastoma’ predilection for young patients is well-
sion are treatment modalities that most or ‘adamantoblastoma, adenoma type’, established.
often are described in case reports of ‘adeno­ameloblastoma’, ‘adenomatoid It is unique among odontogenic
squamous odontogenic tumor. Clini­ ameloblastoma’, ‘adenomatoid odonto­ tumors and unexplainable that:
Odontogenic Tumors 651

• More than two-thirds (69%) are


diagnosed between the ages of 10
and 19 years
• More than half (53%) are diagnosed
in teenagers
• Twenty-one percent are diagnosed
between ages 20 and 29
• Altogether, 88 percent are diagnosed
in the second and third decades.
Pericoronal (dentigerous, follicular)
AOTs are diagnosed at an earlier age
than lesions that are not in a peri­
coronal relationship to a tooth, pro­
bably because affected patients seek
consultation concerning failure of the A B
associated tooth to erupt. The early Figs 28.20A and B: AOT involving the maxillary anterior area in a 20-year-old female
detection of gingival (peripheral, extra­
osseous) AOTs is likely due to the
discovery of a variably obvious anterior follicular or extrafollicular type as they Peripheral lesions present as a
maxillary gingival mass. Although the are peripheral and more conspicuous. gingival-colored mass that ranges from
average age at the time of excision of The peripheral AOT are often found 1 to 1.5 mm in diameter (the size was
gingival lesions is 13 years (and ranges associated with unerupted permanent listed in only 4 of 18 reported cases).
from 3 to 19 years), the fact that some teeth. Unerupted permanent teeth They are 10 times more prevalent in the
lesions had already been present for 3 found in association with the follicular maxillary gingiva than in the mandibular
to 5 years suggests that gingival AOTs AOT, are all four canines accounting gingiva; all but 3 of the 18 reported cases
develop at an early age. for 59 percent and the maxillary canine were located adjacent to an incisor—
alone for 40 percent. usually the maxillary central incisor.84
Gender83,84
The tumor is diagnosed approximately Clinical Features Clinical Differential Diagnosis
twice as frequently in women. Although Usually, AOTs are asymptomatic; how­ The diffuse swelling that can accompany
in the third decade AOT is nearly four ever, the tumor is commonly present in central lesions is clinically indistinguish­
times more frequent in women, in the anterior maxillary region, espec­ially able from the maxillary or mandibular
patients who are older than age 30 it is in younger patients. Patients may be enlargement that may occur with:
diagnosed nearly twice as commonly in aware of a gingival swelling or an area • Central odontogenic cysts and tumors
men. It also is interesting and unexpla­ of jaw enlargement. The teeth in the in­ as well as
inable that the female : male ratio for volved area are missing as they are em­ • Benign fibro-osseous lesions
gingival lesions is 1.4 : 1. bedded in the lesion. Nasal obstruc­tion • Benign mesenchymal neoplasms.
is reported in conjunction with rarely As a result, radiographic evaluation
Location encountered large maxillary lesions. is indicated to narrow the differential
The AOT appears in three clinicotopo­ Gingival lesions most often are painless diagnostic considerations.
graphic variations: and slow growing. Gingival lesions cannot be differen­
a. Intrabony or central (including both tiated clinically from gingival fibromas,
follicular and extrafollicular) consti­ Clinical Signs peripheral cemento-ossifying fibromas,
tute 96 percent of all AOTs, out of Most central lesions are discovered on peripheral giant cell lesions or from oth­
which, follicular are 71 percent. routine dental radiographic exami­nation; er peripheral odontogenic tumors such
b. Commonly found in maxilla than in however, delayed eruption of (especially as odontogenic fibroma, ameloblas­
the mandible with a total ratio of 2.1:1. an anterior maxillary) per­manent teeth toma, calcifying odontogenic cyst and
or slow-growing bony expansion (with or calcifying epithelial odontogenic tumor.
Peripheral without displace­ment of adjacent teeth)
They are a rare type and constitute commonly leads to the discovery of the Diagnosis
4.4 percent of all reported AOT cases. intragnathic AOTs. The mobility of teeth,
They almost exclusively occur in the swelling of the cheek85 and asymmetrical Radiographic Features
anterior upper jaw (88%). They are facial swelling has been reported less fre­ A significant number of AOTs are disco­
detected earlier than the AOTs of quently (Fig. 28.20A). vered radiographically because more
652 Neoplastic Conditions of Head, Neck and Face

Enucleation and Curettage


As the tumor is well encapsulated and
usually present in the anterior maxilla,
the surgical access is simple. The tumor
is easily shelled out from the bone and
in most of the cases can be enucleated
in total.

Prognosis
A B C
Adenomatoid odontogenic tumor al­
most is always referred to as ‘slow’ or
Figs 28.21A to C: Radiographic presentation of the AOT
‘very-slowly growing’ but no report of
measurements of growth rate over a
course of time could be located. The re­
than 95 percent occur intraosseously varying size; minimal yellow brown fluid currence after adequate enucleation is
(centrally), usually as small asympto­ to semisolid material; fine, hard ‘gritty’ not common.
matic lesions. granular material; and one to several
The central AOTs present as a well larger calcified masses.
Ameloblastic Fibroma
demarcated, almost always unilocular
radiolucency that generally exhibit a Microscopic Features Ameloblastic fibroma is a relatively rare
smooth corticated border (Fig. 28.20B). The AOTs exhibit diverse histological true mixed tumor in which epithelial
Most lesions are pericoronal or juxta features. The tumor is composed of and the ectomesenchymal elements are
coronal, but the radiolucency may multinodular proliferation of the spindle, neoplastic. The lesion was first reported
extend apically beyond the CE junction cuboidal and columnar cells in a variety by ‘Kruse’86 in 1891. It is an uncommon
on at least one side of the root. Rare, of patterns comprising of scattered tumor and represents only 2 percent
multilocular cases have been reported duct-like structures, eosinophilic mate­ of odontogenic tumors, but the data
and the scalloped borders are observed rial and calcification in several forms, regarding its frequency are difficult to
occasionally. Most cases are between delimited by fibrous capsule of variable evaluate because (particularly in earlier
1 and 3 cm in the greatest diameter. thickness. The typical feature of AOT reports) some lesions that are diagnosed
About 65 percent of reported cases also is numerous duct-like structures with as ameloblastic fibroma may actually
demonstrate faintly detectable radio­ lumina of variable size, which are lined have represented the early developing
paque foci within the radiolucent lesion. by single-layered cuboidal or colu­mnar stage of an odontoma. It is characterized
Occasionally, a more obvious intra­ cells with the nuclei situated away from by the simultaneous neoplastic prolifer­
lesional radiopacity may be iden­tified. the lumen. The duct-like or microcyst ation of the mesenchymal and epithelial
Divergence of roots and displacement lumina are frequently lined by a band of components without formation of
of teeth occurs more frequently than the eosinophilic material of varying thickness dental hard tissues namely dentin and
root resorption. called hyaline rings. Some AOTs contain enamel. Ameloblastic fibroma and rela­
About 71 percent of AOTs are asso­ varying amount of dysplastic dentin, ted lesions were defined by the WHO as:
ciated with the crown of an unerupted dentinoid and osteodentin. Irregular • Ameloblastic fibroma consists of
permanent tooth, including about round calcified bodies, which may odontogenic ecto-mesenchyme re­
6 percent that are associated with two exhibit areas with a concentric layered sembling the dental papilla and epi­
or more unerupted teeth (Fig. 28.20B). pattern (liesegang rings) may be seen in thelial strands and nests resembling
Nearly 60 percent of AOTs are associ­ the parenchymal or stromal zones. dental lamina and enamel organ.
ated with cuspids—40 percent with the • No dental hard tissue is present.
maxillary cuspids (Figs 28.21A to C). Treatment • If there is dentin formation, the
lesion is referred to as ameloblastic
Macroscopic Features Surgical Findings fibrodentinoma.
Unmagnified gross examination of most Although there may be expansion of the In older literature, it is reported as
excisional surgical specimens of central alveolar bone overlying central lesions, ‘soft mixed odontoma’ as it was believed
AOTs reveal a soft, roughly spherical the cortex is almost invariably intact; that it could mature into an odontoma.
mass with a discernible fibrous capsule. however, on rare occasions, penetration
Upon gross sectioning, the tumor may of the cortical plate has been reported. Pathogenesis­
exhibit white to tan solid to crumbly Essentially all cases have a smooth, well- • It is believed to arise de novo during
tissue or one or more cystic spaces of defined capsule of varying thickness. odontogenesis, possibly as a result of
Odontogenic Tumors 653

overproduction of the basal lamina


without odontogenic differentiation.
• Lesions composed of similar ele­
ments, but in which inductive change
has resulted in the deposition of den­
tin alone or dentin plus enamel, are
termed ameloblastic fibrodentinoma
and ameloblastic fibro-odontoma
respectively.

Controversy
Regarding the belief, that these lesions
represent separate entities or are the
same lesion in a continuum representing A B
different stages of evolution. Cahn and
Blum87 (1952) postulated that ameloblas­
tic fibroma represented the least histo­
logically differentiated lesion that evolves
from a moderately differentia­ ted form,
ameloblastic fibro-odontoma to odon­
toma. However, this concept is not widely
accepted. Some investigators believe that
ameloblastic fibroma and ameloblas­
tic fibro-odontoma are variations of the
same process. And some authors con­ C D
sider that ameloblastic fibro-odontoma is Figs 28.22A to D: Ameloblastic fibroma in a 35-year-old man
a variant of ameloblastic fibroma.

Clinical Features tial presentation may include pain, ten­ of the enamel organ and dental papilla,
It is predominantly found in children derness or mild swelling of the jaws. It respectively. It appears to be a true mixed
and young adults, usually within an age is associated with an impacted tooth in tumor and it is noticeable that, unlike the
range of 6 months to 42 years (average about 75 percent of the cases. histologically somewhat similar, appe­
age: 14.6–15.5 years), the mean age being aring ameloblastoma, mali­gnant change
14.8 years.88 It also has been reported in Radiographic Features in ameloblastic fibroma affects the
a 7-week-old infant (Mosby EL89 1998). It appears as a well-defined, unilocular mesenchymal com­ po­
nent and not the
Trodahl90 (1972) reported that there is or multilocular radiolucency with a epithelium.
no gender predilection. Other authors smooth, well defined outline and often
reported a slight male bias. The posterior with a sclerotic opaque border. The large
Rare Variants of Ameloblastic
mandible is the most common site and mandibular lesions are multilocular,
about 70 percent of cases are located in whereas smaller lesions are typically Fibroma
the first permanent molar and second unilocular (Fig. 28.22B). They may range
primary molar area while the remaining in size from 1 to 8 mm.
Granular Cell Ameloblastic
cases are in the posterior maxilla and Trodahl reported no constant sig­ Fibroma
90

rarely in the anterior region of the jaws nificant differences between the appear­ Couch et al.92,93 1962 reported 2 cases of
(Figs 28.22A to D).91 ance of the simple amelobla­stoma and central mandibular lesions composed
Ameloblastic fibroma is a painless, that of ameloblastic fibroma. It may of large round to polygonal stromal
slow growing and expansile neoplasm. mimic a dentigerous cyst when associ­ cells with finely granular, eosinophilic
About 20 percent of the lesions are dis­ ated with unerupted teeth. Radio­graphic cytoplasm and small, often eccentrically
covered on routine radiography. Amelo­ evidence of cortical expan­sion of bone located, ovoid to round nuclei. These
blastic fibroma exhibits slower clinical may not be seen in all cases. granular cells were arranged in lobules
growth than ameloblastomas and does separated by thin, fibrous connective
not tend to infiltrate bone. It enlarges by Histogenesis tissue septa. Within the lobules of
gradual expansion so that the periphery Ameloblastic fibroma arises from odon­ granular cells were small ovoid to
of the lesion often remains smooth. Ini­ togenic epithelial and mesenchymal cells sometimes elongated islands of cuboidal
654 Neoplastic Conditions of Head, Neck and Face

to columnar epithelial cells, with basal are degenerative rather than neoplastic In a revised WHO classification of
to centrally located nuclei. The center of in nature. Such hypothesis is supported odontogenic tumors, the term ‘amelo­
large collections of epithelial cells had a by the fact that no recurrences after blastic fibrodentinoma’ and ‘dentinoma’
loose stellate reticulum like appearance. surgical treatment of the lesions have are used synonymously.
He concluded that, the lesions were been documented in the literature.
ameloblastic fibromas characterized by
differentiation of the mesenchymal com­
Ameloblastic Fibro-odontoma
ponent into granular cells and suggested
Peripheral Ameloblastic Fibroma Hooker100 (1967) made an important
the name ‘granular cell ameloblastic fi­ The peripheral ameloblastoma is an contribution to the understanding of
broma’. White et al. (1978) thought that extremely rare lesion. In making a his­ odontogenic tumors when he showed
granular cell ameloblastic fibromas could topathologic diagnosis of peripheral that two separate tumors with differ­
not represent variants of the ameloblastic ameloblastic fibroma, a distinction be­ ent clinical behavior were previously
fibroma due to following reasons: ­ tween this lesion and the peripheral grouped, together under the term ame­
• The absence of primitive appearing odontogenic fibroma of WHO type or loblastic odontoma. He differentiated
mesenchymal tissue, characteristic odontogenic gingival epithelial hamar­ amelo­blastic fibro-odontoma from the
of ameloblastic fibroma toma (hamartoma of the dental lamina) amelo­ blastic odontoma and used the
• No proliferative activity of the strands needs to be made. (Abughazaleh K98 term ameloblastic odontoma for the
of odontogenic epithelium or his­ mentioned 3 cases, while Darling MR99 more aggressive tumors composed of
todifferentiation towards enamel mentioned 4 cases). an amelo­blastoma and a compound or
organ-like structures as observed in complex odontoma. The latter, which
ameloblastic fibroma. Interrelationship between behaves in the typically invasive man­
They called the lesion ‘Central granu­ ner of the classic ameloblastoma, has
Ameloblastic Fibroma and
lar cell tumor of the jaws’ (White DK94 been termed odontoameloblastoma.
1978). Others suggested: ‘Central granular Other Mixed Odontogenic The revised WHO classification of
cell odontogenic fibroma’ (Vincent SD95 Tumors odontogenic tumor defines ameloblas­
1987) or ‘Central odonto­ genic fibroma, tic fibro-odontoma as “a lesion similar
granular cell variant’ (Shiro BC96 1989). Ameloblastic Fibrodentinoma to ameloblastic fibroma, but showing in­
Ameloblastic fibrodentinoma is de­ ductive changes that lead to formation of
Clinical features fined ‘a neoplasm similar to ameloblas­ dentin and enamel.”
The granular cell ameloblastic fibroma tic fibroma, but also showing inductive The lesion represents approxi­
is most com­mon in woman and occurs changes that lead to the formation of mately 1 to 3 percent of odontogenic
between 50 and 60 years of age. The dentin.’ It is thought that ameloblastic tumors, however, if patients younger
mandible is more commonly involved fibro­­dentinoma is a histologic variant of than 16 years are considered, amelo­
than the maxilla. It is common in molar- ameloblastic fib­ roma in which dentin blastic fibro-odontoma comprises about
pre­molar region and is mostly centrally or dentinoid tissue has formed. In some 7 percent of odontogenic tumors. About
located. cases diagnosed as amelo­blastic fibro­ 80 cases have been reported in the litera­
dentinoma, dentin matrix or dentinoid ture, including a literature review of the
Radiological features tissue is an area of hyalinization around 50 cases published by Slootweg101 (1981).
It presents as a radiolucent lesion, with epithelial compo­nent and some workers
well defined or sometimes irregular bor­ have suggested that such hyalinized zone Clinical features
ders. may not represent a dentin formation. Ameloblastic fibro-odontoma usually
In other cases a hyalinized area is diagnosed in the first two decades
Histopathological features containing entrapped cells has been of life. Philipsen et al. 1997 reported
The ultrastructural findings of granular considered to be an abortive dentin or that the average age in 86 cases was 9
cell ameloblastic fibroma, first reported dentinoid tissue because of its proxi­ years. It has a slight male predilection.
by White et al. 1978, described that their mity to odontogenic epithelium, the Most tumors are found in the posterior
findings indicated the granular cells margins of such zone often shows radi­ mandible, the second most popular
were of connective tissue origin and ally arranged coarse fiber bundles location being the posterior maxilla. It
identical to the cells in the granular cell with elongated cells and rarely found is an exclusively central or intraosseous
myoblastoma. Takeda Y 199997 also tubular structure. It is important to lesion. It usually presents as a painless,
reveals that, the granular cells were of realize that there is no evidence that slow-growing expansile lesion and
mesenchymal origin. The presence of such ameloblastic fibromas with hyali­ often presents with swelling and failure
numerous intracytoplasmic lysosomal nization or abortive dentin exhibit a of tooth eruption. Most ameloblastic
granules and absence of organelles in different biologic behavior than ordi­ fibro-odontomas are associated with an
the granular cells may suggest the cells nary ameloblastic fibroma. unerupted tooth.
Odontogenic Tumors 655

Fig. 28.23: Ameloblastic fibro-odontoma


showing induction of a thin rim of atubular
A B
dentin in the stroma by the ameloblast-like
cells

Radiographic features
Ameloblastic fibro-odontoma presents as
a well-­circumscribed expansile radiolu­
cency that generally contains solitary or
C D E
multiple small radiopaque foci, which rep­
resent the calcified product in the lesion. Figs 28.24A to E: Case of ameloblastic fibroma having recurrence locally and in the neck
• Most lesions are relatively small
when first detected and are not more minimal, the lesion should be removed epithelium embedded in a mature, fi­
than 1 to 2 cm in size. conservatively without removal of the brous stroma (WHO).
• Occasionally, large tumors involving impacted tooth. A case of mandibular
the entire body and ramus of the ameloblastic fibroma which was treated Synonyms
mandible have been reported. earlier by enucleation, and had recur­ Controversy56 exists as to concept and
• Miller et al. (1976) described a case rent tumor in the submadibular re­ definition. At present the term OF is
in which the calcified portion of the gion, extending in the neck is shown in applied to two histological types of le­
lesion alone measured 6 cm × 7 cm, Figs 28.24A to E. The recurrent tumor sions: The epithelium-poor type (formly
causing significant facial deformity. was treated with excision. The tumor was termed simple type) and the epitheli­
perforating through the cortical perfora­ um-rich type (formerly termed complex
Histopathologic features tion in the mandible and thus, has spill­ or WHO type).
The tumor is composed of strands, cords age in the soft tissue and recurrence. It is
and islands of odontogenic epithelium therefore recommended that when the Epidemiology
distributed in a cell-rich, dental papilla­ ameloblastoma or its variants show cor­ • Age: When considering the epithe­
like ectomesenchymal stroma. Varying tical perforation, the dissection should lium—rich type, the age range was
amounts of osteodentin or dentin-like be extended in the soft tissue to take care 11 to 66 years with a mean age of
material and occasionally enamel matrix of the soft tissue extension of the tumor. 40 years.
can be identified. The odontogenic epi­ • Gender: Female predominance of
thelium adjacent to the enamel matrix 2.8:1.
Odontogenic Fibroma
seems to be preameloblast like. More • Localization: There were consider­
calcified lesions exhibit mature dental Odontogenic fibroma has been includ­ ably more cases located in the
hard tissues that resemble rudimentary ed in the classification of odontogenic mandi­ble than in the maxilla, giving a
teeth or a conglomerate of enamel and tumors dating back as early as 1941. maxilla to mandible ratio of 1:6.5. Of
dentin (Fig. 28.23). In WHO classification of odontogenic the mandibular lesions most involved
neoplasm, the odontogenic fibroma were the molar and premolar areas
Treatment and prognosis appears under the subheading mesen­ and out of the maxillary lesions, only
Conservative surgical enucleation is chyme and/or odontogenic ectomes­ the anterior region was affected.
considered to be the treatment of choice enchyme with or without odontogenic
with concurrent removal of the asso­ epithelium. Pathogenesis
ciated unerupted tooth. Extensive le­ Some authors believe the central odon­
sions causing severe undermining of the Definition togenic fibroma to be derived from the
bone require segmental resection of the The odontogenic fibroma (OF) is a rare ectomesenchymal tissue of the peri­
mandible (Figs 28.22A to D). When the neoplasm characterized by varying odontal ligament, dental papilla or den­
hard tissue component in the tumor is amount of inactive looking odontogenic tal follicle. It is the epithelial component
656 Neoplastic Conditions of Head, Neck and Face

of the WHO type of central odontogenic


fibroma and the fact that this tumor
does not occur in an extragnathic loca­
tion that provide the strongest argument
for this tumor being of odontogenic ori­
gin. Gardner102 stated that it is possible
that the WHO type central odontogenic
fibroma arises from the periodontal lig­
ament, while the simple type is derived
from the dental follicle, thus accounting Fig. 28.25: Odontogenic fibroma involving Fig. 28.26: Collagenous cell rich stroma with
for their dissimilar microscopic appear­ anterior mandible numerous strands of odontogenic epithe-
ances. lium without palisading of peripheral cells
The criteria for designating a central the features (stated above) of a desmo­
fibroma as odontogenic are still far plastic fibroma.”
from being defined. It may be difficult,
if not impossible; to decide whether Features
a central fibroma has arisen from the
mesenchyme of the jaws rather than Clinical Features
from the odontogenic apparatus. The The epithelium-rich type presents a
presence of odontogenic epithelium slow growing, progressive but painless
embedded in the tumor tissue may be swelling, often with cortical expansion.
sufficient, because these structures are The tumor is silent when small and
rarely found in the nonodontogenic jaw painless swelling may announce its Fig. 28.27: Calcified material encircles and
lesions. Some authors (WHO, Gardner) presence. A few patients may experience epithelial islands
claim that the absence of odontogenic slight sensitivity. Janssen and Blijdorp104
epithelial remnants does not preclude a in their study reported an associated stance produces a fibromyxoid quality
central fibroma from being odontogenic. palatal depression. Flower et al. found to the background. Scattered remnants
Thus, the histoarchitecture of a that four of five lesions occurring in the of inactive-looking odontogenic epi­
particular central fibroma does not anterior maxilla had a palatal cleft. thelium appear as small irregular is­
prove that the lesion is nonodontogenic lands and cords. Occasionally, variably
unless the following characteristics are Radiographic Features formed calcifications occur (Figs 28.26
found: bundles of abundant collagen • The tumor appears as a unilocular and 28.27).
fibers separated by spindle-shaped radiolucent area with well-defined The epithelium-rich type of central
fibroblasts with elongated or ovoid often-sclerotic borders (Fig. 28.25). odontogenic fibroma is composed of
nuclei103 combined with areas of delicate • Rarely, the occurrence of calcified cellular, fibroblastic connective tissue
collagen fibers aggregating into focal material may produce a mixed radio­ interwoven with less cellular and often
tuft-like bundles and the absence of lucent/radiopaque appear­ance. vascular areas. Islands or strands of in­
odontogenic epithelium and remanants • Larger lesions show scalloping of the active—looking odontogenic epithelium
of calcified material. If the morphologic margins. are an integral component; they may be
pattern occurs in a central fibroma • Many of the cases are locally aggre­ sparse but are often conspicuous. This
that has shown locally aggressive ssive and show external resorption shows foci of calcified material considered
behavior, there is a considerable chance of the roots, displacement of the to be metaplastically produced dysplastic
that the lesion is a non-odontogenic tooth, tooth mobility, mucosal irrit­a­ cementum/osteoid/dentin. A well–de­
desmoplastic fibroma. It is, however tion and displace­ment of the inferior fined capsule is rare. Subvariants of both
possible that a central desmoplastic alveolar canal. histological types of central odontogenic
fibroma may infiltrate or expand into • Some tumors are associated with the fibroma have been described.105,106
an unerupted tooth and in doing so be crown of an unerupted tooth.
intimately associated with its crown. Histogenesis
This situation should not be considered Histopathology It has been suggested that the epithe­
evidence of odontogenic origin, but The epithelium–poor type of central lium poor type of central odonto­genic
must be regarded as coincidental. odontogenic fibroma is a noninfiltrat­ fibroma is derived from the dental fol­
Thus, the idea put forward by Gard­ ing connective tissue lesion resembling licle whereas the epithelium rich type
ner and supported by Slootweg and a dental follicle. It is minimally cellular arises from the periodontal ligament.
Muller that “every jaw fibroma is odon­ with dispersed delicate collagen fibers. Existence of two types of central odon­
togenic if it does not clearly demon­strate A considerable amount of ground sub­ togenic fibroma has been challenged.
Odontogenic Tumors 657

Treatment and Prognosis et al. 61 percent of the patients had a


Treatment for central odontogenic fibro­ history of pain. Of 15 cases of benign
mas, irrespective of type, is enucleation cementoblastomas reported by Jelic
by vigorous curettage. Long-term follow- et al.111 9 were symptomatic and pa­
up of a large series is not available, but tients complained of pain. The type of
the recurrence rate is considered low. pain is usually characterized as a tooth
ache arising in the pulp.
Benign
Radiographic Features
Cementoblastoma Radiographically, benign cementoblas­
Benign cementoblastoma (BC) or true tomas have a characteristic, almost
cementoma was first described by Nor­ patho­gno­monic appearance. The tumor
berg in 1930.107 It is a rare benign odon­ is well-defined and is mainly of a radi­
togenic tumor of the ecto­mesenchymal opaque or mixed-density, surro­unded
origin. It is considered to be the only by a thin radiolucent zone. Root resorp­
true neoplasm of the cem­ental origin tion, loss of root outline and obliteration
and is characterized by pro­liferation of of the periodontal ligament space are Fig. 28.29: Macroscopic view of the surgical
specimen. The lesion is large and extends up
the cellular cementum. common findings (Fig. 28.28).
to the cemento-enamel junction of the tooth
Definition Macroscopy Features
A cementoblastoma is characterized by The tumor consists of a rounded or
the formation of cementum-like tissue nodular mass attached to one or more
in connection with the root of a tooth tooth roots and is surrounded by a
(WHO). gray-to-tan layer of irregular soft tissue
(Fig. 28.29).
Epidemiology
A cementoblastoma occurs from the Histopathology
age of 8 to 44 years of age, the mean age A cementoblastoma consists of dense
being approximately 20 years.108 There is masses of acellular cementum-like mat­
no distinct gender preference. The male: erial in a fibrous, sometimes rather vas­
female ratio was 1:1.2.109 cular stroma containing multinu­clea­ted Fig. 28.30: Cementoblastoma. The root
cells (Fig. 28.30). The tumor mass blends surface is largely destroyed by the cementum-
Localization with the root of a tooth with simultane­ like tissue, while the pulpal tissue of the tooth
The majority of cementoblastomas are ous root resorp­tion. In the more mature still remained vital
located in the mandible, particularly re­ parts of the tumor, basophilic reversal
lated to the permanent first molar; associ­ lines may produce a paget disease-like
ation with a primary tooth is exceptional. pattern. At the periphery, sheets of un­
mineralized tissue may be seen, often be­
Features ing arranged in a radiating column. The
differential diagnosis includes osteoblas­
Clinical Features toma, the only distinctive criterion being
The most common finding is a pain­ the true connection with the surface of
ful swelling at the buccal and lingual/ root of a tooth in case of a cementoblas­
palatal aspect of the alveolar ridges. toma.112 An important differential diag­
The vitality of the involved tooth rem­ nosis is osteo­ sa­rcoma. Without radio­
ains intact. Lower–lip paresthesia or graphs it is difficult to properly diagnose
a pathologic fracture of the mandi­ble a cement­oblastoma. The diagnosis can­
is rarely reported. The benign cemen­ not be made on the biopsy alone.
toblastoma, intimately associated with
a tooth root, generally presents as a
Treatment and Recurrence
slow-growing, unilateral swelling with Rate
the expansion of the affected bone. The recommended treatment of choice
Ulmansky et al.110 recorded swelling and Fig. 28.28: Periapical dental radiograph is early surgical removal due to the
expansion in 70 percent of their cases. showing benign cementoblastoma at the cementoblastomic capabilities for per­
In the survey published by Ulmansky apex of the root of the mandibular canine sistent growth, expansion and involve­
658 Neoplastic Conditions of Head, Neck and Face

ment of the adjacent structures. The tis­­s­ue or as a direct myxo­matous change Features
growth rate has been estimated to be of fibrous tissue in an odontogenic
0.5 cm per year. The tumor is readily fib­r­oma. Clinical Features
enucleated and does not recur. ‘Recur­ Goldblatt’s119 ultrastructural study of Kaffe et al.126 reviewed 164 odontogenic
rence’ is usually the result of incomplete a maxillary myxoma could not verify an myxomas of the jaws and found that
removal. The affected tooth has been odontogenic origin from primitive non- 75 percent occurred between the sec­
removed with the tumor in almost all odontogenic mesenchymal rests. ond and fourth decades (patient age
the reported cases. Slootweg et al.120 concluded from range, 1–73 years; mean 30 years). Seven
their biochemical study on a mandibular percent of the patients were in the first
Myxoma (Odontogenic myxoma that the myxoma matrix differs decade of life. The female to male ratio
from the matrix in dental pulp and was 1.5:1. There were 109 (66%) neo­
Myxoma, Fibromyxoma) perio­d­ontal ligament. plasms in the mandible and 55 (34%)
The uncertainty that the myxoma is in the maxilla. Myxomas can occur any­
Introduction strictly an odontogenic lesion is sustai­ where in the jaws, but have a predilection
The myxoma (fibromyxoma), which is ned by its origin in extragnathic loca­ for the molar and premolar regions of
a benign neoplasm of uncertain histo­ tions and non-tooth bearing area of the the mandible and maxilla. The odonto­
genesis with characteristic histologic jaws. This tumor occurs in sites separate genic myxoma causes cortical expansion
appearance, often behaves in a locally from the odontogenic area, includ­ ing and perforation (Figs 28.31A and B). The
aggressive, infiltrating fashion.113 the sinonasal tract, facial bones, extra­ maxillary myxomas often extend into the
In the head and neck, two forms of cranial skeleton, upper ramus and con­ sinus. Small odontogenic myxomas are
myxomas or fibromyxomas are recog­ dyle of the mandible.121-123 asymptomatic. Large odo­ntogenic myx­
nized: One is derived from the facial Sinonasal myxomas probably arise omas cause painless expansion. Unilat­
skeleton other is derived from the soft from or within bone and the anterior ma­ eral sinonasal obliter­ation may mimic
tissue. The WHO defines myxoma (odo­ x­il­ lary sinus wall is a frequent loc­ation.124 nasal polyposis.
n­­togenic myxoma, myxofibroma) as a Subclassifying myxomas that are The central myxomas are not seen in
locally invasive neoplasm consisting of derived from facial skeleton into: other bones except the jaw bones. The
rounded and angular cells that lie in an • Odontogenic myxoma tumor is infilterative and has tendency
abundant mucoid stroma. • True osteogenic myxomas may bet­ to recur after surgical enucleation.
In the WHO classification of odonto­ ter define their histogenesis.125
genic neoplasms, myxoma appears un­
der the subheading ‘odontogenic ecto­
mesenchyme with or without included
odontogenic epithelium’.114
Myxoma is of odontogenic origin
that has been perpetuated by its:
• Almost exclusive occurrence in the
tooth bearing areas of the jaws
• Frequent occurrence in young indi­
viduals
• Common association with an un­
erupted tooth or a developmentally A B
absent tooth
• Histologic resemblance to dental
mesenchyme, especially the dental
papilla
• Occasional presence of sparse amo­
unts of odontogenic epithe­lium.115-118
The neoplasms odontogenic deri­
vat­ion is believed to originate from the
primitive mesenchymal portion of the C D
deve­loping tooth germ (dental follicle, Figs 28.31A to D: Odontogenic myxoma of mandible: (A and B) Expansion of the bone
dental papilla and periodontal ligament) due to the tumor; (C) Tennis racket appearance on the X-ray; (D) Tennis racket type bony
as an inductive effect of nests of odonto­ trabaculae present on the inner side of the buccal cortical plate that produce typical
genic epithelium on mesenchymal ‘tennis racket’ appearance on X-ray
Odontogenic Tumors 659

jaws including excision, enucleation and


curettage, curettage with and without
electrical or chemical cautery, en-block
resection and wide resection with and
without immediate grafting. A recur­
rence rate of 43 percent in myxomas that
were treated initially by curettage or lo­
cal surgical exicision was documented in
the series reported by Lo Muzio et al.129
A B
Several authors have em­ phasized that
Figs 28.32A and B: Typical tennis racket appearance of odontogenic myxoma on X-ray:
the rate of recurrence is generally higher
(A) Posterior mandible; (B) Anterior maxilla in 14 years old female
with conservatively treated myxomas
within the first 2 years of treatment. How­
Radiographic Features ever, recurrence have occurred several to
many years after the surgery, so follow-
Periapical dental radiographs and pan­ up should be indefinite.
oramic radiographs are often the first
indicators of myxomas of jaw. The radio­
Odontoma
graphic features of the odontogenic
myxoma are variable, ranging from ‘Broca’ first coined the term ‘odontome’
small unilocular lesions to large multi­ in 1866. He defined it as a tumor formed
locular neoplasms, which often displace by an overgrowth of complete dental tis­
teeth or less frequently, resorb roots.117 sue.130
The multilocular trabecular pattern has In the landmark paper Thoma and
Fig. 28.33: Odontogenic myxoma, high
been described as ‘honey comb’, ‘soap power view of randomly arranged spindle- Goldman131 narrowed the term “odon­
bubble’, ‘tennis racket’, ‘wispy’ and shaped, stellate and rounded cells in a toma” to include tumors that were
‘spiderweb’ in appearance (Figs 28.31C loose myxoid stroma com­­­posed of well-differentiated tooth
and D, Fig. 28.32A). struc­ture. Shafer and Gorlin defined
eosinophilic cytoplasm in a mucoid rich, odon­­toma as a tumor that has devel­
intercellular matrix, although some de­ oped and differentiated enough to pro­
Odontogenic Myxoma of the gree of mild nuclear pleomorphism or duce enamel and dentin.132,133
Anterior Maxilla hyperchromatism may exist, including The second edition of the WHO his­
Most multilocular myxomas are greater an occasional mitosis or binucleate cell, tologic typing of odontogenic tumors
than 4 cm; unilocular myxomas tend to there which has no correlation with re­ classifies odontomas under the broad
be smaller (Fig. 28.32B). Only 5 percent currence of the neoplasm (Fig. 28.33).127 category of tumors containing odonto­
of myxomas are associated with uneru­ genic epithelium with odontogenic ec­
pted teeth.126 Kaffe et al. found that 12.5 Treatment and Prognosis tomesenchyme, with or without dental
percent of myxomas were mixed radio­ In Barkers review of literature, the over­ hard tissue formation.
lucent and radiopaque and 7.5 percent all recurrence for myxomas ranged from Under this classification, three types
were radiopaque. 10 to 33 percent. These high recurrence of odontomas are listed:
rates can be attributed to the subtal local 1. Odontoameloblastoma
Gross Pathology invasion of the neoplasm between the 2. Complex odontoma and
The myxoma is usually a well-deline­ated, cancellous bone, beyond radiographical 3. Compound odontoma.
unencapsulated gray-white to tan-yellow visible margins and lack of incapsula­ The odontomas have become to be
mass that can be rubbery soft or gelatani­ tion.128 The production of mucoid ground known as mixed odontogenic tumors be­
ous (slimy) in texture. The margins are substance is believed to be the cause for cause they are composed of both epithe­
usually ill defined in gelatinous speci­ its growth, because enhanced mitotic lial and ectomesenchymal components.
mens. On the cut surface, it is typically activity and high proliferation rates are Both the epithelial and the ectomesen­
glistening, translu­cent and homogeneous. absent. This recurrence rate differences chymal tissues and their respective cells
were related to the method of treatment. may appear normal morphologically,
Histopathology The standard treatment for myxomas is but they seem to have a deficit in struc­
Histologically, the myxoma is bland in ap­ surgical exision. Radiation therapy and tural arrangement. This deficit has led to
pearance and is composed of loosely ar­ chemotherapy are inactive treatments. the opinion that odontomas are hamar­
ranged, evenly dispersed spindle-shaped, A number of surgical methods have been tomatous lesions or malformations rath­
rounded and stellate cells with a lightly advocated for routine myxomas of the er than true neoplasms.
660 Neoplastic Conditions of Head, Neck and Face

Odontoma, Compound Type odontomas develop from the ameloblas­ be made on the basis of macroscopic
Definition (WHO): A tumor-like malfor­ tic fibroma if the later is left untreated is examination.
mation (hamartoma) with varying num­ questionable but still a matter of debate. • Histopathology:
bers of tooth–like elements (odontoids). The compound odon­toma is more dif­ – Histopathological findings: Due
Synonym: Compound composite ferentiated and its pathogenesis is more to a higher degree of morpho­
od­on­­toma. closely related to the creation of supernu­ differentiation than that of com­
merary teeth, especially mesiodens. plex odontoma, compound odo­
Epidemiological Data ntomas are easily recognizable
• Prevalence, incidence and rela­tive Features even macroscopically. Com­
frequency: The compound odon­ pound odontomas are usually
toma is the most common lesion/ Clinical Features small, but large lesions contain­
malformation of odontogenic origin. These are painless, slowly growing les­ ing up to 100 denticles have been
Its relative frequency varies between ions. When fully matured, develop­ment reported. Denticles are com­
4.2 and 73.8 percent. Sato et al.134 ceases. The size usually varies between posed of enamel, dentin, cemen­
recorded odontomas in 47 percent 1 and 2 cm in diameter, but a diameter tum and pulp tissues with a more
of Japanese patients with benign of up to 6 cm has been reported. Swell­ or less regular arrangement.
odontogenic tumors. ing of the jaw is seen in less than 10 per­ Morphodifferentiation and histo­
• Age: Based on the data of the odon­ cent of the cases. Many are located differentiation of the dental hard
toma survey by Philipson et al.135 the close to the incisal/occlusal part of an tissues in compound odon­tomas
mean age at the time of diagnosis impacted tooth, thus impeding erup­ has been studied in detail by Pi­
was 17.2 years; 74.3 percent of the tion. Displacement of erupted teeth is atelli and Trishi.138 Three percent
cases were diagnosed before the age seen in some cases. Some occur in a site of the odontomas may contain
of 20 years with a marked peak in where the permanent tooth is missing. ghost cells (Fig. 28.35).139
the second decade of life. The com­ Multiple compound odontomas have – Histochemical/immunohisto­
pound odontoma is clearly a lesion been reported and they may be part of chemistrical findings: Along
of childhood and adolescence. Gardner syndrome. Peripheral lesions with the other odontogenic tu­
• Gender: The male: female ratio developing entirely within the gingival mors, Gao et al.140 studied com­
varies between 1.2:1 and 1:1 accor­ soft tissues are rare. pound odontomas using im­
ding to the odontoma survey of munohistochemistry. The aim
Phillipson et al.135 Radiographic Features of their study was to describe
• Localization: Compound odonto­ Radiographically, the compound odon­ the expression and distribution
mas may occur in any tooth bearing tomas appear as a collection of tooth-like of the bone morphologic pro­
area of the jaws. The anterior maxilla structures surrounded by a radiolucent teins (BMPs) in odontogenic
is most frequently affected. zone. Adjacent teeth may be displaced but tumors. BMPs, members of the
are never resorbed (Figs 28.34A and B). transforming growth factor-beta
Etiology (TGF-β) superfamily, play a role
The etiology is unknown. Several theo­ Pathology not only in the bone formation,
ries have been proposed, including • Macroscopy: The specimen consists but also in the epitheliomesen­
trauma and infection. It seems that of a number of teeth-like structures chymal interations, tumors and
these conditions are more likely to result enclosed in a fibrous capsule, which lesions of epithelial and/or ec­
in a hypoplastic tooth germ rather than is thin if the lesion has matured. In tomesenchymal origin, includ­
an odontoma. most cases, the final diagnosis can ing the compound odontoma
Lopez-Areal136 documented a case in
which a child developed multiple odon­
tomas after experiencing trauma with
intrusion of the incisor teeth at the age
of 10 months.
Hitchin137 has postulated that odon­
tomas are inherited or developed as a
result of a genetic mutation.

Pathogenesis
As with the complex odontoma, the
compound odontoma is of odonto­genic A B
origin. The theory that the com­pound Figs 28.34A and B: Complex compound odontomas involving the posterior mandible
Odontogenic Tumors 661

Clinical Features
Complex odontomas are painless slowly
growing lesions. The growth stops when
they are fully matured some reaching upto
6 cm in diameter, the majority measures
less than 3 cm. Mild swelling of the jaw
may be evident. But, when they become
large, produces expansion of the bone
and facial symmetry.143 The adjacent teeth
Fig. 28.35: Compound odontoma with may be displaced and impaction of a per­
tooth like structures composed of dentin manent tooth is a common finding.
and enamel matrix supported by dense Fig. 28.36: Complex odontoma
fibrous connective tissue Pathogenesis
The odontogenic origin of the complex
demonstrated positive reactions odontoma has never been questioned.
while epithelial odontogenic tu­ It is considered a self-limiting devel­
mors were negative. opmental anomaly or hamartomatous
malformation, characterized by non-de­
Complex Odontoma script masses of dental tissues. Recently,
Definition: Odontoma, complex type it has been suggested that odontomas
(OC) is a tumor-like malformation (ham­ tend to incease in size with the age of the
artoma) in which enamel and dentin and patient suggesting conti­nous growth.144
sometimes cementum is present (WHO). Several factors may cause anoma­
Synonym: Complex composite odon­ lous tissue development in odontomas.
toma. These include unsuccessful or an alte­ Fig. 28.37: Odontoma, complex type with
red ectomesenchymal interaction in a dense radiopacity and retained molar
Epidemiology the earliest phase of dental germ deve­
Complex odontomas are one of the most lopment and/or alterations in the sub­
common odontogenic tumors. These sequent phases of the development of hollow circular or oval structures with
are primarily diagnosed in children, these tissues. It has also been assumed empty spaces from decalcified mature
adolescents and young adults. Based on that alterations in the mineralization enamel, enamel matrix producing epi­
137 cases from the odontoma survey the mechanisms with modifications of the thelium and connective tissue. The struc­
mean age at the time of diagnosis was 19.9 mineral component in the enamel may ture of hard dental tissue may vary. The
years141 (range 2 to 74 years). About 83.9 lead to incomplete maturation.145 lesion consists mainly of wavy and plicat­
percent of cases occurred before the age ed walls of tubular or dysplastic dentin
of 30 with a peak in the 2nd decade of life. Radiographic Features covered by enamel. Between these walls
The male:female ratio varies from 1.5:1 to Complex odontomas appear as a sphe­ are irregular curvilinear clefts that con­
1.6:6 to 0.8:1 according to different studies. rical or ovoid radiopacity with a fine tain enamel matrix producing epithe­
radiating periphery, surrounded by a lium and connective tissue. Cementum
Etiology radiolucent zone, which may be broader is scarce except on the ‘root’ surfaces of
The etiology is unknown. Several the­ in a developing complex odontoma tooth—like structures. Scattered ghost
ories142 have been proposed including (Figs 28.34, 28.36 and 28.37). cells may be present (Fig. 28.38).
local trauma, infection, family history The distinction between complex
and genetic mutation. It has also been Histopathology and compound odontoma is mainly
suggested that odontomas are inherited In mature complex odontomas, the soft based on the presence of tooth-like
from a mutant gene or interference, tissue capsule consists of a loose connec­ structures in compound odontomas.
possibly postnataly with the genetic tive tissue containing strands or islands The differential diagnosis between a
control of tooth development. of odontogenic epithelium. In develop­ developing complex odontomas and an
ing complex odontomes, the outer part of ameloblastic fibro-odontoma is some­
Localization the odontoma consists of a cell rich zone times impossible.
Complex odontomas occur in tooth of soft tissue with formation of enamel In 1946, Thoma and Goldman146 first
bearing regions, mostly in the posterior and dentin, not resembling tooth mor­ described ghost cells in complex odon­
part of the mandible and the second phology. The lesion appears as a mass of tomas, but Levy147 often is given credit for
most common site is the anterior maxilla. primarily tubular dentin, which encloses extensively studying this phenomenon.
662 Neoplastic Conditions of Head, Neck and Face

29 cases referred to the DOSAK bone and Zussmann and 1:3 in the four
tumor register. cases reported by Wachter et al.152
According to the 1992 WHO criteria, • Localization: The majority of cases
4 cases of OAs and 14 AFOs were classi­ located in the posterior mandible
fied. Kaugars and Zussmann152 described region.
a case of odontoameloblastoma in 1991
and critically reviewed the English Pathogenesis
literature of reported cases, bringing the The OA is clearly of odontogenic origin;
total to 12. All these studies highlight the however, its relationship to other odonto­
rare occurrence of this tumor. genic tumors—the amelobla­ stoma on
Definition: Odontoameloblastoma (OA) the one hand and the odontomas on the
Fig. 28.38: Odontoma, complex type. combines features of ameloblas­ toma other—is not well understood.
Enamel, dentin and cementum-like tissue with those of an odontoma (WHO).
are arranged in a haphazard pattern, in Synonyms: Ameloblastic odontoma, Features
contrast to the regular structures encoun­
Odontoblastomas and adamanto–odo­
tered in compound odontoma Clinical features
ntoma. Soft and calcified odontoma,
Calci­fied mixed odontogenic tumor. Presenting signs may include bone
Treatment and Prognosis expansion (Fig. 28.39A), root resorption,
Conservative surgical excision is the Epidemiology tooth displa­ce­­ment and occasional
treatment of choice for odontomas, be­ • Prevalence, incidence and relative pain, changes in occlusion and delayed
cause such treatment results in little to frequency: Odontoameloblastoma eruption of teeth.
no chance of recurrence. There have appear to be extremely rare and fig­
been noble approaches to the removal ures on incidence, prevalence or Radiographic features
odontomas. In the study of large man­ relative frequency are available. The Odontoameloblastoma appears as a well-
dibular odontomas, Blender et al. de­ situation is complicated even further defined unilocular or multilocular radio­
scribed a lingual approach to the re­ by the fact that a number of cases lucent lesion in which varying amounts
moval of these large lesions. Because the published under the names am­ of radiopaque material may be identified
lingual cortex is thinner than the buccal, eloblastic odon­toma or odontoam­ (Fig. 28.39B). Most cases are associated
it is logical that this approach should be eloblastoma do not meet the strict with displaced unerupted teeth.
considered to avoid unwanted mandib­ histologic criteria of the lesion and
ular fractures. represent instead examples of the Macroscopy
Kamakura et al.148 described an ameloblastic fibro-odotoma. Most odontoameloblastoma are unen­
interesting treatment approach to a large • Age: The mean age is 18.8 years capsulated. On the cut section, the lesion
compound dontoma. The lesion caused (range 3–50 years). has a multinodular architecture with soft
intrusion of the maxillary central and • Gender: The male : female ratio 2:1 and hard tissue components. The amount
lateral incisor teeth. They were able to in the cases reviewed by Kaugars of mineralized tissue may appear as large
remove odontoma and with combined
orthodontic and surgical therapy, bring
the incisor teeth into the proper occlusion.

Odontoameloblastoma
Thoma149 introduced the term odonto­
ameloblastoma (OA) in 1944. It was
considered by some to be yet another
member of the odontoma group, together
with the ameloblastic fibro-odontoma
(AFO), until Hooker150 showed that they
are two separate tumors with different
clinical behavior, though previously
grouped together under the term amelo­
b­l­astic odontoma.
Wächter et al.151 made a critical
attempt to differentiate between the
od­o­n­to­ameloblastoma and the AFO A B
by means of histologic criteria from Figs 28.39A and B: Odontoameloblastoma involving mandible in a 45-year-old male
Odontogenic Tumors 663

due to its biological behavior of low-


grade, well-differenti­
ated, low-grade
car­cinoma.

Management
The metastatic ameloblastoma are pri­
marily managed by surgery. However,
the survival rate does not improve. The
cervical lymph node metastasis is man­
aged by appropriate neck dis­ section.
Fig. 28.40: Nodular masses of odontogenic Fig. 28.41: Area of plexiform ameloblas­ The pulmonary metastasis is managed
mesenchyme adjacent to a proliferating toma adjacent to a nodule of odontogenic by lobectomy, if adequate pulmonary
epithelium that exhibits a plexiform amelo­ mesenchyme
function can be preserved postopera­
blastoma pattern
tively. The chemotherapy is usually inef­
fective but, shows early short-term relief.
lobulated masses or as rudimentary teeth a true neoplasm. They recommended the
scattered within the soft tissues. performance of regular follow-up in order Ameloblastic Carcinoma
to detect ‘recurrences’ early. Ameloblastic carcinoma represents ma­
Histopathology lignant epithelial proliferation associated
The epithelial component consists of is­ MALIGNANT with the ameloblastoma (carcinoma ex-
lands and cords of odontogenic epithe­ ameloblastoma) or histologically resem­
lium demonstrating follicular and plexi­
ODONTOGENIC TUMORS bles the ameloblastoma (de novo am­
form patterns, typical of ameloblastoma. eloblastic carcinoma). The pronounced
In addition to the fibrous stroma, this Metastasizing Ameloblastoma cytologic atypia and mitotic activity is de­
tumor shows a variable amount of cellu­ Traditionally, the ameloblastoma is monstrable in ameloblastic carcinoma.
lar myxoid tissue adjacent to the epithe­ regarded as a benign, locally aggressive Some tumors show basilar hyperplasia
lium, where mineralized dental tissues tumor and does not metastasize, occ­ and increased mitotic activity and are
are formed as in odontomas. Isolated asionally it can metastasize and could designated as atypical ameloblastoma or
small foci of ghost cells may occasion­ be fatal. This triggers the thinking that proliferative ameloblastoma, but these
ally be found (Figs 28.40 and 28.41). ameloblastoma could be a low grade findings are not adequate to diagnose the
malignant tumor. The term metastatic ameloblastic carcinoma. The presence of
Treatment and Recurrence Rate a­meloblastoma is used to describe the the criteria-like nuclear pleomorphism,
Since the OA has been considered an metastatic tumor that shows histologic perineural invasion and other histologic
aggressive lesion, most authors recom­ features of classic ameloblastoma of jaw. evidence of malignancy are needed to
mend a radical treatment as applied diagnose the ameloblastic carcinoma.
for ameloblastomas. In the series Clinical Features The ameloblastic carcinoma is locally
reviewed by Kaugars and Zussman, The primary ameloblastoma arises in invasive and metastasizes to the cervical
three recurrences were noted, including the mandible of a young adult and af­ lymph nodes, lungs and long bones. It is
one case in which the OA recurred ter the mean latency of 10 to 11 years managed on similar lines that for squa­
twice. Wachter et al. did not record any metastatic nodules develop in the lung mous cell carcinoma.
recurrences among their cases. (80%), cervical lymph nodes (15%) and
Kaugars and Zussmann discussed other extragnathic bones. The pulmo­
the similarity of OAs with both amelo­ nary nodules are typically bilateral and
Primary Intraosseous
blastomas and odontomas. While the lo­ multifocal. The mean survival rate after Carcinoma
cation, expansion and recurrence rate ap­ detection of the pulmonary metastasis The primary intraosseous carcinoma
pear to be similar to those of the SMA, the is two years. The pulmonary nodules (PIOC) is the central jaw bone carci­
age at the time of diagnosis is more com­ present as innocuous lung granulomas noma. It is called primary because it is
parable to that of complex odontoma. on routine radiographs. The pulmonary not the metastatic secondary deposit
Wachter et al. considered the OA and the metastasis is thought to be due to ag­ from other sites and to call it as a primary
ameloblastic fibro-odontoma to be one gressive primary tumor or due to tumor intraosseous carcinoma, the metastasis
entity because of similar biologic behavior embolization in the lymphatics or blood from distant primary to the jaw bones
and prognosis. Also, they considered the vessels during the surgery. The meta­ must be ruled out. Similarly, its origin
OA (and ameloblastic fibro-odontoma) to static ameloblastomas are ambiguously from the oral squamous epithelium and
be more of a hamartomatous lesion than termed as malignant ameloblastoma the sinonasal linings must be ruled out.
664 Neoplastic Conditions of Head, Neck and Face

The PIOC produces diffuse enlarge­ Occasionally, they are associated grade ameloblastic carcinoma and has
ment of the jaw. In the presence of with impacted canines. The mean no significant potential to metastasize. It
mucosal ulceration the diagnosis of PIOC age of occurrence is 59 years with is treated with wide surgical excision and
is doubtful. Similarly, once the tumor distinct male predominance. The postoperative radiotherapy. Chemo­
fungates through the bone to involve lesion may become destructive. The therapy may be chosen for exten­ sive
overlying soft tissue then the diagnosis of lesion is treated by surgery. non-resectable tumors.
PIOC is often difficult to make. • Carcinoma exodontogenic kera­
The origin of the PIOC is thought tocyst: The PIOC is reported to de­ Clear Cell Odontogenic
to be secondary to remnants of the velop from the lining of the OKC by Carcinoma
odontogenic epithelium or from the Mokwasi et al. (2001). The clear cell odontogenic carcinoma
incisive canal epithelium. Few varieties • Central mucoepidermoid carci­ is a low-grade carcinoma characterized
of PIOC have been described: noma: It is also called cystic PIOC by presence of uniform cells with clear
• Solid primary intraosseous car­ and supposed to develop from the cytoplasm. Ninety percent tumors are
cinoma: It is rare tumor which lining of a cyst or the remnants of reported in the mandible and have a fe­
presents a painful swelling in the the odontogenic epithelium. The male predilection. The radiological pic­
posterior mandible. The mean age central mucoepidermoid carci­ ture is variable ranging from unilocular
of occurrence is 52 years. The pa­ noma arises from the sequestrated radiolucency with indistinct borders to
tient presents with the complaints salivary gland tissue during the multiloculated lesions having well-cir­
of pain, swelling and paresthesia in development. They are low-grade cumscribed borders.
the distribution of the inferior alveo­ malignancies and demonstrate The tumor has high recurrence rate
lar nerve. The radiological picture well-circumscribed uniloculated or (48%) after resection. It is refractory
is cup-shaped radiolucent lesion multilocuted radiolucent lesions. to curettage. About 20 percent tumors
(42%), irregular moth eaten radiolu­ The high-grade lesions show de­ show cervical lymph node metastasis
cency (26%) and well-circumscribed structive pattern and have meta­ and 17 percent show pulmonary metas­
radiolucent lesion (10%). The inci­ static potential. The prognosis in tasis. The mortality rate is 20 percent in
dence of cervical lymph node me­ low-grade lesions have fair progno­ extensive extraosseous tumors postop­
tastasis is reported to be 31 percent. sis. The death is usually due to un­ erative radiotherapy may be useful.
The lesion is treated with surgical controlled local growth rather than
excision, neck dissection and post­ the metastatic disease. Ameloblastic Fibrosarcoma
operative radiotherapy. The overall A variety of treatment modalities (Odontogenic Sarcoma,
5 year survival rate is 38 percent. have been used which comprise of cu­
• Cystic primary intraosseous carci­ rettage, segmental resection, hemiman­
Ameloblastic Sarcoma)
noma: The cystic PIOC (PIOC ex- dibulectomy. The ameloblastic fibrosarcoma is a
odontogenic cyst) is a squamous malignant connective tissue of odon­
cell carcinoma that demonstrates togenic origin that contains benign
a cystic component with a lumen Ghost Cell Odontogenic odontogenic epithelium similar to
that contains keratin of fluid and the Carcinoma that of the ameloblastic fibroma. The
lining that shows dysplasia. If the Ghost cell odontogenic carcinoma is tumor commonly (80%) occurs in the
cystic lining does not demonstrate considered as a variant of malignant mandibular posterior region and has a
the atypia, then the possibility of ameloblastoma and shows evidence of male predilection. The clinical presen­
gingival carcinoma eroding the ghost cell keratinization. The ghost cells tation is an expansile lesion showing a
bone and colliding with the cystic are immunoreactive to amelogenin, a radiolucency with indistinct margins.
lining or the development of the protein that is unique to enamel matrix The lesion may be unilocular or mul­
carcinoma adjacent to the cyst can be and therefore represent evidence of tilocular and may be associated with
considered. These tumors may mimic ameloblastic differentiation. The ghost an impacted molar. The tumor extends
odontogenic cysts radiologically. cell odontogenic carcinoma is more to the adjoining soft tissue. The tumor
• Carcinoma ex-dentigerous cyst: commonly seen in the maxilla and originates in a pre-existing ameloblas­
The most common odontogenic has male predilection. The mean age tic fibroma in 35 percent cases. The
cyst undergoing transformation into of presentation being 38 years (range mean age of occurrence is 33 years but,
the PIOC is dentigerous cyst. It of­ 13–72 years). Radio­logical picture is not the de novo ameloblastic fibrosarcoma
ten presents as an asymptomatic or characteristic, but may show multilo­ at a younger age (Average 28 years).
painful radiolucent lesion surround­ culated to poorly delineated radioluscent The reported recurrence rate is approx­
ing the crown of an impacted/un­ lesions. The tumor is locally aggressive imately 37 to 40 percent after surgical
erupted mandibular third molar. and behaves like amelo­blastoma or low- excision and 20 percent patients die of
Odontogenic Tumors 665

the disesase within 5 years of diagnosis. Cysts and Ameloblastoma. Dental Cos­ 28. Mintz S, Anavi Y, Sabes WR. Peripheral
The mortality is not due to the meta­ mos. 1934;74:1173. ameloblastoma of the gingiva. A case
static disease, but due to the locally 13. Reichart PA, Philipsen HP, Sonner S. report. Journal of Periodontology.
aggressive tumor. The tumor is treated Ameloblastoma: biological profile of 1999;61:649–52.
with wide local excision and postopera­ 3677 cases. Eur J Cancer B Oral Oncol. 29. Robert S Redman. Peripheral amelo­
tive radiotherapy. Neck dissections are 1995;31B(2):86-99 blastoma with unusual mitotic activ­
not recommended as the tumor is not 14. Neville BW, Damm DD, Allen CM, ity and conflicting evidence regarding
known to metastasize. Bouquot JE. Oral and maxillofacial histogenesis. JOMS. 1994: 52(2):192-7.
pathology. 2nd edn. Philadelphia: WB 30. Moskow BS, Baden E. The peripheral
Saunders; 2002.pp.611-9. ameloblastoma of the gingiva: case re­
15. Joseph BK, Savage NW. Maxillary ame­ port and literature review. J Periodon­
References loblastoma—case report and review of tol. 1982;53:736–42.
the literature. Aust Dent J. 1992;37:98. 31. Kaneko Y, Ueno S. Peripheral amelobl­
1. Sawyer DR, Mosadomi A, Page DG, et al. 16. Small IA, Waldron CA. Ameloblastoma as­toma resembling a papilloma:
Racial predilection of ameloblastoma? of the jaws. Oral Surg. 1955;8:281. report of ca­se. J Oral Maxillofac Surg.
A probable answer from Lagos (Nigeria) 17. Schafer DR, Thompson LDR, Smith BC, 1986;44:737-9.
and Richmond. J Oral Med. 1985;40(1): Weing BM. Primary ameloblastoma of 32. Horowitz I, Hirshberg A, Dayan D,
27-31. the sinonasal tract: a clinicopathologic Peripheral ameloblastoma. A clinical
2. Assael LA. Surgical management of study 24 cases. Cancer. 1998;82(4): dilemma in gingival lesions. J Clin
odontogenic cysts and tumors. Princi­ 667-74. Periodontol. 1987;14:366-9.
ples of Oral and Maxillofacial Surgery. 18. Kessler HP, Schwartz-Dabney C, 33. Gurol M, Burkes EJ Jr. Peripheral am­
Philadelphia: Lippincott; 1992. pp. 692- Ellis III E. Reccurent left mandibular eloblastoma, J Periodontol. 1995;66:
711. enlargement. J Contemp Dent Pract. 1065-8.
3. Broca P. Gaz Leb de Med et de Chir 2003;3(4):127-37. 34. Buchner A, Sciuba J. Peripheral epi­
(Paris). 1868;5:19,70,113. 19. Infante-Cossio P, Hernandez-Guisado thelial odontogenic tumors: A review.
4. Malassez L. Archives de Physiologie JM, Fernandez-Machin P, Garcia-Perla Oral Surg Oral Med Oral Pathol. 1987;
Normale et Pathologique [in French] A, Rollon-Mayordomo A, Gutierrez- 63(7):688-97.
1885;6:379. Perez JL. Ameloblastic carcinoma of 35. Gardner DG. Some current concepts
5. Bland-Sutton JB. Odontomes. Trans the maxilla: a report of 3 cases. J Cra­ on the pathology of ameloblastomas.
Odontol Soc Great. Brit. 1888;20:32-87. niomaxillofac Surg. 1998;26(3):159-62. Oral Surg Oral Med Oral Pathol Oral
6. Thoma KH, Goldman HM. Odonto­ 20. Philipsen HP, Reichart PA. Unicystic Radiol Endod. 1996;82(6):660-9.
genic tumors: Classification based ameloblastoma: a review of 193 cases 36. Philipsen HP, Reichart PA, Nikai H,
on observations of epithelial, mesen­ from the literature. Oral Oncol. 1998: Takata T, Kudo Y. Peripheral amelo­
chymal and mixed varieties. Amer J 34(5): 317-25. blastoma: biological profile based on
Pathol. 1946;28:433. 21. Eversole LR, Leider AS, Hansen LS. 160 cases from literature. Oral Oncol.
7. Spouge JD, Spruyt CL. Odontogenic tu­ Ameloblastomas with pronounced 2001;37(1):17-27.
mors. Histochemical comparison of the desmoplasia. J Oral Maxillofac Surg. 37. Guralnick W, Chuong R, Goodman M.
adenoameloblastoma and developing 1984;42(11):735-40. Peripheral ameloblastoma of gingiva.
tooth. Oral Surg. 1968;25:447-456. 22. Willis RA. Pathology of tumours. Butt­ J Oral Maxillofac Surg. 1983;41:536.
8. Pindborg JJ, Kramer IRH, Tortoni H. erworth, London; 1948. 38. Stevenson AR, Austin BW. A case of
Histological typing of odontogenic tu­ 23. Tsakins PJ, Nelson JF. The maxillary ameloblastoma presenting as an exo­
mors, jaw cyst and allied lesions. Gene­ ameloblastoma: an analysis of 24 cases. phytic gingival lesion. J Periodontol.
va, World Health Organization, 1971. J Oral Surg. 1980;38(5):336-42. 1990;61:378-81.
9. Kramer IRH, Pindborg JJ, Shear M. 24. Raymond J Fonseca, Michael P Powers. 39. Redman RS, Keegan BP, Spector CJ, Pat­
WHO histological typing of odontogen­ Oral and Maxillofacial Surgery. vol.5. terson RH. Peripheral ameloblastoma
ic tumours (2nd edn), Springer-Verlag, Saunders; 1st edition. with unusual mitotic activity and con­
Geneva (1992). 25. David G Gardner. Radiotherapy in the flicting evidence regarding histogenesis.
10. Bares Leveson JW, Reichart P, Sidransky treatment of ameloblastoma. IJOMS. J Oral Maxillofac Surg. 1994; 52:192-7.
D (eds). Pathology and Genetics. Head 1988;17(3):201-5. 40. Robinson L, Martinez MG. Unicystic
and Neck Tumors. WHO, Geneva 2005. 26. Stanley HRJ, Krogh HW, Peripheral ameloblastoma: a prognostically dis­
11. Robinson HB. Ameloblastoma: a survey ameloblastoma: report of a case. Oral tinct entity. Cancer. 1977;40(5):2278-85.
of 379 cases from the literature, Arch. Surg Oral Med Oral Pathol. 1959;12: 41. Ackermann GL, Altini M, Shear M. The
Pathol. 1937;23:831-43. 760-5. unicystic ameloblastoma: A clinico­
12. Churchill HR. Histologic Differenti­ 27. Kuru H. Ueber das Adamantinom. pathological study of 57 cases. J Oral
ation Between Certain Dentigerous Zentralbl Allg Pathol. 1911;22:291-5. Pathol. 1988;17:541-6.
666 Neoplastic Conditions of Head, Neck and Face

42. Gardner DG, Corio RL. Plexiform unicys­ and anatomic principles. Cancer. 1980; tumor. Report of a case .Oral Surg Oral
tic ameloblastoma. A variant of amelo­ 46: 2514-9. Med Oral Pathol. 1962;15:843-8.
blastoma with a low-recurrence rate af­ 56. Ueno S, Mushimoto K, Shirasu R. Progno­ 69. Robert K Goode. Calcifying epithelial
ter enucleation. Cancer. 1984;53: 1730-5. stic evaluation of ameloblastoma based odontogenic tumours. Oral Maxillofa­
43. Leider AS, Eversole LR, Barkin ME. Cys­ on histologic and radiographic typing. J cial Surg Clin N Am. 2004;16:323-31.
tic ameloblastoma: A clinicopathologic Oral Maxillofac Surg. 1989;47:11–5. 70. Goode RK. Calcifying epithelial odon­
analysis, Oral Surg. 1985;60: 624–30. 57. Feinberg SE, Steinberg B. Surgical togenic tumor. Oral Maxillofac Surg
44. Li TJ, Wu YT, Yu SF, Yu GY. Unicystic management of ameloblastoma: cur­ Clin North Am. 2004;16(3):323-31.
ameloblastoma: a clinicopathologic rent status of the literature. Oral Surg 71. Houston GD, Fowler CB. Extra­osseous
study of 33 Chinese patients. Am J Surg Oral Med Oral Pathol. 1996;81:383-8. calcifying epithelial odontogenic
Pathol. 2000;24:1385-92. 58. Bredenkamp JK, Zimmerman MC, tumor: Report of two cases and review
45. Philipsen HP, Reichart PA. Unicystic Mickel RA. Maxillary Ameloblastoma: A of the literature, Oral Surg Oral Med
ameloblastoma. A review of 193 cases potentially lethal neoplasm. Arch Otolar­ Oral Pathol Oral Radiol Endod. 1997;
from the literature. Oral Oncol. 1998; yngol Head Neck Surg. 1989; 115:99-104. 83:577.
34:317-25. 59. Lee PK, Samman N, Ng IO. Unicystic 72. Bouckaert MMR, Raubenheimer EJ,
46. Eversole LR, Leider AS, Strub D. Radio­ ameloblastoma—use of Carnoy’s solu­ Jacobs FJ. Calcifying epithelial odonto­
graphic characteristics of cysto­ genic tion after enucleation. Int J Oral Maxil­ genic tumor with intracranial extension:
ameloblastoma.Oral Surg Oral Med lofac Surg. 2004;33(3):263-7. report of a case and review of the litera­
Oral Pathol. 1984;57:572-7. 60. Stoelinga PJ, Bronkhorst FB. The inci­ ture. Oral Surg Oral Med Oral Pathol
47. Reichart PA, Philipsen HP, Sonner S. dence, multiple presentation and Oral Radiol Endod. 2000;90:656-62.
Ameloblastoma:biological profile of recur­rence of aggressive cysts of the 73. Pullon, et al. Squamous odontogenic
3677 cases. Eur J Cancer B Oral Oncol. jaws. J Craniomaxfac Surg. 1988;16. tumor: report of six cases of a previous­
1995;31B:86-99. 61. Pindborg JJ. A calcifying epithelial ly undescribed lesion. Oral Surg Oral
48. Waldron CA, El-Mofty SK. A histopatho­ odontogenic tumor. Cancer. 1958;11: Med Oral Pathol Oral Radiol Endol.
logic study of 116 ameloblas­tomas with 838-43. 1975;40:616-3.
special reference to the desmoplastic 62. Pindborg JJ. Calcifying epithelial odon­ 74. Unal T, Gomel M, Gumel O, squamous
variant. Oral Surg. 1987; 63: 441-51. togenic tumors. Acta Pathol Microbiol odontogenic tumor like islands in a
49. Ashman SG, Corio RL, Eisele DW, et al. Scand. 1955;Suppl 11:71. radicular cyst; report of a case. JOMS
Desmoplastic ameloblastoma: A case 63. Philipsen HP, Reichart PA. Calcifying 1987;45: 346-9.
report and literature review. Oral Surg epithelial odontogenic tumor: biologi­ 75. Goldblatt LI, et al. Squamous odon­
Oral Med Oral Pathol. 1993;75:479. cal profile based on 181 cases from the togenic tumour. Report of five cases
50. Thompson IO, Van Rensburg LJ, Phil­ literature. Oral Oncol. 2000;36:17-26. and review of the literature. Oral Surg
lips VM. Desmoplastic ameloblastoma: 64. Peter A Reichart, Hans P Philipsen. Oral Med Oral Pathol. 1982; 54:187-96.
correlative histopathology, radiol­ Odontogenic tumors and allied lesions. 76. Wright Jr JM. Squamous odontogenic
ogy and CT-MR imaging. J Oral Pathol Quintessence, London; 2004. tumor like proliferations in odonto­
Med. 1996;25:405-10. 65. Houston GD, Flower CB. Extraosse­ genic cysts. Oral Surg Oral Med Oral
51. Philipsen HP, Reichart PA, Takata T. ous calcifying epithelial odontogenic Pathol. 1979;47:354-8.
Desmoplastic ameloblastoma (includ­ tumor. A review and analysis of 113 77. Melrose RJ. Benign epithelial odonto­
ing “hybrid” lesion of amelo­blastoma). cases. Oral Surg Oral Med Oral Pathol genic tumors. Semin. Diagn Pathol.
Biological profile based on 100 cases Oral Radiol Endol. 1997;83:577-83. 1999;16:271-87.
from literature and own files. Oral On­ 66. Mesquita RA, Lotufo MA, Sugaya NN, 78. Ide F, Shimoyama T, Horie N, Shimizu
col. 2001;37:455-60. De Araujo NS, D Araujo VC. Peripheral S. Intraosseous squamous cell carci­
52. Gardner DG. A Pathologist’s approach clear cell variant of calcifying epithelial noma arising in association with a
to the treatment of ameloblastoma. J odontogenic tumor:report of a case and squamous odontogenic tumor of the
Oral Maxillofac Surg. 1984;42:161-6. immunohistochemical investigation. mandible. Oral Oncol. 1999;35(4):431-4.
53. Mehlisch DR, Dahlin DC, Masson JK. Oral Surg Oral Med Oral Pathol Oral 79. Norris LH, Baghaei-Rad M, Maloney PL,
Ameloblastoma. A clinicopathologic Radiol Endod. 2003;95:198-204. Simpson G and Guinta J. Bilateral max­
report. J Oral Surg. 1972;30:9-22 67. Kaplan I, Buchner A, Calderon S, Kaffe illary squamous odontogenic tumors
54. Holland PS, Mellor WC. The conserva­ I. Radiologic and clinical features of and the malignant transformation of a
tive treatment of ameloblastoma, using calcifying epithelial odontogenic tu­ mandibular radiolucent lesion. J Oral
diathermy or cryosurgery. A 29-year re­ mor. Dentomaxillofac Radiol. 2001; Maxillofac Surg. 1984;42(12):827-34.
view. Int J Oral Surg. 1981;10:32-6. 30:22-8. 80. Baden E, Doyle J, Mesa M, Fabie M,
55. Gardner DG, Pecak AM. The treatment 68. Chaudhary AP, Holte NO, Vickers Lederman D and Eichen M. Squamous
of ameloblastoma based on pathologic RA. Calcifying epithelial odontogenic odontogenic tumor: report of three cases
Odontogenic Tumors 667

including the first extraosseous case. Oral opercula of permanent molars dela­ usual associated giant cell reaction. Oral
Surg Oral Med Oral Pathol 1993;75:733-8. yed in eruption .J Oral Pathol Med. Surg Oral Med Oral Pathol. 1992;73:62-6.
81. Philipsen HE Birn H. The adenomatoid 1992;21:38-41. 106. Odell EW, Lombardi T, Barret AW,
odontogenic tumor, ameloblastic ad­ 94. White DK, Chen SY, Hartman KS, Miller Morgan PR, Speight PM. Hybrid central
enomatoid tumor or adenoameloblas­ AS, Gomez LF. Central granular-cell tu­ giant cell granuloma and central odon­
toma. Acta Pathol Microbiol Scand. mor of the jaws (the so-call granular-cell togenic fibroma–like lesions of the
1969;75:375. ameloblastic fibroma). Oral Surg Oral jaws. Histopathology. 1997;30:165-71.
82. Gardner DG. The concept of hamar­ Med Oral Pathol. 1978;45(3):396-405. 107. Norberg O. Zur kenntnis der dysodonto­
tomas: its relevance to the pathogenesis 95. Vincent SD, Hammond HL, Ellis GL, geneschen Geschwülste der Kieferkno­
of odontogenic lesions.Oral Surg. 1978; Juhlin JP. Central granular cell odon­ chen. Wschr zahnheikd. 1930;46: 321-55.
45(6): 884-6. togenic fibroma. Oral Surg Oral Med 108. Brannon RB, Fowler CB, Carpenter WM,
83. Philipsen HP, Reichart PA, Zang KH, Ni­ Oral Pathol. 1987;63(6):715-21. Cario RL. Cementoblastoma: an innoc­
kai H, Yu QX. Adenomatoid odontogen­ 96. Shiro BC, Jacoway JR, Mirmiran uous neoplasm? A clinico­pathological
ic tumor: biologic profile based on 499 SA, McGuirt WF Jr, Siegal GP. Cen­ study of 25 cases and review of literature
cases.J Oral Pathol Med. 1991; 20:149-58. tral odontogenic fibroma, granular with special emphysis on recurrence.
84. Philipsen HP, Reichart PA. Adeno­ cell variant. A case report with S-100 Oral Surg Oral Med Oral Patho Oral Ra­
matoid odontogenic tumor: facts and immunohistochemistry and a review of diol Endod. 2002;93:311-320.
figures.Oral Oncol. 1998;35:125-31. the literature. Oral Surg Oral Med Oral 109. Piatelli A, Di Albertti L, Scarano A,
85. Takahashi K, Yashino T, Hashimoto Pathol. 1989;67(6):725-30. Piatelli M. benign cementoblastoma
S.Unusually large cystic adenomatoid 97. Takeda Y. Review: Ameloblastic Fi­ associated with an unerupted third
odontogenic tumor of the maxilla: case broma and related lesions: Current molar. Oral Oncol. 1998;34:229-31.
report. Int J Oral Maxillofac Surg. 2001; Pathologic concept. Oral Oncology. 110. Ulmansky M, Hjørting-Hansen E, Prae­
30(2):173-5. 1999;35:535-40. torius F, Haque MF. Benign cemento­
86. Kruse A. Uber die Entwicklung cysti­ 98. Abughazaleh K, Andrus KM, Katsnelson blastoma. A review and five new cases.
scher Geschwlste im unterkiefer.Arch A, White DK. Peripheral ameloblastic Oral Surg Oral Med Oral Patho. 1994;
Pathol Anat. 1891;124:137-89. fibroma of the maxilla: report of a case 77:48-55.
87. Cahn LR, Blum T: Ameloblastic odon­ and review of the literature. Oral Surg 111. JS Jelic, MJ Loftus, AS Miller, et al. Be­
toma: Case report critically analyzed. J Oral Med Oral Pathol Oral Radiol Endod. nign cementoblastoma: Report of an
Oral Surg. 1952;10:169. 2008;105(5):e46-8. Epub 2008 Mar 4. unusual case and analysis of 14 ad­
88. Philipsen HP, Reichart PA, Praetoius F. 99. Darling MR, Daley TD. Peripheral ame­ ditional cases, J Oral Maxillofac Surg.
Mixed odontogenic tumors and odon­ loblastic fibroma. J Oral Pathol Med. 1993;51:1033.
tomas. Considerations on interrela­ 2006;35(3):190-2. 112. Slootweg PJ. Cementoblastoma and
tionship. Review of the literature and 100. Hooker SP. Ameloblastoma odontoma osteoblastoma: A comparison of hios­
presentation of 134 new cases of odon­ an analysis of twenty six cases. Oral tological features. J Oral Pathol Med.
tomas.Oral Oncol. 1997;33:86-99. Surgery. 1967;24:275. 1992;21:385-9.
89. Mosby EL, Russell D, Noren S, Barker 101. Slootweg PJ, et al. An analysis of the 113. Wenig BM. Atlas of head and neck
BF. Ameloblastic fibroma in a 7-week- inter-relationship of the mixed odon­ pathology. Philadelphia: WB Saunders;
old infant: a case report and review of togenic tumors-ameloblastic fibroma, 1993:29-95.
the literature. J Oral Maxillofac Surg. ameloblastic fibro-odontoma, and the 114. Kramer IRH, Pindborg JJ, Shear M.
1998;56(3):368-72. odontomas. Oral Surg Oral Med Oral Histological typing of odontogenic
90. Trodahl JN. Ameloblastic fibroma. A Pahto. 1981;51:266-76. tumors. 2nd edn. New York: Springer-
survey of cases from the Armed Forces 102. Gardner DG. Central odontogenic Verlag; 1992.
Institute of Pathology. Oral Surg Oral fibroma current concepts. J Oral Pathol 115. Slootweg PJ, Van den Bos T, Straks W.
Med Oral Pathol. 1972;33(4):547-58. Med. 1996;25:556-61. Glycosaminoglycans in the myxoma
91. Kusama K, Miyake M, Moro I. Peri­ 103. Slootweg PJ, Muller H. Central Fib­roma of the jaw: a biochemical study. J Oral
pheral ameloblastic fibroma of the of the jaw, odontogenic or desmoplas­ Pathol. 1985;14:299-306.
mandible, report of a case. J Oral tic. A report of five cases with reference 116. Zachariades N, Papanicolaou S. Treat­
Maxillofac Surg. 1998;56:399-401. to differential diagnosis. Oral Surg Med ment of odontogenic myxoma: review
92. Couch RD, Morris EE, Vellios F. Gran­ Oral Pathol. 1983;56:61-70. of the literature and report of three
ular cell ameloblastic fibroma. Report 104. Janssen JH, Blijdorp PA. Central odon­ cases. Ann Dent. 1987;46:34-7,40.
of 2 cases in adults, with observ­ations togenic fibroma :a case report .J Maxil­ 117. Barker BF. Odontogenic myxoma.
of its similarity to congenital epulis. lofac Surg. 1985;43:666-74. Semin Diagn Pathol. 1999;16:297-301.
Am J Clin Pathol. 1962;37:398-404. 105. Allen CM, Hammond HL, Stimson PG. 118. Halfpenny W, Verey A, Bardsley V.
93. Philipsen HP, Thosaporn W, Reichart Central odontogenic fibroma, WHO Myxoma of the mandibular condyle: a
PA, Grundt G. Odontogenic lesions in type. A report of three cases with an un­ case report and review of the literature.
668 Neoplastic Conditions of Head, Neck and Face

Oral Surg Oral Pathol Oral Radiol epithelial, mesenchymal, and mixed of odontomas. Oral Oncol. 1997;33:
Endod. 2000;90:348-53. varities. Am J Pathol. 1946;12:433-71. 86-99.
119. Goldblatt LI. Ultrastructural study of an 132. Shafer WG, Hine MK, Levy BM. Cysts 142. Owen BM, Schumann NJ, Mincer HH, et
odontogenic myxoma. Oral Surg Oral and tumors of odontogenic origin. In: al. Dental odontomas; A retrospective
Med Oral Pathol. 1976;42:206-20. A textbook of oral pathology. 4th edn, epidemiological study of 104 cases J
120. Slootweg PJ, Van Den Bos T, Straks Philadelphia: WB Saunders; 1983;258- Clin Pediatr Dent. 1997;21:261-4.
W: Glycosaminoglycans in myxoma of 317. 143. Blinder D, Peleg M, Taicher S. Surgical
jaw: A biochemical study. J Oral Pathol. 133. Gorlin RJ, Chaudrey AP, Pindborg JJ. considerations in case of large mandi­
1985;14:299. Odontogenic tumors: classification, bular odontomas located in the mandi­
121. McClure DK, Dahlin DC. Myxoma of histopathology and clinical behavior bular angle. Int J Oral Maxillofac Surg.
bone: report of 3 cases. Mayo Clin Proc. of man and domestic animals. Cancer 1993;22:163-5.
1977;52:249-53. 1961;14:73-98. 144. MacDonald–Jankowski DS, Odon­ to­
122. Heffner DK. Problems in pediatric oto­ 134. Sato M, Tanaka N, Sato T, Amagasa mas in a chinese population. Dento­
rhinolaryngic pathology: I. Sinonasal T. Oral and maxillofacial tumors in maxillofac Radiol. 1996;25:186-92.
and nasopharyngeal tumors and mass­ children: a review. Br J Oral Maxillofac. 145. Marchetti C, Piacentini C, Menghini
es with myxoid features. Int J Peditr 1997;35:92-5. P, Reguzzoni M. Observations on
Otorhinolaryngol. 1983;5:77-91. 135. Philipson HP, Reichart PA, Praeto­ the enamel of odontomas. Scanning
123. Johnson LC, Yousefi M, Vinh TN, rius F. Mixed odontogenic tumors and Microsc. 1993;7:999-1007.
Heffner DK, Hyams VJ, Hartman KS. odontomas. Considerations on inter­ 146. KH Thoma, HM Goldman. Odonto­
124. Heffner DK. Sinonasal myxomas and relationship. Review of literature and genic Tumors. Amer J Path.
fibromyxomas in children. Ear Nose presentation of 134 new cases of odon­ 1946;22:433-71.
Throat J. 1993;72:365-8. tomas. Oral oncol. 1997;33:86-99. 147. Levy BA. Ghost cell and odontomas.
125. Landa LE, Hedrick MH, Nepomuceno- 136. Lopez-Areal L, Silvestre DF, Gil LJ. Oral Surg Oral Med. Oral Pathol. 1973;
Perez MC, Sotereanos GC. Recurrant Compound odotoma erupting in the 36:851-5.
myxoma of the zygoma: a case report. mouth: 4-year follow-up of a clinical 148. Kamakura S, Matusi K, Katou F, Shirai
J Oral Maxillofac Surg. 2002;60:704-8. case. J Oral pathol Med. 1992;21:285-8. N, Kochi S, Motegi K. Surgical and orth­
126. Kaffe I, Naor H, Buchner A. Clinical and 137. Hitchin AD. The aetiology of the calci­ odontic management of compound
radiological features of odontogenic fied composite odontoma. Br Dent J. odontoma without removal of the im­
myxomas of jaws. Dentomaxillofacial 1971;130:475-82. pacted tooth. Oral Surg Oral Med Oral
Radiol. 1997;26:299-303. 138. Piattelli A, Trisi P. Ghost cells in com­ Pathol Radiol Endod. 2002;94:540-2.
127. Slootweg PJ, Wittkampf AR. Myxoma pound odontoma: a study of undemin­ 149. Thoma KH, Johnson GJ, Ascario N.
of the jaws: an analysis of 15 cases. J eralized material. Bull Group Int Rech Case 43: Adamanto-odontoma. Am J
Maxillofac Surg. 1986;14:46-52. Sci. Stomatol Odontol. 1991; 34:145-9. Orthod Oral Surg. 1944;30:244.
128. Pahl S, Henn W, Binger T, Stein U, 139. Sedano H, Pindborg JJ. Ghost cell epi­ 150. Hooker SP. Ameloblastic odontoma:
Remberger K. Malignant odontogenic thelium in odontomas. J Oral Pathol. An analysis of twenty-six cases. Oral
myxomas of the maxilla: case with 1975;4:27-30. Surg. 1967;24:375-6.
cytologic confirmation. J Largyngol 140. Gao YH, Yang LJ, Yamaguchi A. Im­ 151. Wächter R, Remagen W, Stoll P. Is it
Otol. 2000;114:533-5. munohistochemical demonstration of possible to differentiate between odon­
129. Lo Muzio L, Nocini PF, Favia G, et al. bone morphogenetic proyein in odon­ toameloblastoma and fibro-odonto­
Odontogenic myxoma of the jaws. Oral togenic tumors. J Oral Pathol Med. ma? Critical position on basis of 18
Surg Oral Med Oral Pathol Oral Radiol. 1997;26:273-77. cases in DOSAK list. Dtsch Zahnarztl Z.
1996;82:426-33. 141. Philipsen HP, Reichart PA, Praetorius 1991;46(1):74-7.
130. Broka P. Traité des tumeurs, vol 1. F. Mixed odontogenic tumours and 152. Kaugars GE and Zussmann HW. Am­
France: P. Asselin;1866;(1):350. odontomas. Considerations on inter­ eloblastic odontoma (odonto-amelo­
131. Thoma KH, Goldman HM. A classi­ relationship. Review of the literature blastoma). Oral Surg Oral Med. Oral
fication based on the observation of the and presentation of 134 new cases Pathol. 1991;71:371-3.
29 Potentially Malignant
Disorders of the Oral Cavity
Borle Rajiv M, Gadbail Amol

INTRODUCTION early detec­tion and treatment of head and co-exist at the margins of overt oral
neck carcinomas. squamous cell carcinomas.
Although the oral cavity is accessible for • A proportion of these may share mor­
clinical examination by the clinician and phological and cytological changes
the self examination by the patient, the CONCEPT OF PRECANCER observed in epithelial mali­gnancies,
irony is that the early detection of the oral but without frank invas­ion.
malignant lesions is still far from desired. Cancer being a genetic disorder invo­ • Some of the chromosomal, genomic
Although majority of cases of OSCC are lves multiple alterations of the genome and molecular alterations found
preceded by precancerous/potentially progressively accumulated during a in clearly invasive oral cancers are
mali­­gnant lesions and conditions which protracted period, the overall effect of detected in these presumptive ‘pre­
stay in place for the long time, early which surpasses the inherent reparative cancer’ or ‘Premalignant’ phase.
recognition and treatment of such lesi­ ability of the cell. In the course of its The terms ‘precancer’, ‘precursor le­
ons to prevent their conversion in the progression, visible physical changes sions’, ‘premalignant’, ‘intra epithelial
malignancy or detecting the malig­nancy are taking place at the cellular level neoplasia’ and ‘potentially malignant’
in an early stage is still elusive. A majority (atypia) and at the tissue level (dys­ have been used in the international
of the patients with oral cancer report at a plasia). These changes include gene­tic literature to broadly describe clinical
very late stage and thus, the management changes, epi­ genetic changes, sur­face presentation that may have a potential
of such advanced lesions are often alterations and alterations in inter­ to become cancer. They all convey the
difficult and lead to great morbidity and cellular intera­ ctions. The sum total concept of a two-step or multi step pro­
unfavorable pro­gnosis. The oral squamous of these physical and morphological cess of cancer development.
cell car­ ci­
noma is the commonest oral alterations are of diagnostic and prog­
cancer, which in majority of cases are pre­ nostic relevance and is designated as
ceded by potentially malignant lesions ‘precancerous’ changes. POTENTIALLY MALIGNANT
and condi­ tions like leukoplakia, ery­ ­ The concept of denoting some lesi­ DISORDERS
thro­­
plakia, oral submucous fibrosis, or ons or disorders of the oral mucosa
sideropenic dysphagia particularly in as pre­cancerous are based on the evi­ In the past the potentially malignant
Asian countries. These are the potenti­ denced that:1 disorders were often described as pre­
ally dangerous lesions and can transform • In the longitudinal studies, areas m­alignant lesions and conditions and
into frank squamous cell carcinoma. The of tissue with certain alterations in the gradually the nomenclature chan­
iden­ ti­
fication of potentially malignant clinical appearances identified at ged from Precancer—‘Precursor lesi­
lesions of the upper aero-digestive tract the first assessment as precancerous ons’, ‘Pre­­ malignant’, ‘Intra epithelial
can be possible through proper personal have undergone malignant change ne­o­­pla­sia’ and ‘Potentially malignant
history, clinical exami­ nation. Recently, during follow-up. les­­­­­ion’.
the molecular methods help in to detect • Some of these alterations particularly Recen­tly the term ‘potentially mali­
the malignant potential, the prevention, red and white patches are seen to gnant disor­ders’ was recommended
670 Neoplastic Conditions of Head, Neck and Face

as it conveys that not all lesions and oral mucosa and not only site-specific daughter cells. These patches can be
conditions described under this term predictors.2 recognized on the basis of mutations
may transform to cancer, rather that in TP53 and have been reported for
there is a family of morpholo­ gical head and neck, lung, skin and breast
alterations amongst, which some Risk Factors for Oral cancer. The conversion of a patch
may have an increased potential for Potentially Malignant into an expanding field is the next
malignant transformation.1 Potentially Disorders and Oropharyngeal logical and critical step in epithelial
malignant disorders of the oral mucosa Squamous Cell Carcinoma carcinogenesis. Additional genetic alt­
are also indicators of risk of likely future e­rations
­­­ are required for this step, and
malignancies elsewhere in (clinically • Age older than 45 years. However, by virtue of its growth advantage, a
normal appearing) oral mucosa and not the OSCC is detected at much youn­ proliferating field gradually displaces
only site-specific predi­ctors.1,2 ger patients. the normal mucosa.
The Premalignant lesion was defined • Combined tobacco and alcohol use In the mucosa of the head and neck,
as “A morphologically altered tissue in or abuse as well as the esophagus, such fields
which cancer is more likely to occur than • Nutritional deficiencies like vitamin have been detected with dimensions of
its apparently normal counterpart.” The deficiency, iron deficiency greater than 7 cm in diameter, whereas
examples are: • Betel nut use they are usually not detected by routine
• Leukoplakia • Immunosuppression (disease or ther­ diagnostic techniques. Ultimately, clonal
• Erythroplakia apy related) divergence leads to the development of
• Palatal changes associated with • Genetic susceptibility one or more tumors within a contiguous
reverse smoking • Prior upper aerodigestive tract field of preneoplastic cells. An important
• Actinic chelitis cancer clinical implication is that fields often
• Bowen’s disease. • Sun exposure (lip vermilion) remain after surgery of the primary
• Oral human papillomavirus infec­ tumor and may lead to new cancers,
Premalignant Condition tion designated presently by clinicians as “a
It was defined as “A generalized state or • HIV infection might be associated second primary tumor” or “local recur­
condition associated with significantly with increased risk of oral poten­tially rence,” depending on the exact site and
increased risk for cancer development.” malignant lesions and oropharyn­ time interval.3,4
The examples are: geal squamous cell carcinoma. This phrase has been used to des­
• Oral submucous fibrosis cribe three phenomena:4
• Sideropenic dysphagia The Concept of ‘Field • A wide field of aerodigestive mucosa
• Oral lichen planus that tends to be affected by pre-
• Syphilis
Cancerization’ malignant disease
• Discoid lupus erythematosus The concept of “field cancerization” • The frequent occurrence of multiple
• Dyskeratosis congenita was first introduced by Slaughter et al. primary tumors in epithelial areas
• Xeroderma pigmentosum in 19533 when studying the presence affected by widespread pre-mali­
• Epidermolysis bullosa. of histologically abnormal tissue sur­ gnant disease, and
As per the recent concept the pre­ rounding oral squamous cell carci­ • The possibility of distant related
mali­gnant lesions and conditions are noma. It was proposed to explain the primary tumors in the upper aero­
now called as potentially malignant development of multiple primary tumors digestive tract.
lesions. The potentially malignant les­ and locally recurrent cancer. Organ On the basis of recent molecular
ions can be described as under: systems in which field canceri­ zation findings, Braakhuis et al. (2003)5 pro­po­
It conveys that not all lesions and has been described since then are: head sed the definition of field cancerization:
conditions described under this term and neck (oral cavity, oro­pharynx and “The presence of one or more areas
may transform to cancer, rather that larynx), lung, vulva, esophagus, cervix, consisting of epithelial cells that have
there is a family of morphological alter­ breast, skin, colon and bladder.3 genetic alterations. A field lesion (or
ations amongst, which some may have Recent molecular findings support shortly ‘field’) has a monoclonal origin,
an increased potential for malignant the carcinogenesis model in which and does not show invasive growth
transfor­mation.1 the development of a field with and metastatic behavior, the hallmark
Potentially malignant disorders of genetically altered cells plays a central criteria of cancer.”
the oral mucosa are also indicators of role. In the initial phase, a stem cell These clinical expressions of a “field
risk of likely future malignancies else­ acquires genetic alterations and forms cancerization” phenotype could come
where in (clinically normal appearing) a “patch,” a clonal unit of altered about as a result of:
Potentially Malignant Disorders of the Oral Cavity 671

• Either independent molecular eve­ persistent genetic alterations found hyperkeratosis) is not of significant
nts affecting multiple cells separ­ in clonal patches that give rise to importance in the assessment of dys­
ately. the clinical appearance of wide­ plasia.
• Or as a molecular event in a single spread mucosal alteration may ulti­
clonal progenitor that gives rise to mately be successfully treated by WHO Criteria
this phenomenon, via mechanisms elimination of genetic alterations or Collaborating Centre for Oral Cancer
of widespread clonal expansion or the cells that carry them.4 and Precancer, the Working Group
an alternative means of undergoing The clinical observations also supp­ discu­ssed the 2005 WHO classification
lateral spread across the mucosa of ort the theory of field cancerization as and recommended its adaptation for
the upper aerodigestive tract. more than one primary at the time of wider use. The architecture and cytology
first diagnosis, appearance of second criteria used for grading epithelial dys­
primary at different location, after suc­ plasia in the WHO classification 20056
Implications for Therapy cessful excision of the first primary are (Box 29.1).
• The care providers to be more dili­ reported.
gent about screening and directed Grading of Epithelial Dysplasia
biopsies in these patients. The histopathological interpretation
• Frequent examination should be Dysplasia of potentially malignant lesions show
done for high-risk patients. Epithelial dysplasia is the sum of a presence of dysplastic feat­ ures of
• Molecular techniques may aid in various disturbances of epithelial pro­ epithelium. In spite of num­erous sug­
the analysis of surgical margins. In lifer­ ation and differentiation as seen gested prognostic mole­ cular markers,
the future, the presence of altered microscopically. the presence of epithelial dysplasia as
clones at mucosal margins may be When architectural disturbance assessed by light microscopic exami­
an indication for more aggressive is accompanied by cytological atypia nation is still the strongest predictor
therapy, including chemopreventive (vari­­ aions in the size and shape of of future malignant transformation in
or radiotherapy, to treat altered the keratinocytes), the term epithelial an oral potential malignant disorder.
clonal patches that are unable to be dys­ plasia applies. The combination Epithelial dysplasia is usually divided
detected grossly and are beyond the of cellular and architectural changes into three categories (Box 29. 2):
initial scope of surgical excision. observed in the gradual transition to Recently Warnakulasuriya S. et al.
• Screening studies that take advan­ mali­­ gnancy. Dysplasia is a histopa­ (2008)7 classified epithelial dysplasia in
tage of the known genetic alterations tholo­gical diagnosis made on the basis to:
may also become routine, especially of presence of certain histological and • Low risk dyspalasia (No/Question­
for those people in a high-risk group cytological features in premalignant able/Mild)
(smokers and drinkers). lesions and conditions. The magnitude • High risk dysplasia (moderate or
• The concept of field cancerization, or of surface keratinization (keratosis or severe).
a mucosa rendered more susceptible
to tumor formation, has led to the Box 29.1: Architecture and cytology criteria used for grading epithelial dysplasia in the
notion of chemoprevention, where­ WHO classification 2005
by a compound could be given to
prevent tumor recurrence, prevent Architecture criteria Cytology criteria
the progression of pre-malignant Irregular epithelial Abnormal variation in the nuclear size (anisoneucleosis)
disease into malignancy, or retard stratification
tumor progression. Because sur­ Loss of polarity of basal cells Abnormal variations in nuclear shape (nuclear pleomorphism)
gical excision of the entire affected Basal cell hyperplasia Abnormal variations in cell size (anisocytosis)
mucosa is not feasible, chemical Drop shaped rete pegs Abnormal variations in cell shape (cellular pleomorphism)
compounds delivered systemically Increased number of mitotic Increased nuclear cytoplasmic ratio
or topically can provide a wider figures
range of coverage. Retinoids and Abnormally superficial Increased nuclear size
mitosis
other compounds such as cyclooxy­
genase-2 have been studied exten­ Premature keratinization in Atypical mitotic figures
single cells (dyskera­tosis)
sively with promising results, but
Keratin pearls within the Increase in the number and size of nucleoli
the side effects and efficacy are still rete ridges
being studied. Newer, promising
Hyperchromatism
agents are being tested, but the
672 Neoplastic Conditions of Head, Neck and Face

Box 29.2: Grading of epithelial dysplasia Leukoplakia


Mild: Cellular atypia and architectural disturbance limited to basal and parabasal layer
Definitions of Oral Leukoplakia propo­
(Fig. 29.1 to 29.3) sed in the past decades:
Moderate: Involvement from the basal layer to the midportion of the spinous layer (Fig. 29.4) WHO8 (1978): A white patch or
Severe: Alterations from the basal layer to a level above the midpoint of the epithelium. plaque that cannot be characterized
(Fig. 29.5) clini­cally or pathologically as any other
Carcinoma in situ: The theoretical concept of carcinoma in situ is that malignant transfor­
disease.
mation has occurred, but invasion is not present. It is the most severe form of epithelial
dysplasia and involves the entire thickness of the epithelium (top to bottom change). It is First International Conference on
cytologically similar to Squamous cell carcinoma but architecturally the epithelial basement Oral Leukoplakia Malmo, Sweden9
membrane remains intact and no invasion in to connective tissue has occurred (Fig. 29.6) (1984): A white patch or plaque that
can­not be characterized clinically or
path­olo­gically as any other disease and
is not associated with any physical or
chemical causative agent except use of
tobacco.
International Symposium, Upp­
sala, Sweden10 (1994): A predo­minantly
white lesion of the oral mucosa that
cannot be characterized as any other
definable disease.
WHO11 (1997): A predominantly
Fig. 29.1: No dysplasia/hyperkeratosis: Fig. 29.2: Keratosis, acanthosis, no cellular
Ker­a­tosis, acanthosis, no cellular atypia, no atypia, basal cell hyperplasia, no changes in
white lesion of the oral mucosa that
changes in architectural architectural can­not be characterized as any other
definable lesion.
WHO12 (2005): Not defined–no
dis­
tin­ ction is made from other white
patches.
Warnakulasuriya et al.1 (2008):
Leuk­oplakia should be used to recog­
nize white plaques of questionable risk
having excluded (other) known diseases
or disorders that carry no increased risk
for cancer.
Leukoplakia is a clinical term and
the lesion has no specific histology. It
Fig. 29.3: Mild epithelial dysplasia: Kera­ Fig. 29.4: Moderate epithelial dyspla­
tosis, acanthosis, mild cellular atypia, archi­ sia: Architectural changes extend to
may show atrophy or hyperplasia (acan­
tectural changes (lower 1/3 rd of epithe­ middle third of epithelium. Cellular atypia thosis) and may or may not demon­
lium) is mode­rate strate epithelial dysplasia. It has a
variable behavioral pattern but with
an assessable tendency to malignant
transformation. It must be noted that
oral epithelial dysplasia has no specific
clinical appe­arance and the term should
not be used as a clinical descriptor of a
white lesion.
The following conditions/disor­ders
need exclusion to diagnose leuko­ pla­
kia(1,9) (Table 29.1).

Etiology
Fig. 29.5: Severe epithelial dysplasia: Archi­ Fig. 29.6: Irregular interface between
tectural changes extend to upper third of epithelium and connective tissue with Tobacco: It refers to dried leaves of nico­
epithelium. Cellular atypia is marked pointed projections of epithelium indicated tina tobaccum. Tobacco widely used in
early invasive carcinoma two forms.
Potentially Malignant Disorders of the Oral Cavity 673

Table 29.1: Lesions to be considered in the differential diagnosis of leukoplakia leukoplakia. The source of irritation or
Disorder Diagnostic features Biopsy trauma may be malocclusion, ill-fitting
dentures, sharp broken teeth, hot spicy
White sponge nevus Noted in early life, family Biopsy not indicated food or root piece.
history, large areas involved, Candida albicans: As a possible
genital mucosa may be
etio­
logical factor in leukoplakia and
affected
its possible role in malignant trans­for­
Frictional keratosis History of trauma, mostly Biopsy if persistent after
along the occlusal plane, an elimination of cause mation is still unclear. About 10 per­
etiological cause apparent, particularly in a tobacco cent of oral leukoplakias satisfy the clin­
mostly reversible on removing user ical and histological criteria for chro­nic
the cause hyperplastic candidiasis (candidal leuko­
Morsicatio buccarum Habitual cheek lip biting Biopsy not indicated plakia). Epithelial dysplasia is reported to
known, irregular whitish flakes occur four to five times more frequently
with jagged out line
in candidal leukoplakia than in
Chemical injury Known history, site of lesion Biopsy not indicated leukoplakia general. Various evidences
corresponds to chemical
injury, painful, resoles rapidly have been presented to justify an aetio­
Acute pseudo-membranous The membrane can be scraped Swab for culture
logical role for candida in neoplastic
candidosis off leaving an erythematous/ transformation, which includes among
raw surface others the catalytic transformation
Leukoedema Bilateral on buccal mucosa, Biopsy not indicated in vitro of the carcinogenic nitrosamine,
could be made to disappear N-nitrosobenzyl-methylamine, by strains
on stretching, racial of candida albicans demonstrated to be
Lichen planus (plaque type) Other forms of lichen planus Biopsy consistent with selectively associated with leukoplakia.
(reticular) found in association lichen planus Viruses: The possible contributory
Lichenoid reaction Drug history, e.g. close to an Biopsy consistent with role of viral agents (such as HPV 16
amalgam restoration lichen planus or lichenoid
and 18) in the pathogenesis of oral
reaction
Leukoplakia particularly with regard to
Discoid lupus Circumscribed lesion with Biopsy consistent with
erythematosus central erythema, white lines DLE supported by exophytic verrucous leukoplakia.
radiating immunofloresence and Vitamin deficiency: Serum levels
other investigations of vitamin A, B12, C, beta-carotene and
Skin graft Known history Not indicated folic acid were significantly decreased
Hairy Leukoplakia Bilateral tongue keratosis Specific histopathology in patients with oral Leukoplakia than
with koilocytosis EBV normal control.
demonstrable on ISH Genetic factor: Relatively little
Leukokeratosis nicotina Smoking history, grayish white Not indicated is known yet with regard to possible
palate palate gen­etic factors in the development of
Leuko­plakia.
Age and gender: The onset of leuko­­
1. Smokeless tobacco: Chewable tob­ tissues increasing reddening and plakia usually takes place after the
a­cco and snuff. When tobacco is stippling of mucosal surface. age of 30 years resulting in peak inci­
chewed, various chemical consti­ Alcohol: Whether the use of alcohol dence above the age of 50 years. The
tuents leach out such as nitroso­ itself is an independent etiological fac­ gender distribution in most studies
nor­­ni­cotine, nicotine, pyridine and tor in the development of leukoplakia varies, ranging from a strong male pre­
picoline. Alkaline ph: 8.2–9.3 acts as is still questionable. Its effect, at best, dominance in different parts of India to
local irritants and leads to alterations may be synergistic to other well-known almost 1:1 in the western world.
of mucosa. etiological factors (physical irritants).
2. Smoked tobacco: Cigar, cigarette, • It causes irritation and burning sen­ Clinical Features
beedi and pipe. Smoking tobacco sation of oral mucosa. Leukoplakia may occur either as a single,
is harmful as this smoke contains • It facilitates the entry of carcinogen localized change of the oral mucosa
polycyclic hydrocarbons, beta nap­ into exposed cells and thus, alters the or as diffuse, often multiple lesions.
h­thalamine, nitrosoamines, CO, oral epithelium and its metabolism. The site distribution shows worldwide
nicotine, all of which acts as source Chronic irritation: Continuous tra­ differences, that are partly related to
of irritation. Heat also plays a major uma or local irritation in the oral cavity gender and tobacco habits. In fact, any
role. Heat induces alterations in is suspected as a causative agent for oral site may be affected. In general two
674 Neoplastic Conditions of Head, Neck and Face

clinical variants of leukoplakia are being


recognized, the homogeneous and the
nonhomogeneous type. Transition or
changes among the different clinical
variants of oral leukoplakia may occur.
Homogeneous leukoplakia: It has
been defined as a predominantly white
lesion of uniform flat, thin appearance
that may exhibit shallow cracks and a
smooth wrinkled or corrugated surface
with a constant texture throughout. The
adjective homogeneous not only applies Fig. 29.7: Preleukoplakia Fig. 29.8: ‘Homogeneous or thick
to the homogeneous whitish color of (‘mild or thin leukoplakia’) leukoplakia’
the lesion, but also above all to a flat
thin and rather smooth surface. A more
elaborate sub-division may be used
such as13–16
• Homogeneous Smooth (Figs 29.7
and 29.8)
• Homogeneous Furrowed (fissured)
• Homogeneous Ulcerated
Non-homogeneous leukoplakia:
It has been defined as predominantly
white or white-red lesions that may be
irregularly flat, nodular or exophytic.
(Figs 29.9 and 29.10). The nodular
lesions are characterized by white pat­
ches or nodules on erythematosus
base, while the exophytic lesions have Fig. 29.9: Homogeneous to slightly Fig. 29.10: Speckled leukoplakia, or
irregular blunt or sharp projections. nodular leukoplakia nonhomogeneous leukoplakia
The adjective nonhomogeneous is
applicable both to the aspect of color, i.e.
a mixture of white and red changes and
to the aspect of texture, i.e. exophytic,
papillary or verrucous.
Leukoplakia begins as thin, gray, or
gray-white plaques that may appear some­
what translucent, are sometimes fissured
or wrinkled, and are typically soft and flat.
They usually have sharply demarcated
borders but occasionally blend gradually
into normal mucosa. This early stage is
sometimes referred as ‘preleukoplakia’
A B
but preferable desi­g­­nated ‘mild or thin
leukoplakia’ (Fig. 29.7). Figs 29.11A and B: (A) Nodular; (B) Speckled leukoplakia
Thin leukoplakia may disappear
or continue unchanged but as time should be only a few, if any, localized one-third regress or disappear and a
progresses as many as two thirds of nodules or surface projections. At this few become even more severe. The
such plaques slowly extend laterally stage the lesions is severe often called latter lesions begin to develop surface
and acquire a distinctly white appear­ ‘homogeneous or thick leukoplakia’ irregularities of a nodular or granular
ance from a thickened keratinized layer. (Fig. 29.8). nature, and hence are referred to as
They may become leathery to palpation Most thick, smooth lesions remain ‘granular or nodular leukoplakia’
and fissures may deepen, but there inde­finitely at this stage, as many as (Fig. 29.11A). Occasionally, pointed
Potentially Malignant Disorders of the Oral Cavity 675

pro­jections develop on the surface and cell carcinoma usually within 8 years Identification of apppropriate
may be so numerous that the resul­ting of initial PVL diagnosis. These lesions biopsy site
lesions are called ‘verruciform leuko­ rarely regress despite therapy. PVL • To improve the sensitivity and
plakia’. is unusual among the leukoplakia speci­ ficity of lesion identification
An additional change can occur over variants in having a strong female and appropiate biopsy site showing
a time however, multiple circular or oval predilection (1:4 male to female ratio) maximum dysplastic changes, vital
patches of non-blanching redness or and minimal association with tobacco tissue staining is often used.
erythroplakia begin appearing in scatt­ use.19 • Toludine blue is most commmonly
ered areas. Such areas represent sites in used and the intensly stained areas
which epithelial cells are so immature Diagnostic Procedure should be considered for biopsy
that they are no longer able to produce site. Toludene blue is an acidophilic
keratin. These intermixed red and white
(Flow chart 29.1) metachromatic thiazin dye which
lesions are called ‘eryth­roplakia, speckled Elimination of possible causes: In a selectively stains tissue acids and
leukoplakia, or nonhomogeneous leuko­ pati­ent with a white lesion of the oral particularly DNA and RNA. The
plakia’. (Fig. 29.11B). These are the most mucosa, the clinician should first try to rationale for use of this vital stain is
worri­some form of the lesions and carry rule out any of the definable white lesion that dysplastic cells usually contain
an extre­ mely high risk of malignant listed in the above table before accepting more nucleic acid than normal cells.
transfor­mation.17 the definative diagnosis of leukoplakia. • Lugol’s iodine solution is also used.
A special high-risk form of leuko­ The biopsy: In homogeneous leu­ It produces the brown black stain
plakia, ‘proliferative verrucous leuko­ ko­­plkia, the taking of a biopsy should by reaction of the iodine with the
plakia’18 (PVL) is characterized by the be the standard rule. The biopsy may be glycogen, which is inversly related to
development of multiple keratotic incisional or a conservative excisional the degree of keratosis.
plaques with roughened surface projec­ biopsy, if feasible. • The use of vital stains with good
tions (Fig. 29.12). The relationship of In non-homogeneous leukoplakia, mea­ sure of clinical experience is
PVL to cases described as verrucous that are usually symptomatic, epithelial of value in accurate diagnosis and
leukoplakia is uncertain. The multiple dysplasia or even carcinoma in situ or deciding where to perform biopsy.
PVL plaque tends to spread slowly and early squamous cell carcinoma is rather • Oral brush biopsy: Computer assis­
involve additional oral mucosal sites. common. The biopsy should be taken at ted analysis of oral brush biopsy is
Although the lesions typically begin the site of symptoms, if present, and or at an aid to the oral examination which
as simple, flat hyperkeratosis that are a site of redness or induration. Biopsy of helps to determine the significance
indistinguishable from ordinary leuko­ exophytic, verrucous or papillary lesions of oral lesions with an epithelial
plakic lesions, PVL exhibits persis­ should be taken deep enough to include abnormality. Its utility is limited as
tent growth, eventually becoming a sufficient amount of underlying con­ it doesnot provide desired details
exo­phytic and verrucous in nature. nect­ive tissue and preferably from the beyond dysplasia and may be non
As the lesions progress, they may go mar­gins. conclusive in border line cases. It is
through a stage indistinguishable from
verrucous carcinoma, but they later
usually develop dysplastic changes and Flow chart 29.1: Schematic representation of the steps in the diagnosis of oral
transform into full fledged squamous leukoplakia

Fig. 29.12: Proliferative verrucous


leukoplakia
676 Neoplastic Conditions of Head, Neck and Face

expensive technique and hence, not Histo-pathological Features depends upon clinical appearance, site
affordable to majority of population The histopathological aspects of leuko­ and etiological factors.15,20
who need it more. plakia may vary from atrophy of the The incidence of malignant transfor­
• The exfoliative cytology are of limi­ epithelium to hyperplasia with or with­ mation of 07 to 13 percent was reported
ted value when dealing with leu­k­o­ out hyperkeratosis. Epithelial dys­pl­­asia, by Lee et al.20 while Angadi et al.21
plakia. if present, may range from mild to severe. reported the incidence of 11.6 percent.
In some instances, carcinoma in situ Warnakulasuriya22 reported inci­
Identifying malignant change and even squamous cell carcinoma are dence of malignant transformation in
The advanced molecular investigation encountered histo­logi­cally. A his­to­ the leukoplakia is 0.3 to 5.6 percent
like DNA ploid, p53 mutation and chro­ pathological report of exophytic, verru­ while other workers23-26 reported it to be
mosome 3 and 9 changes can indicate cous or papillomatous lesions, in spite between reported 15.6 to 39.2 percent.
significantly increased chances of mali­ of the absence of epithelial dysplasia • Clinical appearance: The homo­
g­nancy. may in time progress to squamous cell gen­eous leukoplakia has low mali­
More than the investigations it is carcinoma and that long-term follow up gnant potential. The presence of
very important to identify the clinical should be considered. The histological dysplasia more or less correlating
changes in the long standing oral report of a leukoplakia should include a with a clinical non-homogeneous,
precancerous lesion which warrants statement on the absence or presence of erythroleukoplakia subtype seems
biopsy for making early diagnosis of epithelial dysplasia and an assessment to be more important indicator of
malignant transformations in the lesion of its severity. malignant potential (Table 29.2).
so that the treatment can be given at a Dys­ pl­as­
tic lesions carry a 5-fold
very early stage to ensure good out come greater risk than non-dysplastic
Malignant Potential of
and prognosis. By and large too much ones. Seven percent of the dysplastic
dependence is shown by the clinicians Leukoplakia lesions progressed to cancer in a
on the investigations and in the bargain Certain features have been reported mean observation period of 7 years.
the clinical findings are often ignored. to be associated with increased risk of In two studies from India (Gupta PC
There is no doubt that biopsy still malignant transformation. et al. 1980,27 Silverman S28 et al. 1976)
remains the gold standard in making • Gender, particularly women seem to low malignant transformation rate of
the diagnosis but when to suspect a be at risk oral leukoplakia have been reported,
malignant change and to take a biopsy • Long duration of the leukoplakia 0.3 percent and 0.06 percent, res­
is purely clinical judgment. The rough • Leukoplakia in non smokers (idio­ pectively. In reports from western
guidelines for clinical diagnosis are pathic leukoplakia) country (Axell T 198729) reported
shown in Box 29.3. • Location in the floor of the mouth, somewhat higher figure.
retro molar area or/and on the ton­ – Around 2 to 5 percent of leuko­
gue plakia becomes malignant in
Box 29.3: Routine guidelines for • Non-homogeneous type 10 years.
diagnosis of leukoplakia • Presence of Candida albicans – 5 to 20 percent of leukoplakias
• Presence of epithelial dysplasia are dys­plastic.
• Every case should be kept under perio­ Of the above-mentioned factors the – 10 to 35 percent of dysplastic leu­
dic follow up and during every follow
up thorough clinical examination is
malignant potential depends on mainly koplakia proceed to carcinoma.
required.
• Any change in the color of the lesion Table 29.2: Phase I to IV leukoplakia subtype and risk of
especially red is highly suspicious (when malignant transformation
the lesion turns fiery and red it is the
time to scratch your head!). Phase Various diagnostic descriptive terms used for phase I Risk of
• Any fissuring or ulceration in the lesion to phase IV leukoplakia subtype and risk of malignant malignant
which fails to heal even after removal of transformation12 transformation
the cause like sharp cusp or tooth.
• Presence of induration in the lesion. I Thin leukoplakia, Preleukoplakia, +/–
The induration is a perception that a Homogeneous leukoplakia
palpating finger gets and this is the II Thick, smooth leukoplakia, fissured leukoplakia ++
most reliable finding but needs lot of Homogeneous leukoplakia
practice and experience. III Granular, verruciform, rough leukoplakia, Candidial epithelial +++
• Fixity of the lesion to the deeper hyperplasia,
stru­ctures. Homogeneous leukoplakia
IV Erythroplakia, Speckled leukoplakia, Candida leukoplakia, ++++
* If any of the above changes are noticed in Nonhomogeneous leukoplakia
the lesion a biopsy is indicated.
Potentially Malignant Disorders of the Oral Cavity 677

• Site: The soft palate complex, ventro­ Treatment and with conservative treatment (Flow
lateral surface of tongue, retro molar Every leukoplakia does not neces­ chart 29.2).
area and floor of mouth has the sarily transform into a malignancy. • The leukoplakia can be treated
high-risk malignant potential. Subli­ The leukoplakias, which are induced with conservative treatment com­
ngual keratosis is more common in by the smokeless tobacco, are more prising of removing the cause and
women. dangerous and tend to resist the con­ medicines. The other modality being
• Etiological factors: Proliferative servative treatment. Those, which are excision. The leukoplakias that are
leukoplakia associated with human precipitated secondary to chronic diffuse and involve large area are
papilloma virus, which have an irritation (sharp tooth, chronic trauma often difficult to excise.
inexorably slow progression over from occlusion), respond, and are • The conservative line of treatment
one or two decades to verrucous or reversible on removing the cause comprises of removing the cause
squamous cell carcinoma. by smoothening the sharp cusps,
– Idiopathic leukoplakias where Box 29.4: Staging system for oral correcting overhanging edges of the
there is no obvious etiological leukoplakia30 restoration/prosthesis or discon­
factor have noted to have a signifi­ tinuation of the habits.
cantly increased risk of malignant L (Size of the lesion) • The medicinal treatment compri­
transformation in comparison • L1–size of leukoplakia < 2 cm. ses of prescription of vitamin A, B
with leukoplakias where there • L2–size of leukoplakia 2–4 cm. com­plex, and iron preparations as
• L3–size of leukoplakia > 4 cm.
are associated causative agents. imp­erical therapy. The vitamin A is
• Lx–size not specified.
While tobacco is the most impor­ P (Pathology i.e. Presence or absence of epithelial conditioner and helps in
tant risk factor associated with dysplasia) healing. The preparations like topical
leukoplakia, lesions in non- • P0–No epithelial; dysplasia. anesthetists (Lidocaine, benocaine)
tobacco users seem to be at inc­ • P1–Distinct epithelial dysplasia. can be prescribed to alleviate the
reased risk of developing oral • Px–Dysplasia not specified in the burning sensation while taking the
pathology report.
squamous cell carcinoma. OLEP staging system
food. Topical steroid preparations
– Candidal leukoplakia has incre­ • Stage I–L1P0 are also used. The patients are often
ase risk of malignant potential. • Stage II–L2P0 prescribed antioxidants like alpha
Chronic candidal infection is • Stage III–L3P0 or L1L2P1 tocopherol, beta-carotene, ascorbic
common in speckled leuko­ • Stage IV–L3P1 acid, and selenium, Zinc in an
plakia and Candida albicans can
cause or colonies on keratosis,
parti­
cularly smokers and is Flow chart 29.2: Management of leukoplakia
especially likely to form speckled
leukoplakia at lip commissures.
They may be dysplastic and have
high malignant potential than
some other keratosis. Candidal
leuko­plakia responds to anti­
fungal therapy and smoking
cessation.
– Syphilitic leukoplakia has high
malignant potential especially
seen on the dorsal surface of
tongue.
– Hairy leukoplakia caused by
Epstein bar virus usually has a
corrugated surface and affects
margins of the tongue almost
exclusively. This is associated
with HIV infections. The condi­
tion appears benign and is self-
limiting.
The staging of the oral leukoplakia is
depicted in Box 29.4.
678 Neoplastic Conditions of Head, Neck and Face

attempt to scavenge free radicals and cryoexcision and surgical excision. The elderly syphilitic patient with a com­
prevent carcinogenesis. The patients smal­ler defects are allowed to granulate parable pre-malignant tendency. Oral
are concealed to discontinue the and heal by secondary epithelization erythroplakia is clinically and histo­
habits and are kept under long term, while as the larger defects recovered pathologically similar to the genital
periodic follow-up. with split thickness skin grafts. The en­ patches. Erythroplakia may also occur
• The surgical treatment comprises of tire excised patch is subjected for the in conjunction with leuko­ plakia and
excision of the patch. The criteria for histopathologically examination and has been found concurrently with a
deciding surgery are: screened thoroughly to rule out malig­ large proportion of early invasive oral
a. Lesions which fail to respond to nancy including carcinoma in situ. carcinoma.16-17
the conservative treatment The malignant potential of erythro­
b. Fast growth Erythroplakia plakia is much higher than the leuko­
c. Development of ulceration Erythroplakia is rare condition, while plakia and the red color if often attri­
d. Color change leukoplakia is a relatively common con­ buted to tall rete pegs and increased
e. Indurations in the lesion dition. In contrast to leukoplakia, eryth­ vascularity, suggestive of high metabolic
f. The moderate and severe epi­ roplakia is almost always asso­ciated with lesion. It is therefore said that “when the
the­
lial dysplasia considered as premalignant changes histologically and lesion appears fiery and red, it is the time
Risky dysplasia and should be is therefore a most important precancer­ to scratch your head” meaning that the
removed surgically. ous lesion. The term ‘erythroplakia’ is erythroplakia should be more carefully
The lesion should be biopsied from used analogously to leukoplakia to des­ dealt.
the suspected areas (hot areas) and ignate lesions of the oral mucosa that
any malignant transformation, deg­ree, present as “a bright red velvety plaque Etiology
severity of dysplasia should be ascer­ or patch which cannot be characterized The etiology of erythroplakia is unkn­
tained, and the potentially dan­gerous clinically or pathologically as being due own, although same as for leukoplakia
lesions should be excised. to any other condition”. smoking and alcohol abuse are impor­
The modalities of excision com­ Described originally as “erythro­ tant etiological factors.
prises of excision with electrocautery, plasia” by Queyrat31 in 1911, as a les­
LASER excision, (Figs 29.13A and B) ion occurring on glans penis of an Clinical Features
Erythroplakia is predominantly a disease
of older men, with peak prevalence at 65
to 74 years. Predilection for sites: Floor
of the mouth, retromolar area, followed
by tongue, soft palate and especially in
Indian, population mandibular sulcus
(Figs 29.14 and 29.15).
The altered mucosa appears as a well-
demarcated erythematosus macule or
plaque with a soft, velvety texture. Many
of these lesions are irregular in outline,
A B and some contain islands of normal
Figs 29.13A and B: LASER excision of the leukoplakia mucosa within areas of erythroplakia, a

A B
Figs 29.14A and B: (A) Well demarcated erythematous plaque on lateral border of Fig. 29.15: Case of erythroplakia in a
tongue; (B) Floor of mouth patient with SMF of palate
Potentially Malignant Disorders of the Oral Cavity 679

Box 29.5: Differential diagnosis of erythroplakia1 form of cigar) smoking practiced among
females of Srikakulam district of Andhra
Nature of condition Diagnostic category
Pradesh, recorded a prevalence of
Inflammatory/immune disorders Nonspecific mucositis, Desquamative gingivitis,
Erythematous lichen planus, Dyscoid lupus 8.8 per­cent of leukoplakia, 4.6 percent of
erythematosus, pemphigoids, hypersensitivity pre­leukoplakia and 17.9 percent leuko­
reactions, Reither’s disease keratosis nicotine palate (Daftary,
Infections Erythematosus candidiasis, histoplasmosis et al. 199235). Palatal changes associated
Hamartomas/neoplasms Hemangioma, Kaposi’s sarcoma with reverse smoking thus, exhibited a
spectrum of clinical changes, and it was
not satisfactory to group under leuko­
plakia, preleukoplakia, or leukoker­atosis
phenomenon that has been attributed Treatment nicotina palate.16-17,36
to coalescence of a number or precance­ • Red lesions of the oral mucosa,
rous foci. It is usually asymptomatic especially those of the oral floor Clinical Features
and may be associated with an adjacent and ventral or lateral tongue, and According to Daftary et al. 1992, the
leuko­plakia. Clinically erythroplakia can in Indian populations should be incidence of palatal changes (encom­
mimic conditions shown in (Box 29.5) viewed with suspicion and a biopsy passing all components) was 24.9/1000
and biopsy often required to distinguish should be performed. among men and 39.6/1000 among
between them. • If a source of irritation can be iden­ women and the peak incidence was in
Several clinical variants of erythr­ tified and removed, biopsy of such the 55 to 64 year age group.
oplakia have been described by different lesions may be delayed for two weeks The regression rate was higher,
investigators, but there is no general to allow a clinically similar infla­ when habit was discontinued or reduced
agreement on classification. Shear,32 in mmatory lesion time to regress. substantially (Gupta PC et al. 198021).
1972, described: • As with leukoplakia, the treatment Malignant transformation was observed
• Homogenous form of erythroplakia is guided by the for 0.3 percent of the palatal lesions. In
• Erythroplakia interspersed with pat­ definitive diagnosis obtained by 10-year intervention study in the same
ches of leukoplakia, and biopsy. area, the malignant potential of various
• Granular or Speckled erythroplakia • Lesions exhibiting moderate dyspla­ components of palatal changes was
(identical to speckled leukoplakia). sia or worse must be removed com­ evaluated: red patches were found to
Homogeneous erythroplakia has pletely or destroyed by the methods exhibit a high potential for malignant
more malignant transformation rate used for leukoplakia. transformation (Fig. 29.16).
than speckled erythroplakia. The car­ • The excised specimen must send for Palatal changes comprise several
ci­no­genic potential of erythro­plakia is microscopic examination because com­­ponents16:
considered to be higher (14–50%)33,34 of the possibility that a focal invasive • Keratosis: Diffuse whitening of en­
than leukoplakia and SMF. carcinoma might be missed in the tire palatal mucosa.
initial biopsy material. • Excrescences: 1 to 3 mm elevated
Histopathological Features • Recurrence and multifocal oral mu­ nodules, often with central red spots.
Different studies have demonstrated cosal involvement are com­mon with • Patches: Well defined, elevated white
that 80 to 90 percent of erythroplakia erythroplakia; hence, long-term plaques.
are histologically either severe epithe­ follow up is suggested for treated
lial dysplasia, carcinoma in situ, or patient.17
superficially invasive squamous cell
carcinoma. The epithelium shows a
Palatal Changes Associated
lack of keratin production and is often
atrophic, but it may be hyperplastic. with Reverse Smoking
This lack of keratinization especially A diffuse thickening of the palatal mu­
combined with dropped pushing rete cosa occurs in reverse smokers. In several
pegs along with deep long connec­ countries, cigars or cigarettes are smoked
tive tissue papillae with overlying with the glowing end inside the mouth.
thin epithelium allows the visibility The largest numbers of reverse smokers
of underlying microvasculature. This is found in certain areas of India, but
explains the red color of the lesion. the habit is also practiced in some Latin Fig. 29.16: Diffuse whitening of palatal
The underlying connective tissue often American countries, in Sardinia and in mucosa with small elevated nodules with
demonstrates chronic inflammation. the Philippines. Reverse chutta (crude central red spots
680 Neoplastic Conditions of Head, Neck and Face

• Red areas: Well defined reddening and inflammation of the palate. Later, exposure to the ultraviolet component
of the palatal mucosa. grayish-white, thickened, multinodular, of sunlight. It is problem confined pre­
• Ulcerated areas: Crater like areas or papular appearance with a small red do­minantly to light com­plexi­oned
covered by fibrin, and spot in the center of each tiny nodule is people with a tendency to sunburn
• Non-pigmented areas: Areas of representing the dilated and sometimes easily. Outdoor occupation obviously
palatal mucosa that are devoid of partially occluded orifice of an accessory is associated with this problem, lead­
pigmentation. palatal salivary gland duct. The mucosa ing to the popular use of terms such as
that covers the papules frequently ‘Farmers lip’ and ‘Sailor’s lip’. A person
Histological Features appears whiter than the surrounding with chronic sunlight exposure and
Histopathologically hyperkeratosis and epithelium. The palatal keratin may compromised immunity, especially a
epithelial dysplasia is noted. Epithelial become so thickened that fissured or transplant recipient, has an elevated
dysplasia was observed in 52 percent of dried mud appearance is imparted. risk of developing a cancer of the lower
red areas, 25 percent of excrescences, It is histopathologically characteri­ lip vermilion.
20 percent ulcerations, 10 percent zed by hyperkeratosis and acanthosis of
of patches and in 19 percent of non- ductal and palatal epithelium. Epithelial Pathogenesis
pigmented areas. (Comprises data from dysplasia is very rarely seen. The ducts Cumulative ultraviolet radiation can
only one study i.e. by Daftary et al.). of minor salivary glands show dilatation produce mutations in the p53 tumor
Palatal changes associated with and inflammation around them. suppressor gene,38 an alteration frequ­
reverse smoking are characterized by ently found in this and other precancers
hyperorthokeratosis, epithelial dysplasia Treatment and cancers of the head and neck region.
and inflammatory cells in the connective It is completely reversible even when
tissue. Melanin deposits is seen in the it has been present for many decades. Clinical Features
lamina propria of most of them. The Although this is not a precancerous Actinic cheilosis seldom occurs in per­
epithelium is either atrophic or shows lesion, the patient should be encouraged
son with 45 years and above. It has strong
epithelial dysplasia in red areas. to stop habit and any suspicious areamale predilection (male : female = 10 : 1
should be examined closely by biopsy.in some studies).
Treatment Any white lesions or the palatal mucosa
• The earliest clinical changes include
The treatment comprises of discon­tinu­ that persist after one month of habit atrophy of the lower lip vermilion
ation of habit and follow-up of the patient. cessation should be considered a true border, characterized by a smooth
If suspicious red areas, ulcer­ations, pat­ leukoplakia and managed accordingly. surface and blotchy pale areas.
ches persist, then biopsy should be carried • Typical blurring of margin between
out. If possible, conservative exci­ sional Bowen’s Disease the vermilion zone and cutaneous
biopsy is the treatment of choice. Bowen’s disease is a special form of in­ portion of lip is seen.
traepithelial carcinoma occurring with
• As the lesion progresses, rough scaly
Nicotina Stomatitis some frequency on skin, particularly in areas develop on the drier portions
(Pipe Smoker’s Palate) patients who have had arsenical therapy. of the vermilion. These areas thicken
It is a specific mucosal change of palate, and may appear as leukoplakic le­
which is frequently seen in heavy pipe Clinical Features sions especially when they extend
smokers. Because pipe smoking gener­ It is often associated with the internal and near the wet line of the lip. The pa­
ates more heat on the palate than other extracutaneous cancer. On rare occasion tient may report the scaly material
forms of smoking. Similar changes can as reported by Gorlin37 Bowen’s disease can be peeled off with some difficulty.
also be produced by the long term use may occur in the oral cavity. It may be • With further progression, chronic
of extremly hot beverages. Although this seen as leukoplakia or a combination of focal ulceration may develop in one or
lesion is a white keratotic change, obvi­ leukoplakia and erythroplakia or as an more sites, especially at places of mild
ously associated with tobacco smoking, it ulcerated lesion intraorally. It is usually trauma from cigarettes or pipe stems.
does not appear to have a premalignant seen in elderly persons and somewhat Such ulcerations may last for months
nature, perhaps because it developes in more common in males than women. and often suggest progression to early
response to heat rather than the chemi­ squamous cell carcinoma.
cals in tobacco smoke.16-17, 27 Usually well-differentiated squamous
Actinic Cheilosis cell carcinoma develops over a time in 6
Clinical Features (Actinic Chelitis) to 10 percent of actinic che­il­osis cases.
Nicotine stomatitis most commonly Actinic cheilosis is a common pre­malig­ Such malignant transformation seldom
is found in men older than 45 years of nant alteration of the lower lip vermilion occurs before 60 years of age, with the
age. It is first manifested as redness that results from long term or excessive resulting carcinoma typically enlarging
Potentially Malignant Disorders of the Oral Cavity 681

slowly and metastasizing only at late clinically effective. All therapies, propria, with epithelial atrophy leading
stage.10 with the exception of chemical peel­ to stiffness of the oral mucosa causing
ing, appear to have a low clinical trismus and inability to eat.”
Histopathological Features failure rate. Histological clearance of
It is usually characterized by an atrophic disease was demonstrated in carbon
stratified squamous epithelium, often dioxide laser-treated patients. 5-Flu­ Etiology
demonstrating marked keratin produc­ o­rouracil failed to achieve complete The pathogenesis of the disease is be­
tion. Varying degrees of dysplasia may removal of histologic dysplasia. lieved to be multifactorial. Present
be encountered. The carbon dioxide laser may be evidence indicates that chewing areca
It is usually associated with increa­sed associated with less scarring and nut, tobacco, slaked lime or other spic­
degree of epithelial change: acan­thosis, an improved cosmetic outcome in es is an important risk factor for OSF.
basophilic change within the connec­ comparison with the scalpel vermi­ Many etiologic factors,37,49 hypoth­
tive tissue, the presence of inflammation lionectomy. esized to trigger the disease process
within the connective tissue, perivascu­ include:
lar inflammation, and thickness of the ORAL SUBMUCOUS FIBROSIS • Betel nut/Areca nut with or without
keratin layer.39 tobacco
Oral submucous fibrosis (OSF) has been • Excessive consumption of chilies
Treatment and Prognosis well established in Indian medical lit­ (capsaicin) or spices
• Many of the changes associated erature since the time of Sushruta as vi­ • Vitamin B deficiency
with actinic cheilosis are probably dari.41 In modern literature, Schwartz42 • Protein deficiency
irreversible, but patient should be first described this condition in 1952 • Iron deficiency
encouraged to use lip balms with while examining five Indian women • Trace element deficiency such as
sunscreens to prevent further dama­ from Kenya, to which he ascribed the iron, zinc and essential vitamins
ged. descriptive term “atrophia idiopathica • Genetic susceptibility
• Areas of indurations, thickening, mucosa oris’. Later in 1953, Joshi43 from • Autoimmunity and hypersensitivity
ulceration, are leukoplakia/erythro­ Bombay redesignated the condition states.
plakia should be submitted for as ‘oral submucous fibrosis’ implying It is apparent that fibrosis and hyali­ni­
biopsy to rule out carcinoma. predominantly its histologic nature. Its zation of sub epithelial tissues account for
• In clinically severe cases without precancerous nature was reported by most of the clinical features encountered.
malignancy; a lip shave procedure Paymaster44 in 1956. Pindborg et al.45 re­ Since the increased collagen synthesis or
(vemilionectomy) may be perfor­ ported a prevalence of OSF in India to be reduced collagen degradation as possible
med. The vermilion mucosa is re­ about 0.2 to 0.5 percent with an estimate mechanisms in the development of the
moved, and portion of the intra­oral of no fewer than 2.5 million cases and disease. It is likely that the normal regu­
labial mucosa is pulled forward or demonstrated a malignant transforma­ latory mechanisms are either down regu­
the wound lip allowed healed by tion rate of 4.5 percent. The reported in­ lated or up regulated at different stages of
secondary intentions. cidence of malignant transformation is 7 disease.
• Alternative treatments include CO2 to 13 percent in the literature.46,47
laser ablations and electrodessi­ This condition is predominantly
Various Mechanisms Suggested
cation. Long-term follow up is reco­ seen in the Indian subcontinent and
mm­ended. people of this origin settled elsewhere for the Etiopathogenesis of OSF
• If a squamous cell carcinoma is in the world. There has been an incre­ • Stimulation of fibroblast prolifer­
iden­ti­fied, the involved lip is treated ase in the use of areca nut, particularly ation and collagen synthesis by
accor­dingly. pan masala in the younger group in areca nut alkaloids (Harvey W et al.50
• Focal actinic cheilitis is easily treated India, due to easy access, effective 1986)
with cryosurgery or electrosurgery. price changes, and marketing strategies • Clonal selection of fibroblast with a
Extensive actinic cheilitis requires leading to increasing incidence of OSF. high amount of collagen production
5-fluorouracil, carbon dioxide laser, In 1966, Pindborg48 defined OSF as during the long term exposure to
or scalpel vermilionectomy for ade­ “an insidious chronic disease affecting arecanut ingredients (Meghji S
quate treatment. The carbon dioxide any part of the oral cavity and sometimes et al.51 1987)
laser offers some advantages over the pharynx; occasionally preceded by • Stabilization of collagen structure by
scalpel vermilionectomy.40 and/or associated with vesicle forma­ catechin and tannins from arecanut
• Cryosurgery, electrocautery, 5-fluo­ tion, it is always associated with juxta- (Scutt A et al.52 1987)
ro­uracil, carbon dioxide laser, and epithelial inflammatory reaction follow­ • Decreased secretion of collagenase
scalpel verimilionectomy were all ed by a fibro elastic change of the lamina (Shieh TY et al.53 1992)
682 Neoplastic Conditions of Head, Neck and Face

• Production of stable collagen (type I and a fibrosis induction phase, fibrosis extending deep into the pillars
trimmer) by OSF fibroblasts (Kuo characterized by diminished acute with strangulation of the tonsils.
MYP et al.54 1995) symptoms and blanching as the • Difficulty in mouth opening, inability
• Increase in collagen cross linking by vesicles heal and fibrous tissue is to whistle or blow out a candle and
up regulation of lysyl oxidase (Ma formed. difficulty in swallowing due to dense
RH et al.55 1995) • Focal vascular dilatations manifest fibrosis involving the tissues around
• Deficiency in collagen phagocytosis clinically as petechiae in the early the pterygomandibular raphae,
(Tsai CC et al.56 1999) and stages of the disease. This may be with progressive fibrosis and the
• Effect of fibrogenic cytokines secre­ the part of vascular response due to sti­f­­fening of certain area of mucosa
ted by activated macrophages and T hypersensitivity of the oral mucosa (Fig. 29.17A).
lymphocytes on fibroblasts (Haque towards some external irritant like • Impairment of tongue movement
MF et al.57 2000). areca nut products. with atrophy of the tongue papillae
• Pain in areas where submucosal and some times loss of gustatory
Clinical Features fibrotic band are developing when sensation.
The onset is insidious, over two to five palpated is a useful clinical test. • Involvement of esophagus can lead
years. to progressive dysphagia and re­
Advanced OSF duced oesophageal mobility.
Early OSF • As the disease progresses, the oral • In extensive cases throat pain, ear
• Burning sensation of the mouth, mucosa become blanched and slight­ pain and losses of auditory acuity
particularly while eating spicy foods. ly opaque, and white fibrous bands due to stenosis of the eustachian
• Followed by the formation of vesicles appear. In patients, who spit the are­ tube are noted.
(often on the palate), ulcerations, or ca nut, tobacco and lime, the buccal • The fibrosis of nasopharynx leads to
recurrent generalized stomatitis, mucosa and lips may be affected at an referred pain to the ear and a nasal
with excessive salivation, defective early stage where as in patients who voice as one of the later signs in
gustatory sensation, and xerostomia. swallow the areca nut, tobacco, lime some patient.
• There are periods of exacerbation and quid the palate and the faucial
manifested by the appearance of pillars are the areas involved first.
Precancerous Nature and
small vesicles in the cheek and • The buccal mucosa is involved sym­
palate with intervals of three months metrically and the fibrous bands in Malignant Transformation
to one year. The vesicles heal the buccal mucosa run in a vertical Paymaster35 first described the precan­
within few days and the burning direction. cerous nature of OSF in 1956 by obser­
sensation diminishes. The healing • The fibrosis varies from a slight whit­ ving the slow growing squamous cell
of the vesicles is characterized by ish area of the soft palate, causing no carcinoma in one third of the patient
blanching, indication induction of symptoms, to a dense fibrosis result­ with the disease. Various groups con­
fibrosis. Borle (1991) proposed two ing in fixation and shortening or even firmed this and Pindborg58 in 1972 put
distinct cyclic phases in OSF, an deviation of the uvula and soft palate forward five criteria to prove that the
erruptive phase, characterized by (Fig. 29.17 B and C). disease is precancerous.
increased burning sensation and • The fibrosis in the faucial pillars varies 1. High occurrence of OSF in oral
formation of vesicles (Fig 29.17D) from slight submucosal to a dense cancer patient

A B C D
Figs 29.17A to D: (A) Interincisal opening of 22 mm; (B and C) Blanching on the buccal mucosa and palate with atrophic uvula;
(D) Vesicles on the palate
Potentially Malignant Disorders of the Oral Cavity 683

2. Higher incidence of SCC in-patient genesis in OSF was hypothesized by secondary to SMF is generally seen in
with OSF Tilakaratne WM et al.60 2000. the retro­molar areas (probably due to
3. Histological diagnosis of cancer • OSF and coexistent leukoplakia: chro­nic irritation from the buccally
with­out any clinical suspicion in OSF Leukoplakia is precancerous lesion; tilted and malposed maxillary third
4. High frequency of epithelial dyspla­ its coexistence with OSF implies the molars), tongue and the floor of
sia, and high risk for oral cancer. More fre­ the mouth and always makes the
5. Higher prevalence of leukoplakia quently homogeneous and nodular identi­fication and assessment very
among OSF cases. leukoplakias occur. difficult due to presence of severe
Malignant transformation rate of • OSF and coexistent oral cancer: The tris­mus (Figs 29.18A to D). Maj­
OSF was found to be in the range of 7 coexistence of the oral squamous ority of the cases are diagnosed at
to 13 percent.59 According to long term, cell carcinoma and the OSF is well stage III or IV making the prognosis
follow up studies a transformation rate documented in the literature and very poor. The disease is usually
of 7.6 percent over a period of 17 years various studies have shown it to be resistant to treatment and early
was reported by Murti PR et al. in 1985.48 between 5 to 42 percent.61 Of late recurrence is a common occurrence.
The dense fibrosis and less vascul­ in the clinical practice more and In some cases second primary after
arity of the corium, in the presence of an more cases of OSCC are seen to be the treatment of the first carci­
altered cytokine activity create a unique associated with pre existing, long nomatous lesion or at the time of first
environment for carcinogens from both standing OSF. As OSF is generally diagnosis more than one primary are
tobacco and areca nut to act on the of a long duration the presence of seen suggesting the phenomenon of
epithelium. So that carcinogens from oral cancer implies that it is a later field cancerization (Fig. 29.18E).
areca nut accumulate over a long period development i.e. a consequences of
either on or immediately below the the malignant transformation of OSF. Histopathological Features
epithelium, allowing the carcinogens to The peculiarity of such association The excessive fibrosis in the mucosa
act for longer duration before it diffuses is that it is seen in rela­tively younger seems to be the primary pathology in
in to deeper tissues. Less vascularity patients, and the youngest patient OSF. The atrophic changes in the epi­
may deny the quick absorption of carc­ reported at our center (SPDC, thelium are secondary.
inogens in to the systemic circu­lation. Wardha, India) was 18 years of age Epithelial changes: In the differ­
This possible mechanism of carci­ no­ (mean age 31.3 years). The OSCC ent stages of OSF are predominantly

A B C

D E
Figs 29.18A to E: (A) SMF with OSCC of retromolar area and lower lip (two primaries); (B) Tongue and retromolar area; (C) Red patch on
buccal mucosa in SMF is warning sign of malignant transformation; (D) Malignant growth in the retromolar area due to cronic trauma
from occlusion in a case of SMF; (E) Multiple primaries in a case of SMF shown in a ressected specimen of wedge mandibulectomy and
SOHD on left side
684 Neoplastic Conditions of Head, Neck and Face

hyper­plasia (early), atrophy (advanced), characterized by vesiculation and inc­ Group III: Moderately advanced cases
and loss of rete pegs of epithelium, asso­ reased burning sensation and (2) A • Trismus evident, with an interincisal
ciated with an increasing tendency for fibrosis induction phase characterized distance of 15 to 25 mm
keratinizing metaplasia. The epithelial by diminished burning sensation and • Buccal mucosa appears pale and
dysplasia without carcinoma is found in blanching due to healing of vesicles by firmly attached to underlying tissues
10 to 15 percent of cases and carcinoma fibrosis. They claimed that these phases • Atrophy of vermilion border
is found in at least five percent of cases. come in cyclic manner and the stage 1 is • Vertical fibrosis bands palpable at
However, the concomitant association induced by irritants like betel nut, lime the soft palate, pterygomandibular
of OSCC and SMF was found in 28 per­ and tobacco.62 raphe, and anterior faucial pillars.
cent cases at our center (SPDC, War­dha, Recently Khanna JN and Andrade
India). NN63 (1995) developed a group classifi­ Histology
Subepithelial changes: In early cation system for the surgical manage­ • Juxtaepithelial hyalinization present
stages juxtaepithelial chronic inflam­ ment of OSF. • Thickened collagen bundles faintly
matory cell infiltrate with dilated blood discernible, separated by very slight,
vessels and rise in mast cells. In ad­ Group I: Very early cases residual edema
vanced cases submucosal deposition • Common symptom is burning sensa­ • Blood vessels mostly constricted
of extremely dense and avascular col­ tion in mouth • Mature fibroblast with scanty cyto­
lagenous tissues with variable numbers • Acute ulceration and recurrent sto­ plasm and spindle shaped nuclei
of chronic inflammatory cells is seen matitis. • Inflammatory exudates consist main­
(Figs 29.19 and 29.20). ly of lymphocytes and plasma cell
Several classification have been put Histology • Epithelium markedly atrophy with
forth by various researchers, based on • Fine fibrillar collagen network inter­ loss of rete pegs
different aspect of Borle R M and Borle spersed with marked edema • Muscle fibers seen interspersed
S R have suggested two clinical stages • Dilated and congested blood vessels with thickened and dense collagen
in the SMF (1) An eruptive phase— • Large aggregate of plump, young fibers.
fibroblasts present with abundant
cytoplasm Group IVA: Advance cases
• Inflammatory cells mainly consist of • Trismus is sever with interincisal
polymorphonuclear leukocytes with distance of less than 15 mm
few eosinophils • The fauces thickened, shortened
• Normal Epithelium. and firmed on palpation
• Uvula is shrunken and appears as
Group II: Early cases small, fibrous bud
• Buccal mucosa appears mottled and • Tongue movement limited
marble-like • On palpation of lips, circular band
• Widespread whets of fibrosis pal­ felt around entire moth.
pable
Fig. 29.19: Atrophic stratified squamous epi­ • Patient is with an interincisal dis­ Group IVB: Advance cases with
thelium with fibrosis in underlying connective tance of 26 to 35 mm. premalignant and malignant changes
tissue stoma involving muscle fibers Hyperkeratosis leukoplakia, squamous
Histology cell carcinoma can be seen.
• Juxtaepithelial hyalinization present
• Collagen present as thickened but Histology
separate bundles • Collagen hyalinization as smooth
• Blood vessels dilated and congested sheet
• Young fibroblast seen in moderate • Extensive fibrosis obliterated muco­
number sal blood vessels and eliminated the
• Inflammatory cell mainly consists melanocytes
of polymorphonuclear leukocytes • Fibroblast were markedly absent
with few eosinophils and occasional within the hyalinized zone
plasma cells • Total loss of epithelial rete pegs
Fig. 29.20: Mild epithelial dysplasia with • Flattening or shortening of epithelial • Mild to moderate atypia present
fibrosis in underlying connective tissue rete pegs evident with varying degree • Extensive degeneration of muscle
stoma involving muscle fibers of keratinization. fibers evident.
Potentially Malignant Disorders of the Oral Cavity 685

Differential Diagnosis • Surgical treatment: Modalities incl­ the condition in 1869. The disease is
OSF has a characteristic clinical ap­ ude excision of fibrous bands with or relatively common affecting approxi­
pearance and there are few conditions without grafting. Grafts inclu­ded, split mately 1 to 2 percent of the population.
that need to be differentiated from it. thickness grafts, placental grafts,64 In the majority of instances cutaneous
One is oral manifestation of scleroder­ ton­­gue flaps,65 buccal fat pad66 (Fig. lesion of LP are self limiting and cause
ma. More often pale mucosa coupled 29.21A). They also have been largely inching, oral lesions in LP are chronic,
with pigmentation seen in anemic con­ unsuccessful due to graft rejections rarely undergo spontaneous remission,
ditions, may be mistaken for blanching and development of secondary scar are potentially malignant and are often
in OSF. contracture in the raw buccal mucosa source of morbidity.10
and ptery­gomandibular raphae areas.
Treatment modalities The involvement of tongue and palatal Etiopathogenesis
• The reduction or even elimination mucosa in advanced cases of OSF The OLP is a T-cell mediated autoimm­
of the habit of areca nut chewing is precludes its use as a flap to recons­ une disease in which cytotoxic CD8+ T
an important preventive measure. truct the defect in buccal mucosa. cells trigger the apoptosis of oral epi­thelial
In the early stage of OSF it could Advanced cases of OSF require apart cells.69 The CD8+ lesional T-cells may
probably slow the progress of the from surgical release of fibrosis, bilateral recognize an antigen associated with the
disease. temporalis myotomy and coronoi­ dec­ major histocompatibility comp­lex (MHC)
• Nutrition support: Mainly for high tomy. Reconstruction of the defect can class I on keratinocytes. After antigen
proteins and calories and for vitamin be performed by the application of the recognition activation, CD8+ cytotoxic
B complex and other vitamins and nasolabial skin island flap67 to provide T-cells may trigger kera­tinocyte apopto­
mineral. supple skin and subcutaneous tissue to sis. Activated CD8+ T-cells (and possibly
• Immunomodulatory drugs: Local interpose in the defect (Fig. 29.21B). keratinocyte) may release cytokines that
and systemic applications of gluco­ The advantages of this technique is attract additional lymphocytes into the
corticoids and placental extracts are that the donor site is in the same oper­ developing lesion. The lichen planus an­
commonly used. These also prevent ating field, reliable, and rich vascu­larity, tigen unknown, although it may be self-
or suppress inflammatory reaction, versatility in design, proximity to defect, peptide. The over expression or unmask­
thereby preventing fibrosis by de­ ease of flap elevation, supple skin thus ing of the OLP antigen may be induced by
creasing fibroblastic proliferation aiding in increased mouth open­ing, the drugs, contact allergens in dental restor­
and deposition of collagen. donor site can easily be under­mined and ative materials or toothpastes, mechani­
• Local drug delivery: Local injec­ closed linearly with minimal deformity. cal trauma (Koebner phenomenon70), vi­
tions of corticosteroids and placental ral infections specially hepatitis C virus or
extract have been tried in addition LICHEN PLANUS unidentified agents. Patient with OLP ex­
to hyaluronidase, collagenase and hibit the higher levels of anxiety, greater
similar substance which break down Lichen planus (LP) is a relatively com­ depression and increased vulnerability to
intercellular cement substance and mon, chronic immunologic inflamma­ psychic disorder. Other causes suggested
also decrease collagen formation. tory mucocutaneous disorder that varies include malnutrition and infection.
• Physiotherapy: This includes mea­ in appearance from keratotic (reticular Grinspan has described an interes­
sures such as forceful mouth open­ or plaque like) to erythematous and ul­ ting association of lichen planus, diabe­
ing and heat therapy. Heat has been cerative. The British physician Erasmus tes mellitus, and vascular hyper­tension.
commonly used and the results have Wilson68 provided the strange name of The triad being described as “Grinspan
been described as satisfactory.
• Combined therapy: Medical line of
treatment includes usage of Gold,
Iodides, Hyaluronidase, Hydrocor­
tisone, Placental extracts, Triam­
cinolone, Vitamins, and Iron supple­
ments. Peripheral vasodilators like
Buflomedial hydrochloride and Nyl­
h­ydrin hydrochloride. They are use­
ful in early stages of OSF. They are of
temporary benefit in advanced stag­
es of OSF and do not offer any long-
term relief to the patients, also have I II
no role in advanced stages in OSF. Fig. 29.21A: Case of SMF treated with Buccal flap pad grafting.
686 Neoplastic Conditions of Head, Neck and Face

I II III IV V VI

VII VIII IX X

XI XII XIII XIV


Fig. 29.21B: Bilateral fibrotomy and reconstruction by bipedaled nasolabial flap (Sawangi protocol)

syndrome”71 by Grapper. The oral liche­


noid lesions develops as an adverse
reaction to the drugs used for the
treatment of hypertension and diabetes
mellitus.72

Clinical Features
Oral lichen planus develops most
commonly in the fifth to sixth decade
of life and in women more than twice
as often as men. It is rarely affected in
children. Oral lichen planus lesions usu­
ally have recognizable and distinctive
clinical features and a characteristic A B
distribution. OLP may manifests in Figs 29.22A and B: Bilateral reticular lichen planus: The network of connecting and
one of four clinical forms: (a) Reticular, overlapping thin white lines on both right and left side of buccal mucosa
(b) Erythematous (atro­phic) (c) Erosive
(ulcerated) and (d) Bullous forms.73
Where as reticular lesions occur as iso­ which are characterized by isolated papules, or plaques in some ins­
lated lesions and are often the only areas of erythema and/or erosions. tances (Figs 29.22A and B).
clinical manifestations of the disease, • The patients with reticulate lesions
erythematous lesions are accompanied The Reticular Lesions rarely complain of symptoms and
by reticular lesions, and erosive lesions • The most recognized form, encom­ often, are unaware of their prese­nce.
are accompanied by reticular and ery­ pass white lesions, which appear as • These lesions are typically not static,
thematous lesions in almost all cases. a network of connecting and over­ but wax and wane over weeks or
This feature helps clinically differentiate lapping white lines (also referred months.
from other vesiculo-erosive diseases to as Wickham’s striae,74 however • The reticular form usually invol­
such as pemphigus and pemphigoid, the white lesions may appear as ves the posterior buccal mucosa
Potentially Malignant Disorders of the Oral Cavity 687

bila­
terally. Other oral mucosal ped and occasionally polygonal in • This is accompanied by juxtaepithe­
surfaces may also be involved con­ form. A network of fine lines often lial intense band of chronic inflam­
currently such as the lateral and overlies many of the papules. matory cell infiltrate predominantly
dorsal ton­ gue, the gingiva, the • The lesions are distributed in a bilat­ of T lymphocytes.
palate, and ver­milion border of lip. erally symmetrical pattern, most of­ • Degenerating keratinocytes may be
ten on flexor surfaces of wrist, fore­ seen in the area of the epithelium and
Erythematous and Erosive OLP arms, inner aspect of knees, thighs, connective tissue interface and have
• Although not as common as reti­ trunk and sacral area. been termed colloid, cytoid, hyaline,
cular form, are more significant for • Typically, cutaneous lesions develop or civatte bodies (Figs 29.23A and B).
the patient because the lesions are within several months after the • Dysplastic changes are sometimes
usually symptomatic. appearance of the oral lesions, and seen.
• Clinically there are atrophic, ery­ the severity of the oral lesions does
thematous areas with central ulcer­ not seem to correlate with the extent
Immunofluorescence
ations of varying degrees. The periph­ of cutaneous involvement. of Perilesional Mucosa
ery of the lesions is usually bordered • Other sites of extraoral involvement • Fibrin and shaggy fibrinogen in a
by fine, white radiating striae. include the glans penis, the vulvar linear pattern at the basement mem­
• Sometimes the atrophy and ulcer­ mucosa, and the nails. brane zone
ation are confined to the gingival • Cytoids deposition in the absence of
mucosa, producing the reaction Histopathological Features deposition of fibrinogen.
pattern called desquamative gin­ The histopathological features of OLP
givitis. In such cases, biopsy speci­ are characteristics but may not be spe­ Diagnosis
mens should be obtained for light cific, because other conditions such The characteristic clinical aspects of OLP
microscopic and immunofluores­ as lichenoid drug reaction, lichenoid may be sufficient to make a correct diag­
cent studies of perilesional tissues, amalgam reaction, lupus erythemato­ nosis if classic skin lesions are pre­sent.
because cicatricial pemphigoid and sus, and chronic ulcerative stomatitis It is important that other lesions, which
pemphigus vulgaris may appear in a may also show a similar histopathologi­ bear superficial resemblance to OLP,
similar fashion. cal pattern. include lichenoid reaction, leukoplakia,
• If erosive component is severe, epi­ • Varying degrees of orthokeratosis erythroplakia, candidiasis, pemphigus,
thelial separation may occur. This and parakeratosis and sometimes- cicatricial pemphigoid, erythema mul­
results in relatively rare presentation atrophic epithelium depending on tiforme, syphilis, recurrent aphthae and
of bullous OLP. biopsy taken from erosive or reticu­ lupus erythematosus. An oral biopsy
lar lesion. with histopathological study is recom­
Cutaneous Manifestations • The rete ridges may be absent or hy­ mended to confirm the clinical diagnosis
• Approximately 15 percent of patient perplastic but they classically have a and mainly to exclude dysplasia and ma­
with OLP develop cutaneous lesions. pointed or “saw toothed” shape. lignancy. The diagnosis of OLP is based
• The classic appearance of skin les­ • Destruction of the Basal cell layer of on clinicohistopathological correlation.
ions consists of erythematous to the epithelium (hydrophic degen­ Sometimes immunofluorescence can be
violaceous papule that are flat top­ eration) is also present. used as an important diagnostic tool.

A B
Figs 29.23A and B: Hyperparakeratotic stratified squamous epithelium with degeneration of basal cell layer and subepithelial band of
chronic inflammatory cell infiltrate
688 Neoplastic Conditions of Head, Neck and Face

Oral Lichenoid Reactions important to monitor all patients with • Other topical agent such as topical
The concept of oral lichenoid reac­tions OLP carefully over the long term.79 retinoids or cyclosporine has
or lesions, eruptions in the oral cavity occasionally been advocated for
that have an identifiable etiology and that Possible Risk Factors for erosive/atrophic lichen planus.
clini­
cally and histologically resemble Malignant Transformation in OLP • For intractable erosive OLP lesions
OLP, is well recognized but controversial. intralesional steroids such as triam-
Other authors use the term oral lichenoid • Habit of tobacco and betel nut, cinolone acetonide (10–20 mg/mL)
reaction when several clinical and his­ smoking and alcohol consumption. injections can be effective and re­
tological features are present but the • Atrophic-erosive forms of OLP pre­ peated every 2-4 weeks.
diagnosis remains inconclusive. disposed to cancer development as • Systemic steroids should be reserved
Dental restorative materials includ­ it enhance the action of carcinogens for recalcitrant erosive or erythema­
ing amalgams, composite resins, cobalt, on epithelium. tous OLP, where topical approaches
gold and even flavoring and plastics • OLP lesions on tongue has increased have failed, or for widespread OLP
can be important in the pathogenesis. risk for cancer. with concomitant skin, genital,
Drug induced oral lichenoid reactions • Gender and age risk is higher in esophageal or scalp involvement.
have been reported most commonly to women than in men frequently • Surgical excision is usually not in­
non-steroidal, anti-inflammatory, the develop between sixth and seventh dicated except in cases where con­
angi­otensin-converting enzyme inhi­ decade of life. comitant dysplasia is identified.
bitors, beta-blockers, methyldopa, and • After OLP diagnosis, the increased
penicillamine. malignant transformation risk after Dyskeratosis Congenita
Clinically the oral lichenoid lesions 3 to 6 years duration. Dyskeratosis congenita is a rare, inherit­
are unilateral and erosive. Histologically • Modification in diet (less fresh veg­ ed disorder, with premature aging, bone
shows more diffuse lymphocytic infi­ltrate etables and fruit especially citrus marrow failure, and malignancy:
and contain eosinophils and plasma cell fruit) imposed by symptoms espe­ It consists of Triad of:
and there may be more colloid bodies cially in erosive and atrophic forms. • Nail dystrophy
than in classical OLP.19 • Infections: • Skin pigmentation and
– Candida albicans may be an • Mucosal Leukoplakia
Malignant Potential impor­­ tant factor in OLP mali­ The syndrome often proves fatal due
The reported frequency of malignant gnant transformation. to Bone marrow failure or Malignant
transformation varies greatly bet­ – Hepatitis C virus infection may changes within areas of mucosal leuko­
ween 0.4 percent to over 5 percent over increases the risk of cancer. plakia.80
peri­ods of observation from 0.5 to over
20 years.75-78 There is considerable con­ Treatment Clinical Presentation
tro­versy regarding the malignant trans­ • Reticular lesions that are asymp­
formation of OLP. Many investigators tomatic generally require no therapy Nail dystrophy, Leukoplakia and skin
have questioned the criteria utilized for but only observation for change. hyper pigmentation tend to appear in
diagnosing OLP in published reports. Occasionally patient may have super­ the first decade of life with medial ages
Some published cases of OLP associated imposed candidiasis in which patient of onset of six, seven and eight years
with malignant transformation, diag­ may complain of burning sensation respectively.
nosed clinically as OLP may actually of the oral mucosa. Antifungal ther­
have been lichenoid dysplasia, pre­ apy necessary in such cases. Mucocutaneous Features
malignant condition with lichenoid • Any etiological agent should be Reticulated skin hyper pigmentation
features. The patient with lichenoid removed or stopped. affecting the neck, face chest and arms
dysplasia often displays erythematous • Psychological counseling of patient. (app. 90% of patient)
and erosive lesions clinically to identical • An optimal oral hygiene program • Can be either a localized or florid
to OLP lesions. Where as other studies should be instituted in-patient with generalized form.
with strict diagnostic criteria for the gingival disease. • A variety of other changes: Cuta­
disease demonstrated significant risk • Topical corticosteroids (e.g. fluoc­ neous atrophy, hyperhidrosis of
for OLP patient to develop squamous inonide, betamethasone, clobetasol the palms and soles, telagiectasia,
cell carcinoma. The uncertainty of the gel) applied several times per day cracking, fissuring, bulla formation,
premalignant nature of OLP and the to the most symptomatic areas is loss of dermal ridges, hair tufts with
fact that early detection of oral cancer usually sufficient to induce healing keratotic plugs on the limbs and ke­
results in improved survival, so that it is within 1 or 2 weeks. ratinized basal cell papillomas.
Potentially Malignant Disorders of the Oral Cavity 689

Dystrophic changes in the nails (90% of • Skeletal anomalies in 20 percent • Identification of the gene responsible
patient) of cases include mandibular hypo­ offers the potential for
• More severed in fingers than toes plasia, osteoporosis, abnormal bone – Improving diagnosis
• Begin with longitudinal ridging and trabe­culation, avascular necrosis, – Monitoring progression of the
splitting and may progress to nail and scoliosis. disease once diagnosed and
loss. • Other manifestations of oral cavity – Novel forms of therapy for this
Leukoplakia (80% of patient) occurs any are hyperpigmentation of buccal muc­­ inherited disorder.68
mucosal surface osa, severe periodontal disease, hypo
• Most frequently reported on oral calcified teeth and tauro­dontism. Syphilis
mucosa, tongue being the most • Genitourinary abnormalities include Syphilitic leukoplakia was a characteris­
frequently affected other include hypoplastic testes, hypospadias, phi­ tic complication of tertiary syphilis but is
lingual mucosa, buccal mucosa and mosis, urethral stenosis and horse­ now rare due to the early and intensive
the palate. shoe kidneys. treatment of the disease with antibiotics
• Increased risk of malignant trans­ • Gastrointestinal abnormalities in­ since 1940. Leukoplakic lesions may de­
formation app. 35 percent with peak clude, developmental oesophageal velop in the atrophic epithelium associ­
in third decade of life. webs in the postcricoid region re­ ated with the glossitis often seen in tertia­
Malignant disease reported include, sulting in dysphagia which have ry syphilis. In later stages, the prediction
solid tumors of the tongue, buccal muc­ been associated with malignant for syphilitic glossitis associated with
osa, nasopharynx, rectum, cervix, vag­ina, transformation, hepatomegally and leukoplakic changes to undergo carcino­
skin, oesophagus and pancreas.Hem­a­­­ cirrhosis. matous transformation has been recog­
tological malignancies include mye­­l­­o­ • Other abnormalities include altered nized for many years. The incidence of
dysplasia and Hodgkin’s lym­phoma. mental status and learning difficul­ such malignant trans­formation has been
ties, microcephaly, intracranial cal­ as high as 30 percent in various reported
cifications, alopecia, hair greying, series.20
The Non-mucocutaneous deafness and amyloidosis, peripher­
Features al neuropathy and choanal atresia.21 Clinical Features
• Bone marrow failure (BMF) resul­ting Syphilitic leukoplakias have no dis­
in peripheral cytopenias of one or The Diagnosis of Dyskeratosis tinctive features but typically affect the
more lineages (85%). Pancy­ topenia dorsum of the tongue and spare the
75 percent, onset in less than 20 years
Congenital margins. Lesions have an irregular out­
of age (80%), with half develop before • Diagnosis may not be so easy, for line and surface and are usually regarded
10 years. example with the presentation as having a high risk of malignant
• Principle cause of death in 70 percent of aplastic anaemia without any change. Carcinoma developing near the
of cases is as a consequence of mucocutaneous features. center of the dorsum of the tongue may
bleed­ing or opportunistic infections • Screen for the DKC1 gene if the be a sequel to syphilitic leukoplakia.
with cytomegalovirus, pneumonia. patient is male with two of the Cracks, small erosions or nodules may
• Some times it is initially diagnosed following features of the disease: prove on histology to be foci of invasive
as idiopathic aplastic anemia. The abnormal skin pigmentation, nail carcinoma.
clinical features also overlap with dystrophy, leukoplakia, and bone
Fanconi’s anemia characterized by marrow failure. Pathology
BMF and predisposition to mali­ • Any patient presenting with idio­ In addition to hyperkeratosis, acanthosis
gnancy. pathic aplastic anaemia should with dysplasia is the characteristics
• Pulmonary complication in 20 per­ undergo chromosomal breakage features. Of late syphilitic chronic infla­
cent of patients are reduced diffusion analysis with mitomycin-C or die­ mmatory changes with plasma cell
capacity with or without a restrictive poxybutane to exclude Fanconi’s predominantly may be seen. Giant
defect. Abnormalities of pulmonary anaemia. cells and rarely granulomas may be
vasculature and abnormally high • If this chromosomal breakage analy­ present. Endarteritis of small arteries
levels of pulmonary fibrosis. sis is normal (i.e., negative for Fan­ is particularly characteristic. However,
• Ophthalmic abnormalities epipho­ coni’s anaemia) then progression to distinctive features of a syphilitic tissue
ria secondary to nasolacrimal duct analyse hTERC gene is appropriate. reaction may be lacking.
obstruction, conjuctivitis, blephari­ • Although rare, Dyskeratosis congeni­
tis, pterygium formation, ectropion, ta should be considered and excluded Behavior and Management
loss of eyelashes, strabismus, cata­ whenever a child presents with oral The diagnosis is confirmed mainly
racts and optic atrophy. leukoplakia. by the serological findings. However,
690 Neoplastic Conditions of Head, Neck and Face

even if positive, biopsy is still essential, underlying predisposing factors in oral Epidermolysis Bullosa
as minute areas of malignant change cancer. The entire oral mucosa is red, Epidermolysis bullosa, particularly the
may be found and the management is shiny, and atrophic. Leukoplakias as welldystrophic type, is an inherited disorder
affected accordingly. In particular, the as multiple oral carcinomas may devel­ of either autosomal or recessive pat­
presence of syphilitic endarteritis may op, predominantly in the posterior part tern. The disease is characterized by
be a contradiction to the radiotherapy. of the mouth and in the oropharynx. formation of bullae of the skin and
Antibiotic treatment of syphilis does not oral mucosa. Oral scarring results in
cure the leukoplakia, which permits and Treatment loss of the oral vestibule, ankyloglossia
can undergo malignant change even • Dietary iron supplementation for and microstomia. Carcinoma of the
after serology has become negative.16,20 the correction of iron deficiency tongue has been described in cases of
anemia. This therapy resolves the dystrophic epidermolysis bullosa.
Sideropenic Dysphagia anemia, relives the glossodynia,
Sideropenic dysphagia (Paterson-Brown- and may reduce the severity of the
REFERENCES
Kelly or Plummer81-Vinson82 syndrome) esophageal symptoms.
mainly affects middle-aged women,83 • Occasionally, esophageal dilation 1. Warnakaulasuriya S, Newell, Johnson W,
with iron deficiency being the underlying is necessary to help improve the et al. Nomenclature and Classification of
cause. Iron deficiency is endemic in many symptoms of dysphagia. Potentially Malignant Disorders of The
tropical countries where oral cancer is • The patient should be evaluated Oral Mucosa. J Oral Pathol Med. 2007;
also common. The iron deficiency is periodically for oral hypopharyngeal, 36:575-80.
due to chronic blood loss as result of and esophageal carcinoma. 2. Napier SS, Speight PM. Natural History
hookworm infestation and nutritional of Potentially Malignant Oral Lesions
deficiencies. Discoid Lupus Erythematosus and Conditions: An Overview of the Lit­
Patient suffering from sideropenic Oral lesions in discoid lupus erythema­ erature. J Oral Pathol Med. 2008;37: 1-10.
dysphagia generally complain of fati­ tosus may show pseudoepithelioma­ 3. Slaughter D, Southwick H, Smejkal W.
gue and difficulty in swallowing. The tous hyperplasia and consequently are “Field cancerization” in oral stratifide
dysphagia is due to the formation of described in classification with other squamous epithelium: clinical impli­
an esophageal web (the presence of precancerous conditions is necessary cations of multicentric origin. Cancer.
abnormal band of tissue). The com­ because a few cases of squamous cell 1953;6:963-8.
mon oral mucosal changes seen in this carcinoma developing in discoid lupus 4. Ha PK, Califano JA. The Molecular
syndrome are angular cheilosis, mucosal erythematosus have been reported, es­ Biology of Mucosal Field Cancerization
pallor, and atrophy which gives tongue a pecially in atrophied epithelium on the of the Head And Neck. Crit Rev Oral
smooth glossy appearance. Histologically, vermilion border of lower lip. Biol Med. 2003;14(5):363-9.
the mucosa of the whole aerodigestive 5. Braakhuis BJ, Tabor MP, Leemans CR,
tract is often atrophic with varying degree Xeroderma Pigmentosum et al. Second primary tumors and field
of submucosal chronic inflammation. In Xeroderma pigmentosum is a rare cancerization in oral and oropharyn­
advanced cases, evidence of epithelial geno­dermatosis in which cutaneous geal cancer: molecular techniques
atypia and dysplasia may be seen. mali­gnancies develop at an early age provide new insights and definitions.
The relationship between siderope­ with a recessive mode of inheritance. Head Neck. 2002;24:198-206.
nic dysphagia and the subsequent devel­ One of several defects in the excision 6. Kujan O, Oliver RJ, Khattab A, et al.
opment of carcinoma of upper alimenta­ repair and/or post replication repair Evalu­ ation of a new binary system
ry tract is well documented. Five to fifty mechanism of DNA causes the disease. of grading oral epithelial dysplasia
percent prevalence of upper aerodiges­ As result of the inability of the epithelial for prediction of malignant transfor­
tive tract malignancy has been reported cells to repair ultraviolet light induced mation. Oral Oncology. 2006;42:987-93.
in affected persons.84 The carcinoma of damage mutation in the epithelial cells 7. Warnakaulasuriya S, Reibel J, Bouquot
buccal mucosa and tongue is well recog­ occur, leading to the development of J. et al. Oral epithelial dyspalsia classifi­
nized. Iron deficiency, whether it is sever skin cancer at a rate 1000 to 4000 times cation systems: predictive value, utility,
enough to cause anemia or not leads what would normally be expected in weak­ness and scope for improvement.
to mucosal atrophy. Iron deficiency people under 20 years of age. The lips J Oral Pathol Med. 2008;37:127-33.
leads to changes in the cell kinetics and are mainly affected. Epithelial atrophy, 8. WHO Collaborating Centre for Oral
increases the susceptibility to topically tela­
ngiectasia and hyperpigmentation, Precancerous Lesions. Definition of
applied carcinogens. It has been sug­ which may occasionally also be observed leukoplakia and related lesions: An aid
gested that mucosal atrophy, increased on the oral mucosa. Squa­ mous cell to studies on oral precancer. Oral Sur­
mitotic activity, and diminished repair carcinoma of the oral mucosa had been gery, Oral Medicine, Oral Pathology.
capacity are among the major common observed in some affected individuals. 1978;46(4):518-39.
Potentially Malignant Disorders of the Oral Cavity 691

9. Axéll T, Holmstrup P, Kramer IRH, 19. Cawson RA, Odell EW. Oral premalig­ 30. Vander Waal I, Axell T. Oral leuko­
et al. International seminar on oral nancy. In essentials of oral pathology plakia: A proposal for uniform
leukoplakia and associated lesions and oral medicine. Sixth edition. 2002. reporting. Oral Onco. 2002;38:521-6.
related to tobacco habits. Community Churchil Livingstone. pp. 216-27. 31. Queyrat L, Erythroplasia du gland, Bull
Dent Oral Epidemiol. 1984;12:145-54. 20. Lee Koyc CH, Huang HL, Chao YY, et Soc Fr Dermatol Syphiligr. 1911;22:
10. Axéll T, Pindborg JJ, Smith CJ, et al. al. Precancer risk of betel chewing, 378-82.
and an International Collaborative tobacco use and alcohol consumption 32. Shear M, Erythroplakia of the mouth.
Group on OralWhite Lesions. Oral in oral leukoplakia and OSMF in Int Dent J. 1972;22(4):460-73.
white lesions with special reference southern Taiwan, Br J Cancer. 2003; 33. Bouquet JE, Ephros H. Erythroplakia
to precancerous and tobacco-related 88:366-72. the dangerous red mucosa. Pract Per-
lesions: conclusions of an international 21. Angadi Punya V, Rekha KP. Oral iodontics Aesthet Dent. 1995;7:59-67.
symposium held in Uppsala, Sweden, submucous fibrosis, a clinicopathologic 34. Shafer WG, Waldron CA. Erythroplakia
May 18–21, 1994. J Oral Pathol Med. review of 205 cases in Indians. Oral and of the oral cavity. Cancer. 1975;36:
1996;25:49-54. Maxfac Surg. 2011;15:15-19. 1021-8.
11. Pindborg JJ, Reichart PA, Smith CJ, 22. Warnakulasuriya S, Kovacevic T, 35. Daftary DK, et al. Primary prevention
et al. World Health Organization Inter­ Madden P, et al. Factors predicting trial of oral cancer in India: A 10-year
national Histological Classifi­cation of malignant transformations in oral follow-up study. J Oral Pathol Med.
Tumours. Histological typing of cancer potentially malignant disorders among 1992;21:433-9.
and precancer of the oral mucosa. patients accrued over ten year period 36. Prabhu SR, Wilson DF, Daftary DH,
Berlin: Springer, 1997. in south eastern England. J Oral Path et al. Oral precancerous lesions
12. World Health Organization. World and Med. 2011;40:677-83. and condition of topical interest. In
Health Organization Classification of 23. Shafer WB, Waldron CA. A clinical oral diseases in the tropics. Oxford
Tumours. In: Barnes L, Eveson JW, and histopathologic study of oral University Press. 1992;402-24.
Reichart P, Sidransky D, eds. Pathology leukoplakia. Surg Gynecol and Obst. 37. Robert J. Gorlin. Bowen’s disease of
and Genetics. Head and Neck Tum­ 1961;112:411-20. the mucous membrane of the mouth:
ours. Lyon: International Agency for 24. Waldron CA, Shafer WG. Leukoplakia A review of the literature and a
Research on Cancer (IARC) IARC revisited: A clinicopathologic study of presentation of six cases. Oral Surgery,
Press. 2005;177-9. 3256 oral leukoplakias. Cancer 1975; Oral Medicine, Oral Pathology. 1950;
13. Vander Waal I, Schepman KP, Vander 36:1386-92. 3(1):35-51.
Meij EH, et al. Oral leukoplakia: a 25. Pindborg JJ, Ranstrup G, Poulsen 38. Dalva R, Neto P, et al. Actinic cheilitis:
clinicopathological Review. 1997;33 HE, et al. Studies in oral leukoplakia. Histopathology and p53. Journal of
(5):291-301. V. Clinical ansd histologic science Cutane Path. 2006:33(8):539-44.
14. Rajendran R. Oral leukoplakia (leuko­ of malignancy. Acta Odontol Scand. 39. George E. Kaugars. Actinic cheilitis:
keratosis): complication of facts and 1963;21:407-14. A review of 152 cases. Oral Surg Oral
figures. J Oral And Maxillo Facs Patho. 26. Feller L, Altini M, Slabbert H. Prema­ Med Oral Pathol Oral Radiol Endod.
2004;6(2):58-68. lignant lesions of the oral mucosa in a 1999;88:181-6.
15. Shafer WG, Hine MK, Levy BM. Benign south African sample: A clinicopatho­ 40. Raymond G. Dufresne. Actinic cheilitis:
and malignant tumors of the oral logic study. J Dent Assoc South Africa. A treatment review. Dermatologic
cavity. In textbook of oral pathology. 1991;46:261-5. surgery. 1997:23(1);15-21.
Fourth edition. 1993. Saunders. 92-109. 27. Gupta PC, Mehta FS, Daftary DK, et al. 41. Mukherjee AL. Oral submucosal
16. Neville BW, Damm DD, Allen CM, et al. Incidence rates of oral cancer and fibrosis. A search for aetiology. Ind J
Epithelial pathology. In oral and maxi­ natural history of oral precancerous Otolaryngol. 1972;24:1:11-5.
llofacial pathology. Second Edition. lesions in a 10-year follow-up study of 42. Schwartz J. Atrophia idiopathica
2009. WB Saunders and Co. NY. 337-53. Indian villagers. Community Dentistry mucosa oris. Presented at the 11th
17. Bouquot BE, Whitaker SB. Oral leuko­ and Oral Epidemiology. 1980;8:287-33. International Dental Congress, London;
plakia—rationale for diagnosis and 28. Silverman Sol jr, Bhargava K, Mani NJ, 1952.
prognosis of its clinical subtypes or et al. Malignant transformation and 43. Joshi SG. Submucous fibrosis of the
”phases”. Quintessence Int 1994;25: natural history of oral leukoplakia in palate and pillars. Ind J Otolaryngo.
133-40. 57,518 industrial workers of Gujarat, 1953;4:1.
18. Hansen LS, Olson JA, Silverman S. India. 1976;38(4):1790-5. 44. Paymaster JC. Cancer of the buccal
Proliferative verrucous leukoplakia. A 29. Axell T. Occurrence of leukoplakia and mucosa: A clinical study of 650 cases in
longterm study of thirty patients. Oral some other oral white lesions among Indian patients. Cancer 1956;9:431-5.
Surg Oral Med Oral Pathol. 1985;60: 20333 adult Swedish people. Commu­ 45. Pindborg JJ, Mehta FS, Gupta PC, et al.
285-9. nity Dent Oral Epidemiol 1987;15:46-51. Prevalence of oral submucous fibrosis
692 Neoplastic Conditions of Head, Neck and Face

among 50915 Indian villagers. Br J 58. Pindborg JJ. Is submucous fibrosis a 72. Lodhi G, Scully C, Carrozzo M, et al.
Cancer. 1968;22(4):646-54. pre-cancerous condition in the oral Current Controversies In Oral Lichen
46. Paymaster JC. Cancer of buccal mu­ cavity? Int Den J. 1972;22:472-80. Planus: Report of An International Con­
cosa: A clinical study of 650 patients. 59. Murti PR, Bhonsle RB, Pindborg JJ, sensus Meeting. Part 1. Viral Infections
Cancer, 1956;9:431-5. et al. Malignant transformation rate And Etiopathogenesis. Oral Surg Oral
47. Angadi Punya V, Rekha KP. Oral sub­ in oral submucous fibrosis over a 17- Med Oral Pathol Oral Radiol Endod.
mucous fibrosis: A clinicopa­thologic year period. Community Dent Oral 2005;100:40-51.
review of 205 cases in Indians. Oral and Epidemiol. 1985;13:340-1. 73. Eisen D, Carrozzo M, Bagan Sebastian
Maxfac Surg. 2011;15:15-19. 60. Tilakratne WM, Klinikowski Saku T, JV, et al. Number V Oral lichen planus:
48. Pindborg JJ, Sirsat SM. Oral submucous Peters TJ, et al. Oral Submucous Fibro­ Clinical features and management.
fibrosis. Oral Surg Oral Med Oral sis: Review on Aetology and Pathogen­ Oral Dis. 2005;11:338-49.
Pathol. 1966;22(6):764-79. esis. Oral Oncology. 2006;42: 561-8. 74. Wickham LF. Sur un signe pathogno­
49. Canniff JP, Harvey W. The aetiology of 61. Mehta, James E. Hamner. Tobacco- monique delichen du Wilson (lichen
oral submucous fibrosis: The stimula­ related oral mucosal lesions and con­ plan) stries et punctuations grisatres.
tion of collagen synthesis by extrats ditions in India: Basic Dental Research Ann Dermatol Syph. 1895;6:17-20.
of areca nut. Int J Oral Surg. 1981;10: Unittata Institute of Fundamental Re­ 75. Kaz RW, Brahim JS, Travis WD. Oral
163-7. search Bombay. 1993. squamous cell carcinoma arising in
50. Canniff JP, Harvey W, Harris M. Oral 62. Borle RM, Borle SR. Management of a patient with long-standing lichen
submucous fibrosis: Its pathogenesis Oral sub mucous fibrosis - A conser­ planus. Oral Surg Oral Med Oral
and management. Br Dent J. 1986;160: vative approach. J Oral Maxillo­fac Surg. Pathol. 1990;70:282-5.
429-34. (USA). 1991;49(8):788-91. 76. Lozada-Nur F, Miranda C. Oral lichen
51. Meghji S, et al. An in-vitro comparison 63. Khanna JN, Andrade NN. Oral Sub­ planus: Epidemiology, clinical charac­
of human fibroblasts from normal and mucous Fibrosis: A New Concept teristics, and associated diseases. Sem
oral submucous fibrosis tissue. Arch In Surgical Management: Report of Cutan Med Surg 1997;16:273-7.
Oral Biol. 1987;32:213-15. 100 Cases. Int J Oral Maxillofac Surg. 77. Krutchkoff DJ, Eisenberg, E. Lichenoid
52. Scutt A, et al. Stabilisation of collagen by 1995;24(6):433-9. dysplasia: A distinct histopathologic
betel nut polyphenols as a mechanism 64. Gupta D. Oral submucous fibrosis—A entity. Oral Surg Oral Med Oral Pathol.
in oral submucous fibrosis. Cellular new treatment regimen. J Oral Maxil­ 1985;30:308-15.
and Molecular Life Sciences. Volume lofac Surg. 1988;46(10):830-3. 78. Onofre MA, Sposto MR, Navarro CM,
1987;43:(4). 65. Tepan MG, Use of tongue flap in sub­ et al. Potentially malignant epithelial
53. Shieh TY, Yang JF. Collagenase activ­ mucous palatal fibrosis. The Journal of oral lesions: Discrepancies between
ity in oral submucous fibrosis. Proc Laryngology and Otology. Cambridge clinical and histological diagnosis. Oral
Natl Sci Counc Repub China B. 1992; University Press. 1986;100:455-60. Dis. 1997;3:148-52.
16(2):106-10. 66. Chin-Jyh Yeh. Application of the buc­ 79. Scully et al. OLP and malignant transfor­
54. Kuo MYP, Chen HM, Hahn LJ, et al. cal fat pad to the surgical treatment mation. Oral diseases. 2008;14; 229-43.
Collagen biosynthesis in human oral of oral submucous fibrosis. Int J Oral 80. Handley TPB, McCaul JA, Ogden GR.
submucous fibrosis fibroblast cultures. Maxillofac Surg. 1996;25(2):130-3. Dyskeratosis Congenita. Oral Oncol­
J Dent Res. 1995;74:1783-8. 67. Borle RM, Nimonkar PV, Rajan R. Ex­ ogy. 2006;42:331-6.
55. Ma RH, Tsai CC, Shieh TY. Increased tended nasolabial flaps in the manage­ 81. Plummer S: Diffuse dilatation of the eso­
lysyl oxidase activity in fibroblasts cul­ ment of oral submucous fibrosis. Br J phagus without anatomic stenosis (car­
tured from oral submucous fibrosis Oral Maxillofac Surg. 2009;47(5):382-5. diospasm). A report of ninety-one cases.
associated with betel nut chewing in 68. Wilson, E. On lichen planus. J Cutan J Am Med Assoc. 1912;58:2013-2015.
Taiwan. J Oral Pathol Med. 1995. Med Dis Skin. 1869;3:117-32. 82. Vinson PP. A case of cardiospasm
56. Tsai CC, Ma RH, Shieh TY. Deficiency in 69. Sugerman P. Oral lichen planus. Clinics with dilatation and angulation of the
collagen and fibronectin phagocytosis in Dermatology. 2000;18(5):533-9. esophagus. Med Clinics North Am.
by human buccal mucosa fibroblasts in 70. Joshi A. Koebner Phenomenon Due 1919;3:623-7.
vitro as a possible mechanism for oral to Sacred Thread in Lichen Planus. J 83. Vinson PP. Hysterical dysphagia.
submucous fibrosis. J Oral Pathol Med. Dermatol. 2000;27(2):129-30. Minnesota Med. 1922;5:107-8.
1999;28:59-63. 71. Grinspan D, Diaz J, Villapol LO, 84. Larsson LG, Sandström A, Westling
57. Haque MF, et al. Oral submucous et al. Lichen ruber planus of the buccal P. Relationship of Plummer-Vinson
fibrosis patients have altered levels mucosa. Its association with diabetes. disease to cancer of the upper ali­
of cytokine production. J Oral Pathol Bull Soc Fr Dermatol Syphiligr. 1966; mentary tract in Sweden. Cancer Res.
Med. 2000;29(3):123-8. 73(6):898-9. 1975;35(11 Pt. 2):3308-16.
30 Oral Cancer
Borle Rajiv M, Arora Aakash, Bhola Nitin

The oral cancer is one of the common all cancers among women.6 In Indian Although the understanding regar­ding
cancers in the Indian subcontinent population incidence rate of oral squ­ the oral cancer has improved signi­ficantly
due to rampant abuse of tobacco. Oral amous cell carcinoma is slightly high and the management moda­ lities have
cancer is the sixth most common cancer because of greater exposure to its evolved and are avail­able widely, still the
in the world.1 It accounts for about 4 known predisposing factors and is most prognosis of oral cancer has not improved
percent of all cancers and 2 percent of common of all cancers. About 94 percent significantly in India. The basic reason for
cancer deaths worldwide.2 of all oral malignancies are squamous the same is that although the mouth is
There is a wide geographical variation cell carcinomas.7 accessible for the self-examination and the
(approximately 20-fold) in the incidence Gingivobuccal sulcus malignancies clinical examination and the fact it does
of this cancer. The areas characterized accounts for about 80 percent of oral not require any sophisticated facilities,
by high incidence rates for oral cancer cancers in Indian population. Tongue is the early diagnosis of oral cancer is still
(excluding lip) are found in the South the most common site for intraoral cancer a dream. In the west, the early detection
and Southeast Asia (Sri Lanka, India, among European and the US populations, of the breast cancer has improved signi­
Pakistan and Taiwan), parts of Western amounting to 40 to 50 percent of oral ficantly following awareness towards the
(France) and Eastern Europe (Hungary, cancers.3 Buccal mucosa cancer is more self-examination. Most of the patients
Slovakia and Slovenia), parts of Latin common among Asian populations due with oral cancer report in stage III or IV
America and the Caribbean (Brazil, to betel quid/tobacco chewing habits.8 In with wide spread cervical nodal metastasis
Uruguay and Puerto Rico) and in Pacific Sri Lanka, 40 percent of oral cancers are making the prognosis poor. This is due to
regions.3 found on buccal mucosa.9 Other intra­oral ignorance and illiteracy. Although the
In the United States, Europe and sites for mouth cancer include floor of government and social organizations
Australia it accounts for 0.6 to 5 percent mouth, gingiva and palate. have launched a massive awareness drive
of all cancers, but it accounts for up to Although the oral cavity is readily and the hazards of tobacco have been
30 to 50 percent of all cancers in India. accessible for self-examination, the ear­ widely publicized, it has not achieved the
However, it ranks number one among ly detection of the oral cancer is still desi­red results. In the rural set up there
men and number three among women illusive. Most of the cases report with is paucity of trained clinicians who are
in India. Usually 91 percent of the cases advanced disease, thus the management able to diagnose a precancerous lesion
occur after the age of 40 years and becomes very challenging and difficult. or an early malignancy and thus, the
highest incidence is found between ages The OSCC of the gingivobuccal sulcus patient does not get proper advice and is
60 and 70 years. Langdon4,5 (1977) stated is commonest due to use of smokeless not referred to the specialist on time. The
that ninety five percent of patients with tobacco in the form of ghutka, pan, testimony to this fact is that in the clinical
oral cancer are over 40 years of age at first khaini, kharra, pan masala, etc. which is practice, it is observed that the teeth,
diagnosis and the mean age at diagnosis consumed not only frequently, but also which are involved in a malignant growth
is 60 years (males 63.5 years, females kept in the buccal vestibule for prolonged and become mobile are extracted without
60.6 years) with the male: female ratio periods of time. In the western countries, detecting the cancerous growth.
between 1.3:1 and 2:1. the habit of smoked tobacco is more The oral submucous fibrosis is a
Oral cancer constitutes 12 percent common, thus the cancers of the tongue com­ mo­nly encountered clinical con­
of all cancers in men and 8 percent of and pharynx are more common. dition in India and it has chronic course.
694 Neoplastic Conditions of Head, Neck and Face

The patients and clinicians tend to take rural population as compared to the The smokeless tobacco is the pre­ferred
it lightly and patient continues with cigarettes and other forms like cigars and form of tobacco use in India. Smoking is
the habits. Clinicians tend to treat this pipe, which are seen to be more popular considered a taboo and there are statutes
condition conservatively and when­ in urban areas. The bidi not only has the banning it in public places and thus,
ever the mali­gnant transformation takes smoke, but invariably the heat genera­ people resort to tobacco chewing habits.
place, it is invariably missed and the pati­ ted during smoking also produces burns The tobacco is still offered to guests as
ents often report very late with advanced on the vermilion and palate. The chutta a social custom. The use of tobacco
malignancy. (reverse smoking) habit is seen in Andhra in this form is common throughout
Pradesh,10 a south Indian state, where the country, but more commonly in
even females smoke the bidi keeping Maharashtra, Madhya Pradesh, UP, Bihar
ETIOLOGY the burning end inside the mouth. The and most northern states. The habit of
palatal lesions like nicotina palatini are ghutka or kharra is common amongst
Tobacco commonly associated with this habit. the youngsters including the school
The tobacco still remains the major The smoked tobacco generally leads to going children as this habit is picked up
etiological factor for the oral squamous precancerous lesions like leukoplakia quite early in life and is not considered
cell carcinoma. The tobacco is con­ and erythroplakia commonly on sites like as bad as smoking. Even women are
sumed in various forms such as: cheek mucosa, palate, tongue, anterior addicted to tobacco in a smokeless
• Smoked form—bidi, cigarette, pipe, mandibular gingiva, tongue and the floor form. The habituated individual often
cigar, hukka, chutta, out of which of mouth and subsequently leads to oral keeps the tobacco lime mixture in the
cigar and pipe is uncommon in India. squamous cell carcinoma (OSCC) of anterior gingivobuccal sulcus of the
• Non-smoked tobacco one of these sites (Figs 30.1A to D). The mandible, leading to precancerous
– As chewable tobacco in the form smoked tobacco additionally carries a risk or cancerous lesions of this site (Figs
of tobacco lime mixture, kharra, of developing the carcinoma of pharynx, 30.1B to D) and the kharra or khaini is
khaini, ghutka, pan, kimam, posterior one third of the tongue, kept in the mandibular buccal vestibule
cakes, pan masala, jarda, etc. larynx and broncogenic carcinoma. It in the posterior area for a long period
– Inhaled form—tobacco snuff. is important to know the duration of (Fig. 30.1A). Sometimes the kharra
– As dentifrice—tobacco snuff. the habit, frequency and quantity of chewers sleep at night keeping the
Out of the smoked forms, bidi is the the bidi or cigarette smoking as it has tobacco in the buccal vestibule. These
most common cause of oral cancer in the direct bearing on the development of habits facilitate the contact of tobacco and
India due to its affordability to poor and precancerous or cancerous lesions. other materials used in the kharra/ghutka
to remain in contact with the mucosa for a
long time, causing chronic irritation. Some
of the ingredients like lime are caustic and
in addition to irritation induce chemical
burns on the mucosa. Thus, this habit
produces precancerous or cancerous
lesions of posterior gingivobuccal sulcus.
The habituated individual consumes
the tobacco as many as 20 to 30 times
a day, posing a greater risk of inducing
A B precancerous or cancerous lesions.

Betel Nut Chewing


The betel nut is a major cash crop of
the tropical region. The betel nut chew-
ing in various forms is a social custom
in India and not considered dangerous
or hazardous. It is consumed by males,
females, children, adults, rich and poor
alike. The betel nut alkaloids (areco-
line, arecolidine, arecaidine, guvacine
and guvacoline) have been investigated
C D by various authors11,12 to establish their
Figs 30.1A to D: (A) OSCC of posterior GB sulcus due to kharra/mawa; (B) At gingivo labial role in the etiology of submucos fibrosis
sulcus tobacco/lime chewing habits; (C and D) At the labial sulcus with extensive leukoplakia (SMF) and oral cancer. The betel nut is
Oral Cancer 695

consumed unripe, processed and pro- anemia, sideropenic dysphagia and Plum­­ • Initiation
cessed forms with addition of various fla- mer-Vinson’s syndrome. The deficiency • Promotion.
voring and sweetening agents. It is con- of vitamins especially the vitamin A, – Initiation phase: Normal cells
sumed alone or with tobacco and pan. B complex and iron leads to inflammatory are changed into dormant tumor
Although the carcinogenic potential of changes, dysplasia and transformation cells by some carcinogenic influ­
betel nut is disputed,13 but still it remains into malignancy. ences in a short period of time.
a fact that majority of the patients who Oral syphilis15 and lichen planus16 Tissue may appear clinically and
have SMF are habituated to betel nut are also implicated in the etiology of histo­logically, normal.
chewing in some form or other and some OSCC. – Promotion phase: Subsequent
of the patients with OSCC give history of expo­sure of the initiated tissue
betel nut chewing alone, without tobac- Exposure to the UV Rays17 to cocarcinogens changes the
co. The fact remains is that the SMF is an The exposure to UV rays induces the dormant tumor cells to visible
established precance­rous condi­tion and carcinoma of the vermilion of the lower tumor mass in longer period.
the association of OSCC with SMF is in- lip (Figs 30.2A to C). It is commonly Recent advances in oral mucosa
creasing. Thus, the carcinogenic poten- seen in the farm laborers who work in rese­
arch suggest the modified concept
tial of betel nut can not be denied. the sun for long times. The basal cell of carcinogenesis. The conventional two
carcinomas have also been implicated stage theory was expanded to three stages.
Alcoholism to sun exposure (UV rays). It is more • Progression phase: It is a process
Most of the chronic alcoholics are often commonly seen on skin above the ala- whereby a neoplasm develops by
heavy smokers, too. The alcoholics derive tragus line, however the lesions have one or more permanent qualitative
energy from the alcohol and eat poorly been reported from the skin of the upper irreversible changes into its consti­
leading to nutritional deficiencies, which lip. It is more common in Caucasian tuent cells. The progression phase
could be a predisposition to development population due to less melanin pigment. once initiated continues to pro­gress
of chronic stomatitis and OSCC. Alcohol even if the cause, which had initiated
may influence the proliferative cells by the same, has been eliminated. Once
PATHOGENESIS
both intracellular (e.g. endocytosis) and the changes in the cells are pro­
intercellular (permeability) pathways. The etiology, clinical behavior, inci­dence gressive, they can not be reversed
The carcinogenic exposure of the pro­ of malignant transformation behavior even if the stimulus that has promoted
lifer­ating stem cells in the basal layer and malignant potential, concept of field the changes has been withdrawn.
may be regulated through these path­ cancerization and oxidative damage, etc. • Oncogenes: They are the genes
ways.14 are discussed in the previous chapter on that promote cell growth in cancer
the premalignant lesions and conditions. cells. They are characterized by the
Chronic Irritation ability to promote cell growth in the
The chronic irritation from sharp or mal­ absence of normal mitogenic signals.
CARCINOGENESIS
posed teeth (Trauma from occlusion), • Proto-oncogenes: They are the
over hanging restorations and ill fitting Carcinogenesis is a multistep process at normal counter part of oncogenes.
dentures, etc. leads to frequent mucosal both phenotypic and genotypic levels, They are physiologic regulators of
ulceration. The chronic irritation brings where the tumor progression occurs in a cell proliferation and differentiation.
about the dysplastic changes in the step wise fashion (Flow chart 30.1). They may be converted to cellular
epithelium, which initially are reaction­ Goldhaber and Berenbaum studied oncogenes by a process known as
ary dysplasia, but subsequently become development of cancer in animal skin and insertional mutagenesis, where the
irreversible and may change into leuko­ mucosa and suggested two stage mech­ mutated proviral DNA is inserted
plakia or OSCC. anism hypothesis for carci­noge­nesis near the proto-oncogene.

Nutritional Deficiencies
Malnourishment, secondary to poor
intake, lack of balanced diet, mala­bsor­
ption syndromes, chronic GI infec­
tions or due to parasites such as worm
infestations, amoebiasis/giardiasis are
common causes of nutritional deficien­
cies in India. Apart from this the chronic
blood loss due to menorrhagia, piles and A B C
hemorrhoids leads to iron deficiency Figs 30.2A to C: Carcinoma of the vermilion border of the lower lip
696 Neoplastic Conditions of Head, Neck and Face

Flow chart 30.1: Carcinogenesis vi. Sustained angiogenesis (vascular


endothelial growth factor, VEGF)
vii. Ability to invade and metastatize.

CLINICAL PRESENTATION OF
ORAL CANCER
• A red indurated patch: A red indu­
rated patch is usually the preexisting
erythroplakia or leu­ko­­plakia, which
changes into malignancy (Figs 30.3A
to E). There may not be any exu­
berant growth or an ulcer, but a
perceptible change in color (white
to red), fissu­ring, change in size and
the most important; presence of
induration. The lesions are slightly
raised from the surface and may have
slightly granular appear­ ance on its
surface. The most important finding
is presence of induration and fixity
and hence, the lesions cannot be
suspec­ted or detected without pal­
pa­tion. The lesions require be­ ing
biopsied to establish the final diag­
nosis. These lesions could be early
malig­nant trans­formation and sub­
sequently change into an ulcera­
ted or exo­phytic growth, which is a
classical presentation of OSCC. The
malignant potential of these growths
should not be underestimated as
they may have widespread lymph
Oncoproteins—are the products of virus, have been implicated in the node metastasis.
oncogenes and proto-oncogenes. etiopathogenesis of oral cancer. • An ulcerated growth: The OSCC pre­
sents mostly as an ulcerated growth.
Carcinogens18 The malignant ulcer has classical
Carcinogens are the factors which initiate
Cocarcinogens everted or rolled out edges (Figs 30.4A
conversion of normal cells into tumor Cocarcinogens are the factors which and B). This is due to rapid division
cells or cause initiation of the carcinoma. convert altered cells to visible mass, of the cells at the periphery, where
They include various chemical, physical e.g. chronic irritation, trauma, vitamin the tumor grows optimally and
and viral carcinogens. deficiency and poor oral hygiene. excessive cellular bulk leads to
• Chemical carcinogens: Most of oral compaction of the cell mass, which
neoplasms are caused by chemical Seven Fundamental Changes produces elevation or evertion of
carcin­ogens. Nickel chrome com­ the edges. The ulcer is irregular in
in Cell Physiology Essential
pound, cigarette smoke, betel nut, shape and the floor is covered with
tobacco quid, asbestos, benzene, cer- for Malignant Transformation whitish materia alba composed of
tain tars, soots, oils and arsenic com- i. Self-sufficiency in growth signals desquamated cells and food debris
pounds. (oncogene activation) with projecting red granulomatous
• Physical carcinogens: Actinic ra- ii. Insensitivity to growth-inhibitory areas. The palpatory findings are
diation, ionizing radiation. signals (TGF-β, inhibitors of CDK’s) indurated edges due to compaction
• Viral carcinogens: Human T-lym­ iii. Evasion of apoptosis (inactivation of the cell mass, indurated and friable
pho­ tropic virus type I (HTLV I), of p53 and other changes) base and bleeding on provocation.
Human papilloma virus (HPV), iv. Defects in DNA repair The ulcer has fixity to the deeper
Epstein-Barr virus (EBV), Hepatitis B v. Limitless replicative potential structure. The ulcerated growths are
Oral Cancer 697

A B C D E
Figs 30.3A to E: Leukoplakia changing into a red lesions, on biopsy they were found to be well differentiated
squamous cell carcinoma

more aggressive as compared to the


exophytic growths in their behavior
and as they readily infiltrate into the
deeper tissue, the bulk (i.e. depth of
infiltration) of the tumor is greater
with early and widespread cervical
metastasis. It is being said that
whenever the tumor bulk increases
beyond 2 mm, the chances of lymph
A B node metastasis increase significantly.
• Exophytic growth: The third picture
Figs 30.4A and B: (A) Classical malignant ulcer with everted/rolled out edges;
(B) Infilterative character is an exophytic growth, which is
often described as ‘cauliflower’—like
growth. The tumor grows more out­
wards and although the out­ward gro­
wth is more the rela­tive deeper infil­
tration is less (Figs 30.5, 30.6, 30.7 and
30.8). Such growths are less aggres­
sive and also metastasize to regional
nodes. The metastasis is late as com­
pared to the ulcerative growths. The
tumor has a multilobulated, with gran­
ular appearance, firm in con­sistency
and friable causing bleed­ ing on
provocation or trauma from occlusion
Fig. 30.5: Early exophytic growth Fig. 30.6: Advanced exophytic growth during mastication. It also infiltrates
into the deeper tissue, but to a lesser
extent than the ulcera­ted growths.
The verrucous carcinomas also
present as exophytic cauliflower-like
growths (Figs 30.9 and 30.10). The
verrucous carcinomas do not metas-
tasize as the basement mem­ brane
is intact. The verrucous carci­noma
is characterized by acan­thosis. The
behavior of the tumor is not very
aggressive and usually wide local
excision, without add­ ressing the
neck is adequate. However, although
Fig. 30.7: Advanced exophytic growth on Fig. 30.8: Exophytic growth on tongue the tumor is labeled as verrucous
tongue carcinoma histopathologically, a
698 Neoplastic Conditions of Head, Neck and Face

Fig. 30.9: Early exophytic growth,


verrucous carcinoma A B
Figs 30.10A and B: Verrucous carcinoma
tran­sitional change to invasive squa-
mous cell carcinoma may be present
in some parts of a large lesion, which • Metastatic tumor in neck nodes either case, the patch should also be
will be often missed if the biopsied with obscure primary: Rarely, the excised along with the primary tumor
tissue does not include this part of squamous cell carcinomas primarily to get adequate surgical clearance.
the lesion. The same is applicable to present as a metastatic mass in the The lesions associated with SMF are
the in situ carcinomas, as both these cervical nodes and the primary is more difficult to evaluate clinically
lesions are border line and have a not detectable in the oral cavity. due to the presence of trismus and
threshold to change into an invasive The fine needle aspiration cytology altered tissue consistency due to
squamous cell carcinoma. Hence, it (FNAC) of the involved lymph which the induration is difficult to
is imperative that these lesions be nodes shows deposits of squamous elicit. The common sites of OSCC
evaluated thoroughly for regional cell carcinoma. A thorough clinical secondary to SMF are retromolar
metastasis and the entire excised evaluation of not only the oral cavity, area (probably due to trauma from
lesion be thoroughly screened his- but of nasal cavity, nasopharynx and occlusion [TFO] from the buccally
topathologically to find out any area oropharynx is needed. The possi­ placed maxillary third molars and loss
of invasive changes in the lesion. bility of primary intraosseous carci­ of elasticity of the cheek mucosa) and
The cases of verrucous carcinomas noma should also be ruled out. Four tongue and both cannot be evaluated
should be kept under long term quadrant incisional biopsy from properly, if trismus is present. The
follow-up to detect any locoregional most common sites of develop­ presence of trismus in the retromolar
recurrence. ment of OSCC like tongue, floor of malignancies could also be due to
• A mixed growth with both ulcerated mouth, cheek and tonsils is taken tumor infiltration in the muscles,
and exophytic areas: Some tumors in an attempt to locate the obscure but this cannot be ascertained if the
present with such a mixed picture. primary, which is rarely productive. patient has tri­smus due to SMF and
The behavior in spite of the dual The chances of distant lymphatic invariably the growths are extensive,
presentation is aggressive similar to metastasis from viscera like upper involving the infratemporal fossa
the ulcerated growth. GI tract are there and warrant to be and surgical clearance is difficult. A
• As a nodule: It is not a very usual ruled out. The treatment strategies com­puterized tomography (CT) scan
presentation of the OSCC except in are definitely altered, if the primary with contrast is ideal to assess the
some cases of the carcinoma of the is obscure. tumor extent in such cases.
tongue. It may present as a small The tumor may be associated with When the tumor infiltrates full
ulcer on the venterolateral margin leukoplakic or an erythroplakic patch thickness of the cheek, it inva­des the
of the tongue, but when palpated, a at the periphery, which suggests that overlying skin. Initially it produces
nodular lump may be felt in the sub- the tumor might have originated in ‘peau d’orange’ or orange peel ap-
stance of the tongue, which could the pre-existing premalignant les­ pearance. Then the skin becomes
be appreciably large involv­ing large ions, but some tumors are without eroded and finally the tumor fun­
area of the tongue. It is the reason such picture. Whenever such patches gates extraorally (Figs 30.11A to C).
why evaluation of tongue is done are present, they should also be Such open growths get infected
with a magnetic resonance imag- biopsied and evaluated. Sometimes sec­ondarily, leading to formation
ing (MRI), in addition to the clinical they may show severe dysplasia or of orocutaneous fistulas and foul
examination (see Figs 30.27A to D). frank invasive carcinoma and in smell. The grow­ths can get infected
Oral Cancer 699

A B C
Figs 30.11A to C: Extraoral fungation

as carotid artery making them unre-


sectable and the chances of major
vessel blow outs and life threatening
hemorrhage during the surgery are
increased.

PRIMARY INTRAOSSEOUS
CARCINOMA
Primary intraosseous carcinoma (PIOC)
is an uncommon neoplasm. According
to the most recent edition of the World
Fig. 30.13: Extraoral fungation of the OSCC
Health Organization (WHO) classi­
with secondary infection, presenting as a
Fig. 30.12: Extraoral fungation with cutaneous sinus like osteomyelitis fication for histological typing of odon­
maggots togenic tumors, it is defined as a
squamous cell carcinoma arising within
the jawbone without connec­tion to the
oral mucosa, probably from odontogenic
epithelial residues. This tumor was first
described by Loos in 1913. Pindborg
coined the term PIOC in the first edition
of the WHO classification for histological
typing of odontogenic tumors. Affecting
more males than females (M:F, 3:2),
PIOC is more frequent in the 6th and 7th
decades of life. It occurs more frequently
in the mandible (especially the posterior
section) than in the maxilla.
A B Since PIOC essentially occurs only in
Figs 30.14A and B: External fungation of the metastatic lymph nodes the tooth bearing areas of the jawbone,
the hypothesis of odontogenic epithe­
lial origin is theoretically acceptable,
with myasis, which is a common careful clinical evaluation and histo­ except in the maxillary incisive canal.
presentation in such growths in ru- pathological examination for correct At termination of the odontogenesis,
ral India (Fig. 30.12). The fungation diagnosis. Similarly, the meta­­static remnants of the odontogenic epithelium,
with pus discharge due to the sec- cervical lymph nodes can also fun- derived from different origins such as the
ondary infection often mimics the gate on the skin surface (Figs 30.14A tooth germ, remain in the oral tissues as
presen­tation of chro­nic suppurative and B). Such lymph nodes also infil- epithelial rests. Occasionally, owing to
osteo­myelitis (Fig. 30.13) and needs trate the deeper vital struc­tures such some unknown stimuli, these epithelial
700 Neoplastic Conditions of Head, Neck and Face

rests are activated and, either alone or in Once the diagnosis is made, the
conjunction with mesodermal tissues, PIOC should be treated as any other
they then proliferate and develop into squamous cell carcinoma and treated
odontogenic cysts or carcinomas. In in the similar fashion. Due to its intra­
contrast to the classic oral mucosa squa­ osseous nature, radiotherapy as primary
mous cell carcinomas, the risk factors modality of its treatment is not recom­
of alcohol, tobacco or betel quid abuse mended.
are usually not present in PIOC patients.
The most common risk factor for indu­
Modalities of Spread of the
cing neoplastic formation of PIOC is Oral Squamous Cell Carcinoma
assumed to be a reactive inflammatory The modes of spread of the oral squa­
stimulus, with/without a predisposing mous cell carcinoma are:
genetic cofactor. Fig. 30.15: Carcinoma of maxillary sinus
Local Spread fungating through the alveolus and exten­
The WHO has published criteria to
ding to the buccal mucosa
differentiate PIOC from other pri­mary The local spread of the OSCC is as a result
and metastatic squamous cell carci­ of the direct infiltration of the tumor in
nomas of the jaw bone such as: the adjacent tissues. The tumor spread The OSCC of lower gingivobuccal
• Intact oral mucosa before diagnosis. occurs along the path of least resistance. sulcus infiltrates the alveolar bone and
• Microscopic evidence of squamous The anatomical barriers try to restrict the extends to the lingual gingiva and there-
cell carcinoma without a cystic com­ tumor spread, but soon their integrity is on involves the floor of the mouth caus-
ponent or other odontogenic tumor violated by the tumor infiltration. The ing widespread lymph node metastasis
cells. spread of the tumor in the cancellous bilaterally, changing the clinical course
• Absence of another primary tumor bone is faster than the cortical bone. and management of the malignancy
on chest radiographs obtained at the The tumors of retromolar area spread (Figs 30.16A and B).
time of diagnosis and during a follow- to the pterygomandibular space and
up period of more than 6 months. the infratemporal area rapi­ dly due to Regional Lymph Node Spread
Therefore, exclusion of the possi­ the potential spaces present there and The OSCC are known to metastasize
bility of metastatic lesion from a distant infiltrate the muscle like medial pterygoid to the regional lymph nodes quite
primary tumor is always necessary for resulting in trismus. Simil­ arly, due to early necessitating the management
the final diagnosis of PIOC. the presence of more spongy bone, the of the me­ t­
astatic nodes imperative for
Although the clinical features of tumors of the maxillary sinus or those the effe­ctive locoregional control of the
PIOCs are non-specific, still most of originating in the maxillary gingivobuccal disease. The carcinomas originate from
them are associated with complaints vestibule, spread rapidly involving large the epithelium and once the base­ment
of sensory disturbances like paresthesia areas. The tumor rapidly extends to the membrane is broken the cancerous
and numbness, mimic­king facial neuro- para­nasal sinuses and the involve­ment cells enter the underlying connective
logical problems. When solely neurolog- of ethmoidal and sphenoidal sinuses tissue. The area of the connective tissue
ical disturbances are present and there is leads to the involvement of the base of which lies just below the epithelium
absence of any obvious mucosal abnor- anterior cranial fossa. The involve­ment has rich network of lymphatics and the
malities within the oral cavity, especially of the posterior wall of maxilla leads cancer cells ingress in to the lymphatic
in case of the early lesion, increases to extension of the tumor in the infra­ channels and reach the regional lymph
the probability of delayed diagnosis. temporal fossa and renders it virtually nodes. Thus, the lym­ phatic spread is
Delay in correct diagnosis will worsen unresectable. The tumors of the maxillary more common in the carcinomas. More
the prognosis; hence, it is important to sinus involving the infe­rior wall, fungate the tumor bulk, more are the chances of
consider intraosseous carcinoma in the through the alveolar bone and the exten­ lymph node metastasis. The groups of
jawbone in the differential diagnosis for sion of such tumors on to the buccal lymph node draining a particular area are
all cases of facial paresthesia and numb- mucosa after crossing the buccal vesti­ most likely to be involved in metastasis.
ness to facilitate the early identification bule changes the clinical behavior of The carcinomas of the tongue and floor
of PIOC and enabling prompt institution the tumor (Fig. 30.15). The maxillary of the mouth have optimum tendency
of suitable treatment. sinus malignancies do not frequently for widespread lymphatic metastasis,
Radiographic examination is one of metastasize in the regi­onal lymph nodes, and in the latter case they could be
the most effective methods for detecting but extension of this tumor on the buccal bilateral. This is because both these
PIOCs. A lesion that is completely sur­ mucosa causes lymph node metastasis, sites have rich lymphatic networks and
rounded by bone can be regarded as of which war­ rants neck dissection along there is crisscrossing of the lymphatics
intraosseous origin. CT scan can also with the maxillectomy thus, changing the from the contralateral side. Similarly,
facilitate correct diagnosis. treat­ment requirements. the malignancies of the midline tend to
Oral Cancer 701

tumor cells proliferate in the lymphatic


nodules present in the subcortical area
and compaction of the cell mass takes
place. As a result of this, the lymph node
becomes round in shape and the node
becomes non-compressible and stony
hard in consistency (Fig. 30.17).
The cervical lymphatics are located
along the major veins of the neck. The
lymphoid sinuses roughly around 80
A B to 90 in number develop around the
Figs 30.16A and B: Gingivobuccal carcinoma extending on to the floor of mouth by developing venous channels in the
direct infiltration, changes the behavior of the tumor neck. Over a period of time they reduce
in number and form aggregates, which
metastasize bilaterally. The retromolar along with the excision of the primary. develop in the nodes, which have diffe­
area malignancies are also known to The other indications for the elective rent locations around the veins in the
metastasize in deep cervical nodes neck dissection being, the anaplastic neck. The various locations at which the
more often than the gingivobuccal or carcinoma and malignant melanoma. cervicofacial lymph nodes are present
buccal mucosa carcinomas. Thus, the The metastatic lymph nodes are firm are (Fig. 30.18):
carcinomas of the tongue, floor of the to hard in consistency as the metastatic • Occipital
mouth and the retromolar area are cells reach the cortex of the lymph node • Retroauricular (mastoid)
often treated by elective neck dissection through the afferent lymphatics. The • Parotid

Fig. 30.17: Structure of the lymph node. The metastatic cells reach the lymph node through the afferent
lymphatic to get lodged in the subcortical area, making the node hard in consistency and round earlier
702 Neoplastic Conditions of Head, Neck and Face

of the internal jugular vein (Jugulo-


diagastric) and the adjacent spinal acce­
ssory nerve.
Level IIA: Lymph nodes are located an-
terior (medial) to the spinal accessory
nerve. These nodes are present at the lev-
el, where the posterior belly of digastric
crosses the internal jugular vein and thus
are referred to as jugulo digastric nodes.
Level IIB: Lymph nodes are located
posterior (lateral) to the spinal accessory
nerve.
III (middle jugular): Lymph nodes
located around the middle third of the
internal jugular vein; nodes are located
between the inferior border of the hyoid
bone and the inferior border of the cricoid
cartilage. They are present at the level,
Fig. 30.18: Various groups of cervical lymph nodes19 where the superior belly of the omohyoid
crosses the internal jugular vein and
are also designated as jugulo-omohyoid
group of nodes or midjugular nodes.
IV (lower jugular): Lymph nodes located
around the lower third of the internal
jugular vein; nodes extend from the infe­
rior border of the cricoid cartilage to the
clavicle.
V (posterior triangle): Lymph nodes
located along the lower half of the spi­
nal accessory nerve and the transverse
cervical artery; supraclavicular nodes
are located in this group of lymph nodes.
Level V A: Along the lower half of the
spinal accessory (above the inferior
Fig. 30.19: The hyoid bone and cricoid belly of omohyoid).
cartilage are the important landmarks in Level V B: They are present along the
determining the lymph node levels transverse cervical artery (below the
inferior belly of omohyoid).
• Facial VI (central compartment): Lymph
• Submandibular nodes in the prelaryngeal, pretracheal,
• Submental Fig. 30.20: Classification of neck nodes paratracheal and tracheoesophageal
• Superficial cervical according to levels groove; boundaries are the hyoid bone to
• Deep cervical. the suprasternal notch and between the
The lymph nodes of the neck can be by the stylohyoid muscle and the medial borders of the carotid sheaths.
further classified as per the levels as19: inferior border of the mandible. These They are not commonly involved in the
(Figs 30.19 and 30.20) nodes are not present in single location OSCC, but are involved in thyroid and
IA (submental): Lymph nodes but are distributed superficial, anterior, laryngeal malignancies.
within the triangular boundary of the posterior to the submandiblar salivary VII (superior mediastinal): Lymph
anterior bellies of the digastric muscles gland and also with in the glandular nodes in the anterior superior medi­
and the hyoid bone. parenchyma. Thus, for excising these astinum and tracheoesophageal grooves,
IB (Submandibular): Lymph nodes nodes, the submandibular gland needs extending from the suprasternal notch to
within the boundaries of the anterior to be excised. the innominate artery.
belly of the digastric muscle, posterior IIA and IIB (upper jugular): Lymph The lymphatic drainage of the oral
belly of digastic muscle, complemented nodes located around the upper third structures is primarily in the particular
Oral Cancer 703

Box 30.1: Lymphatic drainage of oral structures (Fig. 30.21). The metastasis can occur
to the bones as well like the vertebra,
Floor of mouth Anterior part—upper deep cervical nodes, either directly or via submental cranial bones, or long bones. The distant
nodes
hematogenous spread of the disease is a
Remaining part—submandibular and upper deep cervical nodes
poor prognostic sign (Fig. 30.22).
Maxillary sinus Drains in the submandibular nodes
Paranasal sinuses—upper deep cervical nodes, directly or through
retropharyngeal nodes Contact Spread
Teeth Lower incisors—submental and therefore to submandibular or lower deep Contact spread is a rare type of spread
cervical nodes of OSCC. It is more common in the
Rest lower teeth and all upper teeth—submandibular lymph nodes and malignancies of vulva. In the oral cavity
upper deep cervical nodes contact spread could take place in the
Occasionally upper and lower teeth also drain into the buccal and
malignancies involving vermilion, where
mandibular lymph nodes
the tumor can spread to the opposing
Tonsil Do not possess afferent lymphatics or lymph sinuses
Dense plexus of fine lymphatic vessels surround each follicle, forming lip or occasionally from gingiva to the
efferent lymphatic, which drain to upper deep cervical lymph nodes, buccal mucosa.
especially the jugulodigastric nodes
Hard palate Anterior part—submandibular lymph nodes TNM Classification of Oral
Posterior part—upper deep cervical nodes and to the retropharyngeal
nodes Squamous Cell Carcinoma
Soft palate Lymphatics drain partly to the retropharyngeal and partly to the upper (Box 30.2)
deep cervical nodes
The TNM system for the classification
Tongue Tip of tongue—bilaterally to submental nodes of malignant tumors was developed by
Anterior 2/3rd—unilaterally to submandibular nodes
Central vessels—jugulodigastric or jugulo-omohyoid nodes Pierre Denoix20 in France between 1943
and 1952 and eventually was adapted by
the International Union against Cancer.21
The objectives of such classification
groups of lymph nodes as mentioned along the bloodstream in this way also. are as follows:
above (Box 30.1). However, there can The cellular emboli can get lodged at • To aid the clinician in treatment
be variations due to crisscrossing of distant sites and start proliferating there, planning.
the lymphatics, aberrant lymphatic producing metastatic disease. Usually • To provide prognostic value.
channels, anastomosis and due to a the richly vascular visceral organs like • To evaluate the results of treatment.
phenomenon called skip metastasis. lungs, liver, kidneys and the brain are • To facilitate exchange of information
involved in hematogenous metastasis between surgical teams.
Hematogenous Spread
The hematogenous spread of OSCC is a
rare and late occurrence. The tumor cell
seeding in the bloodstream can occur if
a tooth involved in the malignant growth
is extracted. The cells can invade the
blood vessels during surgery. In cases of
advanced disease, the tumor cells involve
deeper connective tissue and spread
hematogenously. The other causes of
the hematogenous spread could be
that the lymph nodes are located along
the venous channels right from their
development. This proximity can make
a metastatic node involve the adjacent
vein and the tumor cells can spread via
the bloodstream. Lastly the lymph drains
in to the venous compartment through
the efferent channels or finally through
the ductus chylus and the tumor cells
present in these channels can spread Fig. 30.21: Drainage of lymph in the veinous system
704 Neoplastic Conditions of Head, Neck and Face

Box 30.2: TNM classification

T staging for tumors of the lip and oral cavity


• TX: Primary tumor cannot be assessed
• T0: No evidence of primary tumor
• Tis: Carcinoma in situ
• T1: Tumor 2 cm or less in greatest dimen­sion
• T2: Tumor >2 cm but not >4 cm in great­est dimension
• T3: Tumor >4 cm in greatest dimension
• T4a: Lip Tumor invades through cortical bone, inferior alveolar nerve, floor of mouth,
or skin of face (i.e. chin or nose). Oral tumor invades through cortical bone, into deep
Fig. 30.22: An advanced case of OSCC with [extrinsic]. Cavity muscle of tongue (genioglossus, hyoglossus, palato­ glossus, and
secondaries in the brain styloglossus), maxillary sinus, or skin of face
• T4b: Tumor involves masticator space, pterygoid plates, or skull base and/or encases
internal carotid artery
• To contribute to the continuing in- N staging for all head and neck sites except the nasopharynx and larynx
• Nx: Regional lymph nodes cannot be assessed
vestigation of human cancer.22
• N0: No regional lymph node metastasis
• N1: Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension
Staging of OSCC • N2: Metastasis in a single ipsilateral lymph node, >3 cm but not >6 cm in greatest
The staging of the tumor is as shown in dimension; or in multiple ipsilateral lymph nodes, none >6 cm in greatest dimension; or
Box 30.3. in bilateral or contralateral lymph nodes, none >6 cm in greatest dimension
• N2a: Metastasis in a single ipsilateral lymph node >3 cm but not >6 cm in greatest
dimension
Clinical Features of the Oral • N2b: Metastasis in multiple ipsilateral lymph nodes, none >6 cm in greatest dimension
• N2c: Metastasis in bilateral or contralateral lymph nodes, none >6 cm in greatest
Squamous Cell Carcinoma as dimension
per the Site of Involvement • N3: Metastasis in a lymph >6 cm in greatest dimension
Although the general presentation of the M staging for head and neck tumors
OSCC is common to all the sites, there • Mx: Distant metastasis cannot be assessed
• M0: No distant metastasis
are site wise clinical features, which are • M1: Distant metastasis
described below.

General Clinical Features


• An ulcerated growth with rolled out in the earlier stage, but get fixed to Detailed History
edges or an exophytic growth, (cauli­ adjacent structures in the advanced In the clinical practice, arriving at a
flower like) details are given above disease diagnosis is always a sequential process.
• Rapid growth • Weight loss, cachexia in the advan­ It requires a methodology. The history
• Infiltrative nature ced stages. taking is an essential step for leading to
• Fixity to underlying and overlying a proper diagnosis. The relevant findings
tissues Site-wise Clinical Features in the history pertaining to the OSCC are:
• Friability Site-wise clinical features are shown in • Age: Commonly seen in 40 to
• Tendency to metastasize to cervical Box 30.4. 60 years of age. However, of late
lymph nodes the patients developing the OSCC as
• Metastatic nodes are round, stony Diagnosis and Clinical early as 20 to 30 years of age, secon­
hard in consistency and are discrete dary to SMF have been seen.
Examination of the Oral • Sex: More commonly seen in males.
Squamous Cell Carcinoma • Signs of malnourishment, iron defi­
Box 30.3: Staging of oral cancer
The diagnosis of the OSCC with adva­ ciency, vitamin deficiency.
Stage 1 T1 N0 M0 nced stage is straight forward due to • Habits: Tobacco, betel nut, alcoho­
Stage 2 T2 N0 M0 its peculiar presentation and common lism are commonly associated
Stage 3 T3 N0 M0 occurrence. The early lesions and the with the OSCC. The duration of the
T 1/T 2 N1 M0 malignant transformations in pre­ habits, frequency and quantity are
Stage 4 T4 N0 M0 cancerous lesions or conditions pose also noted. The carcinomas of the
T4 N1 M0 great challenge and require clinical tongue have been reported in females
Any T N2 M0 skill and expertise. The diagnosis of the without associated habits, but having
Any T N3 M0 OSCC can be arrived at following the chronic iron deficiency anemia,
Any T N0 M1
steps mentioned below. perimenopausal age or having sharp
Oral Cancer 705

Box 30.4: Site-wise clinical features or condition such as leukoplakia,


lichen planus or SMF, etc.
Gingivobuccal sulcus Loosening of the teeth/exfoliation • Color and size change in the precan-
Inability to masticate
cerous lesion.
Involvement of the bone and inferior alveolar nerve producing
numbness • Development of induration and
Tongue Commonly involving the venterolateral surface and rarely the fixity. The induration is hall mark
dorsum of malignancy. The elicitation of
Salivation this sign needs practice. A palpating
Hypomobility of tongue finger can tell the nature of lesion
Inability to swallow accurately. Due to the infiltrative
Fixity of the tongue (ankyloglossia), which is poor prognostic sign
nature of the lesion fixity to the
(Fig. 30.23)
Lump in the tongue adjacent structures develops.
Bilateral and widespread lymph node metastasis • Neurological deficit: When a gingi­
Floor of mouth Inability to swallow vobuccal growth infiltrates the man­
Involvement of tongue leading to hypomobility dible, the inferior alveolar nerve
Bilateral and widespread lymph node metastasis gets involved leading to paresthesia
Cheek Inability to chew of the inferior alveolar nerve. This
Fixity to the skin sign is absent in large benign lesions
Extraoral fungation
like ameloblastoma, which tend to
Posterior one third of Inability to swallow
displace the neurovascular bundle
the tongue Fixity of the tongue, lack of protrusion
Microaspiration leading to chest infections than involving it.
Spread to adjacent structures like larynx which can lead to change • Signs of involvement of paranasal
in speech sinuses like epistaxis and foul smel­
Late detection ling discharge.
Maxillary sinus Details given in the chapter no. 14 • Presence of trismus due to involve­
Retromolar trigone Trismus due to involvement of muscles of mastication ment of muscles of mastication,
Spread to the infratemporal fossa especially in the retromolar trigone
Deep cervical lymph node metastasis
and maxillary sinus malignancies.
Poor prognosis
• Peau d’orange of the skin and extra­
Primary intraosseous Rare
carcinoma Absence of other primary oral fungation.
Irregular, oesteolytic lesion in the bone • Presence of cervical lymph node
Mobility of the teeth metastasis: The OSCC are open
Involvement of nerve leading to paresthesia growths in oral cavity and are liable
Metastatic disease from other sites must be ruled out. to get secondarily infected and also
tend to metastasize in the regional
cervical lymph nodes depending
upon their anatomical location. A
teeth or over hanging restorations, or careful clinical evaluation of the
chronic TFO. lymph nodes is required.
• Lack of pain and tenderness, unless
signs of secondary infection are pre­
Assessment of Cervical Lymph
sent.
• Nature of growth: Whether it is an Nodes
ulcerated or exophytic growth. If it is The OSCC often metastasize to the
an ulcerated growth it has indurated cervical lymph nodes. The secondaries
everted or rolled out edges indurated in the neck, i.e. metastatic disease in the
base, fixity to deeper structures, cervical lymph nodes need to be evalu­
friability. The exophytic growths are ated carefully. If the primary disease
sessile and friable. They are rapidly is present in the oral cavity and the
growing and develop fixity to the examination of the neck nodes reveals
underlying structures. that the lymph nodes are either not
Fig. 30.23: Carcinoma anterior 2/3rd of • Short history and rapid growth or palpable or insignificant, the neck is then
tongue with ankyloglossia long standing precancerous lesion labeled as N0 neck. However, the N­0 neck
706 Neoplastic Conditions of Head, Neck and Face

I II III
Fig. 30. 24A: Clinical examination of the nodes

and not yet lodged in the recipient lymph


node. Thus, the examination of the neck
has to be methodical and comprehensive.
With the advancement in techniques and
technology, the accuracy, sensitivity and
specificity has increased significantly, but
still the assessment is not cent percent
accurate. Thus, in some cases the surgeon
has to make a decision of undertaking
an elective neck dissection (electing to
perform the neck dissection in presence
of N0 neck) or advising the postoperative
I II
radiotherapy to take care of occult meta­
stasis or to do a second surgery, if the
metastatic nodes are detected during the
follow-up.
• Clinical evaluation: The neck is
flexed to relax the muscles and the
lymph nodes are carefully palpated.
The palpation starts from level one,
i.e. from the submental group and
then descends down level wise. All the
groups should be palpated, bilaterally
and any lymphadenopathy should be
noticed along with the characteristics
III IV of the nodes. Simultaneous bilateral
Fig. 30.24B: Intra operative photographs: (I and II) Note the submandibular LN are smaller palpation facilitates the comparison
but rounded and hard in consistency and turned out to be metastatic, while as the upper of findings (Fig. 30.24A). The infla­mm­
jugular nodes are larger, soft and oval and were found to be negative for metastasis; atory nodes are enlarged, soft, oval and
(III) Specimen of round, hard lymph node highly suspicious of secondaries; (IV) Oval node tender. The metastatic nodes are often
mostly inflammatory
round, stony hard, initially discrete,
but subsequently become adherent
does not necessarily mean that the tumor metastasis. Similarly, some times the (Fig. 30.24B). The tubercular lymph
has not metastasized in the neck nodes as metastatic disease may not be present in nodes are often matted.
micrometastasis cannot be ascertained the group of nodes draining that site, but The findings that are required to
clinically and in such cases additional may be present in the subsequent group be noted on the clinical examination
evaluation of the neck nodes using of nodes due to skip metastasis. The are:
other modalities as mentioned below, metastasis in transit implies when the – Site/level
may be required to ascertain the nodal cancer cells are present in the lymphatics – Size
Oral Cancer 707

• Computed tomogram scan26 (CT)


and magnetic resonance imaging27,28
(MRI) (Figs 30.26 and 30.27).
These are more effective not only
in determining the extent of primary,
but also in assessing the deep cervical
nodes than the UGC. The MRI scans
are particularly more useful in the
assessment of the carcinomas of the
tongue (Figs 30.28A to C).
• Sentinel node biopsy (SNB): It is
the first euchlion lymph node that
is most likely to drain a part. If this
lymph node is biopsied there are
optimum chances of detecting the
Fig. 30.25: USG of malignant lymph node
nodal metastasis. The first successful
SNB in a head and neck SCC was
performed, in 1996, by Alex29 and
Krag on a patient with a laryngeal
supraglottic carcinoma.
Rationale:
– Cervical metastasis is the single
most important prognostic factor
in patients with oral cancer, with
the presence of nodal spread de-
creasing the 5-year disease-free
survival rate by approximately
50 percent.
– SNB is a staging tool.
– Improved the accuracy of stag­
ing, while reducing the mor­bidity
caused by unnecessary lympha­
Fig. 30.26: Axial computerized tomography (CT) scan showing central necrosis within a
denectomy in melanomas and
left cervical lymph node metastasis contrast enhanced axial CT image showing enlarged
jugulodigastric lymph node breast cancers.
Preoperative technique: Lym-
– Shape phoscintigraphy (SPECT) and gam-
– Extent – Central necrosis—present in ad- ma probe-guided localization have
– Number vanced disease emerged as useful techniques for
– Consistency – Perinodal infilteration (extra- identification of the sentimental
– Fixity capsular spread) lymph node (SLN). Lymphoscintig-
– Tenderness – Fixity to vessels. raphy30 is typically performed in the
– Matting. • Fine needle aspiration cytology25 nuclear medicine suite. A radiotracer
• Ultrasonography23,24: It is an effec- (FNAC): The lymph nodes which is injected at several sites around the
tive method for evaluation of the are 1 cm plus in size and have tumor and gamma camera images
deep cervical nodes, lying below clinical or USG features suspicious depict the laterality and approximate
the sternocleidomastoid muscle of metastasis are further evalua­ anatomic location of the SLN(s).
(Fig. 30.25). The USG criteria for ted by FNAC. The cytology may The nuclear medicine physician
iden­ti­fying the metastatic node are: not be always be confirmatory and marks the area(s) that corresponds
– Size—more than 1 cm accurate, but is effective in most to the SLN(s) on the patient’s skin. In
– Shape—round cases to determine type of the neck the operating room, the surgeon uses
– Number dissection required in a particular a gamma probe trans­cutaneously to
– Echogenicity—hypoechogenic case. The FNAC could be USG gui­ confirm the location of the SLN(s).
– Intactness of phylum—it is dis­ ded or CT guided to enhance its Next, blue dye is injected intra­
torted sensitivity and accuracy. dermally and the SLN exposed.31
708 Neoplastic Conditions of Head, Neck and Face

A B

A B

C
Figs 30.28A to C: PET scan of neck showing
posi­tive node (the yellow node is postive
C D node)
Figs 30.27A to D: MRI of the tongue for the carcinoma of tongue is a good modality to
see tumor infiltration in the tongue – Lymphoscintigraphy revealed
un­expected bilateral or contra-
lateral disease in about 14 per-
SLNs are identified by the pre­ – In June 2001, the conclusions of cent of patients.34
sence of blue staining and/or radio­ the 1st International Conference – Up to 46 percent of SLN harbor
tracer uptake, as detected by the on SNB of head and neck SCC, metastases (data for breast can­
gamma probe. Concurrent use of held in Glasgow, underlined that cer metastasis)
blue dye and radiotracer is currently results were significantly better i Fine section frozen analysis
recommended; in view of the fact in those centers that performed increases sensitivity to about
that many studies suggest that the more than 10 cases a year: over- 95 percent
SLNs are not always blue, or always all sentinel node identification ii. Immunohistochemical stain-
radioactive. was 98 percent, and sensitivity of ing.
Having two methods to identify the procedure was 90 percent.33 – False negative rate is roughly
the SLN intraoperatively increase Reliability of SNB was confirmed 10 percent and the grossly invo­
the identification rate and probably 2 years later, at the 2nd Inter- lved nodes less likely to take up
account for the sensitivity and national Conference held in tracer.
specificity reported in recent stu­ Zurich. Pooled data on 397 cN0 – Better sensitivity for T1/T2 lesi­
dies. The SLNs are removed and head and neck patients from ons: Most false negative results
sent to the pathologist for histologic 20 centers have been presented: associated with larger T3 lesions.
and immuno­histochemical analysis. the identification rate was 97 • Positron emission tomography
Therapeutic node dissection is per­ percent (range 90–100%), with (PET) scan: The positron emission
for­med only in patients whose SLN a 96 percent (range 88–100%) tomography with flurodeoxyglucose
is positive. negative predictive value of a is functional imaging modality that
Silent features: negative sentinel node for the used abnormal tissue metabolism
– Sentinel nodes found in more remainder of the neck using to detect neoplasms and metastatic
than 90 percent of cases.32 both preoperative lymphos- node. The radioactive glucose ana-
– 56 percent success in SLNB (*data cintigraphy and intraoperative logue FDG is metabolized in nor-
in relation to breast cancer) hand-held gamma probe.32 mal tissue and neoplastic tissues in
Oral Cancer 709

proportion to the rate of tissue glu-


cose metabolism. FDG is meta-
bolically trapped in the intracel-
lular space, this occurs more in
the tumors than in normal tissues
and can be used to identify tumors
based on accelerated glycolytic rates A B
(hyper­metabolic lesions) using PET
Figs 30.29A and B: Mouth eaten, irregular radioluscency with floating teeth and
(Figs 30.28A to C).
pathological fracture
• Radiographic examination: The
mali­gnant lesions produce typical ra-
diological appearance on X-ray, the
irregular, mouth-eaten radiolucency.
The destruction of the periodonitium
leads to a typical floating teeth ap-
pearance (Figs 30.29A and B).
• Biopsy: The biopsy still remains the
gold standard in the final diagnosis
of the OSCC. The oral cavity tumors
are readily accessible and the biopsy
is easy to obtain. It is economical
and most importantly confirmatory. Fig. 30.30: Well differentiated SCC Fig. 30.31: Moderately differentiated SCC
The types of the biopsy are:
1. Punch biopsy
2. Incisional biopsy • Moderately differentiated (Fig. 30.31)
3. Excisional biopsy • Poorly differentiated, based on the
4. Fine needle aspiration cytology/ degree of differentiation of the cells
biopsy (FNAC/FNAB). (Fig. 30.32).
The incisional biopsy is obtained Apart from the degree of differen­
from the lesion, mostly under local tiation, the depth of involvement or the
anesthesia as an out door procedure. bulk of the tumor is also important. As
The guidelines for the biopsy are: the depth increases beyond 2 mm in
• As far as possible take a piece of 1 cm × the connective tissue, the chances of
1 cm × 1 cm, as the wide represen­ the regional lymph node metastasis are
tation of the tumor is available and Fig. 30.32: Poorly differentiated SCC enhanced and the lymph node metas­
the depth of the biopsy should also tasis compromises the prognosis.
be adequate for ascertaining the for transporting in the laboratory for
depth of penetr­ation of the tumor. further processing. General Examination
• The biopsy should be taken from the Although OSCC originates in the oral
periphery of the lesion and certain cavity, it has systemic ramifications as it
Histopathological Grading
amount of normal tissue should tends to spread to regional lymph nodes
also be included for the comparative of OSCC and its Clinical and occasionally to the distant sites by
purposes. The lesion grows at the Relevance hematogenous metastasis. Thus, the
periphery and has optimum mitotic The histopathological diagnosis alone is clinical examination is necessary to detect
activity and is more representative not adequate in the management of the the distant metastasis. The examination of
rather than the center, where the OSCC, but the histopathological grading the chest and X-ray of the chest is required
exfoliated, necrotic cells are present. of the lesion is important to know its to rule out pul­monary metastasis. The
• The representative area is one where biological behavior. Generally the well clinical exami­ nation of the abdominal
the optimum induration is present differentiated squamous cell carcino­ viscera to rule out organomegaly and
and it should be biopsied. Hence, mas are less aggres­sive than the poorly in sus­pected cases USG or CT scan may
out of the edge of the ulcer, the area differentiated and highly anaplastic gro­ be useful. The biochemical assessment
which is more indurated should be wths.35 like renal function test or liver function
included in the biopsy. The histopathological grading of test could be of value. The neurological
• The biopsy specimen should be fixed OSCC can be done as: examination to detect any neurological
in 10 percent formaldehyde solution • Well differentiated (Fig. 30.30) deficit is done in cases suspected to have
710 Neoplastic Conditions of Head, Neck and Face

cerebral metastasis followed by a CT scan frozen sections are of immense value in than the cancel­ lous bone and hence
or MRI. determining adequacy of the surgical in selected, early cases the wedge
resection. The malignancies involving the madi­ bulectomy could be adequate
mandibular bone are also treated with and avoid morbidity in the patients
MANAGEMENT OF OSCC
a segmental resection of the involved (Figs 30.35A and B). The growths involving
The modalities for the management of segment keeping two centimeter mar­ the anterior region and the body of the
oral squamous cell carcinoma are: gins as the tumor can extend beyond the mandi­ble can be treated with segmental
• Surgery radiological margins through the can­ mandibulectomy with adequate soft
• Radiation therapy cellous bone. The cor­ tical bone offers tissue clearance (Fig. 30.36). The malig­
• Chemotherapy more resistance to the tumor spread nancies involving the retromolar area
• Combination of above.

Surgery
The surgery is still the most prefer­
red primary treatment modality of all
resec­ table cancers. The wide surgical
exci­sion of the growth along with the
2 cm margins of normal tissue all around
is recommended for adequate surgical
clearance. The surgical clearance has
to be three dimensional, i.e. apart from
periphery adequate clearance in the
depth should also be achieved. The tumor
excision not only removes the primary, but A B
also abolishes the chances of further spread Figs 30.33A and B: Wide local excision of a very early (T1) growth
and metastasis. Surgical management
of the cancer not only revolves around
the excision of the primary, but a com­
prehensive surgical management com­
prising of excising the metastatic lymph
nodes with block dissection and recons­
truction of the defect.
The purpose of the cancer surgery
is not only to eradicate the disease, but
also to ensure the quality of life post­
operatively. The surgery is intended
to establish the locoregional control
and the term cure may not be always A B
applicable. The locoregional control Figs 30.34A and B: (A) Preoperative photograph of a case of verrucous carcinoma of
is better in the early malignancies, lower lip; (B) Wide local excision
i.e. the stage I and stage II rather than
the advanced malignancies with wide
spread regional lymph node metastasis.
The presence of regional lymph node
metastasis itself is taken as a sign of
guarded or poor prognosis. Rather than
the term ‘cure’ the disease free period
or locoregional control with minimum
5 years life expectancy is realistic.

Management of Primary
The primary growth is treated surgically
by wide local excision keeping ideally
2 cm margins—into the normal tissue A B
all around (Figs 30.33 and 30.34). The Figs 30.35A and B: Wedge mandibulectomy
Oral Cancer 711

tumor load for subsequent therapy. In Table 30.1: Co-relation between site of
cases of extraoral fungation, gross un- primary tumor and percentage of cases
having nodal metastasis
hygienic conditions due to secondary
infection, the debulking of the tumor is
Site of Percentage of
indicated.
primary cases having
If the excision of the primary tumor nodal metastasis
is planned with the neck dissection as
is the case in majority of the patients, Lip 12%
Floor of mouth 72%
it is desirable to excise the neck block Buccal mucosa 32%
along with the primary enblock (i.e. in Gingivobuccal sulcus 43%
Fig. 30.36: Segmental mandibulectomy continuity) to ensure that all the inter­ buccal vestibule
vening lymphatic channels are removed, Gingivobuccal sulcus 67%
so that any metastasis in transit is not linual vestibule
Tongue 71%
are treated by resecting the mandible left behind.
Maxillary sinus 8%
along with disarticulation of the condyle. Retromolar area 63%
The condylar stump preservation could
be helpful in reconstruction for fixing
Regional Lymph Node Metastasis
the screws for a reconstruction plate; Management Box 30.5: Incidence of lymph node meta­
however, it should not be at the cost of The OSCC metastasize to the cervical stasis as per the clinical stage of OSCC
adequate surgical clearance. ‘There is lymph nodes. The incidence of nodal (statistics at SPDC, Wardha, India)
no scope of conservative surgery, while metastasis also depends upon the site
treating the malignancy’ and ‘the first of tumor, the nature of the tumor, the Stage Percentage
chance is the best chance for the surgical histopathological grading of the tumor Stage I 2%
resection’. The recurrence will always be and the clinical stage of the tumor. Stage II 2%
unplanned and the salvage surgery may Stage III 13%
not be possible. A thorough presurgical Site Stage IV 83%
evaluation of the case to ascertain the The tumors of the floor of mouth tend to
resectability is mandatory. It is desirable metastasize early and bilaterally due to
to have the facilities of frozen section rich lymphatic supply and crisscrossing exophytic growths due to their deeper
biopsy to determine adequate surgical of the contrala­ teral lymphatics. The invasion. The tumor bulk also plays a
margins of the ressected tumor. While tongue is also lymphatic rich organ major role in the nodal metastasis. The
obtaining the specimen for the frozen and wide spread cervical lymph node more the bulk of the tumor, the more
section, it should be taken from edge metastasis is commonly seen upto are the chances of the lymph node
of the surgical defect rather than the deep cervical nodes and level IV and metastasis (Table 30.2).
specimen to ascertain that what is left V also. The tumors in midline tend to
in situ is disease free. metastasize bilaterally and the tumors of Histopathological Grading
Those growths where the doubts the retromolar region also metastasize to The poorly differentiated lesions are
pertaining to safe surgical margins ex- the lymph nodes of deep cervical chain. highly anaplastic and tend to have more
ist preoperatively are relatively unre- The incidence of lymph node metastasis incidence of nodal metastasis than the
sectable. In such cases, the surgery is amongst the cases of OSCC in relation to well differentiated growths (Box 30.6).
not free of risk of early recurrence and the site of the primary as depicted in the The surgery for excising the cer­
have guarded prognosis. They may re- table given below (Table 30.1). vical lymph nodes is termed as the neck
quire postoperative chemoradiations. dissection or cervical block dissection
The preoperative chemotherapy or ra- Clinical Stage as the entire block of the fibrofatty tissue
diotherapy certainly reduces the tumor The stage III and IV tumors have more along with the lymph nodes is excised
bulk, but their ability to shrink the sur- incidence of cervical lymph node meta­ in continuity. The concept of block
gical margins is doubtful and hence the stasis as compared to the stage I and II dissection was introduced by Sir George
surgical margins do not shrink is the tumors as observed in a study carried Crile36 who demonstrated classical radi­
dictum. Hence, the surgery could serve out at our center (Box 30.5). cal neck dissection under local anes­
only debulking purpose and residual thesia (LA) for a case of oral cancer in
tumor mass can be managed with 1906. However, the history of cervical
chemoradiation as a palliative resort. Clinical Presentation lymphadenectomy prevailed from the
The debulking surgeries tend to recur The ulcerative growths tend to meta­ year 1839 when Warren,37 removal of
fast, but serve the purpose of reducing stasize to the neck nodes faster than the submandibular lymph node in a case of
712 Neoplastic Conditions of Head, Neck and Face

Table 30.2: Incidence of lymph node metastasis as per the clinical presentation of OSCC
(statistics at SPDC, Wardha, India)

Lesion No of cases/100 Node positive Percentage

Ulcer 82/100 31 37.80%


Exophytic growth 18/100 5 27.78%
Total 100 36 36%

Box 30.6: Incidence of L N meta­ stasis excision/sacrifice of the spinal accessory


according to grade of biopsy (statistics at nerve lead to shoulder dysfunction, which Fig. 30.37: Radical neck dissection (RND) the
SPDC, Wardha, India) is ill afforded by the patients, especially SCM, IJV and spinal accessory are sacrificed
in the subcontinent who are poor and do
Incidence of L N metastasis
according to grade of biopsy physical labor to earn their livelihood. The
excision of the IJV leads to facial edema
Well differentiated SCC 18%
and raised intracranial pressure especially
Moderately differentiated SCC 53%
Poorly differentiated SCC 100% in bilateral neck dissections as it is one
of the major veins draining the cranial
cavity and the face, it is more pronounced
as the other draining channels, i.e. the
carcinoma of the tongue. M von Chelius,38 lymphatics are also excised.
1847 gave the first systematic description The types of the neck dissections
of cervical lymph nodes in HNF cancers. that are commonly undertaken are:
Subsequent to demonstration of the clas­ • Suprahyoid neck dissection: It
sical neck dissection by George Crile, is the excision of the lymph node Fig. 30.38: Modified radical neck dissec­
many authors did research in the field groups, which are present above the tion, type I (MRND-I) preserving the spinal
of neck dissection and the technique, hyoid bone, i.e. the level I and IIA accessory nerve
understanding and practices evolved. nodes along with the submandibular
Hayes Martin,39 1951 considered the salivary gland. It is often considered – Modification III: Selectively
pro­­
phylactic neck dissection to be to be inadequate and the supra pre­­serves SCM, IJV and spinal
illogical in the cases of HNF cancers, omohyoid neck dissection is more acce­ssory nerve (Fig. 30.40).
whereas Bocca and Pignataro,40 1967 preferred. Extended neck dissection: When the
introduced a concept of ‘functional neck • Selective neck dissection: When procedure removes other lymph node
dissection’ to avoid morbidity secondary one or more lymphoid groups are groups or non-lymphoid structures dif-
to neck dissection. Initially the concept of preserved. The examples are: ferent from those removed in the radical
‘commando operation’ was very popular – Supraomohyoid neck dissection neck dissection.
in which the primary and neck node block – Lateral neck dissection The neck dissections can be further
were excised in continuity without much – Postereolateral neck dissection categorized as
emphasis on the postoperative morbidity – Anterior neck dissection. • Therapeutic: When the positive
and quality of life. But, with the better • Radical neck dissection: Excision nodes exist and are excised.
understanding of neck node levels and of fibrofatty tissue along with level • Elective or prophylactic: In the N0
their involvement, the biological behavior I to V lymph nodes along with the neck the surgeon elects to perform
of the cancer it was felt that the neck SCM, IJV and spinal accessory nerve the prophylactic neck dissection
dissection can be selective and functional (Fig. 30.37). (for carcinoma of tongue, floor of
without compromising the outcome. The • Modified radical neck dissection: mouth, retromolar trigone or where
structures like sternomastoid muscle, One or more of the above mentioned the patient compliance is poor and
internal jugular vein (IJV) and spinal struc­tures are preserved, while doing he/she is unlikely to come for follow-
accessory nerve are excised in a classical clearance from level I to level V nodes. up as seen in Indian conditions,
radical neck dissection are now preserved, – Modification I: Selectively preser­ which is due to illiteracy, poverty
unless their excision is indicated as they ves only spinal accessory nerve and ignorance).
may be involved in the disease or come (Fig. 30.38).
in the way of adequate surgical clearance. – Modification II: Selectively pre­ Incisions for the Neck Dissection
The excision of the sternomastoid muscle serves IJV and spinal access­ory Various incisions for the neck dissection
leads to neck morbidity, while the nerve (Figs 30.39A and B). have been described in the literature.
Oral Cancer 713

A B
Fig. 30.39: MRND-II, preserving the IJV and spinal accessory nerve

Fig. 30.43: Schobinger’s incision

Fig. 30.40: MRND-III, preserving the SCM,


IJV and the spinal accessory nerve

The ideal requirements of an incision


are:
• It should provide good, liberal access
to the deeper structures of neck.
• The flaps should have good vascul­ Fig. 30.41: Crile’s ‘Y’ incision
arity to avoid ischemic necrosis.
Fig. 30.44: Modified Conley’s incision
• As far as possible the triangular
edges in the flaps should be avoided
as they are liable to undergo ische­
mic necrosis. Similarly, the sharp
edges and curves should be avoi­
ded. (Nature does not like sharp
edges and curves, if you make them
sharp nature makes them round by
inducing ischemic necrosis at the
edges).
• The vertical legs in the incision
should be avoided as they produce
unsightly scars and contractures,
which produce neck morbidity.
Fig. 30.45: McFee’s incision
• The triangular edges of the incision
lines should not fall on the major
vessels as dehiscence can lead to dis­section is to be carried out upto
major vessel exposure (Figs 30.41 Fig. 30.42: Hay-Martin’s double 'Y' incision level IV and V. The McFee’s ladder
and 30.42). incision produces very good cosmetic
The other incisions taken for neck (Fig. 30.44), Hay-Martin's double 'Y' results and the chances of marginal
dissection are Schobinger’s incision incision (Fig. 30.42) and McFee’s incision necrosis are also very less as the incision
(Fig. 30.43), modified Conley’s incision (Fig. 30.45) which are taken when the falls in skin creases and there are no
714 Neoplastic Conditions of Head, Neck and Face

therapy, chemoradiation therapy, or


previous selective neck dissection.
Relevant preoperative evaluations
are essential before performing classical
radical neck dissection. This includes
contrast-enhanced computed tomo­
gra­phy scan and fine needle aspiration
cytology for confirmation of tissue diag­
nosis. Frank invasion or encasements
of the internal carotid artery or invasion
A B of the deep prever­ tebral musculature
by metastatic cancer are contraindica­
tions to radical neck dissection. Thus,
preoperative radiological evaluation to
assess these areas is desirable; however,
often the extent of such involvement
is only apparent during intraoperative
explor­ation.

Surgical Technique
The patients are operated under Gen­
eral anesthesia through suitable endo­
tracheal intubation with adequate
muscle relaxation. The patient typically
is in the supine position, and neck is
hyper­ extended by placing sand bag
under the shoulder to make the struc­
tures prominent. The head is turned to
C the opposite side. The head and chest are
Figs 30.46A to C: (A and B) Apron for unilateral; (C) Bilateral SOHD elevated to 30° to prevent excessive blood
loss. Hypotensive anesthesia is preferable
triangular areas. However, the neck diss­ vein and the sub­mandibular salivary gland to avoid blood loss (Fig. 30.47). Alth­
ection through this incision demands in a mono block fashion. In certain cases, ough the skin incision is influenced by
greater skills. The apron incision is good the extent of resection must be exten­ded the planned resection of the primary
for the Supraomohyoid neck dissection to include adjacent soft tissues, cranial tumor and subsequ­ ent reconstruction,
(dissection upto level III) and produces nerves, overlying skin, or the major vessels
adequate exposure and preservation
good cosmetic results and has negligible in the neck because of the extranodal of cutaneous vas­ cular supply must
chances of marginal necrosis (Figs 30.46 spread of the metastatic growth. This is be ensured. Most commonly, a single
A to C). called an extended radical neck dissection.trifurcate incis­ion is used, extending
However, anything less than a classical
Radical Neck Dissection radical neck dissection is considered a
Radical neck dissection is a technique of ‘modified’ or ‘selective’ neck dissection.
monoblock removal of regional cervical Despite the resultant esthetic and
lymph nodes from the lateral neck for functional morbidity of a classical radical
malignant tumors involving the upper neck dissection, certain indications do
aerodigestive tract. This technique was exist for using this surgical procedure.
first described by Sir George Crile in 1906. The current indications41 for a classical
The classical radical neck dis­ section radical neck dissection are:
includes excision of cervical lymph nodes • N3 disease in the upper part of the
at all the five levels of the lateral neck. neck.
This entails clearance of essentially all • Gross invasion of the spinal acces­
of the fibrofatty and lymphatic tissue in sory nerve by metastatic lymph
the lateral neck, as well as resection of nodes at level II in the neck. Fig. 30.47: The extension of the neck by
the spinal acces­ sory nerve, the sterno­ • Recurrent or persistent metastatic providing a sand bag below the shoulder
cleidomastoid muscle, the internal jugular carcinoma after previous radiation for performing the neck dissection
Oral Cancer 715

ligated. The transverse cervical artery


and vein are identified, divided between
clamps and ligated inferiorly. Care is
taken to identify the brachial plexus
between the middle and anterior sca­
lene muscles, and the phrenic nerve
on the surface of the anterior scalene
muscle. The thin fascia covering the
scalen­ious table may be preserved as
it ensures preservation of these impor­
A B tant structures. The identification of
Figs 30.48A and B: (A) Sub platysmal dissection exposing SCM, EJV and greater auricular the phrenic nerve is made due to its
nerve; (B) Identification of spinal accessory nerve using greater auricular N as a guide. The unique anatomical feature that it is
spinal accessory N lies deep to SCM and within 1 cm superior to the greater auricular nerve the only nerve in the neck which runs
from the lateral to the medial direction
(Figs 30.49A and 30.50).
from the ipsi­­lateral mastoid tip along an
the anterior border of the trapezius This is facilitated by division of the
upper neck skin crease up to the midline muscle, which should be exposed from inferior belly of the omohyoid and its
at the level of the thyrohyoid membrane, the mastoid to the clavicle and rep­ retraction medially. Cutaneous cervical
approximately two fingers breadths resents the posterior limit of dissection. nerve branches are identified coming off
below the mandible. If the platysma is invaded by metastasis, of the cervical roots as dissection proceeds
The descending limb of the incision it is resected and dissection therefore cephalad. (Erb’s point) (Figs 30.49A and
begins at the posterior border of the proceeds superficial to the platysma in B). The cutaneous branches are divided,
ipsilateral sternocleidomastoid muscle a subcutaneous plane (Figs 30.48A and carefully preserving the motor branches
and travels in a curvilinear fashion to the
B). Cou­n­tertraction is applied and the to the posterior com­partment muscles
midclavicular point. The skin incision is soft tissue is divided from the anterior and the phrenic nerve (Fig. 30.51). The
made with a scalpel and the dissection border of the trapezius muscle and cutaneous roots are legated along with
proceeds thereafter with electrocautery. elevated off of the floor of the posterior their accom­panying small blood vessels
At the beginning of the procedure, triangle of the neck, with sequential (veina commitance). The superior att­
only the posterior half of the transverse exposure of the splenius capitis, levator ach­ ment of the sternocleidomastoid
incision and the descending limb are scapulae and scalene muscles. During mus­cle to the mastoid tip is divided and
incised; the remaining incision is made this dissection the peripheral cutaneous the specimen is allowed to rest in situ.
after the posterior triangle dissection branches of the cervical plexus and the
has been completed. spinal accessory nerve are divided. The Anterior Triangle Dissection
external jugular vein which is superficial The remaining transverse skin incis­
Posterior Triangle Dissection in location and runs superior-inferiorly, ion is then completed and attention
The posterior skin flap is elevated initi­ and gently curls posteriorly, is also is turned anteriorly. The anterior flap
ally, in the subplatysmal plane, up to divided between the two clamps and is elevated in the subplatysmal plane

A B C
Figs 30.49A to C: (A and B) Descendens hypoglossi, Ansa cervicalis and branches of C3 and C4 cervical roots, (black arrow) and greater
auricular nerve (white arrow), (C) Spinal accessory nerve running deep (black arrow) to SCM
716 Neoplastic Conditions of Head, Neck and Face

Fig. 30.50: Spinal accessory nerve (black Fig. 30.51: Elevation of the fibrofatty Fig. 30.52: Dissection of the carotid triangle,
arrow), phrenic nerve running over the and lymphatic tissue of the floor of the carotid sheath, apex of the posterior tri­
anterior scalene muscle and the branches reveals the inferior belly of the omohyoid, angle. The submandibular triangle dis­
of the brachial plexus running in the groove transverse cervical vein and brachial plexus section above the digastricus is started with
between anterior and middle scalene between the middle and anterior scalene mobilization of the submandibular salivary
mus­cles muscles gland

until the sternal and clavicular heads omohyoid is identified. The dissection
of the sternocleidomastoid muscle are anterior to the common Carotid artery
exposed and divided. Retraction of and superiorly, leads to dissection of
this detached muscle superiorly allows the carotid triangle. The fibrofatty tissue
identification of the carotid sheath in the carotid triangle is raised and the
(Fig. 30.52). Meticulous sharp and bifurcation of the carotid is identified.
blunt dissection exposes the contents This area is susceptible to handling as
of carotid sheath, the common carotid there are baroreceptors in this area and
artery and the vagus nerve, which are thus, needs careful handling to prevent
preserved, and the internal jugular vein,
bradicardia. The external and internal
which is divided at its lower end and carotid arteries are identified, the former
doubly ligated. lies superiorly and anteriorly to the
Fig. 30.53: Branches of the ECA, from
Care is taken to identify and ligate
former. The superior thyroid artery is
infe­r­ior to superior, superior thyroid, lingual
lymphatic vessels on either side of thepreserved as it runs deep to the block. The and facial arteries
neck, with particular attention to con­middle thyroid vein is ligated. At the level
trolling the thoracic duct on the left side of
of the greater cornue of hyoid bone, the omohyoid, anteriomedialy. Once the
the neck. The thoracic duct lies posterior
common facial vein which runs deep to lower border of the digastric muscle is
to and passes deep to the IJV and at times
the posterior belly of the digastricus and exposed completely, the specimen is
there are multiple ducts which are thinis seen merging with IJV. It is identified allowed to rest in the surgical field. All the
and fragile. They should be identified and ligated. Along with the common major vessels run deep to the digastric.
and ligated. In case of the doubt aboutfacial vein and several pharyngeal veins The attention is turned to the post­
its adequate ligation the anesthetist is
crossing the digastric muscle are divided erior triangle block elevated previously.
asked to ventilate the patient, during the
to expose the posterior belly and tendon The block is raised from the mastoid,
inspiration as the intrathoracic pressure
of the digastric up to the hyoid bone. along the posterior belly of digastric and
increases, milky white chyle leak can be
The hypoglossal nerve after crossing the the fibrofatty contents of the Bocca’s
observed which facilitates the ligation.
carotid bifurcation may loop around the triangle (spinal accessory chain of Ly­
The proximal stumps of the transverse occipital branch of the external carotid mph nodes, i.e. 2B nodes) are cleared
cervical art­ery and vein are divided and
artery (Fig. 30.53). The descendens and the root of the spinal accessory,
ligated. The entire block of ligated IJV
hypoglossi to the strap muscles is often a (see Fig. 30.49C) greater auricular nerve
and divided sternomastoid muscle is good guide, leading up to the hypoglossal are divided. The internal jugular vein
raised cephalad. nerve (Fig. 30.49A). is clamped and divided 2 cm below the
The upper border of carotid triangle skull base before it enters the jugular
Dissection of Carotid Triangle dissection ends at the level of the foramen and double ligation of the
The dissection reaches the midpoint of common tendon of digastric muscle, cephalic end is done to prevent slipping
the neck and the common tendon of the superiorly and at the superior belly of of ligature, bleeding and retraction of
Oral Cancer 717

digastric is divided to visualize the cut


end of the artery.
As the submandibular gland is lifted
from the mylohyoid and hyoglossus
cur­tain, the deep part leading into the
Wharton’s duct is identified. The lingual
nerve and submandibular ganglion lie
close to the deep part near the origin
of the duct. The lingual nerve is identi
fied, and its postganglionic secretomotor
fibers are divided, as is Wharton’s duct
(Fig. 30.58). Any remaining veins of
the pharyngeal venous plexus accom­
Fig. 30.54: Bocca's triangle, the posterior Fig. 30.56: Identification of the hypoglossal panying the hypoglossal nerve must be
belly of the digastricus, spinal accessory nerve below the posterior belly of digastric divided between claps and ligated. The
nerve running deep to IJV (black arrow) dissection is then carried out anteriorly
in the sunbmental trangle and the
the vein intracranially (Fig. 30.54). Some is mobilized. The hypoglossal nerve lies submental block between the two anter­
surgeons prefer to divide the posterior deep to the posterior belly of digastric ior bellies of the digastric muscles upto
belly of digastric to visualize the IJV and inferiomedial to the submandibular the body of the hyoid bone, is ressected.
and some retract the muscle superiorly. gland, after it crosses the external carotid The terminal branch of anterior jugular
The block is now raised anteriorly and artery and runs medially and superiorly, vein and the submental branch of the
the dissection of the tissue at the tail of it should be identified and protected facial artery are ligated.
parotid is done. The retromandibular (Fig. 30.56). The facial artery and comm­ Meticulous hemostasis is achieved
vein is ligated. on facial vein are present deep to the and the wound is closed over two suction
sub­ mandibular salivary gland and drains. One drain is tacked posteriorly
Digastric and Submental Triangle after lifting the gland, blunt dissection along the trapezius muscle with a loop
Dissection is carried out to identify these vessels. of catgut suture. The anterior drain lies
Attention is then turned to the superior They are identified and ligated. The facial along the strap muscles. These drains
flap, which is also elevated in the sub­ artery originates from the external carotid are brought out through separate stab
platysmal plane with care taken to artery at the level of greater cornu of hyoid incisions inferiorly.
identify and preserve the marginal bone and runs deep to posterior belly of The platysma is closed with 3-0
mandibular branch of the facial nerve digastic muscle (Figs 30.57A and B). If cut chromic catgut interrupted sutures
as it crosses the facial artery and vein. accidentally it gets retracted below the and the skin with 3 or 4 ‘0’ proline or
Retraction of the superior stumps of posterior belly of diagnostic and bleeds silk suture. Care is taken to achieve an
these vessels after their division further sizably. It is difficult to clamp and ligate airtight closure and to initiate suction
protects the nerve (Fig. 30.55). it, in such cases the posterior belly of on the drains during closure to prevent
Dissection continues anteriorly along
the inferior border of the mandible. The
superomedial limit of dissection is the
an­terior belly of the contralateral dig­
astric muscle. The submandibular gland

A B
Fig. 30.55: Identification of the marginal Figs 30.57A and B: The lower pole of the submandi­bular salivary gland, posterior belly
mandibular nerve of digastric and facial artery and vein identified
718 Neoplastic Conditions of Head, Neck and Face

Functional Neck Dissection fascial dissection, but it was justified


Functional neck dissection is not a as nodal groups are only a schematic
technique, but it is a concept wherein representation of the lymphatic system
the neck dissection is carried out pre­ of the neck, which is really configured in
serving certain structures, preserving different chains that follow the course of
the optimum function and preventing the major cervical vessels and nerves.
postsurgical morbidity, without com­
pro­mising the surgical clearance. Rationale and Anatomical Basis
for Functional and Selective
Origin of Functional Neck Neck Dissection
Dissection Functional neck dissection, as described
The main goal of the ‘functional’ appro­ by Osvaldo Suárez,42 is based on the
Fig. 30.58: The submandibular salivary ach to neck dissection proposed by existence of a fascial barrier between
gland is lifted from the submandibular Suárez42 in 1963 and popularized by the lymphatic tissue and the muscular,
triangle. The Wharton’s duct is ligated Bocca43 is the removal of all lymphatic glandular, neural and vascular struc­tures
before excising the gland. The lingual nerve tissue in the neck, preserving the rem­ of the neck. This anatomical separation
is often identified deep to the mylohyoid, aining neck structures. This is achi­eved allows the creation of a sur­gical plane
inferior to the duct by using the fascial planes of the neck of dissection. The fascial layer invests
that surround most cervical structures muscles and organs in the neck, forming
clots from forming within the drains. and separating them from the adjacent planes and spaces, where many important
Postoperatively, the drains are removed lymphatic tissue. As long as the tumor structures are crowded together. This fact,
when there is minimal serous drainage. cells remain confined within the known as fascial compartmentalization,
Complications unique to radical lymphatic system of the neck, they can holds the rationale for functional neck
neck dissection are related to the sacri­ be safely removed by carefully stripping dissection.
fice of the sternocleidomastoid muscle the neck structures from their fascial Fascial compartmentalization allows
and the spinal accessory nerve. This may covering. There is no oncological benefit the removal of cervical lymphatic tissue
result in shoulder dysfunction and the from removing the sternocleidomastoid by separating and removing the fascial
resultant “Frozen shoulder syndrome” muscle, internal jugular vein, or any walls of these ‘‘containers’’ along with
can be debilitating and requires diligent other important neck structure, when their contents from the underlying vas­
physical therapy. cancer is locked up inside a partially cular, glandular, neural and muscular
Bilateral radical neck dissection can isolated lymphatic space. The situation structures.
result in significant facial lymphedema, changes when the lesion invades the
which dissipates only slowly. walls of this anatomical container, Selective Neck Dissections: Types
If combined with laryngectomy, fixing the nodes to surrounding stru­
simultaneous bilateral resection of the ctures. Then, the tumor is no longer
and Indications
internal jugular veins can result in acute a ‘nodal cancer’ but becomes a ‘neck The anatomical studies of Rouviere44
obstruction to both intra- and extra­ cancer.’ This situation invalidates the demon­strated that the lymphatic drai­
cranial venous drainage and massive ‘functional’ spirit and justifies the use of nage from normal head and neck muc­
venous edema. The extent of resection of a classic radial approach with removal osal sites is relatively predictable. Later
soft tissue in a radical neck dissection can of the involved neck structures. clinical studies concluded that oral
leave the carotid artery relatively exposed Therefore, the spirit of functional cavity cancers mostly metastasized to
and subsequent radiation therapy incr­ neck dissection is to take advantage the jugular digastric and midjugular
ea­ses the risk of hemo­rrhage. of the particular anatomy of the neck nodes. Cancers of the anterior tongue,
A regional musculocutaneous flap to remove all or part of the lymphatic floor of the mouth and buccal mucosa
can provide some protection from this. system, with preservation of the remain­ metastasize first to the nodes in the
Current indications for radical neck ing neck structures. submandibular triangle. Some meta­
dissection are such that only patients It may be argued that preservation stasis may skip the submandibular
with extensive disease, or disease that of some nodal groups requires cutting and upper deep jugular nodes and go
has failed prior treatment, undergo the through the fibrofatty tissue that con­ directly to the midjugular nodes on
procedure. Thus, their postoperative tains the lymphatic system of the neck, either side of the neck. The Lindberg45
risks, both of complication and recur­ something that seems to be in con­ study and a subsequent study by
rence, are significant. tradiction with the basic principle of Skolnik,46 observed that oral cavity and
Oral Cancer 719

oropharynx tumors rarely metastasize to Table 30.3: Nodal groups at greatest risk of developing metastases according to location
posterior or lower deep jugular nodes in of the primary tumor
the absence of metastases in the upper
jugular and submaxillary nodal groups. Nodal region Location of the primary tumor
Shah’s47 (1990) retrospective review Area I: Submental nodes Floor of mouth, anterior oral tongue, anterior mandibular
of radical neck dissection specimens     Submandibular nodes alveolar ridge, lower lip
from patients with oral, laryngeal and Oral cavity, anterior nasal cavity, soft tissue structures of
the midface, submandibular gland
pharyngeal cancers concluded that oral
Area II: Upper jugular nodes Oral cavity, nasal cavity, nasopharynx, oropharynx,
cavity cancers metastasize most often to hypopharynx, larynx, parotid gland
levels I, II and III, whereas oropharynx
Area III: Middle jugular nodes Oral cavity, nasopharynx, oropharynx, hypopharynx,
cancers most often go to levels II, III and larynx
IV (Table 30.3). Area IV: Lower jugular nodes Hypopharynx, larynx, cervical esophagus
Based on these findings, several se- Area V: Posterior triangle Nasopharynx, oropharynx
lective neck dissections have been pro- Area VI: Anterior compartment Thyroid gland, larynx (glottic and subglottic), apex of the
posed. piriform sinus, cervical esophagus
Area VII: Upper mediastinal group Thyroid, larynx (glottic and subglottic), lung
Supraomohyoid Selective Neck
Dissection
This procedure is used for oral cavity
cancers. The submental, submandi­bular,
upper and midjugular groups of nodes
are the usual sites of metastases from
the oral cancers (Figs 30.59 to 30.61).
Supraomohyoid neck dissection removes
levels I, II, III (Figs 30.62A and B) and at
times (oral tongue cancer) level IV. The
level V is excluded. Bil­ateral dissection
is recommended for midline, floor of
the mouth, ventral surface of the tongue
tumors, provided that there is clinical
evidence of lymph node metastasis on
the either side of neck. In patients with Fig. 30.59: Clearance of Bocca’s triangle Fig. 30.60: Exposure of spinal accessory,
significant (N2) nodal metastases in the with sparing the spinal accessary nerve, vagus, branches of ext. carotid artery
ipsilateral neck, bilateral dissection or notice the hypoglossal nerve running
contralateral neck radiation is crucial. It deep to IJV and crossing the carotid artery.
is suggested that if there are metastases Notice the descending hypoglossi and Ansa
in level II, then the level IV and V should cervicalis
be dissected.

A B C
Figs 30.61A to C: Bilateral supraomohyoid neck dissection
720 Neoplastic Conditions of Head, Neck and Face

(see Fig. 30.48). The greater auricular


nerve is a very important landmark for
the identification of the spinal accessory
nerve. The spinal accessory nerve lies
within 1 cm distance superior to the
greater auricular nerve at the point where
it curls around the posterior border the
SCM (see Fig. 30.48B). Careful blunt
dissection in this area shows the spinal
accessory nerve which lies deep and
superiorly to the greater auricular nerve
(see Fig. 30.49B). The inferior flap is also
raised in the subplatysmal plane for its
entire length taking care not to damage
A B the anterior jugular vein or the external
Figs 30.62A and B: (A) Supraomohyoid; (B) Anterolateral neck dissection jugular vein. The venous perforators
going to the platysma are cauterized.
The lower level of the dissection ends
Most of the squamous cell carcino­ comm­only practiced while treating the inferior to the intersection of the SCM
mas of oral cavity in India are due to gingivobuccal SCC. It is indicated when and the superior belly of the omohyoid
smokeless tobacco and manifest in the the metastasis is restricted to upper muscle. The latter runs obliquely, deep
gingivobuccal sulcus. The com­mon lym- cervical nodes up to level I and II. It is to the SCM and superiorly to the IJV. The
phatic metastasis pattern is involvementshown to be equally effective as the posterior border of the SCM is dissected
of level I and II nodes, except where the
RND or MND, while treating Stage I to free from the adjoining fibrofatty tissue
tumor is originating from tongue or floor
III SSC of the gingivobuccal sulcus. It from its superior aspect going inferiorly
of mouth, where the tumor may have me- comprises of excising the lymph nodes up to the inferior extent of the flap. As
tastasis in deep cervical chain and con-at level IA, IB, IIA, IIB, level III and the the spinal accessory nerve is already
tralaterally also. The involvement of 2Boccasionally the dissection is extended identified earlier, the chances of the
nodes is also rare in the gingivobuccal up to level IV for the SSC involving damage to it are minimum during the
malignancies and hence, supraomohy- tongue and floor of mouth. Although the sharp dissection. The external jugular
oid neck dissection is usually adequate apex of the posterior triangle is cleared vein is ligated at the level of the inferior
in majority of cases. The dissection mayduring the SOHD, the VA nodes may extent of the dissection. The spinal
be extended to level IV or V if there isnot be completely removed. Usually an accessory nerve is carefully dissected
evidence of involvement of level III or apron incision is taken (see Figs 30.46A inferiorly as it runs posterioinferiorly
obvious metastasis in level IV or V nodes.
to C). The skin flap is raised in the towards the anterior border of the
In cases of midline tumor, crossing the subplatysmal layer up to the inferior trapezius muscle. The attention is then
midline, supraomohyoid dissection is border of the mandible anteriorly and shifted to the anterior border of the
very useful and avoids morbidity. The up to the tip of the mastoid process in SCM. The anterior border of the SCM is
post surgical radiotherapy can take carethe posterior region. As the flap is raised carefully dissected for its entire exposed
of micrometastasis, if any at Level IV the platysma ends just posterior to the length. The SCM is then lifted and all
and V. sternocleidomastoid muscle and the the fascial attachments inferior to it
The supraomohyoid neck dissec- tissue is more adherent and tenacious are carefully separated. While doing so
tion is very acceptable method. As all in this region. While reflecting the flap care should be taken to stay close to
the structures like sternocleidomastoid over the SCM, the external jugular vein the inferior surface of the muscle to
muscle, IJV, spinal accessory including is seen running anteriosuperiorly over avoid damage to the IJV. Minor venous
the Ansa cervicalis and greater auricular
the SCM, which is dissected superiorly perforators are seen inferior to the SCM
(see Fig. 30.59) can be preserved, with-up to the tail of the parotid as it enters which are cauterized and the entire SCM
out compromising the outcomes. The the parotid. The greater auricular nerve muscle is mobilized. Once an access is
patient has negligible morbidity and theis also seen entering the parotid and created the mobilization of the entire
quality of life after surgery is acceptable.
lies posterior to the external jugular muscle can be done by gentle finger
vein, which is also dissected carefully. dissection. The SCM is skeletalized
Supraomohyoid Neck Dissection As this nerve is dissected inferiorly, it and retracted posteriorly, the carotid
(SOHD) is seen running over the SCM muscle sheath is opened by blunt dissection
The supraomohyoid neck dissection and it curls around the posterior and the next step is skeletalization of
is a type of selective neck dissection, border of the SCM and goes deep to it the IJV. The middle thyroid branch and
Oral Cancer 721

the common facial veins are identified fibro-fatty tissue is mobilized sup­eriorly dissection is carried superiorly into
and ligated. The veins are fragile and over the scalenus table, preserving the the Bocca’s triangle. All the fibro-fatty
thus, should be handled carefully to fascia covering the anter­ ior, midius, tissue around the spinal accessory nerve
prevent their avulsion. The end of the posterior scalenus muscles and the is carefully dissected taking care not
vein towards the IJV should be ligated levator scapulae muscle. This is very to damage the IJV, which is protected
and smaller peripheral branches can important to prevent damage to the by retraction with vessel retractor and
be cauterized with bipolar cautery. phrenic nerve and the branches of the the posterior belly of digastrics is also
There are no branches originating brachial plexus as they lie deep to this retracted superiorly to facilitate proper
from the common carotid artery. The fascia. The phrenic nerve runs from dissection in this area (see Figs 30.54
carotid bifurcation (carotid bulb) area lateral to medial side over the scalenus and 30.59). A branch of occipital artery
has baroreceptors, and handling dur­ anterior muscle. is often encountered in this area which
ing the dissection in this area can The dissection is carried cephald in can be coagulated using bipolar cautery.
lead to bradycardia and hypotension. the posterior triangle. The skeletalized The entire block is lifted as the lower
Spraying two percent lidocaine solution spinal accessory nerve is retracted and border of the deep lobe of parotid is
in this area can reduce the chances protected. The IJV and common carotid reached. The dissection then goes
of bradiacardia. The branches of the artery are retracted and guarded using superiorly to the posterior belly of the
external carotid (superior thyroid, the vessel guard to protect them while digastrics muscle. The tail of the parotid
lingual, facial arteries) are given at dissecting the lymph nodes and fibro- gland should be carefully palpated
the level and superior to the greater fatty tissue below them. The carotid and if the lymph nodes are present
cornue of the hyoid bone but, unlike the artery does not give any branches, they should be excised as they are
branches of the IJV they lie deeper and posteriorly. The IJV also seldom gives known to produce recurrence in some
should be preserved. Hypoglossal nerve branches posteriorly and even if they are cases due to metastatic growth, which
is seen running horizontally, deep to the present, they should be either ligated or remains unaddressed. Some surgeons
IJV at its intersection with the posterior cauterized. The cutaneous branch of the deliberately excise the portion of the tail
belly of the digastricus and should be C3 and C4 roots are seen entering into of the parotid to excise the lymph nodes
preserved. The descending hypoglossi the lifted block and are divided. The in this region. The dissection is then
(Ansa cervicalis) is seen originating from greater auricular nerve can be easily carried anteriorly, the retromandibular
the hypoglossal nerve at this point and it protected. The spinal accessory nerve vein is ligated. The rest of the dissection
runs inferiorly, anterior to the IJV and it is dissected deep to the SCM, after it for clearing the submandibular triangle
should also be preserved (see Fig. 30.59). emerges deep to the IJV at the level and the submental triangle remains the
After the entire fibro-fatty tissue along of the posterior belly of the digastrics same as described under the radical
with the embedded lymph nodes is freed (see Fig. 30.49C). It runs clinging to neck dissection.
from the anterior aspect of the IJV and the deep surface of the SCM. It gives a Lateral selective neck dissection: The
the carotid artery, the superior belly of branch to the SCM and gets a twig from lateral dissection (Fig. 30.63) remo­ ves
the omohyoid is identified as it crosses the cervical plexus all these braches can nodal groups II, III and IV, leaving levels
the IJV in the mid portion of the neck. be easily protected by proper retraction I and V undissected. The lateral operation
This point marks the lower limit of the while dissecting around them. The is recommended for oropharyngeal,
supra omohyoid neck dissection. The
dissection is carried superiorly along
this muscle and all the fibro-fatty tissue
and lymph nodes between the superior
belly of the omohyoid and the anterior
aspect of the IJV are mobilized enblock
from the base of the carotid triangle up
to the level of digastricus muscle and
its common tendon. The block is left
in situ and the attention is shifted to the
posterior side of the IJV.
The inferior level of the posterior
triangle dissection also ends at the level
of the superior belly of the omohyoid.
The SCM is retracted anteriorly with L
A B
retractor or by passing a red rubber ca­t­h­
eter around it (see Figs 30.49A and C). The Figs 30.63A and B: (A) Lateral; (B) Anterior neck dissection
722 Neoplastic Conditions of Head, Neck and Face

hypo­ pharyngeal and laryngeal cancers confined within the lymphatic tissue. have disappeared as a consequence of
and should be done bilaterally if there are Thus, this approach is ideal for the previous treatment. Thus, fascial
proven metastases to one side of the neck. N0 cases with a high risk of occult dis­section is not possible anymore. In
Posterolateral neck dissection: metastasis. An additional advantage these cases, modified radical neck dis-
This operation removes the nodes of of functional neck dissection is that section appears as an alternative to
levels II, III, IV and V, the suboccipital it may be performed simultaneously radical neck dissection as a means to
and the postauricular nodal groups. It on both sides of the neck without preserve structures not involved by the
is recommended for metastases from increasing morbidity. In all midline tumor. The dissection will be made ac-
skin malignancies of the posterior scalp, head and neck lesions with high cording to the basic principles of radical
posterior neck and some parotid salivary risk of cervical metastasis (floor neck dissection, but preservation of un-
gland cancers that have metastasized of the mouth, base of the tongue, involved neck structures will be accom-
posteriorly. The dissection differs from supraglottic larynx and gingivolabial plished according to the surgical scenar-
the dissections favored for aerodigestive malignancies crossing the midline) io. This is a clear example that illustrates
system metastases. It removes the functional neck dis­section is the best the difference between functional and
lymph nodes and lymphatics containing surgical option for N0 cases. modified radical neck dissection.
fibrofatty tissue of the posterior neck, the • In patients with small palpable
subdermal fat and fascia between the nodes functional neck dissection is Reconstruction of Surgical Defects
primary site and nodal compartments, still a valid option as long as some The ablative cancer surgeries produce
where there are no distinct fascial principles are carefully observed. large surgical defects. The defects can­not
compartments. The nodes should not be greater be planned as the wide excision of the le-
Anterior neck dissection: This dis­sec­­ than 2.5 to 3.0 cm in greatest dia­ sion with safe margins is the goal of the
tion removes only area VI, which includes meter. This is justified by the need to surgery and the surgeon does not have
the paratracheal nodes, perithyroid and have all metastatic disease confined many options. The reconstruction of the
precricoid (Delphian) groups (Figs 30.63A within the lymph node capsule. defect needs to be planned prior to the sur-
and B). The procedure is favored for thy- Although extracapsular spread is gery with an appropriate flap. The recon-
roid cancer, cervical trachea, subglottic possible in lymph nodes of all sizes, struction should not only plug the effect
laryngeal cancer (subglottic or transglot- it is well known that chances of with the tissue, but also serve the cosmetic
tic), cervical esophagus and hypopharynx extra­capsular spread increase with needs and help in the restoration of the
cancer. The procedure is usually bilateral increasing lymph node size.48 Gross function. The lack of reconstruction leads
for cervical esophageal and large hypo- extracapsular extension results in to lot of morbidity and cosmetic compro-
pharyngeal cancer. It can be combined lymph node fixation to contiguous mises. The small defects which are seen
with a lateral dissection and occasionally structures. In no instance should only in early malignancies can be closed
needs to be extended to the upper medi- func­tional neck dissection be attem­ primarily by mobilizing the local tissue.
astinum. pted in patients with fixed nodes. However, too much tension across the
Extended neck dissection: There are • The number of palpable nodes and suture line invariably leads to dehiscence
situations where none of these selective location of primary tumor is not a and orocutaneous fistula. The dribbling
operations will fit a clinical scenario. contraindication for functional neck saliva, secondary infection, foul smell and
This requires another category called the dissection as long as all nodes fulfill unhygienic conditions lead to poor social
extended neck dissection. The extended the previously mentioned criteria. acceptance of such patients. The osseous
neck dissection is defined as selective • It is generally recommended to ex­ defects and large soft tissue resections
dissection plus something more like the tend the neck dissection one level leads to microstomia, ina­bility to masti-
removal of a non-lymphatic structure, below the clinically palpable lymph cate and swallow making the overall nu-
such as the internal jugular vein or the nodes. The last level that is excised tritional status severely compromised and
sternomastoid muscle. Other extensions should be subjected to frozen section the patient becomes malnourished and
that include, in a descriptive block, the biopsy and if found positive then cachexic. Thus, the resection of the tumor
upper mediastinum, the axilla, or the the dissection can be appropriately should not be the only goal, but to pro-
retropharyngeal space, are examples of extended to the lower levels. vide adequate reconstruction and quality
the extended neck dissec­tion. of life by restoring function and esthetic
Contraindication of Functional should also be kept in high priorities.
Indications and Limitations of the Neck Dissection The surgical defects could be osse­
Functional neck dissection is not pos­ ous and soft tissue and both require to
Functional Approach
sible in patients previously treated with be addressed.
• To be safe, functional neck surgery radiotherapy or other types of neck sur- The modalities for the osseous
requires all metastatic disease to be gery. In these patients the fascial planes reco­nstruction are:
Oral Cancer 723

• Implants: Reconstruction plates graft is the most popular and artery, common facial vein or
made up of stainless steel or titani- widely used graft (Figs 30.65A jugular vein by either end-to-
um, titanium mesh, custom made ti- to D). The graft is harvested end or end-to-side anastomosis
tanium prosthesis using CAD/CAM along with a vascular pedicle of technique). The advantage with
technology, etc. regional artery and the vein and the free tissue transfer is that it
The problem with the cancer anastomosed to the neck artery provides good reconstruction,
surgery is that due to the loss of large and vein (Figs 30.66A and B) (e.g. healing and contour. The survi­
portion of the soft tissue, the implants facial artery, external carotid val of the graft is predictable
do not get adequately covered by soft
tissue and the tight closure might
lead to wound dehis­cence, exposure
and infection of the implant. The
reconstruction of the midline defect
of the mandible, which is recon­
structed with the reconstruction
plate invariably fails and the plate
dehis­cence through the mucosa or
skin takes place due to the erosion
of these structures due to the friction
from the plate during the movements
(Figs 30.64A and B). Thus, if the cortical
bone at the inferior border is not
invol­ved, a wedge mandibulectomy
should be performed for the midline A B
mali­gnancies of the mandible as far Figs 30.64A and B: Reconstruction of the mandibular osseous defect with the SS and
as possible. If the patient is required titanium recon plates
to be subjected to the postoperative
irradiations, the metallic implants
interfere with the radiation therapy
by either scattering the radiations
or absorbing the radiations and
induc­ing tissue necrosis around the
implant. Hence, either they are avoi­
ded or removed prior to the radiation
therapy.
• Grafts:
– Free bone grafts—rib graft, iliac
crest bone grafts. As the water A B
tight cover of the wound cannot
be always achieved due to the
loss of the soft tissue, there is
high risk of graft rejection due to
infection and thus its not a good
option.
– Vascularized bone grafts (free
tissue transfer, microvascular
free grafts): The popular options
for the osseous reconstruction
are microvascular fibular grafts
based on the peroneal vessels,
iliac crest graft based on the
circumflex iliac artery and vein
and the lateral scapular graft. C D
Out of these, the free fibular Figs 30.65A to D: Free fibular graft with skin pearl used for mandibular reconstruction
724 Neoplastic Conditions of Head, Neck and Face

• Distant flaps: Deltopectoral flap


(Fig. 30.69A), pectoralis major myocu­
taneous flap (Fig. 30.69B), pectoralis
major myocutaneous-osseous com­
posite flap, latissimus dorsi myo­
cutaneous flap, sternomastoid myo­
cutaneous flap, platysmal flap, etc.
• Free tissue transfer: Radial forearm
flap (thin flap very good for the floor
of mouth, tongue, for lining and cov­
ering of other moderate defects)
(Figs 30.70A to E), rectus abdominous
flap, fibular flap with the skin pedal, etc.

A B Complications
• Wound infections and wound
Figs 30.66A and B: Forehead flap used to reconstruction of surgical defect of upper lip
breakdown: Incidence higher in ir-
radiated tissue; soilage of wound by
saliva, tracheal aspirates, or gastric
secretions; tight wound closure; im-
munocompromised and malnour-
ished states and presence of a foreign
body, hematoma, or seroma.
Treatment: Aggressive antibiotic
regimen, monitor for fistula, control
diabetes, maximize nourishment,
meticulous wound care (debride-
ment, wet to dry dressings), evaluate
A B
potential for carotid blow out.
• Flap necrosis: Poorly planned incis­
ion that compromises vascular sup­
ply may result in tissue loss, wound
infection, fistulas, or vessel exposure
(Figs 30.71A to C).
To avoid the same, properly
designed neck incisions are reco­
mmen­ded (e.g. curvilinear, MacFee,
modi­ fied Schobinger incision and
the trifurcation should begin at right
angles from the main incision).
C D The posterior leg of the flap should
be smaller than the anterior and
Figs 30.67A to D: Local eastlander flap linear incisions should be avoided
and gentle curvatures should be
after the successful anastomosis Soft Tissue Reconstruction incorporated to ensure tension free
and the most important thing is approximation.
that such a stable bone can be The soft tissue reconstruction can be • Shoulder syndrome: Injury or sacri­
used for dental rehabilitation done in: fice of spinal accessory nerve leads to
by placement of implants in this • Local tissue advancement (Figs 30.67A shoulder dysfunction and pain. The
transferred bone, which is not to D), local pedicled flaps like myo­­ shrugging and abduction is hampers
possible with other modalities. mucosal tongue flaps, nasolabial and the winged scapulas are seen
The free tissue transfer is a speci­ flaps, (Figs 30.68A and B) temoralis (Figs 30.72A and B).
alized facility, which is not universally muscle fascia flap and forehead flap The treatment comprises of phy­
and widely available. (see Fig. 30.66). sical therapy, may also consider early
Oral Cancer 725

A B
Figs 30.68A and B: Bipedaled nasolabial flap for the reconstruction of anterior alveolar defect

I II III

IV V
Fig. 30.69A: DP flap used for the reconstruction of the surgical defect of anterior region. The raw area on the chest is skin grafted
726 Neoplastic Conditions of Head, Neck and Face

I II III IV

V VI VII
Fig. 30.69B: PMMC flap used for the reconstruction

A B

C D E
Figs 30.70A to E: Radial forearm bases on radial artery and vein used for the reconstruction of the floor of mouth
Oral Cancer 727

A B C
Figs 30.71A to C: Flap necrosis and dehiscence

Treatment: The best treatment


is careful dissection and avoiding
the damage during the surgery. If it
is discovered intraoperatively imm­
ediate neurorrhaphy should be per­
formed and may consider facial reani­
mation procedures.
• Hematoma/Seroma: Prevented with
meticulous hemostasis and place­
ment of suction drains.
Treatment: Consider reopening
for major hematomas with removal
of clot and controlling bleeding; for
A B
minor hematomas may wait 7 to
Figs 30.72A and B: Shoulder morbidity 10 days to allow for liquification then
aspirate; may also consider pressure
dressings and prophylactic antibiotics;
seromas may also be aspirated.
• Injury to the brachial plexus: While
dissecting the fibrofatty tissue over
the sceleneal table at the base of
the posterior triangle, the dissection
should be carried out carefully to
avoid the damage to the branches
of the brachial plexus. The phrenic
nerve should be identified and
preserved (Figs 30.73A and B). The
A B damage to the phrenic nerve leads
Figs 30.73A and B: Identifying the branches of the brachial plexus to paralysis of the diaphragm. The
phrenic nerve is the only nerve in
cable grafting or orthopedic recon­ Treatment: The treatment may the neck, which runs from lateral to
struction. require tracheotomy for airway medial side.
• Injury to the vagus nerve: Injury mana­gement (especially for bilateral Chylous fistula: Chylous leakage
results in varying presentations vocal fold paralysis), management of is an uncommon complication, with
dep­en­ding on level and branch of aspiration and vocal fold paralysis. a reported incidence of 1 to 2.5 per-
injury; superior laryngeal nerve • Injury to the marginal mandibular cent. It is much more frequent on
injury typi­cally may present with branch of the facial nerve: At risk the left side of the neck. When the
only subtle voice changes, recurrent during elevation of the cervical flap, thoracic duct is to be ligated during
laryngeal nerve injury may result in should be identified and protected surgery, it should be surrounded by
hoarseness, aspiration, or airway (see Fig. 30.55), bilateral injury may muscle, fascia, or adipose tissue to
com­promise. result in oral incompetence. avoid sectioning its thin wall with
728 Neoplastic Conditions of Head, Neck and Face

the ligature. After ligation, the lower be avoided. It is important to note • Neurosurgery consultation
part of the left side of the neck must that preservation of the sternoclei- • Consider corticosteroids
be carefully inspected for chyle pool- domastoid muscle in functional and • Lumbar drainage
ing. Asking the anesthesiologist to selective neck dissection constitutes • Hyperventilation
inc­rease the intrathoracic pressure an important obstacle for successful • Hyperosmolar agents (mannitol)
and placing the patient in the Tren­ compression. Insertion of a pressure and diuretics.
delen­burg position are helpful in packing impregnated with irritant The bilateral IJV ligation can be
the intraoperative identification of solution, like Betadine or tetracy- avoided by choosing modified radical
chyle leak in the area of the thoracic cline, into the area of the thoracic neck dissection on at least one side and
duct. It is important to note that in duct has also been recommended preservation of the IJV there in.
most patients developing postopera- as a nonsurgical method to stop • Blindness: Caused by optic nerve
tive chyle fistula, this was previously chylous leak. The daily volume of infarction (uncertain etiology, may
identified and apparently controlled the leak has been reported to range be from hypotension and increased
intraoperatively. In the postopera- from 80 to 4500 mL. When more than intracranial pressure) and is a rare
tive period, chylous fistula is recog- 500 mL of chyle drain per day, non- complication.
nized by the appearance of a milky surgical stop is unlikely.49 • Postoperative dyspnea: Possible
fluid in the drains. This is usually If no response is found upon etiologies include pneumothorax,
evident within the first 5 days of sur- con­ser­
vative treatment, the lower phrenic nerve injury, intrinsic lung
gery. The chylous origin of the fluid part of the neck should be surgically disease (atelectasis) and congestive
can be confirmed by measuring the explored. Before surgery is attem­pted, heart failure.
content of triglycerides, usually over it may be helpful to put the patient • Carotid blowout: Typically occurs
100 mg/dL. When chylous leak is on a high lipid enteral diet to give secondary to infected wound site
suspected, dietary modifications can chyle a thick and milky consistency, and wound breakdown and has high
be prescribed. Low fat diet, either which will improve the intraoperative mortality rate (approximately 10%).
enteral or parenteral, is usually rec- identification of the leak. The treatment comprises of airway
ommended, because medium-chain • Cerebral and facial edema: Higher management, compression, large-bore
triglycerides are absorbed directly risk with internal jugular vein lig­ catheters with fluid replacement, imme-
into the portal venous circulation, ation (especially bilateral internal diate blood replacement, intraoperative
avoiding the thoracic duct. The pa- jugular vein ligation), (Figs 30.74A ligation and venous grafts for repair.
tient should be given paren­ teral and B) may present with syndrome of
feeding rather than gastric feeding. inappropriate antidiuretic hormone Chemotherapy
Elevation of the head, repeated as- secretion (SIADH) or mental status The chemotherapy of cancer differs
piration, and pressure dressing are changes. from the chemotherapy of infection.
also recommended. However, use The treatment of cerebral edema The microorganisms have distinct
of indwelling vacuum drains should must be undertaken urgently: metabolic pathways as compared to
the human cells and thus, they can be
selectively targeted and eliminated by
the antibiotics. However, the meta-
bolic pathway of the malignant cells is
similar to that of normal cells and thus,
this specificity is not present. Hence,
the chemotherapeutic agent affects the
malignant cells and normal cells alike
and induces high toxicity. The division
rate of the malignant cells is very high
as compared to the normal cell and
thus, this rapidity of the cell cycle ren-
ders the malignant cell more vulnerable
to the chemotherapeutic agents. The
hematological malignancies respond
well to the chemotherapy, but in the
A B management of the OSCC, the role of
the chemotherapy as a primary modal-
Figs 30.74A and B: Lymphedema of face following RND due to ligation of veins and
ity is questionable. It is often used as an
lymphadenectomy
Oral Cancer 729

Advantages: Simultaneous thera­


pies may synergistically maximize thera­
peutic effect (chemotherapy sensitizes
cells to radiation and simultan­ eously
kills micro­metastatic disease).
Disadvantages: Results in increased
side effects from concurrent therapies
(mucositis, infection, malnutrition, hem­
a­­topoetic depression).

Radiation and Chemotherapies


• Chemotherapy inhibits the repair
A B of cells that may otherwise recover
Figs 30.75A and B: (A) Clinical photograph prior to neoadjuvant chemotherapy; from radiation
(B) Post treatment photograph showing reduc­tion of tumor size • Concomitant radiation and chemo-
therapies result in synchronization
adjuvant therapy with other modalities is practiced with variable success. The of cell cycles increasing the effec-
like radiation therapy or surgery or as a tumor shrinks significantly with the tiveness of both therapies
palliative therapy in the management of neoadjuvant chemotherapy (Figs 30.75A • Resistant cells of one mode of the­
advanced, unresectable cancers. and B). The reduction in size of the tumor rapy may be susceptible to the other
A chemotherapeutic agent affects certainly improves the tumor handling, mode of therapy thus, producing
a cell in its dividing cycle and induces reduces blood loss during the surgery synergistic action
irreparable damage to the DNA to and also facilitates the endotracheal • Shrinking the tumor with radiation
induce cell death. intubation. However, whether the improves drug delivery for increased
tumor margins also shrink or not is not effectiveness of chemotherapy
Indications for Chemotherapy certain. Second disadvantage is that • Combined therapy may initiate
• Nasopharyngeal cancer the texture of the tissue in the shrunken cells from G0 phase to active phases
• Unresectable head and neck cancer area of the tumor gets altered following rendering the cells more susceptible
• Laryngeal organ preservation the chemotherapy, which makes clinical to therapy
• Pyriform sinus cancer organ preser- decision of the safe surgical margins • Concomitant modalities damage
vation difficult. The frozen section biopsy can cells in different ways and increase
• Recurrent and distant metastatic be of great help in such cases. chances of cells’ death.
dise­ase: Original traditional role in The concept of organ salvage was
head and neck cancer, essentially primarily induced to salvage the visceral Adjunctive
pro­vides palliation for recurrent unr­ organs by reducing the tumor bulk and Definition: Chemotherapy after pri­mary
e­­sectable disease or incurable cancer reducing the quantum of resection. treatment modality to control micro­
with distant metastatic disease. The same concept is not applicable to scopic disease.
OSCC as the tumor bulk may shrink Indications: Locally advanced dis-
Chemotherapy Strategies with the preoperative chemotherapy, ease, multiple positive regional neck
but the resection margins do not and the nodes, nodal extracapsular spread,
Neoadjuvant (induction)
quantum of resection remains the same. posi­tive margins, recurrence.
Definition: Sequential chemotherapy Disadvantages: Postchemotherapy Advantages: May improve survival.
before local treatment modality (surgery patients are often more debilitated, Disadvantages: Exposes patient to
or radiation). which may increase complications of side effects of chemotherapeutic agents.
Advantages: Initial chemotherapy surgical intervention or radiotherapy If it is given after the surgery, the pen­
may allow better drug penetration prior and the margins are difficult to access. etration of the drug in the operated
to impaired vascularity secondary to area is questionable due to disturbed
radiation effects, initial chemotherapy Concominant (Radiation Therapy vascularity and fibrosis in the operated
may also reduce tumor bulk or ‘cure’ and Chemotherapy) area. It will have more side effects than the
patient of disease (organ preservation Definition: Concurrent chemotherapy therapeutic effects. However, the distant
or organ salvage). The neoadjuvant and radiation (chemotherapy may be metastasis and nodal micro­ metastasis
chemotherapy in the management of the given continuously or interrupted [split may be treated with this modality, which
oral SSC is not very popular modality. It course]). is away from the primary surgical site.
730 Neoplastic Conditions of Head, Neck and Face

Chemoprevention50 Carboplatin Bleomycin


• Retinoids (analogues of vitamin A) Mechanism of action: Similar to cis­ It is an antibiotic having antineoplastic
have been shown to reduce mali­ platin (less reactive). pro­ perties. It is a mixture of glyco­
gnant potential of premalignant oral Common side effects: Better toler- peptides. It acts on a cell specifically in
lesions51 (54% reversal of dysplasia ated than cisplatin (less nephrotoxicity, G2 and mitotic phase.
with retinoids versus 10% for con­ nausea, neurotoxicity and ototoxicity). Mechanism of action: Causes DNA
trols, P = 0.01) and prevent the Indications: Not been fully investi- breakage in susceptible malignant cells
development of second primaries gated in head and neck cancer, often used through an activated free radical mech-
in a single-institution phase III trials in combination with taxol 5-fluorouracil anism.
(4% developed second primaries (5-FU). Dose: 10 to 15 mg/m2 IV daily for
with retinoids versus 24% in controls, Mechanism of action: Antimetabolite 3 to 4 days every 3 to 4 weeks.
P = 0.005)52; the effect, however, is not that binds to thymidylate synthetase
sustained once treatment is stopped. blocking the conversion of uridine to Vinca alkaloids
• Mechanism of action: Regulate thy­midine preventing DNA synthesis in They are the vinca alkoloids, derived
cellular differentiation and proli­ S-phase. from the plant and include vincristine,
feration in epithelial tissue (via reti­ Common side effects: Anorexia and vinblastine, vindesine.
noic acid receptors) and modulate nausea, mucositis, diarrhea, alopecia, Mechanism of action: Bind to the
neoplastic cell growth differentiation myelosuppression, cardiac toxicity. protein tubulin, preventing polymer-
and apoptosis. Indications: Similar to cisplatin ization to form microtubules and is M-
(cisplatin and 5-FU is the most studied phase specific.
Common Side Effects of combination chemotherapy regimen in Dose: 1-2 mg/m2 weekly IV.
Chemotherapy head and neck cancer). Disadvantages
• Mucous membrane and skin dryness • No selectivity
• Alopecia Methotrexate • Hematopoetic depression
• Conjunctivitis Mechanism of action: Antimetabolite • Immunosuppression.
• Transitory elevated transa­min­ases that binds to dihydrofolate reductase
• Hyperlipidemia preventing DNA synthesis in S-phase. Radiation Therapy
• Myalgia Its action is similar to the action The ionizing radiations are known to
• Teratogenicity of the ionizing radiations and thus induce damage to the nucleotide chains
• Skeletal effects reffered to as radiomimetic drug and of DNA and induce cell death. When a
• Hematopoetic depression it potentiates the action of the radi­ single chain is damaged, the damage is
• Leucopenia ations. repairable, but when the double strand-
• Immunosupression Common side effects: Bone mar- ed damage occurs the cell death results.
• Superinfections row suppression, gastrointestinal distur-
• GI bleeding due to erosive changes. bances, mucositis, alopecia, dermatitis, Mechanism of Injury
nephrotoxicity, teratogenicity, intersti- • Direct mechanism of radiation
Common Chemotherapeutic tial pneumonitis. injury: Direct damage of radiation
Agents and Combinations in Indications: ‘Standard’ palliative ther­ with critical elements in a cell (e.g.
apy for recurrent or metastatic disease. DNA, cell membranes).
Head and Neck Cancer
Leucovorin (tetrahydrofolic acid): • Indirect mechanism of radiation
Cisplatin Utilized as a ‘rescue’ agent, competi­ injury: Secondary damage from
Mechanism of action: Heavy metal that tively overcomes increases intracellular direct radiation effects on other
acts as an alkylating agent, covalently pools of dUMP (also used with 5-Fluo­ cell moieties; primary mechanism
binding with DNA and RNA. rouracil). of cell death (e.g. DNA injury from
Common side effects: Nausea, neph- production of free radicals).
rotoxicity, peripheral neuropathy, ototox- Taxanes (paclitaxel and docetaxel)
icity, electrolyte disturbances, anorexia. Mechanism of action: Prevent normal Determinants of Sensitivity
Indications: Best single-agent against microtubular reorganization. of Radiation Therapy
squamous cell carcinoma of the head and Common side effects: Neutropenia, Radiotherapy is not considered to be
neck in recurrent disease; common com- alopecia, mucositis. the first line of treatment yet it can
bination agent for neo­adjuvant, adjuvant Indications: Currently being inves- be quite useful if following principles
and concomitant chemotherapy of the tigated for recurrent disease and as a are understood before instituting the
head and neck; radiation sensitizer. potential radiation sensitizer. patient for radiotherapy.
Oral Cancer 731

• Larger tumors have a more hypoxic External beam radiotherapy tissue in 3 dimensions. The maximum
center, therefore, are less sensitive to (teletherapy) dose can be given to target tumor tissue
radiation because less free radicals It is usually cobalt-60 radiations given in with precision avoiding radiation to
are generated (1 cm tumor = 109 cells; a dose of 2 Gy/day for 5 days in a week surrounding vital structures.
3 cm tumor = 1,010). total of 30 cycles (total dose of 60–70 Gy).
• Oxygenated cells are more suscep- Disadvantage: Since beam directed Fractionation
tible to radiation than hypoxic cells through skin, it causes skin reactions, Conventional fractionation: In frac­
(exophytic tumors are typically well ORN and thus, the incidence of adverse tiona­tion, radiotherapy is given in small
vascularized and therefore, more reactions is very high. interval doses rather than the whole dose
susceptible to radiation injury, ul- at once. It allows cells to proceed in their
cerative and infiltrative tumors are Neutron beam therapy cycle to more radiosensitive stages in their
less vascularized and therefore, It is a heavy particle therapy, which was cell cycle and allows for reoxygenation
more resistant to radiation). popular for its penetration in the tissue. of previously more hypoxic cells (more
• Cell death occurs with proliferation However, this therapy is most damaging susceptible), pro­longed waiting between
(usually 4–5 times before lysis), to normal cells, as well as tumor cells fractions results in regrowth of tumor cells
therefore, rapidly growing tumors leading to ORN. It is rarely used today from sublethal damage. Furthermore,
are more susceptible to injury. because of its complications of signifi- normal tissue tends to have better repair
• Cells tend to be more radiosensitive cant muscle and deep tissue fibrosis. than tumor cells, therefore, recovery
in mitosis and late G1 and early more quickly from sublethal damage.
S-phases. Interstitial radiotherapy Fractionation results in total less
(brachytherapy)
• The intrabony tumors are relatively biological injury due to the greater opp­
radioresistant than the soft tissue The word brachytherapy is derived from ortunity for repair, therefore, requires a
tumors. The term radioresistant is a Greek word, brachy meaning ‘short higher total dose than single or hypo­
little misnomer as all the tissues range’. This term is used to des­cribe the fractionated dosing, hypofract­ionization
are affected by the radiations with a treatment of malignant disease by inter- (less fractions) are used for tumors with
variable degree. Those tissue or tu- stitial, intracavitary and surface applica- good reparation of sublethal injury (ma-
mors which are affected to a greater tion of sealed radio­isotopes. lignant melanoma).
extent by radiations are termed as
Sources Methods of fractionation
radiosensitive and those which are
not affected significantly are termed •Radium-226 • Conventional fractionation: Typi­
as radioinsensitive due to various •Caesium-137 cally uses one treatment per day
factors mentioned above. •Cobalt-60 (generally 1.8–2.2 Gy) for 5 days a
•Iridium. week
Types of Radiation Advantage: Maximum radiation • Pure hyperfractionation: Increases
• Electromagnetic radiation dose is delivered to selectively targeted rate of treatment (e.g. 2-times a day
For example, radiowaves, heat waves, tumor tissue with sparing of surround- dosing), smaller dose per fraction,
light waves, UV waves, X-rays and ing vital structures. same duration of therapy, higher total
gamma-rays. Disadvantage: ORN. dose than conventional fractionation;
• Particulate radiation decreases late side effects.
For example, electrons, protons, alpha- Hyperfractionated radiation therapy • Accelerated (standard) fractiona­
rays, neutrons, negative pi-mesons. • Rationale: To allow normal cells tion: Decreases duration of therapy,
to proliferate and to suppress the increa­ses rate, higher dose per frac­
Types of Radiotherapy tumor cells in between the fractions. tion, with same decreased total
• Dose: 1 Gy twice daily, for total dose as conventional fractionation;
Radical radiotherapy
dose of 60 to 70 Gy over a period of increases acute side effects, decreases
• Radiotherapy given at high dose 7 weeks. late side effects, increases tumor cell
with curative intent. kill (prevents tumor cell proliferation)
• Dose delivered is the highest that Intensity modulated radiotherapy • Accelerated hyperfractionation:
(IMRT)
can be delivered without undue Incre­ ases rate of treatments, de-
functional consequences. It is a type of CT-CRT (CT guided con­ creases duration of therapy, increas-
• Palliative therapy: Seeks to control formal radiotherapy). The delineation es total dose.
symptoms in which the cancer of target tissue by CT and MRI is better • Concomitant boost accelerated
is deemed incurable or in which and the computer controlled delivery frac­tionation: Changes rate to twice
the patient is not sufficiently fit to of radiation is ensured. It is a conformal a day dosing in the last 2 weeks of
withstand. radiotherapy: it conforms to the tumor therapy.
732 Neoplastic Conditions of Head, Neck and Face

Radiation Strategies Disadvantages: Requires higher dental caries, change in taste and
• Shrinking fields: Selective radiation dose of radiation due to hypoxia in oper- tenacious oral secretions; Rx: fluids
dosing to varying region depending ated tissue, microscopic disease may be with meals, artificial saliva, pilo­
on primary size and shape (e.g. within scar tissue resulting in decreased carpine, fluoride treatment, aggres­
7,000 cGy to primary site as primary radiosensitivity, requires larger fields sive oral hygiene (prevent with
therapy, 5,000–5,500 cGy to N0 neck than preoperative radiation therapy. preoperative dental evaluation).
or adjuvant treatment) • Osteoradionecrosis of the mandible/
• Brachytherapy: Delivery of radiation Advantages of Radiotherapy cartilage radionecrosis of the larynx:
to malignant tissue by placement of • No tissue defect causing final or Hypocellularity, hypovascularity, and
permanent radioisotopes intraopera- cosmetic problem ischemia of tissue (not infectious); Rx:
tively via a temporarily placed radio- • Mortality rate less than in surgery initially should treat conservatively
active source within tumor bulk • Both local and regional diseases are with antibiotics, analgesics, meticu­
• Three-dimensional multiple treat­ taken care simultaneously. lous oral hygiene and soft diet; debri­
ment beam therapy: Utilizes CT and dement may be required; may also
MRI imaging, multiple treatment Side Effects consider hyperbaric oxygen therapy.
fields arranged to maximize radia­ Cutaneous reactions: May result in dry- • Radiation induced cancer: Increa­
tion dose to target area yet achieve ness, erythema, hyperpigmentation, de­ sed risk of thyroid, salivary gland
maximum normal tissue sparing s­q­­uamation, telangiectasias, or subcu- cancer, leukemia, sarcomas (may
• Concomitant radiation therapy and taneous fibrosis; Rx: skin moisturizers, have lag period of 20 years).
chemotherapy (Chemoradiation) mild skin cleaning, oral diphenhydr- • Otologic sequelae: Increased inci­
• Hyperfractionation amine (pruritis), corticosteroid creams. dence of otitis externa, sterile otitis
• Neutron beam therapy: ‘Heavy’ Mucositis: Presents as tender, ery­ media and auricular chondritis.
neu­tron particle that result in greater the­matous and swollen mucous mem-
direct mechanisms of injury, less de- branes; increased risk of coexisting in-
pendence on cell cycling and prolifer- fections with Candida, herpes simplex
CACHEXIA IN MALIGNANCY
ation; however, less repair of sublethal virus and other bacteria; may result in Cancer cachexia occurs most frequently
damage by normal tissue. sepsis for severe cases; Rx: aggressive in malignancy and accounts for more
oral hygiene (oral irrigations), adjust than 20 percent of cancer deaths. Patients
Preoperative Radiation Therapy dental appliances, smoking and alcohol with cancers of oral cavity and upper
Advantages: May reduce tumor bulk, cessation, cool food, nutritional supple- aerodigestive tract are most likely to suffer
which may cause inoperable les­ ions ments, oral and topical anesthetics from substantial weight loss (Figs 30.76
to become operable, reduce sur­ gical (viscous lidocaine, diphenhydramine, and 30.77). The word ‘cachexia’ comes
ex­ci­
sion area, or cure (organ preser­ aluminum hydroxide-magnesium hy- from the Greek words ‘kakos’ and
vation); requires smaller portals than droxide-simethicone mixture). ‘hexis’, meaning ‘bad conditions’.
pos­t­
operative radiation therapy; micr­ • Alopecia: Temporary hair loss may Cach­ exia is a complex metabolic sta­
os­copic tumor is more sensitive than occur in radiation field, may be tus with progressive weight loss and
postoperative residual tumor (micro­ permanent at higher doses. de­pletion of host reserves of adipose
scopic disease may be in scar tissue, • Xerostomia/dental caries: Salivary tissue and skeletal muscle. Cachexia
there­f­ore, more hypoxic). acinar cells are extremely sensitive should be suspected if involuntary
Disadvantages: Increased difficulty to radiation therapy causing irrever­ weight loss greater than 5 percent of
in operating in irradiated tissue due to sible xerostomia, increased risk of pre­morbid weight occurs within a
fibrosis, which makes the clinical as-
sessment more difficult and the tissue
planes are lost, which makes the dissec-
tion more difficult, increased postopera-
tive complications (wound infections,
carotid blowout).

Postoperative Radiation Therapy


Advantages: Allows for adequate post­
operative healing prior to beginning
adjuvant therapy, accurate assessment
of pathologic staging and factors for
recurrence. Fig. 30.76: Cachexia of malignancy Fig. 30.77: Severe cachexia of malignancy
Oral Cancer 733

6-month period. Cachexia represents lysis in murine adipocytes. A recent ponents and/or oral, and parenteral
the clinical consequence of a chronic, study showed that this lipolytic pro­cess is nutritional supplement.
systemic inflammatory response, with mediated through the β-3 adrenoceptors. For the correction of cancer related
high hepatic synthesis of acute-phase LMF produces a signi­ficant increase in malnutrition, enteral and parenteral
proteins resulting in depletion of essen­ the mitochondrial uncoupling proteins administration of nutrient solutions has
tial amino acids. In contrast, in starva­ (UCPs) in brown adipose tissue, skeletal been widely used. In patients with oro-
tion only fat metabolism is increased, muscle and liver. pharyngeal dysfunction from head and
while the organism tries to conserve Despite the controversial discussion neck neoplasm or esophageal obstruc-
lean body mass. In addition to metabolic of cachexia-inducing mechanisms uncer­ tion, blenderized food and liquid sup-
changes, cachexia is often associated tainty over what causes cachexia, it plement can often achieve an adequate
with anorexia. In cancer patients there is quite clear that proinflammatory level of nutritional repletion, although
can be mechanical interference such cytokines are linked to all pathways percutaneous gastrostomy or jejunos-
as obstructions, as well as treatment- that induce cachexia. As mentioned, tomy offer bypass-feeding methodology
related toxicity. In patients receiving cachexia is associated with a chronic when necessary. For patients who can-
chemotherapy or radiation, subsequent systemic inflammatory response and the not tolerate the use of the gastrointes-
nausea, vomiting and diarrhea can elevation of acute phase proteins. High tinal tract because of nausea, vomiting,
contribute to weight loss. But the lack serum levels of IL-1, IL-6 and INF gamma obstruction, malabsorption, or absence,
of nutrients alone cannot explain the are present in many cancer patients and it may be necessary to begin total par-
metabolic changes seen in cachexia. the levels of these cytokines seem to enteral nutrition (TPN, hyperalimenta-
correlate with tumor progression. tion).
These cytokines stimulate the ex­ Parenteral nutritional support is
Theories Related to
pression of leptin and/or mimic the an intensive method of clinical care,
Pathophysiology of Cachexia hypothalamic effect of negative feed­ requir­ing physicians, pharmacists, die­
The first theory is the pathological back from leptin by disarranging the ticians and experienced nurses who,
alteration of control cycles. Food intake signaling pathway of NPY, resulting in as a team, must make daily rounds to
is regulated through a complex system long-term inhibition of food intake. IL-1 evaluate nutritional status and check
of hormones and neuropeptides. Inui antagonizes NPY-induced feeding in for complications. Complications from
et al. demonstrated that neuropeptide Y rats and disrupts the orexigenic pathway parenteral nutrition can be multiple.
(NPY), the most potent feeding stimul­ of NPY. On the other hand, central corti­ Among them, the com­plications from
atory peptide in this cycle, is deregulated cotropin-releasing factor (CRF), which is infection are the most problematic
in the hypothalamic orexigenic network, upre­gulated by IL-1, seems to influence when long-term nutri­tional support is
leading to decreased energy intake but satiety and is a potent anorexigenic used. In addition, the costs of nutrient
high metabolic demand for nutrients. signal. solutions, prolonged hospitalization,
High levels of leptin, a hormone secreted and/or frequent visits to a special clinic
by adipocytes, block the release of NPY. or office are formidable medical and
Treatment
In cachexia the leptin feedback loop financial burdens.
seems to become out of control, altering Supportive Care
the neuropeptidergic control cycles.53 In clinical trials, nutritional supplemen­ Newer Pharmacotherapy
The second theory is based on the tation and dietary counselling failed to Many trials have been performed in the
idea that tumor-derived factors maintain increase body weight. Several appetite- search for a treatment for cachexia, but
the cachectic syndrome. Tisdale et al.54 stimulating drugs have been tested in most therapies have not fulfilled expecta-
postulated a factor that was extracted an attempt to increase the food intake of tions. Currently, eicosa­pent­aenoic acid
from the urine of cachectic patients and cachexia patients, but most of them had is being tested in cachectic patients.55
which induces protein degradation in little or no effect on body weight. Eicosapentaenoic acid seems to interfere
skeletal muscle by upregulation of the Patients with anorexia from decre­ with the signaling pathway of PIF and
ubiquitin-proteasome pathway. This ased physical activity, concomitant first results are promising. Future thera-
proteolysis-inducing factor (PIF) is infection and toxicities from chemo­ pies may consist of anticatabolic and
closely related to weight loss in cachexia therapy and radiotherapy are managed anabolic drugs in combination with ap-
and in a recent study, it was shown that symptoma­ tically for maintenance of petite stimulants.
PIF is produced in human colon cancer. nutritional status and quality of life.
A second factor extracted from the Such management includes the use
BASAL CELL CARCINOMA
urine of cachectic patients is the lipid of mouthwash for stoma­titis, frequent
mobilizing factor (LMF). It is closely small volume feedings, anti­ emetics, Basal cell carcinoma is a nonmela­
related to weight loss and induces lipo­ antibiotics, transfusions of blood com­ nocytic, low grade, slow growing and
734 Neoplastic Conditions of Head, Neck and Face

locally invasive carcinoma of the basal agent, predominantly Fowler’s sol­ 3. Nodular basal cell carcinoma,
layer of the epidermis. Basal cell car­ ution of potassium arsenite, which which essentially include most the
cinoma is particularly liable to occur was used to treat many disorders, remaining categories of basal cell
in fair and dry skinned people and it including asthma and psoriasis. A cancer. It is not unusual to encoun-
typically appears on sun-exposed skin contaminated water source has been ter morphologic features of several
and rarely metastasize. the most common source of arsenic variants of basal cell cancer in the
Basal cell carcinomas have a typical ingestion. same tumor.
body distribution: 70 percent on head • Immunosuppression: A modest in-
(most frequently on face), 25 percent on crease in the lifetime risk of basal cell Clinical Features
trunk, and 5 percent on penis, vulva, or carcinoma has been noted in chroni- • Elderly people are usually affected,
perianal skin.56 cally immunosuppressed patients, especially in middle or late age.
such as recipients of organ or stem • Males are more affected than fem­
Etiology cell transplants. ales.
The exact cause of basal cell carcinoma • Xeroderma pigmentosum: This • Particulary seen in whites residing in
is unknown. Environmental and genetic auto­somal recessive disease results tropical countries.
factors that are believed to predispose in the inability to repair UV-induced • Grow slowly over a course of years.
patients to basal cell carcinoma skin DNA damage. Pigmentary changes • It is particularly prevelant in Aus­
cancer. Basal cell carcinoma has a high are seen early in life followed by the tralia and is confined to white
frequency in older men who have a development of basal cell carcinoma, people of the labor class whose skin
long history of unprotected exposure to squamous cell carcinoma and mali­ is exposed to bright sunlight of high
ultraviolet (UV) light. In a few patients, gnant melanoma. Other features actinic value.
the contributing factors are contact with include corneal opacities, eventual • Frequently multiple and multiple
arsenic,57 tar, coal, paraffin,58 certain types blindness and neurological deficits. growth may be confined to one area
of industrial oil, radiation exposure, scars Basal cell carcinoma can be divided or may occur in different areas.
(i.e. burn complications), xeroderma into three groups, based on location and • 90 percent of the basal cell carci­
pigmentosum,59 vaccinations, or even difficulty of therapy: noma is seen in the face above a
tattoos. 1. Superficial basal cell carcinoma, or line from corner of the mouth to the
• Exposure to sunlight: The sunlight some might consider to be equi­ lobule of the ear, the commonest
is the most frequent association and valent to in situ. Very responsive site being around the inner canthus
risk is associated with the amount to topical chemotherapy such as of the eye (Figs 30.78A and B). The
and nature of accumulated sun Aldara, or fluorouracil. It is the only common sites are:
exposure over a lifetime, especially type of basal cell cancer that can – Inner canthus of the eye
during childhood. UVB, 290 to be effectively treated with topical – Outer canthus of the eye
320 nm, which causes sunburn, is chemotherapy. – Nose
believed to play a greater role in the 2. Infiltrative basal cell carcinoma, – On and around nasolabial fold
development of basal cell carcinoma which often encompasses morphea­ – On the forehead—more common
than UVA. form and micronodular basal cell in females.
• Gene mutations: Recent studies cancer. More difficult to treat with Rodent ulcer is seen more com­
demonstrate a high incidence of conservative treatment methods monly in places of the face over
p53 gene mutations in basal cell car­ such as electrodessiccation and cur- where tear roll down. That is why it
cinoma. Researchers speculate that rettage, or with currettage alone. is often called ‘tear cancer’.
UV sunlight may play an important
role in the genesis of this mutation;
however, genetic involvement has
been demonstrated on chromosome
9 only in patients with familial basal
cell nevus syndr­ome.
• Exposure to artificial ultraviolet
light (e.g. tanning booths, ultraviolet
light therapy).
• Ionizing radiation exposure (e.g.
X-ray therapy for acne). A B
• Arsenic exposure through inges- Figs 30.78A and B: Basal cell carcinoma in the infraorbital area treated by wide local
tion: Arsenic was used as a medicinal excision
Oral Cancer 735

• Principle complaint is persisting that has brown-black macules in Pathophysiology


lesion—either as a nodule or an some or all areas, often making Although the exact etiology of basal cell
ulcer. It is not painful in the begin- it difficult to differentiate from carcinoma is unknown, a well-established
ning, though it may itch. The lesion mela­noma. Typically, some ar- relationship exists between basal cell
grow slowly and show little bleed- eas of these tumors do not retain carcinoma and the pilosebaceous units,
ing. If untreated, it may become pigment; pearly, raised borders as tumors are most often discovered on
big and deep. It may then cause with telangiectases that are typi- hair-bearing areas. Tumors are currently
pain and bleeding and become in- cal of a nodular basal cell carci- believed to arise from pluripotent cells
fected. noma can be observed. This aids (which have the capacity to form hair),
• The tumor always starts as nodule. clinically in differentiating this sebaceous glands and apocrine glands,
Gradually, the center of the nodule tumor from a melanoma. Tumors usually arise from the epidermis
dies and an ulcer results. Such a Morpheaform (sclerosing) basal or the outer root sheath of a hair follicle.
ulcer has rolled edges, i.e. raised and cell carcinoma: It is an uncom- Sun light exposure leads to the for­
rounded. As the growth spreads, the mon variant in which tumor cells mation of thymine dimers, a form of DNA
shape of the ulcer becomes irregular. induce a proli­ feration of fibro­ damage. While DNA repair removes
An irregular raised edge around a blasts within the dermis and an most UV-induced damage, not all cross­
flat white scar is sometimes called increased collagen deposition links are excised. There is, therefore,
field fire BCC. (sclerosis) that clinically resem- cum­­ulative DNA damage leading to
• Appears as deeply eroding ulcer with bles a scar. The tumor appears as mut­a­­tions. Apart from the mutagenesis,
typical rolled edges, often beaded a white or yellow, waxy, sclerotic sun­light depresses the local immune sys­
and floor shows scabbing over some plaque that rarely ulcerates. The tem, possibly decreasing immune sur­
areas and breaking at the others and morpheaform subtype is the most veillance for new tumor cells.
is covered with coat of dried serum difficult subtype to diagnose. Be- Basal-cell carcinoma also develops
and epithelial cells. cause the tumor infiltrates in thin as a result of basal-cell nevus syndrome,
• Regional lymph nodes are usually strands between collagen fibers, or Gorlin syndrome.
not involved. treatment is difficult and the clini-
• Although it is called rodent ulcer, cal margins are difficult to distin- Histologic Findings
many of the lesions are non-ulcerat- guish. Mohs micrographic surgery Usually, basal cell carcinomas are well
ed. Clinical presentation of basal cell is the treatment of choice for this differentiated and cells appear histo­
carcinoma varies by type: type of basal cell carcinoma. logically similar to basal cells of epidermis.
– Nodular basal cell carcinoma: – Superficial basal cell carci- It consists of densely packed islands
Nodular basal cell carcinoma is noma: It is often multiple, most of darkly stained cells, which extend
the most common type of basal often developing on the up- down from the epidermis, although no
cell carcinoma and usually pres- per trunk or shoulders. It grows connection with the epidermis may be
ents as a round, pearly, flesh-col- slowly and appears clinically as seen. The cells on the periphery of the
ored papule with telangiectases. an erythe­matous, well-circum- islands are more deeply stained and
As it enlarges, it frequently ulcer- scribed patch or plaque, often have ‘palisade’ arrangement. There are
ates centrally, leaving a raised, with a whitish scale. Occasion- no cell rests or keratinization. Prickle
pearly border with telangiectases. ally, minute eschars may appear cells are also absent. Mitotic figures are
– Cystic basal cell carcinoma: An within the patch or plaque. The usually absent. Stromal component is
uncommon variant of nodular tumor appears multicentric, with composed of benign fibrovascular tissue
basal cell carcinoma, cystic basal areas of clinically normal skin and chronic inflammatory cells.
cell carcinoma is often indistin- intervening among clinically in- Histologically, basal cell carcinoma is
guishable from nodular basal cell volved areas. divided into two categories: Undifferenti-
carcinoma clinically, although it – Field fire or forest fire or geo­ ated and differentiated. Basal cell carci-
might have a polypoid appear- graphic variety: With advancing noma with little or no differentiation is
ance. Typically, a bluish-gray edges and healing center. It has referred to as solid basal cell carcinoma
cyst-like lesion is observed. The irregular raised edge around flat and includes pigmented basal cell carci-
cystic center of these tumors is white scar. noma, superficial basal cell carcinoma,
filled with clear mucin that has a About two-thirds of basal cell car­ sclerosing basal cell carcinoma and infil-
gelatin-like consistency. cino­mas occur on sun-exposed areas of trative basal cell carcinoma (a histologic
– Pigmented basal cell carcino- the body. One-third occurs on areas of subtype). Differentiated basal cell car-
ma: Pigmented basal cell carci- the body that are not exposed to sunlight, cinoma often has slight differentiation
noma is an uncommon variant emphasizing the genetic susceptibility toward cutaneous appendages, includ-
of nodular basal cell carcinoma of basal cell cancer patients. ing hair (keratotic basal cell carcinoma),
736 Neoplastic Conditions of Head, Neck and Face

sebaceous glands (basal cell carcinoma • Infiltrative basal cell carcinoma is a • Stage III: The cancer has spread
with sebaceous differentiation), or tubu- common type of basal cell carcinoma to tissues beneath the skin (e.g.
lar glands (adenoid basal cell carcinoma). in which strands of basaloid tumor muscle, bone, cartilage) and/or has
Noduloulcerative (nodular) basal cell car- cells are seen infiltrating between spread to regional lymph nodes, but
cinoma is usually differentiated. Histolog- collagen bundles. has not spread to other organs.
ic types can be summarized as follows:60 • Morpheaform or sclerosing basal • Stage IV: The cancer can be any size
• Nodular or noduloulcerative basal cell carcinoma consists of elongated and has spread to other organs.
cell carcinoma, which is the most strands of basaloid cells that lead to
common type, generally consists of the adjacent formation of a dense Treatment
large, round or oval tumor islands fibrous stroma. Standard surgical excision with either
within the dermis, often with an epi- • Superficial basal cell carcinoma frozen section histology, or parafin
dermal attachment. Artificial retrac- consists of buds of basophilic cells embedded fixed tissue pathology. This
tion of the tumor islands from the sur- within the papillary and occasion­ is the preferred method for removal
rounding stroma is commonly seen. ally superficial reticular dermis, of most BCCs. The cure rate for this
• Micronodular basal cell carcinoma but they are attached to the epi­ method is totally dependent on the
is similar to the noduloulcerative dermis. surgical margin. Unlike the SCC, when
type, although the tumor islands are standard surgical margin of 4 mm or
small (often < 15 cells in diameter). Clinical Staging more61 is taken, a high cure rate can be
• Pigmented basal cell carcinoma • Stage 0: Cancer involves only the achieved with excision.62 A weakness
consists of large, round or oval tumor epi­dermis and has not spread to the with standard surgical excision is the
islands containing large amounts of dermis. high recurrence rate of basal cell cancers
melanin within melanocytes and • Stage I: Cancer is not large (i.e. of the face, especially around eyelids,
melanophages. < 2 cm) and has not spread to the nose and facial structures63 (Figs 30.79
• Cystic basal cell carcinoma consists lymph nodes or other organs. and 30.80). On the face, or on recurrent
of large, round or oval tumor islands • Stage II: The cancer is large (i.e. basal cell cancer after previous surgery,
within the dermis with mucin present > 2 cm), but has not spread to lymph complete circumferential peripheral
within the center of the island. nodes or other organs. and deep margin assessment using

A B C
Figs 30.79A to C: Surgical excision of basal cell carcinoma of lower lip and reconstruction with local flap

A B C
Figs 30.80A to C: Basal cell carcinoma of pinna
Oral Cancer 737

frozen section histology is employed64 accurately utilized with a temperature due to the physical properties of light
(Figs 30.79A to C and 30.80A to C). probe and cryotherapy instruments, it absorption and reflection described by
can result in very good cure rate. Dis­ the Tyndall light phenomenon or effect.
Moh’s Surgery advantages include lack of margin Oral conditions with increased melanin
Moh’s surgery65 (or Moh’s micrographic control, tissue necrosis, over or under pigmentation are common; however,
surgery) is an outpatient procedure in treatment of the tumor and long recovery melanocytic hyperplasias are rare.
which the tumor is surgically excised time. In contrast to cutaneous melan­omas,
and then immediately examined under which are etiologically linked to sun ex-
a microscope. It is claimed to have the Electrodessication and Curettage posure, risk factors for mucosal mela-
highest cure rate of 97 to 99.8 percent by Electrodessication and curettage (EDC) nomas are unknown. These melanomas
some individuals.66 The base and edges is accomplished by using a round knife, have no apparent relationship to chemi-
are microscopically examined to verify or curette, to scrape away the soft cancer. cal, thermal, or physical events (e.g.
sufficient margins before the surgical The skin is then burned with an electric smoking; alcohol intake; poor oral hy-
repair of the site. If the margins are current. This further softens the skin, giene; irritation from teeth, dentures, or
insufficient, more is removed from the allowing for the knife to cut more deeply other oral appliances) to which the oral
patient, until the margins are sufficient. with the next layer of curettage. The mucosa constantly is exposed. Although
cycle is repeated, with a safety margin benign, intraoral melanocytic prolif-
Chemotherapy of curettage of normal skin around the erations (nevi) occur and are potential
Some superficial cancers respond to visible tumor. This cycle is repeated 3 to sources of some oral melanomas; the se-
local therapy with 5-fluorouracil, a che­ 5 times and the free skin margin treated quence of events is poorly understood in
motherapy agent. Topical treatment with is usually 4 to 6 mm. Cure rate is very the oral cavity. Currently, most oral mela-
5 percent imiquimod cream, with five much user dependent and depends on nomas are thought to arise de novo.
applications per week for 6 weeks has a the size and type of tumor. Infiltrative Although most melanomas occur on
reported 70 to 90 percent success rate at or morpheaform BCCs can be difficult skin, they may develop at any site where
reducing, even removing, the BCC (basal to eradicate with EDC. Generally, melanocytes are present.67 Malignant-
cell carcinoma). Chemotherapy often this method is used on cosmetically melanoma is a neoplasm of epidermal
follows Mohs surgery to eliminate the unimportant areas like the trunk. melanocytes in that OMM has a more
residual superficial basal cell carci­noma aggressive course, because tumors tend
after the invasive portion is remo­ved. Malignant Melanoma to metastasize or locally invade tissue
Oral melanomas are uncommon and more readily than other malignant
Immunotherapy they are thought to arise primarily from tumors in oral region.68
Immunotherapy research suggests that melanocytes in the basal layer of the In oral cavity, the most common site
treatment using Euphorbia peplus, may squamous mucosa. Melanocytic density is palate (32%), followed by maxillary
be effective. has a regional variation. Facial skin has gingiva (16%) (Fig. 30.79A and B); man­
the greatest number of melanocytes. di­
bular gingiva (7%), buccal mucosa
Radiation In the oral mucosa, melanocytes are (7%), lips (7%), and alveolar gingiva
Radiation therapy is appropriate for all observed in a ratio of about 1 melano­cyte (5%).69,70 In one-third of cases, melanosis
forms of BCC as adequate doses will to 10 basal cells. Pigmented entities are precedes the tumor, thus pigmented oral
eradi­cate the disease. Although radioth­ relatively common in the oral mucosa lesions should be viewed with suspicion
erapy is generally used in older patients and arise from intrinsic and extri­ nsic and biopsy is mandatory when clinical
who are not candidates for surgery. sources. Conditions such as mela­notic diagnosis is uncertain. Oral melanoma
macules, smoker’s melanosis, amalgam reportedly occurs more commonly
Photodynamic Therapy and graphite tattoos, racial pigmen­ in the Japanese than in other groups.
Photodynamic therapy is a new modal- tation, and vascular blood-related pig­ Oral malignant melanoma, although
ity for treatment of basal cell carcinoma, ments occur with some frequency. rare in whites, is still more common
which is administrated by application Addison disease and Peutz-Jeghers syn­ in whites than in the pigmented races.
of photosensitizers to the target area. drome also appear in perioral and oral The incidence of primary OMM has
When these molecules are activated by locations as pigmented macules. Oral been between 0.2 to 8 percent of all
light, they become toxic; therefore, de- pigmentations may range from light melanomas. Oral melanoma occurs
stroy the target cells, e.g. methyl ami- brown to blue-black, red, or purple. more often in males (2.8:1) in all ages.71
nolevulinate. The color depends on the source of the Oral malignant melanoma is largely a
pigment and the depth of the pigment disease of those older than 40 years,
Cryosurgery from which the color is derived. Melanin and it is rare in patients younger than
Cryosurgery is an old modality for the is brown, yet it imparts a blue, green, 20 years. The average patient age at
treatment of many skin cancers. When or brown color to the eye. This effect is diagnosis is 56 years. Oral malignant
738 Neoplastic Conditions of Head, Neck and Face

melanoma is commonly diagnosed in regional, or lymph node metastasis Staging


men aged 51 to 60 years, whereas it is is present. The American Joint Committee on Cancer
commonly diagnosed in females aged • Studies such as bone scanning with does not have published guidelines for
61 to 70 years. a gadolinium-based agent and chest the staging of oral mali­gnant melanomas.
radiography can be beneficial in ass­ Most practitioners use general clinical
Clinical Features ess­ing metastasis. stages in the assessment of oral mucosal
• Because oral malignant melanomas • Magnetic resonance imaging (MRI) melanoma as follows:
are often clinically silent, they can is used to diagnose melanoma in • Stage I: Localized disease
be confused with a number of asym­ soft tissue. • Stage II: Regional lymph node
ptomatic, benign, pigmented lesions. Biopsy is mandatory for establishing metastasis
• Oral melanomas are largely macular, the diagnosis. • Stage III: Distant metastasis
but nodular and even pedunculated Histologically, primary OMM is indi­ • Tumor thickness and lymph node
lesions occur. stin­­guishable from cutaneous-mela­ metastasis are reliable prognostic
• Pain, ulceration, and bleeding are noma; as its pathogenesis differs from indicators
rare in oral melanoma until late in latter which causes them to be more • Lesions thinner than 0.75 mm rarely
the disease. aggressive, and may permit blood ves- metastasize, but they do have the
• The pigmentation varies from dark sel invasion, hematogenous dissemina- potential to do so. On occasion, a
brown to blue-black; however, mu- tion early in the course of the disease. small primary lesion is discovered
cosa-colored and white lesions are Mali­ gnant-melanoma metastasizes via after a symptomatic lymph node is
occasionally noted, and eryth­ ema lymphatic and vascular channels, while harvested.
is observed when the lesions are in- cutaneous-melanoma spreads to four
flamed. main lymph nodes intraparotid, cervi- Histologic Findings
• The palate and maxillary gingiva are cal, axillary, and ilioinguinal.72 Primary Although any of the features of cutaneous
involved in approximately 80 per- OMM has marked propensity to metasta- malignancy can be found, most oral mel-
cent of patients, but buccal mucosa, size locally to submucosa and to regional anomas have characteristics of the acral
mandi­bular gingiva, and tongue le- lymph nodes.73 However, distant metas- lentiginous (mucosal lentiginous) and,
sions are also identified. tases occur to lungs, brain, liver, kidneys, occasionally, superficial spreading types.
• The oral mucosa is primarily invo­ and bones. Mucosal-melanoma may be The malignant cells often nest or
lved in fewer than 1 percent of mel­ primary or metastatic from other loca- cluster in groups in an organoid fashion;
anomas. tions in the body, it is therefore important however, single cells can predominate.
• Metastatic melanoma most frequ­ to rule out the possibility of a primary The melanoma cells have large nuclei,
ently affects the mandible, tongue, malignant-melanotic lesion. The criteria often with prominent nucleoli, and show
and buccal mucosa. for diagnosis of a primary OMM are fol- nuclear pseudoinclusions due to nuclear
• Features of long-standing lesions lowing: membrane irregularity. The abundant
include elevation, color variegation, • Demonstration of clinical and micro­ cytoplasm may be uniformly eosinophilic
ulceration, and satellite lesions that scopic tumor in the oral mucosa, or optically clear. Occasionally, the
may have the appearance of physi­ • Presence of junctional activity in cells become spindled or neurotize in
ologic pigmentation. lesion, and areas. This finding is interpreted as a
• A neck mass may be present, indi­ • Inability to show any other primary more aggressive feature, compared
cating regional metastasis; how­ever, site. with findings of the round or polygonal
this is rare unless the primary tumor The difficulty of applying cutaneous- cell varieties. In the oral mucosa, the
is extensive. melanoma classification to oral-mela­ prognosis is dismal for patients with any
no­mas has been noted by several inves­ type of malignant cell.
Evaluation ti­gators.74 The use of Clark’s criteria for Melanomas have a number of histo­
The evaluation is done following imaging degree-of-invasion and prognosis are pathologic mimics, including poorly
techniques: not applicable to oral-melanomas as differentiated carcinomas and ana­
• Imaging studies, such as computed there is no intraoral counterpart for plastic large-cell lymphomas. Diff­­er­­
tomography (CT), may be of benefit reticular and papillary dermis.75 OMM en­tiation requires the use of immuno­
in determining the extent of the were classified as: histochemical techniques to highlight
tumor when contrast enhancement • Pigmented-nodular intermediate filaments or antigens spec­
is used. • Non-pigmented nodular ific for a particular cell line.
• Contrast-enhanced CT can be • Pigmented-macular Leukocyte common antigen and
used to determine the extent of • Pigmented-mixed and Ki-1 are used to identify the lympho­
the melanoma and whether local, • Non-pigmented mixed type. cytic lesions. Cytokeratin markers, often
Oral Cancer 739

cock­tails of high- and low-molecular- show brown of black discoloration of the mucosal-melanoma is less than cuta-
weight cytokeratins, can be used to lymph nodes and the visceral organs at neous-melanomas.69 Negative surgical
help in the identification of epithelial the site of metastasis (Fig 30.82B). margins and size of primary lesion do
malignancies. In one-third of cases, melanosis not appear to be predictive of outcome.
S-100 protein and homatropine meth­ precedes the tumor, thus pigmented The only clinical finding that appears
yl­­bromide (HMB-45) antigen posit­ivity oral lesions should be viewed with to have definitive prognostic signifi-
are characteristic of, although not specific suspicion and biopsy is mandatory cance is presence of distant metastasis
for, melanoma. S-100 protein is frequent- when clinical diagnosis is uncertain. The at the time of diagnosis.75 In the case of
ly used to highlight the spindled, more mainstay of treatment is wide surgical primary oralmalignant melanoma aris-
neural-appearing melanocytes, whereas resection aiming at complete resection of ing from the maxillary gingiva, shown
HMB-45 is used to identify the round cells. pri­mary tumor and any positive cervical in Figures 30.81 and 30.82, a solitary
Melanomas, unlike epithelial lesions, are lymph nodes; however, this could metastatic lesion was detected within 2
identified by using vimentin, a marker of also be in combination with chemo- months of surgery. The patient was ad-
mesenchymal cells. Recently, microph- radiotherapy or radiotherapy alone in ministered chemotherapy but he died
thalmic tran­ s­
cription factor, tyrosinase, inoperable tumors or in the elderly. due to widespread distant metastasis,
and melano-A immunostains have been The management of clinically negative within one year of surgery, depicting the
used to highlight melanocytes. The inclu- nodes still remains controversial. In- aggressive behavior of the tumor.
sion of these stains in a panel of stains for spite of aggressive treatment modalities,
melanoma may be beneficial. survival in patients with advanced-
REFERENCES
In the test named “rubbing-with- stage-disease remains poor. Because of
gauze” the surface of lesion was rubbed lack of data, the biological behavior of 1. Shah JP, Singh B. Keynote comment:
with a piece of gauze and was considered these lesions still remains unpredictable why the lack of progress for oral cancer?
positive if gauze stained brown/black and its outcome is dismal, probably due Lancet Oncol. 2006;7(5): 356-7.
due to presence of melanin-laden to its long, ‘silent’ course. 2. Hawkins RJ, Wang EEL, Leake JL.
cells on epithelial surfaces; however, The prognosis is generally poor, Preventive health care, 1999 update:
a negative result does not exclude this with a 3-year mortality rate higher than prevention of oral cancer mortality. J
neoplasm. The metastatic disease also 50 percent. The survival of patients with Can Dent Assoc. 1999;65.
3. Warnakulasuriya S. Global epide­mio­
logy of oral and oropharyngeal cancer.
Oral Oncol. 2009;45(4):309-16.
4. Langdon JD, Rapidis AD, Harvey PW,
et al. STNMP-a new classification for oral
cancer. Br J Oral Surg. 1977;15(1): 49-54.
5. Langdon JD, Harvey PW, Rapidis AD,
et al. Oral cancer: The behaviour and
response to treatment of 194 cases. J
Maxillo Fac Surg. 1977;51227-37.
6. Hamada GS, et al. Comparative epi­
A B der­­nio­logy of oral cancer in Brazil and
Figs 30.81A and B: (A) Primay oral malignant melanoma arising from maxillary gingiva; India. Tokai J Exp. Clin Med. 1991;
(B) Mirror image 16(1):63-72.
7. Abdul Wahid. Pattern of carcinoma of
oral cavity reporting at dental depart­
ment of Ayub medical college. J Ayub
Med Coll Abbottabad. 2005; 17(1):65-6.
8. Pathak KA, Nason R, Talole S, et al.
Cancer of the buccal mucosa: a tale of
two continents. Int J Oral Maxillafac
Surg. 2009;38(2):146-50.
9. Siriwardena B. Demographic, aetiol­
ogical and survival differences of oral
A B squamous cell carcinoma in the young
and the old in Sri Lanka. Oral Oncol.
Figs 30.82A and B: (A) Resected specimen of maxilla; (B) Neck dissection block showing
2006;42(8):831-6.
black lymph nodes due to metastatic disease.
740 Neoplastic Conditions of Head, Neck and Face

10. Gupta PC, Mehta FS, Pindborg JJ. 24. Hodder SC, Evans RM, Patton DW, 35. Nakazawa Mitsuhiro. The significance
Mortality among reverse chutta smo­ et al. Ultrasound and fine needle of histological malignancy grading and
kers in south India. Br Med J (Clin Res aspiration cytology in the staging of its clinical use in oral squamous cell
Ed). 1984;289(6449):865-6. neck lymph nodes in oral squamous carcinoma. Head and Neck Cancer.
11. Bhavana J Dave. Role of areca nut con­ cell carcinoma. Br J Oral Maxillofacial 2004;30(1):25-32.
sumption in the cause of oral cancers. Surg. 2000;38(5):430-36. 36. Crile, George. Excision of cancer of
A cytogenetic assessment. Cancer. 25. Lee RE, et al. Lymph node examination the head and neck. J Am Med Assoc.
1992;70(5):1017-23. by FNA in patients with known or sus- 1906;47:1780-6.
12. Yi-Shan Tsai. Arecoline, a major alka­ pected malignancy. Acta cytological. 37. Warren JC. Surgical Observations on
loid of areca nut, inhibits p53, represses 1987;31:563-71. Tumours, With Cases and Operations.
DNA repair, and triggers DNA damage 26. Sarvanan Y. Computed tomography London, England: John Churchill; 1839.
response in human epithe­ lial cells. and ultrasonographic evaluation of 38. Chelius JM. A System of Surgery. Trans­
Toxicology. 2008;249(2-3):230-7. metastatic cervical lymph nodes with lated by John F. South, Volume 3. (Phil­
13. Ramesha Rao A, Padma Das. Evalu­ surgicoclinicopathologic correlation. J a­delphia: Lea and Blanchard. 1847.
ation of the carcinogenicity of different Laryngol Otol. 2002;116(3):194-9. 39. Martin H. The case for prophylactic
preparations of areca nut in mice. Int J 27. Miwako Oomori. Dynamic magnetic neck dissection. Cancer. 1951;4:92-7.
Cancer. 2006;43(4):728-32. resonance imaging of cervical lymph 40. Bocca E, Pignataro O. A conservation
14. Graham R. Ogden. Alcohol and oral nodes in patients with oral cancer: utility technique in radical neck dissection.
cancer. Alcohol. 2005;35(3):169-73. of the small region of interest method in Ann Otol Rhinol Laryngol. 1967;76:975-
15. Lund CL. Syphilis in relation to cancer evaluating the architecture of cervical 87.
of the buccal mucosa. J Med. 1933; lymph nodes. Oral Radiol. 2008;24(1). 41. Shah JP (Ed). Cervical lymph nodes, in
209:131-4. 28. Ding ZX, Liang BL, Shen J, et al. Mag- Color Atlas of Operative Techniques
16. Lozada-Nur F. Oral lichen planus and netic resonance imaging diagnosis of in Head and Neck Surgery: Face,
oral cancer: Is there enough epidemio- cervical lymph node metastasis from Skull, and Neck. Orlando, FL. Grune &
logic evidence? Oral Surg Oral Med lingual squamous cell carcinoma. Ai Stratton. 1987.pp.353-94
Oral Pathol Oral Radiol Endod. 2000; Zheng. 2005;24(2):199-203. 42. Suárez O, El problema de las metastasis
89(3):265-6. 29. Alex JC, Krag DN. The gamma-probe- linfáticas y alejadas del cáncer de lar-
17. IARC monographs on the evaluation of guided resection of radiolabeled pri- inge e hipofaringe. Rev Otorrinolarin-
carcinogenic risks to humans: Solar and mary lymph nodes. Surg Oncol Clin N gol. 1963;23:83-99.
ultraviolet radiation. IARC Monogr Eval Am. 1996;5(1):33-41. 43. Bocca E, Pignataro O, Sasaki CT. Func­
Carcinog Risks hum. 1992;55:01-316. 30. Vigili MG, Tartaglione G, Rahimi S, et al. tional neck dissection: a description of
18. Ramzi S Cotran, Stanley L Robbins. Lymphoscintigraphy and radioguided operative technique. Arch Otolaryngol.
Basic Pathology, 6th edition. W.B. sentinel node biopsy in oral cavity 1980;106:524-7.
Saun­ders Company, New York, 1997. squamous cell carcinoma: same day 44. Rouviere H. Anatomie des lympha­
19. Lindberg R. Distribution of cervical protocol. Eur Arch Otorhinolaryngol. tiques de l’homme. Paris: Masson et
lymph node metastases from squa­mous 2007;264(2):163-7. Cie; 1932.
cell carcinoma of the upper respiratory 31. KT Pitman. Sentinel lymph node biop- 45. Lindberg R. Distribution of cervical
and digestive tracts. Cancer. 1972;29(6): sy in head and neck cancer. Oral Oncol. lymph node metastases from squa­
1446-9. 2003;39(4):343. mous cell carcinoma of the upper
20. Denoix PF. The TNM staging system. 32. Stoeckli SJ, Pfaltz M, Ross G, et al. The respiratory and digestive tracts. Cancer.
Bull Inst Nat Hyg (Paris). 1952;7:743. second international conference on 1972;29:1446.
21. Sobin LH, Wittekind C. TNM Classifi­ sentinel node biopsy in mucosal head 46. Skolnik E. Metastatic neck disease:
cation of Malignant Tumours, 6th and neck cancer. Ann Surg Oncol. Evaluation by computed tomography.
edition. Hoboken, New Jersey: John 2005;12:919-24. Arch Otolaryngol. 1984;110:443-7.
Wiley and Sons; 2002. 33. Ross GL, Shoaib T, Soutar DS, et al. 47. Shah JP. Patterns of cervical lymph
22. Marx RE, Stern D. Oral and maxil­lofacial The first international conference on node metastasis from squamous carci-
pathology: a rationale for diagnosis and sentinel node biopsy in mucosal head nomas of the upper aerodigestive tract.
treatment. Hanover Park (IL): Quintes- and neck cancer and adoption of a Am J Surg. 1990;160(4):405-9.
sence Publishing; 2003.pp.284-9. multicenter trial protocol. Ann Surg 48. Kadir Imre. Predictors of extracapsular
23. Lawrence E. Ginsberg. The Role of Oncol. 2002;9:406-10. spread in lymph node metastasis. Eu-
Diagnostic Imaging in Identifying Cer- 34. Uren RF. The Role of Lympho­scinti­ ropean Archives of Oto-Rhino-Laryn-
vical Metastases in Oral Cavity Cancer. graphy in the Detection of Lymph gology. 2008;265(3).
Oral Cancer Metastasis. New York: Node Drainage in melanoma. Surg. 49. Scorza LB, Goldstein BJ, Mahraj RP.
Springer. 2010:pp.33-48. Oncol Clin N Am. 2006;15(2):285-300. Modern management of chylous leak
Oral Cancer 741

following head and neck surgery: a 59. Mohanty P, Mohanty L, Devi BP. Mul- Primary Malignant Melanoma of the
discussion of percutaneous lym­ ph­ tiple cutaneous malignancies in xero- Oral mucosa. J Oral Maxillofac Surg.
an­giography-guided cannulation and derma pigmentosum. Indian J Derma- 2007;65:1117-20.
embolization of the thoracic duct. Oto- tol Venereol Leprol. 2001;67(2):96-7. 69. Pandey, Mathew, Iype, Sebastian,
laryngol Clin North Am. 2008;41(6): 60. James, William D, Berger. Timothy G, Abraham, Nair. Primary malignant
1231-40. Andrews’ Diseases of the Skin: Clinical mucosal melanoma of the head and
50. Takuji Tanaka. Chemoprevention of Dermatology. 11th Ed. W.B. Saun­ders neck region: pooled analysis of 60
oral carcinogenesis. Eur J Cancer B Co Elsevier. 2005. published cases from India and review
Oral Oncol. 1995;31B(1):03-15. 61. Wolf DJ, Zitelli JA. ‘Surgical margins for of literature. European Journal of
51. Hong WK, Endicott J, Itri LM, et al. basal cell carcinoma’. Arch Dermatol. Cancer Prevention. 2002;11:3-10.
13-cis-retinoic acid in the treatment of 1987;123(3):340–4. 70. Gao Man Gu, Epstein JB, Morton
oral leukoplakia. N Engl J Med. 1986; 62. Silverman MK, Kopf AW, Bart RS. TH. Intraoral melanoma: Long-term
315:1501-05. ‘Recurrence rates of treated basal cell follow-up and implication for dental
52. Hong WK, et al. Prevention of second carcinomas. Part 3: Surgical excision’. clinicians. A case report and literature
primary tumors with isotretinoin in J Dermatol Surg Oncol. 1992;18(6): review. Oral Surg Oral Med Oral Pathol.
squamous-cell carcinoma of the head 471-6. 2003; 96:404-13.
and neck. N Engl J Med. 1990; 23(323): 63. Sigurdsson H, Agnarsson BA. ‘Basal 71. Barker BF, Carpenter WM, Daniels
795-801. cell carcinoma of the eyelid. Risk of TE. Oral mucosal melanomas: The
53. Inui A. Neuropeptide Y: a key molecule recurrence according to adequacy of WESTOP Banff proceedings. Oral Surg
in anorexia and cachexia in wasting surgical margins’. Acta Ophthalmol Oral Med Oral Pathol 1997;83:672-9.
disorders? Mol Med Today. 1999;5:79-85. Scand. 1998;76 (4):477-80. 72. Patton LL, Brahim JS, Baker AR, et al.
54. Tisdale MJ. Cachexia in cancer pati­ 64. Dhingra N, Gajdasty A, Neal JW. Metastatic malignant melanoma of the
ents. Nat Rev Cancer. 2002;2:862-71. ‘Confident complete excision of lid- oral cavity. Oral Surg Oral Med Oral
55. Zuijdgeest-Van Leeuwen SD. Eicosa- margin BCCs using a marginal strip: Pathol. 1994;78:51-6.
pentaenoic acid ethyl ester supple- an alternative to Mohs’ surgery’. Br J 73. Rapidis AD, Apostolidis C, Vilos G,
mentation in cachectic cancer pa- Ophthalmol. 2007;91(6):794-6. et al. Primary Malignant Melanoma
tients and healthy subjects: effects on 65. Mohs. Frederic Edward. Chemosurgery: of the Oral Mucosa. J Oral Maxillofac
lipolysis and lipid oxidation. Clin Nutr, microscopically controlled surgery for Surg. 2003;61:1132-9.
2000;19(6):417-23. skin cancer. Springfield, Ill: Thomas. 74. Patton LL, Brahim JS, Baker AR, et al.
56. Mulvany NJ, Allen DG. Differentiated 1978.pp.3-6. Metastatic malignant melanoma of the
intraepithelial neoplasia of the vulva. 66. Bene NI, Healy C, Coldiron BM. ‘Mohs oral cavity. Oral Surg Oral Med Oral
Int J Gynecol Pathol. 2008;27(1):125-35. micrographic surgery is accurate 95.1% Pathol. 1994;78:51-6.
57. Cabrera HN, Gómez ML. Skin cancer of the time for melanoma in situ: a pro- 75. Jeevan Lata, Satya Narain. Primary
induced by arsenic in the water. J spective study of 167 cases’. Dermatol mucosal melanoma of oral mucous
Cutan Med Surg. 2003;7(2):106-11. Surg. 2008;34(5):660-4. membrane—A report of two cases.
58. Romao-Correa RF, Maria DA, Soma M, 67. Neville, Damm, Allen, Bouquot. Oral J Maxillofac Oral Surg. 2005;4:28-30.
et al. Nucleolar organizer region stain­ and Maxillofac Path. 2nd ed. W.B.
ing patterns in paraffin-embedded Sounders Co; 2004. pp.377-80.
tissue cells from human skin cancers. 68. Midion Mapfumo Chidzonga, Leonard
J Cutan Pathol. 2005;32(5):323-8. Mahomva, Rudo Makunike-Mutasa.
Section 11
Important Tips for
Postgraduate Students

n Thesis Writing
n Seminar and Journal Club Presentation
31 Thesis Writing
Gaidhane Abhay, Quazi Syed Zahiruddin

It is science alone that can solve the problems of hunger and poverty, insanitation and illiteracy, of superstition and deadening
custom and tradition, of vast resources’ running to waste, of a rich country inhabited by starving people.
—Jawaharlal Nehru

One of the major components of the the thesis. The synopsis initially has • Feasibility
Postgraduate curriculum is writing thesis. to be submitted to the Institutional • Availability of relevant infrastructure
Work for writing the thesis is aimed at Ethical Committee and/or Animal and facilities
contributing to the develop­ ment of a Ethical Committee as applicable, for • Availability of adequate clinical
spirit of enquiry, besides exposing the the approval. After clearance from mate­rial to constitute a sample size,
candidate to the techni­ques of research, the Institutional Ethical Committee, which can be processed statistically
critical analysis, acquain­tance with the the synopsis is communi­ cated to the to generate cognigible data
latest advances in medical science and concerned university for approval of the • Possibility of completing the work in
the manner of identifying and consulting thesis. The work on any research project the prescribed time frame
available literature. A postgraduate can be started only upon the ethical • Considering ethical aspects
student is required to carry out work on committee clearance. The purpose • Considering financial feasibility.
an assigned short-term research project of this exercise is to allow the next 18 It is not feasible to fix the sole
under the guidance of a recognized months to the students to undertake the responsibility on the postgraduate stu­
postgraduate teacher, the result of which study according to the protocol (data dent to search for the topic of rese­
shall be written up and submitted in collection). As the study is completed in arch as he/she has no insight in the
the form of a thesis. Thesis should be the 18 months, over the next 6 months speciality nor he/she is acquainted to
submitted at least six months before the the collected data can be compiled, the facilities and other protocols. The
theory and clinical/practical examination. processed and interpreted and finally role of the postgraduate student should
A candidate shall be allowed to appear the text is prepared in the form of be facilitative. The research topic is
for the theory and practical/clinical thesis. This allows the student complete often selected by the student, while
examination only after the acceptance of 2 years for the thesis work after the doing a doctoral research (PhD) and
the thesis by the examiners. ethical committee clearance. not during the postgraduation. Once the
topic is finalized the student is entrusted
PREPARING SYNOPSIS OUTLINE OF THE a responsibility of making a synopsis
under the due guidance and supervision
STUDY PROTOCOL
As per the existing statute, a postgra­ of the postgraduate teacher.
duate student is assigned to a reco­ At the postgraduate level the concerned The ideal way for starting on thesis
gnized postgraduate teacher. Within postgraduate teacher is expected to allot is working on study protocol. This
first 6 months from the date of comm­ a suitable and feasible research topic to approach gives clarity and guide to
ence­ ment of the academic term, the the postgraduate student. The viability select the research work for the thesis.
postgraduate student has to prepare of the study must be ascertained in The candidate can work on the study
synopsis and submit for approval of terms of: protocol as given in Table 31.1.
746 Important Tips for Postgraduate Students

Table 31.1: Study protocol designing Inter­ven­­tion/exposure if any; C–Com-


parison; O–Outcome).
Sr. No. Element Purpose Do anticoagulant agents improve
1. Research question What question will the study address? outcomes in patients with acute isch­emic
2. Background and significance Why are these questions important? stroke compared with no treat­ment?
3. Design How the study is structured? In this example, the type of target
a. Time frame person/population on whom study is
b. Epidemiological approach being conducted is patients with acute
4. Subjects Who are the subject and how they will be ischemic stroke. It should be during the
a. Selection criteria selected? process of making type of target person/
b. Sampling design population in the RQ decided, what you
5. Variables What measurement will be made? meant by acute ischemic stroke, what
a. Predictor variables age, sex, severity of patients you will
b. Confounding variables
c. Outcome variables include, by what means will be your
6. Statistical issues How large will be the study?
clinical diagnosis for acute ischemic
a. Hypothesis testing How it will be analyzed? stroke, whether you will include Outpa­
b. Sample size tient/Inpatient; and within 48 hours of
c. Analysis approach stroke onset (Flow chart 31.2).
The type of exposure (anticoagulant
agents) whether it will be unfractionated
START WITH RESEARCH Once you are ready with your RQ and heparin, low-molecular-weight heparin,
QUESTION sub research question, you will be able hep­a­ri­noids, oral anticoagulants, etc. It
to write research objectives, hypothesis, should be very clear initially when mak­
define key variables and select study ing a research question of what type of
A question well stated is half ans­
design, make dummy tables and what exposure/intervention is being given in
wered; but a question that is poorly
statistics to apply. the study or should be known that there
stated or unstated is not likely to be
is no exposure nor any interv­ention is
answered at all.
—Charles Franklin Kettering A POORLY FRAMED given.
The type of comparison what type of
RESEARCH QUESTION control or comparison is in the study. In
Remember the most important task is Example of poorly framed RQ, it only this example there is control group, i.e.
to identify and clearly define the rese­ describes type of intervention (antico­ no anti-coagulation is given to the study
arch question (RQ) of the study. To agulant agent) and on what type of target group.
decide the research question the stu­ population (patient who had stroke) but The type of outcome anticipated
dent should consult teachers, discuss does not explain what is the outcome in the study is to be described. In this
with colleagues, go through literature which needs to be studied and whether example, outcome can be death, disab­
review, identify problems that are faced there is any comparison in the study ility, major hemorrhage, recurrent stroke
in clinical practice, identify researchable with another group (Flow chart 31.1). or deep vein thrombosis (DVT).
area, look at your personal interest, go
for divergent thinking. Try to think…..
A Nicely Framed Research
outside the box. Question Flow chart 31.2: An example of nicely
framed research question
A RQ should have sound biologic One way of making research question
rationale and plausibility. The RQ should is by seeing whether the RQ contains
be feasible, have adequate number of PICO (P–Population/person/thing; I–
subjects, technical expertise, affordable
in time and money and manageable in Flow chart 31.1: Example of poorly
scope. The research question should framed research question
be novel, confirms or refutes previous
findings, extends previous findings and
provide new findings. Research question
should be ethical and should be relevant
to scientific knowledge, clinical and
health policy, and should be able to
provide future research direction.
Thesis Writing 747

Table 31.2: Sampling error


HYPOTHESIS
Decision
The great tragedy of Science—the Null hypothesis
Accepted Rejected
slaying of a beautiful hypothesis by
True Correct conclusion Type I or (α) error
an ugly fact.
—Thomas Henry Huxley False Type II or (b) error Correct conclusion

Once the research question or rese­


arch problem is identified, the next step gation in the related area are essential to An error that occurs in hypothesis
would be to make guess/guesses (based conceptualize the logical outcome/answer testing is called as ‘sampling error’.
on review of literature and experience of our research question. Other things that These can be of two types:
survey) about the possible answer. These could add up to this understanding is
guesses are hypothesis, which either solve our experience, observation (Intuitions), Type I Error
problem or guide for further investigation. reasoning, insight and logical derivation Type I error also called α error: When
Thus, hypo­thesis is a provisional formu­ from the theory. HO is rejected even if it is true, then
lation, a tentative solution to the problem Research hypothesis are of two types: type I error is committed. The α error is
fac­ing the researcher. In other words, 1. Null hypothesis: Denoted by the defined as 5 percent.
hypothesis is a statement about an expec­ symbol HO.
ted relationship between two or more 2. Alternative hypothesis: Denoted by Type II Error
variables that permits empirical testing. the symbol HA. Type II error also called β error: When
While ultimate objectives iden­ tify the Null hypothesis (HO) is the hypo­ HO is accepted even if it is false, then
anticipated contributions ari­sing from a thesis in which the sample or populations type II error is committed. The β error
study and immediate objectives (stated being compared in a study or test are is usually defined as 20 percent and is
in behavioral terms) specify what will be similar. If there is any difference, it is due linked to power of the study (1-β = power
done or measured in the study, hypotheses to chance, not due to measurable factor. of study; 100 – 28 = 80 Power of study).
specify the expected relationship among HO is initially accepted and considered For ease of understanding refer the
the vari­ables. Hypothesis statements are true for analytical comparison. An Alter­ following example and figure.
most appropriate for field intervention or n­ative hypothesis (HA) is the hypo­thesis
evaluative studies. Diagnostic or explo­ to be tested and must be stated, before
ratory studies do not normally require the study is designed (Table 31.2).
Sampling Error
hypothesis statements because they HO is used to define significant differ­
Sampling is done to determine the chara­
gene­rally do not test relationships bet­ ence. A significant difference occurs, if cteristics of a whole population, the diff­
ween variables. HO is disproved and HA is accepted. erence between the population values
Descriptive studies can formulate and the sample is considered as sampling
hypothesis, but for testing it if is true or Testing of Hypothesis error. Statistics on the samples differ from
false, we need to undertake the analytical It means accepting or rejecting HO. This the parameters on the entire population
studies. Descriptive and analytical stu­ is usually done on statistical analysis. since the sample does not include all the
dies are discussed subsequently in detail. For testing the level of confidence for members of the population.
A well formulated hypothesis of ana­ rejecting HO is arbitrary, usually fixed
lytical studies can: at 5 percent. Type of statistical test Example:
• Help researcher proceed in corr­ect used for testing and its interpretation A study to estimate the hemoglobin
direction. is also different for unidirectional (one level in high-school students was
• Guide the researcher for order among tailed) hypothesis and bidirectional conducted. The results showed that
facts. (two tailed) hypothesis. There could be the mean Hb level in one school was
• Give points to the inquiry (helps three situations on hypothesis testing: 14 g/dL and in other school 13 g/dL.
rese­ar­
cher to know specifically, 1. If HO is rejected and HA is accepted, On analysis it was observed that the
what he has to find out). the two population, sample are signi­ probability that it is due to chance alone
• Help in selection of pertinent or ficantly different. is 15 percent. The Interpretation would
rele­vant facts. 2. If HO in not rejected, the two pop­ul­ be that the difference is not significant.
• Help in drawing conclusion. ation, sample are similar (no differ­ Therefore; the null hypothesis is not
To formulate a good hypothesis, ence). rejected, as α  error (also called as level
extensive literature search on related 3. If HO is not rejected, even if the two of significance) is defined as 5 percent.
topics is most essential, because the population, sample are different— If the same study is repeated 100 times
facts established by previous investi­ an error is committed. and 5 out of 100 studies showed
748 Important Tips for Postgraduate Students

significant difference. This means that that is linked to measurement (rate, fi­cation is needed as a blue print of the
the probability, that it is due to chance prevalence, frequency, etc.) study planning.
alone is less than 5 percent and HO • Measurable: Objective unit that can
is rejected. The type I error is made in indicate achievement
these five studies. • Achievable: With a reasonable amo­ PLANNING THE RESEARCH
To understand type II error, consider unt of effort, can this be done?
this, if there is a difference between • Relevant: Appropriate impact, out­ After deciding the research question/
Hb level of students, the probability put, products? thesis topic formulation of hypothesis
of the study detecting the difference is • Time-bound: Indicates target dates and objectives, the next step is to plan for
80 percent whereas not detecting the and study context. the research. In planning, the researcher
difference is 20 percent. needs to consider the different options
Examples to Understand available to investigate the research
question/hypothesis/objectives. In other
Objectives More Clearly
words, the investigator needs to finalize
OBJECTIVES the suitable research design. The various
Example 1: A Survey of Diabetes to
issues that need to be looked into for
be Conducted in the Community planning the research are:
“The successful man is the average
Objective 1: To establish the exact • Selecting the suitable study design
man, focused.”
number of diabetics in the comm­unity. • Calculating sample size and defining
—Anonymous
Comment: Statement is clear, but the sampling methodology (random
formulation is incomplete (prevalence error and level of significance and
Objective indicates the accomplish­ment rate, age, gender, etc). power of study)
of the study. Just by reading an objective, Objective 2: To discover the undiag­ • Data collection: Tools and tech­
other persons must get a sense of what you nosed cases of diabetes. niques (methods)
are doing (even if they do not understand Comment: Not a complete state­ • Data quality
technical terms). Thus, objectives must ment (--- and to compare their age • Data analysis.
be clearly linked to problem and question and sex distribution with that of known
and framed in clinical/epidemiological cases).
terms that measure outcome, rates, Objective 3: To investigate the possible SELECTING THE SUITABLE
incidence, mortality, morbidity etc. This hereditary factors. STUDY DESIGN
will allow us to evaluate the success of Comment: Too non-specific for
the research project. The study objective blue print for study planning. Did the The study objective can be achieved by
also influences the study design, data investigator want to—study a familial number of alternative designs. Resear­
collection and interpretation. clustering of cases, association with an cher has to select the most appro­priate
Hint: While, reading the research occurrence of genetic markers, compare and feasible design. Selection of the
paper in any journal, the objective(s) the frequency of the positive family study design may depend upon the
is usually the last sentence of the histories of diabetes among diabetic, follow­ing issues:
‘introduction’ section. newly detected, or non-diabetics. • What is the research question/hypo­
To formulate a good objective, use thesis/objective.
no more or less than one verb each, Example 2: A Report on National • Time available for study.
(i.e. an objective is an action and must • Resources available for the study.
Study of Cerebral Palsy in
clearly and strongly reflect that). The • Common/rare disease or production
objective should be clear about whether Adolescent and Adulthood problem.
they call for testing a hypothesis (e.g. ‘we Objective 1: To learn about the extent • Type of outcome of interest.
are going to compare….’) or they call for and nature (of the problem) and spe­ • Quality of data from various sources.
measuring a quantity (e.g. we are going cific need of the cerebral palsied young­ • Often there are multiple approaches,
to describe….’) ster and adult through socio-medical which will all work.
Be careful not to get too broad or you study. • Choosing an established design
can lose focus. Too general formulations, Objective 2: Collect an epide­mi­olo­gical gives you a huge head start in design,
“e.g. to study the health status of ------” data of cerebral palsied individuals. analysis and eliminating biases.
will not be useful at all. To make good Objective 3: To evoke the interest of Broadly the research designs can
quality study objectives we can make public agencies and local communities be classified as observational and inter-
use of pneumonic ‘SMART ’: in the program. ventional/experimental. Observational
• Specific: Specify what you want to Comments: These formulations may studies could be either descriptive or
achieve. Describe a precise outcome be OK as a starting point, but much speci­­ analytical.
Thesis Writing 749

Descriptive Studies be weak in terms of empirical evidence. compared with the frequency in those
These studies describe the patterns of The lack of a comparability can lead to not exposed.
diseases with regards to person, place misleading conclusions. In addition, the Cross-sectional studies are especi­
and time. Descriptive studies are a nec- number of individuals involved in case ally useful for defining the health needs
essary antecedent of analytic studies and series is often small. of a population at a particular point
are less expensive than analytic studies. Case report and case series studies in time, and as the first step in more
Descriptive studies help in formulating may describe: detailed etiological investigations. How­
research questions or hypothesis, but • A previously described disorder ever, as they are based on prevalent
they cannot be used for testing hypoth- involving a new population or sub- (existing) cases rather than incident
eses. They can also be used to assess the group (new) cases, they are of limited value for
associations between putative risk fac- • A known disorder with unusual clin- investigating etiological relationships.
tor and disease, but cannot comment on ical presentation or clinical course Correlation studies are also called
causation by doing descriptive studies. • A condition in which novel treatment as ecological studies. In these studies
The different types of descriptive studies methods are used we consider populations as unit of
are—case reports, case series, cross-sec- • A previously unknown condition analysis and use database from entire
tional surveys, correlation studies. • A index case in an epidemic situ­ populations to compare frequency of
ation. a particular disease. In other words,
Case Reports Example of case report: Thalido­ we look to see whether the outcome
The most basic descriptive study with mide tragedy in 1957, thalidomide was is more frequent in groups where the
no control group. They describe the created by West German company exposure is more frequent. For each
experience of a single patient. Case Cheme Gruen­thal to treat hyperemesis group, the exposures and outcomes are
reports are used for documenting the gravi­darum. Developmental deformities measured for the group as a whole. So,
unusual medical occurrence and may possibly due to thalidomide. A Case it is not possible to link the exposure
lead to identification of new disease. Report Ihno Y. Russell WJ, May 1963. of any particular individual to his or
They can be done quickly with little Example of case series: ‘Human her outcome. Ecological studies can be
money. Immunodeficiency Virus (HIV) and done quickly and inexpensively using
PCP pneu­monia’ Gottlieb, Michael existing data such as, vital statistics,
Case Series et al, “Pneumocystis carinii pneumo- hospital discharge data, product con­
Descriptive studies, which focus on nia (PCP.) and mucosal candidiasis in sumption data, environmental data,
individuals. They examine the experi­ previously healthy homosexual men,” etc. Because of this, correlation study
ence of a group of individuals sharing NEJM, 1981:305:1425-31. are often used as a first step in the
a common experience. This may be a investigation of a possible exposure-
shared exposure (or risk factor) or a Cross-sectional Surveys outcome relationship. However, it can
shared outcome (perhaps symptoms, or Cross-sectional surveys are also called be difficult to interpret the results of an
a disease). A key characteristic of case Prevalence Surveys. Exposure and ecological study.
series is that there is no comparison disease are measured simultaneously.
group. Case series are common in These surveys provide a ‘snapshot’ of Analytical Studies
clinical medicine, where they are often the popul­ation. The analytical studies are conducted
used to highlight unusual or inter­ In a cross-sectional study, measure to test the hypothesis and to find out
esting findings. They may be used to the frequency of a particular exposure(s) the association between the risk factors
describe a new disease or a rare mani­ and/or outcome(s) in a defined popu­ or predictors and disease or outcome.
festation of an existing disease. Case lation at a particular point in time. The most commonly used analytical
studies can also be used to help detect Cross-sectional studies can either be study designs in health research are
the effects (adverse or beneficial) of descriptive or analytical. case control studies, cohort studies and
a new treatment. Case series can be In a descriptive cross-sectional study, nested case control studies. Interven­
particularly useful for generating hypo­ simply describe the frequency of the tional/experimental studies are also
theses, which can then be explored exposure(s) and/or outcome(s) in a de- type of analytical studies.
in larger, well-designed studies. Case fined population.
series are attractive as they can usually In an analytic cross-sectional study, Cohort Study
be conducted quickly and cheaply. the information is simultaneously colle­ This study is started by selecting a
However, despite their popularity in cted on both the outcome of interest and study population or cohort of people
clinical medicine, case series are less exposure to potential risk factor(s). The who do not initially have the outcome
commonly used in epidemiology. This frequency of the outcome in the people of interest. The members of the cohort
is largely because they are considered to exposed to each risk factor is then are then according to whether they
750 Important Tips for Postgraduate Students

have been exposed to the potential risk Examples of cohort studies (to give factors. These studies can measure the
factor or not. The entire cohort is then the source for these studies) association between the risk factor and
over time followed and comparison • Framingham Heart Study outcome. The case control studies are
is made between the incidence of the • National Health and Nutrition Exam­ useful, if the disease is rare. The big
outcome(s) in the exposed individuals i­­nation Surgery (NHANES) Studies advantage of case-control studies is
with the incidence in those not exposed. • Physicians’ Health Study that past exposures and outcomes are
The cohort studies are particularly useful • Nurses’ Health Study measured at the same time. Because of
for investigating the rare exposures • Ndoll R, Peto R, Boreham J, this, these studies can be done quickly,
or rare risk factor or rare cause and in Sutherland I. Smoking and dementia without the need to wait for the
situations, where we are interested in in male British doctors: prospective outcome to occur. Another advantage
studying more than one outcome. The study. BMJ 2000;320:1097-1102. of case-control studies is that they are
limitation of cohort study is that they a good way to study rare outcomes and
are time consuming and expensive to Case-control Studies outcomes with a long induction period.
carry out. They are also inefficient for Case-control studies are retrospective This is because the starting point is
investigating rare outcomes. studies. The case-control study is started the identification of people with the
by identifying individual cases of the outcome in question.
Design of Cohort Study outcome of interest. A representative The major difference between case-
Cohort study can be prospective, retro­ group of individuals is then identified control studies and cohort studies is the
spective or ambidirectional. This is given who do not have the outcome. These way that the study subjects are chosen.
in the flow chart below (Flow chart 31.3 individuals act as controls. Cases and In a cohort study, subjects are selected
and 31.4). For more information readers controls are compared to assess whether before they have had a chance to develop
are requested to refer the suggested there were any differences in their past the outcome of interest. They are classi­
reading. exposure to one or more possible risk fied according to their exposure or non-
exposure to the possible risk factor. We
then follow them over time to see, if they
Flow chart 31.3: Design of cohort study
develop the outcome. In contrast, in a
case-control study we select subjects on
the basis of the presence or absence of
the outcome. We then look to see if they
were exposed or not to the possible risk
factor (Flow chart 31.5).

Nested Case Control Study


In cohort study when enough individuals
have developed the outcome of interest,
they can be compared to controls. In
other words a case-control study is
Flow chart 31.4: Schematic representation of concurrent, retrospective and inserted into a cohort study. This type
ambidirectional cohort studies of design is called as nested case control
study. Such design allows interim
evaluation of the association between
the variables (Fig. 31.1).

Flow chart 31.5: Case control study design


Thesis Writing 751

Fig. 31.1: Cohort study design

Clinical Trials
These are experimental studies (RCTs)
(Flow chart 31.6). Clinical trials are con­
ducted in different phases:
• Phase l: Initial testing in healthy
human volunteers following animal
studies. In this phase the dose limi­
ting toxicities, tolerated doses etc.
are studied.
• Phase ll: Testing in subjects with
disease to determine activity and
therapeutic efficacy. In this toxicity
Fig. 31.2: Intervention study design and dosage data of the drug is valid­
ated.
• Phase lll: Randomized trials for
Interventional/Experimental of potential benefit to patients, such as com­parison. In this phase the effi­
Studies preventive or therapeutic measures. cacy of the drug on patients is
In an interventional study, the distri­ Most commonly used experimental measured.
bution of the exposure and outcome in studies are the randomized clinical • Phase IV: Post marketing trials. These
a population is observed. The exposure trial or randomized trial or randomized are post-marketing surveill­ ance for
(or intervention) to one of the study control trial (RCT ). These are similar to monitoring the long-term adverse
groups is then actively allocated. The a cohort study as individuals are studied effect of drugs, if any.
group that is allocated not to receive the on the basis of exposure. However the
intervention acts as a control group. If main difference between observational Single Blind Trials
the intervention is a type of treatment, and intervention studies are that indivi­ Single-blind describes experiments, where
the control group can be described duals in the intervention study have no information that could introduce bias or
as receiving standard treatment. The control over the exposure they receive. otherwise skew the result is withheld from
groups are then followed over a period In RCT study participants are assigned the participants, but the experimenter will
of time. The frequency of the outcome treatment group and control group by be in full possession of the facts.
in the group allocated to receive the randomization. This ensures that the In a single-blind experiment, the
intervention is compared with the allocation of the intervention is deter­ individual subjects do not know wheth-
frequency of the outcome in the group mined by chance alone. er they are so-called ‘test’ subjects or
who were allocated not to receive the RCT can be used to: mem­ bers of an experimental control
intervention (Fig. 31.2). • Evaluate new drugs. group. Single-blind experimental design
Intervention studies provide strong • Evaluate new treatment procedures. is used, where the experimenters either
evidence about causation, because • Testing efficacy of new health care must know the full facts (for example,
when designed well (with random allo­ program. when comparing sham to real surgery)
cation) they minimize the possibility • Assess preventive measures. and so the experimenters cannot them­
of selection bias and confounding. • Assess new program for screening. selves be blind, or where the experi­
However, for ethical reasons we can only • Assess new ways to deliver health menters will not introduce further bias
use them to study interventions that are services. and so the experimenters need not be
752 Important Tips for Postgraduate Students

Flow chart 31.6: Design of RCT Furthermore each design has sub-
types. Even though there is some hi-
erarchy in study designs; no study de-
signs are gold standard, but the design
should be such that, it will give the most
definitive answers to the research ques-
tion planned. None of the study designs
are free of bias/errors or confounding.
Therefore the results of the studies need
to be interpreted cautiously considering
the potential bias. However, the discus-
sion on bias is beyond the scope of this
chapter. For more information on bi-
ases, readers are requested to refer the
suggested reading mentioned at the end
of the chapter.

DEFINING THE SAMPLING


METHODOLOGY AND
CALCULATING SAMPLE
SIZE (RANDOM ERROR AND
blind. However, there is a risk that sub- to is kept by a third party and not given LEVEL OF SIGNIFICANCE
jects are influenced by interaction with to the researchers until the study is over.
AND POWER OF STUDY)
the researchers—known as the experi­ Double-blind methods can be app­
menter’s bias. lied to any experimental situation where
there is the possibility that the results will Sampling Methodology
Double-blind Trials be affected by conscious or unconscious Sampling methodology is that part of
Double-blind describes an especially bias on the part of the experimenter. statistical practice concerned with the
stringent way of conducting an experi­ selection of individual observations
ment, usually on human subjects, in an Design of RCT intended to yield some knowledge about
attempt to eliminate subjective bias on In health research, various study design a population of concern, especially for
the part of both experimental subjects and options available, with regards to their the purpose of statistical inference.
the experimenters. In most cases, double- hierarchy, from weakest to strongest
blind experiments are held to achieve a design, can be arranged as under:
Population, Sample and
higher standard of scientific rigor. • Case Report
In a double-blind experiment, nei­ • Case Series Sampling Frame (Fig. 31.3)
ther the individuals nor the researchers • Correlational Study Population: Population means people
know which subject belongs to the con­ • Cross-Sectional Study from whom the sample is drawn. There
trol group and the experimental group. • Opinion/KAP Study (health social are five dimensions of population:
Only after all the data have been recorded sciences) • Size, could be infinite or finite
(and in some cases, analyzed) do the • Longitudinal Study • Geographic area
researchers learn, which individuals • Case-control study–observational • Structure that could be either homo­
belong to which group. Performing an anal­­y­tical retrospective studies genous or heterogeneous
experiment in double-blind fashion • Cohort Study • Nature that could be static or dyna­
is a way to lessen the influence of the • Ecologic Study mic
prejudices and unintentional physical • Research on Diagnostic Tests • The time frame.
cues on the results (the placebo effect, • Economic Evaluation Sampling frame: Sampling frame
observer bias, and experimenter’s bias). • Program Evaluation is the list of ultimate sampling entities,
Random assignment of the subject to • Health System Research which may be people, households, orga­
the experimental or control group is a • Experimental Study (trials) nizations or other units of analysis. For
critical part of double-blind research • Systematic Reviews (meta-analysis) example, the list of registered students
design. The key that identifies the • Methodologic Research may be the sampling frame for a survey
subjects and which group they belonged • Hybrid Designs. of the student body at a university. To
Thesis Writing 753

that assures that the different units in Multi-stage or cluster sampling: It is


population have equal probabilities of where the researcher divides the popu­
being chosen. Humans have long prac­ lation into strata, samples the strata, then
ticed various forms of random selection, stratifies the samples and then resamples,
such as picking a name out of a hat, or repeating the process until the ultimate
choosing the short straw. These days, sampling units are selected at the last of
computers are used as the mechanism the hierarchical levels. When the strata
for generating random numbers as the are geographic units, this method is
basis for random selection. sometimes called area sampling. For
Simple random sampling: The sim- instance, at the top level, states may be
plest form of random sampling is called sampled (with sampling proportionate to
simple random sampling. In a simple state population size); then cities may be
random sample of a given size, all such sampled; then schools; then classes; and
Fig. 31.3: Concept of target population or
subsets of the frame are given an equal finally students.
universe, sampling population/frame and
sample probability. Each element of the frame,
thus has an equal probability of selec- Nonprobability sampling
select the representative sample, first tion—the frame is not subdivided or The difference between non-probability
the sampling frame should be prepared partitioned. and probability sampling is that non-
from the population of interest. Stratified sampling: Where the pop- probability sampling does not involve
Sample: Sample is a proportion of ulation embraces a number of distinct random selection and probability sam-
population selected by a pre-decided categories, the frame can be organized pling does. Does that mean that non-
and scientific method (different types by these categories into separate ‘strata.’ probability samples are not representa-
of sampling methods). In other words A sample is then selected from each tive of the population? Not necessarily.
sample is a drawn from a population of ‘stratum’ separately, producing a strati- But it does mean that nonprobability
interest so that by studying the sample fied sample. The two main reasons for samples cannot depend upon the ratio-
the results may fairly be generalized using a stratified sampling design are: nale of probability theory. At least with a
back to the population from which they 1. To ensure that particular groups probabilistic sample, we know the odds
were chosen. within a population are adequately or probability that we have represented
represented in the sample. the population well. Nonprobability
Sampling Methods 2. To improve efficiency by gaining sampling methods can be divided into
Sampling methods can be categorized greater control on the composition two broad types—accidental or purpo-
as: of the sample. In the second case, sive. Most sampling methods are pur-
• Probability or random sampling: major gains in efficiency (either posive in nature because we usually
– Simple random lower sample sizes or higher pre­ approach the sampling problem with a
– Stratified cision) can be achieved by varying specific plan in mind. The most impor-
– Systematic the sampling fraction from stratum tant distinctions among these types of
– Multi-stage/multi-phase to stratum. The sample size is sampling methods are the ones between
– Cluster usually proportional to the relative the different types of purposive sam-
– PPS (population proportional to size of the strata. pling approaches.
size). Systematic sampling: Selecting (say) Accidental, haphazard or conven­
• Non–probability or non-random sam- every 10th name from the telephone direc- ience sampling: One of the most com-
pling: tory is called an every 10th sample, which mon methods of sampling goes under the
– Accidental/haphazard is an example of systematic sampling. It is various titles listed here. The traditional
– Convenience easy to implement and the stratification ‘man on the street’ (of course, now it is
– Purposive—modal instance, ex- induced can make it efficient, but it is es- probably the ‘person on the street’) inter-
pert, quota, heterogeneity, snow- pecially vulnerable to periodicities in the views conducted frequently by television
ball. list. If periodicity is present and the period news programs to get a quick (although
is a multiple of 10, then bias will result. It non-representative) reading of public
Probability sampling is important that the first name chosen is opinion can be included in this category.
A probability sampling method is any not simply the first in the list, but is chosen Purposive sampling: In purposive
method of sampling that utilizes some to be (say) the 7th, where 7 is a random sampling, sampling is done with a
form of random selection. In order integer in the range 1–10-1. Every 10th purpose in mind. Usually would have
to have a random selection method, sampling is especially useful for efficient one or more specific predefined groups
some process or procedure must be set sampling from databases. that we are seeking. For instance, run
754 Important Tips for Postgraduate Students

into people in a mall or on the street men and that you want a total sample the population, it is more important to
who are carrying a clipboard and who size of 100, you will continue sampling under­stand the cause system of which
are stopping various people and asking until you get those percentages and then the population is outcomes and to en-
if they could interview them? Most likely you will stop. So, if you’ve already got sure that all sources of variation are
they are conducting a purposive sample the 40 women for your sample, but not embraced in the frame. Large number
(and most likely they are engaged in the 60 men, you will continue to sample of observations is of no value, if major
market research). men, but even if legitimate women sources of variation are neglected in the
Modal instance sampling: In stati­ respondents come along, you will not study.
stics, the mode is the most frequently sample them because you have already The desired sample size can now
occurring value in a distribution. The ‘met your quota.’ easily be calculated with the help of
most frequent case, or the ‘typical’ Heterogeneity sampling: We sample statistical computer programs, but the
case is sampled. In a lot of informal for heterogeneity, when we want to principles underlying the calculation and
public opinion polls, for instance, they include all opinions or views and we the limitation must be clearly under­stood
interview a ‘typical’ voter. There are a are not concerned about representing by the researcher. To put this in simple
number of problems with this samp­ these views proportionately. Another way, if the sample is too small, even the
ling approach. First, is to identify the term for this is sampling for diversity. In most rigorously executed study may fail
‘typical’ or ‘modal’ case? The modal many brainstorming or nominal group to answer its research question. Study
voter can be a person who is of average processes (including concept mapping), may fail to detect important effects or
age, educational level and income in we would use some form of heterogeneity associations, or may estimate those effects
the population. But, it is not clear that sampling because our primary interest or associations too imprecisely. If the
using the averages of these is the fairest is in getting broad spectrum of ideas, sample is too large, the study will be more
(consider the skewed distribution of not identifying the ‘average’ or ‘modal difficult and costly than necessary, it will
income, for instance). And, how do we instance’ ones. In effect, what we would be waste of resources and may even lead
know that those three variables—age, like to be sampling is not people, but to a loss in accuracy, as it is often more
education, income—are the only or ideas. difficult to maintain high data quality.
event the most relevant for classifying Snowball sampling: In snowball Thus, calculating the precise sample size
the typical voter? What if religion or sampling, you begin by identifying is important in any health research.
ethnicity is an important discriminator? someone who meets the criteria for For calculating the desired sample
Clearly, modal instance sampling is only inclusion in your study. You then ask size before beginning the study, we need
sensible for informal sampling. them to recommend others who they to do exercise in reverse. We have to
Expert sampling: Expert sampling may know meeting the criteria. Altho­ decide beforehand the level of probability
involves the assembling of a sample of ugh this method would hardly lead or uncertainly (allowable error) that
persons with known or demonstrable to representative samples, there are we are willing to accept for the study
experience and expertise in some area. times when it may be the best method and then we find the desired sample
Often, we convene such a sample under available. Snowball sampling is espe­ size to provide that level of statistical
the auspices of a ‘panel of experts’. There cially useful when you are trying to reach significance. For most stu­dies, the level
are actually two reasons you might do populations that are inaccessible or hard of significance is set at 0.05 or 5 percent,
expert sampling. First, because it would to find. For instance, if you are studying it means that accepting the chance of
be the best way to elicit the views of the homeless, you are not likely to find 5 percent of an association that is not
persons who have specific expertise. In good lists of homeless people within a actually there. In general the researcher
this case, expert sampling is essentially specific geographical area. However, if should aim for a lower probability of
just a specific sub-case of purposive you go to that area and identify one or error, when it is particularly important to
sampling. two, you may find that they know very avoid making a false positive statement
Quota sampling: In quota sampling, well who the other homeless people in about the findings.
you select people nonrandomly accor­ their vicinity are and how we can find As discussed earlier in section of
ding to some fixed quota. There are two them. sampling error, the power of study (1β)
types of quota sampling: also depends upon the sample size.
1. Proportional Larger the sample size, higher will be the
Calculating Sample Size (How
2. Nonproportional. statistical power of the study. For most
In proportional quota sampling Much Sample is Needed?) studies, the power is set at 80 percent,
you want to represent the major chara­ Where the frame and population are means that accepting 20 percent chance
cteristics of the population by sampling identical, statistical theory yields ex- of missing a difference or an association
a propor­tional amount of each. For act recommen­dations on sample size. that is actually there.
instance, if you know the population However, where it is not straightfor- The other issue that needs consi­
has 40 percent women and 60 percent ward to define a frame representative of deration for calculating the sample size
Thesis Writing 755

is a prior estimate of the frequency of the • World Medical Assembly Declar­ check the box, if you spend more than
condition under study and the degree of ation (ethical issues) 30 minutes daily, since the last episode
variation in the data. Some information • Guidelines for Clinical Trials on of chest pain?
may be available from the previous studies Pharmaceutical Products in India • Walking
to guide the estimates. If not, it is up to the (MOH, GOI, 2001) • Cycling
researcher to come up with a tentative We have to apply to the Institutional • Jogging
estimate that statistician can use. Ethical Committee for Clearance and • Swimming
The other term we need to under­ only after the approval we can proceed • Racket sports
stand, particularly for calculating sam­ to data collection. • Yoga
ple size of analytical studies, is Effect • Other (specify------------------------).
Size. It refers to the actual size of the DATA COLLECTION: If we wish to study attitude of the
difference observed between the groups respon­dent to a certain statement, we
or the strength of relationship between
TOOLS AND TECHNIQUES may use either Likert Scale (strongly
the variables. The likelihood that a study (METHODS) agree, undecided, disagree or stro­
will be able to detect an association ngly disagree) or Forced Choice Format
between predictor and outcome vari­ Tools (strongly agree, agree, disagree, strongly
able depends upon the magnitude of Much of the data in clinical research is disagree). This format does not allow an
the association we decided to look for. gathered using questionnaires or inter­ undecided answer (Plogar and Thomas
Larger sample size is needed to detect views. A questionnaire or the interview 2000).
smaller differences. The choice of effect schedule is a document designed for If questionnaire or interview sche­
size is difficult and arbitrary, but it must the purpose of seeking specific infor­ dule has to be in local language, then first
be set beforehand and must make a mation from the respondents. The prepare it in English, translate it into local
meaningful difference. term questionnaire is mainly used for language and then again translated it into
In making final estimation of the self-administered document, whereas English. This is usually done to ensure
sample size, factors such as drop outs, the interviews schedules are usually correct translation. A questionnaire must
attrition and loss to follow-up should adminis­tered by interviewer. The self- be pre-tested in a pilot study, before
also be accounted. If the calculated administered questionnaire approach using it in a main study.
sample size is larger than that can be is cheap, less susceptible interviewer For many studies, the validity of the
practically obtained, then we may con­ bias and can be administered by mail, results depends on the quality of these
sider increasing effect size or decrease but there may be high non-response or instruments, therefore is important
the power of study (increase allowable some incomplete responses. to develop the questionnaire or inter­
error) or change the design or give up There are two major formats for de- view schedule correctly to address the
the study. For calculating the sample veloping the questionnaire/interview research question or hypothesis. To
size readers are requested to consult schedule—the open ended and closed develop a good data collection instru­
statistician or refer the WHO manual response types. In closed response ques- ment, we need to consider the following
(Lwanga) after considering the entire tions, the respondent is provided with issues:
perquisite as discussed above. the pre-determined response options. Ask one question at a time: A
Closed ended questions can enhance double-barrelled question asks more
Ethical Issues in Thesis the participant recall. Open ended ques- than one question, making it difficult
Various ethical guidelines are available tions elicit more elaborate responses, to know which part of the question is
to which strict adherence is required. but the researcher required much effort answered.
Main guidelines are: to encode it for data analysis. The open Example: Is the water in your com­
• Guidelines for Institutional Ethics ended questions can pick up unantici- mu­nity contaminated or does it smell?
Committee (ICMR) pated situations. A data collection tools This question is asking two different
• Guidelines for Care and Use of Ani­ can include the both types of questions things, contamination of water and odor
mals in Scientific Research (Indian formats. and do not lead us anywhere. The better
National Science Academy, New way of asking the same thing could be—
Delhi) Example can you drink the water coming out of
• Guidelines for Exchange of Human Open ended question: What physical your faucets without getting diarrhea?
Biological Material for Biomedical activities/sports you undertake daily on Use accessible language: Avoid
Purpose (MOH and FW, GOI) regular basis (at least 30 minutes) since ques­­tions with prolonged jargon that
• GCP-ICH Guidelines last episode of chest pain? may be unfamiliar to the respondents.
• Nuremberg Code (ethical issues) Closed ended question: For each of Example: Do you take any of the
• Helsinki Declaration (ethical issues) the following physical activity/sports, following drugs?
756 Important Tips for Postgraduate Students

• Pain killer may be difficulty in recalling the height. valid/accurate we need to check for
• Anti dyspeptic No option for ‘Can not remember’ and measure­ment, transcription and non-
• Diuretics. the respondent may be forced into sampling errors.
The respondent may not understand inaccurate responses.
the medical terms, in such cases it is A typical questionnaire or interview Reliability
better to ask open ended question to list schedule include following section: Refers to the degree of similarity of in-
names of the current medication. • An introductory statement by the formation obtained when the measure­
Keep questions simple: Use syno­ interviewer to introduce herself/ ment is repeated in the same subject
nyms for longer words. himself and explain the purpose of (consistency), i.e. the data are measured
Example: What is your current the study (study objectives). and collected consistently.
occu­pation, if not currently employed, • The respondents should also be
please put your most recent job? This informed about the confidentiality Precision (Precise)
question is too vague concerning the of their responses. The data have sufficient detail and are
amount of detail required. The question • Sociodemographic questions to coll­ at the appropriate level of detail. The
needs to be very specific, requesting the ect the relevant information about expected change being measured is
organization/firm and exact job title. the background of the respon­dents. greater than the margin of error.
Avoid using biased questions: Bia­ • Factual questions.
sed or leading questions can indicate to • Opinion questions—answering the Timeliness
the respondent that they are expected opinion questions require a reflec­ Data are up-to-date (current) and infor­
to answer in certain way. Leading tion; it is generally easier for the mation is available on time. Perfor­
questions are different from the probe, respondents to answer factual ques­ mance data are available on a frequent
which we used most of the time in in- tions. Putting the factual questions enough basis to regularly inform pro­
depth interview for qualitative research. first serve as a warm up to the opi­ gram management decisions.
Example: Since last episode of chest nion questions.
pain, you undertake walking (at least 30 • Closing statement by the interviewer Integrity
minutes) daily, didn’t you? to thank respondents and wherever The data are protected from deliberate
Yes/No appropriate if she/he wants to bias or manipulation for political or
This question hint’s the respondent provide any additional information. personal reasons.
to answer “Yes”. Reliability of the results obtained
Be specific in wording question: by the questionnaire can be studied by Confidentiality
The more concrete and specific your looking for the internal consistency, Study subjects/participants are assured
wording, the more confident you can be which is the extent to which the different that their data will be maintained accor­
that the question will be answered in the questions related with each others. ding to national and/or international
way you intended. Nowadays this can be done using the standards for data.
Example: Is consumption of Iodine computer programs.
salt useful? This is less specific question.
The appropriate one would be—has
DATA QUALITY (FIG. 31.4)
consumption of iodine salt been useful
in reducing the number of new goitre In any health research the accountability
patients in your community? for results reported is increasingly
Pick up an appropriate number of important as it may have implications
res­ponse choices: The options/choice on either clinical care of patients, or
should be appropriately given. Too few desi­
gning the preventive intervention Fig. 31.4: Valid and reliability of data due
can lead to over simplification of the and influence on the health policy to good quality
issue; whereas too many choices can and programs. Therefore the quality
lead to confusion about and minimize of colle­c­ted data is of utmost important. DATA ANALYSIS AND BASIC
the difference between responses. To ensure the quality data, following BIOSTATISTICS PRINCIPLES
Usually aim for four to five choice issues needs to be looked into:
and offer ‘do not know’ or ‘can not Some measures used in research for
remember’ or ‘Not applicable’, as it may Validity/Accuracy analysis of the health data are:
be needed sometime to avoid inaccurate Refers to the extent to which a measure The list below is not exclusive. There
responses. actually measures what it is meant to are many measures that can be used in
Example: What was your height at measure (accuracy). Valid data are epidemiology and health research for
age 25 years? In such questions there consi­dered accurate. For data to be data analysis. The measures to be used
Thesis Writing 757

depend upon the research question, Broadly two types of statistics can be • Mean
objectives, hypothesis, study design used for analyzing the health data: • Median
and type of data collected. Therefore, • Mode.
it is essential that in the planning stage Descriptive Statistics The mean, the median, and the mode
itself, one should define what measure It summarizes the data by describing are measures of central tendency. The
to be used for analysis. In other words, what was observed in the sample mean is simply an arithmetic average. It
we have to plan the study depending numerically or graphically. is the sum of individual scores divided by
upon the measures that we will be using the number of individuals. The median
in analysis stage. Inferential Statistics is the midpoint measure in a group of
• Numbers of cases Uses patterns in the data to draw measures—half of the observations fall
• Proportional mortality inferences about the population repre­ above the median and half below. The
• Proportional mortality ratio sented, acco­unting for randomness. mode is the most frequently occurring
• Prevalence rates Before moving on the actual data figure in a set of figures. Each of these
• Incidence rates analysis, let us have a look at various statistical measures describes the typical
• Specific prevalence and incidence types to study variables and scales of characteristic or tendency of a group in
rates measurement, because the choice of a slightly different way.
• Standardized rates statistics depends on the type of the
• Standardized ratios variables studied and scale used for Variance in the Data
• Relative risk measuring these variables. Measures of dispersion refer to those
• Odds ratio measures, which describes the spread
• Attributable risks and population Analytic Procedures I or dispersion of data points. These are
attributable risk The purpose of data analysis is to provide as follows:
• Numbers needed to treat and pre­ answers to the research questions being • Range
vent studied. The research question also • Variance—average squared distance
• Number needed to harm dictates the type of data to be collected of any value from its mean
• Relative risk reduction during a study and the type of analyses • Standard deviation—square root of
• Absolute risk reduction to be performed. For almost all studies, variance.
• Life years lost we want to describe what is typical of the Often a researcher is interested
• Disability adjusted life year (DALY) group studied and how the cases differ not only in the average characteristic
• Quality adjusted life year (QALY). from each other. Our measure of what of a group, but also in the variance or
Discussion on each study measures is typical is called the Central Tendency. dispersion within the group, i.e. how
are beyond the scope of this chapter. Our measure of how the cases differ is individuals in a group differ from the
Readers are requested to refer the sug- called the Variance or Dispersion in the average or central tendency of the
gested reading at the end of this chapter. data. group. For example, if the mean age of
Before examining the central tend­ first voluntary HIV testing is 28, what is
Basic Biostatistics ency and variance of data, you must the age range of the group? What is the
Statistics is fundamental to epidemiology first decide on the type of measurement age of the youngest person tested and
and contributes to the majority of studies that you will use. For example, is it more the oldest person tested? A group with
published in the medical literature. It is appropriate to use a median or a mean? a mean of 28 years, but with a range of
essential for anyone studying epidemi­ Can you calculate the variance in the 24 to 30 years at first testing is probably
ology to have an understanding of the data? The type of analytic procedure or quite different from another group with
key statistical principles and methods. measurement that you can apply to a a mean of 28 years, but with age at first
Statistics are most essential to move variable depends on the characteristics testing that range from 15 to 59. The
data (crude information) to knowledge of the variable. term variance is used when researchers
in three steps. First the data becomes measure dispersion around a mean. A
information when they become relevant common statistical measure of variation
to decision problem. In second stage
Central Tendency or within a group is the standard deviation.
information become facts when the Characteristic of the Data This measure gives the average distance
data is summarized into different A measure of central tendency is a cen- of individual measurement observations
characteristics or measures and finally tral value, which describes the distribu- from the group mean. The larger the
in third step facts become knowledge tion of a particular variable in terms of standard deviation, the greater the
when they are used in the successful its location. It is the aggregate measure variation in the individual observations.
completion of the decision process. of the values of a variable: The formulas of some commonly used
758 Important Tips for Postgraduate Students

statistical tests of differences between posi­tive status (positive or negative) or because interval variables do not have
means such as the t test and the F test, sex (male or female). a true zero point. At best, they have
also called the analysis of variance Only very limited statistical mani­ zero points that are set by convention
(ANOVA), use variance estimates pul­
a­tions are possible with nominal or convenience.
to establish whether differences are vari­ables. While examining central ten­ The lack of a true zero point means
statistically significant. dency, we can calculate the mode (the that you cannot calculate ratios with
most frequently occurring number). In interval data. However, you can calculate
Other Measures of Dispersion looking at dispersion, we can calculate all of the measures of central tendency
You can obtain other measures of a percentage or frequency distribution. and dispersion that are allowed with
disper­sion in the data by counting the But we cannot calculate a mean or a nominal and ordinal variables plus the
number of cases in each category. The standard deviation. It makes no sense to mean and standard deviation.
resulting count is called frequency distri­ speak of the ‘mean sexually transmitted
bution. disease,’ or the average distance from Ratio Scale
Variables can be of two types: ‘female.’ Numbers represent magnitude, equal
I. Categorical: interval and an absolute zero point, For
a. Records, such as several groups Ordinal Scale example, number of living children,
or categories to which an indi- Numbers represent the rank order of number of sexual partners, etc.
vidual belongs. If there are two the variable being measured. However As you can see, the characteristics
possible categories we called it these numbers do not represent the of the four measurement scales are
as a binary variable. magnitude of the difference between cumulative. All the statistics that we can
b. Example: Gender, marital status, two subjects, only which one is higher use in analyzing nominal data can be
socioeconomic status (SES), etc. or lower. For examples, disease stages used in analyzing ordinal data, plus we
II. Quantitative: (stage I, stage II, stage III and stage IV). can use additional analyses that cannot
a. Numeric values With ordinal variables, you can use be used with nominal data. Similarly,
b. Example: Age, height, income, all the statistical manipulations appro- all the analyses that you can use with
etc. priate for nominal variables (such as the nominal, ordinal and interval data can
mode and the frequency distribution). also be used with ratio data. In addition,
Classification of Variables Because there is a rank order to the ratio data permits use of additional
Although variables can be characterized numbers, you can also use the median analyses that the lower level of scales
in many ways, for the purposes of data and the percentile. But you cannot use a does not.
analysis we classify variables by a mean, or a standard deviation. It makes
measurement scale. A scale is a rule for no sense to speak about the mean atti- Analytic Procedures II
assigning numbers to objects or events. tude of respondents to condom adver-
The type of scale that characterizes tising. The reason is that the distance Descriptive Statistics
a variable also determines the types or interval between the categories is not All studies should describe the characte­
of analyses or measurements that known. ristics of the group being studied. Basic
can or cannot be performed on that descriptive statistics include fre­quency
variable. The four levels of variable Interval Scale distributions, percentages and percen-
mea­surement are nominal, ordinal, Numbers indicate relative amounts tiles, means and standard deviations,
interval and ratio. of the attribute, also, equal distances and contingency tables (cross-tabula-
between numbers assigned to subjects, tions) (Flow chart 31.7).
Nominal Scale reflect equal differences in the amo­unts
In nominal measurements, the cate­ of the attribute measured. Temper­ Differences within the Data
gories of variables differ from one ature and calendar dates are examples Most often, you want to know whether
another in name only. In other words, of interval variables. For example, the differences between groups or
one category of a variable is not neces­ the difference between the beginning observations can be attributed to the
sarily higher or lower, or greater or of day 1 and the beginning of day intervention or whether they could have
smaller than another category; it is just 2 is 24 hours, just as it is between day occurred by chance alone. The three
different in name. For example, gender, 3 and day 4. With interval variables common significance tests that we will
race, blood types, etc. such as temperature, you can say that discuss are the chi-square (χ2) test,
A special type of nominal variable a temperature of 80°F is 40°F warmer t test and analysis of variance (ANOVA
is a dichotomous variable, which can than a temperature of 40°F. However, or F test).
take only one of two values. Examples an important point is that 80°F cannot All statistical tests of significance
of dichotomous variables include sero­ be said to be twice as warm as 40°F assume that differences are produced
Thesis Writing 759

Flow chart 31.7: Various statistical tests used for data processing with ordinal data and can be used with
ratio data, but it is less powerful than
statistics that make use of the mean and
variance of the data. The chi-square test
is used to determine whether frequency
distributions differ significantly. When
using χ2 you first prepare a cross-tabul­
ation of the variables. The chi-square
test can then be applied to the cross-
tabulation to determine whether there
is a significant difference between distri­
butions.

t Test of Means
The t test is used to determine whether
the difference between two means is
Flow chart 31.8: Correlations between variables statistically Significant. A t test can be
used only with interval or ratio data.

F Test (Analysis of Variance)


The F test, or analysis of variance
(ANOVA) is usually used to determine
whether the difference between three or
more means is significant. We can use
an ANOVA test whenever we do a multi-
ple group experiment. For example, will
peer educators perform better, if they
are given one, two or three days of re-
training? Both t tests and F tests require
interval or ratio data because they use
variance estimates in calculating statis-
tical signifi­cance.
by chance alone. This assumption is of the time. You will be committing a The statistical test and its appli­
called the null hypothesis. The stati­ Type I error when the results of the test cation is shown in Flow chart 31.7.
stical tests tell us the probability that lead you to reject the null hypothesis,
the observed differences could have when in fact the result was due to chance.
Correlations between Variables
occurred by chance. This number is You commit a Type II error, when you
called significance level. The convention accept the null hypothesis, when in fact (See Flow chart 31.8)
for writing the significance level is the intervention did affect the results. In a descriptive study (a design that does
p < followed by the probability that the A small significance level decreases the not include an experimental treatment),
result could have occurred by chance. probability of making a Type I error, but researchers often look for ‘correlations’
Thus, p < 0.05 means that the probability increases the probability of making a between variables to determine whether
that the result is due to chance alone Type II error. A common way to decrease there is an underlying relationship bet­
is less than 1 in 20. By convention, the probability of making a Type II error ween them or whether one factor (for
researchers do not usually reject the is to hold the significance level constant example, age of positive HIV test) is
null hypothesis unless they find p < 0.05. and increase your sample size. related to another (such as years of
Obviously, if you choose a very small A common misconception is that sta- survival) factor. If you have interval
p value for your significance level, you tistically significant also means impor­ or ratio data, you can use Pearson’s
decrease the probability of rejecting the tant. This is not true. correlation coefficient to measure the
null hypothesis. The statistical test also degree of association between the vari­
tells you how often you will be wrong in Chi-Square (χ2) Test ables. When you have ordinal data,
rejecting the null hypothesis. If p < 0.05, The chi-square (χ2) test is the only Spearman’s and Kendall’s rank correl­
you will be wrong 5 percent of the time. If significance test that can be used with ation tests are appropriate for measuring
p < 0.75, you will be wrong three-fourths nominal data. It is also frequently used association.
760 Important Tips for Postgraduate Students

Table 31.3: Choice of statistical test and its purpose the probability that the degree of the
observed relationship is different from 0.
Parametric test Purpose of application Non-parametric Be careful to note that correlation does
equivalent not mean causality. In using correlational
‘t’ test for independent Comparison of two Mann-Whitney ‘U’ test techniques, the researcher needs to keep
samples independent groups in mind that the correlation between two
‘t’ test for paired samples To test the difference between Wilcoxon signed rank test or more variables does not necessarily
paired observations (before
imply that variation in one variable
and after)
causes variation in the other variables.
Analysis of variance Comparison of several groups Kruskal Wallis test
In other words, just because variable A
Pearson’s correlation (r) To quantify the linear Spearman’s rank correction (p) is correlated, associated, or related with
relationship between variable B does not necessarily mean
variables that variable A causes variable B. To use
a silly example, drinking tea is usually
associated with the use of sugar and milk.
Table 31.4: Sample measurement
But tea drinking does not cause sugar and
milk use; rather, it is only associated with
Measurement Examples Appropriate Some appropriate
it. The statistical test and its application is
scale measures of measures of
central tendency comparison and shown in Flow chart 31.8.
and variation association
Nominal Assigning classes like Number of cases Chi-square Choosing the Statistical Test
‘HIV-negative’ or ‘HIV- Mode
Choice of statistical test and its purpose
positive’ to numbers
of application is given in Table 31.3.
Ordinal Median Percentiles Chi-square
Mode Number of Tests of rank order
cases correlation
Scales of Measurement
Interval Mean Standard t test
deviation Median Analysis of variance Table 31.4 shows sample measurements.
Percentiles Mode Pearsons’(r)
Number of cases
Ratio Geometric mean t test Multivariate Analysis
Coefficient of variation Analysis of variance
Unlike the bivariate (only two variables)
Mean Pearson’s(r)
Standard deviation statistical measurements described
Median Percentiles above, multivariate analysis is used to
Mode Number of examine the relationship between more
cases than two variables.
Typically, we are concerned with the
relationships between multiple inde­­pen­
The tests produce numbers called to –1.0), the stronger the relationship or dent variables and a single dependent
correlation coefficients that range from association between the two variables variable. But this is not always the case.
–1.0 to +1.0. When the correlation (for example, a correlation of 0.2 implies Multivariate techniques also exist for
coefficient is negative (i.e. preceded by a a weaker relationship than a correlation exami­ ning the relationship bet­ ween
minus sign), it means that the relationship of 0.7). A correlation coefficient of 0 multiple dependent variables and a
is such that one variable decreases as means that no relationship between the single independent variable, as well
the other increases. In the example two variables exists and a coefficient as multiple independent and multi­
above, a negative correlation would of 1.0 means that the two variables are ple dependent variables. Multi­ vari­
mean that the older people are at age of perfectly related or correlated. Tests ate analysis is sometimes used with
HIV diagnosis, the shorter their survival of significance can be applied to the quasi-experiments and is often used
time and vice versa. If the correlation correlation coefficient. However, ins­tead in descriptive, diagno­stic studies. For
coefficient is positive (preceded by a + of testing the probability that differences example, suppose you complete a
sign), it means that when one variable is between groups could have been the quasi-experiment to determine whether
high, so is the other and that when one result of chance, as is the case in making a training intervention to improve
variable is low, so is the other. The closer comparisons between experimental provider competence results in better
the correlation coefficient is to +1.0 (or groups, measures of asso­ ciation test patient adherence to antiretroviral drug
Thesis Writing 761

treatment regimens. You perform a t test Graphical Presentation particular technique for the analysis
and discover that the patients of providers of Data of the data?
in the training intervention group have • Provide examples of important
significantly better adherence than did Graphical presentation of data gives dummy tables.
the comparison group. In selecting the the reader immediate and overall view/ • Be sure that your plan of analysis
intervention and comparison groups, perspective without having to read each clearly explains how you will meet
you matched the clinics on the type of column/row in a table. all your study objectives, use all your
antiretroviral treatment regime most Some common forms of graphical study variables, and test all your
often used by patients. However, you presentation are given in Figure 31.5. study hypotheses.
did not match the clinics on patient age
or education. When you analyze the Plan of Analysis WRITING THE THESIS/
data, you find that age and education • Describe in detail each of the
DISSERTATION REPORT
differences between groups are statis­ analytical techniques and statistical
tically significant. Our provider training measures you plan to use, indicating
intervention is confounded with patient how each technique and measure
Research Spiral
age and education, which means that will help you meet your study Title
the difference in groups may be due to objectives. What variables will be Indicate the study’s design with a com­
the age or education differences rather involved? Why have you selected a monly used term in the title.
than to the training intervention. In this
situation, you might be able to separate Table 31.5: Multivariate procedures
the effects of client age, education and
provider training by doing a multivariate Measurement Measurement scale of dependent variables
analysis. If the relationship between the scale of Dichotomous Nominal (more Ordinal (more Interval and
intervention and adherence continues independent (two than two than two ratio
variables categories) categories) categories)
to be undimi­nished (statistically signi­
ficant), even when the other two factors Dichotomous, Logistic Multinomial Multinomial Multiple
are held constant, you could conclude nominal and regression logistic logistic regression with
that age and education have little or ordinal regression regression dummy
no influence on adherence and you ordered independent
variables
may attribute the differences between
Interval and ratio Logistic Multinomial Multinomial Multiple
groups to provider training. However,
regression logistic logistic regression
if the relationship between provider regression regression
training and adherence disappears (is ordered
no longer statistically significant), when Mixed Logistic Multinomial Multinomial Multiple
you control for the other two variables, (any regression logistic logistic regression
you must conclude that your interven­ combination regression regression
tion was not successful in improving of measurement ordered
scales)
patient compliance. In addition to deter­­
mining, which independent vari­ ables
are significantly related to a depen­
dent variable, multivariate tech­ niques,
like simple correlations, may also allow
you to measure the strength of the rela­
tionship. There are several multi­variate
techniques. The one you should use
depends, just as with bivariate tech­
niques, on the measurement scale of the
variables.
The five of the more commonly
used multivariate procedures for differ-
ent com­binations of independent and
depen­dent variables.
Table 31.5 shows multivariate proce­
d­ures. Fig. 31.5: Various graphical depictions of data
762 Important Tips for Postgraduate Students

Concise titles are easier to read than the whole document. A number is allo­ • Evaluate the ‘success’ of your pro­
long, convoluted ones. Titles that are cated to a source in the order in which ject.
too short may, however, lack important it is cited in the text. If the source is • Influences your study design, data
information. Readers should be able to referred to again, the same number is collection and interpretation.
easily identify the design that was used used. • Hint: this is usually the last sentence
from the title. An explicit, commonly Example:...as one author has put of the ‘introduction’ section of a
used term for the study design also it ‘the darkest days were still ahead’ journal article.
helps ensure correct indexing of articles [1]: which is well documented in the • Should be clear about whether:
in electronic databases. Title should be literature. [2–5] This proves that ‘the – They call for testing a hypo­
specific, but comprehensive. Should darkest days were still ahead’. [1] The thesis (e.g. ‘we are going to
be short, but should be sufficiently author’s name can also be integrated compare….’).
descriptive. No abbreviations should be into the text, e.g. Scholtz [2] has argued – They call for measuring a quan­
used. that... tity (e.g. we are going to descr­
ibe….’).
Introduction Objectives – Can be created to measure
The Introduction section should descri­ State specific objectives, including any process, impact, outcome.
be, why the study was done and what prespecified hypotheses. Objectives are – May be sorted out as primary
questions and hypotheses it addresses. the detailed aims of the study. Well- and secondary.
It should allow others to understand the crafted objectives specify populations, – Be careful not to get too broad or
study’s context and judge its potential exposures and outcomes and parameters you can lose focus.
contribution to current knowledge. that will be estimated. They may be • M-A/R-S-T is often the best way.
formulated as specific hypotheses or as – Measurable is the most impor-
Background/Rationale questions that the study was designed to tant consideration. You will know
Explaining the scientific background of address. In some situations, objectives that you have achieved your ob-
the study provides important context for may be less specific, e.g. in early disco­ jective.
readers. It sets the stage for the study and very phases. Regardless, the thesis – A non-‘A’ non-‘R’ objective will
describes its focus. It gives an overview of should clearly reflect the investigator’s not get beyond paper (has it been
what is known on a topic and what gaps intentions. For example, if important done before?, other resources?)
in current knowledge are addressed by subgroups or additional analyses were or will have little use.
the study. Background material should not the original aim of the study, but – The devil is in the ‘S’ details—
note recent pertinent studies and any arose during data analysis, they should avoid assumptions and jargon,
systematic reviews of pertinent studies. be described accordingly. Both the define terms, use appropriate
It does not include review and history main and secondary objectives should and understandable language.
of the subject. Does not identify all be clear and any prespecified subgroup – T relates to S, M, and R—provides
the other gaps in knowledge. Does not analyses should be described. a frame-work.
include methods, results and discussion.

Literature Review How to Make and Write Example Objectives


The ‘literature’ means the works con­ Objectives
Study Objectives Examples
sulted in order to understand and Accomplish the following in the study:
investigatin our research problem. A • Be specific (SMART). • Estimating a quantity or burden:
good literature review is an argument • Make use of only one verb (i.e. an – To determine the prevalence of
that is more purposeful than a simple objective is an action and must diabetes among South Indian
review of rele­vant literature. clearly and strongly reflect that). children from 2000 to 2005
How to quote review of literature: • Anybody should get a sense of • Testing a hypothesis/association:
Either square [ ] or curved brackets ( ) your objectives (even if they do not – To estimate the relative frequ­
can be used as long as it is consistent. understand technical terms). ency of iodine deficiency among
Numbers should be inserted to the left • Must be clearly linked to problem poorer people
of colons and semi-colons. Full stops and question. – To estimate the effect of vitamin
are placed either before or after the • Frame the problem in clinical/ A supplementation on cure rates
reference number. Whatever format epidemiological terms. of tuberculosis patients in Peru.
is chosen, it is important that the • Measure outcome, rates, incidence, The Objective should be SMART/
punctuation is consistently applied to mortality, morbidity, etc. RUMBA (Box 31.1).
Thesis Writing 763

Box 31.1: SMART/RUMBA objective main study types, there is an additional sources and methods of case ascertain­
need for clarity. For instance, for a ment and control selection. Give the
S-Specific R-Relevant case-crossover study, 1 of the variants rationale for the choice of cases and
M-Measurable U-Understandable of the case-control design, a succinct controls.
A-Achievable M-Measurable
description of the principles should be Cross-sectional study participants:
R-Relevant/Reliable B-Behavioral
T-Time Bound A-Achievable given. Give the eligibility criteria and the sources
We recommend that investigators and methods of selection of parti­cipants.
refrain from simply calling a study Detailed descriptions of the study
SMART Objective: ‘prospective’ or ‘retrospective’, because participants help examiner/readers un-
• Specific: Specify what you want to these terms are ill defined. We reco­ derstand the applicability of the results.
achieve. Describe a precise outcome mmend that, whenever investi­gators use Investigators usually restrict a study
that is linked to an epi measurement these words, they define what they mean. population by defining clinical, demo-
(rate, prevalence, frequency, etc.) Most importantly, we recom­mend that graphic and other characteristics of
• Measurable: Objective unit that can investigators describe exactly how and eligible participants. Typical eligibility
indicate achievement when data collection took place. criteria relate to age, gender, diagnosis
• Achievable: With a reasonable amo­ and comorbid conditions. Despite their
unt of effort, can this be done? Setting importance, eligibility criteria often are
• Relevant: Appropriate impact, out- Describe the setting, locations and rel­ not reported adequately.
put, products evant dates, including periods of recruit­ Eligibility criteria may be presented as
• Time-bound: Indicates target dates ment, exposure, follow-up and data col­ inclusion and exclusion criteria, although
and study context. lection. this distinction is not always necessary or
Examiner or reader needs infor­ useful. Regardless, we advise authors to
Methodology mation on setting and locations to as- report all eligibility criteria and also to
The methods section should describe sess the context and generalizability of describe the group from which the study
what was planned and what was done a study’s results. Exposures, such as en- population was selected (for example,
in sufficient detail to allow others to vironmental factors and therapies, can the general popu­ lation of a region or
understand the essential aspects of the change over time. Also, study methods country) and the method of recruitment
study, to judge whether the methods may evolve over time. Knowing when a (for example, referral or self-selection
were adequate to provide reliable and study took place and over what period through adver­ti­sements).
valid answers and to assess whether any participants were recruited and followed Knowing details about follow-up
deviations from the original plan were up places the study in historical context procedures, including whether pro­ced­
reasonable. and is important for the interpretation of ures minimized non-response and loss
results. to follow-up and whether the procedures
Study Design Information about setting includes were similar for all parti­cipants, informs
Present key elements of study design early recruitment sites or sources (for ex- judgments about the validity of results.
in the paper. ample, electoral roll, outpatient clinic,
We advise presenting key elements cancer registry or tertiary care center). Variables
of study design early in the methods Information about location may refer Clearly define all outcomes, exposures,
section so that readers can understand to the hospitals or practices where the predictors, potential confounders and
the basics of the study. For example, investigation took place. We advise stat- effect modifiers. Give diagnostic criteria,
authors should indicate that the study ing dates rather than only describing the if applicable.
was a cohort study, which followed length of time periods. There may be dif- Disease outcomes require adequately
people over a particular time period ferent sets of dates for exposure, disease detailed des­ cription of the diagnostic
and describe the group of persons that occurrence, recruitment beginn­ing and criteria. This applies to criteria for cases
comprised the cohort and their exposure end of follow-up and data collection. in a case-control study, disease events
status. Similarly, if the investigation used during follow-up in a cohort study, and
a case-control design, the cases and Participants prevalent disease in a cross-sectional
controls and their source population Cohort study participants: Give the study. Clear definitions and steps taken to
should be described. If the study was a eligibility criteria and the sources and adhere to them are particularly important
cross-sectional survey, the population methods of selection of participants. for any disease condition of primary
and the point in time at which the cross- Describe methods of follow-up. interest in the study.
section was taken should be mentioned. Case–control study participants: Data sources/measurement: For
When a study is a variant of the three Give the eligibility criteria and the each variable of interest, give sources of
764 Important Tips for Postgraduate Students

data and details of methods of assess- • No reference of standard methods otherwise require a lengthy description,
ment (measurement). Describe compa- • No reference of manufacturer’s as in the example above. The diagram
rability of assessment methods, if there instru­ctions may usefully include the main results,
is more than one group. • No approval of Insti­tutional Ethical such as the number of events for the
Committee primary outcome. While, we recom­
Bias • Not taking consent mend the use of a flow diagram, parti­
Describe any efforts to address potential • Not using corrective abbreviations cularly for complex observational stu­
sources of bias. and SI units dies, we do not propose a specific format
Biased studies produce results that • Missing essential details for the diagram.
differ systematically from the truth. • Use of lab jargon
It is important for a reader to know • Incorrect word usage Discussion
what measures were taken during • No mechanism of data quality checks The discussion section addresses the
the conduct of a study to reduce the • No confidentiality of the information. central issues of validity and meaning
potential of bias. Ideally, investigators of the study. Surveys have found that
carefully consi­der potential sources of Statistical Methods discussion sections are often dominated
bias when they plan their study. At the Describe statistical methods with by incomplete or biased assessments of
stage of reporting, we recommend that enough detail to enable a knowledgeable the study’s results and their implications
authors always assess the likelihood of reader with access to the original data to and rhetoric supporting the authors’
relevant biases. Specifically, the direc­ verify the reported results. When possi- find­ings. Structuring the discussion
tion and magnitude of bias should be ble, quantify findings and present them may help authors avoid unwarranted
discussed and if possible, estimated. with appropriate indicators of measure- speculation and over interpretation of
For instance, in case-control studies, ment error or uncertainty (such as con- results, while guiding readers through
information bias can occur, but may fidence intervals). Avoid relying solely the text. Investigators structure the discu­
be reduced by selecting an appropriate on statistical hypothesis testing, such as ssion section by presenting the following:
control group. p values, which fail to convey important • A brief synopsis of the key findings
information about effect size. References • Consideration of possible mech­
Study Size for the design of the study and statistical anisms and explanations
Explain how the study size was arrived methods should be to standard works • Comparison with relevant findings
at. when possible (with pages stated). De- from other published studies
A study should be large enough to fine statistical terms, abbreviations and • Limitations of the study
obtain a point estimate with a suffi­ most symbols. Specify the computer • Brief section that summarizes the
ciently narrow confidence interval to software used. implications of the work for practice
meaningfully answer a research ques- and research.
tion. Large samples are needed to dis- Results
tinguish a small association from no as- The Results section should give a factual Key Points
sociation. Small studies often provide account of what was found, from the • Past tense
valuable information, but wide confi- recruitment of study participants, the • Focus, then discuss the bigger picture
dence intervals may indicate that they description of the study population, to • Be critical of the literature
contribute less to current knowledge the main results and ancillary analyses. • Be specific in pointing out where
in comparison with studies providing It should be free of interpretations and further gaps in knowledge can
estimates with narrower confidence discursive text reflecting the author’s be fulfilled instead of just writing
intervals. Also, small studies that show views and opinions. ‘further research is needed’
‘interesting’ or ‘statistically significant’ • What gaps in knowledge remain to
associations are published more fre- Participants be filled?
quently than small studies that do not Report the numbers of individuals at • Only mention previous results or
have ‘significant’ findings. While, these each stage of the study, e.g. numbers pot­ comments, which illuminate or
studies may provide an early signal in entially eligible, examined for eligi­bility, which are illuminated by the present
the context of discovery, readers should confirmed eligible, included in the study, results.
be informed of their potential weak- completing follow-up and analyzed. • Final paragraph in which the mess­
nesses. Give reasons for non-participation at age of the article is firmly stated.
each stage.
While Writing Methodology— Consider use of a flow diagram. Discussion—Common Mistakes
Common Mistakes An informative and well-struc­tured • Repetition—introduction and results.
• Grammar not consistent flow diagram can readily and trans­ • Lack of organization, no logical flow
• Do not follow a logical order parently convey information that might • Not addressing the key points.
Thesis Writing 765

Summary those enrolled in the study with regard sis statement? Leave a final impres­sion on
Summarize key results with reference to to age, sex, ethnicity, severity of disease the reader. Summarize new obser­vations,
study objectives. and comorbid conditions? Are the nature new interpretations and new insights
It is good practice to begin the discu­ and level of exposures comparable and that have resulted from the present work.
ssion with a short summary of the main the definitions of outcomes relevant to Include the broader implications of your
findings of the study. The short summa- another setting or population? Are data results. Do not repeat word for word from
ry reminds readers of the main findings that were collected in longitudinal studies introduction or discussion.
and may help them assess whether the many years ago still relevant today? Are
subsequent interpretation and implica- results from health services research in Recommendations
tions offered by the authors are support- one country applicable to health systems Remedial action to solve the problem.
ed by the findings. in other countries? Write in brief of further research to fill in
The question of whether the results gaps in our understanding and specify in
Limitations of a study have external validity is often a which directions for future investigations
Discuss limitations of the study, taking matter of judgment that depends on the on the topic or related topics is needed.
into account sources of potential bias or study setting, the characteristics of the Investigators should suggest ways in
imprecision. Discuss both direction and participants, the exposures examined which subsequent research can improve
magnitude of any potential bias. and the outcomes assessed. Thus, it is on their studies rather than blandly
The identification and discussion of crucial that authors provide readers with stating ‘more research is needed’.
the limitations of a study are an essential adequate information about the setting
part of scientific reporting. It is impor- and locations, eligibility criteria, the Bibliography
tant not only to identify the sources of exposures and how they were measured, It should be written as per the guidelines
bias and confounding that could have the definition of outcomes and the set by the university. Follow the men­
affected results, but also to discuss the period of recruitment and follow-up. tioned order. Authors (use et al. after
relative importance of different biases, The degree of non-participation and the 6 authors, if there are more than six
including the likely direction and magni- proportion of unexposed participants authors, complete names should not be
tude of any potential bias. in whom the outcome develops are also written). Article title (should be exact
relevant. Knowledge of the absolute risk as existing). Journal name (should be
Interpretation and prevalence of the exposure, which in standard PubMed abbreviations, full
Give a cautious overall interpretation will often vary across populations, are journal name should not be written).
considering objectives, limitations, multi­ helpful when applying results to other Year, Volume, Page numbers (325–327
plicity of analyses, results from similar settings and populations. to be written as 325–27) (Fig. 31.6).
studies and other relevant evidence. Example: As shown in Fig. 31.6.
The heart of the discussion section is Conclusion Use full internet resources for how to
the interpretation of a study’s results. Over- Refer back to Research Question posed write references:
interpretation is common and human; and describe the conclusions that you • http://www.nlm.nih.gov/bsd/uni­
even when we try hard to give an objective reached from carrying out this inve­ form_requirements.html
assessment, reviewers often rightly point stigation. Stress the importance of the the­ • http://www.icmje.org/
out that we went too far in some respects.
When interpreting results, authors should
consider the nature of the study on the
discovery to verification continuum and
potential sources of bias, including loss to
follow-up and nonparticipation.

Generalizability
Discuss the generalizability (external
validity) of the study results.
Generalizability, also called external
validity or applicability, is the extent to
which the results of a study can be applied
to other circumstances. There is no external
validity per se; the term is meaningful only
with regard to clearly specified conditions.
Can results be applied to an individual,
groups, or populations that differ from Fig. 31.6: Bibliographic method for journal article
766 Important Tips for Postgraduate Students

Appendices 11. Freedman B. Equipoise and the ethics 23. Leon Gordis. Epidemiology. 5th edition.
• The study questionnaire of clinical research. N Engl J Med. Philadelphia: Pennsylvania; 2013.
• The informed consent form 1987;317:141-5. 24. Lilienfeld AM. Foundations of Epide­
• A copy of the approval from the 12. Greenland S, Neutra R. Control of miology. New York: Oxford University
Insti­tu­tional Review Board. confounding in the assessment of Press; 1976.
medical technology. International 25. Lohr SL. Design Effects (Chapter 7.5).
Journal of Epidemiology. 1980;9:361-7. Sampling: Design and Analysis. Pacific
Dissemination and Utilization
13. Greenland S. Randomization, statistics, Grove: Duxbury Press. 1999.
of Research Findings and causal inference. Epidemiology. 26. MacMahon B, Trichopoulos D. Epid­
• The utilization of research results is 1990;1:421-9. emiology, principles and methods. 2nd
the goal of every research. 14. Guyatt G, Rennie D. User’s guide ed. Boston: Little, Brown and Co.; 1996.
to medical research: a manual for p. 81.
evidence based clinical practice. 3rd ed. 27. Maldonado G, Greenland S. Simul­
BIBLIOGRAPHY
Chicago (IL): AMA Press Printing; 2002. ation study of confounder-selection
1. Als-Nielsen B, Chen W, Gluud C, 15. Hanson BP. Designing, conducting and strategies. American Journal of Epide­
Kjaergard LL. Association of funding reporting clinical research. A step by m­iology. 1993;138:923-36.
and conclusions in randomized drug step approach. Injury 2006;37:583-94. 28. Miettinen OS. Theoretical Epidemio­
trials: a reflection of treatment effect or 16. Haynes RB, Sackett DL, Guyatt GH, logy: principles of occurrence research
adverse events? JAMA. 2003;290:921-8. et al. Clinical epidemiology: how to do in medicine. New York: Wiley; 1985.
2. Altman DG, De Stavola BL, Love SB, clinical practice research. 3rd ed. New 29. Mullner M, Matthews H, Altman DG.
Stepniewska KA. Review of survival York (NY): Lippincott Williams and Repor­ ting on statistical methods to
analyses published in cancer journals. Wilkins; 2007. adjust for confounding: a cross-secti­onal
Br J Cancer. 1995;72:511-8. 17. Hulley S, Cummings S, Browner W, survey. Ann Intern Med. 2002;136:122-6.
3. Altman DG. Categorizing continuous et al. Designing clinical research. 30. Olson SH, Voigt LF, Begg CB, Weiss NS.
variables. In: Armitage P, Colton T, 3rd ed. Philadelphia (PA): Lippincott Reporting participation in case-control
editors. Encyclopedia of biostatistics. Williams and Wilkins; 2007. studies. Epidemiology. 2002;13:123-6.
2nd ed. Chichester: John Wiley; 2005. 18. International Committee of Medical 31. Pocock SJ, Collier TJ, Dandreo KJ,
4. Black N, Brazier J, Fitzpatrick R, Journal Editors (ICMJE). Uniform req­­ et al. Issues in the reporting of epide­
and Reeve B. (Eds). Health Services uire­­ments for manuscripts sub­mit­ miological studies: a survey of recent
Research Methods. A Guide to Best ted to biomedical journals. Electr­onic practice. BMJ. 2004;329:883.
Practice. London: BMJ Publishing; 1998. version updated February 2006, avail­ 32. Rigby AS, Vail A. Statistical methods
5. Bland JM, Altman DG. One and two able at http://www.icmje.org. The New in epidemiology. II: A commonsense
sided tests of significance. BMJ 1994; England Journal of Medicine 1997;336: approach to sample size estimation.
309:248. 309-15. Disabil Rehabil. 1998;20:405-10.
6. Brian Haynes R. Forming research 19. Jan Jonker, Bartjan Pennink. The Ess­ 33. Robins JM. Data, design, and back­
questions. J Clin Epidemiol. 2006;59: ence of Research Methodology A Con­ ground knowledge in etiologic infer­
881-6. cise Guide for Master and PhD Stud­ ence. Epidemiology. 2001;12:313-20.
7. Carlin JB, Doyle LW. Sample size. J ents in Management Science. Springer 34. Rothman KJ, Greenland S, Lash TL.
Paediatr Child Health. 2002;38:300-4. Heidel­ berg Dordrecht London, New Modern Epidemiology, 3rd edition.
8. Dales LG, Ury HK. An improper use York; 2010. Philadelphia, PA: Lippincott, Williams
of statistical significance testing in 20. Jenicek M. Clinical Case Reporting. and Wilkins; 2008.
studying covariables. International Evidence-Based Medicine. Oxford: 35. Rothman KJ, Greenland S. Precision
Journal of Epidemiology. 1978;7:373-5. Butt­er­worth-Heinemann; 1999; p. 117. and Validity in Epidemiologic Studies.
9. Fisher, Andrew A. Designing HIV/AIDS 21. Krimsky S, Rothenberg LS. Conflict of In: Rothman KJ, Greenland S (Eds).
intervention studies: an operations interest policies in science and medical Modern epidemiology, 2nd edition.
research handbook/Andrew. Popul­at­ journals: editorial practices and author Lip­pincott Raven; 1998.pp. 120-5.
ion Council. New York, Washing­ton, disclosures. Sci Eng Ethics. 2001;7:205- 36. Rothman KJ, Greenland S. Types of
DC; 2002. 18. Epidemiologic Studies. In: Rothman
10. Fisher CG, Wood KB. Introduction 22. Last JM. A Dictionary of Epidemiology. KJ, Greenland S (Eds). Modern Epi­
to and techniques of evidence based 4th edition. New York: Oxford de­­
miology. 2nd edition. Lippincott
medicine. Spine 2007;32(Suppl): S66-72. University Press; 2000. Raven; 1998. pp. 74-5.
Thesis Writing 767

37. Sackett D, Strauss S, Richardson man­datory and mystical. Lancet. 2005; 43. Vandenbroucke JP. Prospective or
W, et al. Evidence-based medicine: 365:1348-53. retrospective: what’s in a name? BMJ.
how to practice and teach evidence- 40. Taubes G. Epidemiology faces its 1991;302:249-50.
based medicine. 2nd ed. Edinburgh limits. Science. 1995;269:164-9. 44. Von Elm E, Altman D, Egger M, Pocock
(UK): Churchill Livingstone; 2000. 41. Temple R. Meta-analysis and epidemio­ S, Gøtzsche PC, Vandenbroucke JP.
38. Schulz KF, Grimes DA. Case-control logic studies in drug development and The Strengthening the Reporting
studies: research in reverse. Lancet. postmarketing surveillance. JAMA. of Observational Studies in
2002;359:431-4. 1999; 281:841-4. Epidemiology (STROBE) Statement:
39. Schulz KF, Grimes DA. Sample size 42. Vandenbroucke JP. In defense of case guidelines for reporting observational
calculations in randomised trials: reports and case series. Annals of studies. Epid­em­iology. 2007;18:800-
Internal Medicine. 2001;134:330-4. 804.
32 Seminar and Journal
Club Presentation
Borle Rajiv M

allied reading is very important at the through the ability to present. The goal
Introduction postgraduate level for better under- of the two modalities are different. The
standing. For example, if a patient is presen­tation apart from the depth of
There is a significant difference between admitted in the ward and it is presented the reading done by the presenter, will
the level of the undergraduate (UG) and by the postgraduate student during the also test his communication skill, abil-
postgraduate (PG) training. Although clinical case discussion or if the case is ity to condense a vast topic in to a small
most of the topics that are covered in to be operated all the details of the pre- time bound presentation without miss-
the curriculum are same, the length senting pathology along with treatment ing out the key points, understanding
and depth at which they are required modalities and operative procedure of the basics, capability to organize the
to be studied at the postgraduate level must be read. While performing any presentation for better understanding
are different. The topics taught in a bedside procedure or even during the and effectiveness for audience and skill
didactic manner at the undergraduate monitoring of the cases postoperatively of being able to summarize the topic.
level are required to be studied by the all details pertaining to procedures and The ability to answer the accrued ques-
postgraduate student himself in greater allied literature must read and under- tions out of the presentation is another
depth. As the postgraduate student is stood. If a drug is prescribed to the aspect, which highlights the present-
already sensitized to these topics dur- patient the pharmacological properties, er’s under­standing of the subject. This
ing the undergraduate level, and it is actions, indications, adverse reactions, aspect is vital as the current postgradu-
expected that the knowledge should get and precautions must be read. This is ate student is the teacher of the future
consolidated. The student should under- a very sound habit of augmenting the and thus, inculcating these skills in the
stand the subject rather than reading it knowledge as simultaneously the clini- student is imperative. The postgraduate
only as the things which are understood cal exposure is also gained, which pro- training is not restricted to just acquir-
are seldom forgotten. It means that the vides better insight in the subject and ing information, but, the student should
learner should not only gather informa- consolidates the knowledge. The UG be able to implement this knowledge in
tion or should get structured training, but student is expected to acquire the basic clinical practice and for the same should
he should know the reasoning, should be understanding through the textbooks, acquire matchable skills and he should
able to analyze on the basis of evidence, but the objective of postgraduate train- be able to communicate the acquired
think and articulate the subject. He ing is not served until the other sources knowledge in the most effective way.
should develop ability to take decision of information like journals, internet, The good presentation is not always
and make appropriate alterations in the attending continuing medical educa- a result of individual brilliance nor it is
treatment plan as per the situation and tion programs and workshops are also accidental. A scientific planning, repeat-
condition of patient. He should develop utilized. After acquiring the informa- ed practice and learning by imitating the
ability for lifelong learning. In nutshell tion the post­graduate student should good presenters can enhance the aver-
the student should be “Educated” and be able to interpret, organize, apply age skills of the beginner, to make him/
not only trained. The training at the post- and present the same information in a her more accom­ plished presenter in
graduate level is guided or supervised systematic manner. There can be two due course of time. The purpose of this
learning. It requires initiative on part ways of evaluating the theoretical acu- chapter is to give few important tips to
of the student. The didactic component men of the postgraduate student, the the budding postgraduate students, to
of training at the postgraduate level is first is through the formative and sum- enhance their abilities to make an effec-
marginal. The incidental learning and mative examinations and the second is tive scientific presentation.
Seminar and Journal Club Presentation 769

students is required. The topic should should be selected. For example, rather
Seminar
be based on the level of the training the than selecting straight forward topics like
postgraduate student is going through odontogenic cyst or tumors, topic like
Definitions (i.e. whether he/she is junior, senior or differential diagnosis of multi­ loculated
A seminar can be defined as: the chief resident). For example, if the lesions of the jaw be given to make it more
“Any meeting for exchanging infor­ presenter is the junior resident he should interesting. As it is not straightforward,
mation and holding discussions”. be given topics based on the basic sci- the presenter will have to refer wider
Or ences. It is irrelevant for the junior resi- literature to search for such pathologies,
“A course or subject of advanced dent to straight away talk on the treat- their salient features so as to discuss
students”. ment modalities, alternative techniques differential diagnosis. In case of topics
Or of management or the cur­rent advances. that require multidisciplinary approach,
“A small group of students, engaged It is also desirable to distribute the topic the concerned specialties should also
in advanced study and original research amongst 2 to 3 postgraduate students, be involved. One must remember that
under a member of faculty and meeting according to the level of training of the the horizons of the knowledge are so
regularly to exchange information and residents so that the junior resident wide, that they can­not be restricted in
hold discussions”. talks about basic sciences, senior resi- small water tight compartments. As the
Or dent talks about the clinical features and knowledge has no barriers, the student
“A class held for advanced studies in management and the chief resident talks and teacher also do not have any barrier.
which students meet regularly to discuss about complications and their man- Any input from any body if enhances,
original research, under the guidance of agement along with recent advances to the quality must be accepted with open
a professor”. make the presentation complete. mind. There should be a good example of
Or It is desirable to talk about common horizontal and vertical integration.
“A meeting held for the exchange topics first than talking about rare, but
of useful information by members of a important topics. Look at the phrase Purpose
common business community’. ‘bread and butter’ or ‘cake and icing’, it The purpose of the seminar activities
If we look at the definition of the means bread or the cake (common) has at the postgraduate level have already
seminar a few key words catch our at- to be first and then the luxury of butter been discussed earlier. They can be
tention like ‘exchange of information’, or icing (rarities). This is a practical summarized as:
‘discussion’, ‘guidance of professor’. approach, as the common topics are not • No didactic teaching at the post­
These terms are self-explanatory and only routinely required in the clinical graduate level
it can be easily gathered that it is not a practice, but are also commonly asked • Requires own efforts under guidance
mere speech or a didactic activity, it has in the examination by majority of the • To know the topic in a broader sense
a dimension of interactiveness. It means examiners. Hence, it also serves the pur­ • To learn to search literature
that both the presenter and audience pose of preparing the student for the • To compile the literature
must be equally prepared for free flow- examination. • To analyze the literature
ing discussion and interaction to give However, advances are equally • To develop understanding and con­
completeness to this activity. The other important. The common topics fall in cept.
dimension is ‘guided’ by the teacher. the category of ‘must know’ and the
The teacher has a vital role to play. He advanced topics fall in the category of Topic Elaboration
should ensure that the set objectives of ‘desirable to know’ or ‘nice to know’ cat- Once the topic is identified for the pre-
the seminar are met with; the student is egory. Hence, any presentation should sentation/seminar, it needs to be elabo-
not missing vital points and not deviat- be a good blend of basics and advances, rated in the systematic way. Haphazard
ing from the objectives. A beginner will however the degree of emphasis may presentations may cover lot of things,
always require this guidance until he vary depending upon the level of the but loose its impact as the communica-
gains that maturity. training of the presenter and the level of tion value is poor and generate negative
the audience. impact. It must be remembered that all
Guidance for Seminar While selecting the topics for the the aspects pertaining to the topic must
seminars, it must be ensured that wider be covered. The degree of emphasis on
Topic Selection coverage of topics is made, so as to com- certain areas may be more or less, de-
The selection of the topic is essential for plete the entire curriculum in a phased pending upon the purpose of presenta-
a meaningful activity. It should be based manner rather than sticking to the same tion, time limits, level of audience. Any
on the relevance of the topic to the pre- areas. presentation that is too lengthy, loses its
senter and the audience. At a postgradu- Apart from the standard topics some impact. An ideal seminar should be con-
ate level step by step grooming of the innovative, thought provoking topics structed under the following headings:
770 Important Tips for Postgraduate Students

• Introduction: Should spell out the • To practice: As the final draft is information and many important
outline of the topic and the objec- made it is necessary to practice the points on a single slide. It looses
tives of presentation presentation. ‘Practice makes a man the focus of the audience and the
• Historical aspects perfect’ holds true. The practice presenter as well. The information
• Brief review covering wider areas should be done as follows: may be added verbally.
• Controversies – First practice yourself with time • Amount of information per slide—
• Current advances limit and audit. less the better: The large amount of
• Summary – Then in front of friendly audi- information on single slide has the
• Bibliography. ence. same drawbacks as the preceding
– Then again yourself. point. In addition to that more the
Contents The practice will make the pre­ lines and more the words per line,
The contents of the seminars should be senter well versed with the topic, smaller becomes the font. The slide
enriched using wider sources of litera- contents of the presentation, sequ­ appears staggering due to packed
ture such as: ence of points and provide insight information and the focus is lost. It is
• Books (lesser) as to what to speak for each slide. better that each slide has 4 to 6 lines
• Journals It also brings about fluency in and each line has 4 to 6 words. The
• Internet. presentation and facilitates time best way is to elaborate the points by
The bibliography given at the end of auditing. It is always better if the speaking (Fig. 32.1).
the seminar should be able to depict the slides have only key points and the • Number of slides, less minutes
quantum of efforts done by the presenter elaboration is done by the presenter you speak: The time frame of the
in preparation of the seminar. It also in his own words in an extempore presentation must be taken into
validates the information incorporated manner. Practice will facilitate this, account. Too lengthy presentations
in the seminar. The seminar would as every individual may not be good are often less effective and unable
never be capable of causing cognigible at extempore manner and may to generate the desired impact. It is
impact, unless it is prepared with lot struggle to find effective and appro­ an established fact that the audience
of involvement and effort. It is simply priate words on time. rapport cannot be obtained beyond
governed by the old quote ‘no pain no • Emphasis on important areas: A 45 minutes. On an average in 1 min­
gain’. presenter must identify important ute not more than two slides can
or key areas of the presentation and be presented by an experienced
Presentation lay more emphasis on them rather and established speaker and for a
• To discuss with the concerned than wasting time on discussing the beginner, this ratio is even more
teacher: Once the topic is allotted issues, which are not so vital. critical and he/she may require
it must be discussed with the con- • Tell the objectives first: more than 1 minute and hence the
cerned teacher, so as to formulate – A talk is not a mystery novel slides should be less in number than
the objec­ tives and make the out- Before starting the presentation the minutes for which you speak.
line of the presentation. The infor- always spell out the contents and • Slides with best contrast (light fore-
mation can be searched, compiled objectives rather than starting and ground and dark background):
and organized under appropriate ending abruptly. The color scheme and contrast is
heads. Once the rough draft is made • One major point per slide—you can very important. What appears good
it should be again discussed with the always add the points verbally: Do on the screen of the computer may
concerned teacher and then the nec- not flood your slides with too much not look good on projection. The
essary editing (additions, deletions
be made). The final draft should be
approved by the teacher before it is
taken up for the presentation.
• To be prepared well in advance:
It is a good practice to prepare the
seminar well in advance, so that you
get plenty of time for practice and
refinement. Rushing at the eleventh
hour reflects poor practice, lack
of commitment/involvement and
a casual attitude. Anything done
half-heartedly is never going to be Correct Incorrect
effective. Fig. 32.1: Correct and incorrect way of making a powerpoint slide
Seminar and Journal Club Presentation 771

Fig. 32.2: Dark background and faint Fig. 32.3: Dot not make slides unnecessarily colorful. Only matter to be highlighted can
foreground is easy to read be of separate color

scientific presentation should be illustrations as-long-as they serve the monotony should be avoided. A pause
sober. The impact is created by desired purpose. The general guidelines at the right place, when important
contents and quality of presentation for use of diagrams and illustrations are: diagrams or clinical photographs are
and not by the flashy slides devoid • No imitation for use projected and ability to brush through
of substance. The slides should be • Preferably self-designed through your less important points is real test of the
soothening to eyes and easy to read. own imagination rather than copied skill. Some people are gifted, but those
Usually the dark backgrounds and • Use sketches along with the photo- who are not can always acquire these
faint foreground (letters) is preferred graphs or book diagrams skills by practice. The positive body
(Fig. 32.2). • Maintain originality language is generally an out come of
• Do not use more colors than is • Use of computer animations. confidence generated within you as a
needed to be effective: Flashy color result of thorough knowledge of the
schemes and designs do not add Audience Rapport subject. Few important tips to engage
to the value of the presentation. It The involvement of the audience is the audience are as follows:
should have minimum required color equally important as is the involvement • Engage the audience—make eye
scheme. The colors are very effective of the presenter. It is an art to involve the contact, but do not linger on one per-
means of communication provided audience in your presentation. Presenters son
that they are used judiciously. Rather would appreciate undivided attention • Use humor, but do not force it
than making the entire presentation and less interruptions. Primarily the • Be spontaneous in your humor punch
use different colors to highlight the presentation should be rich in contents. and talk
salient features of key points, only it Secondly the effective communication • Be a good story teller.
will create more impact. Red, pink skill should be demonstrated by way
and other shades of the red appear of body language, command over the Conclusions
clear on the computer screen, but are language and speed of presentation, After the presentation the presenter
hard to see when projected (Fig. 32.3). accent and clarity of pronunciation. should be able to generate a summary
• Font size preferably more than Rushed speed of presentation is not well or conclusion of the presentation in
24 pt: Too small font size is not conceived by the audience and similarly the condensed manner. Similarly the
easily visible especially when it is
presented before large gathering.
It is desirable to have a font size of
greater than 24. Similarly the font
pattern should be simple and easy
to read for establishing an effective
communication (Fig. 32.4).

Diagrams
The illustrations and diagrams should
be liberally used in the presentation
provided, that they are relevant and able
to simplify and explain the subject. There Proper Improper
is no upper limit for use of diagrams or Fig. 32.4: Font type should be easy to read
772 Important Tips for Postgraduate Students

presenter should be able to deliver the preparation of the presenter. When ever might lead to new research or to new ap-
take home message out of the presen­ a question is asked take a pause, think plications.
tation. and compose your answer, so that you Journal clubs are also used in the
are to the point and precise. education of graduate or professional
Role of Audience students. These help make the student
The seminar activity should be inte­ractive Journal Club become more familiar with the adva­
in nature and not like monologue. The nced literature in their new field of study.
role of audience is also very important,
Presentation In addition, these journal clubs help
they should not be only passive listeners, Another important aspect of the post- improve the student’s skills of under­
but their active participation in the graduate training is a journal club activ- standing and debating current topics
seminar is very important. The semi­ ity. The purpose of this activity is ‘criti- of active interest in their field. This
nars are always mutually beneficial. The cal appraisal’ and ‘analysis of an article’. type of journal club may sometimes be
presenter gets an opportunity to study The primary goal of journal club is to taken for credit. Research laboratories
the topic in depth and the audience improve the resident’s ability to criti- may also organize journals clubs for
gets readymade information. The topic cally evaluate the medical literature and all researchers in the lab to help them
needs to be discussed threadbare, which how it applies to clinical practice. keep up with the literature produced by
is not possible without active involve­ The earliest references to a journal others who work in their field.
ment of the audience. It is therefore club is found in a book of memoirs and
necessary for the audience also to letters by the late Sir James Paget, a Selection of Article
come prepared with the given topic. British surgeon, who describes a group for Journal Club
The topic for presentation must be at St. Bartholomew’s hospital in London The article that are selected for the
informed to other participants well in in the mid-19th century as “a kind of journal club must not be routine case
advance to facilitate them to prepare club—a small room over a baker’s shop reports, rather they should be the arti­
the topic. The audience should not ask near the Hospital-gate where we could cles generated out of:
questions just for the sake of asking, sit and read the journals.”1 • Structured scientific studies
but the quality of questions should be Sir William Osler established the • Innovative ideas
such that they should throw light on first formalized journal club at McGill • Modification of techniques
the unaddressed, unexplained areas or University in Montreal in 1875. The • Thought provoking
should help in bringing completeness to original purpose of Osler’s journal club • Topics, which are rare and not includ-
the discussion. The audience can share was ‘for the purchase and distribution of ed in routine curricular activities.
any added information if the presenter periodicals to which he could ill afford
has missed that during the presentation. to subscribe.’2 Presentation of the
The criticism if any must be constructive A journal club is a group of indi- Journal Club
and logical. The levels of the audience viduals who meet regularly to critically The journal club activity is not a group
are variable, some are beginners and evaluate recent articles in scientific lit- reading of an article, but it is the critical
some are established and accomplished erature. Journal clubs are usually orga- appraisal of a study. The entire text of
people. nized around a defined subject in basic the article must not be projected on
or applied research. For example, the the screen, but the article should be
Anticipate Questions application of evidence-based medicine presented in the form of a condensed
While preparing for the seminar, think if to some area of medical practice can be powerpoint presentation. This appro­
you were on the other side of the table, facilitated by a journal club. Typically, ach enhances the ability of the trainee
anticipate questions that are likely to be each participant can voice their view to critically read, summarize, pickup
asked by the audience and be prepared relating to several questions such as the important key areas of the study.
with the answers. The testimony of com- appropriateness of the re­search design, The hard copy of the article may
pleteness of preparation of the topic lies the statistics employed, the appropriate- be kept handy for any reference, if
in the ability of the presenter to answer ness of the controls that were used, etc. needed. There should be a structured,
the questions asked by the audience. There might be an attempt to synthesize chronological, analytical approach in
The level of the questions asked by them together the results of several papers, the presentation.
is also variable for example the begin- even if some of these results might first The presentation of the article should
ners tend to either keep quiet or ask very appear to contradict each other. Even if include:
basic things, but the more accomplished the results of the study are seen as val- • Brief background of the study
people like teachers may ask advanced id, there might be a discussion of how – Explain the rationale for under­
questions sometimes just to assess the useful the result are and if these results taking the study.
Seminar and Journal Club Presentation 773

– What is the context for the study? Critique the Study look forward and use this opportunity
– What previous work has led up to This component of the presentation will to “think outside the box”. Do you en-
experiments done in the study? define the success of your journal club. A vision these study results changing
– Focus on key studies leading useful and widely accepted approach to the landscape of clinical practice or
to this set of experiments and this analysis has been published in Journal redirecting research in this field? If so,
explain the importance of the of American Medical Association series how? Or do you find the results of this
problem in a wider context. “User’s guide to the medical literature.” study to be counterproductive or inap-
• Research question asked and main The Centre for Health Evidence in plicable in your clinical practice? If yes,
outcome of interest in the present Canada has made the complete full-text why?
study. set of these user’s guides available online. Good journal club discussions are
• Methodology used—case-control The important areas that are addressed, integral to the educational experience
study, case series, randomized trial, while one critiques the study are: of postgraduate trainees. Following
etc. a. Remember to critique (critically dis- the above approach, while utilizing
• Subjects used including inclusion cuss) the study. Strengths and weak- the resources available, will lay the
and exclusion criteria. nesses. ground work for an outstanding pre-
• How the study was done and how the b. Are there alternative interpretations sentation.
outcome of interest was measured? for the data presented?
• Describe the results of the study and c. Can you think of additional controls
References
statistical tests used. that should have been done?
• What conclusions were drawn by d. What other approaches could be 1. Esisi, Martina. “Journal clubs.” BMJ
the authors? undertaken to improve on the study? Careers. 13 Oct. 2007. Web. 09 Jan. 2010.
• Comparison of results with other <http://careers.bmj.com/careers/
studies—It means the resident advice/view-article.html?id=2631#ref2>
Summary and Conclusion
cannot present a journal club by 2. Milbrandt Eric B, Jean-Louis Vincent.
referring only one article, but has to of Journal Club Presentation “Evidence-based medicine journal
widely search articles on the similar Restate the author’s take-home mes- club.” Critical Care (2004): 401-02.
subject and compare the current sage followed by your own interpreta- PubMed. U.S. National Library of
study with other studies to discuss tion of the study. Provide a personal Medicine, 3 Nov. 2004. Web. 10 Jan.
the merits and demerits, differences perspective, detailing why you find this 2010. <http://www.ncbi.nlm.nih.gov/
in results and reasons thereof. paper interest­ing or important. Then, pmc/articles/PMC1065082/.
Section 12
Appendices
Commonly Prescribed Investigations
in Surgical Practices, their Values
and Interpretation
Borle Rajiv M

Appendix-I: Hematology

Common Hematological Investigations

Sr. No. Name of Sample collection Normal values Interpretation


investigation
1. Hemoglobin 2 mL of blood sample Male: 12–14 g% A decreased value is indicative of anemia. The
is taken by method of Female: 10–12 g% most common cause of anemia is iron deficiency
venous puncture in bulb due to decreased intake of essential compounds,
containing 0.2 mL of EDTA like vitamin B1, B6, B12, iron, vitamin C.
Bone marrow depression, acute blood loss,
chronic blood loss as in bleeding piles, gastric/
duodenal ulcers, heavy menstrual flow,
hemoptysis and postpartum bleeding are also
other causes.
2. Complete 2 mL of blood sample RBC: Male: 4.5–6.2 million/cumm A decrease in the RBC count is seen in anemia,
blood count is taken by method of Female: 4.5–5.5 million/cumm pellagra, hemorrhage, liver disease.
venous puncture in bulb An increase is seen polycythemia and extreme
containing 0.2 mL of EDTA dehydration.
A physiologic increase in the RBC count is seen
in high altitude, hypoxia, emotional stress,
pregnancy.
WBC: 5000–10000/cumm WBC is increased in acute infections, uremia,
leukemia and with steroid therapy.
WBC is decreased in aplastic anemia, radiation
therapy, infectious mononucleosis, malaria,
AIDS, enteric fever, and drug poisoning.
DLC: Neutrophils—50–62% Increase in infection, granulocytic, leukemia,
postsurgery, severe hemorrhage and burns.
Decrease in aplastic anemia, viral infection and in
patient undergoing radiation or dialysis.
DLC: Eosinophil—2–8% Increase in allergies, parasitic infection, collagen
vascular diseases, Addison’s disease and
malignancy.
Decreased in stress, steroid therapy, ACTH excess
and Cushing’s syndrome.
Monocytes—1–3% Increased in tuberculosis, chronic inflammation,
collagen diseases, malaria, typhoid, kala azar and
protozoal infections.
Contd...
778 Appendices

Contd...

Sr. No. Name of Sample collection Normal values Interpretation


investigation
Lymphocytes—25–30% Increased in viral infection, tuberculosis, syphilis,
whopping cough.
Decreased in stress, uremia and steroid therapy.
Basophils—0–1% Increased in polycythemia and chronic myeloid
leukemia.
Decreased in stress, steroid therapy and
thyrotoxicosis.
Platelet count: 1,50,000– Increased in allergic conditions, asphyxia,
4,00,000/cumm hemorrhage, bone fractures, surgical operations,
splenectomy, rheumatic fever and trauma.
Decreased in acute infections, acute leukemia,
aplastic and pernicious anemia, chicken pox,
small pox, splenomegaly, scarlet fever, typhoid
and tuberculosis.
3. Erythrocyte 2 mL of blood sample Males: 17–50 years 10 mm Increased in tuberculosis, malignant tumors, rheu-
sedimentation is taken by method of >50 years 12–14 mm matoid arthritis, rheumatic fever and liver disease.
rate (ESR) venous puncture in bulb Females: > 50 years 19–20 mm Decreased in allergic conditions, sickle cell
containing 0.2 mL of EDTA (Westergren’s method at 1 hour) anemia, peptone shock, polycythemia.
4. MCV (Mean 2 mL of blood sample 85 ± 8 fl Lesser than lower limit of normal: Microcytic
corpuscular is taken by method of anemia
volume) venous puncture in bulb Within normal range: Normocytic anemia
containing 0.2 mL of EDTA Greater than normal: Macrocytic anemia
5. MCH (Mean 2 mL of blood sample 29.5 ± 2.5 pg Lesser than normal: Hypochromic anemia
corpuscular is taken by method of Within normal range: Normochromic anemia
hemoglobin) venous puncture in bulb Greater than normal: Hyperchromic anemia
containing 0.2 mL of EDTA
6. MCHC (Mean 2 mL of blood sample 32.5 ± 2.5 g/dL Since MCHC is independent of RBC count and
corpuscular is taken by method of size, it is considered to be of greater clinical
hemoglobin venous puncture in bulb significance, compared to absolute values. It
concentration) containing 0.2 mL of EDTA is low in iron deficiency anemia but is usually
normal in macrocytic anemia.

Peripheral Smear

Name of investigation Sample collection Indications


Peripheral smear 2 mL of blood sample Platelet count, TLC, DLC, • Platelet count in parasitic and viral infections. De-
is taken by method of anemia typing, septicemia, crease in count < 70,000 is suggestive of thrombo-
venous puncture in bulb parasitic infections like cytopenia, patient has spontaneous bleeding ten-
containing 0.2 mL of mala­ria or filiriasis, sickling dency when the count is < 30,000–40,000.
EDTA or finger puncture in sickle cell anemia • Normochromic, hypochromic, microcytic, macrocytic
chara­cter of the RBCs help in typing the anemia.
• The morphological anomalies of the RBCs can be
detected.
• On addition of the reducing agent, classical sickling
of RBCs can be seen in sickle cell disorders.
• PS in a patient with septicemia shows immature
WBCs in the form of band cells and intracellular
eosinophilic granules termed as septic granules.
• Peripheral smear detects malarial parasite in the
RBCs when the sample is taken during the spike
of fever and chills as the parasites come in the
peripheral circulation. The filarial parasite can
be seen if the sample is taken at the night as the
parasites are present in the peripheral blood during
night.
Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 779

Peripheral Blood Smear Cell picture

Cells Interpretation
Target cells Decreased osmotic fragility
Deficiency of an enzyme called lecithin cholesterol acyl transferase
Hemoglobin abnormalities (hemoglobinopathies)
Iron deficiency
Liver disease
Spleen removal
Thalassemia
Spherocytes Autoimmune hemolytic anemia
Hereditary spherocytosis
Increased osmotic fragility
Elliptocytes Hereditary elliptocytosis or hereditary ovalocytosis
Schistocytes Artificial heart valve
Disseminated intravascular coagulation
Hemolytic uremic syndrome (HUS)
Microangiopathic hemolytic anemia
Thrombotic thrombocytopenic purpura (TTP)
Normoblast Cancer that has spread to bone marrow
Erythroblastosis fetalis
Leukoerythroblastic anemia (myelophthisis process)
Miliary tuberculosis
Myelofibrosis
Removal of spleen
Severe hemolysis
Thalassemia
Echinocytes (Burr cells) Uremia
Acanthocytes (Spur cells) Abetalipoproteinemia
Severe liver disease
Teardrop-shaped cells Leukoerythroblastic anemia
Myelofibrosis
Severe iron deficiency
Thalassemia major
Howell–Jolly bodies Myelodysplasia
Post splenectomy
Sickle cell anemia
Heinz bodies Alpha thalassemia
Congenital hemolytic anemia
G6PD deficiency
Unstable form of hemoglobin
Few reticulocytes (immature RBCs) Anemia with bone marrow recovery
Hemolytic anemia
Hemorrhage
Basophilic stippling Lead poisoning
Myelofibrosis
Myelophthisic process
Neutrophilic hypergranulation (toxic granulation) Severe inflammation, septicemia, burns, trauma, and upon exposure
to hematopoietic growth factors such as granulocyte-colony
stimulating factor (G-CSF)
Döhle bodies Infection, burns, uncomplicated pregnancy, toxic states, or during
treatment with hematologic growth factors such as G-CSF
780 Appendices

Appendix-II: Biochemical Investigations

Liver Function Test

Sr. No. Name of investigation Sample collection Normal values Interpretation


1. Alanine Plain Bulb: Blood samples Normal Adult Increased levels
aminotransferase are allowed to clot at Range: 0–48 I.U./L • Hepatocellular disease
(ALT) 15–24°C for minimally Optimal Adult • Active cirrhosis (mild increase)
Serum glutamic 30 minutes and maxi­ Reading: 24 I.U./L • Metastatic liver tumor
pyruvic transaminase mally one hour. Male: 0–40 I.U./L • Obstructive jaundice or biliary obstruction (mild
(SGPT) For serum samples— Female: 0–36 I.U./L to moderate increase)
specimens should • Bone metastasis
be centrifuged at a • Congestive heart failure
temperature 15–24°C • Muscle inflammation
for 10 minutes at • Shock, trauma
1500 gravity within • viral, infectious or toxic hepatitis (30–50x nor­
1 hour after blood mal)
collection. • infectious mononucleosis
Drugs that increase
ACE inhibitors, acetaminophen, anticonvulsants,
antibiotics, heparin, NSAID’s
2. Aspartate Male: (10–55 I.U./L) Reflects damage to the hepatic cell
aminotransferase Female: (7–30 I.U./L) Less specific for liver disease
(AST) Children: 2–3 times adult Elevated in viral hepatitis, mononucleosis, and
Serum glutamic normal values. acute hepatotoxicity, ischemia.
oxalaoacetic SGPT:SGOT = 1:1 SGOT > x 2 higher than SGPT characteristic of
transaminase (SGOT) alcoholic liver disease; also in cirrhosis, hepatitis,
pancreatitis, liver CA
SGPT > SGOT viral or drug induced hepatitis and
hepatic obstruction other than malignancy
3. Bilirubin–Total Male: (0.3–1) mg% • H epatogenous/obstructive jaundice (increased
Female: (0.3–1) mg% total and conjugated bilirubin)
• Hemolytic jaundice (increased total bilirubin
but conjugated bilirubin does not rise)
• Not a sensitive indicator of hepatic dysfunction
• Must exceed >2.5 mg/dL to produce clinical
jaundice
• >10 mg/dL hepatocellular jaundice
• >20 mg/dL in obstructive jaundice (neoplastic/
intrahepatic)
• <30 mg/dL in extrahepatic jaundice after which
there is a plateau due its renal excretion
• >50 mg/dL in severe heptaocellular jaundice
Unconjugated Male: (0.2–0.7) mg% Increased unconjugated bilirubin: increased he­
bilirubin Female: (0.2–0.7) mg% mo­ lysis, decreased hepatic uptake/conjugated
(e.g. Gilbert’s syndrome), cirrhosis, erythroblastosis
fetalis, malaria
Conjugated bilirubin Male: (0.1–0.3) mg% Elevated conjugated bilirubin: biliary obstruction,
Female: (0.1–0.3) mg% cirrhosis, pregnancy.
4. Alkaline phosphatase Adults: 65–306 I.U/L Increased
Children: Less than 645 I.U/L • Cholestasis, biliary obstruction, bone meta­
stasis, calcium deficiency, cirrhosis, high fat
intake, hyperparathyroidism, infectious mono­
nucleosis, leukemia, osteogenic carcin­ oma,
vitamin D deficiency, fibrous dysplasia, Paget’s
disease.
• Infiltrative diseases of liver

Contd...
Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 781

Contd...

Sr. No. Name of investigation Sample collection Normal values Interpretation

• Serum ALP by osteoblast-rapid growth of bone


(growth, healing of fracture, osteosarcoma,
bone metastasis, Paget’s disease, fibrous dys­
plasia, multiple myeloma, rickets).
Decreased in—Cystic fibrosis, excessive vitamin
D intake, hypophosphatemia, pernicious anemia,
celiac disease, chronic nephritis, scurvy.
Drugs that increase—ACE inhibitors, anti­con­vul­
sant, heparin, NSAID’s, estrogens
Drugs that decrease—Fluorides, propranolol.

5. Gamma glutamyl Female: 5–29 U/L Elevated levels (> 10–30 IU/L) are observed in:
transferase (GGT) Male: 5–38 U/L Chronic alcoholism, acute pancreatic disease,
Enzyme Child: 3–30 U/L myo­­cardial infarction, renal failure, chronic obstru­c­
Newborn: 5 times child’s tive pulmonary disease and in diabetes mellitus,
normal value biliary obstruction, cholecystitis, cholelithiasis, renal
cancer, SLE.
Drugs that increase: Aminoglycosides, barbi­tura­
tes, NSAID’s, phenobarbital, phenytoin.
Drugs that decrease: Oral contraceptive.

6. Serum protein Male: (6–8) g% • Proteins levels are nonspecific for liver disease
Female: (6–8) g% • No changes in protein levels in acute liver
dis­ease but evident changes in chronic liver
disease like cirrhosis, hepatocellular damage.

Serum globulin Male: (2.5–3.5) g% Decreased in malnutrition, severe illness,


Female: (2.5–3.5) g% nephritic losses and protein losing enteropathies.

Serum albumin 4.0 to 5.7 g/dL Hypoprotienamia: Decreased serum protein dec­
re­­ases the osmotic pressure of the blood, lead­
ing to loss of fluid from the intravascular com­
partment, or the blood vessels, to the interstitial
tissues, resulting in edema. This is termed as hypo­
proteinemia.

RA factor

Name of test Collection of blood Normal values Interpretation


samples

RA factor Venous blood in plain • Less than 40–60 u/mL High levels of rheumatoid factor occur in rheumatoid arthritis
sterile bulb or and Sjögren’s syndrome. The higher the level of RF the greater
• Less than 1:80 (1 to 80) titre the probability of destructive articular disease.
It elevates in chronic hepatitis, primary biliary cirrhosis,
any chronic viral infection, bacterial endocarditis, leukemia,
derm­a­tomyositis, infectious mononucleosis, systemic sclero-
sis, and systemic lupus erythematosus (SLE)
782 Appendices

Kidney Function Test

Sr. No. Name of Sample collection Normal values Interpretation


investigation

1. Serum creatinine Plain sterile bulb Male: (0.7–1.5) mg% Increased


• Blood samples are allowed to clot at Female: (0.5–1.2) mg% • Renal parenchymal damage and
15–24°C for minimally 30 minutes cata­­bolic disorders muscle
and maximally one hour. • More sensitive indicator of GFR than
• For serum samples—specimens blood urea nitrogen
sho­uld be centrifuged at a tempera­
ture 15–24°C for 10 minutes at
1500 g within 1 hour after blood
coll­ection

2. Serum potassium Male: (3–5) mEq/L Hyperkalemia: Urine potassium level


Female: (3–5) mEq/L above 40 mEq/L suggest intact renal
excretory mechanism. Implying that
high intake or failure of cell uptake is
the major mechanism for hyperkalemia.
Seen in dehydration, kidney failure,
acidic blood pH, burns, diabetes, drugs
like ACEI (Angiotensin converting enz­
yme inhibitor)
Hypokalemia: Is a metabolic disorder
that occurs when the level of potassium
in the blood drops too low. Seen in
severe burns, cystic fibrosis, alcoholism,
Cushing’s syndrome, dehydration, mal­­
nu­trition, vomiting, diarrhea and cer­
tain kidney diseases, such as Bartter’s
syndrome.

3. Serum sodium Male: (136–145) mEq/L Increased: (Hypernatremia)


Female: (136–145) mEq/L Hypotonic fluid loss—diarrhea, vomi­ting,
Chronic renal failure
Decreased: < 135 mEq/L (Hypon­ata­tre­
mia)
Hypothyroidism, Addisons disease, pro­
lon­ged vomiting, decreased oral intake,
severe diarrhea, SIADH (Syndrome of
inappropriate antidiuretic hormone sec­
re­tion)

4. Serum urea Male: (18–40) mg% Increased


Female: (18–40) mg% Renal parenchymal disorder
Decreased GFR
Decreased
Advanced liver disease
Low protein diets
Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 783

Other Biochemical Investigations

Name of the Method of sample collection Normal values Interpretation


investigation
Serum calcium For total and ionic serum cal­ Total: 9–11 mg/dL Hypercalcemia: malignancy, hyperpara­thy­
cium, blood collected in RA roi­­dism, hyperthyroidism, osteomyalacia,
tubes, centrifuged to draw pagets disease.
serum Hypocalcemia: hypoparathyroidism, vitamin
D deficiency, excess of fluid loss from body.
Ionized Ca++ Ionized calcium of An ionized calcium value within the refe­
1.1–1.4 mmol/L or (4.5–5.6 mg/dL) r­
ence range implies adequate calcium
home­ostasis, as this is a direct measure of
calcium in its active form.
Decreased levels: Hyperparathyroidism,
multi­­ple myeloma, sarcoidosis
increased levels: Hypoparathyroidism,
acidosis, hypoalbuminemia, malignant neo­
plasm.
Serum phosphorus Adults: 3.0–4.5 mg/dL Hyperphosphatemia: liver disease, renal
Children: 4.5–6.5 mg/dL failure, excess of vitamin D, hypocalcemia,
and hypoparathyroidism.
Hypophosphatemia: malnutrition, low in­take
of vitamin D, hypercalcemia, and hyper­
parathyroidism
Acid phosphatase Male: 0–0.8 U/L It is a type of enzyme used to free attached
phosphate groups from other molecules dur­
ing digestion. It is stored in lysosomes.
Different forms of acid phosphates are found
in different organs, their levels are used to
evaluate the success of the surgical treatment
of prostate cancer.
Alkaline phosphatase Discussed earlier in liver function tests

Blood Glucose Test

Name of investigation Normal values (range) Sample Interpretation


Random blood sugar (RBS) 80–140 mg/dL 1 mL venous blood sample in Increased in diabetes
fluoride bulb Decreases in states of hypoglycemia
Fasting blood sugar (FBS) 70–110 mg/dL 1 mL venous blood sample in Increased in diabetes
fluoride bulb
Post prandial blood sugar or post meal <140 mg/dL 1 mL venous blood sample in Increased in diabetes
blood sugar (PPDS/PMBS) fluoride bulb

Glycosylated Hemoglobin (Hba1c)


Glycosylated hemoglobin testing is recommended for both
i. Checking the blood sugar control in people who might be prediabetic.
ii. Monitoring blood sugar control in patients with more elevated levels, termed diabetes mellitus. It provides accurate
assessment of glucose control of past four months, thus helps in titrating anti diabetic medications.
Glycosylated hemoglobin measurement is not appropriate when there has been a change in diet or treatment within
6 weeks. Likewise, the test assumes a normal red blood cell aging process and mix of hemoglobin subtypes (predominantly
HbA in normal adults). Hence, people with recent blood loss, hemolytic anemia, or genetic differences in the hemoglobin
molecule (hemoglobinopathy) such as sickle-cell disease and other conditions, as well as those that have donated blood
recently, are not suitable for this test.
784 Appendices

Investigation Reading Type of sample Interpretation


HbA1c Test <7% Venous blood sample Good diabetic control
10% Venous blood sample Fair control
13–20% Venous blood sample Poor control

Oral Glucose Tolerance Test


The test is usually used to test for diabetes, insulin resistance, and sometimes reactive hypoglycemia and acromegaly or rare
disorders of carbohydrate metabolism.

FBS (For >8 hours) <100 mg/dL Venous blood and urine sample Increased in diabetes mellitus
FBS (Two hours after 75 g oral glucose load) <140 mg/dL Venous blood and urine sample Increased in diabetes mellitus
RBS >200 mg/dL Venous blood and urine sample Diabetes mellitus

Thyroid Function Test

Test Method Normal range Interpretation


“TSH” test—thyroid 2 mL venous blood 0.4–6 µIU/mL < 0.4 µIU/mL can indicate possible hyperthyroidism. Over
stimulating in plain sterile bulb 0.3–3.0 µIU/mL 6 µIU/mL is considered indicative of hypo­thyroidism.
hormone/serum (as of 2003) Note: the American Association of Clini­cal Endocrinologists
thyrotropin has revised these guide­lines as of early 2003, narrowing the
range to .3–3 µIU/mL.
Total T4/serum 4.5–12.5 µIU/mL < 4.5 µIU/mL can be indicative of an under functioning
thyroxine thyroid when TSH is also elevated. > 12.5 µIU/mL can indicate
hyperthyroidism. Low T4 with low TSH can sometimes
indicate a pituitary problem.
Free T4/free 0.7–2.0 ng/L < 0.7 ng/L is considered indicative of possible hypothyroid-
thyroxine-FT4 ism.
T3/serum triiodo­ 1–9 years: 94–269 ng/dL < 80 pg/mL can indicate hypothyroidism.
thyronine 10–19 years: 102–220 ng/dL
> 20 years old: 80–220 ng/dL
Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 785

Appendix-III: Coagulation

Coagulation Profile

Sr. No Investigations Method of Normal Interpretations


sample collection values

1. Bleeding time Finger prick 3–8 min Prolonged in Aspirin therapy


Duke’s method (Blotting paper) Thrombocytopenia
Ivy method Capillary blood Disorders of platelet function
von Willebrand disease
Vascular abnormalities (Ehlers Danlos syndrome)
Severe deficiency of factor V and IX
2. Clotting time Finger prick 9–14 min Prolonged in cases of Hemophilia A and B vitamin K deficiency
Capillary blood Coagulation disorders in liver disease
3. Prothrombin time (PT) Venous blood in 12–15 sec Evaluation of extrinsic and common pathway (deficiency of factors I,
Quick’s one stage PT the ratio of (blood: V, VII and X)
anticoagulant) 9:1 Prolonged in cases of
Oxalate bulb Oral anticoagulant therapy
DIC, liver diseases
4. Partial thromboplastin Venous blood in 30–40 sec Evaluation of intrinsic and common pathway (deficiency of factors I,
time (PTT) oxalate bulb II, V, VIII, IX, X, XI and XII)
Prolonged in cases of
Prolonged parenteral heparin therapy
DIC, liver diseases
5. aPTT + PT aPTT prolonged, PT normal
Deficiencies of intrinsic pathway fac­tor(s) VIII, IX, XI or XII
PT prolonged, aPTT normal
Deficiency of extrinsic pathway factor VII
Occasionally, mild to moderate deficiency of common pathway
factor(s) fibrinogen, II, V or X
Both PT and aPTT prolonged
Deficiency of common pathway factor(s) fibrinogen, II, V, or X
Multiple factor deficiencies
6. Thrombin time (TT) Venous blood in 8–12 sec Evaluation of common coagulation pathway
the ratio of (blood: Prolonged in
anticoagulant) 9:1 • Afibrinogenemia
oxalate bulb • DIC
• Parenteral anticoagulant therapy
7. D–Dimer test 1 mL of platelet 110–250 n D-dimers are not normally present in human blood plasma, except
(Latex agglutination poor plasma g/mL when the coagulation system has been activated, for instance
test) incubated with 3.2% because of the presence of thrombosis or disseminated intravascular
sodium citrate in coagulation. The D-dimer assay depends on the binding of a
plastic vial monoclonal antibody to a particular epitope on the D-dimer fragment.
It is useful in diagnosis of DVT, pulmonary embolism and DIC.
8. INR (international Maintaining an INR of 2.0 to 3.0 is advised for prophylaxis/treat­ment
normalized ratio) to of venous thrombosis and thromboem­bolic complication associated
express the intensity with atrial fibrillation, for pulmonary em­bo­lism, for prophylaxis of
of anticoagulant systemic embolism after myocardial infarction and for prosthetic
therapy. cardiac valves. A higher INR of 2.5 to 3.5 is recommended for cardiac
INR = patient PT/ valve replacement which involves mechanical valves and anti­
lab PT phospholipid antibody syndrome. Range of INR > 2.0 can cause
serious bleed­ing sequences.
9. Clot retraction time 3 mL in sterile 0–2 hrs A normal value means that outside-in signaling through integrin
plain bulb αIIbΒ3 in the clotting process is normal. This generalizes that overall
platelet func­tion is normal, although it does not test every factor.
Contd...
786 Appendices

Contd...

Sr. No Investigations Method of Normal Interpretations


sample collection values
A long clot retraction time is abnormal and suggests an abnormality
some­where in the coagulation cascade after integrin αIIbΒ3 interacts
with fibrin. This suggests a prolonged bleeding time and abnormal
platelet thrombus formation, such as can be seen with acquired or
hereditary platelet disorders. Integrin αIIbΒ3 receptor dysfunction is
specifically implicated in Glanzmann thrombasthenia.
Low plate­lets or fibrinogen as well as high RBC concentrations prolong
clot retraction time. Anitplatelet medi­cations can also prolong clot
retraction time. A low value, or short clot retraction time, may suggest
tendencies toward thrombosis and other pathologies. This could also
be due to nonstandardized conditions for the test.

Individual Factor Assay


Sr. No. Test performed Sample collection Normal range Inference
1. Factor I assay Coagulation citrated Normal range Fibrinogen levels are reduced in: DIC due to the consumption of clotting
samples obtained by 1.5–4.0 g/L factors.
clean venipuncture Liver disease due to decreased synthesis.
An abnormal fibrinogen may also be found in patients with liver disease
due to an abnormal (increased) sialic acid content.
Massive transfusion leading to a dilutional coagulopathy.
Inheri­
ted deficiencies e.g. hypofi­ bri­
nogenemia, afibrinogenemia
and dysfibrinogenemia [the latter is often associated with reduced
fibrinogen levels as well as activity].
Following thrombolytic therapy.
In some patients following treatment with asparaginase.
Fibrinogen levels are increased in:
Increasing age.
Female sex, pregnancy, oral contraception.
In postmenopausal women.
Acute phase reaction.
Disseminated malignancy [but may also be decreased if this is
associated with DIC].
2. Factor II assay Coagulation citrated Normal range Intracranial hemorrhage, disseminated intravascular coagulation (DIC)
samples obtained by 50–150 u/dL both PT and PTT prolonged, to evaluate a prolonged PT (with normal
clean venipuncture PTT), vitamin K deficiency
3. Factor V assay Coagulation citrated Normal range Both PT and PTT prolonged, to evaluate a prolonged PT (with normal
samples obtained by 50–150 u/dL PTT)
clean venipuncture
4. Factor VII assay Coagulation citrated Normal range to evaluate a prolonged PT (with normal PTT), liver dysfunction vitamin
samples obtained by 50–150 u/dL K deficiency, thrombosis
clean venipuncture
5. Factor VIII assay Coagulation citrated Normal range von Willebrand disease evaluation, hemophilia A (Factor VIII defi-
samples obtained by 50–150 u/dL ciency), PTT prolonged, PT normal, thrombosis, increase during preg-
clean venipuncture nancy
6. Factor IX assay Coagulation citrated Normal range Hemophilia B, to evaluate a prolonged PTT (with normal PT), Warfarin
samples obtained by 50–150 u/dL or vitamin K deficiency
clean venipuncture
7. Factor X assay Coagulation citrated Normal range Both PT and PTT prolonged, to evaluate a prolonged PT (with normal
samples obtained by 50–150 u/dL PTT), Warfarin or vitamin K deficiency
clean venipuncture
8. Factor XI assay Coagulation citrated Normal range PTT prolonged, PT normal, thrombosis, decrease during pregnancy,
samples obtained by 60–150 u/dL liver dysfunction, proteinuria
clean venipuncture
9. Factor XII assay Coagulation citrated Normal range PTT prolonged, PT normal, liver dysfunction, proteinuria
samples obtained by 40–150 u/dL
clean venipuncture
Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 787

Appendix-IV: Arterial gas analysis

Arterial Blood Gases


Blood gas analysis, also called arterial blood gas (ABG) analysis, is a test which measures the amount of oxygen (O2) and
carbon dioxide (CO2) in the blood, as well as the acidity (pH) of the blood.
Blood gas studies are usually done to assess respiratory disease and other conditions that may affect the lungs, and to
manage patients receiving oxygen therapy (respiratory therapy) and the patients on assisted ventilation.
In addition, the acid-base component of the test provides information on kidney function too.

Indications
There is no single method for deciding the ABG to be done. It needs to be determined after proper evaluation of individual
patient.

When ABG is needed


a. In emergency critical and unstable patients where significant acid base disorder is suspected, ABG is needed immediately.
b. If history examination and serum electrolytes suggests severe or progressive acid base disorders.
c. Sick patient with significant respiratory distress secondary to acute respiratory diseases or exacerbation of chronic res­
piratory diseases.

How to Collect blood for ABG


Technique for radial artery puncture:
1. Perform modified Allen’s test.
2. Under proper asepsis 21 gauge needle heparin flushed syringe is used.
3. Palpate artery with one hand and enter the skin at 45° angle
4. Obtain 2–4 mL of blood without aspiration.

After a pulse is found, a blood sample is taken from the artery

Information provided by an ABG

Parameter Significance Normal value Interpretation


PaCO2 This is the partial pressure of The normal range for a healthy A high PaCO2 (respiratory
carbon dioxide dissolved within person is 4.7–6.0 kPa or acidosis) indicates
the arterial blood. It is used 35–45 mm Hg although in underventilation, a low PaCO2
to assess the effectiveness of chronic pulmonary diseases it (respiratory alkalosis) indicates
ventilation. may be considerably higher and hyper- or overventilation.
still normal for that patient.
PaO2 This is the partial pressure of The normal range is 9.3–13.3 kPa It is of vital importance but
oxygen dissolved within the or 80–100 mm Hg. is not used in determining
arterial blood and will determine patients’ acid base status and
oxygen binding to hemoglobin normally low readings indicate
(SaO2). hypoxemia.
Contd...
788 Appendices

Contd...

Parameter Significance Normal value Interpretation


SaO2 Oxygen saturation measures The normal levels are 97% and Reduced in hypoxia
Oxygen saturation how much of the hemoglobin above, although levels above
(Hb) in the red blood cells is 90% are often acceptable in
carrying oxygen (O2). Although critically ill patients.
similar to SpO2 (measured by
a pulse oximeter), it is more
accurate.
pH The pH measures hydrogen ions The pH of blood usually between A pH of less than 7.0 indicates
(H+) in blood. 7.35 to 7.45. acidosis and pH greater than 7.4
indicates alkalosis.
HCO3 (Bicarbonate) Bicarbonate is a chemical (buffer) Normal range is 22–26 mmol/l. A low HCO3– indicates metabolic
that keeps the pH of blood from acidosis, a high HCO3– indicates
becoming too acidic or too metabolic alkalosis. HCO3– levels
basic and indicates whether a can also become abnormal
metabolic problem is present when the kidneys are working
(such as ketoacidosis). to compensate for a respiratory
issue so as to normalize the
blood pH.
Base excess (BE) The base excess is used for the Normal range is Low value indicates metabolic
assessment of the metabolic –3 to +3 mmol/l. acidosis and high value indicates
component of acid-base metabolic alkalosis.
disorders.
Anion gap (AP) The charge difference between Anion gap (AP) = Na (Cl + HCO3) AG in metabolic acidosis:
unmeasured anion and cation is    = 12 ± 2 mEq/L anion gap is most useful to
termed the anion gap (AP). establish etiological diagnosis
of (hyperchloremic) acidosis is
diarrhea. While important cause
of increased anion gap acidosis
are lactic acidosis, ketoacidosis
and CRF.
Increased anion gap acidosis is
characterized by two factors:
1. low HCO3 and
2. Increased anion gap. It is
important to remember that fall
in HCO3 = Rise in anion gap.
Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 789

Appendix-V: Urine Examination

Gross and biochemical examination

Name of Sample collection Normal values Interpretations


investigation
Color In human medicine, 4–10 mL Many things affect urine color, including fluid balance, diet, medi­
of urine is used as the standard cines, and diseases. Vitamin B supplements can turn urine bright
volume in sterile plain bulb. yellow. Some medicines, blackberries, beets or blood in the urine
Early morning, mid stream urine (hematuria) can turn urine red-brown.
sample is collected.
Turbidity Urine is normally Turbidity or cloudiness may be caused by excessive cellular mat­
clear erial or protein in the urine (proteinurea) or may develop from
crystallization or precipitation of salts upon standing at room
temperature or in the refrigerator. Clearing of the specimen after
addition of a small amount of acid indicates that precipitation of
salts is the probable cause of turbidity.
Odor Nutty odor Some diseases cause a change in the odor of urine. For example, an
infection with E. coli bacteria can cause a bad odor, while diabetes
or starvation can cause a sweet, fruity odor.
Specific Specific gravity between 1.002 This test detects the ion concentration of urine. Small amounts of
gravity and 1.035 on a random sample protein or ketoacidosis tend to elevate the urine’s specific gravity
should be considered normal if (SG). This value is measured using a urinometer and indicates
kidney function is normal hydration or dehydration. If the SG is under 1.010, the patient is
hydrated; an SG value above 1.020 indicates dehydration.
pH of urine The pH of A diet high in meat can decrease urine pH (more acidic). Cranberries,
urine can vary popularly thought to decrease the pH of urine, have actually been
between 4.6 shown not to acidify urine. Drugs that can decrease urine pH include
and 8, with ammonium chloride, chlorothiazide diuretics, and methenamine
neutral 7 being mandelate
normal
Bence-Jones They are the light chain gamma This protein is precipitated at 40° and at 50–60°C redissolves. It
protein globulins (kappa and lambda) precipitates again on cooling. It is pathognomonic of multiple
(BJ proteins) myeloma. It is also seen in leukemia, hypergammaglobulinemia,
lymphoma and carcinomatous metastasis in bones, injured
glomerular membrane. Bence Jones proteins are particularly
diagnostic of multiple myeloma in the context of end-organ
manifestations such as renal failure, lytic (or “punched out”) bone
lesions, anemia, or large numbers of plasma cells in the bone
marrow of patients. Bence Jones proteins are present in 2/3 of
multiple myeloma cases.
Certain nonmalignant diseases, such as rheumatoid arthritis,
systemic lupus erythematosus, and chronic renal insufficiency, can
have Bence Jones proteins in the urine. High doses of penicillin or
aspirin before collecting the urine can give a false positive result.
Ketone bodies Ketone bodies When Ketone bodies are present in urine it is termed as ‘Ketoneuria’
are normally With carbohydrate deprivation, such as starvation or high-protein
absent diets, the body relies increasingly on the metabolism of fats for
energy. This pattern is also seen in people with diabetes mellitus,
when a lack of the hormone insulin prevents the body cells from
using the large amounts of glucose available in the blood. This
happens because insulin is necessary for the transport of glucose
from the blood into the body cells. The metabolism of fat proceeds
in a series of steps. First, triglycerides are hydrolyzed to fatty acids
and glycerol. Second, the fatty acids are hydrolyzed into smaller
intermediate compounds (acetoacetic acid, betahydroxybutyric
acid, and acetone). Thirdly, the intermediate products are used

Contd...
790 Appendices

Contd...

Name of Sample collection Normal values Interpretations


investigation
in aerobic cellular respiration. When the production of the
intermediate products of fatty acid metabolism (collectively known
as ketone bodies) exceeds the ability of the body to metabolize
these compounds, they accumulate in the blood and some end up
in the urine (ketonuria).
Ketone bodies are present in urine in conditions like diabetic
ketoacidosis and nondiabetic ketonuria, febrile illness, hyperemesis
in pregnancy, cachexia, excessive fatty acid metabolism and failing
anesthesia, on exposure to cold, severe exercise and fasting.
Bile pigments In trace amounts The fixed phagocytic cells of the spleen and bone marrow destroy
old red blood cells and convert the heme groups of hemoglobin
to the pigment bilirubin. The bilirubin is secreted into the blood
and carried to the liver, where it is bonded to (conjugated with)
glucuronic acid, a derivative of glucose. Some of the conjugated
bilirubin is secreted into the blood and the rest is excreted in the
bile as bile pigment that passes into the small intestine. The blood
normally contains a small amount of free and conjugated bilirubin.
An abnormally high level of blood bilirubin may result from an
increased rate of red blood cell destruction, liver damage (as
in hepatitis and cirrhosis), and obstruction of the common bile duct
as with gallstones.
Increased urobilinogen (conjugated form of bilirubin) in urine
is diagnostic of hemolytic jaundice. Urobilinogen is a colorless
product of bilirubin reduction. It is formed in the intestines
by bacterial action. Some urobilinogen is reabsorbed, taken up
into the circulation and excreted by the kidney. This constitutes the
normal “enterohepatic urobilinogen cycle.”
Increased amounts of bilirubin are formed in hemolysis, which
generates increased urobilinogen in the gut. In liver disease (such
as hepatitis), the intrahepatic urobilinogen cycle is inhibited also
increasing urobilinogen levels. Urobilinogen is converted to the
yellow pigmented urobilin apparent in urine.
The urobilinogen (also known as stercobilinogen) in the intestine
is then oxidized to brown stercobilin, which gives the feces their
characteristic color.
In biliary obstruction, below-normal amounts of conjugated bili­
rubin reach the intestine for conversion to urobilinogen. With
limited urobilinogen available for reabsorption and excretion, the
amount of urobilin found in the urine is low. High amounts of the
soluble conjugated bilirubin enter the circulation where they are
excreted via the kidneys. These mechanisms are responsible for the
dark urine and pale stools observed in biliary obstruction.
Low urine urobilinogen may result from complete obstructive
jaundice or treatment with broad-spectrum antibiotics, which
destroy the intestinal bacterial flora. (Obstruction of bilirubin passage
into the gut or failure of urobilinogen production in the gut.)
Low urine urobilinogen levels may result from congenital enzymatic
jaundice (hyperbilirubinemia syndromes) or from treatment with
drugs that acidify urine, such as ammonium chloride or ascorbic acid.
Elevated levels may indicate hemolytic anemia (excessive break­
down of red blood cells), overburdening of the liver, increased
urobilinogen production, reabsorption—a large hematoma, restric­
ted liver function, hepatic infection, poisoning or liver cirrhosis.
The most common cause of bilirubinuria is hepatocellular disease.
More rare causes include inherited disorders, such as Dubin-
Johnson syndrome and Rotor syndrome.

Contd...
Commonly Prescribed Investigations in Surgical Practices, their Values and Interpretation 791

Contd...

Name of Sample collection Normal values Interpretations


investigation
Proteins Dipstick method with indicator <150 mg/day Since proteins are very large molecules (macromolecules), they
dye, Bromphenol blue. or are not normally present in measurable amounts in the glom­e­
Heat precipitation test. 10 mg/100 mL of rular filtrate or in the urine. More than 150 mg/day is defined
or single specimen as proteinuria, proteinuria >3.5 g/day is severe and known as
Sulfosalicylic acid test nephotic syndrome. This may be caused by renal infections or by
other diseases that have secondarily affected the kidneys, such as
hypertension, diabetes mellitus, jaundice, or hyperthyroidism.
Glucose Dipstick method Normally • The renal threshold for glucose is 180 mg/dL. When blood sugar
Benedict’s test absent or is > the renal threshold the glucose appears in urine (glycosuria).
present in • Glycosuria leads to excessive water loss into the urine with
traces resultant dehydration, a process called osmotic diuresis.
Normal glucose • However the glycosuria can be seen in pregnancy (gestational
range in urine: glycosuria), ailimentary glycosuria secondary to transient
0–0.8 mmol/l elevation of blood sugar after ingestion of large quantity of
(0–15 mg/dL) sweets (carbohydrate rich diet), or it could be renal glycosuria,
i.e. due to renal pathology the glucose appears in urine inspite
of normal blood levels. Glycosuria alone does not mean that the
patient is diabetic but it can be a useful screening and monitoring
investigation. It is an unreliable indicator.

Microscopic Urine Analysis

Cellular casts RBC Normally not present They may stick together and form red blood cell casts. Such casts are
indicative of glomerulonephritis, with leakage of RBC’s from glomeruli,
or severe tubular damage.
WBC Normally not present They may stick together and form red blood cell casts. Such casts are
indicative of glomerulonephritis, with leakage of RBC’s from glomeruli,
or severe tubular damage.
Cells RBC Normally not present Hematuria is the presence of abnormal numbers of red cells in urine.
or Indicating damage to renal parenchyma and urinary tract. It may be due
1–2 /HPF is considered to a generalized bleeding diathesis or a urinary tract-specific problem
normal (trauma, stone, infection, malignancy, etc.) or artifact of catheterization
in case the sample is taken from a collection bag, in which case a fresh
urine sample should be sent for a repeat test.
If the RBCs are of renal or glomerular origin (due to glomerulonephritis),
the RBCs incur mechanical damage during the glomerular passage, and
then osmotic damage along the tubules, so get dysmorphic features.
WBC Less than 5 WBC/HPF is Pyuria refers to the presence of abnormal numbers of leukocytes that
commonly accepted as may appear with infection in either the upper or lower urinary tract or
normal with acute glomerulo nephritis. Nonseptic causes on inflammation such
as uroliths and tumors, also must be considered. It is an indication for
urine culture.
Epithelial cells Normally not present Indicator of normal tubular cell renewal or regeneration.
or Renal tubular epithelial cells, usually larger than granulocytes, contain a
< 2/HPF considered normal large round or oval nucleus and normally slough into the urine in small
numbers.
Squamous cells ≤ 15–20 squamous epithelial Squamous epithelial cells: Squamous epithelial cells from the skin surface
cells/HPF or from the outer urethra can appear in urine. It indicates improper meth-
od of urine collection and possible contamination with perigenital skin.
Bacteria Bacterial species which are Bacteria are common in urine specimens because of the abundant
commensals to urinary tract normal microbial flora of the vagina or external urethral meatus.
are present Bacteriuria can be confirmed if a single bacterial species is isolated in
a concentration greater than 100,000 CFU/mL of urine in clean-catch
midstream urine specimens (one for men, two consecutive specimens
with the same bacterium for women).
Contd...
792 Appendices

Contd...

Yeast Normally not present Yeast cells may be contaminants or represent a true yeast infection. Most
often they are Candida, which may colonize in bladder, urethra, or vagina.
Crystals Common crystals may be Crystalluria indicates that the urine is supersaturated with the com­
seen in healthy individuals. pounds that comprise the crystals. Common crystals seen even in healthy
Uncommon crystals patients include calcium oxalate, triple phosphate crystals and amor­
are present in cases of phous phosphates.
nephrolithiasis Uncommon crystals such as calcium oxalate are present in cases of neph­
rolithiasis

Bibliography
1. Dacie and Lewis, Practical hematology; 7th Ed, 1991, Churchill Livingstone Elsevier.
2. De Gruchy, Clinical hematology in medical practice; 3rd Ed, 1970, Blackwell Willey.
3. June and Cella Junaitha Watson, Manual of laboratory tests; 1st Ed, 2006, AITBS.
4. Pagana, Kathleen Deska. Mosby’s Manual of Diagnostic and Laboratory Tests, 1998, St. Louis: Mosby, Inc.
5. Todd, Sanford Davidsohn, Clinical diagnosis and management by Laboratory investigation; 17th Ed, 1989, W B Saunders Philadelphia
Inc.
Index

Page numbers followed by f refer to figure and t refer to table, respectively.

A and chronic osteomyelitis, treatment Airway 481


for 368 in maxillofacial surgery, management
Abbe flap 525f
and secondary chronic osteomyelitis, of 131
ABC See Aneurysmal bone cyst
surgical management of 369f maintenance of 132
Abdominal thrust 121f
complications of burn 481 Alar fascia 331
Abnormal attachment of palatal
hemorrhage 85 Alarm clock headaches 170
musculature in cleft palate 501f
migraine headache 174 Albumin 81
Abrasions 388, 488
pericoronitis, management of 225 Alcohol 673
types of 489 pseudo-membranous candidosis 673 Alcoholic hand rubs 16
Abrasive wound, age of 489, 489t respiratory distress syndrome 73 Alcoholism 695
Abscess 330f suppurative osteomyelitis 365 Alimentary glycosuria 105
drainage, principles of 349 Adamanto-odontoma 662 Alkaline phosphatase 783
Absence of sepsis 3 Addison’s disease 198 Alkalosis 79t
Absidia 357 Adenocarcinoma 304 Al-kayat Bramley’s incision
Absorbable synthetic suture 37 Adenoid cystic carcinoma 302 advantages of 63
Acanthocytes 779 Adenomatoid odontogenic tumor 650-652 closure of 63f
Acanthomatous 649 age 650 Alkylene oxide copolymers 216
Acanthosis 672f controversy 653 Allergy 117
Accelerated introduction 650 Allie’s
fractionation, standard 731 treatment 652 forceps 22
hyperfractionation 731 Adenosine triphosphate 87, 178 tissue holding forceps 26f
Acetylcholine, release of 106 Adequate surgical margins, specimen Allogeneic amnion 484
Acid phosphatase 783 radiographs 637f Alloplastic augmentation
Acid-base Adjacent genioplasty 557, 561f
balance 71 teeth 211 Alveolar
buffering systems 78 vital structures 211 bone 330
disorders, classification of 78 Adjunctive 729 grafting 517, 518, 518f
homeostasis and disorders 77 Adjuvant therapy 88 clefts 532
Acidemia 77 drugs 88 osteitis 219
Acidosis 79t mast garment 88 ridge distraction 269
Acinic cell carcinoma 303 steroids 88 Alveolectomy 261
Acriflavine 9 vasopressors 88 Alveoloplasty 259
Acrylic obturators 287 Adrenal types of 259
Actinic crisis 102 Alveolotomy 261
cheilosis 680 deficiency 102 Ameloblastic
treatment 681 insufficiency, management of 102t carcinoma 663
chelitis See Actinic cheilosis Adrenaline IP fibrodentinoma 654
Actinobacillus actinomycetemcomitans 375 adverse reactions 124 fibroma 652, 653, 653f
Actinomyces 375 dose 122 recurrence in neck 655f
israelii 374 Adrenocorticotrophin 87 fibro-odontoma 655, 655f, 662, 663
osteomyelitis 374 Age of fractures 492f fibrosarcoma 664
Active jaw exercise 596 Air odontoma 662
Acute conditioning system 14 sarcoma 664
adrenal insufficiency 101 embolism 186 Ameloblastoma 631, 634, 635, 663
794 Textbook of Oral and Maxillofacial Surgery

benign tumor 634 Antidiuretic hormone 87 precautions 125


from cystic lining into connective tissue Antihistaminics 181 side effects 125
wall of cyst 643 Anti-inflammatory drugs 594 Atwood’s classification of ridge
incidence 631 Antiseptic resorption 246f
introduction 631 action of different 10t Atypia 669
malignant tumor 634 solution 6 Audience, role of 772
management 635 care of 11 Augmentation genioplasty 556
of anterior maxilla 645 technique 10 Auriculotemporal syndrome 562
of mandible Antitetanus serum 410 Austin’s retractor 27f, 232f
in anterior area 640f Antithyroid drugs 110 Autogenous bone graft 269f
treated with segmental resection and Anuric renal failure 82 Autonomic nervous system 86
reconstruction with AOT, radiographic presentation of 652f Avulsive injuries 391
reconstruction plate 638f Apertognathia 532, 581 AXO lever elevator 204f
pathogenesis 631 Apex of root of mandibular canine 657f Axonal recovery 167
presentations of 632f Apical
radiosensitivity of 646 curettage 327f
severe thinning of cortex 633f fragment ejector 205f B
surgical management of 644 Apicoectomy 322, 327 Babcock’s
treatment decisions for 644 Apicoectomy See also Periapical surgery, forceps 26f
Amikacin 351 indications for gland 22
Amniotic membrane 32 Apisectomy 322 Bacillus subtilis 148
Amoxicillin 328, 351 Aponeurosis of zuckercandl 344 Bacteremia 90, 332, 356, 484
action of 351 Appiani’s incision 67, 67f Bacteroides melaninogenicus 356
Amoxyclox 351 Appropriate biopsy site, identification Baillarger syndrome 162
Ampicillin 328, 351 of 675 Balanced salt solutions 81
Ampiclox 351 Apron Ballistic injuries 491
Analgesia, stage of 182 for bilateral SOHD 714f Balloon rhizotomy 157f
Analytic procedures I 757 for unilateral 714f Bandage 33
Anaphylactic incision of Freund 69, 69f uses of 33
reaction treatment 189 and Latyshevsky 69f Bands of Büngner 166
shock 92 Arbeitsgemeinschaft für Bard-Parker
acute management 94 osteosynthesefragen 417 blades 54f
causes 92 Arch bar 414 handles 54f
management 94 advantages of 414 and blades, types of 21f
treatment of 94 Architecture criteria 671 Barrier, removal of 589
Anaphylactogen 92 Armamentarium 44 Basal cell
Anaphylactoid reaction 92 for third molar surgery 231f carcinoma 635, 733
Anaphylaxis 94 needle holder 44 etiology 734
symptoms of 94 Around orbit, incisions 64 in infraorbital area wide local
Anesthetic vapors 185 Arterial excision 734f
Aneurysmal bone cyst 605, 621, 621f blood gases 787 of lower lip and reconstruction with
treatment 621 gas analysis 787 local flap 736f
Anginal attack in dental office 110 Arteriovenous fistulas 393 of pinna 736f
management of 110 Arthrocentesis, advantages of 597 hyperplasia 672f
Ankylosis 576 Article for journal club, selection of 772 Basic biostatistics 757
in child with temporal muscle fascia and Artificial ultraviolet light, exposure to 734 Basophilic stippling 779
CCG interposition, management ASCH Battle’s sign 437f
of 587f forceps application 466f Bayonet flap 56f
release of 586f septal forceps 466 Bell’s palsy 159, 160, 305
with interpositional arthroplasty, surgical septum forceps 466, 466f management 159
management of 586f Aseptic technique 3, 12 medicinal treatment 159
Ankylotic Ashley’s palatal Bell’s sign 159, 159f
bony mass removed 584 flap 285f Bellies of digastric muscles 335
mass, exposure of 586f pedicle flap 284 Benadryl 174
Anosmia 277, 436 Aspiration 610 Benign
Ansa cervicalis 721 of blood stained 343 cementoblastoma 657
Antacids 181 of foreign body 120 definition 657
Antemortem and postmortem laceration management 120 epithelial tumors 296
490, 491t prevention 121 mixed tumor 299
Anterior neck dissection 721f Assessment of cervical lymph nodes 705 oncocytomas 301
Anterolateral Asthma 106 Betel nut 694
neck dissection 720f Atraumatic forceps 26f chewing 694
wall, involvement of 280f Atrophic mucosa 378 Bevel, direction of 328f
Anticholinergic drug 184 Atropine sulfate 100 Bias 764
Index 795

Bibliographic method for journal fracture 403 flap 283, 284


article 765f graft 287, 638 frenectomy 255, 256f
Bicoronal in midface advancement, use of 520 incision 549f, 550f
approach 59, 470 placement into alveolar defect 518f osteoperiosteal flap 287f
incision 456, 470, 546f use of 287 osteotomy cut 548f
incisions See also Unicoronal loss in edentulous jaw 246 pad of fat, use of 286
Bifocal transport distraction 571f marrow failure 689 space
Bifurcated palatal beak engages single metabolizing unit 430 boundaries of 341
palatal root 207f morphogenetic proteins 430 management 341
Bilamellar zone, laxity of 592f morphologic proteins 660 source of infection 341
Bilateral removal of 211f, 232 sulcular incision 242
advancement flap on forehead 396f repair unit 430 with vestibular extension 242
black eye 436f resorption 605 Buccopharyngeal fascia 331
fibrotomy and reconstruction by scanning 367 Bull’s eye 228, 228f
bipedaled nasolabial flap 686f scintigraphy 367 Bupivacaine 129
gap arthroplasty 581f transport 639 Bureau of Indian standards 148
Le Fort II fracture, management of 446f wax, composition of 216 Burger’s flap 284, 284f
parasymphysis fracture 131 Bony Buried sutures 49, 50f
partial cleft lip, repair of 512f callus Burn
reticular lichen planus 686f formation 427, 429f contracture of
sagittal split osteotomy 549 stage 429f face 486f
advantages 551 orbit, anatomy of 461f neck 486f
complications 551 window, preparation of 327f extent of 477
surgical procedure 550, 551 Borrelia vincentii 219 in inpatient department, management
supraomohyoid neck dissection 719f Bowen’s disease 680 of 481
Z approach 470, 472f Boyle’s injury 481
Bimanual palpation of submandibular apparatus 184 on outdoor basis, management of 481
gland 297f machine 184f severity, classification of 478, 482
Binder, syndrome 503f Brachial Burr cells See Echinocytes
Biochemical investigations 780, 783 cyst 623
Biologic wound dressings 484 plexus, injury to 727
Biological dressings 32 sinus 623 C
Biomedical waste Brachy facial 532 Cachexia
components of 145 Brachytherapy 732 in malignancy 732
definition 145 Brachytherapy See Interstitial radiotherapy newer pharmacotherapy 733
management 145 Brain abscess 358 of malignancy 732f
Biopsy 675, 709 Branches of ext. carotid artery, treatment 733
Bipedaled nasolabial flap for reconstruction exposure of 719f Cadaveric specimen of TMJ ankylosis 575f
of anterior alveolar defect 725f Branchial Calcified material encircles and epithelial
Bipedaled nasolabial flap for intraoral arches 622 islands 656f
closure 399f cleft cysts 622 Calcifying epithelial odontogenic
Birn’s hypothesis 219f cyst 622 cyst 616, 641
age incidence 623 tumor 646, 648
Bjork flap 138
development 622 introduction 646
Black eye 437f
pathology 623
Blair incision 66 Calcium
symptoms 623
Blanching on buccal mucosa and palate abnormalities 77
treatment 623
with atrophic uvula 682f gluconate
Branchial cleft cyst, excision of 623f
Bleomycin 730 dose 129
Brawny induration 352
Blindness 728 indications 129
Brisement force 579
Blood 484 Caldwell-Luc operation 279, 279f, 455, 462
Bristow’s
brain barrier 117, 356, 449 incisions for 279f
elevator 453f, 454
glucose test 783 Callus
zygoma elevator 454, 454f, 460
soaked sponge 621 formation 430
Brodie’s abscess 370
supply in anterior maxillary region, stage of 430
Bronchospasm 94, 106, 186
direction of 324f Campbell-Trapnell lines 446f
treatment 186
vessels, involvement of 437 Canal, deflection of 229f
Bruxism 175
Blow out fracture of orbit 461, 461f Cancellous bone 362, 429, 637
Buccal
Bocca’s triangle with sparing spinal graft 560f
alveoloplasty 260
accessary nerve 719f Cancer cachexia 732
cortex 404
Body osteotomy 556f Candida albicans 673, 676
decortications 607f
Bomb blast injuries 491 exostoses 263 Candidal leukoplakia 677
Bone fat pad Candidal leukoplakia See Chronic
AWL 415 for closure of OAF, use of 287f hyperplastic candidiasis
expansion 206f to close palatal fistula 523f Candidiasis 687
796 Textbook of Oral and Maxillofacial Surgery

Canine space 342 Cefoxitin 351 Chewable tobacco in form of tobacco lime
anatomical boundaries of 342f Ceftriaxone 351 mixture 694
boundaries of 342 Cell body 163 cakes 694
source of infection 342 Cellulitis 329, 332, 332f ghutka 694
Cannon’s observations 85 and abscess 332t jarda 694
Canthoplasty 471 case of 32 khaini 694
Canulation of parotid duct 397f of submental 354f kharra 694
Cap splints 415 Cementoblastoma 657f kimam 694
Capsule consists 657 pan 694
application procedures 589 Cemento-enamel junction of tooth 657f masala 694
tightening procedures 597 Central Cheyne-stokes breathing 86
Carbolic acid, solution of 35 granular cell tumor of jaws 654 Chin
Carbon dioxide 77 mucoepidermoid carcinoma 664 deformities 532
Carbonic acid 78 nervous system 182 retractor 27f
Carboplatin 730 regeneration 167 Chlorhexidine 9, 18
Carcinogenesis 696 odontogenic fibroma 654 gluconate 6, 379
Carcinogenesis of salivary gland tumors 299 treatment for 657 Chloroform 393
Carcinogens 696 type of 656 Chloromycetin 90
Carcinoma tendency 757 Choosing statistical test 760
anterior 2/3rd of tongue with venous Chromic
ankyloglossia 705f catheterization 187 acid 37
ex-ameloblastoma See Ameloblastoma pressure 87 method 37
ex-dentigerous cyst 664 Cephalexin 351 catgut 40f
exodontogenic keratocyst 664 Cephalometric analysis 536 Chronic
ex-pleomorphic adenoma 304, 305f Cephalosporin, chemical structure of 93f alcoholics 695
of maxillary sinus 279 Cerebral edema 82, 728 candidal infection 677
fungating alveolus and extending to Cerebrospinal fluid rhinorrhea 436f hyperplastic candidiasis 673
buccal mucosa 700f Cervical inflammatory cell infiltration in
management 280 deep cervical fascia 330 lining 619f
surgical treatment 280 fascia irritation 673, 695
of vermilion border of lower lip 695f anatomy of 330 obstructive pulmonary disease 180
Cardiac arrest 111, 115 in cross section of neck, layers of 331f osteomyelitis 366, 366f, 371f
chest compressions 112 lymph node paroxysmal hemicrania 171
definition 111 groups of 702f sclerosing osteomyelitis 374
identification of 112 metastasis 705 suppurative otitis media 576
management 112 necrotizing fasciitis 356 Chutta 679, 694
Cardiac life support, advanced 114 cause of 356 Chylous fistula 727
Cardiopulmonary resuscitation 112 superficial fascia 330 Cidex 8
for children 114 Cervicofacial Circum-mandibular wiring, procedure
Cardwell-Luc operation 283 disease 375 for 415
Carnoy’s solution 615 infections 131 Circumorbital
after enucleation of unicystic Champhy’s ecchymosis 437f, 451f
lines 420f
ameloblastoma, use of 645 edema 450
miniplates, fixation of 421f
Carotid Circumzygomatic wiring 442, 443f
monocortical plates 419
arteries 168 Cisplatin 730
osteosynthetic lines 419
blowout 728 Civilian bomb blast injuries 491
plates and screws 420f
sheath 331, 332 Clark’s
Characteristic of data See also Central
triangle, dissection of 716f rule 228
tendency
Cartilage radionecrosis of larynx 732 technique 251, 252
Cheek
Cartilaginous Classic eagle syndrome 168
advancement flap 396, 397f
callus formation 427 Clavulanate 351
retractor 27f
pointer of conley 293f Clear cell odontogenic carcinoma 664
Chemical
Case-control study participants 763 Cleft lip
carcinogens 696
Casoni’s test 628 and palate 532
cauterization 609
Cat’s paw retractor 22, 25f surgical procedures for 511
condylotomy 594
Catecholamines, release of 106 deformity, repair of 511
indicator strips 6f
Cavernous sinus thrombosis 354, 356f epidemiology 498
injury 673
CCG introduction 497
vapor sterilization 6
advantages of 582 Chemoprevention 730 repair, surgical procedures for 511
disadvantages of 583 Chemotherapy 728, 729 surgical anatomy 498
Cefadroxil 351 indications for 729 Cleft soft palate and uvula 506f
Cefazolin 351 side effects of 730 Cleidocranial dysostosis 222
Cefepime 351 strategies 729 Clindamycin 90, 351, 356
Cefotaxime 351 Chest compression techniques 113, 114 Clinical presentation of oral cancer 696
Index 797

Closed osteotomy 567 Cracker burst injury 397f


gloving technique 17f unilateral cleft lip Cranial
reduction alveolus and palate 505f fossa, anterior 436, 463, 467
advantages of 411 and alveolus 504f nerves 436
disadvantages of 411 Complex Craniofacial
in mid-face fractures, method of 448f compound odontomas involving disjunction 446
indications for 411 posterior mandible 660f skeleton 195
Clostridium odontoma 661, 661f Craniopharyngioma See Pituitary
tetani 14 etiology 661 ameloblastoma
welchii 14 treatment 662 Cricoid
Closure of OAF, method of 283 type with a dense radiopacity and cartilage 702f
Cloxacillin 351 retained molar 661f hook 139f
Cluster headache 169 Compound Cricothyroidectomy 131, 133
hypothalamus 169 bone fracture 402 procedure 134
pain 169 comminuted bone fracture 403 Cricothyrotomy 133
signs 169 composite odontoma 660 Crile’s ‘Y’ incision 67, 68f, 713f
smoking 169 Concentrated cresol solution 7 Crista galli 467
symptoms 169 Concious sedation 143 Cross nerve innervation 161f
treatment 170 Concominant 729 Cross-sectional surveys 749
triggers 169 boost accelerated fractionation 731 Crow’s feet incision 66
CNS mucormycosis 360 Condylar Crown, destruction of 210f
Coagulation 785 fractures 424 Crude form of cigar See Chutta
profile 785 retractor 28f, 581 Crush injury
Cocarcinogens 696 Condylectomy 580 of hand 392, 490
Coccidioides immitis 348 Congenital heart diseases 502 syndrome 391
Codman’s triangle 363 Conley’s incision 713 Cryosurgery 609, 737
Coexistent leukoplakia 683 Conscious sedation 144 Crystalloid solutions 81
Cohort study 749 indications for 144 CSF rhinorrhea 447, 449
design of 750, 751f Contact healing 430 Cuboidal
participants 763 Continuous cells 649
Cold IVY loop wiring 413 epithelial cell, layers of 612
shock See also White shock, stage of locking suture 48, 49f Cupid’s bow correction 525f
sterilization 6 mattress 49 Curettage of cystic lining 328f
advantages 6 Contused lacerated wound on upper Curreri formula 485t
disadvantages 6 lip 490f Curvilinear incision 57, 58f
Collagenase Contusion 389, 489 Custom made implants 639
resistant glycoprotein 428 over right side of chest 489f Cutaneous
cell rich stroma with numerous strands Conventional and unicystic manifestations 687
of odontogenic epithelium without ameloblastomas, differences mucormycosis 360
palisading of peripheral cells 656f between 642 Cyclophosphamide 172
Collett technique 251 Cooley technique 251 Cyst
Collodion gauze 467f Corner of mouth, drooping of 159f and tumor formation 226
Colloid classifications of 604
Cornoy’s solution 645
osmotic pressure 73 contents of 614
Cornu of hyoid bone 335
solution 79, 81 development of 603
Coronectomy 237
Colman’s sign 406, 406f diagnosis of 605
Coronoidectomy, role of 583
Columella enlargement, theories of 605
Correct and incorrect way of making a
lengthening 526 formation, stages of 604t
powerpoint slide 770f
point 539 growth of 605f
Correlations between variables 759f
Combined local flaps 285, 286f in relation to stage of development
Corrugated
Comminuted of tooth 603t
portex drain 30f
bone fracture 402 of oral cavity, classification of 603
rubber dam drain 30f
fracture 403f of soft tissue of
Cortical
of symphysis, management of 420f face 621
alveoloplasty 259
infraorbital rim plated with orbital head 621
chipping of medial pole of condyle 424f
plate 456f neck 621
expansion 607f
Common treatment modalities of 606
to ameloblastoma and paper thin
causes of pulpal pathologies 321 Cystic
cortices 633f
chemotherapeutic agents 730 basal cell carcinoma 735
Cortication of canal, loss of 229f cavity after enucleation 607f
salivary gland neoplasm 299
Comparison, type of 746 Corticocancellous bone grafts 638 lesions in mandible 605f
Complete Coston’s syndrome 590 odontogenic tumor 633
bilateral cleft lip, alveolus and Cotton wool filaments, deflection of 282f pioc 664
palate 505f Cough 277 primary intraosseous carcinoma 664
blood count 777 Coup-counter-coup injury 435 WHO 2005, classifications of 604
798 Textbook of Oral and Maxillofacial Surgery

Cysts of odontogenic origin, Dentigerous cyst 605, 609, 610 Dish face deformity 445, 445f, 447
developmental 609 associated with impacted third Displaced disc, anteriorly 595f
Cytogenic ameloblastoma See also molar 226f Displaced unsupported premaxilla and
Unicystic type in mandibular body 612f palate 501f
Cytology criteria 671 undergoing ameloblastic changes 612f Distant
Cytomegalovirus 299, 484 with maxillary metastasis 297
canine treated with enucleation 611f metastatic disease 729
premolar managed by Distobuccal gutter, preparation of 233
D enucleation 611f Distraction
Dancing distraction 565 with severely displaced unerupted osteogenesis 519, 562, 566, 570
Danger triangle 354, 355f molars 610f concept of 562
Darkening of roots 229f Dentistry drug-related emergencies 118 rhythm 562
Dash board injuries 435 Dentoalveolar fracture 438 Distractor
Data management of 439 mandible 564
analysis and basic biostatistics midface and maxilla 564
with traumatic avulsion of incisors 438f
principles 756 nonsubmerged device 564
Denture fibroma 259
collection: tools and techniques 755 submerged device 564
Depiction of abnormal musculature
quality 756 technique 564
surrounding cleft lip 499f
Dautry’s procedure 590f type of 563
Depth of burn injury 477
Davis and Ritchie’s classification of Distruction
Dermoid cyst 624, 626
clefts 503 osteogenesis
age 625
DCP with tension introduction 562
causes 626
band 419f treatment planning 563
history 626
plate 419f vector 563
near medial canthus of eye 626f
De novo ameloblastic carcinoma Divergent roots 211f
of head neck area 626f
See Ameloblastoma Docetaxel 730
Dean alveoloplasty 259, 260 sex 625
treatment of 627, 628 Döhle bodies 779
Deep Doppler ultrasound and color-flow
cervical facial 337f Desmoplastic
ameloblastoma 642, 644f imaging 297
anterior layer of 331 Double
layer of deep cervical fascia 331 involving maxilla 643f
apexo elevator technique 205, 205f
partial thickness burn 480f variant 649
blind trials 752
second-degree burn 480 Desquamative gingivitis 687
lip
temporal Dettol composition 7
excision 257f
fascia 161f Development of tooth, stage of 604
surgery 257f
exposure of 586f Developmental odontogenic cyst, type
sliding
space of 617
genioplasty 557
management 343 Deviated nasal septum 465, 468
horizontal genioplasty 560f
boundaries of 343 Dextran 70, 81
Down syndrome 222, 503f
Deepest point of cupid’s bow 513f Dextrose 81
Doyen’s mouth gag 23f
Definition odontoameloblastoma 662 Diabetic
Drains
Definition of exodontia 195 coma 105
advantage, types of 28
Deformed condyle and ankylosis 578f ketoacidosis 105 cotton gauze, types of 28
Degenerative joint disorder 586 ketosis 105 disadvantages, types of 28
Degloving Diagnostic nerve block, role of 154 removal of 27
incision 57, 57f Diastema 547 types of 28
injury 411f Diazepam 199 uses, types of 28
laceration in lower labial vestibule 490f Diethyl ether 179 wicks
Delaire’s Difluoromethoxy 178 advantages, types of 29
philosophy to repair cleft lip and Digastric disadvantages, types of 29
palate 512 and submental triangle dissection 717 types of 29
technique for cleft lip 513f triangle 334 Dressing, types of 32
Denker’s procedure 279f Digastricus 403 Dry
Dental Dihydrothiazine ring 92 dressing 32
and periodontal injuries 559 Dilaceration roots 211f heat of sterilization 3
evaluation and dental health 532 Dingman’s mouth gag 23f hot air oven 4
follicle 658 Diphenhydramine 174 advantages 4
model surgery 541 Diphenylhydantoin disadvantages 4
advantages 541 dose 126 open flaming 3
disadvantages 541 side effects 126 socket 219
surgical splints 541 Diplopia 452 causes 219
advantages 541 Disarticulated facial bones 434f definition 219
technique 541 Discoid lupus erythematosus 690, 673 management 219
papilla 658 Diseases of maxillary sinus, classification Duct-like structures 650
wiring 412 of 276f Dulcolax 181
Index 799

Dumbbell tumor 292, 301f Enucleation Extended


Dupuy syndrome 162 advantages of 608 maxillectomy with orbital
Dynamic compression plates 418 and curettage 635 exenteration 282f
Dysesthesia 165 cystic lining 607f neck dissection 712, 722
Dyskeratosis congenital 688 disadvantages of 608 radical neck dissection 714
diagnosis of 689 Envelope incision 231 External
Dysphagia 627 EO sterilization beam radiotherapy 731
Dysphonia 627 advantages of 11 carotid artery 576f
Dysplasia 669, 671 disadvantages of 11 fixators 416
treatment 677 Epidermis 480f fungation of metastatic lymph nodes 699f
Dysplastic cells 675 Epidermoid cysts 621, 626 ophthalmoplegia 436, 459f
Dyspnea 110, 627 Epidermolysis bullosa 690 Extracellular fluid volume imbalance 75t
Episodic cluster headache 170 Extracted tooth with fractured
E Epistaxis 277 tuberosity 213f
Epithelial dysplasia 671 Extraction
Eagle’s syndrome 168, 594
grading of 671, 672 contraindications for 197
treatment 169
Epithelium of odontogenic cysts 631 of tooth, indications for 197
Ear
Epstein-Barr viruses 299, 696 Extraoral
injury on 399
Ergot alkaloids 174 barrel bandage 410
lobule repair 400f
Erruption of canine through grafted distraction
Early
bone 518 mandibular widening 566
exophytic growth 697f, 698f
Eruption cyst 617 maxillary distraction 568
OS 682f
Erythema See Superficial burn wounds distractor 566
prophylactic removal 230
Erythematous and erosive OLP 687 components 521f
advantages 231
Erythrocyte sedimentation rate 778 fungation 699f
disadvantages 231
Erythroplakia 675, 678, 687 with maggots 699f
warm shock 89
differential diagnosis of 679 incisions 58
Eccentric dynamic compression plates 419
etiology 678 Extraosseous
Echinococcus
in patient with SMF of palate, CEOT anterior maxilla female 647f
granulosus 627
case of 678f peripheral ameloblastoma 639
infection 627
treatment 679 Eyeball 438
Echinocytes 779
Ectodermal origin, congenital cysts of 627 Escharotomy 483 retractor 28f
EDCP eccentric holes 419f Escherichia coli 89, 330, 356, 377, 485 Eyebrow
Edentulous ESR See Erythrocyte sedimentation rate closed primarily, injury of 400f
geriatric fractures 424 Essig’s wiring 412 injury of 400f
jaw fracture 416, 416f Ethical issues in thesis 755 reconstruction of 400
Edinger-Westphal nucleus 436 Ethmoidal Eyelid 401
Eikenella corrodens 375 air cells 448
Elective tracheostomy, incisions for 138f bone 467 F
Electrolyte imbalance 74 Ethylene oxide gas sterilization 11
Elevation of fibrofatty 716f Facial
Ethylene trioxide 6
Elevator, use of 202 artery 310f
Eusol composition 8
Elliptocytes 779 asymmetry 532, 536
Evaluation of nasal cavity 182
Emergency axis angle 537
Excedrin migraine 174
drugs 122, 123t burn 477, 485
Excessive pain 218
kit etiology 477
Excision of dermoid cyst 626f
composition of 122f introduction 477
Excitement, stage of 182
in office, maintenance of 121 convexity 538
Exodontia
management of anaphylaxis 95 deformities, classification of 532
complications of 212
Eminectomy 589, 589f depth angle 538
contraindications for 198t
Endaural edema 728
indications for 197
approach 63, 64f excision 485
intra-alveolar extraction 200
incision 579 features 535
method of 200
Endodontically treated tooth 210f nerve 168, 388f, 576
presurgical assessment 199
Endogenous hormones 299 branches of 293f
transalveolar extraction 200
Endotoxin shock 85 identification of 293
Exophytic
Endotracheal involvement 305f
cauliflower-like growths 697
intubation 140, 483 paralysis 158
growth 697
fiberoptic bronchoscope 579f paralysis classification 158
advanced 697f
tubes 141 infranuclear lesions 159
on tongue 697f
Enophthalmos 461f nuclear lesions 158
advanced 697f
Enterobacteriaceae 375 supranuclear lesions 158
Expert sampling 754
Entonox 179 paralysis on right side 159f
Exposure, type of 746
800 Textbook of Oral and Maxillofacial Surgery

scars 562 Fluorodeoxyglucose 298 Functional neck dissection 718


skeleton in three parts, division of 434f Foley’s catheter 31, 462f anatomical basis for 718
Factors predisposing osteomyelitis 364t Forced duction test 452f contraindication of 722
Failure of pump 85 Forceps Functional superficial parotidectomy 308
Fascia lata slings 160 extraction 206, 208f advantages of 308
Fascial parts of 206f Fungal infections 329
boundaries 348f Forehead flap used to reconstruction of of maxillofacial area 357
compartmentalization 718 surgical defect of upper lip 724f Furlow
spaces 332 Forensic ballistics 491 double opposing Z-palatoplasty 517
Fasciotomy 483 Formalin solution 8 technique 516f, 517f
incision 359f composition 8 Furosemide 127
Favorable fracture 405f Fourth degree burns 481f Fusarium 484
Fever 277 Fracture 405 Fusobacterium 356, 484
Few reticulocytes 779 direct 404, 406f
Fiberoptic broncoscope 354f
Fibrin tissue glue 43
fragments 403 G
healing 426
Fibrinolytic alveolitis 219f Gamma-amino butyric acid 178
complications of 431
Fibromyxoma 658 Gap arthroplasty 580
delayed union and nonunion 432
Fibro-osseous Gap healing 429
infection 431
disease 633 Garre’s osteomyelitis 374
malunion 432
dysplasias 631 treatment 374
osteomyelitis 431
Fibrous Gastric inflation 114
stage of 430 Gastrointestinal tract 71
ankylosis 580f in maxillofacial surgery 417
hyperplasia of oral tissues 258 Gender 651
indirect 404, 406f Gene mutations 734
membrane 136
management of 408 General anesthesia 181
Field
mandible, classification of 402 complications of 185, 186
cancerization, concept of 670
of alveolar bone 213 indications for 180
fire BCC 735
of mandible 214, 227, 227f, 402, 409, 409f stage of 182
Figure of-eight
in geriatric 423 Genetic factor 673
suture 49, 50f
of maxilla 439 Genial tubercle reduction 262
wiring 412
tuberosity 213 Genioglossus muscle 254f
Filiary sequestra 376
of middle third Geniohyoid 403
Final tube placement 139f
classification of 438 muscle 337
Fine needle aspiration
cytology 698, 707 of facial skeleton 434 Genioplasty 556
cytopathology 298 of nasal bone 464f, 465f Gentamicin 351
First of pediatric mandible 423 pmma beads 369
aid treatment 478 of tooth 213 Geriatric fractures 423
degree burn 480f of zygoma 452f Ghost cell 616
Fistula See also Brachial sinus of zygomatic arteritis See Temporal arteritis
Fistula repair, techniques of 521 arch 459 odontogenic carcinoma 664
Fixed dilated pupil 459f bone 449 Gillies temporal approach 454, 460
nonresponsive to light 436f and bleeding in sinus 453f Gilmour’s wiring 413, 414f
Flap telescoping of 406 Gingival
designing of 231, 324 Fractured abscess 329
dimensions of 324 reconstruction plate 638f cyst 616
like laceration 391, 391f teeth, conservation of 439 hyperplasia 259f
necrosis 724 Free fibular graft with skin pearl for retraction 202
and dehiscence 727f mandibular reconstruction 723f Gingivolabial sulcus tobacco/lime
reflection 232f Free microvascular fibular grafts 638 chewing habits 694f
Flattening of malar prominence 451f Frey’s syndrome 162 Gingivobuccal carcinoma extending on to
Flip genioplasty 556 treatments 162 floor of mouth direct infiltration 701f
Floating maxilla 439 Frey-Baillarger syndrome 162 Ginwalla’s
Floor of Frictional keratosis 673 incision 58, 58f
maxillary sinus 276f Frontal face analysis 534 inverted ‘Y’ incision 155f
mouth 678f Frontonasal buttress 434f Girard-Carroll screw 453, 453f
Fluid Frontozygomatic suture 457f GIT mucormycosis 360
and electrolyte and buttress 458f Glabella 539
imbalance 73 Fulcrum 426 Gland, irradiation of 317
therapy 79 Full thickness Glenoid fossa 402
excess 73 burn See Third degree burn of temporal bone 402
hypovolemic shock, loss of 85 excision of superior retrodiskal Glial scar 167
volume, disorders of 73 lamina 598f Globulomaxillary cyst 619
Index 801

Glossopharyngeal landmarks 536, 537f Horner’s syndrome 346


nerve 168 procedures 259 Hospital
neuralgia 157 Harris-benedict’s formula 485, 485t acquired infection 146
causes 157 Hartman’s solution 81 gangrene 356
treatment 158 Harvesting Hot
Glycerine fascia lata graft 161f air oven and glass bead sterilizer 4f
and magsulf dressing 350f of bfp 523 and cold and cemental caries 226
magsulf solution 9 skin graft 399 How to collect blood for ABG 787
Glyceryl trinitrate 169 temporal muscle fascia flap 586f Howell-Jolly bodies 779
Glycogenolysis 103 Harvestion buccal pad of fat 309f H-shaped incision 471f
Glycosuria 105 Haversian system Hudson’s classification 365
Glycosylated hemoglobin 783 formation of 428f Human
Gnathion 537 of bone 363f bite of lower lip 392f
Godwin’s technique 250, 251 Hayes martin incision 68, 68f cadaveric allografts 484
Goldenhar syndrome 503f Hay-Martin’s double 713 papilloma virus 696
Gomori methanamine silver stain 360 Y incision 713f t-lymphotropic virus 696
Gomphosis 195 Hayton-William’s Humby knife used for harvesting skin
Good modality to tumor infiltration disimpaction forceps, application of 441f grafts 399f
in tongue 708f forceps 441 Hurler’s syndrome 222
Gorlin’s cyst 616 application of 441 Hyaline membrane disease 187
Gorlin’s cyst See Calcifying epithelial maxilla holding forceps 441 Hyaluronic acid 247
odontogenic cyst HBO therapy, complications of 373 Hydatid
Gorlin-Goltz syndrome 614 Head and neck cancer, combinations in 730 cyst 627
Goulian knives 485 Healing of abrasion 389f disease 627
Granular Heimlich maneuver 121f cases of 627
cell for infants 121f sand 628
ameloblastic fibroma 653, 654 Heinz bodies 779 Hydrocolloid dressings 484
variant 654 Heister’s jaw exercises 583f Hydrogen peroxide 8
or nodular leukoplakia 674 Hemarthrosis 575 composition 8
Granulation tissue, stage of 430 Hematogenous spread 703 plasma sterilization 11
Green stick bone fracture 403, 404f Hematologic disease 199 Hydrophic degeneration 687
Grievous injuries 488 Hematology 777 Hydrostatic cyst enlargement 605
Gross and biochemical examination 789 Hematoma 727 Hydroxyl starch 88
Growth in maxillary sinus 281f stage of 430 Hyoid bone 702f
Grummon’s analysis 538 Hemifacial microsomia 570 Hyperbaric oxygen 373, 380
Guardsman’s fracture 404 Hemimandibulectomy 636 chamber 373
Guérin Hemoglobin 777 therapy 373
fracture 439 Hemolytic streptococcal gangrene 356 contraindications for 373
sign 440, 440f Hemorrhagic shock 85, 86 in osteoradionecrosis 380
Guidance for seminar 769 therapy of 87 Hypercalcemia 77
Gunning splint 416, 416f Hepatic disorders 198 Hypercarbia 186
Gutierrez incision 67f Hesitation cuts 490 Hypercementosis 211f
Heterogeneity sampling 754 Hyperchromatic
High points of cupid’s bow of cleft 513f and polarized basal cells 643f
H High subcondylar fracture 425f columnar nuclei 616f
H2O2 Hind’s postramal approach 64, 64f Hyperfractionated radiation therapy 731
advantages of 11 Histogenesis Hyperglycemia 105
disadvantages of 11 extraosseous 649 management 105
Haberman nipple 508f intraosseous 649 Hyperkalemia 77, 82
Hairy leukoplakia 673, 677 Histopathological features 676 Hyperkeratosis See also Keratosis
Halothane 180 Histopathological types 635 Hypermetabolic syndrome 189
vapor 180 Homicidal wounds 492 Hypermobility management 589
Hamartoma See Tumor-like malformation Homogeneous 674, 674f Hypernatremia 76
Hamartoma leukoplakia 674 correction of 76
of dental lamina 654 to slightly nodular leukoplakia 674f Hyperparakeratotic stratified squamous
versus neoplasm 650 Honey comb 659 epithelium with degeneration of basal
Hamartomatous 630 Hooding of eye 452 cell layer 687f
Hand scrubbing 14 Horizontal Hypersensitive carotid sinus 122
Happy gas 178 augmentation genioplasty, surgical Hypertension 180
Hard procedure for 558f Hyperthyroidism 109
callus formation 427 genioplasty with advancement 558f Hypertonic
tissue mattress 49, 49f hyponatremia 75
analysis 536 osteotomy for interpositional bone graft saline 81, 88
cephalometric analysis for augmentation 265f Hyperventilation 107
orthognathic surgery 538f skeletal profile analysis 539 management of 107, 108t
802 Textbook of Oral and Maxillofacial Surgery

Hypervolemia 73 diagnostic aids 238 hydrocortisone 125


with decreased intravascular volume 73 management 238 lasix 127
with increased intravascular volume 74 surgical lignocaine 128
Hypocalcemia 77 anatomy 222 mephentine 128
Hypodermoclysis 79 procedure 231 morphine 126
Hypoglossal nerve 168 Impaction, theories of 222 noradrenaline 124
below posterior belly of digastric, Implantation dermoid 625 of aminophylline 107
identification of 717f Important planes in cephalometric pethidine 126
Hypoglycemia 103, 104, 104 analysis 539 potassium chloride 128
management of 103t Impure blow out fracture 462f promethazine hydrochloride 126
shock Inadequate distraction infection 570 propranolol 125
causes 91 Incised wound 389, 489 sodium bicarbonate 127
in conscious patient, management over nose and eyelid 390f Injuries, types of 488, 488t
of 91 over upper eyelid 489f Injury, types of 388
in unconscious patient, management Incision and drainage of lateral pharyngeal Insertional mutagenesis 695
of 92 space 346f Interdental bone, removal of 260f
management 91 Incision Interfragmentary compression 418f
prevention 91 Adson and OTT 67f Interincisal angle 537
treatment of 104 Al-kayat Bramley’s 61, 62f, 63f, 66, 585f Intermaxillary
Hypoglycemic shock 91 making, principles of 54 fixation 142, 414
Hypokalemia 77 Inclusion cysts 619 using screws 414
Hypomochlion 426 Individual screws for IMF 415f
Hyponatremia 74 coagulopathy, treatment for 217t Internal
with decreased extracellular volume 75 factor assay 786 jugular vein 168, 332
with hyperglycemia 75 Infantile osteomyelitis 373 ophthalmoplegia 457
with increased extracellular volume 75 Infection Internasal suture 463
with normal extracellular volume 75 management, principles of 349 Interpositional
without hypotonicity 75 stage of 332t arthroplasty 581
Hypothesis 747 Infectious waste 146 bone graft augmentation 266
Hypovascularity of irradiated tissue 378 management plan 146 Interpositioning temporal muscle fascia
Hypovolemia 73 treatment and disposal methods 147 flap 586f
Hypovolemic shock 85, 88 types of 146 Interrelationship between ameloblastic
causes 85 Inferior fibroma and other mixed odontogenic
type of 85 alveolar canal 266 tumors 654
Hypoxia 378 dental nerve 218 Interstitial radiotherapy 731
Hypoxic vena cava in supine position, Intervention study design 751f
cells 731 compression of 101f Interventional/experimental studies 751
tissue 329 Inferiorly based nasolabial flap 398 Intraepithelial neoplasia 669
Infiltrative basal cell carcinoma 734 Intra-abdominal dermoid cysts 625
I Inflamed duct 314f Intra-articular injections of
Inflammatory corticosteroids 594
Identifying
diseases 312 Intrabony fissural cyst 619
branches of brachial plexus 727f
hyperplasia of vestibular mucosa 259 Intracerebral hematoma See also Subdural
malignant change 676
papillary hyperplasia of palate 257 hematoma
Idiopathic trigeminal neuralgia 153
Information provided by ABG 787 Intracranial
Idiosyncrasy 118
Infraorbital hematomas 393
IJV and spinal accessory nerve 713f
canal 197 intraspinal, or intra-abdominal dermoid
Illiac crest
extension 61f cysts 626
corticocancellous graft 636f
incision 64, 64f Intraoral
exposure 518f
nerve 197, 436 degloving incision 281f
Immature RBCs 779
rim suspension wiring 442, 442f distractors 521f
Immunofluorescence of perilesional
space infection 342, 342f mucosal incision 346f
mucosa 687
Infraorbital and Borle’s temporal transport distraction device 572
Immunomodulatory drugs 685
extension 61f vertical ramus osteotomy 553
Impacted
Infundibulum 621 Intraosseous wiring 417, 444f
mandibular third molars 222
Inhalation injury management 483 techniques for 417f
maxillary third molar 239
Injection Intraseptal alveolectomy 259
classification of 242f
aminophylline 125 Invasive hemodynamic monitoring 482
teeth, management of 222
atropine sulphate 125 Inverted l osteotomy 553, 553f
third molar
avil 126 Involucrum 363
impactions, classification of 223
side effects 126 Ionic aqueous solution 315
pressure symptoms 226
calcium gluconate 129 Ionized Ca++ 783
tooth 222, 231, 238, 241
diazepam 126 Ionizing radiation exposure 734
classification 238
diphenylhydantoin 126 Ipsilateral coronoidectomy 583f, 586f
diagnosis 241
Index 803

Ischemic Lack of extraocular movements 459f Liesegang rings 652


attack in dental office 111 Lag screws 421, 421f Ligating clips disadvantages 44
management of 111 over bone plates, advantages of 422 Ligation of erich’s arch bars 413f
heart disease 110, 180, 198 Lagophthalmos 159 Ligatures 51
Island pedicle flap 284 correction of 160 Lignocaine
Islands of ameloblastoma 643 Langenback’s retractor 24f dose 128
Isotonic saline 81 Langer’s lines 55 precautions 128
Ivy loop wiring 412, 414f Langerhans lines 55f Lincoln’s highway
limitation of 413 Large lipoma in parotid area 301f anterior 332
Large radicular cyst with enucleation, of neck, anterior 346
management of 618f
J Laryngeal mask airway 143f
Lingual
cortex 404
Jaw Laryngoscopy and insertion of ETT 143f flap 232f
thrust chin lift Laryngospasm 186 incision 56
head tilt maneuver 132f treatment 186 frenectomy 256f
maneuver 132 Laryngotracheal area, anatomy of 134f myomucosal pedicle flap 286
tumors 631 Laser excision of leukoplakia 678f nerve 338
benign 631 Lasix shelf for mandibular third molars 223f
malignant 631 dose 127
Journal club presentation 772 split technique 237
side effects 127 sulcoplasty 253, 254f
Jugulo digastric nodes 702 Late tori excision 263f
cartilaginous stage 429f Lining epithelium ameloblastomatous 643
K cold shock 90 Lip
fibroblastic stage 428f injury of 399
Kaban’s protocol 579, 580
therapeutic removal 231
Kapetansky-Juri advancement flap 524, scar revision, procedure for 523
Lateral
525f, 526f with nasal injury 390f
and inferior cortex removal 372f
Kazanjian technique 250, 251 Liver function test 780
brow incision 66, 66f
Keen’s intraoral approach 453, 454 Local
cephalometric X-ray 522f
Keratocyst drug delivery 685
periodontal cyst 617, 617f
enlargement of 612 eastlander flap 724f
pharyngeal space 344
management of 615 tissue flaps 521
contents of 344
multiloculated radiluscent Localized buccal space abscess 341f
rhinotomy 59
appearance 615f Long face syndrome 532, 535
incision 60f
types of 613, 613f Low
selective neck dissection 721
Keratocystic odontogenic tumor 614, 614f subcondylar fracture 425f
tension test 469f
Keratosis 671, 672f velocity fracture 450
trephnization 226
Ketamine 177 Lower
Latham’s appliance 506, 509f
Kidney function test 782 anteriors degloving incision, flap
Laughing gas 178, 179
Kiesselbach’s plexus 464 design for 324f
Le Fort
Kinetic exercises 596 chest 121
I fracture 439, 440f
Klebsiella 356, 485 facial asymmetry 532
management of 441
Kno-pull tensile strength 35 incisor
I osteotomy 542, 543f
Knot inclination 537, 537f
II fracture 444, 444f
indicated for different suture material, protrusion 537, 537f
management of 446
types of 47 lip paresthesia 657
II osteotomy cuts 546f
tying 47 pole of submandibular salivary
types of 47, 47f III advancement osteotomy 546
III fracture 446, 447f gland 717f
Korsolex 6 Ludwig’s angina 325f, 352, 353f
Krishner’s wire 417, 417f III osteotomy cuts for total advancement
of zygomatic complex 546f Ludwig’s angina, treatment of 353
Kruger’s modification 285f
Leucovorin 730 Luebke-Ochsenbein submarginal flap 325f
Kussmaul breathing respiration 105
Leukoedema 673 Lumpy jaw 375
Leukokeratosis nicotina palati 673 Luxated teeth 412
L Leukoplakia 672, 674, 687 Lymph
Labial changing into red lesions 697f in veinous system, drainage of 703f
alveoloplasty 260 differential diagnosis of 673t node 22
frenectomy 254, 255f management of 677 structure of 701f
inferius 539 subtype and risk of malignant Lymphatic
sulcus with extensive leukoplakia 694f transformation 676t drainage of oral structures 703
superius 539 Liberal gingival retraction 202f tissue of floor 716f
Laceration Lichen planus 685 Lymphedema of face RND to ligation of
on chin 411f treatment 688 veins and lymphadenectomy 728f
types of 490 Lichenoid reaction 673 Lynch extension 60
804 Textbook of Oral and Maxillofacial Surgery

M AP deficiency 532 Meleney’s gangrene 356


bone 196 Mendelian’s theory 222
Macfee’s
canine impactions 237 Meningoencephalitis 358
incision 68, 69f
defects, reconstruction of 639 Meniscus without reduction, anterior
ladder incision 68f
deficiency 535 dislocation of 593f
Macrogenia 532
deformities 532 Mental
Magill’s forceps 143f
Magnesium sulfate, solution of 9, 32 depth angle 538 nerve 218
Malar bone 449 excess 535 neurectomy 156
fractures 450 forceps 206 repositioning 258f
Malignancies of maxillofacial region 378 hypoplasia, correction of 519 surgical repositioning of 258
Malignant length 538 neurovascular bundle 555
epithelial tumors 296 molar forceps 207f Mesenchymal cells 653
hyperthermia 178, 189 osteomyelitis 370f Mesial eruption path 241
melanoma 737 osteotomies 542 Metabolic
odontogenic tumors 663 osteotomy acidosis 78, 82
pleomorphic adenoma of left parotid anterior 547 alkalosis 78
gland 305f Wassmund technique, anterior 547 Metal suture
potential 688 Wunderer technique, anterior 548 advantages 43
of leukoplakia 676 pinch grasp 208f and clips 43
Mallampati ridge augmentation 264 clearon 44
classification 182, 183f segmental distraction 568 ethistrips 44
score 182, 183 sinus 275, 323f ligating clips 43
Malleable retractor 28f diseases of 213, 275 skin staples 43
Malposed teeth 211 surgical anatomy 275 surgical staples 43
Mandible various walls of 275f tissue glues 43
along Champhy’s lines 420f sinusitis 276 vacuum-assisted closure 44
resection of 636 treatment of 278 Metallic
surgical anatomy of 402 subapical osteotomy, anterior 554f oropharyngeal airway 137f
Mandibular third molars tracheostomy tube 137f
alveolar bone 196f surgical exposure 241 Metastasizing ameloblastoma 663
AP deficiency 532 treatment 241 Metastatic ameloblastoma
AP excess 532 tuberosity reduction 261 management 663
asymmetry 532 tumors 636 Methotrexate 730
body osteotomy 555 Maxillofacial Metronidazole 351
deficiencies 532 infections 331 Microgenia 532
deformities 532 complications of 352 Microscopic urine analysis 791
management of 584 injuries 434 Microvascular anastomosis 638
distraction 565 region, infections of 319 Microwave diathermy 595
excess 535 surgery, incisions in 54, 579 Middle
extraction forceps 208f Maxillo-mandibular fixation 412 cranial fossa 402, 424
forceps 206, 207 Mcfee’s incision 713f layer of deep cervical fascia 331
nerve 338 MCH See Mean corpuscular Midface deficiencies 532
plane angle 538 hemoglobin 778 Midline vertical approach 472f
prognathism 532 MCHC See Mean corpuscular hemoglobin Midpalatal
retromolar pad reduction 258 concentration cysts 619
sling grasp 208f MCV See Mean corpuscular volume raphae cyst of infants 616
step osteotomy 556, 557f Mean corpuscular Midpalatine split 548
subapical osteotomy, anterior 554, 554f hemoglobin 778 Migraine 172
Marey’s reflex 86 concentration 778 attacks 174
Marginal mandibular volume 778 aura phase 172
branch of facial nerve, injury to 727 Mechanical fumigator 14f diagnosis 173
nerve, identification of 717f Medial management 174
Marsupialization 608 canthal neural theory 174
advantages of 608 anatomy 471 pain phase 172
disadvantages of 608 tendon 468 postdromal phase 173
Marx-university of miami protocol 380 displacement of lateral pharyngeal prodromal phase 172
Masseter muscle 404 wall 345f serotonin theory 173
Masticatory space management 338 pterygoid muscle 403 signs 172
Matrix metalloproteinases 613 Median palatal cyst 620f symptoms 172
Mattress suture 48 Medical emergencies, classification of 99 triggers 174
Mature complex odontomas 661 Medicinal treatment of osteomyelitis 368 unifying theory 174
Maxillary Medicolegal aspects of injury 488 vascular theory 173
alveolar bone 196f Medullary paralysis, stage of 182 Migrating periosteal cells 427
Index 805

Mild Mucormycosis 357 dissection 67


epithelial dysplasia 672f Mucosal advancement 249 anterior 722
with fibrosis in underlying connective Mucositis 378 incisions for 712
tissue stoma involving muscle Mucous membrane 136 examination of 182
fibers 684f Multiloculated nodes, classification of 702f
hemorrhagic shock 86 cystic lesion with displacement and Necrosis
or thin leukoplakia 674 resorption of roots 606f of hard and soft tissues 562
or thin leukoplakia See Preleukoplakia lesion, with bony septae 615f zones of 481f
Mill wheel’ murmur 188 Multivariate analysis 760 Necrotic
Millard Mural growth theory 605 bone 363
rotation advancement repair 512 Muscle fascia, debridement of 359f
rotational flap technique 513f attachments of mandible 405f Necrotizing fasciitis 77, 356
Minor salivary gland relaxants 185, 594 Needle
of palate 303f Mycobacterium tuberculosis 348 body, parts of 45
tumors, management of 310 Myelinated nerve 163 curvature 45
Mixed structure of 163f holder to hold needle, placement of 44f
odontogenic tumors 659 Myocardial parts of 45
salivary gland 299 infarction 111 point, parts of 45
Mock surgery 541 management 111 swage, parts of 45
Moczair’s flap 284, 284f ischemia 111, 186 to curvature, types of 46f
Modal instance sampling 754 treatment 186 track infections 339
Moderate Myofacial pain dysfunction Neoglucogenesis 103
and severe hemorrhagic shock 86t syndrome 590, 594 Neoplasias See Jaw tumors
epithelial dysplasia 672f Myxedema 108 Neoplasms See Tumors
shock 86 Myxoma 658 Neoplastic disease 367
Moderately differentiated SCC 709f gross pathology 659 Nerve
Modified introduction 658 damage 218
austin’s retractor 202f prognosis 659 management 218
blair incision 66f treatment 659 hook 24f
Conley’s incision 713f injuries
Kernahan classification 504f
radical neck dissection 712
N axonotmesis, classification of 164
classification of 163
visor osteotomy 267 Nagpur classification 506
neuropraxia, classification of 163, 164
Moh’s surgery 737 Narrow nostril floor, correction of 526
involvement of 435
Moist heat sterilization 4 Narrowing of roots 229f
regeneration 166
autoclaving 4, 6 Nasal
supply of
advantages 6 and pharyngeal evaluation 536
mandibular teeth 196
disadvantages 6 antrostomy 278
maxillary teeth 196
boiling 4 bone fractures 463
Nested case control study 750
advantage 4 classification 464
cavity Neurogenic shock 85
disadvantages 4 Neurological
chemiclaving 6 examination of 469
involvement of 358 deficit 705
Monoamine oxidase inhibitors 125 disorders 199
discharge 277
Monomorphic adenoma 301 of face 153
injuries, treatment of 465
Monosodium glutamate 174 Neuromuscular blocking agents 176
regurgitation of fluid 282
Moore gilby’s collar technique 233 Neuropeptide Y 733
spine, anterior 536
Morpheaform basal cell carcinoma 735 Neutron beam therapy 731, 732
trauma 536
Morphine Neutrophilic hypergranulation 779
Nasoalveolar moulding 506, 509, 510
dose 126 Nicely framed research question 746
Nasoethmoidal
side effects 126 example of 746
complex
Morsicatio buccarum 673 Nicotina
fractures, classification of 468
Moth-eaten appearance 366 palatini 694
injuries 467
Mouth eaten, irregular radioluscency with stomatitis 680
management of 469
floating teeth and pathological treatment 680
fractures 467
fracture 709f Nidus of infection 394
region, anatomy of 467f
Mouth props 23f Nitroglycerin 169
Nasolabial flap 398
Mouth-to-mask technique 114 Nitronox 179
Nasomaxillary hypoplasia
Mouth-to-mouth breathing 113 with cleft lip-palate deformities 536 Nitrous oxide 178, 179
MRND-II, preserving IJV and spinal with prognathic mandible 535 No cellular atypia 672f
accessory nerve 713f Nasopharyngeal airway 132, 132f, 481 Nocardia asteroides 375
Mucoceles of tongue and lower lip 312f Neck Nociceptive trigeminal inhibitor 175
Mucocutaneous features 688 by providing sand bag below shoulder Nodine theory 222
Mucoepidermoid carcinoma 302 for performing neck dissection, Nodular
of submandibular salivary gland 302 extension of 714f basal cell carcinoma 734, 735
806 Textbook of Oral and Maxillofacial Surgery

masses of odontogenic mesenchyme Odontogenic leukoplakia, definitions of 672


663f and nonodontogenic cysts of lichenoid reactions 688
Nodule of maxillofacial region 603 potentially malignant disorders and
ameloblastoma projects in lumen 643 carcinoma 648 oropharyngeal squamous cell
odontogenic mesenchyme 663f cyst 603, 604, 648 carcinoma 670
NOE fracture definitions 603 squamous cell carcinoma 694, 704
complications of 473, 473t etiopathogenesis 604 modalities of spread of 700
exposure of 470f of inflammatory origin 617 site of involvement 704
with bone graft, management of 471f features of 604 submucous fibrosis 681
Nonabsorbable suture material 41 epithelium 630 etiology 681
Nonadjacent teeth 211 fibroma 655 Orbicularis
Nonhomogeneous leukoplakia 674, 675 definition 655 oculi muscle 401
Nonhomogeneous leukoplakia See also involving anterior mandible 656f oris muscle 399
Speckled leukoplakia infections 329, 330, 335 Orbit, involvement of 437
Noninvasive medical treatments 175 cause of 329 Orbital
Nonmyelinated nerve 163 local barriers 330 apex syndrome 360, 457
Non-neoplastic surgical anatomy 330 cellulitis 358
jaw lesions 631 keratocyst 612 floor removed 281f
tissue See also Hamartomatous reclassified keratocystic odontogenic fractures 460
Nonodontogenic tumor 613 Organic osmolytes 76
and fissural cysts 604 myxoma 659f Origin
cysts 619 myxoma See odontogenic myxoma of functional neck dissection 718
Nonprobability sampling 753 myxofibroma 658 theories of 620
Nonsteroidal anti-inflammatory of anterior maxilla 659 ORN, treatment of 381
drugs 174, 328 of mandible 658f Oroantral
Noradrenaline origin 661 communication 213
dose 124 fistula 281, 283
sarcoma See Ameloblastic fibrosarcoma
etiology 281
side effects 124 tumors 630, 631
management 283
Normal saline 81 introduction 630
Oropharyngeal, insertion of 132
Normoblast 779 Odontoma 659, 661f, 662f
Orthodontic
North pole tube 141f compound type 660
extraction 207
Nutrient foramen in retromolar area 223f etiology 660
surgical aid to 541
Nutrition support 685 OLEP staging system 677
treatment 517
Nutritional Oleum dulcis vitrioli 179
Orthognathic surgery 519, 531, 570t
deficiencies 695 Olfactophobia 173
clinical features 535
support 485 Olfactory nerve 435
complications of 559, 568
Nylon suture 42, 42f Oligemic shock 85 definition 531
state of 482 device failure 570
Oliguria 186
O Oncocytoma 301
introduction 531, 542, 568, 570
operative procedures 542
Obwegeser Oncogenes 695 Orthokeratinized OKC 614f
bone awl 443f Onion skin 374 Orthostatic hypotension 102
modified linguosulcoplasty 255f Onlay bone graft 264 Orthognathic surgery 532
secondary epithelization vestibuloplasty Open OSCC
252, 253 bite deformity 581f management of 710
submucous vestibuloplasty 249, 249f, 250 anterior 581 of posterior GB sulcus to
technique 260f flaming 4f kharra 694f
for alveoloplasty 260 reduction mawa 694f
for skin grafting 254 indications for 417 staging of 704
Occlusal splint 59, 595f of fracture 455 with secondaries in brain, case of 704f
Oculomotor Operculum 225 OSF
nerve 436 Oral advanced 682
palsy See Third cranial nerve brush biopsy 675 and coexistent oral cancer 683
Odontectomy 233 cancer 693 Osmophobia 173
for distoangularly impacted tooth 234f carcinogenesis 695 Osteoarthritis 586
for horizontally impacted tooth 234f etiology 694 treatment 587
for mesioangularly impacted tooth 234f pathogenesis 695 Osteomyelitis 219, 362, 367f, 368
for vertically impacted tooth 234f staging of 704 etiology 364
Odontoameloblastoma 662 cavity maxillaries neonatorum 373
macroscopy 662 concept of precancer 669 moth-eaten appearance 366f
treatment 663 introduction 669 of facial bones 362
Odontoblastomas See also Ameloblastic preparation of 17 of mandible 335
odontoma glucose tolerance test 784 in sickle cell disease 376
Index 807

sequestrum formation 369 Partial dendrites 163


surgical management 369 bilateral cleft lip and alveolus 505f introduction 162, 163
symptoms of 220 cleft lip 504f management of 167
treatment of 220, 367 and alveolus 504f nervous system 166
types of 373 maxillectomy 280 odontogenic keratocyst 613
Osteoplasia 643 superficial parotidectomy 308, 308f smear 778
Osteoprogenitor cells 427 Participants 763 vascular
Osteoradionecrosis 220, 378, 380 Partsch’s operation 606, 608 diseases 357
complications of 378 Paterson-Brown-Kelly syndrome 690 resistance/vasodilatation, loss of 85
definition 378 Pathophysiology of cachexia 733 Periradicular surgery 323
management 220 Pediatric contraindications for 323
of mandible 379f, 732 fractures 423 indications for 323
Osteotomy cut 521f jaw fractures 415 Periradicular tissues, reaction of 322
for gap arthroplasty 584f mandibular fracture 423f Persistent
for modified visor osteotomy 267f Pedicle island flap 285 airway tract obstruction/hypotension,
for SSO on mandible 551f Pell and Gregory’s classification 224, management of 95
for total mandibular subapical 224f, 225 labial groove 498
ostetomy 555f Pemphigus 687 Pethidine
Ostium maxillare 275 Pen grip 21f, 55f dose 126
Otologic sequelae 732 Penetrating injuries 392 side effects 126
Outline of study protocol 745 Penicillin 328 Pharyngeal See also Branchial arches
Overlay grafting for augmentation chemical structure of 93f Pharyngomaxillary space 344
genioplasty 561f Penicillinase 351 Pharyngoplasty 519
Ozone gas sterilization 11 Penrose drain 31 technique 520f
disadvantages of 12 Peptostreptococcus 356 Phencyclidine derivative 177
Ozone gas sterilizer, advantages of 11 Phenergan 181
Periapical
Pheniramine maleate 126, 181
abscess, case of 322f
Phentolamine mesylate 117
P cyst 327f
Pheochromocytoma 125
dental radiograph benign
Packaging of infectious waste 147 Phleboliths, formation of 621
cementoblastoma 657f
Paclitaxel 730 Photodynamic therapy 737
infection
Paget’s Photomicrograph of
anatomical considerations 323
disease 211, 364, 657 parakeratinized OKC 614f
causes 321
test 624 radicular cyst 619f
fate of 321
Palatal Physical carcinogens 696
management of 321 Pierre Robin sequence 503f
changes associated with reverse surgeries 321, 322
smoking 679 Pigmented basal cell carcinoma 735
surgery, indications for 323 Pindborg’s tumor 646
fistula 521 zone of
anterior 523f Pipe smoker’s palate See Nicotina
contamination 322 stomatitis
flap 284 infection 322
design 325f Pitcher plant extract 170
irritation 322 Pituitary ameloblastoma 640
gingiva and maxillary ridge 258 stimulation 322
hinged flap 285, 286f Planning
Pericoronitis 225, 225f and design of operating room 12
mucosa with small elevated nodules 679f Peridontal abscess 322f research 748
root of maxillary molar 334f Periodontal Plaque type See also Lichen planus
rotational-advancement flap 285, 285f ligament 658 Plaster of Paris 443
tor, removal of 262f pocket formation 226 Platelet-derived growth factors 431
Palate Perioperative complications of Pleomorphic adenoma 299, 301f, 310f
development of 499f tracheostomy 140 of palate 309f
formation of 499 Periorbital burns 485 of parotid 309f
Pancuronium 185 Periosteal Plummer-Vinson’s syndrome 695
Papillary cystadenoma lymphomatosum 301 blood supply 424 Plunging ranula 312
Parade ground fracture 404 reaction 367f PMMC flap for reconstruction 726f
Paranasal Periosteum 330 Pneumothorax 186
access incision 546f muscle 254f treatment 186
air sinuses, involvement of 437 of bone 250f Poliglecaprone 25 monocryl 41
Paresis of facial nerve 159f Peripheral Polydioxanone 41
Parkland formula for estimation of fluid 482 ameloblastic fibroma 654 Polyester fiber suture 42
Parotideomassetric fascia 331 ameloblastoma 639 Polyglycolic acid 37
Parotid blood smear cell picture 779 advantages 37
gland 66, 292f cell division 605 uses 37
surgical anatomy of 292 circulatory failure 86 Polyglyconate 40
tumors, management of 307 nerve injuries 162 Polymorphous low-grade
Parotitis, case of 312f axon 163 adenocarcinoma 306
808 Textbook of Oral and Maxillofacial Surgery

Polyomavirus 299 Premalignant Pyogenic osteomyelitis 377


Polyproline suture 42 and malignant changes, advance cases Pyramidal fracture 444
advantages 42 with 684 Pyriform fossa wiring 442, 442f
uses 42 condition 670
Poor type of central odontogenic Preoperative radiation therapy 732
fibroma 656 Preparing synopsis 745 Q
Poorly Preprosthetic surgery, scope of 245 Quadripoid fracture 450
differentiated scc 709f Presentation of journal club 772
framed research question 746 Presurgical orthodontics 506, 517, 540 R
Pop splint 466, 467f advantages of 540
Ra factor 781
Porosity of bone 245 Prethyroid fascia 331
Portex drainage tube 31 Pretracheal fascia 331 Raccoon’s eye 436f
Positron emission tomographic scan 367f Prevertebral fascia 331 Radiation
Postanesthetic care 189 Primary and chemotherapies 729
Postauricular approach 63, 63f bone healing 417, 429 induced cancer 732
Postauricular incision 580f canine, extraction of 238 therapy 729
Postdental extraction hemorrhage 218, 218t intraosseous carcinoma 663, 699 Radical neck dissection 712, 714
Posterior rhinoplasty 525 SCM, IJV and spinal accessory 712f
lincoln’s highway 331f squamous cell carcinoma 304 Radicular cyst 617, 617f
maxillary osteotomy 548 Primordial cyst 604, 609 with incisors presenting as a palatal
complications 549 Prior to neoadjuvant chemotherapy 729f sinus 618f
surgical technique 549 Priorities in management of anaphylactic with nonvital
nasal spine 537 shock 95 maxillary incisors 618f
segmental maxillary osteotomy, Priorities in management of polytrauma tooth 606f
variations of 549 patient 473 Radiopaque sequestrum 367f
Posteroanterior cephalometric analysis 538 Prognathic mandible 535 Ramus
Posterolateral neck dissection 722 Prolene suture 43f of mandible 337
Postirradiation dental care 380 Proliferative verrucous leukoplakia 675, 675f with preservation of neurovascular
Postoperative Promethazine 181 bundle, enucleation of 612f
dyspnea 728 Prophylactic Ranula 311
radiation therapy 732 space augmentation 238 Rare variants of ameloblastic fibroma 653
Postramal treatment 170 Rathke’s pouch 641
approach 425 Propofol 176 tumor 640
hind’s approach for fixation of fractures Prosthion 536 RCT, design of 752
with miniplates 425f Proto-oncogenes 695 Receptor activator of nuclear factor-KB 613
Post-styloid or retro-styloid compartment Pseudarthrosis 432 Reconstruction plate
344 Pseudoanaphylaxis 94 fixation of 638f
Postsurgical lip deformities, evaluation Pseudocyst 604 with condylar prosthesis 638f
of 522 Pseudohypertelorism See also Traumatic Red
Post-trauma ectropion, correction of 401f telecanthus indurated patch 696
Post-traumatic osteomyelitis 377 Pseudomonas 14, 484 rubber corrugated drain 29
Post-treatment reduction of tumor size 729f aeruginosa 485 advantages 29
Postural hypotension 102 Pterygomandibular space, boundaries of disadvantages 29
management of 103t 339, 339f Redivac drain 31
reflex mechanisms 102 Pterygoid plexus 453 Redon and vaillant incision 67f
Poswillow’s hook 453, 453f Pterygomandibular space 338 Reduction
Potassium drainage of 339 genioplasty 556
abnormalities 76 management 339 glossectomy 552f
chloride sources of infection 339 of dislocated condyle 214f
dose 128 Pterygomaxillary fissure 537 of dislocation 589f
side effect 128 Ptosis of of knife-edged 261
permanganate 9 eye 457 of mucoperiosteal flap 211f
Potentially malignant upper eyelid 436f of mylohyoid ridge 261
disorders 669 Pulmonary Regional lymph node 296
of oral cavity 669 edema 82 metastasis management 711
lesions 670 mucormycosis 358 spread 700
Preanesthetic medication 180, 181 support 88 Regional muscle transfer 160
Preauricular incision 61, 580f wedge pressure 82 Regulation of osmolality 72
Precancerous nature and malignant Pulpal tissue of tooth still remained Relation of basilar artery 154f
transformation 682 vital f 657 Relaxed skin tension lines 55
Precervical sinus 622 Pure hyperfractionation 731 Removing
Pregnancy glycosuria 105 Purse-string suture 50 class III impacted canine, surgical
Preirradiation dental care 380 Push-back technique 514f approach for 241f
Preleukoplakia 674, 674f PVC tracheostomy tubes 137f gloves 20
Index 809

Renal disorders 98, 198 S Seddon’s


Repositioning splint, anterior 595f and Sunderland’s classification 165t
Saboraud’s glucose agar 360
Resected specimen of maxilla 739f axonotmesis 164
Sagittal split osteotomy 549, 551f
Resection without continuity 636 classification 165
modification of 551
Residual deformity treated by mandibular Segmental
Salivary
distraction 567f mandibulectomy f 711
caruncle 292
Respiratory maxillary osteotomy 547
duct, dilation of 313
acidosis 78 maxillectomy 280
fistula 316
alkalosis 79 osteotomy cut 547
gland 22
distress syndrome, adult 82 Selecting suitable study design 748
diseases of 291, 297
tract emergencies 106 Selective neck dissection 712
embryological development 291
Resting skin tension lines 55 anatomical basis for 718
pathologies, classification of 295
Retromandibular incision 59, 60f indications 718
swellings 299f
Retropharyngeal space 347, 348f types 718
tumors 295t, 299, 301
Reverse smoking 694 Semilunar incision 57, 57f, 325f
incidence of 295
treatment 680 Seminar 769
management of 307, 310
Reversible hemorrhagic shock 86 and journal club presentation 768
viruses 299
Rheumatoid arthritis 587 definitions 769
injuries 562
treatment 588 Sensitivity of radiation therapy,
Samengo incision 67f
Rhinocerebral mucormycosis 358 determinants of 730
Sample measurement 760t
Rhinoplasty 524, 525 Sensory and motor
Sampling error 747t
nerve injuries 559
Rhizotomy 157 Sampling methodology 752
neurons 162t
Rhombic flap 398 Sandwich
Sentinel node biopsy 707
Rhyrocricotomy 133 genioplasty 557, 560f
Septal-mucosal flaps 515
Ribbon gauze pack 466, 466f osteotomy 266
Septic
Rickett’s analysis 538 technique 267f, 441
shock 89
Ridge Saucerization, surgical technique for 370
syndrome 89
augmentation procedures 263 Sawangi protocol 686f
Septicemia 332
extension procedures 248 Sawhney’s grading 578t
Sequelae of impacted third molars 225
Rigid Saw-tooth ridge 261
Sequence of tooth extraction 201
arch bars 414 Scales of measurement 760
Sequencing naso-orbito-ethmoidal
internal fixation 417 Scalp rotation flap 481f
fractures 472t
Ringer’s solution 81 Scar
Sequestration dermoid 625
Risdon’s contractures of lips and buccal mucosa,
Seroma 727
approach 339f, 425 correction of 256
Serum
submandibular of stellate laceration 390f
calcium 783
approach 59 revision of cleft lip 522
creatinine 782
incision 59f, 341 Schistocytes 779
phosphorus 783
wiring 412, 413f Schobinger’s incision 68, 68f, 713, 713f
potassium 782
Rochon-Duvigneaud syndrome 457 Schuchardt’s transversal flap 286, 286f
sodium 782
Rodent ulcer 735 Scintillating scotoma 172
urea 782
Romovac drain 31 Sclerosing 735
Seven fundamental changes in cell
Root Sebaceous
physiology essential for malignant
canal treatment 324 carcinoma 306
transformation 696
cone implants 248 of parotid gland 306f
Severe
cyst 603, 621
into antrum, displacement of 214 cachexia of malignancy 732f
classical black punctum 622f
resorption of second molar 226 epithelial dysplasia 672f
excision of 622f
Rotational flap technique 395f nasoethmoidal injury 469f
Sebum 621
Routine guidelines for diagnosis of odontogenic infections 338
Second molar
leukoplakia 676 paranasal hypoplasia 544
paramarginal flap with vestibular
Row’s periodontal disease 197
extension 56
disimpaction forceps, application of 441f shock 86
sulcus incision 56
maxillary disimpaction forceps 444 trismus 577f
Secondary
zygoma elevator, application of 455f Sevoflurane 179
aneurysmal bone cysts 621
Rowe and Sharpey’s fibers 195
bone
Killey classification 464 Shen gray pallor 86
healing 417
Williams’ classification of midface Shobinger’s incision 69f
repair 427
fractures 438t Shock 85
epithelialization vestibuloplasty 252
Rowe’s zygoma elevator 454 type of 85
rhinoplasty 525
Royal demolition explosive 491 Short face syndrome 532
Securing
Rule of two 102, 331 Shoulder
medial canthal tendon, method of 472f
Rushton’s hyaline bodies 618 morbidity 727f
tendon, method of 471
syndrome 724
810 Textbook of Oral and Maxillofacial Surgery

Sialadenitis, cause of 313 corrective surgeries 254 Straight


Sialolith in injuries, management of 387, 393, 410 advancement flap 285f
orifice of Stensen’s duct 313f landmarks 539, 540f elevator used as lever 203f
Warton’s duct 314f menton 539 pull tensile strength 35
Sialolithiasis 313 nasion 539 Stranc and robertson classification 465, 465f
Sickle cell pogonion 539 Stress reduction with anxiolytic agents 594
disease 376, 377 reconstruction 724 Stridorous breath sounds 183
osteomyelitis 377 Sole removal of sequestrum 370 Strokes hand scrubbing 15f
Sideropenic dysphagia 690, 695 Solid Structures involved in superior orbital
Sideropenic dysphagia treatment 690 primary intraosseous carcinoma 664 fissure syndrome 459f
Silk suture 41f variant of ameloblastoma in ramus Stylocarotid syndrome 168
Silver perforating cortex 637f Subacute suppurative osteomyelitis 365
nitrate 9 Solutes in extracellular and intracellular Subciliary
sulfadiazine 483 water, composition of 72 extension 60, 60f, 61f
Simple South pole tube 141f incision 64, 65f
alveoloplasty 259 Space Subcondylar fracture 406
bone fracture 402 around causing open bite 426f
closure of small oac 283f jaw bones 333t Subconjunctival hemorrhage 450, 451f, 437f
comminuted bone fracture 402 mandible 333 Subcuticular sutures 49, 50f
interrupted suture 48f maxilla 333, 341 Subdural hematoma 128
random sampling 753 boundaries of 335 Subepithelial band of chronic inflammatory
Single cell infiltrate 687f
Specimen of enucleated lining 607f
blind trials 751 Subeschar clysis 483
Speckled leukoplakia 674f, 675
pedicle advancement flap 396 Sublingual
Spherocytes 779
tooth osteotomy 547 gland 337
Spinal
advantages 547 surgical anatomy of 294
accessory
disadvantages 547 tumor, management of 308
exposure of 719f
tooth wiring 413 hematoma step deformity 406f
nerve 716f
Sinus, roof of 280f ranula 312f, 608
injury 488
Sinusitis 277 salivary gland 303f
Spirit composition 8
classification of 277 space infection 336, 337f, 338f
Site predilection for occurrence of OKC 613f Splinting nasal bone fracture 467f
management 337
Skeletal convexity, degree of 539 Splints 415 space, boundaries of 337
Skin construction of 542 spread of infection 337f
adnexa 625 Spread of periapical infection 335f Submandibular
graft 253, 673 Spur cells See acanthocytes abscess, case of 336f
hook 25f Sputum 484 gland 293, 294f, 310f, 313
Skip metastasis 703 Squamous surgical anatomy of 293
Sliding genioplasty 556, 559f cell carcinoma 304, 675, 679, 698 space infection 334
Sluder’s odontogenic tumor 649 swelling in sialolithiasis 314f
neuralgia 169 histogenesis of 649 tumor, management of 308
syndrome 168 history 649 Submarginal incision 57, 57f
SMF introduction 649 Submasseteric
treated with buccal flap pad grafting 685f treatment 650 space
with OSCC of retromolar area and S-S intranasal splint 466 abscess 340f
lower lip 683f Staging system for oral leukoplakia 677 infection 339
Smoked tobacco 673 Standard weber-ferguson incision 60f Submental space 336
Smokeless tobacco 673 Staphylococcus aureus 348, 483 anatomical boundaries of 336f
Snowball sampling 754 Start with research question 746 management 336
Soap Status source of infection 336
bubble 659 asthmaticus 107 Submucosal
appearance 633 migrainosus 174 suturing, advantages of 253
Sodium bicarbonate Steinman’s pins 416 vital root retention 247
dose 127 Stellate reticulum 616f technique of 247
side effects 127 Steps in diagnosis of oral leukoplakia 675 Subnasale 539
Soft Sterile Subspinale 537
metal sheet 467f gown, application of 16 Subtarsal incision 64, 65f
of flexible arch bars 414 suture 35 Sub-zygomatic fracture 439
palate repair 516 technique 3 Suction drain 31
tissue Sterilized instruments, handling of 12 Suicidal
cephalometric Sterillium composition 7 and homicidal injuries 492t
analysis 539 Sternocleidomastoid muscle 346f wounds 492
parameters 540t Strabismus 452f Sulcoplasty 248
Index 811

Sulcular incision 56, 56f Swan-Ganz catheter 89 Teratoid cysts 624


Sulfur granules 375 Sweet’s diagnostic criteria 155 Teratomatous dermoid cyst 625
Suncope, stages of 99t Swelling Terms in infection 332
Sunderland’s classification 165 and trismus 218 Tessier’s classification
Superficial of lips 92 bony clefts 507f
basal cell carcinoma 734, 735 Swiss cheese 303 of craniofacial clefts 506f
burn wounds 483 Syndromic clefts 502 soft tissue clefts 507t
dermis 480f Synergestic necrotizing cellulitis 356 Testing of hypothesis 747
layer of deep fascia 331 Synovial joint 575 Tetanus
partial thickness 478 Synthetic tissue engineered dressings 484 immunization 393
second-degree burns damaging dorsa Syphilis 689 prophylaxis 483
of fingers 480f management 689 Tetrahydrofolic acid See also Leucovorin
temporal space 343 Syphilitic Thermocoagulation of ganglion 157f
boundaries of 343 leukoplakia 677, 689 Thick leukoplakia See also Homogeneous
Superior osteomyelitis 376 Thiopental sodium 177
dental plexus 197 Systemic Third cranial nerve 436f
mediastinal 702 factors compromising host immunity 364 Third degree burn 481f
orbital fissure syndrome 457 hormones 430 Third molar
ptosis of eyelid 459f removal of 243f
Superiorly based nasolabial flap 398f surgery
Support to fractured lower jaw using four T complications of 237
tailed bandage 410f Tactoids 376 evaluation of 227
Suppurative parotitis 312 Target cells 779 Thoma’s angulated vertical incision and
Suprahyoid Tarsal plates 460 hockey stick incision 61f
muscles 403 Taxanes 730 Three-D CT scan multiple cortical
neck dissection 712 Tear cancer 734 perforations 615f
Supramentale 537 Tear type of laceration over face 490f Throat, angle of 539
Supramucosal vital root retention 247 Teardrop-shaped cells 779 Thyroglossal
Supraomohyoid 720f Teeth, extraction of 380 cyst 603, 624, 624f
neck dissection 714, 720 Telecanthus 468 tract 624
selective neck dissection 719 Teletherapy See External beam cyst 623
Supraorbital rim radiotherapy symptoms 624
suspension wiring 443 Telodendria 163 Thyroid
wiring 443f Temporal function test 784
Surgery, principles of 3 arteritis 171 storm 109
Surgical signs 171 Thyrotoxic crisis 125
anesthesia 182 symptoms 171 Thyrotoxicosis 109
cotton 43 tests 171 management 109
advantages 43 treatment 171 Tic douloureux 153
disadvantages 43 fascia 62f Timing for staged reconstruction of cleft
defects, reconstruction of 722 pouches, anatomical boundaries of 343f deformities 510t
emergencies 118 space 343 Tinel’s sign 167
hemorrhage 118 Temporalis muscle 339, 404 Tissue
management 118 fascia, use of 286 dissection of 22
systemic treatment 120 flap 61f growth factor 428
Suspensory ligament of lockwood 438f harvested for interpositional handling and tissue respect 20
Suture 35 arthroplasty 584f matching 492
and properties, types of 38t sutured over zygomatic arch 584f retraction 22
classification of 40t Temporary fixation of fracture with Titanium mesh and fixation of fracture using
lacerated wound 480f horizontal stay wire across fracture miniplates 463f
material line 410f TMJ
catgut 37 Temporomandibular joint 61, 131, 196, 536 ankylosis 567f
chromic catgut, types of 37 ankylosis 575 management of 579
plain catgut, types of 37 classification 576 arthrocentesis 597
parts of 46f complications 584 indications for 597
principles 46 dislocation of 213 TNM
properties of 35 disorders 575, 585 classification 704
removal 51 arthritis 585 and staging of salivary gland
technique of 51 management 586 neoplasms 295
selection, principles of 36 surgical anatomy 575 of oral squamous cell carcinoma 703
size 37 Temporozygomatic suture 456 Toggle bone 472
technique, removal of 53f Tennis racket 659 Toludine blue 675
Suturing techniques 48 Tennison and randall triangular flap Tongue
Swage, types of 45 repair 511 and retromolar area 683f
812 Textbook of Oral and Maxillofacial Surgery

facilitate bilateral spread of infection Transcutaneous electrical nerve U


337f stimulation 160
protrusion and lifting of 338f Transfixing suture 52f Uncommon dentofacial deformities 532
stitch 133f Transforming growth factor-beta 431, 660 Undisplaced fractures 450
application of 133 Transmyelohyoid 470 Unfavorable fracture 405f
Tools 755 Transoral removal of calculus in duct of Uni and bicoronal incisions 58f
Tooth or root into tissues, displacement submandibular salivary gland 315f Uni/hemicoronal approach 58
of 214 Transport bone distraction osteogenesis 570 Unicoronal 579
Topazian’s Transudation and exudation 605 incision 456, 580f
classification 576 Transverse Unicystic
protocol for antibiotic regimen for incision 262f ameloblastomas 635, 641
osteomyelitis 369 palatal cut 548f involving anterior mandible 643f
Topical wound agents 483 Trapezoid flap 325f management 644
Torus Traumatic prognosis 641
mandibularis 263 arthritis, hemarthrosis 585 type 641
on occlusal radiograph 263f bone cyst 619, 620 Unilateral
palatinus 262 treatment 620 cleft palate 517
Total DNS 465 epistaxis 450
body water 71 telecanthus 468 TMJ ankylosis
interpositional bone graft 264 theory 619 of left side 577f
intraveinous anesthesia 185 Trauner’s technique 253, 254f with deviation of chin treated with
mandibular Treacher Collin’s syndrome 468 extraoral mandibular distraction
onlay bone grafting 265f Treated with hypomochlion and anterior device 567f
subapical osteotomy 554 elastic traction 426f Uniphasic reactions 95
maxillary Treatment planning and timing of United States pharmacopeia
onlay bone grafting 264f surgery 507 classification 37
osteotomy with advancement 264 Trendelenburg position 101f Universal
maxillectomy 281f Treponema denticola 219 precaution suit 15f
onlay graft 265 Triangle dissection, anterior 715 symbol of hazardous biomedical
osteotomized maxilla, advancement Triangular flap technique 512f waste 146f
of 265f Trifluoroacetic acid 180 Unstable systemic disease 198
parenteral support 485 Trifocal transport distraction 571f Unsupported and hypermobile gingiva 258
parotidectomy with facial nerve Trigeminal Untractable asphyxiation 483
preservation 308 nerve 153 Upper
respiratory obstruction 120 neuralgia 153 bionet forcep used for extraction of root
Toxic descriptions of 153 fragments 207f
granulation See Neutrophilic Triggering agents treatment 189 cowhorn forceps for molars 207f
hypergranulation Tripod left side 207f
shock syndrome 356 fracture 404 right side 207f
Toxicology 492 grip of needle holder 45f eyelid 390f
Trachea Triradiate incision See also Crile’s ‘Y’ injury of 400f
exposure of 139f incision jugular 702
surgical anatomy of 135 True hamartomas 626 lid blepharoplasty incision 66, 66f
Tracheal Tube molar, position of 537
dilator 139f drain 30
Urinary tract infection 484
intubation position of 142
Urine 105, 484
contraindications for 141 shift technique 228, 229f
examination 789
indications for 140 Tuberculous osteomyelitis 375
USG of malignant lymph node 707f
Tracheostomy 131, 134 Tubes, type of 142
UV rays, exposure to 695
decanulation of 140 Tubulodermoid 625
indications for 136 Tumors 630
set 138f benign 631
surgical anatomy 135 changes behavior of 701f
V
tube 137 like malformation 661 Vacuum drain 31
subsequent care of 139 malignant 631 Vagal nerve 168
types of 137 necrosis factor, TNF-alpha 87 Vagoglossopharyngeal neuralgia 157
uses of 136 spread 635 Vagolytic drugs 101, 181
Traditional narcotic analgesics 185 Turner’s hematoma 474 Vagus
Transalveolar extraction 210 Turpentine IP 9 exposure of 719f
indications for 200 Two flap palatoplasty 514, 516 nerve 332
Transantral Type of cyst formed, stages of 604t injury to 727
approach 454 Typical Valid and reliability of data to good
palatal osteotomy 549f basal cell carcinoma 635 quality 756f
Transconjunctival incision 65, 65f dumbbell-shaped swelling in temporal Van der Woude syndrome 503f
with lateral canthotomy 66f pouch infection 344f Variables in distraction 563
Index 813

Varieties of Viruses 673 WHO classification of


dentigerous cyst 610f Visceral fascia 331 biomedical waste 146
central 610f Visor osteotomy 266 odontogenic tumors 630
circumferential type 610f technique for 267f Wick drain 29f
lateral 610f Vitamin deficiency 673 Wickham’s striae 686
Various dye agents Volkmann’s canals 362, 366 Wide
advantages 315t Vomer flaps 515 flaring nostril, correction of 526
disadvantages 315t von Langenbeck procedure 516 unilateral cleft lip with depressed
Various mechanisms suggested for nose 500f
etiopathogenesis of OSF 681 Winter’s
Vaseline gauze dressing 32 W classification 223
Vasoactive drugs 90 Waldron operation 606, 608 lines 224
Vasodepressor syncope 99, 101 Waldron’s method 608 Wispy 659
Vasogenic shock 85 advantages 609 Wolff’s law 428
Vasovagal disadvantages 609 Worth’s criteria 366
shock 99 Wallace’s rule of nine 478f Wound
management 100 Wallerian degeneration 166 debridement 394, 394f
syncope, management of 100 Walsham’s forceps 466f definition of 387
Veau’s classification 503 application of 466f dressings, classification of 33
Vemilionectomy 681 Walsham’s nasal 466 for closure, preparation of 235
Venous air War lines 225f infections and wound breakdown 724
emboli Wardill-Kilner pushback palatoplasty 514 management 483
signs 188 Warm shock, stage of 89 types of 388
symptoms 188 Warthin’s tumor 301 Woven bone 428, 430
treatment 188 Washing sink, design of 16f Wrinkling on forehead, loss of 159f
embolism 186 Water W-shaped approach 471, 472f
Ventricular fibrillations 114 and electrolyte therapy, principles of 79
Vermilion deficiency 524f deficit, calculation of 76
oropharyngeal airway 189
X
Vermillion margins 523
view 465 Xeroderma pigmentosum 690, 734
Verruciform leukoplakia 675
Verrucous carcinomas 697, 698f Weak iodine solution 7
Versajet water dissector 485 Weakening eye sight 199 Z
Vertical Weapon, types of 492 ZMC, classification of 451f
body osteotomy 556, 557 Webbing, correction of 526 Z-plasty
loading autoclaves 5f Weber-Ferguson for correction of step deformity of
mattress 49 incision 60, 60f, 61f, 645 vermilion border 524f
sutures 49f for partial maxillectomy 281f technique, stage of 398f
maxillary with lynch extension 60, 60f Zygomatic
deficiency 532, 535 Wedge arch fracture 460f
excess 532, 535 mandibulectomy 710f type of 459f
osteotomies, anterior 549f principle 206f bone 64, 439, 454
reduction genioplasty 558f Well demarcated erythematous plaque on fracture, management of 452
surgical procedure for 559f lateral border of tongue 678f buttress 442, 456f
skeletal profile analysis 539 Well differentiated SCC 709f fracture 458f
subsigmoid osteotomy 555, 556f squamous cell carcinoma 650 management of 458f
Vesicles on palate 682f Wet dressing 32 suspension wiring 442
Vesiculo-erosive diseases 686 Wheel and axle principle 204 Zygomaticomaxillary
Vestibular extension 56 White buttress 449
Vestibuloplasty procedures 249 shock, stage of 90 complex fractures 450
Vicryl suture 40f sponge nevus 673 suture 449
Vinca alkaloids 730 Whitish lining of hydatid cyst 628f Zygomaticotemporal branch of
Viral carcinogens 696 Whitnall’s tubercle 438, 448, 450 facial nerve 587f

You might also like