EDITED BY GAUNT, TANG AND WALSH

GENERAL SURGERY
OUTPATIENT DECISIONS
second edition GENERAL SURGERY
OUTPATIENT DECISIONS
second edition

OUTPATIENT DECISIONS
GENERAL SURGERY
Few doctors receive formal training in how to conduct an outpatient consultation or how to compose
and dictate an outpatient letter. Trainee surgeons in each new speciality spend their first few weeks in
outpatient clinics learning by experience with all the pitfalls this entails. Much work involves seeing
patients who have been brought back for review by their predecessors. Problems are caused by
inexperience, unfamiliarity, fear of making mistakes, the pressure of patient numbers and lack of training.
New doctors will find little help in the standard textbooks on how to follow-up patients. This book
provides the necessary background information to enable rational decision making in a concise and
economical style. It describes reasonable and safe lines of management suitable for most patients, ideal for
when discussion with a senior colleague is not possible.
The information in this new edition has been revised, expanded and presented in the context of today’s
specialist clinics and multidisciplinary teams. This new edition is multi-authored to take account of the
multidisciplinary approach.
As well as an overall review of general outpatient issues, every major speciality is covered, with clear notes
for each condition covering history, examination, investigations, results, treatment, follow-up and post-
operative follow-up. The book can be read before or during clinics, and enables trainees to have an action
plan in mind before they walk into a consultation.
All surgeons have to be trained to go through the process of dealing with unfamiliar clinical conditions
for the first time. Surgeons will use this book as a useful foundation on which to build their own personal
knowledge.
other radcliffe books of related interest
Handbook of General Surgical Emergencies
Sam Mehta, Andrew Hindmarsh and Leila Rees second edition
Safe Sedation for All Practitioners
a practical guide
James Watts
Treating Common Diseases
Hugh McGavock and Dennis Johnston

EDITED BY MICHAEL GAUNT, TJUN TANG AND STEWART WALSH

www.radcliffe-oxford.com
foreword by stephen brearley
Electronic catalogue and
worldwide online ordering facility.

9781846191916_gaunt_pb.indd 1 8/9/08 10:32:04

General Surgery Outpatient Decisions
SECOND EDITION
This page intentionally left blank
 General Surgery
Outpatient Decisions
SECOND EDITION

Edited by
MICHAEL GAUNT MD, FRCS
Consultant Vascular Surgeon, Cambridge University Hospitals NHS
Foundation Trust, Cambridge, UK
Associate Lecturer, Cambridge University, UK

TJUN TANG MRCS

Specialist Registrar in General & Vascular Surgery, Eastern Deanery, UK
Clinical Research Associate, Cambridge Vascular Unit, Cambridge University
Hospitals NHS Foundation Trust, Cambridge, UK
and

STEWART WALSH MSc, MRCS

Specialist Registrar in General & Vascular Surgery, Eastern Deanery, UK
Clinical Research Associate, Cambridge Vascular Unit, Cambridge University
Hospitals NHS Foundation Trust, Cambridge, UK

Foreword by
STEPHEN BREARLEY MChir, FRCS
Consultant Surgeon
Director, The Whipps Cross Higher Surgery Course

Radcliffe Publishing
Oxford • New York
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742
© 2008 by Michael Gaunt, Tjun Tang and Stewart Walsh
CRC Press is an imprint of Taylor & Francis Group, an Informa business

No claim to original U.S. Government works

Version Date: 20160525

International Standard Book Number-13: 978-1-138-03088-6 (eBook - PDF)

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Contents

Foreword viii
Preface to second edition ix
Introduction x
About the editors xii
List of contributors xiii
List of abbreviations xv

1 General outpatient issues 1

Michael Gaunt, Tjun Tang and Stewart Walsh

2 Breast 10
Fiona MacNeill
Breast lump
Breast pain
Nipple discharge
Nipple retraction/inversion
Post-investigation follow-up
Male breast problems
Post-operative clinic visit
Breast cancer follow-up visit

3 Neck and endocrine 30

Bill Fleming
Thyroid lump
Thyroid lump results clinic
Post-thyroid surgery follow-up visit
Hyperparathyroidism
Cervical lymphadenopathy
Salivary gland lumps
Post-operative salivary gland lump
Thyroglossal duct cyst
MEN
Disorders of the adrenal gland

4 Oesophagus 57
Edward Cheong
Hiatus hernia
Congenital diaphragmatic hernia
Traumatic diaphragmatic hernia
Reflux oesophagitis
Non-reflux oesophagitis
Benign oesophageal stricture
Achalasia
 Vigorous achalasia
Diffuse oesophageal spasm
Nutcracker oesophagus
Pharyngeal pouch
Motility disorders secondary to systemic disease
Oesophageal cancer

5 Stomach and duodenum 75

Richard Hardwick
Dyspepsia/epigastric pain
Dysphagia
Post-gastric surgery/potential complications
Gastric tumours
Gastric cancer

6 The small intestine and vermiform appendix 94

Alastair Windsor
Intestinal bleeding
Intestinal malabsorption
Short gut syndrome
Crohn’s disease
Carcinoid tumours
Carcinoid syndrome
AIDS enteropathy
Radiation-induced bowel disease
Post-appendicectomy follow-up

7 The spleen and lymph nodes 115

Neville Jamieson
Follow-up following splenectomy
Referral by another speciality for possible splenectomy
Assessment and management of left upper quadrant pain/mass
Conservative trauma management
Lymphadenopathy

8 Liver, biliary system and pancreas 127

Satyajit Bhattacharya and Adrian O’Sullivan
RUQ pain
Jaundice
RUQ/epigastric mass/hepatomegaly
Liver tumours/metastases
Post-cholecystectomy
Post-pancreatitis
Pancreatic Tumours
Rare HPB disorders

9 Colon, rectum and anus 190

Henry Tilney and Paris Tekkis
Rectal bleeding
Diarrhoea
 Constipation
Diverticular disease
Polyps
Colorectal carcinoma
Irritable bowel syndrome
Proctitis
Radiation proctitis
Rectovaginal fistula
Rectourinary fistula
Rectal prolapse
Anorectal fistulas
Pruritis ani
Incontinence
Haemorrhoids
Anal carcinoma
Pilonidal sinus disease
Stomas

10 Vascular 239
Umar Sadat and David Cooper
Assessment of painful legs
Carotid artery disease
Buerger’s disease
Aortic and iliac aneurysms
Peripheral artery aneurysms
Vasospastic disorders of the arteries
Primary varicose veins
Superficial thrombophlebitis
Recurrent varicose veins
Chronic venous insufficiency
Leg ulceration
The swollen limb
Lymphoedema
The diabetic foot
Arterial disease of the upper limb
Thoracic outlet compression syndrome
Amputation

11 Lumps and bumps 294

Miles Banwell and Michael Irwin
Skin lumps
Groin lumps
Lymph nodes
Ingrowing toenails
Scrotal lumps/testicular swellings

Index 321
Foreword
Doctors in clinical practice spend most of their time making decisions, often without
realising it. The decisions most often recognised as such are those concerning treatment
– not simply what treatment to recommend but whether to recommend any treatment
at all – but decision making starts whenever a doctor first meets a patient, not when the
patient’s work up has been completed. Doctors are constantly having to decide what ques-
tions to ask in the light of the patient’s presenting complaint, what physical examination
to undertake, whether to investigate further, what investigations to do, what explanation
to give to the patient at each stage, whether the information gleaned is sufficient to make
a sound diagnosis and develop a treatment plan, and so on.
In order to be soundly based, all these decisions need to be founded on an understand-
ing of the pathology of surgical and other diseases, the symptoms to which they may give
rise, the physical signs which they may produce and the investigations which may be used
to detect them, including the reliability of those investigations. Much of this informa-
tion is conveniently brought together in this book, which aims to lead the inexperienced
surgical trainee systematically through the assessment and management of a wide range
of conditions frequently seen in surgical outpatient clinics, pointing out some common
pitfalls along the way.
That such a book is needed is beyond doubt. Just as well-informed and thoughtful
decision making leads to optimal patient care, poor decision making, even over apparently
trivial matters, may lead to patients being harmed and to litigation. Many more actions
in medical negligence result from poor decisions than from poor surgical technique. Yet
it is still not rare for young surgeons to be asked to see patients in clinics without direct
supervision and without their having been given any specific training in how to meet
the particular demands of outpatient work. The decisions these doctors make, whether
to investigate, to treat, to follow-up or to discharge, may not be systematically checked.
Surgical trainees who may be about to face the challenge of outpatient work for the first
time, or in an unfamiliar speciality, are likely to find that the advice and wisdom con-
tained in this volume gives them the framework they need to perform effectively from
the outset.
The book may also be useful to those approaching surgical exams. Nowadays, surgical
viva voce examinations tend to focus not on surgical topics but on clinical scenarios. The
examiners want to find out whether candidates can analyse clinical information logically,
draw appropriate conclusions and propose rational management strategies. These are
precisely the intellectual processes which this book seeks to inculcate and to foster.
Sadly, there are still a few surgeons who see outpatient clinics as a regrettable necessity
in order to recruit patients on whom they can operate. Often this point of view seems to
go hand in hand with an unsophisticated and unthinking approach to decision making.
The reflex response which equates one hernia with one operation or bleeding at stool with
a flexible sigmoidoscopy is neither stimulating for the doctor nor good for the patient.
Sophistication in diagnosis and decision making not only leads to optimal patient care
but enormously increases the job satisfaction of the doctor. I hope that readers of this
book will find that it increases their enjoyment of outpatient work, as well as helping
them to perform to a high standard in the clinic.

Stephen Brearley MChir, FRCS

Consultant Surgeon
Director, The Whipps Cross Higher Surgery Course
August 2008

viii
Preface to second edition
Welcome to the second edition of General Surgery Outpatient Decisions. I found
publication of the first edition a very rewarding experience, especially when people
who had read the book took time to contact me and tell me how much they enjoyed it.
Occasions that stick in the memory include when a professor of surgery from Turkey who
was visiting Cambridge tracked me down in Addenbrooke’s Hospital to tell me that he
had found my book in the library and had spent three hours sitting on the floor reading
it. More recently a delegate approached me after a teaching session at another hospital to
tell me how he used the book every day and recommended it to all his junior colleagues.
The book was now dog-eared and full of his notes, written in the margin, which was
exactly how I envisaged the book would be used.
Since the first edition was published, surgical outpatient services have undergone
tremendous change. The traditional general surgical clinic has largely been replaced by
specialist clinics where decisions on patient management are taken by multidisciplinary
teams (MDTs). Breast clinics are the most striking example of this approach and there
is no doubting the improvement in care and outcomes that has resulted. Therefore, this
new edition is a multi-author edition to take account of the multidisciplinary approach.
However, working in MDTs brings its own challenges, not least because surgeons are still
expected to take overall responsibility for the patient, especially when things go wrong.
Increasing sub-specialisation also brings challenges to the trainee surgeon experiencing
that speciality for the first time. MDTs develop their own way of working and decision
making, which can be difficult to understand for the newcomer. In order to reflect
this new way of working, I have recruited two surgical registrars of the highest calibre:
Tjun Tang and Stewart Walsh, whose experience of working in this environment is still
current.
Once again, this book attempts to provide the necessary background information
to enable rational decision making in a concise and economical style. I hope you find
this book useful in your everyday practice and in preparation for your professional
examinations, where the question, ‘Yes the theory is all very well but what would you
actually do?’ can be the most difficult to answer; and may make the difference between
success and failure.
When I wrote the first edition I had no idea how far across the world it would spread.
A medical secretary from our hospital, on holiday in Vietnam, wandered into a bookshop,
found my book for sale there and took a photograph to prove it! Although this book is
written by surgeons working in the British National Health Service, I believe the medical
problems described in this book are common to all healthcare systems. All surgeons have
to be trained and go through the process of dealing with unfamiliar clinical conditions
for the first time. Therefore, I hope surgeons from all countries will use this book as a
useful foundation on which to build their own personal knowledge.
Finally, I would like to thank my fellow editors and the expert contributors to this book
for their hard work and dedication to the cause.

Michael Gaunt
Cambridge, UK
August 2008

ix
Introduction
A new batch of trainee surgeons attends their first outpatient clinic of a new speciality.
They are anxious. They may have had some experience of this speciality as medical
students and, like all good doctors, have read a textbook about the subject before starting
in the post. However, they have yet to acquire a ‘feel’ for the speciality and to obtain
the practical knowledge necessary to enable them to identify the crucial issues in each
consultation and to function efficiently. The result of this uncertainty is that in outpatient
clinics all over the world as the jobs rotate, trainee surgeons spend the first few weeks
seeing patients who have been brought back for review by their predecessors. They in
turn, unable to identify anything specifically wrong with the patients but not confident
enough to discharge them, bring the patients back for their successors to do the same. The
cycle continues at great inconvenience to the patients and at great cost to all healthcare
systems. The clinics are crowded and time available to see those patients who are in real
need is reduced, thus increasing the possibility of mistakes.
In general, few doctors receive any formal training in how to conduct an outpatient
consultation or how to compose and dictate an outpatient letter. The result of poorly
structured consultations and difficulties with communication is letters such as this one:
Dear Dr. I reviewed Mrs Smith who is a delightful old lady in the outpatient clinic
today her symptoms do not seem too bad at the moment although she is getting more
pain now so I advised her just to increase the painkillers if and when she thought it was
necessary and we will review the situation again at her next outpatient visit.
Despite the lack of punctuation, this doctor is trying to project the image of a bright and
confident clinician who is constantly amused by the stream of old characters referred
to him by the kind-hearted GP. However, any doctor who does not know the patient
will have gained no useful information from this letter. The diagnosis is not mentioned
or put into context with regard to other co-existing conditions or the patient’s overall
prognosis. The current dose of painkiller is not mentioned and no attempt has been made
to explain why Mrs Smith is getting more pain. What is the overall treatment plan and
what are the alternative therapeutic options if increasing the painkillers does not work?
The only plan is to review the patient again, but when – next week, next month, next year?
Unfortunately, these types of letters are often attached to very large sets of notes, which
the next clinic doctor has to spend valuable time reading in order to ascertain the exact
purpose of the consultation. Also, when the GP is called to see ‘this delightful old lady’
as an emergency because she has reached the maximum dose of painkiller and is still in
pain, the GP may be more inclined to admit her to hospital, because the latest outpatient
letter does not suggest any alternative course of action.
Mr Jones is 41 years old and is attending the surgical clinic to have his piles injected.
He has been coming every three months for the past two years. On his first visit he saw
the senior surgeon, who thought his small amount of rectal bleeding was probably due
to haemorrhoids and would settle down with injection sclerotherapy. Injecting piles is
an unpleasant task, which is often delegated to the most junior member of the team.
Therefore, Mr Jones has seen several different trainee surgeons who have each injected
the piles every three months. Each time, the bleeding improves for a few weeks after
the injection but then returns. Unfortunately, as well as piles Mr Jones also has a rectal
carcinoma at 10cm from the anal margin. At the time of his first consultation it was small
and obscured by faeces and therefore not seen by the consultant. Now it is much bigger,
but still not visible to the trainee surgeon injecting his piles. If the senior surgeon had
known that the bleeding had not settled down he would have investigated further and the

x
 INTRODUCTION xi

carcinoma would have been detected. Unfortunately, the senior surgeon is busy seeing
the new referrals and the ‘difficult’ cases, and the clinic nurse automatically sends the
‘piles’ down to the trainee surgeon. By the time the cancer is diagnosed it will probably
be inoperable.
These are just a few examples of the kinds of things that can go wrong in outpatient
clinics of all specialities. They are problems caused by inexperience, unfamiliarity, the fear
of making mistakes, the pressure of patient numbers and a lack of training.
Doctors tend to learn by experience, with all the pitfalls that entails. Most public
healthcare systems are so busy that not every patient can be seen by the senior surgeon
every time; and junior medical staff are integral to the running of the outpatient service.
Inevitably the level of ability and experience of junior staff will vary, but for the patient
only one level of care is acceptable – the best. Some may say this is well known and junior
staff are expected to deal only with straightforward new cases or routine follow-ups. But
straightforward cases are only straightforward up to the point where the patient reports
a new symptom or complication. Follow-ups are considered easy, but is this true? In
standard textbooks the new doctor will find little help on how to follow up patients. The
new doctor may be faced with the choice of either walking down to the senior doctor’s
room, past the crowded waiting area full of disgruntled patients and exasperated clinic
nurses, to ask the advice of the busy consultant for the fifth time this clinic; or ignoring
the new symptom; or bringing the patient back to clinic after a time to see someone else;
or perhaps ordering an investigation to buy some time – what do you do?
These problems are not easily solved, but we hope this book may help in some small
way. Research for this book has been difficult because the information on the outpatient
management of patients, especially follow-ups, is difficult to obtain. There is no standard
management of each condition in every patient and this book does not aim to set one.
The aim of this book is to describe a reasonable line of management suitable for most
patients, but one which the reader should modify to take account of individual patient
factors and local variations and preferences in practice.

Michael Gaunt
Tjun Tang
Stewart Walsh
Cambridge, UK
August 2008
About the editors
Tjun Tang graduated from Cambridge University in 2000 with distinction in surgery.
He undertook house jobs and his basic surgical training in Cambridge and he joined
the East Anglian specialist registrar rotation in General Surgery in 2004. He is currently
completing his MD thesis on imaging carotid plaque inflammation using contrast-
enhanced MRI, and he wishes to sub-specialise in vascular surgery. He has published
over 50 peer-reviewed manuscripts and has co-written several revision books for the
MRCS examination. He is actively involved in undergraduate teaching at Addenbrooke’s
Hospital in Cambridge and has been an examiner for the Final MB.

Stewart Walsh graduated from University College Dublin in 1997. After completing
house jobs in Northern Ireland, he undertook basic surgical training in the north-west
of England. He joined the Cambridge specialist registrar rotation in General Surgery in
2002. In 2006, he obtained an MSc from the University of Liverpool. He has published
over 50 peer-reviewed papers and, at present, is completing his Master of Surgery thesis
on the peri-operative care of vascular surgery patients. He teaches on both the Basic
Surgical Skills course and the Care of the Critically Ill Surgical Patient course.

Michael Gaunt qualified in medicine with distinction at Leicester University in 1988 and
undertook his surgical training in hospitals around the Midlands. He was elected Fellow
of the Royal College of Surgeons of England in 1992 and undertook a period of research
leading to the award of a doctorate of medicine with distinction. During his training he
received a number of research awards, including the Moynihan Medal of the Association
of Surgeons of Great Britain and Ireland the Founders Prize of the Vascular Society of
Great Britain and Ireland, and the European Vascular Surgery Prize. Mr Gaunt was elected
Hunterian Professor of Surgery of the Royal College of Surgeons of England in 1996.
In 1999 he was appointed consultant vascular surgeon at Addenbrooke’s Hospital
and associate lecturer at Cambridge University. Mr Gaunt has published over 100 peer-
reviewed research papers and is actively involved in both undergraduate and postgraduate
medical education.

xii
List of contributors
Miles Banwell PhD, FRCS
Specialist Registrar in Plastic Surgery
Eastern Deanery

Satyajit Bhattacharya MS, FRCS

Consultant Surgeon
Hepato-Biliary and Pancreatic Surgery Unit
The Royal London Hospital, London

Edward Cheong BSc(Hons), BMedSc, MD, FRCS (Gen Surg)

Specialist Registrar in Upper GI Surgery
Norfolk and Norwich University Hospital, Norfolk

David Cooper MA, MS, FRCS

Specialist Registrar in Vascular Surgery
Cambridge Vascular Unit
Cambridge University Hospitals NHS Foundation Trust, Cambridge

Bill Fleming FRACS, FRCS

Consultant Endocrine Surgeon
Hammersmith Hospital
Imperial College Healthcare NHS Trust, London

Richard Hardwick MD, FRCS

Consultant Surgeon and Lead Clinician for Upper GI Cancer
Cambridge Oesophago-Gastric Centre
Cambridge University Hospitals NHS Foundation Trust, Cambridge

Michael Irwin FRCS, FRCS (Plast)

Consultant Plastic and Reconstructive Surgeon
Department of Plastic and Reconstructive Surgery
Cambridge University Hospitals NHS Foundation Trust, Cambridge

Neville Jamieson MD, FRCS

Consultant Hepatobiliary and Transplant Surgeon
Cambridge University Hospitals NHS Foundation Trust, Cambridge

Fiona MacNeill MBBS, FRCS, MD

Consultant Breast Surgeon and Breast Tutor
Royal College of Surgeons of England
Royal Marsden Hospital, London

Adrian O’Sullivan MB, FRCSI

Specialist Registrar
Hepato-Biliary and Pancreatic Surgery Unit
The Royal London Hospital, London

xiii
xiv LIST OF CONTRIBUTORS

Umar Sadat MRCS

Clinical Research Associate
Cambridge Vascular Unit and University Department of Radiology
Cambridge University Hospitals NHS Foundation Trust, Cambridge

Paris Tekkis BMedSci, BM BS, MD, FRCS

Senior Lecturer and Consultant Colorectal Surgeon
Imperial College London

Henry Tilney MBBS, MRCS

Specialist Registrar in General Surgery
South West Thames Higher Surgical Training Rotation

Alastair Windsor MD, FRCS, FRCS(Ed)

Consultant Surgeon and Honorary Senior Lecturer
University College London Hospitals, London
List of abbreviations
131
I radio-iodine
131
MIBG meta-iodobenzylguanidine
5-ASA 5-aminosalicylate
5FU 5-fluorouracil
5-HIAA 5-hydroxyindoleacetic acid
5-HT 5-hydroxytryptamine
99m
Tc technetium-99m
AAA abdominal aortic aneurysm
ABPI ankle-brachial pressure index
ABS Association of Breast Surgery
ACE angiotensin-converting enzyme
ACTH adrenocorticotropic hormone
ADH atypical ductal hyperplasia
AFP alpha-foetoprotein
AIDS acquired immunodeficiency syndrome
ALP alkaline phosphatase
ALT alanine transaminase
ANA antinuclear antibodies
ANCA antineutrophil cytoplasmic antibody
ANCA antineutrophil cytoplasmic autoantibodies
APA aldosterone-producing adenoma
APT prothrombin antigen
ARDS acute respiratory distress syndrome
ASCA anti-Saccharomyces cerevisiae antibodies
AST aspartate aminotransferase
AXR abdominal X-ray
BASO British Association of Surgical Oncology
BBC benign breast change
BC breast cancer
BCN breast care nurse
beta hCG beta human chorionic gonadotropin
BP blood pressure
BT Breslow thickness
BU breast unit
C&S culture and sensitivity test
C14 glycocholate
CA 19-9 carbohydrate antigen 19-9
CAD cystic adventitial disease
CBD common bile duct
CBT carotid body tumour
CCA common carotid artery
CE capsule endoscopy
CEA carcinoembryonic antigen
CHOP cyclophosphamide, doxorubicin, vincristine and prednisone
CML chronic myeloid leukaemia
CRP C-reactive protein
CT computed tomography
CTA/MRA computed tomography angiography/magnetic resonance angiogram
CTD connective tissue disease/disorders
CWD continuous wave Doppler

xv
xvi LIST OF ABBREVIATIONS

CXR chest X-ray

CXR-PA chest X-ray, posterior anterior view
DCIS ductal carcinoma in situ
DF118 dihydrocodeine
DMSA dimercaptosuccinic acid
DSA digital subtraction angiography
DVT deep-venous thrombosis
ECA external carotid artery
ECG electrocardiogram
EHIDA 99Tcm-diethyl-IDA
ELISA enzyme-linked immunosorbent assay
ENT ear, nose and throat
EPO evening primrose oil
ERCP endoscopic retrograde cholangiopancreatography
ER/PR oestrogen/progesterone receptors
ESR erythrocyte sedimentation rate
EUA examination under anaesthetic
EUS entoscopic ultrasound
EVAR endovascular repair
EVLA endovenous laser
F/A fibroadenoma
FACS follow-up after colorectal surgery
FAP familial adenomatous polyposis
FBC full blood count
FHH familial hypercalcaemic hypocalciuria
FMD fibromuscular dysplasia
FNAC fine-needle aspiration cytology
FNH focal nodular hyperplasia
FOB faecal occult blood test
GA general anaesthetic
gamma GT gamma-glutamyl-transpeptidase
GIST gastrointestinal stromal tumour
GnRH gonadotropin-releasing hormone
GOJ gastro-oesophageal junction
GORD gastro-oesophageal reflux disease
GTN glyceryl trinitrate
H2RA H2-receptor antagonist
Hb haemoglobin
HBsAg hepatitis B surface antigen
HCC hepatocellular carcinoma
HDL high-density lipoprotein
HHT hereditary haemorrhagic telangiectasia
HIB Haemophilus influenzae type b
HNPCC hereditary non-polyposis colorectal cancer
HPV human papillomavirus
HPZ high-pressure zone
HRT hormone replacement therapy
IBD inflammatory bowel disease
ICA internal carotid artery
IgA immunoglobulin A
IgG immunoglobulin G
IgM immunoglobulin M
IMA inferior mesenteric artery
INR international normalised ratio
 LIST OF ABBREVIATIONS xvii

IPA idiopathic hyperaldosteronism

IPSID immunoproliferative small intestine disease
IVC inferior vena cava
LCIS lobular carcinoma in situ
LDL low-density lipoprotein
LDS lipodermatosclerosis
LFT liver function test
LIF left iliac fossa
LN lymph node
LUQ left upper quadrant
MALT mucosa-associated lymphoid tissue
MAOI monoamine oxidase inhibitor
MC&S multi culture and sensitivity
MCV mean corpuscular volume
MDM multidisciplinary meeting
MDT multidisciplinary team
MEN multiple endocrine neoplasia
MI myocardial infarction
MIBG meta-iodobenzylguanidine
MLD manual lymphatic drainage
MRCP magnetic resonance cholangiopancreatography
MRI magnetic resonance imaging
MST morphine sulphate
MTBE methyl tert-butyl ether
MTC medullary thyroid cancer (medullary carcinoma of thyroid)
NAC nipple areolar complex
NHSBSP National Health Service Breast Screening Programme
NICE National Institute for Health and Clinical Excellence
NIDDM noninsulin-dependent diabetes mellitus
NP59 6-beta-iodomethyl-19-norcholesterol
NSAID non-steroidal anti-inflammatory drug
OA osteoarthritis
OCP oral contraceptive pill
OGD oesophago-gastro-duodenoscopy
OPD outpatient department
OPSI overwhelming post-splenectomy infection
PAIR percutaneous fine-needle puncture, aspiration, injection of hypertonic
saline and reaspiration
PAN polyarteritis nodosa
PAS p-aminosalicylic acid
PDT photodynamic therapy
PEC percutaneous endoscopic colostomy
PET positron emission tomography
PG12 prostacyclin
PGE1 prostaglandin E1
PID pelvic inflammatory disease
P-J Peutz-Jeghers syndrome
PPAM post-amputation mobility
PPI proton-pump inhibitor
PPPD pylorus-preserving pancreatoduodenectomy
PTC percutaneous transhepatic cholangiography
PTFE polytetrafluoroethylene
PTH parathyroid hormone (parathormone)
PV polycythaemia vera
xviii LIST OF ABBREVIATIONS

PV/ESR plasma viscosity/erythrocyte sedimentation rate

PVD peripheral vascular disease
RA rheumatoid arthritis
RAS renal artery stenosis
RET proto-oncogene reticuloendothelium
RFA radiofrequency ablation
RT radiotherapy
RUQ right upper quadrant
SBE small bowel enema
SBFT small bowel follow through
SCC squamous cell carcinoma
SeHCAT test 75-selenium homotaurocholic acid retention test
SFA superficial femoral artery
SFJ saphenofemoral junction
SGOT serum glutamic oxaloacetic transaminase
SGPT serum glutamic pyruvic transaminase
SLE systemic lupus erythematosus
SMA superior mesenteric artery
SOB shortness of breath
SOD sphincter of Oddi dysfunction
SPECT single photon emission computed tomography
SS systemic sclerosis
SSV short saphenous vein
TAA thoraco-abdominal aneurysms
TACE transarterial chemoembolisation
TART transanal resection of tumour
TBPI toe-brachial pressure index
TED thromboembolic disease
TEM transanal endoscopic microsurgery
TENS transcutaneous electric nerve stimulation
TIA transient ischaemic attack
TIPS transjugular intrahepatic portosystemic shunt
TOCS thoracic outlet compression syndrome
TPN total parenteral nutrition
TSH thyroid-stimulating hormone
U&E urea and electrolyte
UC ulcerative colitis
UCSF University of California, San Francisco
USS ultrasound scanning
UTI urinary tract infection
VNUS® radiofrequency ablation procedure developed by VNUS
VIPoma vasoactive intestinal peptide tumour
VBI vertebrobasilar ischaemia
VA vertebral artery
VLDL very low-density lipoprotein
WCC white cell count
ZE Zollinger-Ellison syndrome
ZN Ziehl-Neelsen
General outpatient issues
Michael Gaunt, Tjun Tang and Stewart Walsh

ONE
The outpatient consultation
Purpose of the outpatient consultation
It is worth emphasising the simple but fundamental point that each consultation has
a purpose. If the doctor cannot identify a purpose for another consultation then the
patient should be discharged. Discharging a patient does not mean casting them off into
the wilderness. Patients should be discharged with a plan and instructions for re-referral
if appropriate.
The structure of the consultation
Each consultation should have a structure, which becomes routine. In this way important
stages and information are not overlooked. Doctors develop their own routine, but a
simple structure might consist of the following.
✧ Read the referral letter.
✧ Read the previous clinic letters and old notes.
✧ Be clear about the purpose of the consultation before entering the room.
✧ Introduce yourself and who you work for.
✧ Put the patient at ease; ascertain who has accompanied the patient.
✧ Explain what you are going to do, e.g. take a history then perform an examination.
✧ Take the history.
✧ Perform the relevant examination.
✧ Have a think and decide what to do.
✧ Discuss any investigations or treatments with the patient.
✧ Answer any questions.
✧ Give concluding remarks and instructions.
✧ Insert a handwritten entry in the notes, include diagrams etc.
✧ Dictate the clinic letter.

The referral letter

The consultation begins before the patient is seen, when the doctor reads the referral
letter in the case of new patient or the last clinic letter in the case of follow-ups. For new
patients, the referral letter usually contains the reason the patient has been sent to the clinic
and other useful information such as a list of co-existing medical conditions and a list of
current medication. The referral letter sets the scene and provides useful information, but
this should n.ot be allowed to unduly influence the consultation. Once patient contact is
made the diagnostic process starts again from scratch with the history and examination.
The previous clinic letter and notes
The previous notes are in the clinic for a purpose – they are there for you to read. In
general it is better to have as much information as possible before starting a consultation.
Reading the notes puts the current presenting illness in context and prevents any repeti-
tion of investigations. An apparently successful consultation can be undermined by the
patient informing you that they have already had the investigations you were proposing
and they were all normal. You are embarrassed and the patient leaves with the impres-
sion that you didn’t know what you were doing. Reading a very large set of notes during
a busy clinic is not feasible. This is where a detailed previous clinic letter is invaluable in
summarising what has gone before.

1
2 GENERAL SURGERY OUTPATIENT DECISIONS

Purpose of the consultation

New patients
In the case of new patients the objectives of the consultation are either to reach a diagnosis
or to exclude any serious pathology related to that speciality. If it is suspected that the
patient’s symptoms may be caused by a potentially serious or malignant condition,
investigations will need to be performed and reviewed promptly.
Follow-up patients
Seeing the follow-up patients is a task often delegated to junior staff, who may lack a
clear understanding of the consultation objectives. In surgery, follow-up patients fall
into three categories: those with new undiagnosed conditions who are returning for the
results of investigations; those with chronic conditions that are being monitored; and
post-operative patients.
New conditions under investigation
These patients are returning to clinic to receive the results of investigations performed so
far. The patient will have been seen previously, either by you or by a colleague. Read the
previous clinic letter and review the notes to remind yourself of the case. It is useful to
ensure that the results of all investigations are available before you meet the patient. This
may involve telephoning for the results, out of earshot of the patient. Decide whether
the results are diagnostic or whether further investigations are necessary. If the results
are diagnostic and the outcome is bad news, e.g. cancer, plan how you are going to
break the news. If the results are equivocal it may be necessary to repeat the history and
examination to detect new features that may have developed and will aid the diagnosis.
Think about possible further investigations and the timescale for obtaining these results.
It may be that the results are not diagnostic but serious causes have been excluded
and the need to obtain a diagnosis is less urgent. If the results are diagnostic and good
news, decide whether further follow up will be required or whether the patient can be
discharged with advice.
Chronic conditions
The purpose of the consultation in the case of these patients is to detect whether the
patient’s condition is stable, improving or deteriorating and to detect any complications
of the underlying condition or treatment. Ideally the previous clinic letter should contain
the reason for the follow-up, what to look for and an objective description of the clinical
condition at that time to allow comparison with the present. It may be time for a routine
investigation to be performed, e.g. yearly mammogram, three-monthly FBC. If the
patient’s condition has been stable for some time it may be appropriate to decrease the
frequency of outpatient consultations or to discharge the patient, with clear instructions
to the GP and the patient on when to re-refer. Do not automatically bring the patient
back at the same time interval as did the last clinic doctor.
Another useful option is the ‘open appointment’. With an open appointment the
patient is not given another clinic date but has open access to make an appointment
directly if his or her condition recurs. This system works best for sensible patients,
familiar with their clinical condition, who have been stable for a long period but who may
relapse and require prompt treatment. Usually, open appointments have a time limit, e.g.
a year, after which a new referral through the GP is required if the condition recurs. Open
appointments must be used sparingly; otherwise the clinic can become overloaded and
open to abuse. Some patients make appointments for an opinion on unrelated conditions
or even for other members of their families! Never underestimate the importance of the
GP as gatekeeper to the proper functioning of the health service.
 GENERAL OUTPATIENT ISSUES 3

Post-operative patients
The purpose of these consultations is to decide whether the operation has been successful
in achieving its objectives, e.g. relieving the patient’s symptoms or completely removing a
tumour. Prior to seeing the patient, read the notes to determine the operation performed
and whether there were any intra-operative or post-operative complications that require
long-term follow-up, e.g. damage to the common bile duct. If tissue was removed at the
time of operation and sent for histology, make sure you read the histology report even if
this was routine. Occasionally, routine histology can reveal occult cancer that was never
suspected but that may necessitate further management.
If the operation was to remove cancer, determine whether this was all removed or
whether the tumour extended to the radial or longitudinal resection margins, indicating
residual disease requiring further surgery or adjuvant therapy. The histological grade of
the tumour and any evidence of lymph node spread or vascular invasion may indicate
that adjuvant radiotherapy/chemotherapy is required. Decide on the outlines of a treat-
ment plan before breaking any bad news to the patient. The patient may modify the
plan according to their own preferences, but uncertainty on the part of the doctor at this
difficult time is to be avoided.
Meeting the patient
Thoroughly prepared, the doctor enters the consultation room. Ascertain which person
in the room is the patient, and introduce yourself. Many patients will be expecting to
see the consultant, because that is the name on their appointment card. Who you are
and your position in the hierarchy needs to be explained. Determine the relationship of
other people in the room to the patient. Do not automatically assume they are relatives.
In this way you will avoid an embarrassing exposure of a patient in front of a neighbour
or volunteer driver.
It may be appropriate to put the patient at ease with some friendly comments before
launching in to the consultation proper, e.g. apologise for the long wait. It is often useful
to explain the structure of the consultation to the patient: ‘What I’d like to do is to ask you
some questions, then examine you and then we’ll discuss what we are going to do.’
History and examination
Obtain the relevant history and perform the relevant examination. Examination in the
outpatient clinic can be difficult. The patient may be relatively immobile and encased
in numerous layers of clothing, which take a long time to remove. It is frustrating to
wait – but more frustrating to miss an obvious and vital clinical sign due to inadequate
examination.
Have a think: the management plan
Many doctors seem embarrassed to be seen thinking, but it is actually what we are paid
to do. Once the history and examination are complete and the patient is getting dressed,
there is time to record and reflect on the findings and formulate a management plan. For
simple and routine problems this will be brief, but for more complicated problems this
may be the time to obtain more senior advice or consult a helpful text.
Medicine is a partnership between patient and doctor. The more the patient under-
stands about what you are trying to achieve, the more likely they are to comply with the
investigations or treatment. Therefore, although you have a management plan, you must
be prepared to modify it depending on the patient’s preferences. Always allow time for
the patient to ask any questions, and answer them as fully as you can.
Concluding remarks
The consultation has to be brought to an end. Ideally this occurs when all questions are
4 GENERAL SURGERY OUTPATIENT DECISIONS

answered and everyone understands what is involved. However, there may be occasions
when a more formal signal that the consultation is drawing to a close is needed. Usually
standing up and closing the notes folder is taken as the relevant cue. Final remarks may
consist of: ‘You’ll receive an appointment for the ultrasound scan through the post in a
few weeks’ time and we’ll see you again in the clinic a week after the scan to discuss the
results.’
Handwritten entry in the notes
A handwritten entry in the notes is necessary as a contemporaneous record of the consul-
tation and the management plan. Diagrams can be included to illustrate clinical findings,
which are difficult to incorporate in the typed letter. Also, a detailed handwritten note is
invaluable some days later when the audio-typist reports that the tape from the clinic is
corrupted and you need to dictate the letters again.
Dictating the clinic letter
Matters concerning the composition of clinic letters and other forms of communication
are covered in the next section.

Communication
Good communication is at the heart of good medicine, and this is particularly the case
in outpatient medicine. A doctor needs to communicate effectively with the patient and
the patient’s relatives at the time of the consultation. The importance of this has been
recognised in most medical schools, and communication with patients, in particular
breaking bad news, now forms part of most courses. However, a more neglected area is
communication with other healthcare professionals. The most common means of com-
munication in the clinic is the outpatient letter.
Communication with the patient
This consists mainly of verbal communication during the consultation itself. The
importance of introductions and determining the relationship to the patient of any
accompanying person has already been emphasised. If the patient is accompanied by a
member of staff from a nursing or residential home, this person may be a useful source
of information and may be able to relay instructions back to the nursing home. Relatives
may be another useful source of information but, alternatively, may try to dominate the
consultation with their own interpretation of events. Generally if the patient is capable of
answering questions they should be allowed to do so without interference, and relatives
should be encouraged to keep quiet. However, the relative may be an important carer
for the patient, so it is worth avoiding alienation. Explaining that you wish the patient to
answer their own questions at this point in the consultation – but you would be interested
in the relative’s observations at the end – may control the situation.
Breaking bad news
This usually means a diagnosis of cancer or other serious disease. Prior to the consultation
decide how certain the information is or whether further investigation is needed. If there
is no reasonable doubt, then a plan of how to break the news is needed.
There are numerous helpful texts on the subject of how to break bad news, which
cover the subject in more detail than can be given here. But several basic principles,
which are applicable to the outpatient setting, will be described. If possible a patient
should not be given bad news in isolation. Ideally a relative or close friend should be
there when the news is given. Hospitals vary in their provision for these circumstances,
but a trained counsellor or nurse in attendance is also useful for providing comfort and
further explanation if required.
 GENERAL OUTPATIENT ISSUES 5

Another principle is that bad news should be tempered with good news. One of the
first questions a patient tends to ask after receiving an adverse diagnosis is, ‘Is there
anything that can be done?’ It is reassuring to be told that reasonably effective treatment
is available and that the hope of cure exists. The best interpretation should be put on the
situation without instilling false hopes. Uncertainty on the part of the doctor at this stage
will make a bad situation worse. Therefore, the management plan needs to be decided
before the consultation begins. This may involve talking with the consultant and deciding
on the best course of action before meeting the patient.
Answer as many questions as you can and then withdraw, giving the patient some time
to come to terms with what has been said and to receive the comfort and reassurances of
relatives and nurses. During this time further queries may occur and the nurse can relay
these so that you can return to answer them. The nurse should also determine how the
patient is getting home. Probably no patient should be allowed to drive immediately after
receiving this kind of news. They are unlikely to be concentrating fully on their driving.
It may be more sensible to order a hospital taxi and for the patient or relative to arrange
for the car to be picked up the following day.
The outpatient letter
This letter is unusual because one letter is written to several different potential readers
who require different information and may interpret the same information differently.
The first person you are writing the letter to is yourself. This letter is your record of
what happened during the consultation, which you can refer to if a query arises. The letter
is best dictated immediately after a consultation, when all the details are fresh in your
memory. There may be the temptation not to record certain facts in the belief that you
will remember them. This may be true for a week or two, but six months and possibly
a thousand patients later this will not be the case. If you think that something might be
relevant, note it down.
The next person you are writing to is the GP, who receives a mountain of mail every
week and does not have the time to wade through a lot of flowery prose. The GP basically
wants to know the diagnosis and the management plan, including further investiga-
tions, treatment and timing of the next outpatient appointment. The GP also wants this
information as soon as possible after the consultation – not two months down the line.
Some GPs prefer letters that consist of a list of headings, such as diagnosis, investigations,
treatment, follow-up; this removes the need to compose a letter at all.
The next person to read the letter is the next outpatient doctor, who has never seen the
patient before. This doctor requires a summary of the original complaint or symptoms,
what has happened in terms of investigations or interventions and an outline of the
current management plan. The alternative to a letter summarising this information is the
task of wading through the whole set of notes trying to read other people’s handwriting
and trying to find pathology/radiology reports – a considerable waste of time that could
have been spent with the patient.
Finally, remember this letter may be read by a hospital manager investigating a com-
plaint, or ultimately by a prosecution lawyer. Humorous or apparently witty statements,
which seemed funny at the time, may appear at best insensitive and at worst patronising
and disparaging when read in the light of subsequent adverse events.
Most letters are dictated onto tape (dictaphone) and typed some time after the clinic
by an audio-typist.
Dictating the letter
There are many different makes and models of dictating machine around, so before
dictating a whole clinic’s worth of letters make sure you know how the machine operates.
Check that the tape and the machine are compatible, and that what you are saying is
6 GENERAL SURGERY OUTPATIENT DECISIONS

recording and can be played back in an intelligible form. Nothing is worse, after a long
clinic, than to find that none of your carefully composed letters have been recorded and
you have to do it all again.
Decide whether you are going to state the punctuation as you dictate (comma), or
leave it to the secretary to put in the punctuation based on your sentence construction
and voice intonation (full stop). If possible, discuss this with the secretary who is going
to be typing the letters to find out what the secretary prefers. Some secretaries are expert
at making sense of the worst dictation. Secretaries can also advise you as to the preferred
style of your consultant.
Start the tape by stating the date; the title of the clinic, e.g. Mr Big’s Endocrine Clinic;
and who you are, e.g. Mr Small dictating. Then say: ‘The first patient is . . . etc.’ This
enables the tape to be identified even if it becomes separated from the notes.
At the start of each letter state the patient’s name and hospital identification number
or date of birth. Next, state to whom the letter is being sent, e.g. letter to the GP Dr Good,
with a copy to the stoma care sister.
The style of the letter may be largely determined by the ‘house style’ of the firm you are
working for. It may be a structured letter under set headings, with or without a section
of text. For text it is a good idea to allocate a new paragraph to the introduction, history,
examination, investigations and treatment.

Letter to the general practitioner

The GP wants to receive answers to the following questions: What is the diagnosis, or
which investigations are being performed to reach a diagnosis? When do you expect to
make a diagnosis? What should be done about the symptoms in the meantime? What
have you told the patient? If the diagnosis has been made, what is the treatment plan and
what is the prognosis?
As stated earlier, the average GP receives a mountain of mail every week, so short,
concise communications are appreciated. Try to limit one consultation to one sheet.
The style of letter varies from hospital to hospital. The style you adopt will be deter-
mined largely by the preferred format of the department you are working in. Increasing
in popularity is the formulated letter, consisting of a series of headings such as diagnosis,
investigations awaited, results, medications and so on. This is a very efficient letter, but
some consider it too impersonal and not sufficiently explanatory. At the other end of
the scale is flowery prose consisting of long sentences and paragraphs, which many GPs
skip to read the bottom line. A combination of the two exists. It starts with a structured
summary under relevant headings and then includes a section of text explaining how the
diagnosis was reached and why a series of investigations has been requested. Whatever
the style, all good letters contain the following information:
✧ a summary of why the patient was referred
✧ a summary of the history
✧ a summary of examination findings
✧ a list of differential diagnoses
✧ a list of investigations
✧ the treatment plan
✧ the time course for investigations or treatment
✧ what the patient and relatives were told
✧ arrangements for follow-up, open appointment, or, if the patient has been discharged,
the conditions under which the patient should be re-referred.

Follow-up patients
For follow-up patients, letters should include the following information:
 GENERAL OUTPATIENT ISSUES 7

✧ a summary of the course of the illness and any interventions so far, which sets the
consultation in context
✧ a reason why the patient is being followed
✧ current history and examination findings
✧ results of recent investigations
✧ an explanation of the symptoms and signs to look out for
✧ how long the follow-up is likely to continue
✧ when the patient is likely to be discharged.
Letter to the next OPD doctor
It is important to write the OPD letter bearing in mind that the next doctor to see the
patient may not be yourself. In the case of new patients returning for the results of
investigations, the needs of the next clinic doctor are the same as the GP and a letter
containing the information outlined in the previous section is adequate.
Follow-up letters, which consist of: ‘I have reviewed Mrs Smith and her condition is
unchanged and we will see her again in three months’ time,’ are completely unhelpful.
Each letter should start with a summary, which sets the consultation in context, e.g. ‘I
reviewed this 43-year-old lady who, in April 1996, underwent a right simple mastectomy
with a level 1 axillary node clearance. Her prognostic factors revealed this to be a 1cm
tumour, which was a moderately differentiated (Bloom & Richardson grade II) ductal
carcinoma with 3 out of 8 axillary lymph nodes involved. Following surgery she was
treated with a full course of adjuvant CMF chemotherapy, from which she made a
good recovery and on her last two outpatient visits she has been well with no signs of
recurrence . . .’.
The next doctor now knows exactly what the original problem was without having to
search for the operation note, the oncology notes or the several histology reports. Once
this trend is established it is a simple matter for the next doctor to use the same paragraph,
modified appropriately, to start the next letter.
Referrals to other clinicians
There may be occasions when referral of a patient to another speciality is indicated,
either because the original complaint is not your speciality or the original complaint is
your speciality but there is a co-existing condition which merits treatment in its own
right. Many GPs have their preferred referral pathways, and therefore non-urgent cases
should be referred back to the GP with reasons why a referral is indicated. However, on
other occasions a referral may be urgent, or closely related to surgical treatment, e.g. a
cardiology assessment prior to a surgical procedure in a patient with an existing heart
condition. In these instances it is probably advisable to refer the patient yourself, but send
a copy of the referral letter to the GP.
Prior to referring to another speciality, it is wise to discuss the case with your consultant,
who can confirm a referral is indicated and advise you as to the correct referral pathway.
In this case the referral letter should start by indicating that your consultant has been
involved in the decision to refer. Then outline the reason why the patient was referred to
your speciality and what your main findings have been. Explain why a referral to another
speciality is indicated and how this affects the condition, if at all. Finally, express a time
by which you would like the patient seen and explain how this fits in with your own
timetable for follow-up and treatment.
Ordering investigations
Investigations tend to be classified as either urgent or routine. Difficulty arises in the case
of patients who are not urgent – but if the result was positive the surgeon would want to
know immediately. For example, in an investigation of rectal bleeding the decision may
8 GENERAL SURGERY OUTPATIENT DECISIONS

be made to investigate the condition further with a barium enema. The investigation is
performed to exclude a colonic carcinoma. There may be an eight- to ten-week waiting
list for routine barium enemas. If the result is negative there are few consequences, but
if a colonic cancer is detected two months have been wasted, during which potentially
life-saving treatment could have been administered. When deciding on whether a case is
urgent or not, one must always consider the consequences of a positive result.
Routine investigations
Routine investigations are usually arranged by completing the relevant request form. An
experienced clinic nurse can usually advise you as to the correct form. If not, you can
always telephone the relevant department and ask their advice. One assumes there is no
pressing need to know the results as long as they are available for the next consultation.
However, for certain investigations there may be very long waiting times indeed – once
again, contact the relevant department for more advice.
Urgent investigations
Obtaining urgent investigations is an art-form. Just writing ‘urgent’ on the request form
is no guarantee that the request will be treated as urgent. Clearly stating when the result
is needed helps investigating departments plan and prioritise their work appropriately.
However, many departments have set procedures for dealing with urgent requests and
unless these procedures are followed precisely the request fails. This information is often
known to the people who have worked in the hospital for many years, but is a labyrinthine
mystery to newly rotated doctors. A telephone call to the relevant department to obtain
advice regarding these procedures, or a specific appointment time, is useful. Always
record the name of the person you spoke to, in case of future difficulties. Telephone calls
can use up a lot of time in the clinic and it may not be possible to contact the relevant
person. It may be possible to delegate such calls to the clinic clerk and get involved only
if difficulties arise.
In very difficult cases, admitting the patient to the hospital and performing the investi-
gations with them as an in-patient is one option. However, in many cases it may be
inappropriate and it is often wasteful of hospital resources.
In the end, a dictated letter to the consultant in charge of the department in question,
explaining the clinical features and asking them to ensure the investigation is performed
within a certain time, tends to ensure the right result – even if you get a less than friendly
written reply.
Performing procedures in clinic
Performing procedures in clinic may be an integral part of the investigation or treatment
of the patient’s condition. Procedures commonly performed in the OPD include
fine-needle aspiration, Tru-cut biopsy, rigid sigmoidoscopy, proctoscopy, injection of
haemorrhoids and rectal biopsy. Other procedures may be performed depending on the
speciality. Details of these procedures are given in the relevant chapters.
Obviously one should never perform an invasive procedure unless one has been
trained to do so. Also, consider the issue of consent. It is unusual for patients to sign a
consent form prior to these procedures. However, there may be occasions when this is
appropriate. Usually, informed verbal consent is sufficient, but this situation may change
in the future.
The discharge plan
Discharging patients from clinic can be a contentious issue. On the one hand, if all
patients were followed up indefinitely, the clinics would soon become overburdened
and cease to function. On the other hand, if discharge is handled insensitively there
 GENERAL OUTPATIENT ISSUES 9

can be criticism that the patient has been abandoned, or that an unfair onus of further
management has been placed on the GP.
The decision to discharge a patient from the clinic is easy when the patient originally
presented with a relatively simple condition, which was treated and the symptoms
resolved. However, with other patients the decision to discharge can be more difficult.
Earlier in the text, I emphasised that if a reason for follow-up cannot be identified the
patient should be discharged. This seems like common sense and for an experienced
clinician it is a relatively simple decision. But junior surgeons may fear that they cannot
identify a reason for follow-up because their knowledge is deficient – they suspect a good
reason does exist, but they fear they are ignorant of it. In this situation there is a strong
temptation to ‘play safe’ and follow the course of the previous clinic doctor, reviewing
the patient in the clinic at the same interval as before. Inappropriate outpatient visits are
wasteful of NHS resources and cause an inconvenience for patients and their carers, so
every effort should be made to reserve outpatient consultations for those patients who
really need them.
Another problem with multiple inappropriate clinic visits is that some patients
become accustomed to attending the hospital and may actually look forward to their
appointments. These patients may have adopted the sick role, and frequent hospital
visits legitimise their ‘illness’. There may be certain sociological and economic benefits,
e.g. people are excused from work, or receive social security benefits that they feel may
be threatened if they are discharged. These can be difficult patients to manage. To avoid
conflict it may be necessary to delay discharge until they have seen the consultant at the
next appointment.
For some chronic conditions or after major surgery, follow-up intervals become very
long, e.g. yearly. In these situations the doctor should question whether further hospital
follow-up is appropriate. After all, it is unlikely that the occurrence of new symptoms
will coincide with the next appointment date. It is more likely that if new symptoms arise
within that time the patient will seek the advice of their GP, who in turn will ask for the
appointment to be brought forward. The original appointment will become irrelevant. If
the patient had been discharged with instructions to consult their GP if new symptoms
arose, the same procedure would have been followed and the patient seen in the same
time but without the inconvenience of the original clinic appointment.
An alternative arrangement is the time-limited open appointment, where the patient
has open access to the clinic to make their own appointment if the symptoms recur within
a certain time after discharge, e.g. one year.
Patients should be discharged with a plan, which includes instructions as to when they
should seek a medical opinion. The instructions should be included in the clinic letter,
stating what the patient was told and giving additional instructions to the GP.
 Breast
Fiona MacNeill
TWO

Introduction
In the United Kingdom, the female breast has a cultural, psychological and sociological
significance far beyond its function as a milk-producing organ. As well, breast health
issues have become increasingly politicised as a consequence of powerful advocacy and
lobbying and high media involvement.
Although the incidence of breast cancer is rising slowly (especially in those aged over
70), mortality is declining rapidly (13 000 deaths per annum) and many patients now
survive their cancer in extended remission. The five-year survival for screen-detected
cancers is more than 95%.
The team
Breast cancer is a high-stake diagnosis: women fear a diagnosis that is associated with
reduced life expectancy and disfiguring surgery, with a perception of reduced feelings
of femininity and sexuality. They may also fear rejection from their husband or partner.
Patients with a breast symptom or breast change are often terrified they might have
breast cancer – no matter how low the likely risk – and the time spent waiting for a breast
clinic appointment or results of breast investigations is stressful and full of uncertain-
ties. Consequently, modern breast units have developed a specialist, streamlined and
efficient breast assessment service. Specialist multidisciplinary care has been shown to
improve patient outcomes as well as to enhance the quality of care and overall patient
experience.
The core multidisciplinary team (MDT) consists of individuals who specialise, often
exclusively, in ‘breast’, especially breast cancer: surgeons (breast/general, oncoplastic,
plastic), radiologists and imaging teams, pathologists, oncologists, breast care nurses and
an extensive clerical and management staff. The delivery of high-quality care is rarely
dependent on the skills of one clinician; it is mainly the result of good organisation and
a functional, patient-focused team.
Practical tips for the trainee
It is suggested that trainees take note of the following tips.
✧ Be aware of the National Institute for Health and Clinical Excellence (NICE) Breast
Cancer Outcome guidelines: www.nice.org.uk.
✧ Read and understand the Association of Breast Surgery (ABS) and National Health
Service Breast Screening Programme (NHSBSP) symptomatic assessment guidelines
and Quality Assurance (QA) standards: www.baso.org.uk.
✧ Find out the latest government diagnostic and treatment targets for breast services, e.g.:
∝ all women with a symptomatic breast problem to be assessed within two weeks
∝ thirty-one days from referral to diagnosis and 62 days from referral to treatment.
✧ Multidisciplinary meetings (MDM) have a strong educational value and are a
powerful learning resource for new team members. You will be able to learn how to
function within a MDT and watch the complexity of team dynamics and leadership
styles. Collaborative working represents the future model of healthcare. Working
within the MDT means you will never be making decisions in isolation.
✧ Draw from the experience of the whole team.
✧ Each unit will have its own protocols for breast triple assessment. Ask if these are
available, as they are a useful guide.

10
 BREAST 11

✧ At your first clinic, ask if you can sit in and watch someone more experienced or senior
do the first few assessments.
✧ If possible, in the early days of your attachment follow a patient through the whole
process of triple assessment. It will give you the opportunity to:
∝ understand the process from the patient’s perspective
∝ see the rest of the unit and introduce yourself to the whole team
∝ attend as many different types of breast clinic as possible.

Breast assessment
Breast referrals are made for a wide variety of breast/chest wall and axillary problems,
pain being the most common symptom and a lump the most common sign. Most patients
(90%) will have normal breasts: the breast is a dynamic organ under constant hormonal
influence, especially from puberty to menopause, so the majority of breast changes are
functional or physiological alterations secondary to puberty, pregnancy/lactation or the
menopause. From 35 years onwards the breast starts to involute. This accelerates after
the menopause.
Pain is not a symptom of breast cancer (BC) but is usually what draws the patient’s
attention to their breast. A lump is more likely to be breast cancer as the age of the woman
increases. In the teenage to twenty-year age group most breast lumps are fibroadenomas
(F/A). In the thirty to forty-year age group, as the breast involutes, a focal area of benign
breast change (BBC) is the commonest cause. Above the age of fifty, BC is more common,
and in the sixty-plus age group most breast lumps will be cancer.
The safest course of action is to assume each lump might be a cancer whatever the
patient’s age, until proven otherwise by triple assessment. Table 2.1 shows the percentage
of symptoms that turn out to be cancer.
TABLE 2.1
SYMPTOM % BC
Breast lump 36
Painful lumpiness 33
Pain alone 17.5
Nipple discharge 5
Nipple retraction 3
Family history of breast cancer 3
Others 2.5

TABLE 2.2
AGE RISK OF BREAST CANCER
20 1:20 000
30 1:2000
40 1:200
50 1:50
60 1:25
70 1:15
80 1:10
90 1:8
12 GENERAL SURGERY OUTPATIENT DECISIONS

Table 2.2 shows the age-related risk of breast cancer in the general population. (These
risks are likely to be slightly higher in a symptomatic breast-clinic population.)
Triple breast assessment
Triple assessment (clinical assessment, mammography/ultrasound and cytology/biopsy)
is the core of breast assessment. The principles of triple assessment underpin all breast
assessment. It allows rapid and accurate diagnosis of cancer prior to surgery and, con-
versely, reliable exclusion of cancer, allowing most patients to be discharged back to their
GP after one clinic visit.
The appropriate use of these three modalities will reduce but not eliminate the chance
of missing a cancer, as no modality is 100% sensitive or specific. Not all cancers present
as discrete changes or with classical clinical or radiological features; this is especially
true now that women are more breast aware and present with early-stage disease with
minimal signs.
Clinical skills and experience remain an important aspect of triple assessment, espe-
cially when reviewing the concordance of the assessment process.
The cancer most commonly ‘missed’ is lobular; clinical and radiological presentation
can be subtle and cytology may have a bland appearance. The most common cause of
a delay in BC diagnosis (and therefore of litigation) is failure to use triple assessment
appropriately and failure to recognise non-concordance. This is usually due to poor
departmental processes and procedures rather than poor individual competence.
The following notes describe the use of triple assessment in the symptomatic breast
clinic. Symptomatic cancers are usually larger than 2.5cm but screen-detected cancers
may be smaller than 15mm and are usually asymptomatic. Women with solid, screen-
detected lesions (that are usually impalpable) also undergo full triple assessment in
separate NHSBSP assessment clinics.
Triple assessment scores
As shown in Table 2.3, each modality of triple assessment is scored 1–5, i.e. normal to
malignant. The aim is to try to bring objectivity into a subjective area. If there is any diag-
nostic doubt, repeat investigations or further ‘second stage’ investigations are arranged.
TABLE 2.3
IMAGING BIOPSY
CLINICAL (R – RADIOLOGY) C – CYTOLOGY
(P – PATIENT) (U – ULTRASOUND) B – CORE BIOPSY
Normal 1 1 1

Benign 2 2 2

Uncertain 3 3 3

Suspicious 4 4 4

Malignant 5 5 5a Ductal carcinoma in situ (DCIS)

5b Invasive disease
 BREAST 13

A score of ‘1’ can also indicate inadequate assessment, so it needs to be interpreted with
caution.
No definitive cancer treatment should be undertaken unless two of the three triple
assessment modalities are positive for cancer, one of which must be cytology or, ideally,
histology. A false positive diagnosis of cancer is rare, but may result in unnecessary cancer
treatment with far-reaching physical and psychological consequences.
Triple assessment stage one: Clinical
Breast history
Introduce yourself and explain your status. It is important the patient understands you
will see them first and then discuss their management with the senior doctor/consultant,
who may also wish to see them.
You and the patient should ideally be seated during the history taking. The patient’s
breasts must not be exposed at this stage of the consultation. They must be covered, either
with the patient’s own clothes or with a specially designed Breast Unit (BU) top.
Whilst taking a history you have the opportunity to assimilate other ‘softer’ issues, for
example, your patient’s concerns and fears: what drove them to report their symptoms
and come to see you? What do they want from you? It is not always the obvious.
Try to establish rapport, as the patient may already be nervous and embarrassed about
the intimacy of the forthcoming breast examination. Make lots of eye contact, smile, and
try to appear friendly and relaxed as well as confident and calm, as patients are often very
scared and tearful.
Occasionally a female patient will refuse to see a male doctor. Usually the nursing staff
will have anticipated and managed the situation. This can be hurtful and seem personal.
It isn’t – be sensitive, not offended.
The stressful consultation
Sometimes the consultation is tense and stressful – usually because the patient is terrified
of what you may find. A patient may scrutinise your face, and over-interpret (usually
negatively) words and actions. Alternatively, they may be cold and withdrawn or angry
and aggressive. Occasionally they may cry continuously. Patients may ask repeatedly if it
is all OK. You may feel intimidated and pressurised, but try not to give bland reassurances
or distance yourself. Try to understand their vulnerabilities, but be honest. If it feels OK,
say so; if you are not sure, say so; if you are concerned, express your concerns. Explain
that the examination is one part of the assessment process and you may not be able to
confidently tell what the problem is until the imaging has given you some clues – hence
the importance of a thorough assessment.
Taking the history
Age is the most important factor in assessing the likelihood of a new breast change being
cancerous.
Pain may be cyclical or non-cyclical. Note when the pain first started, duration, site,
severity, relieving and exacerbating factors and associated symptoms.
Cyclical breast pain is related to ovarian function. Breasts are swollen and tender
and/or lumpy 3–10 days (can be longer) prior to menstruation, with pain relieved by
menstruation.
Non-cyclical breast pain is pain caused by specific conditions of the breast not related
to ovarian function, e.g. trauma and fat necrosis, infected cyst, mastitis (periductal or
lactating), abscess, fistula.
Reasons for non-breast pain include angina, cholelithiasis, cervical spondylosis, hiatus
hernia, nerve entrapment, Tietze’s syndrome, oesophageal lesions and lung conditions.
If there is a lump, get the patient to describe it to you – ‘pea’, ‘marble’, ‘grape’ and
14 GENERAL SURGERY OUTPATIENT DECISIONS

‘torpedo’ are useful comparisons. How was the lump noticed? How long has it been
present?
Nipple discharge may be spontaneous or on stimulation (e.g. after the bath). Ask about
colour (blood, bloody, watery, yellow/sticky, pus-like, green). Is it associated with pain?
(Consider papilloma, infection, ectasia.)
History of presenting problem: determine the time course of each symptom and any
variation within the menstrual cycle, as this is often a clue to the diagnosis. Getting bigger
or smaller, varies in size with periods? Associated pain or tenderness?
Any previous breast imaging: date and location of last mammogram.
General: general health and co-morbidities. Smoking is important in breast sepsis.
BC risk factors: the most powerful risk factor is family history.
∝ Family history: maternal and paternal, first- and second-degree.
∝ Past history of radiation to the chest wall (mantle radiotherapy (RT) for Hodgkin’s).
∝ Any previous breast problems – nature, investigation and outcome.
∝ We ask about other risk factors but in reality these are of little help in assessing an
individual’s risk in the symptomatic breast clinic. However, such information helps
to build a picture of your patient and if your unit runs a database the information
may be useful for future analysis.
∝ Endogenous oestrogen exposure: menarche, menopause, age at first pregnancy,
number of pregnancies, breast-feeding history.
∝ Exogenous oestrogen exposure: oral contraceptive pill (OCP), hormone replace-
ment therapy (HRT).
Breast examination
Always have a chaperone, regardless of your gender. The room and your hands must be
warm. Explain at each stage what you are going to do and why and obtain verbal consent.
There are many breast examination techniques. You need to watch a variety and develop
your own. Consistency and reliability are the objectives.
A common technique is to imagine the breast as a clock and work your way around
the clock face from 12 to 12, examining the breast from the outer margin towards the
nipple (see Figure 2.1).
The signs of locally advanced cancer are difficult to miss when a patient undresses:
ulceration; fixation to chest wall (ribs, muscles); erythema of the skin; satellite nodules;
peau d’orange; invasion of the skin; matted, fixed axillary lymph nodes; lymphoedema.
Try not to look shocked: remain professional. The patient already knows the diagnosis
and is gauging your reaction. However, it is unusual to see advanced breast cancer (fewer
than 10% present with stage IV disease).
✧ Ask the patient to expose their whole torso, displacing long hair and jewellery, and to
sit on the right side of the couch facing you.
✧ Ask them to point to the area they are concerned about: the patient’s use of hand and
fingers will give you a clue to whether it is a focal or generalised problem.
✧ Look for asymmetry, visible lumps, skin dimpling or peau d’orange. Inspect the nipple
areolar complex (NAC).
✧ Look for skin dimpling or distortion as the patient slowly raises both hands above
the head.
✧ Ensure the patient is lying supine but not flat, with a pillow under the head, arms
elevated with elbows flat on the bed and hands tucked under the head.
✧ Examine the asymptomatic breast first to gain some idea of the normal texture of
the breast.
✧ Palpate breast tissue.
∝ Palpate all breast tissue with the flat of the fingers. Focus on the area of patient
concern, remembering the axillary tail and the NAC.
 BREAST 15

12

Upper outer Upper inner

Lower outer Lower inner

RIGHT breast

FIGURE 2.1 Breast quadrants. Most breast glandular tissue lies in the outer quadrants,
especially the upper outer quadrant.

∝ If you find a lump consider its site, size, consistency, surface and skin/muscle
tethering.
∝ If the problem is nipple discharge, ask the patient to massage the breast/nipple to
demonstrate the discharge: assess colour, and number of ducts involved (uniduct
or multiduct).
∝ Palpate the axilla for enlarged lymph nodes (with the patient’s arm supported in
your non-examining hand to allow better access to the axilla).
∝ Palpate infraclavicular and supraclavicular fossa for lymph nodes.

Repeat the process for the opposite side.

What is a lump?
Do not agonise over whether tissue is a lump or not. If the patient feels her breasts have
changed and/or she thinks there is a lump, you need to prove she doesn’t have a cancer.
A lump is tissue or an area that feels prominent or asymmetric. Clinical examination,
although helpful, is unreliable and subjective. All women’s breasts feel very different so it
is important to compare the two breasts, since asymmetry is a useful guide for proceeding
to imaging.
Lumps can be obviously discrete and circumscribed, e.g. an F/A, cyst, lipoma or cancer;
or they can just feel like an area of asymmetric lumpiness, e.g. BBC, F/A, cyst, lipoma or
cancer. A discrete lump deep in the breast will feel like lumpiness because it elevates the
surrounding tissue. The texture of the patient’s tissue and skin and the proportion of fat
16 GENERAL SURGERY OUTPATIENT DECISIONS

to glandular tissue will also affect your ability to feel a lump. A young breast with low
fat content and a tight skin envelope has little laxity and feels generally hard (dense), so
it can be difficult to feel even a superficial discrete lump. An older breast with a greater
fat to glandular tissue ratio and a more lax skin envelope (ptosis) is softer, so lumps are
usually more obvious.
✧ Benign breast changes may show generalised islands of nodularity, occasionally focal
or asymmetric.
✧ Fibroadenoma lumps are firm, round, very mobile and may be multiple. They usually
cannot be compressed.
✧ Breast cyst lumps are firm, round, mobile and may be multiple: as the fluid is
compressed, they may have a ‘bouncy’ feel. They are sometimes tender.
✧ Breast cancer has some classical signs such as hardness, irregularity, dimpling, tether-
ing, ulceration and so on, but now we are seeing smaller, earlier cancers that do not
demonstrate these signs. Virtually any type of breast change can indicate a cancer.
The nipple
Nipple discharge
Pre-menopausal discharge is common and usually settles with the menopause: therefore
all post-menopausal discharge must be regarded as suspicious. In the younger woman,
watery discharge can be a sign of DCIS. There are a number of physiological causes of
nipple discharge.
✧ Multi-duct, multi-coloured (yellow to dark greeny-brown) discharge is common and
normal. It is often secondary to nipple massage or a hot bath/shower. It is occasionally
spontaneous. It is usually seen pre-menopausally.
✧ Ectatic ducts produce a sticky yellow fluid or toothpaste-like material on massage.
✧ Milk-like fluid can be expressed by most pre-menopausal women who have lactated.
True galactorrhoea (pituitary adenoma – raised prolactin levels) is rare and the
discharge is spontaneous and copious.

Pathological discharges are usually watery (blood-stained), single duct, spontaneous and
persistent. They may be pre- or post-menopausal.
✧ Intraduct papilloma usually presents with pure blood discharge.
✧ Cancer (especially a presenting feature of DCIS) discharge is usually watery, with
intermittent pinkish staining.
Nipple inversion/retraction
Understand the differences between inversion (benign) and retraction (malignant).
Inversion and retraction look very different.
Inversion is usually slit-like (letterbox appearance) and often congenital. It is due to
fibrosis and shortening of the periductal tissue and major ducts. The nipple can often be
gently everted with manipulation and the areola is soft and healthy.
Retraction is due to a retro/periareolar cancerous process or mass pulling the NAC
inwards. Often the nipple is visible but distorted and the surrounding areolar tissue is
hard, inflexible and indrawn in a saucer-like manner.
Eczema and Paget’s disease
Eczema and Paget’s can look identical, especially in the early stages of Paget’s. Eczema
usually spares the nipple and affects the areola and surrounding skin. It can be bilateral
and associated with a generalised eczematous skin change.
Paget’s usually starts centrally, destroying the nipple architecture and spreading
outwards onto the areola. However, these signs are not pathognomic and a scaling/
excoriated NAC should undergo a punch biopsy.
 BREAST 17

Record the examination

Record examination findings and score your clinical impression (see Figure 2.2).
✧ Always mark the site of patient concern.
✧ There are standard ways of illustrating your findings.
✧ Imagine the breast as a clock face: describe the site of the lesion accordingly.
✧ Record the distance of the lesion from the nipple.
✧ Give the size of the lesion.

Fibroadenoma 2cm
4 o’clock 1cm from
nipple

Cyst Cancer

Benign lesion xxx Nodularity

xxx

Dimpling/tethering

FIGURE 2.2 Recording the examination.

Triple assessment stage two: Primary imaging

Most women who attend a rapid diagnostic clinic will be offered imaging regardless of
their presenting symptom or sign: clinical examination is poor at discriminating between
cancer and normal changes, particularly in the pre-menopausal woman with a dense
nodular breast.
Indications for imaging
First you should check your local protocols. However, the following recommendations are
commonly used. All women with symptoms who are more than 35 years of age should
have:
✧ mammography: to screen both breasts
✧ targeted ultrasound – focused on the symptomatic area.

Women younger than 35 who have focal lumps, nodularity, pain or tenderness should
have:
✧ targeted ultrasound – focused on the symptomatic area.

Results are scored M1–5 (or R1–5) for mammography and U1–5 for ultrasound. Results
must always be interpreted in combination with the rest of the triple assessment.
Mammography
Mammography uses soft-tissue X-rays to image the breast. The breast is compressed
between two plates while the image is made. Mammography is the gold-standard breast
imaging and screening tool because of its high sensitivity and specificity. Usually two views
(oblique and cranio-caudal) are obtained using 1 mGy of radiation. The breast is more
radio-dense before the age of 35, making mammography less sensitive. Mammography
18 GENERAL SURGERY OUTPATIENT DECISIONS

is particularly good at detecting early non-palpable lesions, microcalcification and

multifocality. It is not very useful for women under 35 (breasts are too dense).
Ultrasound
Acoustic water-based gel, which is a good medium for the transmission of ultrasound
waves, is applied to the breast and an ultrasound probe is manipulated over the breast by
the sonographer. There is no radiation. This is the best imaging for those under 35, and
it looks at retroareolar tissue, which is not well seen using mammography. Ultrasound
gives an accurate size and an indication of how well circumscribed a lesion may be. It is
operator dependent, not as sensitive as mammography and not used as the sole investi-
gation for those over 35. Because it is a poor screening tool, scanning an asymptomatic
breast is not recommended.
Other breast imaging modalities (secondary imaging)
If a patient has changes that are suspicious or diagnostic for cancer, the sonographer will
usually scan the axilla. If a node appears to be suspicious for cancer (local criteria), fine-
needle aspiration cytology (FNAC) is performed. Pre-operative identification of axillary
nodal disease will allow for more appropriate management of the axilla and cancer, for
example axillary clearance, than sentinel node biopsy will.
There are many other breast imaging techniques whose roles are unclear or still in the
research or developmental arena, e.g. positron emission tomography (PET) scanning
and scintiscanning. Magnetic resonance imaging (MRI), with its high sensitivity, is
especially useful in imaging the difficult breast (very young and dense, post surgery and
radiotherapy) or in assessing multifocality, but a low specificity and difficulty in MRI
biopsy restrict use to very specific indications. You should see your local protocols.
Triple assessment stage three: Tissue diagnosis
Techniques for tissue diagnosis include:
✧ fine-needle aspiration cytology (FNAC)
✧ nipple aspiration cytology
✧ punch biopsy
✧ percutaneous wide-bore needle (core) biopsy.

In general you should only proceed to obtaining tissue if there is a focal or discrete solid
change, either on imaging, clinical examination or, as is more usual, both modalities.
Random aspiration of a lumpy area is to be avoided.
Most units prefer to perform FNAC or core biopsy after the clinical exam and imaging,
as any invasive procedure can cause tissue inflammation/bleeding and can reduce the
accuracy of clinical and radiological findings.
Increasingly, core biopsy is the preferred technique for obtaining tissue, as it gives
histology rather than cytology. Histology is the gold-standard diagnostic modality. Core
biopsy will give a definitive diagnosis of benign lesion (e.g. it will confirm if the lesion
is a fibroadenoma and can be safely ignored) and will give more information about the
cancer, so allowing better pre-operative planning.
Aspirate cysts only if they are symptomatic or if patients request aspiration.
Asymptomatic cysts do not require aspiration. After aspiration, cyst fluid can be discarded
if there is no blood-staining or residual mass – which can indicate a papilloma, intracystic
carcinoma or necrotic cancer with cystic degeneration.
Occasionally, on aspiration you will perforate an unseen vessel and blood will enter
the cyst fluid in your syringe. If you are in doubt, request cytology.
Tissue/cyst drainage can be performed either freehand (usually by the surgeon or
nurse practitioner) or under image control (by the radiologist, sonographer or surgeon).
 BREAST 19

Image guidance (ultrasound or stereotactic mammography) is the preferred method,

especially for smaller lesions. It reduces the risk of missing the lesion and limits false
negative results, which can result from poor sampling. This means that the opportunity
to perform FNA and core biopsies now lies in the imaging department. Take advantage
of this training opportunity.
Results are scored C1–5 for cytology and B1–B5a, b for histopathology. Always
interpret the results in combination with the rest of the triple assessment.
Fine-needle aspiration cytology
FNAC requires a 10 ml syringe and a green or blue needle. The patient is positioned as
for examination of the breast and the procedure is explained. Verbal consent is usually
sufficient. Clean the skin and infiltrate with local anaesthetic. The lesion is fixed with
one hand while the other inserts the needle, applying suction to the syringe and passing
5–6 times through the lesion. Suction is released and the needle withdrawn. The sample
is deposited either onto glass slides or into cytological preservative fluid (check your local
protocol).
As soon as the needle is withdrawn, pressure is applied with a cotton wool ball to
the area of aspiration for 3–4 minutes to minimise bruising. A sticking plaster or other
covering is applied to prevent staining of the patient’s garments.
The technique is quick to perform, gives almost immediate results and samples a wide
area. Information provided is limited to ‘cancer’ or ‘benign’. It can be difficult to get an
adequate number of epithelial cells. The results are very dependent on the experience of
the clinician doing the FNAC and on the cytologists interpreting the result. FNAC is not
useful for assessing microcalcifications. ABS standard: less than 20% of FNAC reported
as C1 (inadequate).
Nipple fluid cytology
Nipple fluid can be smeared on a slide and cytology requested. This can be helpful in
distinguishing physiological from pathological discharge.
Punch biopsy
Punch biopsy is useful for the breast skin or very superficial lesions in the skin (e.g. skin
tumour deposit), especially in the area of the NAC if you want to exclude Paget’s disease.
Explain the technique (verbal consent is usually sufficient) and position the patient as
for a breast examination. Clean the NAC skin and infiltrate under the NAC with local
anaesthetic.
Punch biopsy cutting blades are provided on a handle, in a range of sizes from 2–6mm.
Using a screwing motion, push the round cutting blade through the skin and underlying
tissue. Lift the tissue above the skin using forceps or a needle, and cut the tissue free with
scissors. Place the tissue in a formalin pot. Sutures are not required. Apply a suitable
dressing.
Percutaneous wide-needle (core) biopsy
After explaining the technique (verbal consent is usually sufficient), position the patient
as for a breast examination. Clean the skin and infiltrate with local anaesthetic. Make a
small incision with a number 11 blade in the skin over the lesion. Fix the lesion between
thumb and forefinger and insert the special biopsy needle (gun) up to the lesion. After
the gun is fired the needle is removed in the closed position and opened to deposit the
core of tissue into a formalin pot.
As soon as the needle is removed, pressure is applied to the biopsy site with a cotton
wool ball to minimise bleeding and bruising. Take 3–4 cores. A core containing sufficient
breast tissue will sink in the pot. Apply a suitable dressing.
20 GENERAL SURGERY OUTPATIENT DECISIONS

Histological diagnosis is so much more informative, especially if cancer is found: it

gives morphology, grade, oestrogen/progesterone receptors (ER/PR) and HER2 status.
It takes slightly longer to perform than does FNAC, it is slightly more traumatic (more
bruising) and results take 24–48 hours to obtain.
Excision biopsy
This is surgical excision of a lesion or microcalcification, with or without a localising
guidewire. It is performed when triple assessment is non-concordant and biopsy, or
repeat biopsy, is not possible.
Microdochectomy or Hadfield’s procedure (major duct excision) may be useful to
diagnose the underlying cause of a bloody/watery nipple discharge. Microdochectomy
retrieves a large amount of tissue for histology. If the lump is benign the procedure
provides both diagnosis and treatment. The procedure requires a formal operation,
which leaves a scar. If a lump proves to be malignant, a second operation may be needed
for staging and wider excision. Only a small number of lesions require formal surgical
excision to make a diagnosis – usually the smaller screen-detected cancers or small foci
of microcalcification.
Frozen section
This is used only in exceptional circumstances and after full discussion with the pathologist
and patient.
A frozen section involves surgical excision of the lump and immediate processing of
tissue for histological diagnosis while the patient is still anaesthetised. If a lump proves
to be malignant, a further surgical procedure is performed without waking the patient
from anaesthesia, removing the need for a second operation. The procedure has now
fallen into disuse – tissue is no longer available for future, more detailed analysis; and
accurate histological diagnosis is more difficult on frozen sections (especially for subtle
lesions, DCIS, lobular carcinoma in situ (LCIS), and atypical ductal hyperplasia (ADH)).
It is difficult to advise and gain consent from the patient pre-operatively.
Other diagnostic breast investigations
These are determined by the presentation, history and examination, but in general very
few other diagnostic investigations are required (see gyneacomastia).
Multi culture and sensitivity (MC&S)
If the patient has breast sepsis, try to obtain pus for culture before starting treatment.
Staging
If the patient is diagnosed with breast cancer they may require staging. Each unit will
have a specific protocol, but routine pre-operative staging is not recommended and
is reserved for those with advanced disease or specific symptoms and signs that may
indicate metastatic disease.
Staging tests include full blood count (FBC), liver function tests (LFT), chest X-ray
(CXR), bone scan and liver scan.
Triple assessment: Concordance
There are two main questions to answer concerning concordance.
✧ Do the assessment results fit the clinical picture? If not, investigate further, repeat
tests.
✧ Is each aspect of the ‘triple’ assessment in agreement? If not, investigate further, repeat
tests.
 BREAST 21

The rapid diagnostic clinic

Assessment results must be discussed with the senior/responsible clinician during the
rapid diagnostic (RD) clinic especially before discharging a patient. If you are uncertain
about what to do, a follow-up appointment is not the solution – discuss the problem with
the senior clinician, who will be pleased to provide guidance.
The multidisciplinary meeting
Patients who have undergone full triple assessment are usually discussed further at the
weekly MDM. The process and details vary from unit to unit, but in general most units
will discuss the triple assessment results of that week’s new cancers, and will review
all cases that had FNAC or cores. This is to confirm concordance and appropriate
management, be that discharge, definitive treatment or further investigations.
Occasionally review of the assessment process will throw up uncertainties and
surprises, resulting in complex diagnostic problem solving. Try to understand the MDT
decision-making process. If it is not clear – ask.
After triple assessment: what to do next
Advice and education
After appropriate assessment and diagnosis you need to formulate a management strategy
with your patient. This will be mainly in the form of advice and education regarding BBC
and normal age-related breast changes; and guidance on breast awareness and the use
of breast screening. Make sure patients know they are always welcome back if they have
further problems, and explain the local referral mechanisms – usually via the GP. If you
make a patient feel they have wasted your time because they have normal breasts, they
will not report future changes for fear of being made to look foolish.
Most patients do not understand the complex nature of a breast and the hormonal
influences that cause breast changes. Understandably, patients think pain is a sign of
disease rather than function. A simple explanation will transform understanding. A
well-informed patient will have greater confidence in managing their own breast signs
and symptoms in the future, which will help reduce the number of clinic attendances for
minor breast problems such as cyclical breast pain and lumpiness. The breast care nurse
will have copious literature available. Use leaflets judiciously: handing out information
sheets is no substitute for a careful face-to-face explanation.
Breast awareness is more than breast self-examination and looking for a lump. It is
about knowing your breasts, so if there is a change – any change – you will know there has
been a change and can report it to the doctor or nurse. They can then review the change
at a different stage of the menstrual cycle (in a pre-menopausal woman) or refer straight
to a breast clinic (in a post-menopausal woman).
The anxious patient
Occasionally you will meet a patient who finds it difficult to accept they have normal
breasts. Often all that is required is more time and a careful repeat explanation of the
results. Sometimes a patient may have a cancer phobia or other underlying psychological/
psychosocial problems. These patients need to be identified early and seen by the senior
clinician and breast care nurses rather than to have large numbers of unnecessary
investigations or treatments.
The dissatisfied patient
Occasionally a patient will not be satisfied that the assessment has been carried out
properly. This requires careful handling. Always involve the senior clinician and do not
be dismissive. Listen to concerns with courtesy and sympathy – you might be wrong and
the concerns justified. Remember, no test is infallible.
22 GENERAL SURGERY OUTPATIENT DECISIONS

Breaking bad news

You may need to explain the diagnosis of cancer; this is difficult for you, but remember
it is even more difficult for the patient. It is normal for a patient to be distressed at a
diagnosis of breast cancer. Allow them the time to weep. To begin with, sit in with a more
experienced clinician and take guidance from the breast care nurses. Develop your own
style and approach: it is possible to be honest, clear and humane.

Management of specific breast conditions

Each unit has its own protocols – know these.
Breast cancer
The management of breast cancer is beyond the scope of this book.
Normal or benign lumps
Fibroadenoma
If you have histological proof of an F/A (B2) nothing further need be done. The majority of
F/As involute and have no increased cancerous potential. Some women prefer to have the
lump removed. However, this is at the expense of a scar, the possibility of chronic pain and
the risks of surgery. Some F/As will grow. Explain that the patient can always return.
Cysts
After investigations confirm cysts, nothing further needs to be done unless there is a
dominant cyst that is troublesome (pain, infection). Aspiration with a fine needle (blue
or orange) is all that is required. Cytology is not requested unless the fluid is blood-
stained (perhaps from intracystic carcinoma or papilloma) or the lump doesn’t disappear
(consider necrotic cancer with cystic degeneration).
Benign breast change
BBC is normal. Once you have confirmed BBC no further action is required.
Other benign lumps
For other benign lumps, e.g. lipomas, if assessment shows the lump is benign, no further
action is required.
Pain
Most patients with pain have hormonally mediated breast pain. They are usually happy
to cope and self-manage after cancer has been excluded and they have been given an
explanation of the condition. Giving some helpful advice such as trialling the wearing of a
bra 24 hours a day or taking evening primrose oil (EPO) (prescription not required) does
seem to help some women, but the evidence base is flimsy. Simple analgesia is generally
not helpful.
Complementary therapies such as acupuncture or reflexology are non-evidence based,
but help some women cope with their symptoms.
It is possible to reduce breast pain with medication that alters the breast hormonal
axis, e.g. danazol, bromocriptine, tamoxifen and GHRH analogues, but these are powerful
drugs that should never be recommended without consultation with the senior clinician
and a careful and detailed risk-benefit discussion.
Surgery never offers a solution for chronic breast pain.
Nipple inversion
Gentle manipulation may encourage the nipple to evert to allow breast-feeding. Surgery
 BREAST 23

will provide a permanent solution, but at the expense of division of the major ducts,
which will prevent feeding.
Breast sepsis
Pain, redness and swelling are the usual symptoms of breast sepsis, but these symptoms
can also be caused by rare inflammatory breast conditions that are often diagnosed by
exclusion, e.g. granulomatous mastitis.
Inflammatory breast carcinoma may present with the history and appearance of an
acute breast infection.
Breast infections may be present in lactating or non-lactating women.
Breast infection during lactation
Puerperal mastitis/abscess occurs during breast-feeding and weaning. There may be
a history of cracked nipples, allowing bacteria (Staphylococcus aureus, S. epidermidis,
streptococci) to enter.
Breast infection without lactation
There are a number of possible causes.
✧ Periductal mastitis affects young/middle-aged women who have a history of smoking,
which damages the periareolar ducts. Infection of the damaged ducts causes periareolar
inflammation with or without a mass (caused by enterococci, anaerobic streptococci,
Bacteroides and S. aureus).
✧ Mammary duct fistula is a communication between the skin, usually in the periareolar
region, and a major duct. It usually follows a history of periductal mastitis with
periareolar inflammatory mass, which discharges spontaneously. It is occasionally
seen after a biopsy of an area of inflammation, or incision and drainage of a non-
lactating abscess.
✧ Infected sebaceous cysts are common in the sternal and inframammary regions of the
breast.
✧ Variations of Hidradenitis suppurativa can be seen in the breast, especially around the
nipple and axilla.

Other rare causes of sepsis or breast inflammation need to be considered if the sepsis
doesn’t settle with appropriate treatment.
Treatment
If infection is suspected (redness, heat, pain, swelling, fever) it is justified to start treatment
based on clinical judgment and modify according to the results of investigation. If the
patient is toxic they may require admission for intravenous (IV) antibiotics (flucloxacillin
or augmentin).
✧ Abscess – regardless of aetiology, most can be treated in the clinic or A&E with
ultrasound-guided aspiration under local anaesthetic. Overlying thinned or necrotic
skin needs removal to allow free drainage, but this can also be done in the clinic or
A&E. Prescribe antibiotics. Encourage manual expression of milk and/or feeding.
Repeat aspirations every 24–48 hours as required. Surgery is indicated for refractory
or multiloculate abscesses.
✧ Periductal mastitis – try flucloxacillin. If persistent or if anaerobes are cultured, add
metronidazole. If ultrasound shows an abscess, repeat aspiration is better than incision
and drainage, which results in a mammary fistula in up to one-third of patients. The
patient should stop smoking.
✧ Mammary duct fistula requires antibiotics and surgical excision.
24 GENERAL SURGERY OUTPATIENT DECISIONS

Follow-up
Follow-up is determined by the diagnosis and course of the condition. Periductal mastitis
is difficult to treat and may have a relapsing course. Treatment for recurrent disease
is surgical excision of the diseased duct system under antibiotic cover. The cosmetic
outcome can be very poor. Periductal mastitis usually resolves after the menopause.

Male breast problems

Gyneacomastia and breast cancer
More men are attending breast clinics because of increased awareness of male breast
cancer – there are 300 cases in the United Kingdom each year – and because they are
distressed by the appearance of gyneacomastia.
The male breast does not have lobules (glandular) tissue. Gyneacomastia is diffuse,
often tender (in the early stages) enlargement of the breast ductal/stromal tissue behind
the male nipple. The tissue becomes enlarged due to alterations in the male oestrogen/
testosterone ratios.
Causes
The two most common causes of true gyneacomastia are puberty and senescence.
Other causes include virtually anything that will alter the oestrogen/testosterone ratio:
antiandrogen drugs (cimetidine, digoxin, spironolactone), cirrhosis, malnutrition,
primary hypogonadism, secondary hypogonadism, hyperthyroidism, renal disease, lung
cancer and, finally but rarely, testicular tumours.
History and examination
Male breast patients require a full general history with a detailed drug, alcohol and smok-
ing history. A full examination including the genitalia is mandatory. Male BC can mimic
gyneacomastia but usually presents with all the classical features of female BC, i.e. an
asymmetric lump with dimpling and so on. In general the diagnosis of male BC is straight-
forward, as there is no surrounding glandular tissue to cause diagnostic uncertainty.
Investigations
Male BC is rare, especially in men in the under-50 age group with no family history of
the condition, but you should proceed to assessment if concerned. Mammography of the
male breast is possible. If tissue is required, core biopsy is the preferred technique because
cytology can be misleading in the male breast.
There are numerous causes of gyneacomastia. It can be difficult to settle on a realistic
investigative algorithm, as the yield from a series of diagnostic trawling tests is very low.
The history and examination will in general guide any further investigations. Contrary to
what is written in the textbooks, gyneacomastia is often asymmetric and painless.
Treatment
Male BC is treated in a similar fashion to female BC.
Physiological gyneacomastia requires no specific treatment other than explanation
and reassurance. Surgery for gyneacomastia is essentially aesthetic: expectations are very
high and outcomes often poor. Since men go topless far more frequently than women,
surgery should be undertaken only by an appropriately trained and experienced surgeon
(oncoplastic or plastic).

Breast follow-up clinics

The purpose of triple assessment is to exclude cancer and confirm a normal/benign
 BREAST 25

breast, thus allowing prompt discharge of the patient. Women with normal breasts do
not require regular checkups. Ask yourself – why do I want to bring this patient back?
If you are not confident about the concordance of the initial assessment, then go with
your instincts. Repeating tests or getting further tests needs to be done now, not in three
months’ time at review. Discuss with a senior clinician. However, there are exceptions, of
which the following are examples.
✧ Occasionally a patient with a cancer phobia may respond to a structured follow-up
schedule over a few years, until her underlying fears have been addressed through
counselling or other appropriate interventions.
✧ Women who are at high risk of BC due to their family history or to other factors
should be part of a regular quality-assured high-risk screening programme. The
process will vary from unit to unit.
✧ Women with known cysts who get recurrent lumps can find an open-access clinic for
a mini assessment useful.
The post-surgery ‘results’ clinic
The composition of a results clinic may vary, but usually in attendance are the surgeon
and the breast care nurse with or without the oncologist(s).
Histology results are available on average from 7 to 14 days after surgery. Results
clinics should be held after the weekly MDM, with all the necessary information and a
management plan.
Patients can become distraught whilst awaiting results, especially if there is uncertainty
about the diagnosis. The breast care nurses bear the brunt of this distress. Patients with
benign lesions can be contacted by letter or phone to save them a journey or relieve
anxiety before the clinic appointment. However, you need to have a reliable mechanism
in place to ensure this happens.
Procedure at the clinic
Examine the patient for possible complications of surgery before discussing the results.
✧ Once you have completed the examination you can ask the patient to dress.
✧ Ensure the patient is comfortable and sitting next to their partner.
✧ Explain the results.
✧ It can be very helpful to have the breast care nurse (BCN) present, especially if the
information is complicated or the results indicate a poor prognosis.

Never give the results whilst the patient is undressed.

During the consultation, assess your patient’s physical and emotional recovery.
Emotional recovery may be more difficult to judge in the acute stages of recovery, but
the BCN may have invaluable insight.
Pain
Breast and axillary surgery is not painful; pain is generally mild and controlled with
simple analgesia. Neurogenic pain can be difficult to manage, so early involvement of the
pain team is essential to prevent a chronic pain syndrome developing.
✧ If pain has been difficult to control since surgery, consider nerve damage.
✧ If pain was mild but is getting worse, consider infection.
✧ Poor mobility can increase pain due to disuse atrophy and stiffness, so consider
intensive physiotherapy.
Wound
Infection occurs in 5–10% of breast surgery wounds. It is normally minor and self
limiting. Take swabs or aspirate fluid for culture and prescribe antibiotics.
26 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Abscess formation is rare, but needs prompt drainage in the clinic.

✧ Delayed haematoma can occur – the wound will be bulging and oozing blood. The
clot requires evacuation, which can often be done in the clinic.
Seroma formation
This is common after any breast and axillary surgery (>50%). It requires aspiration
only if it is very large and uncomfortable (stretching the wound to dehiscence) or looks
infected. Most seromas will reabsorb over a few weeks. If aspiration is required, use
aseptic technique, insert the needle or trocar through the insensate wound and keep the
needle parallel to the chest wall.
Lymphoedema
Early, very mild, post-operative oedema of the arm or breast is common after axillary
node dissection and improves as other routes for lymph flow are established.
Cording (lymphatic thrombosis) is common and can be traced from the axilla, down
the inner aspect of the arm, across the elbow to the wrist. It is self limiting.
Nerve damage
Intractable pain or hyperparesthesia in the nerve distribution is often the clue.
Physiotherapy may help to lessen any disability.
✧ Intercostobrachial – sensation altered for the inner aspect of the arm, axilla and
posterior axillary fold.
✧ Serratus anterior (long thoracic nerve) – may see winging of the scapula.
✧ Latissimus dorsi (thoracodorsal nerve) – wasted posterior axillary fold.

Shoulder mobility
It is normal to have slightly restricted movements in the first few weeks after axillary
surgery, but the importance of physiotherapy exercises must be reinforced to prevent the
development of a frozen shoulder as the scar tissue starts to mature and contract. Early
identification and referral for intensive physiotherapy of potential shoulder problems is
crucial.
The joint breast/oncology clinic
Patients who have completed their cancer therapy are reviewed on a regular basis in the joint
breast/oncology clinic. The schedule is determined by local protocols, which you should
know, as they can sometimes be very complex. The minimum is usually a yearly exami-
nation and mammography for 2–5 years or whilst the patient is on active treatment.
The value of routine clinical examination in detecting recurrent or new cancers is
debatable, as most recurrences are screen- or patient-detected. It is clear patients value
follow-up consultations, as they provide reassurance and the opportunity to discuss
concerns and worries. The trend is to nurse-led follow-up. In the future this might be
community based.
Once again the structure of the clinics and who performs the follow-up varies from
unit to unit.
Use the clinic to gain a better understanding of cancer treatment protocols – reading
and summarising the patient’s history on the GP letter is a powerful learning tool.
History
The following are a few prompts that may be useful.
✧ How are they? How is their general health? How is life?
✧ Are they menstruating?
✧ Are they taking their prescribed anti-cancer treatment?
 BREAST 27

✧ Do they have any side effects?

✧ Have they noticed any new symptoms or breast changes?
Examination
The examination is mainly focused on checking for loco-regional recurrence in the
breasts and nodal basin, but take general note of the patient’s state of health – advanced
metastatic disease is usually obvious.
✧ Skin and chest wall: local recurrence may present as scattered skin lesions in the
vicinity of the previous surgery or on the chest wall.
✧ Breasts: local recurrence after breast-conserving surgery may be difficult to detect
because of the fibrous changes that occur following surgery and radiotherapy.
Contralateral cancers occur in 5% of patients.
✧ Nodal basin: axillae, infra and supraclavicular fossae, intramammary chain (sternal
intercostal spaces).
✧ Other sites for clinical examination such as the abdomen or chest will be determined
by the history.
Investigations
If the patient is asymptomatic and well, routine follow-up investigations such as bone
scan, CXR or tumour markers are not recommended.
✧ Suspected local recurrence needs to be proven, ideally with targeted imaging and
histology. Systemic recurrence is diagnosed mainly on imaging appearances and
pattern, as histology can be difficult to obtain.
✧ On confirmation of recurrence it is necessary to restage the disease – use local
protocols.
Treatment
Results are discussed at the MDM and a treatment plan is instituted; the details are
beyond the scope of this handbook.
When a patient relapses it is a demoralising experience, and their fears about dying
will resurface. Most patients regard the diagnosis of recurrence as a greater psychological
blow than the original diagnosis. It is important to be honest about the implications of
relapse, especially if the patient has very advanced disease with poor prognosis. Honesty
can be delivered with humanity and is usually appreciated. Realism must always be
tempered with hope – a difficult balance even for the experienced clinician. Considerable
psychological support will be needed and time should be allocated during the clinic to
dealing adequately with all these aspects.
✧ A local relapse may predict for an early systemic relapse in the next year or so, or it
may indicate that the original local control was inadequate and further treatment
may still be curative.
✧ A systemic relapse indicates the disease is not curable. Further treatment is to control
and contain. However, depending on response to second-line treatment, remission
can be measured in terms of years, especially if the disease is bony rather than visceral.
Newer targeted therapies are offering extended remissions.
Finally
In conclusion:
✧ never forget your duty of care is to the patient
✧ do not make decisions beyond your level of training or competence. If you are not sure
check and check again – a patient may pay a very high price for your uncertainty
✧ never be afraid to ask for help or advice. Do not work in isolation – you are a member
of the MDT, and the MDT is there to both train and support you.
28 GENERAL SURGERY OUTPATIENT DECISIONS

Enjoy your time with the breast team. It will be a demanding, but rich and stimulating,
professional and personal experience.

GP guidelines
‘Urgent’ referrals
Fewer than 5% of breast cancers occur in women under 40 years of age.
Urgent referrals should be made for those:
✧ older than 35 years whose symptoms/signs are highly suggestive of breast cancer
✧ between 35 years and menopause for any discrete lump that persists over a menstrual
cycle
✧ after menopause for any discrete lump.

Referral criteria for symptomatic breast clinic

Signs of breast cancer
Signs of breast cancer are:
✧ lump with dimpling/ulceration
✧ nipple retraction (new), distortion, ulceration (unilateral)
✧ others – change in skin contour, peau d’orange, dimpling and fungation.

Lumps
Please do not needle a lump with no recent/proven history of cysts. Signs include:
✧ discrete lump – lumps in post-menopausal women not using HRT are usually
cancers
✧ asymmetrical, discrete nodularity that persists and does not change with cycle
✧ post-menopausal abscess/infection – refer for urgent treatment and investigation.

Nipple discharge
Multi-duct or multi-coloured discharge is innocent – duct ectasia.
Signs of cancer include:
✧ any post-menopausal discharge
✧ bloodstained discharge (although 85% of bloody nipple discharge is benign, e.g.
intraduct papilloma)
✧ persistent single duct discharge, especially if watery
✧ excessive discharge, sufficient to stain clothes (i.e. socially embarrassing)
✧ ‘eczema’: Paget’s ulcerates the nipple then the areola. Eczema usually affects the areola
only.
Pain
(Fewer than 5% of breast cancers present with pain and no lump. Pain is important if it
is:
✧ associated with a lump (usually benign breast changes or cyst)
✧ intractable (but first try reassurance, well-supporting bra, dietary or lifestyle changes,
EPO)
✧ unilateral, persistent (more than three months) pain in post-menopausal women.

Women who can be managed by a GP/practice nurse

The following conditions can be managed by a GP or practice nurse.
✧ Recurrent cysts: GP cyst aspiration should be performed only in women with proven
cystic changes (previous triple assessment at Breast Unit). Always request cytology.
✧ Starting HRT: mammography is not indicated.
 BREAST 29

✧ Most women aged under 30 years: especially with cyclical, tender, lumpy breasts or
symmetrical nodularity, with no focal or discrete abnormality.
✧ Most breast pain: explain its hormonal nature.
✧ Most nipple discharge: especially if multi-duct/multi-coloured.
✧ Most family history: asymptomatic women with average risk.
✧ Simple lactational sepsis that responds to antibiotics.
Breast screening eligibility
Breast screening is suitable only for asymptomatic women.
Familial breast cancer (up to 50 years of age)
Refer www.nice.org.uk.
The following are the minimum referral criteria for moderate or higher risk.
✧ Mantle radiotherapy for Hodgkin’s.
✧ One first-degree relative younger than 40 years with breast cancer or with bilateral
breast cancer at any age.
✧ Two first-degree relatives younger than 50 years with breast cancer.
✧ Three first- or second-degree relatives at any age with breast cancer.
✧ Male relative (first-degree) with breast cancer or with a family history of ovarian/
breast cancer.
NHSBSP (over 50 years of age)
Tel: 01206 744749
✧ Women aged between 50 and 70 receive an automatic invitation to have a three-yearly
mammogram. There is no examination. The first invitation is sent at 49 to 52 years,
depending on the local screening cycle. It is not sent at the fiftieth birthday.
✧ Women aged over 70 should be encouraged to self-refer to NHSBSP if they are
asymptomatic.
 Neck and endocrine
Bill Fleming
THREE

Introduction
The referral pattern of endocrine problems and neck lumps is variable, so general sur-
gery trainees are likely to see these conditions during their training. Endocrine problems
may be seen initially by an endocrinologist who refers suitable cases for surgery, or may
present directly to general or specialist endocrine surgical clinics. In some centres patients
may be referred to multidisciplinary endocrine clinics incorporating both physicians and
surgeons. Neck lumps may be referred to almost any speciality and later be referred to
appropriate specialist surgical clinics for investigation and treatment. Excisional biopsy
may not be the correct course of action. Therefore, the surgical trainee needs a working
knowledge of endocrine conditions so that the patient is managed appropriately.

Assessment of endocrine disorders

If a patient is referred with a lump in an endocrine gland there are certain principles that
need to be followed.
✧ Make the endocrine diagnosis.
✧ Make the patient safe for surgery, if necessary.
✧ Localise the tumour.
✧ Decide whether the patient needs an operation.
✧ Decide what operation is appropriate.
✧ Replace any deficit.

How these principles are applied depends on the particular gland being assessed, and will
be dealt with later in the chapter. In the first instance a careful history and examination
are required, followed by targeted endocrine investigations to make the endocrine
diagnosis.
Endocrine history
Most endocrine problems are found in the thyroid or parathyroid glands, but the adrenal
and endocrine pancreas can also be affected. Unlike most other conditions, there is no
single endocrine history. The symptoms vary widely according to the affected endocrine
system, but the objectives of each consultation are similar: determining whether that
lump is associated with an endocrine abnormality, or with any other lumps elsewhere,
and whether the lump is benign or malignant.
It is not proposed to discuss pituitary disorders in this chapter, and pancreatic
endocrine lesions and the Zollinger-Ellison syndrome are described in the pancreatic
chapter. The carcinoid syndrome is described in the chapter about small intestinal
disorders.
Endocrine examination
The examination is generally directed towards the specific endocrine system, but any
endocrine gland mass may be associated with an endocrine syndrome, producing
widespread effects on the patient, e.g. Cushing’s syndrome. Endocrine masses are
generally palpable only in the neck, as the pancreas and adrenals are relatively out of
reach.

30
 NECK AND ENDOCRINE 31

Investigation of endocrine disorders

As with the history and examination, investigations are targeted towards the endocrine
gland in question, in order to firm up the diagnosis. In general, laboratory investiga-
tions aim to estimate hormone levels in either serum, urine or both, while imaging is
used to localise the tumour, assess function and possibly determine the likelihood of
malignancy.
Tissue biopsy, usually in the form of fine-needle cytology, may help in diagnosis
of malignant lumps and direct the appropriate surgical approach. This is particularly
important in the diagnosis of thyroid lumps.
Some of the specific investigations used in endocrine diagnosis will be described
below.
Laboratory investigations
Biochemistry
Serum tests
Biochemical assays are available to determine the levels of most hormones in the serum
as a measure of disease. Thyroid, parathyroid, adrenal and gut hormones can all be
measured directly to determine over- or under-activity.
In addition, other disease markers can be estimated. Tumour markers are available,
such as thyroglobulin in papillary thyroid cancer, and calcitonin and carcinoembryonic
antigen (CEA) in the case of medullary carcinoma of the thyroid. These are particularly
useful in the follow-up after total thyroidectomy and can act as an early warning of
recurrence.
Urinary tests
These are particularly useful in patients with hyperparathyroidism, when 24-hour
urinary calcium excretion may be elevated. Low excretion of calcium (less than 2 mmol/
day) may indicate the rare condition of familial hypercalcaemic hypocalciuria (FHH),
which can mimic hyperparathyroidism.
Functioning adrenal tumours may well be detected by excess hormone in the urine.
Elevated 24-hour urinary catecholamines are indicative of phaeochromocytoma, while
estimation of urinary cortisol excretion is used in the assessment of Cushing’s syndrome.
Conn’s syndrome is associated with a low serum potassium and elevated excretion of
potassium in the urine.
Provocation tests
Sometimes the standard measurement of serum levels does not accurately identify
the disease or identify the ectopic production of a hormone. Provocation tests involve
administering an agent that stimulates production of the hormone in question. Serum
levels are monitored to determine whether levels of the hormone rise in response to the
stimulus. For example, most ectopic sources of adrenocorticotropic hormone (ACTH)
are not responsive to corticotropin-releasing hormone (CRH), while most pituitary
lesions remain so. Administration of CRH produces a rise in serum ACTH if there is a
pituitary source but no rise if there is an ectopic source.
A provocation test can be combined with selective venous sampling to localise the site
of the lesion producing the hormone. For example, gastrinomas and other pancreatic or
gut tumours can be stimulated to release hormones by administration of calcium into
the arterial supply of the affected part. Selective venous sampling can then localise the
tumour to the area of highest stimulated hormone excretion, even if no lump is visible
on other imaging.
32 GENERAL SURGERY OUTPATIENT DECISIONS

Immunology
Antibodies to thyroid peroxidase (thyroid microsomal antigen) are found in most patients
with Graves’ disease and in those with Hashimoto’s thyroiditis. Thyroid-stimulating
hormone receptor antibodies are found in 90% of patients with Graves’ disease.
Genetic tests
Genetic tests are used mainly to screen first- and second-degree relatives of patients with
multiple endocrine neoplasia (MEN) syndrome. MEN 1 is caused by an abnormality on
the long arm of chromosome 11, while MEN 2 shows an abnormality on chromosome 10.
Referral to a medical genetics department is essential, as pre-test and post-test counselling
is an important part of the process.
Fine-needle aspiration (FNA) cytology
FNA is simple, safe and the most cost-effective method of assessing thyroid lumps. It is a
quick technique that is well tolerated by the patient and well suited to busy clinics. Results
are always interpreted in combination with the clinical and imaging assessments. Reports
may use terms such as malignant, benign, suspicious or inadequate, or may be classified
using the THY numbered classification. Results depend on the experience of the person
performing the technique and the cytologist interpreting the result. Inadequate results
occur infrequently if the FNA is performed by the cytologist or cytology technician.
Generally inadequate FNA means the test must be repeated, with ultrasound guidance
if the lesion is difficult to locate. The technique provides a tissue diagnosis, and in
thyroid disease can accurately diagnose colloid nodules, thyroiditis, papillary carcinoma,
medullary carcinoma, anaplastic carcinoma and lymphoma. Small numbers of cells are
obtained. Follicular lesions on cytology cannot be separated into follicular adenomas and
carcinomas, and usually require excision.
Imaging techniques
Ultrasound
This non-invasive technique is good at differentiating cystic and solid lesions, and it can
detect nodules less than 0.5mm. Fine-needle aspiration can also be performed under
ultrasound control for cytological examination, and the wall of cysts can be aspirated for
cytology. It is a critical part of the localisation of parathyroid tumours. It is also possible
to increase diagnostic yield by the use of contrast agents or microbubble techniques.
Ultrasound is operator dependent and usually cannot distinguish between benign and
malignant disease.
Thyroid isotope scan
The most common agents used in the assessment of the thyrotoxic patient are 123I and
technetium pertechnate 99mTc. The technique can differentiate hot from cold nodules,
but overall it has a very limited role. Detection of metastases in patients after total
thyroidectomy for medullary carcinoma of the thyroid can be achieved using pentavalent
dimercaptosuccinic acid (DMSA), octreotide or meta-iodobenzylguanidine (MIBG).
In a low dose (2–5 mCi), 131I can be used to detect metastatic disease after total
thyroidectomy for the more common forms of thyroid cancer. The patient must have
stopped thyroxine replacement some weeks beforehand or have recombinant thyroid-
stimulating hormone (TSH) administered prior to the test. Detected metastases can
then be treated with a therapeutic dose (150–200 mCi) of 131I. It may be useful, in
the assessment of the thyrotoxic patient, to differentiate single toxic nodules, toxic
multinodular disease and Graves’ disease.
Most metastatic follicular carcinomas and more than 80% of papillary carcinomas
can be imaged. The technique uses radioactivity. Differentiation of nodules into ‘hot’ and
 NECK AND ENDOCRINE 33

‘cold’ does not identify or exclude malignancy and therefore has a limited role assessing
thyroid nodules. Twenty per cent of papillary carcinomas are not imaged by 131I.
Parathyroid isotope scan
Technetium-sestamibi is the investigation of choice in the localisation of parathyroid
tumours, superseding the older method of technetium-thallium ( 210Tl-chloride)
subtraction scanning. Sestamibi accumulates in the mitochondria of parathyroid cells
and has a more favourable emission spectrum, improving the sensitivity of the technique.
Single photon emission computed tomography (SPECT) is also possible with this
technique, allowing better spatial resolution.
Adrenal isotope scan
MIBG is taken up by catecholamine granules and is used mainly for localising phaeo-
chromocytomas in the adrenal and in extra-adrenal sites and for the detection of
metastases. Multiple gland involvement can be found in MEN syndromes. Therapeutic
doses of MIBG can be used to treat some lesions. MIBG is very specific for catecholamine
tumours with very few false positives, although false negatives occur in 5–10%.
Computerised tomography (CT) scans
CT scans are particularly useful in the assessment of large retrosternal goitres, to deter-
mine the relationship to other structures. They may also be used to locate ectopic or
mediastinal parathyroid glands. Most adrenal lesions larger than 3cm can be detected
with CT scanning. It uses ionising radiation.
Magnetic resonance imaging (MRI) scan
MRI scans are particularly useful in the assessment of large retrosternal goitres, to
determine the relationship to other structures. The scan is also useful in detecting small
pituitary, adrenal and pancreatic lesions and in detecting ectopic sites of hormone produc-
tion or metastases. MRI is a useful technique for locating ectopic parathyroid glands,
although angiography and venous sampling are more accurate. The technique is expensive
and generally of limited availability. Many patients find the experience unpleasant.
Selective venous sampling
The technique is usually performed under local anaesthetic. The femoral vein is cannu-
lated using the Seldinger technique, and vascular catheters are inserted and manipulated
under radiological control until positioned correctly. Samples of blood are withdrawn
from the catheter and from a peripheral vein simultaneously and the serum concentra-
tions of hormone are compared. Sometimes an injection of a substance, such as calcium,
is used to stimulate hormone release.
Selective venous sampling is used in difficult or recurrent cases to identify the site
and side of secretion of the particular hormone. It is used in assessment of pituitary
lesions and parathyroid lesions, but it can be used in the assessment of adrenal lesions
and of ectopic production of hormones from other body sites. It is an expensive, time-
consuming and invasive technique with a small but definite morbidity and mortality, so
it is confined to redo surgical patients and some adrenal patients in general.

Neck lumps
The causes of neck lumps can be considered in four main groups: salivary gland lumps,
thyroid lumps, lymph nodes (thyroid lumps and lymph nodes form the bulk of neck
lumps referred to the general surgeon) and then non-thyroid lumps, which contain well-
known but relatively rare causes that everyone learns for exams. The majority of thyroid
34 GENERAL SURGERY OUTPATIENT DECISIONS

lumps can be palpated in the region of the thyroid gland and move on swallowing, while
non-thyroid lumps are in other locations and do not move on swallowing. Differentiating
non-thyroid lumps from lymph nodes requires knowledge of their different characteris-
tics, and these will now be described. If you are unsure of the extent of any of these lumps,
especially recurrent lesions or extensive primary lesions, a high-resolution ultrasound or
MRI scan is extremely helpful.
Lymphangiomas
Lymphangiomas are abnormal collections of lymph-filled tissue that are classified into
three main groups:
✧ lymphangioma simplex (one-third occur in the floor of the mouth, e.g. as a ranula)
✧ cystic hygroma
✧ cavernous lymphangioma (mainly affects the tongue).

The smaller lymphangiomas occur in the lips and cheek, where the tissue planes are
tighter, whereas cystic hygroma has more room to expand in the tissue planes of the neck.
Two-thirds are noted at birth and 90% before the end of the second year. They usually
transilluminate. Cystic hygromas can recur in adulthood at the margins of previous
surgical excision.
Midline dermoid tumours
These are lumps caused by elements of one dermal layer trapped in another, either
congenitally or by trauma.
✧ Epidermoid cysts contain cheesy contents of squamous epithelium only.
✧ True dermoid cysts contain squamous epithelium and skin appendages such as hair.
✧ Teratoid cysts contain endo, meso and ectoderm elements such as nails, teeth and
brain.
These lumps tend to present as solid or cystic masses in the midline of the neck or lateral
to the submandibular gland. Painless swelling is the only symptom, usually presenting
in the second and third decades.
Thyroglossal duct cysts
These are a remnant from the descent of the thyroid from the back of the tongue. They
can occur anywhere from the foramen caecum to the manubrial notch. They are found
in an age range from four months to 70 years, but mean age at presentation is five years.
Most are midline, but up to 10% may be deviated to one side (usually left).
History
Most patients complain of a painless cystic lump. Some present with tenderness and
rapidly increasing size due to infection, while others present with a fistula discharging
fluid.
Examination
Mobile in all directions; usually transilluminates; moves on swallowing or protruding
tongue. Suprahyoid cysts may be mistaken for submental adenitis or a dermoid. Prehyoid
cysts tend to be dumbbell or bar shaped and if large can push the tongue upwards,
causing dysarthria.
Investigations
This is usually a clinical diagnosis. In doubtful cases ultrasound scanning (USS) will
confirm the cystic nature. FNA is usually unnecessary and may introduce infection, but
it may help in difficult cases.
 NECK AND ENDOCRINE 35

Treatment
These cysts are prone to recurrent infection and are best treated by complete surgical
excision.
Follow-up
Review at short intervals (1–4 weeks) until diagnosis is obtained. Arrange surgical
excision promptly to prevent further episode of infection.
Post-operative follow-up
Review with histology to confirm diagnosis and to exclude the extremely rare thyroglossal
duct carcinoma. Examine for general complications of neck surgery. The most common
specific complication is a thyroglossal fistula, which results from infection or failure to
remove the whole cyst. It usually presents as an opening in the lower neck, discharging
clear fluid. Treatment is by further surgical excision.
Thyroglossal duct carcinoma is rare but should be excluded. It is always papillary. Ten
per cent have metastases. Treatment is by local excision, thyroidectomy, radioactive iodine
therapy and tumour suppressive doses of thyroxine.
Lingual thyroid
Lingual thyroid results when an embryological remnant of thyroid fails to descend to
the normal position in the neck. They may be asymptomatic and unnoticed unless
enlargement of the thyroid tissue occurs. The lingual thyroid may be the patient’s only
thyroid tissue, so excision may render the patient hypothyroid.
History
Patients may complain of a lump at the back of the tongue or of respiratory or swallowing
difficulties.
Examination
Examination may be normal, or ear, nose and throat (ENT) examination reveals the
swelling.
Investigations
The diagnostic investigation is 123I scan, which differentiates lingual thyroid from other
causes.
Treatment
It is possible to shrink an enlarged lingual thyroid with thyroxine therapy. If this fails,
therapeutic radio-iodine (131I) should be used. There is seldom any need to resort to
surgery.
Follow-up
Follow-up is at short intervals (1–4 weeks) until diagnosis is obtained and relief of
symptoms is achieved. Then intervals are increased (1–6 months) until the condition is
stable and the patient is symptom-free. Monitor thyroid function tests to ensure adequate
T4 replacement and TSH suppression. The patient may then be discharged, with advice
to return if symptoms recur and for the GP to monitor the thyroid function tests.
Branchial cysts
The exact aetiology is unknown. The cysts may be remnants of branchial clefts, pouches
or squamous metaplasia of a lymph node. Age range is 1–70 years, but peak incidence is
in the third decade. Most occur on the left side and appear anterior to the sternomastoid
muscle in the upper third of the neck.
36 GENERAL SURGERY OUTPATIENT DECISIONS

History
Most patients complain of a continuous swelling, though in some patients the swelling
can be intermittent. Pain affects up to a third of patients but infection occurs in less than
15% and some patients may complain of pressure symptoms.
Examination
Most feel cystic on palpation but do not transilluminate. Approximately one-third are
solid. They tend to not have any attached sinus or fistula track, as branchial fistula is a
separate disease. Branchial fistulas extend from an internal opening in the tonsillar bed,
through the carotid artery bifurcation to an external opening in the lower part of the
anterior triangle of the neck. Sinuses have similar external openings, but no internal
openings. Fibrous tracts can also occur.
Investigations
A CT/MRI scan may be needed to differentiate from a chemodectoma if there is direct
or transmitted pulsation and the cyst feels solid. If there is no pulsation, FNA can be
performed and will reveal aspirates rich in cholesterol.
Treatment
Optimal treatment consists of primary excision surgery. Try to avoid excision drainage
of infected tissue unless there is an obvious cyst that is going to discharge through the
skin. If infection seems to be a problem, pre-operative antibiotics to reduce the amount
of inflammatory tissue are worthwhile.
Follow-up
Review with results at 1–3 months and decide on management.
Post-operative follow-up
Review with results of histology (which, rarely, may contain squamous carcinoma)
to confirm diagnosis and detect complications of the operation. Uncomplicated cyst
removal not complicated by infection can be discharged. If there is doubt about complete
excision, recurrence would normally occur within the first year. Thereafter advise and
discharge.
Laryngocele
This is a rare, air-containing sac arising from the laryngeal saccule. Incidence is one in
2.5 million people per year, with a 5:1 male to female ratio. Peak incidence is 50–60 years.
It may be external, presenting through the thyrohyoid membrane, or internal. The most
important causative factor to exclude is a co-existent carcinoma of the larynx.
History
There may be hoarseness, neck swelling, stridor, dysphagia, sore throat, pain or cough.
Ten per cent are infected.
Examination
There is a large swelling over the thyrohyoid membrane, which can be emptied easily by
squeezing – but do not do it before the X-ray! Arrange for a full ENT examination of
the larynx.
Investigations
Soft tissue neck X-ray shows an air-filled sac.
 NECK AND ENDOCRINE 37

Treatment
Surgical excision – try to avoid emptying the sac before it is identified.
Follow-up
Review with results. Once cancer is excluded, arrange excision if fit for surgery.
Post-operative follow-up
Review once with histology and to detect any complications, e.g. wound infection.
Reassure and discharge if uncomplicated.
Chemodectomas (paragangliomas)
These are tumours of neural crest tissue that occur in the carotid body, the jugular bulb
and the ganglion nodosum of the vagus nerve in the neck.
Carotid body tumours (see vascular section) are rare, with an age range of 35–50 years.
Five per cent are bilateral; 10% are malignant. There is a strong family history and they
may be associated with phaeochromocytomas.
History
There is a long history of a painless lump (typically 4–7 years). Other symptoms include
headache, neck pain, dizziness, hoarse voice and dysphagia caused by local invasion or
cranial nerve compression. Occasional flushing, arrhythmias and hypertension are caused
by neuroendocrine secretion by the tumour.
Examination
There is a lump up to 4–5cm in size that moves from side to side, but not up and down.
It exhibits a transmitted but not an expansile pulse. Bruit may be present and may reduce
in size with carotid compression. Large tumours may involve IX, X, XI and XII nerves
and occasionally the sympathetic chain, causing Horner’s syndrome.
Investigations
Duplex ultrasound and angiogram shows a splayed bifurcation and a ‘tumour blush’
circulation. There may be a feeding vessel from the external carotid or vertebral artery.
CT/MRI may be useful to define the relationship of the tumour to other structures,
especially if local invasion is suspected.
Treatment
Treatment involves surgical excision by an experienced vascular surgeon, in case vascular
reconstruction is required.
Follow-up
Follow up in short intervals of 1–4 weeks, until diagnosis is obtained.
Post-operative follow-up
Review with histology to confirm diagnosis and complete excision and to detect any
complications of wound healing. Exclude bilateral tumours and phaeochromocytoma.
Arrange for genetic counselling and screening if there is a strong family history.
Glomus vagale tumour is a rare cause for a mass at the angle of the jaw. Angiography
may show an abnormal circulation from the external carotid artery.
Neck lymph nodes
The first objective is to determine whether the enlarged lymph node is due to a localised
problem in the head and neck or whether it is part of a generalised lymphadenopathy.
38 GENERAL SURGERY OUTPATIENT DECISIONS

If the cause is localised to the head and neck, the second objective is to determine
whether the cause of enlargement is non-malignant (e.g. infection – acute/chronic) or
malignant (i.e. metastatic from a head and neck carcinoma). Any patient over the age of
50 presenting with a single enlarged lymph node in the upper part of the neck must have
a full examination of the naso-, oro- and hypopharynx before biopsy of the neck node
to exclude occult carcinoma in these areas.
History
Ask about local head and neck symptoms, nasal symptoms, voice change, cough, hoarse-
ness and dysphagia. Ask about recent bouts of sore throat or tonsillitis, which may have
given rise to enlarged draining nodes. General symptoms include weight loss, respiratory
symptoms, abdominal symptoms and night sweats.
Examination
Examine the lump, noting size and consistency. Try to determine whether the node
is isolated or part of generalised enlargement. Site the node in one of the anatomical
triangles of the neck. The anterior triangle is formed by the midline of the neck, the
anterior border of the sternomastoid muscle and the lower margin of the mandible. The
posterior triangle is formed by the posterior border of the sternomastoid, the anterior
border of the trapezius and the upper border of the clavicle. A thorough examination by
an ENT specialist needs to be performed, of the mouth, naso-, oro-, and hypopharynx. A
thorough examination of the thyroid, breast, lung, abdomen (including spleen and liver)
and lower extremities needs to be performed for the site of possible primaries, especially
if the enlarged nodes are in the supraclavicular fossae. All other lymph node sites need to
be examined (axillae, groins, mediastinum and abdomen).
Investigations
Excision biopsy of the enlarged lymph node is not the first investigation. Laboratory tests
include FBC and film (haematological abnormalities), polycythaemia vera/erythrocyte
sedimentation rate (PV/ESR) and Monospot/Paul Bunnell (for glandular fever). Perform
FNA of non-pulsatile lumps for cytology.
If lymphoma is a possibility, ask the laboratory for advice regarding the transport of
specimens for tumour markers and flow cytometry.
Imaging with ultrasonography is useful for the differentiation of solid and cystic
lumps, and for the diagnosis of vascular lumps such as carotid artery aneurysms or
chemodectomas.
FNA is also useful for potentially infective lumps/lymph nodes, when a sample should
also be sent for microbiology. If tuberculosis (TB) is suspected, a sample should be sent
for Ziehl-Neelsen (ZN) stain and culture.
If no primary can be found in the head and neck for a malignant lymph node,
the search has to be continued into the chest. A chest X-ray may indicate a bronchial
neoplasm, TB or hilar/mediastinal pathology. Assessment of the gastrointestinal tract
(GIT) may be indicated, with upper and lower gastrointestinal (GI) endoscopy. Consider
ultrasound of the abdomen and occasionally CT scan of retroperitoneum and pancreas;
consider breast mammogram for impalpable breast neoplasms.
Treatment
Management depends on the results of investigations. The assessment of all lumps
depends on the clinical assessment, imaging and cytology. In children and young people,
once lymphoma has been excluded the causes are usually related to infective episodes and
will settle in time with antibiotics. Similarly, the management of TB lymph nodes is the
relevant chemotherapy and referral to an infectious disease specialist.
 NECK AND ENDOCRINE 39

In cases related to generalised lymphadenopathy, e.g. lymphoma/leukaemia or glan-

dular fever, the management is of the underlying condition.
Occasionally FNA does not supply sufficient histological information, and surgical
excision biopsy is indicated. This should not be undertaken without multidisciplinary
input from ENT or a head and neck specialist.
For a single malignant lymph node presenting in the neck, a primary will be found on
examination in approximately one-third of cases. The primary sites in order of frequency
are: nasopharynx, tonsil, base of tongue, thyroid gland, supraglottic larynx, floor of
mouth, palate, pyriform fossa, bronchus, oesophagus, breast and stomach. In a further
third of patients no primary is evident at the time of presentation but becomes apparent
on follow-up in the following sites: oropharynx, nasopharynx, thyroid, hypopharynx,
lung, abdomen and miscellaneous (10%).
For a head and neck cancer, treatment is of the primary lesion with block dissection of
the relevant lymph node field as indicated. If excision biopsy is necessary this should be
performed by the surgeon who would perform the definitive head and neck surgery.
Follow-up
Follow-up intervals should be short until cancer has been excluded or the primary site
identified.
Post-operative follow-up
Review at 1–2 weeks with the results of the histology and arrange further treatment
if appropriate. Complications include wound infection, which usually responds to
antibiotics. If the lymph node resection reveals TB, infection may be long term and
chronic until antibiotic therapy is effective. Persistent lymph leak can occur, especially
if the lymph node was neoplastic. Most will settle over 4–6 weeks. Some persistent or
copious leaks may be associated with neoplastic lymphatic obstruction, which may
respond to local radiotherapy.
Salivary gland lumps
Causes of salivary gland enlargement are divided into:
✧ enlargement of more than one gland (mumps, echo, coxsackie viruses, Sjögrens)
✧ generalised enlargement of one gland (sialectasis)
✧ localised enlargement of part of one gland
∝ benign tumours – pleomorphic adenomas, monomorphic adenomas (Warthin’s),
oncocytoma
∝ malignant tumours – adenoid cystic carcinoma, adenocarcinoma, squamous
carcinoma, malignant pleomorphic adenoma
∝ potentially malignant tumours – mucoepidermoid, acinic cell, rare tumours.

Twenty per cent of parotid tumours are malignant; 45% of submandibular tumours are
malignant; 65% of minor salivary gland tumours are malignant.
History
The following should be considered.
✧ Age: mumps is more common in children, but if it occurs twice it is more likely to be
congenital sialectasis.
✧ Does the swelling affect one gland or more than one: tumours are unilateral (Warthin’s
is occasionally bilateral).
✧ Is swelling related to eating: calculous disease secondary to sialectasis.
✧ Pain is generally due to duct obstruction from calculous disease. Occasionally adenoid
cystic carcinoma with nerve involvement will be the cause of pain.
40 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Systemic disorders which can cause painless salivary gland enlargement include
myxoedema, diabetes, Cushing’s, cirrhosis, gout and alcohol abuse, sarcoid and TB,
as well as certain drugs, such as thiouracil and high-oestrogen pills.
Examination
Examine all salivary glands. Is one gland affected, or more than one? Is enlargement due
to a localised mass within the gland or is there a generalised enlargement of the gland? Is
there skin involvement? Is there facial weakness? Is the lesion solid or cystic? Is the lesion
irregular? (However, benign pleomorphic adenomas are often irregular and knobbly.)
Benign tumours are usually mobile.
Investigations
If indicated, use laboratory tests to exclude myxoedema, diabetes, Cushing’s, rheumatoid
arthritis.
If sarcoid is suspected, a Kveim test is needed. FBC and ESR may be needed.
Plain X-rays are used if calculous disease is suspected. However, remember that parotid
stones are radiolucent; submandibular stones are radiopaque. Intraoral films may be
required.
Sialography (cannulation of the salivary duct and injection of contrast) is useful for
a diagnosis of sialectasis. Congenital saccular sialectasis gives a snowstorm appearance.
Advanced cystic disease shows large collections of dye. Pure duct stenosis is nearly always
an iatrogenic artifact caused by traumatic cannulisation.
CT scans are useful for determining the extent of spread of malignant salivary tumours
and for planning the surgical approach.
FNA for cytology is mandatory in every case. Avoid excision biopsies unless there is
diffuse enlargement of the gland and no diagnosis has been reached by other methods.
Diagnosis of minor salivary gland tumours is by incisional biopsy performed by the
surgeon who will eventually remove the lesion.
Treatment
The following treatments are used.
✧ Benign parotid tumours are treated by superficial parotidectomy if the tumour is
located in the superficial part of the gland, which happens in 80% of cases. Benign
submandibular tumours are rare and the treatment is removal of the whole gland.
Minor salivary gland tumours are diagnosed by incisional biopsy and then excised.
✧ Malignant parotid tumours are treated by total parotidectomy. If the facial nerve
is involved this is also excised and a decision is made at operation regarding nerve
grafting. If neck nodes are palpable, total parotidectomy is combined with a radical
neck dissection. Post-operatively, radiotherapy is given if the resection margins are
in doubt.
✧ Malignant submandibular tumours are treated by excision of the gland and, if neces-
sary, the mandible, skin and adjacent nerves if involved. Reconstruction is possible.
Post-operative radiotherapy is used if there are doubtful resection margins.
✧ Minor salivary glands are treated by wide excision and reconstruction of the oral
cavity.
✧ Mucoepidermoid and acinic cell tumours are often diagnosed on post-operative
histology after excision of an apparently benign mass. Tumours are graded as either
high grade or low grade, with prognosis determined by the grade. For low grade,
90% have five-year survival; for high grade, it is 20%. Many surgeons give immediate
post-operative radiotherapy. Some surgeons prefer to follow up patients monthly or
bi-monthly for 4–5 years to detect recurrence, and then to treat by wide field excision
and post-operative radiotherapy. Refer for an oncology opinion in every case.
 NECK AND ENDOCRINE 41

✧ Sialectasis has mild and infrequent symptoms, so advise the patient to finish each meal
with a citrus drink and massage the duct to expel debris from it. Many patients have
no further trouble after the diagnostic sialogram, which flushes the ducts.
✧ Submandibular duct stones are treated by surgical removal via the intraoral route
and marsupulisation. Stones in the body of the gland are treated by removal of the
whole gland.
✧ Parotid duct stones are removed intraorally. Persistent severe symptoms are treated
by total parotidectomy (superficial parotidectomy is often insufficient).
Follow-up
Follow-up intervals are short (1–4 weeks) until cancer has been excluded. Generalised
causes of salivary gland enlargement are referred to the relevant specialist. Mild sialectasis
can be discharged with the relevant treatment advice and a plan to return if symptoms
deteriorate. More severe cases can be reviewed at three-monthly intervals or greater until
the patient and surgeon feel that surgery is indicated.
Post-operative follow-up
The success of the operation is determined by the histology, the wound healing and
the absence of complications. Review the histology report to ensure that presumed
benign lumps were benign and did not contain any malignant elements. If the operation
was performed for malignant disease, confirm that the resection margins were clear
of tumour. If not, or if resection margins were very close to the tumour, refer for an
oncology opinion regarding radiotherapy.
✧ Complications of parotidectomy: Frey’s syndrome consists of discomfort, sweating
and redness of the skin over the parotid area during and after eating. This is caused
when the severed ends of parasympathetic secretomotor nerve fibres in scar tissue
are stimulated (as they formerly were to produce saliva) causing vasodilatation and
sweating. Spontaneous resolution within six months is usual. Treatment for severe
persistent cases is an ipsilateral tympanic neurectomy to divide the parasympathetic
pathway.
✧ Facial nerve injury causing facial muscle weakness may respond to rehabilitation.
Occasionally tarsorrhaphy, fascial sling procedures, nerve grafting or a unilateral face
lift are required.
✧ Salivary fistula tends to occur where a sialectatic deep lobe is left in situ with a
cut surface. Most cases settle with time. Anticholinergic drugs may help, as may
radiotherapy for persistent cases. Alternatively, further surgery to remove the deep
lobe is indicated.
Thyroid lumps
Goitre
There is visible or palpable enlargement of the thyroid gland. Causes of thyroid disease
can be divided into diffuse enlargement of the thyroid gland such as physiological goitre
(pregnancy, menarche); endemic goitre (iodine deficiency, Derbyshire neck); sporadic
goitre (goitrogens include cabbage, p-aminosalicylic acid (PAS) and lithium drugs);
autoimmune (Graves’ disease, Hashimoto’s); and focal lumps in the thyroid (non-toxic
nodular goitre, adenomas, carcinomas, lymphoma and medullary cell carcinoma).
History
History of the lump and history of thyroid symptoms are required. Most patients give
a history of painless enlargement. Look at rate of growth and if there has been sudden
recent enlargement. Ask about voice change. Look for symptoms of tracheal compression,
including inspiratory stridor. Hyperthyroid symptoms include sweating, palpitations,
42 GENERAL SURGERY OUTPATIENT DECISIONS

heat intolerance, menstrual irregularities, weight loss, anxiety, diarrhoea and muscle
weakness. Hypothyroid symptoms are the opposite of these. Painful enlargement of the
gland may indicate Hashimoto’s thyroiditis.
Examination
Examination of the lump
Inspect to see if the enlargement is visible, and, if so, whether it moves on swallowing
or protrusion of the tongue. Palpate to determine whether the whole gland is enlarged
or just part of it. Is the enlargement confined to one lobe? Does the gland feel regular
(Graves’) or irregular (nodular goitre)? Are draining lymph nodes enlarged? A thyroid
swelling firm to palpation, either diffuse or one-sided in a post-menopausal female,
usually raises the suspicion of Hashimoto’s.
Undifferentiated thyroid cancers and medullary cancers can present with an enlarging
neck mass involving other neck structures, e.g. recurrent laryngeal nerve. ENT examination
may be required if recurrent laryngeal nerve palsy is suspected.
Examination of thyroid status
Over-activity is indicated by hand tremor, palmar sweating and tachycardia; under-activity
by slow pulse, hoarse voice and slow relaxing tendon reflexes. Features of Graves’ disease
include exophthalmos, lid lag, lid retraction and pretibial myxoedema. Destruction of
the thyroid tissue by the autoimmune process in Hashimoto’s usually renders patients
hypothyroid eventually, although they may be thyrotoxic in the early stages.
Investigations
Management should follow the principles outlined earlier, determining the diagnosis,
localising the lesion and then determining if the patient needs an operation and, it so,
which one.
As with lumps in other body sites, thyroid lumps should undergo triple assessment
consisting of clinical assessment combined with imaging and cytology from FNA and
biochemical assessment of thyroid status: T4, T3 and TSH. Thyroglobulin is available
as a tumour marker, but it is only of use after total thyroidectomy, when it should fall to
zero in the absence of metastases.
Ultrasound examination of the thyroid will determine whether lumps are solid or
cystic and whether lumps are single (suspicious) or multiple (e.g. part of a multinodular
goitre).
123
I isotope scanning can identify thyroid tissue and determine whether nodules are hot
or cold, but this is rarely useful except in the toxic patient. A CT or MRI scan of the neck
and upper chest can identify tracheal deviation and retrosternal extension of thyroid.
FNA biopsy for cytology should be performed in every case.
If medullary carcinoma is suspected, serum calcitonin levels are very high and can
be used as a tumour marker. A rise in levels after treatment may indicate recurrence.
If medullary carcinoma is confirmed, patients should be screened for co-existing
parathyroid adenoma (calcium, phosphate and serum parathyroid hormone (PTH)) and
phaeochromocytoma (urinary catecholamine levels).
Tests for thyroid autoantibodies are performed if Hashimoto’s thyroiditis is suspected,
and they can confirm a diagnosis of Graves’ disease.
Results
✧ Diffusely enlarged gland, euthyroid: physiological and endemic goitre.
✧ Diffusely enlarged gland, hyperthyroid: Graves’ disease. The early stages of Hashimoto’s
may give this appearance but this is rare. In contrast to Graves’, Hashimoto’s does not
demonstrate increased uptake in a radioisotope scan.
 NECK AND ENDOCRINE 43

✧ Focally enlarged gland, euthyroid: diagnosis includes simple cysts; a single dominant
nodule in a multinodular goitre; benign adenomas; and malignant tumours.
∝ Malignant tumours can be classified as papillary, follicular, medullary and
anaplastic. FNA cannot differentiate between follicular adenomas and carcinomas
and all should be regarded as potentially malignant.
✧ Focally enlarged gland, hyperthyroid: thyrotoxic adenoma, thyrotoxic nodule in a
multinodular goitre.
Treatment
All suspicious and malignant lumps require surgery. Cystic lumps which are malignant,
greater than 4cm in size, contain blood or recur after 2–3 aspirations require surgery.
Most retrosternal goitres require surgery.
Benign lumps
✧ Benign cysts should be aspirated and reviewed at six weeks. This can be repeated on
two or three occasions. If they recur, surgery is required. If there is no recurrence,
review at six months, and if there is still no recurrence, discharge.
✧ For a solitary thyroid nodule that is euthyroid and benign, surgery is required only
for treatment of pressure symptoms or from patient preference. Repeat FNA once
or twice over the next 12 months, and if there is no change, the patient could be
discharged.
✧ A solitary thyroid nodule, hyperthyroid, benign and less than 3cm in size can be
treated by radio-iodine or surgery. Those greater than 3cm require surgery.
✧ For a multinodular goitre, euthyroid, if no dominant nodule or pressure symptoms
are present patients should be observed for 12–18 months, then discharged with
advice, unless surgery is indicated for large lesions or the patient is worried by the
cosmetic appearance.
✧ For a multinodular goitre, euthyroid, with a dominant nodule that is benign on FNA
and shows no pressure symptoms, observation is acceptable. If the dominant nodule
is suspicious or malignant, surgery is indicated.
✧ A multinodular goitre, hyperthyroid, for small glands can be treated with 131I. Large
glands are treated with antithyroid drugs and surgery.
Malignant thyroid tumours
These tumours can be classified as papillary, follicular, medullary and anaplastic.
✧ Differentiated thyroid cancer: prognosis is determined by age. Children and young
adults have a 90% five-year survival. The same tumour occurring in mid-life is
associated with a 60% five-year survival. Prognosis is worse if there is a history of
prior neck irradiation. Treatment generally consists of total thyroidectomy, which will
treat frequently multifocal disease, decrease local recurrence and allow post-operative
treatment with 131I and monitoring of thyroglobulin levels. Local enlarged lymph
nodes should also be excised, followed by radio-iodine ablation and suppressive doses
of thyroxine. The patient is then monitored for recurrence using ultrasound and by
measurement of thyroglobulin levels. Metastases are treated with therapeutic doses
of radio-iodine. Treatment of low-risk microcarcinomas (smaller than 1cm) by total
lobectomy is adequate, followed by TSH-suppressive doses of thyroxine.
✧ Undifferentiated thyroid cancer: frequently symptoms of rapid swelling, voice changes
and stridor may require total thyroidectomy to relieve or prevent respiratory obstruc-
tion, but prognosis is grave. Adjuvant radiotherapy can be given but chemotherapy
has no role.
✧ Medullary carcinoma of the thyroid arises from parafollicular cells and has no benign
variant. Calcitonin levels are high and can be used as a tumour marker. Medullary
44 GENERAL SURGERY OUTPATIENT DECISIONS

thyroid cancer (MTC) is sporadic in 80% of patients, but 20% have MEN-2 syndrome,
associated with phaeochromocytoma and parathyroid adenomas, which should be
excluded by estimations of serum PTH and urinary catecholamine levels. Treatment
consists of total thyroidectomy and excision of central compartment lymph nodes.
This tumour is not responsive to radiotherapy, chemotherapy or TSH suppression,
so thyroxine is given in replacement doses.
✧ Lymphoma: primary lymphoma is rare and usually of the non-Hodgkin’s B-cell type,
and it tends to complicate cases of Hashimoto’s thyroiditis of 10–15 years’ duration.
This responds well to radiotherapy and chemotherapy, and if diagnosed early enough
thyroidectomy can be avoided. Surgery is reserved for tracheal decompression. Stridor
can sometimes be successfully managed with dexamethasone and radiotherapy.
Other thyroid conditions
✧ Autoimmune thyroiditis in practice means Hashimoto’s, since other variants, such as
Riedel’s and de Quervain’s, are so rare that some experienced thyroid surgeons have
never seen a case. Surgical intervention is avoided and the condition responds well to
T3/T4 therapy to suppress TSH-stimulated enlargement of the gland.
✧ Graves’ disease: three treatment options are available, but choice depends on individ-
ual circumstances.
∝ Antithyroid drugs such as carbimazole or propylthiouracil can be given for
18 months, which cures fewer than 50% of patients. Nearly 45% relapse in the
first year after stopping, and 20% of the remaining patients relapse in each of the
subsequent five years. Drug toxicity is not uncommon. Beta blockade can also be
used for control of symptoms and is especially useful in patients being prepared
for surgery when given in combination with an antithyroid drug.
∝ Radio-iodine treatment ablates the thyroid tissue and will cure most patients,
although repeat doses may be needed. More than 60% will become hypothyroid
in the first year. Radio-iodine is the favoured method of treatment, but may not
be suitable in young women of child-bearing age or in those with young children.
Others simply prefer to avoid radiation exposure and opt for surgery.
∝ Indications for surgery include patients with recurrence of thyrotoxicosis after
medical therapy; patient preference; pressure symptoms; and the presence of un-
sightly goitres. Generally the author favours total thyroidectomy to guarantee cure
and prevent possible recurrence. Subtotal thyroidectomy, leaving approximately
5 ml of tissue on each side, is difficult to judge successfully, resulting in a small
recurrence rate or hypothyroidism. The patient should be euthyroid before
surgery, so antithyroid drugs are continued up to the day of surgery.
Follow-up
In the diagnostic phase, follow-up intervals should be short (1–2 weeks) until malignant
causes have been excluded. Similarly, any thyrotoxic patient should be reviewed within
1–2 weeks with the results of the thyroid function tests, and at 2–4-weekly intervals to
assess the effect of antithyroid drug therapy. When putting patients on the waiting list for
operation, patients with focal thyroid lumps should be operated on within 4–6 weeks to
exclude malignancy. Known malignant tumours should be removed quickly, as should
those with non-malignant causes but with symptoms of tracheal compression.
Post-operative follow-up
Review the patient with the histology report to confirm the diagnosis and adequate
excision and to detect any complications of thyroidectomy. All patients should be referred
to a multidisciplinary team for further assessment and management.
 NECK AND ENDOCRINE 45

Differentiated thyroid cancer

For those patients who have undergone total thyroidectomy, surveillance for recurrence
is required using either regular estimations of serum thyroglobulin levels, or ultrasound,
or both.
If tumour size is greater than 1cm, the patient undergoes a 131I total-body scintiscan
4–6 weeks post-operatively. If there is evidence of uptake in the neck or elsewhere,
therapeutic radioactive iodine is administered. The scintiscan is repeated six-monthly
for the first two years and then annually for five years.
In the absence of metastases, thyroglobulin falls to zero after total thyroidectomy.
Any rise post-operatively is an indicator of functioning thyroid tissue, either as a local
recurrence or as distant metastases, which requires ablation with radio-iodine. All
patients receive TSH-suppressing doses of thyroxine.
Undifferentiated thyroid cancer
All patients receive TSH-suppressing doses of thyroxine. Patients should be referred to
an oncologist for consideration of adjuvant radiotherapy.
Medullary carcinoma
There is a 90% five-year survival in the absence of lymph node involvement; 45% if
lymph nodes are involved. Patients are monitored for recurrence with regular calcitonin
and CEA levels. A rise in levels can indicate recurrence, which can be detected by USS,
CT/MRI, DMSA, MIBG or selective venous sampling. Recurrences can be treated by re-
operation or radiotherapy, but response rates are poor.
Voice change due to inadvertent damage to the recurrent laryngeal nerve occurs in
less than 1% of cases. Damage to the external laryngeal nerve supplying the cricothyroid
muscle causes difficulty in tensing the vocal cords. It affects the quality of the voice
and may be particularly significant to singers. Damage to the internal laryngeal nerves
– usually during mobilising the upper pole – desensitizes the appropriate side of the
larynx and can cause aspiration or coughing. Referral for an ENT opinion is appropriate.
Hypoparathyroidism occurs in approximately 1%. Temporary hypocalcaemia is common
in the first few days, especially after thyrotoxicosis, due to a combination of venous
congestion and hungry bones demineralised by the thyrotoxic state. Long-term treatment
with vitamin D may be necessary.
Other problems of the wound include haematoma formation, keloid formation and
suture granuloma. Haematomas are uncommon but can be life-threatening if large.
Because sudden respiratory difficulty after thyroid surgery may be due to haematoma
formation, sutures should be removed in the ward to evacuate the clot, including deep
sutures. Most minor haematomas detected in outpatients can be handled conservatively.
Suture granulomas respond to removal of the suture, while keloid scars can be excised
after a year, but can recur.

Parathyroids and disorders of calcium metabolism

The dominant hormone regulating calcium metabolism is parathormone (PTH), and the
total absence of calcitonin has little effect on calcium homeostasis. A fall in serum calcium
level stimulates an increase in PTH secretion, as do a fall in magnesium and an increase
in phosphate. PTH increases serum calcium concentration by increasing resorption of
bone, decreasing excretion by the kidney and increasing absorption from the intestines.
PTH mediates the production of the active 1,25-dihydroxycholecalciferol from vitamin
D precursors in the kidney. The effects of PTH on the bones and intestine do not occur
in cases of vitamin D deficiency.
46 GENERAL SURGERY OUTPATIENT DECISIONS

Hypercalcaemia
The main cause of hypercalcaemia of interest to the surgeon is hyperparathyroidism. Other
causes include bone metastases, excess vitamin D ingestion, milk alkali syndrome, hyper-
thyroidism, multiple myeloma, reticuloses, leukaemias, sarcoidoses, Addison’s disease,
Paget’s disease of bone, renal failure, thiazide diuretics and ectopic secretion of PTH.
History
This usually involves vague symptoms of tiredness, lethargy and muscle pains; it is rare
to see ‘bones, moans, stones and groans’. There may be a change in mood, especially
depression; a history of dyspepsia or peptic ulceration; or polyuria, nocturia or polydipsia.
There may be a history of renal stones; constipation; thiazide diuretic therapy; or vitamin
D ingestion. Symptoms are related to the possible underlying causes.
There may be a family history of hypercalcaemia, e.g. MEN syndrome. There is also
the condition known as familial hypercalcaemic hypocalciuria (FHH), which is due
to a resetting of the sensitivity of the calcium receptor and is unrelated to parathyroid
disease. A low urinary calcium excretion, combined with a family history, should alert
the clinician.
Examination
Parathyroid adenomas seldom produce lumps in the neck large enough to palpate. A
general physical examination is performed, looking for signs suggesting other diagnoses,
e.g. Paget’s. Hypercalcaemia may produce few signs apart from dehydration, myopathy
and, rarely, a calcified ring around the cornea.
Investigations
Confirm the hypercalcaemia. Repeat the serum calcium levels corrected for serum
albumin, and measure the PTH and vitamin D levels. A low serum phosphate and a
raised alkaline phosphatase and chloride suggest a parathyroid cause. A plain CXR, full
blood count and film, urea and electrolytes and serum electrophoresis will exclude many
non-parathyroid cases. A normal or raised PTH level, in the presence of a raised calcium
level, indicates hyperparathyroidism.
Treatment
Mild to moderate hypercalcaemia (2.6–3 mmol/l) usually responds to medical measures
such as avoiding bed rest, keeping well hydrated and consuming a diet containing a
moderate amount of calcium. This is combined with treatment of the underlying cause.
Moderate to severe hypercalcaemia (more than 3 mmol/l) cannot be easily controlled by
these medical measures and may require the use of bisphosphonates or even admission
to hospital for intravenous saline. Investigation and surgical therapy if indicated should
be expedited.
Follow-up
Mild hypercalcaemia can be reviewed at short intervals (1–4 weeks) to monitor serum
calcium levels in response to treatment and to establish the diagnosis. More severe
hypercalcaemia may require admission to hospital for further management.
Hypocalcaemia
Causes include uraemic osteodystrophy; post-operative parathyroid and thyroid surgery;
and vitamin D deficiency. Ureamic osteodystrophy occurs in chronic renal failure, where
calcium is not reabsorbed by the kidneys and phosphate is not secreted, leading to
accumulation. PTH is secreted in excess, the parathyroid glands become hyperplastic and
calcium is resorbed from the bones, leading to osteitis fibrosa cystica.
 NECK AND ENDOCRINE 47

History
Hypocalcaemia gives symptoms of paraesthesia of the fingers and around the mouth.
Long-term hypocalcaemia may lead to the development of epilepsy. There may be a
history of recent neck surgery; of inadequate diet, poor in the fat soluble vitamins; or of
religious clothing preventing adequate exposure to sunlight.
Examination
Signs of hypocalcaemia include positive Chvostek’s sign and positive Trousseau’s sign. In
the long term, hypocalcaemia leads to the development of cataract. There may be signs
of osteomalacia and rickets; of recent neck surgery; or of chronic renal failure.
Investigations
Test for serum calcium, albumin, urea and electrolytes and PTH level. Carry out liver
function tests and a renal ultrasound scan.
Treatment
✧ Uraemic osteodystrophy: correction of hypocalcaemia, then total parathyroidectomy.
✧ Osteomalacia and rickets: Vitamin D (1-alpha-cholecalciferol).
✧ Post-surgery hypocalcaemia: temporary hypocalcaemia is common after thyroidectomy
for thyrotoxicosis, due to venous congestion of parathyroid glands and hungry bones.
In the acute situation, intravenous injection of 10 ml of 10% calcium gluconate
is rarely needed and should only be given via a central line. Patients can generally
be controlled acutely and in the longer term with oral calcium supplements and
1-alpha-cholecalciferol. Regular checking of serum calcium and PTH is essential, as
parathyroid recovery may lead to iatrogenic hypercalcaemia.
Hyperparathyroidism
Primary hyperparathyroidism is due to a parathyroid adenoma or, more rarely, primary
hyperplasia. Secondary hyperparathyroidism is caused by a reactive hyperplasia of the
glands in response to chronic calcium losing states such as malabsorption or chronic
renal failure. Tertiary hyperparathyroidism occurs when a secondary gland becomes
autonomous. Exclude other associated neoplasms (MEN 1, MEN 2). Hyperparathyroidism
pathology consists of a single adenoma (85%), two adenomas (5%), carcinoma (1%) and
hyperplasia (5–10%).
History
Secondary and tertiary causes can generally be excluded if there is no history of
malabsorption or chronic renal failure. A family history of other endocrine neoplasms
should raise the possibility of the multiple endocrine neoplasia syndromes.
Examination
Look for evidence of hypercalcaemia, malnutrition or chronic renal failure.
Investigations
Following the principles of endocrine assessment, diagnosis of hyperparathyroidism is
confirmed on finding a normal or raised PTH level in the presence of hypercalcaemia.
Once the diagnosis has been made, and the patient has a safe calcium level (below
3 mmol/l), the tumour needs to be localised to allow minimally invasive surgery.
Localising investigations consist of high-resolution ultrasound and technetium-
sestamibi scanning, which will find the affected gland in about 75% of cases. For redo
cases, other imaging with MRI or CT scanning and angiography with selective venous
sampling are required.
48 GENERAL SURGERY OUTPATIENT DECISIONS

Treatment
If the tumour has been localised with concordant scans, a minimally invasive surgical
approach is indicated, removing only the affected gland. If the tumour is not localised
or hyperplasia is suspected, surgical exploration of all glands is undertaken and the
abnormal glands are removed. Intra-operative frozen section should always be used to
confirm the appropriate tissue has been removed, and intra-operative PTH measurement
is very useful if available.
✧ Primary parathyroid adenoma: surgical excision by minimally invasive approach.
✧ Secondary parathyroid hyperplasia (four glands): usually excision of all four glands,
or three glands, and leave half of the fourth marked with a metal clip.
✧ Tertiary hyperparathyroidism, autonomously functioning hyperplastic or adeno-
matous: usually total parathyroidectomy and lifelong maintenance on calcium and
vitamin D therapy; or total parathyroidectomy and reimplantation of gland fragments
in the brachioradialis muscle of the forearm.
✧ Parathyroid carcinoma: if recognised pre- or intra-operatively it is treated by para-
thyroidectomy, ipsilateral thyroid lobectomy and lymph node dissection (if nodes
present), followed by radiotherapy.
Follow-up
Bone disease caused by excess reabsorption of calcium by hyperparathyroidism (osteitis
fibrosa cystica) is particularly severe with secondary and tertiary hyperparathyroidism,
and it requires calcium and vitamin D therapy for months.
Post-operative follow-up
Review with histology to confirm the diagnosis. Confirm the biochemical success of
the operation. Persistent hyperparathyroidism is diagnosed if hypercalcaemia recurs
within six months of operation. Recurrent hyperparathyroidism occurs after six months.
The common cause of persistent hyperparathyroidism is unrecognised multiple gland
disease. The source of persistent or recurrent tumour can be localised with angiography
and selective venous sampling. Reoperation is indicated but technically can be very
difficult.
Parathyroid carcinoma is monitored with frequent estimations of serum calcium and
PTH to detect recurrence or metastases. Recurrence in the neck is treated by en bloc
resection if possible, otherwise palliation of hypercalcaemia with calcimimetics.
Multiple endocrine neoplasia (MEN) syndromes
Multiple endocrine neoplasia syndromes are rare, but require screening of family
members for the genetic abnormalities and the appropriate investigation of possible
tumours if the genetic defect is found. Family members without the genetic defect do
not need to be screened.
MEN 1
MEN 1 is an autosomal dominant disease consisting of hyperparathyroidism, pituitary
tumours and pancreatic tumours. It is caused by a defect on the long arm of chromosome
11.
✧ Hyperparathyroidism occurs in 90% of patients, characteristically hyperplasia.
✧ Pancreatic islet tumours occur in 30–75% and tend to be multiple. Gastrinomas occur
in 30–60% and insulinomas in 35%. Others consist of glucagonomas and vasoactive
intestinal peptide tumors (VIPomas).
✧ Pituitary adenomas occur in 15–40%. Prolactinomas are the most common, with
acromegaly (growth hormone) and Cushing’s syndrome (ACTH hypersecretion) less
common.
 NECK AND ENDOCRINE 49

✧ Carcinoid tumours and thyroid neoplasia are more common, and adrenocortical
adenomas are also found, although tending to be non-functional.
Investigations
Screening of affected family members consists of genetic screening, biochemical tests and
imaging. In family members carrying the defective gene on chromosome 11, biochemical
screening is performed yearly after puberty and consists of measuring serum calcium,
PTH, prolactin and gut hormones every 1–3 years. Suspected insulinomas are investigated
by measuring serum glucose, insulin and pro-insulin levels during symptomatic episodes.
MRI scans of the pituitary are performed every five years and combined with estimations
of serum prolactin levels.
Treatment
✧ Hyperparathyroidism is treated by total parathyroidectomy.
✧ Gastrinomas: medical therapy is effective, but needs to be lifelong. Enucleation is
performed for lesions in the head of the pancreas or duodenum. Distal pancreatectomy
is performed for lesions in the body or tail. Recurrent or metastatic disease occurs in
50% and is treated symptomatically.
✧ Insulinoma: enucleation is performed for suitable lesions. Inoperable disease is treated
with diazoxide and chemotherapy. Octreotide is effective.
✧ Pituitary lesions: hypophysectomy and external beam radiotherapy are used.
Bromocriptine and its derivatives are effective for treatment of prolactinomas and
acromegaly.
MEN 2
This is an autosomal dominant condition with a chromosomal defect in the RET proto-
oncogene on chromosome 10. Three forms exist.
✧ MEN 2A represents approximately 90% of cases of MEN 2, consisting of
medullary carcinoma of thyroid (MTC)(25%), phaeochromocytoma (50%), and
hyperparathyroidism (15%).
✧ MEN 2B represents 5% of MEN 2, with an association of MTC, phaeochromocytomas
(often bilateral), a general lack of parathyroid disease, and a Marfanoid body habitus,
multiple mucosal neuromas and gut ganglioneuromas (which can cause severe
constipation and diarrhoea).
✧ FMTC or familial MTC – patients with inherited MTC but no other endocrine
abnormalities.
Investigations
Genetic screening of all first- and second-degree relatives is performed. Affected individ-
uals undergo yearly biochemical screening, consisting of calcitonin levels and screening
for phaeochromocytoma (urinary catecholamine levels) and hyperparathyroidism
(serum calcium, phosphate and albumin, PTH).
Treatment
Total thyroidectomy is performed in all affected children aged 5–7 to prevent metastatic
medullary carcinoma, but it should be done as early as possible in genetic carriers, as
MTC can occur as early as the first year of life. The parathyroids are examined at the
same time and removed if enlarged. Phaeochromocytomas are treated appropriately if
they are detected.
50 GENERAL SURGERY OUTPATIENT DECISIONS

The adrenal gland

The main disorders of the adrenal gland requiring surgical intervention include Cushing’s
syndrome and Conn’s syndrome, which affect the adrenal cortex, and phaeochromocytoma,
which affects the medulla.
Cushing’s syndrome
Excess amounts of cortisol in the blood lead to the characteristic features of Cushing’s
syndrome, which is most commonly caused by long-term steroid treatment. True
Cushing’s disease is adrenocortical hyperplasia caused by a pituitary lesion. The diagnosis
of Cushing’s syndrome is suspected in patients with the characteristic clinical features and
confirmed by finding an inappropriately raised serum and urinary cortisol level. Once
this has been obtained the next objective is to determine whether this is due to a pituitary
lesion, adrenal lesion (adenoma or carcinoma), or ectopic production of ACTH by oat
cell carcinoma of bronchus, branchial carcinoid tumours, thymic tumours, islet cell
tumours or phaeochromocytomas. If an adrenal lesion is implicated the next objective
is to localise it.
History/examination
Look for obesity, especially of face and trunk, with thin extremities, moon face, menstrual
irregularities, osteoporosis, striae, glucose intolerance, myopathy, hirsutism, bruising and
oedema. In ectopic ACTH syndrome the clinical appearance is dominated by the effects
of malignancy – pigmentation and severe proximal myopathy. Patients may also present
with symptoms of diabetes mellitus, polyuria and hypertension.
Investigations
A simple screening test is to measure the cortisol in a 24-hour urine collection.
For definitive diagnosis the patient generally needs more extensive investigation in
hospital, with determination of 24-hour urinary free cortisol and then serum cortisol to
demonstrate loss of circadian rhythm. Low- and high-dose dexamethasone suppression
tests are undertaken as well. Morning serum ACTH levels are measured. They will be high
in pituitary tumours, very high in ectopic production and low in adrenal tumours.
Localisation
If ACTH is not raised, this indicates an adrenal lesion – a CT or MRI scan of the abdomen
localises the adrenal tumour or tumours.
If ACTH is raised, this indicates either a pituitary lesion or ectopic production. A CXR
may reveal a bronchial lesion or a widened mediastinum caused by a thymic tumour. An
MRI scan of the chest for ectopic sources is more sensitive. Similarly, an MRI scan of the
pituitary fossa will identify most pituitary lesions. Most ectopic sources are not CRH
dependent, so an injection of CRH will not cause a rise in ACTH, whereas most pituitary
lesions remain CRH dependent and a rise does occur. Similarly, high-dose dexametha-
sone will decrease cortisol levels in pituitary lesions but not in ectopic lesions. If this does
not resolve the site of ACTH secretion, selective venous sampling of the inferior petrosal
sinuses and the chest, measuring the ACTH levels in response to a dose of CRH injected,
helps to localise pituitary lesions to one side or the other. A rare cause of Cushing’s is
ectopic CRH production.
Treatment
✧ Cushing’s disease: transphenoidal adenectomy or transphenoidal hemihypophysectomy
(based on inferior petrosal venous sampling). Radiotherapy – recurrence rates at
two years are 50%. If these treatments are unsuccessful then bilateral laparoscopic
adrenalectomy may be considered.
 NECK AND ENDOCRINE 51

✧ Autonomous adrenal tumour: surgical excision, usually by laparoscopic approach.

Because of suppression of the normal gland, steroid replacement therapy may be
needed for up to two years. Testing of the hypothalamic-pituitary-adrenal axis (short
synacthen test) at regular intervals over that period is indicated.
✧ Ectopic ACTH: excision of primary tumour if the primary is benign or pancreatic.
For oat cell – palliation. For indolent metastatic carcinoids, bilateral adrenalectomy
is occasionally indicated.

Adrenocortical carcinoma (10% of adrenal tumours) often presents late, with large
tumours and pulmonary metastases. It is often malignant if it occurs in children.
Treatment is surgical debulking of the tumour and/or control of metastatic disease with
mitotane. Partial remissions can be obtained with chemotherapy (fluorouracil (5FU),
doxorubicin, cisplatin).
Follow-up
Follow up at short intervals until diagnosis is obtained. In many cases a planned
admission to hospital is required to perform the investigations in consultation with an
endocrinologist.
Post-operative follow-up
Review with histology to confirm the diagnosis and excision and to detect any complica-
tions of surgery. Exclude adrenal insufficiency and confirm adequate cortisol replacement
under joint management with an endocrinologist. A combination of hydrocortisone and
fludrocortisone is required after bilateral adrenalectomy. Counsel the patient regarding
the need for increased steroid therapy during illness or further surgical procedures. A
patient receiving chemotherapy may also become hypothyroid and require thyroxine.
Cushing’s should gradually improve over a year after surgery. Scaly desquammation
of the scalp is a sign of improvement. Weight loss occurs, muscle strength improves and
diabetes often resolves. Urine and electrolytes return to normal.
Conn’s syndrome
This syndrome consists of hypertension and hypokalaemia caused by an adrenocortical
adenoma secreting aldosterone. Approximately 60% of cases are due to a benign adrenal
adenoma (aldosterone-producing adenoma (APA)) and 40% are due to bilateral hyper-
plasia (idiopathic hyperaldosteronism (IPA)). The occasional case is due to carcinoma.
Secondary causes of hyperaldosteronism include stimulation by angiotensin in
response to decreased circulating volume, which may be caused by cirrhosis, nephrotic
syndrome, diuretic therapy and cardiac failure. Other causes include renal artery stenosis
or a renin-secreting tumour.
History
Patients present because a raised blood pressure has been noticed, which either fails to
respond to treatment or is associated with accompanying symptoms of muscle weakness,
tetany, polyuria, nocturia and thirst.
Examination
May be normal or there may be a raised blood pressure with evidence of muscle weakness
and tetany.
Investigations
Suspect Conn’s in any hypertensive patient with hypokalaemia; however, a third of Conn’s
patients have a normal potassium. Potassium excretion in the urine is inappropriately
52 GENERAL SURGERY OUTPATIENT DECISIONS

high. If hyponatraemia co-exists this may indicate secondary hyperaldosteronism.

Hypernatraemia is more typical of primary aldosteronism. Morning renin and aldosterone
levels are measured from a blood sample taken from an arm vein between 9 and 10am
(after fasting from 10pm the night before). Ideally the patient should have been off all
medications for four weeks prior to the blood test.
Conn’s is diagnosed by an elevated plasma aldosterone level in the presence of a low
plasma renin level. High plasma aldosterone levels are not suppressed by increased intake of
sodium chloride. Glucocorticoid levels should be normal. Secondary hyperaldosteronism
is characterised by high plasma renin levels with hypertension and often renal disease or
sodium depletion.
Localisation
CT scanning plus 131I 6-beta-iodomethyl-19-norcholesterol (NP59) scintigraphy can
distinguish between adenoma and hyperplasia. Occasionally MRI scanning and selective
venous sampling is useful in localising difficult cases.
Treatment
✧ Adrenal tumour: unilateral laparoscopic adrenalectomy. Precede surgery with
1–6 weeks of spironolactone to return serum potassium to normal. Patients will need
cortisone cover peri-operatively.
✧ Adrenal hyperplasia: medical therapy. Treat hypertension with spironolactone 100 mg/
day rising to 400 mg/day until potassium returns to normal, then reduce the dose.
Resistant hyperplasia requires total or subtotal adrenalectomy.
Follow-up
Follow up at short intervals until diagnosis is obtained, hypertension is controlled and
potassium returns to normal. Admission to hospital is often required. Spironolactone
can cause gynaecomastia, decreased libido, impotence and menstrual irregularities but
still not control the hypertension. Second-line therapy with amiloride or triamterene
may be required.
Post-operative follow-up
Review with histology to confirm the diagnosis and excision and to detect any post-
operative complications. Confirm a biochemical return to normal. Exclude adrenal
insufficiency and treat with steroid replacement as required.
Phaeochromocytoma
Ten per cent are malignant, 10% are bilateral and 10% can occur anywhere along the
sympathetic chain from the neck to the pelvis. Phaeochromocytomas may be familial
and associated with other tumours such as neurofibromatosis (10%), acoustic neuroma,
meningioma, glioma, astrocytoma and cerebellar haemangioma (14%). In MEN 2,
phaeochromocytoma is associated with medullary carcinoma of thyroid and parathyroid
adenomas. Adrenal hyperplasia can occur as a precursor of phaeochromocytoma.
History
History includes palpitations, fear, facial flushing; abdominal symptoms such as nausea
and vomiting; diarrhoea and weight loss; glucose intolerance; and cardiac failure. Also
look for attacks of high blood pressure with headaches; nausea and vomiting; chest and
abdominal pain; anxiety; pallor; sweating and palpitations – lasting a few minutes to
several hours.
 NECK AND ENDOCRINE 53

Examination
Hypertension can be sustained or paroxysmal, with periods of normotension or hypo-
tension, so single blood pressure readings can be normal. If the phaeochromocytoma
secretes noradrenaline or dopamine, hypotension can be the presenting sign. Examine
for tachycardia and palpitations, evidence of cardiac failure, dehydration and recent
weight loss.
Investigations
Measuring catecholamines and metanephrines in a 24-hour urine collection is 90%
sensitive. Plasma catecholamine levels are raised, but tests can be rendered inaccurate
by calcium channel blockers, monoamine oxidase inhibitors (MAOIs), phenothiazine,
tricyclic antidepressants and beta-blockers.
Extra-adrenal and malignant phaeochromocytomas tend to secrete noradrenaline,
while benign adrenal phaeochromocytomas tend to secrete adrenaline.
Localisation
Most tumours are usually greater than 3cm in diameter. Take a CT scan of adrenal,
para-aortic and pelvic areas. Meta-iodobenzylguanidine (131MIBG) is taken up by
catecholamine granules and is extremely useful in confirming the site of the tumour
and in diagnosing extra-adrenal and bilateral phaeochromocytomas. It can also be used
therapeutically for treatment of metastases.
Treatment
Phenoxybenzamine (alpha-blocker, 20–80 µg daily) is started when diagnosed, for at
least two weeks prior to surgery or longer in the presence of electrocardiogram (ECG)
abnormalities. Additional therapy with beta-blockers (20–40 µg, 6-hourly) can be used
to control tachycardia. Labetalol (an alpha- and beta-blocker) can also be used.
When hypertension is controlled, unilateral laparoscopic adrenalectomy is
performed.
Follow-up
Follow up at short intervals (1–4 weeks) until diagnosis is achieved. There is a clinical
association with MEN 2, so medullary carcinoma of the thyroid and hyperparathyroidism
should be excluded in all cases of phaeochromocytoma.
Post-operative follow-up
Seventy per cent of patients are cured of hypertension by surgery. Review with histology
to confirm diagnosis and excision and to detect complications of surgery. Patients with
malignancy should be followed up long term to detect recurrence. Recurrence is suspected
by recurrence of symptoms, and confirmed biochemically. Metastases are localised by an
MIBG scan, which is then given in a therapeutic dose. Malignant phaeochromocytomas
that recur can also be treated by surgical debulking. Chemotherapy has been used with
a 50% response rate.
Childhood adrenal tumours
These include neuroblastoma, ganglioneuroma and neurofibroma.
Adrenal incidentaloma
With the increasing availability of abdominal CT scanning, apparently asymptomatic
adrenal masses are being referred for surgical opinion. Over 50% are metastases from
a known primary, 30% are cortical adenomas with potential endocrine symptoms
(phaeochromocytoma, Cushing’s, Conn’s), 5% are metastases from an occult primary
54 GENERAL SURGERY OUTPATIENT DECISIONS

and 5% are adrenal malignancies. Other causes include cysts, haematomas and
myelolipomas.
History/examination
Take a history to elicit symptoms of endocrine conditions, and examine for relevant
clinical signs. In particular, determine any known primary malignancy.
Investigations
Often the CT scan appearance is diagnostic or suggests malignancy due to an irregu-
lar outline, invasion of adjacent structures or lymph node metastases. If not, perform
biochemical tests for phaeochromocytoma, Cushing’s and Conn’s: e.g. urinary catecho-
lamines, serum and urinary potassium and serum and urinary cortisol estimations.
Ultrasound/CT-guided biopsy may be justified.
Treatment
All adrenal masses greater than 4cm require surgical excision because of malignant
potential. Even with metastatic masses, surgical excision may be justified. Cysts are very
rarely malignant and do not require surgery unless large. Haematomas may occur spon-
taneously and resolve over time, but can occur within primary or metastatic tumours.
Myelolipomas are benign and surgery is indicated only if they become large.
Follow-up
Follow up at short intervals (1–4 weeks) until diagnosis is achieved. If all investigations
are normal and surgery is not indicated because of size or other features, serial MRI scan
observation performed every six months initially is justified.
Post-operative follow-up
Review with histology to confirm diagnosis and excision and to detect any complications
of surgery. Follow-ups for specific lesions are described under their relevant sections.
Hirsutism
Plasma testosterone and urinary 17-oxysterol are elevated when there is a virilising adrenal
tumour, but may be elevated in other virilising syndromes such as ovarian tumour. Most
patients have congenital adrenal hyperplasia, which may present as virilisation in male
and female children.
History
Determine the onset of hirsutism. Patients may complain of oily skin, acne and increasing
facial and other body hair. The voice may deepen. There may be menstrual irregularities
or amenorrhoea.
Examination
Perform a general examination. Examine for the male pattern of body hair and acne.
Abdominal examination may reveal an abdominal or pelvic mass. Rectal and vaginal
examination may reveal an ovarian mass.
Investigations
Adrenal imaging by CT or MRI is essential. Simultaneous imaging of the ovaries is
also helpful. Measure plasma testosterone and 17-oxysterol. Serum ACTH is high in
congenital adrenal hyperplasia.
 NECK AND ENDOCRINE 55

Treatment
Benign adrenal tumours are excised, which improves acne and restores menstruation,
ovulation and fertility. Hirsutism usually persists. Malignant tumours may require
chemotherapy.
Congenital adrenal hyperplasia is treated by replacement of deficient adrenal steroids
to reduce the stimulation of the adrenals and the production of virilising by-products
caused by the high levels of ACTH.
Follow-up
Review at short intervals (1–4 weeks) until adrenal or ovarian tumours are excluded.
Monitor the effect of hormone replacement in collaboration with an endocrinologist.
Gynaecological referral is indicated for treatment of ovarian tumours.
Post-operative follow-up
Review with histology to confirm diagnosis and excision and to detect complications of
surgery. Exclude adrenal insufficiency.
Surgical management of obesity
Determine whether the patient is clinically obese, exclude underlying metabolic disorder,
detect complications of obesity and select appropriate patients for surgery.
Surgery should be considered prophylactic in relatively young or middle-aged
patients.
History
Look at types of abnormal eating or binge eating; types of diet; impact of obesity on life;
and psychological upsets. Trials of medical therapy, i.e. diet and exercise.
Examination
Determine the body mass index (BMI): weight (kg)/height2 (m2). A BMI of 20–25 is a
desirable weight. Morbid obesity is defined as a BMI greater than 40–45, or more than
100 lbs (45 kg) overweight.
Examine for conditions caused by obesity, including cardiovascular disease, diabetes
mellitus, osteoarthritis, cancer and respiratory disease.
Examine for underlying metabolic conditions that can cause obesity, include Cushing’s
syndrome and hypothyroidism. Excess weight gain can also be associated with fluid
retention secondary to cardiac, renal or hepatic disease.
Investigations
Look at height, weight, BMI, BP, ECG, full blood count (FBC), lipid levels, CXR,
spirometry, blood gases, glucose tolerance tests, ultrasound gall bladder and thyroid
function tests.
Treatment
Selection of patients suitable for surgery
Criteria are five years or more presence of morbid obesity and BMI greater than
40–45 kg/m2; patient has made serious attempts at losing weight through diet; increasing
immobility; intelligent and working; strongly motivated; mentally stable with no history
of alcoholism, drug addition or attempted suicide; not a high operative risk.
Relative indications include hypertension, hyperlipidaemia, noninsulin-dependent
diabetes mellitus (NIDDM) and osteoarthritis (OA).
Contraindications include unwilling patient, unfit for general anaesthetic (GA),
psychological instability, unable to lose weight on dieting.
56 GENERAL SURGERY OUTPATIENT DECISIONS

Team approach
The team will include the anaesthetist, surgeon, dietitian, and physiotherapist.
Surgical procedures include Lap Band, vertical banded gastroplasty and gastric bypass
with Roux-en-Y leaving a 150 ml reservoir. The patient is then fed on a diet of solid food
requiring chewing and is required to exercise. Operative mortality is approximately 2%.
Morbidity consists mainly of pulmonary atelectasis, venous thrombosis and wound
infection.
Results
Reducing BMI to less than 35 is successful in 40–70% of vertical gastric stapling
procedures.
Follow-up
Review at regular intervals until underlying metabolic disorder is excluded and the need
for surgery is determined.
Post-operative follow-up
Review to detect any complications of surgery and to determine success in terms of
weight reduction.
Oesophagus
Edward Cheong

FOUR
The oesophagus
On a simple level, the oesophagus is a tube whose function is to transport food from the
mouth through the chest and diaphragm into the stomach. Successful completion of this
task requires the co-ordinated function of brain, nerve, muscle and mucosa. Disorders
affecting any of these systems can result in oesophageal symptoms, as may disorders
originating in the chest or the diaphragm.
A particular diagnostic difficulty is the differentiation of pain, which may be cardiac or
oesophageal in origin. Because cardiac pain may represent a potentially life-threatening
disorder, investigation of the cardiovascular system may take priority over oesophageal
investigation in this situation.
Abnormalities in gastric function, such as acid hypersecretion, may first present with
oesophageal reflux rather than gastric symptoms, as may conditions associated with
increased intra-abdominal pressure.
Therefore, the assessment of oesophageal conditions may require the consideration of
a number of different body systems to arrive at the correct diagnosis.

Oesophageal history
Start with a general gastrointestinal history. When the responses indicate a possible
oesophageal problem, a more detailed oesophageal history is required to differentiate
oesophageal problems from cardiac or pulmonary disorders and gastric problems.

Dysphagia
Dysphagia strongly suggests an oesophageal problem and can be due to mechanical or
motility disorders. The site and time course of onset are useful points.
Are symptoms intermittent, and helped by sipping fluids or repeated swallowing
(motility), or are they persistent and progressive, suggesting a mechanical stricture of
the lumen, e.g. carcinoma?
Dysphagia for solids suggests a mechanical cause; dysphagia for fluids only suggests a
motility disorder.

Regurgitation
There is a sour taste in the mouth, it may occur most at night, and in the morning the
fluid has stained the pillow.
Postural regurgitation that is increased by a supine posture or that is worse after large
meals, bending or straining suggests reflux disease.
Overflow at night causing coughing or aspiration might be due to a constricting lesion,
but is more common in a motility disorder, e.g. achalasia.

Odynophagia
Localised pain, usually in the lower sternal region immediately the patient swallows
certain foods and liquids such as hot drinks, suggests organic disease, e.g. oesophagitis.
Heartburn
Due to gastro-oesophageal reflux causing chemical inflammation to the oesophageal
mucosa.

57
58 GENERAL SURGERY OUTPATIENT DECISIONS

Oesophageal anterior chest pain

Angina-like, it can radiate to the back, jaw and arm and may be difficult to differentiate
from cardiac pain. Often relieved by nitrates. Seen in both reflux and motility disorders,
it can be precipitated by meals, emotion and exercise.
Water brash
Excess secretion of saliva, which tastes salty; often experienced in reflux disease.
Atypical presentations
✧ Anaemia.
✧ Haemetemesis.

Twenty to forty per cent of patients with chest pain and normal coronary angiograms
have oesophageal pain.
Oesophageal examination
Perform a general examination. In particular look for:
✧ signs of weight loss
✧ pallor due to anaemia
✧ neck swelling (e.g. pharyngeal pouch)
✧ enlarged lymph nodes in left supraclavicular fossa, which may represent metastatic
spread from a gastrointestinal malignancy.

Percussion and auscultation of the lungs should be performed to detect aspiration

pneumonia.
The presence of an epigastric mass and/or hepatomegaly may represent the presence
of advanced malignant disease.
Perform an examination of the cardiovascular system to detect any cardiac disease if
the presentation includes atypical chest pain.
Investigation of oesophageal disorders
Laboratory investigations
Haematology
✧ Full blood count (FBC) may indicate microcytic anaemia.
✧ Leucocytosis may suggest infection.

Biochemistry
Abnormal liver function tests (LFT) may indicate liver metastases in malignancy.
Microbiology
Microbiology may show candidiasis of the mouth/oesophagus.
Cytology/histology
Cytology is of brushings, or histology of biopsies taken at endoscopy.
Imaging techniques
Chest X-ray
All patients who have oesophageal symptoms should have a chest X-ray (CXR) to look
for:
✧ aspiration pneumonia
✧ mediastinal widening due to lymph node metastases
 OESOPHAGUS 59

✧ suspicious soft tissue shadows (infection or metastatic disease)

✧ fluid/gas levels (large hiatus hernia with intrathoracic stomach, dilated oesophagus
in achalasia).
Oesophago-gastro-duodenoscopy (OGD)
Except for suspected pharyngeal pouch (do a water-soluble contrast study), this should
be the first investigation in all patients with oesophageal symptoms. It allows direct
visualisation of mechanical obstructions and enables biopsies to be taken for histological
diagnosis. It can also visualise oesophagitis, ulceration, varices and so on.
Certain therapeutic manoeuvres, e.g. dilatation of benign strictures, can be
performed.
However, it is an invasive procedure that is unable to diagnose early motility disorders,
which require oesophageal manometric study. Some patients may find it unpleasant and
are unable to swallow the scope. Complications include:
✧ aspiration
✧ trauma to the oesophagus, stomach and duodenum, which may cause bleeding, pain
or occasionally perforation.
Barium swallow/meal
This is the first-line investigation if oesophageal web, oesophageal motility disorder
or pouch is suspected. It is the second-line investigation if OGD fails to provide a
diagnosis.
It is also useful after oesophageal or gastric surgery in symptomatic patients to exclude
a mechanical cause or herniation. The investigation is good for diagnosing:
✧ hiatus hernia
✧ oesophageal perforations (use water-soluble contrast)
✧ abnormalities of the upper oesophageal sphincter and swallowing mechanism.

Double contrast (barium-air) barium meals are useful for the evaluation of oesophageal
cancer, especially the length of the lesion, which may correlate with depth of invasion
and resectability. They are not reliable in the diagnosis of reflux. (Approximately 20% of
normal people exhibit reflux in the Trendelenburg position, but only reflux demonstrated
when upright is significant.)
Computerised tomography (CT) scanning
CT scanning is used in staging oesophageal malignancy to demonstrate:
✧ extent of mural invasion
✧ involvement of adjacent structures
✧ mediastinal lymph node involvement
✧ distant metastases.

It tends to underestimate early mediastinal spread and lymph node metastases, and it is
not totally reliable in differentiating direct metastatic spread from reactive inflammation
surrounding a tumour.
Ultrasound
Ultrasound is mainly used non-invasively with the ultrasound probe applied to the
outside of the body after applying acoustic water-based gel.
Endoluminal ultrasound is a specialised technique where a specialised probe is placed
into the oesophagus to provide images of the oesophageal wall and adjacent lymph
nodes. It is good for determining intramural spread, tumour size (T stage) and lymph
node involvement.
60 GENERAL SURGERY OUTPATIENT DECISIONS

Laparoscopic ultrasound is another specialised technique that uses a special probe

inserted into the abdomen at laparoscopy. It may be applied directly to organs, e.g. liver,
and used to give more detailed information on suspicious liver lesions or suspected nodal
spread. It is operator dependent. CT is required to confirm findings.
Radioisotope scans
These scans are used to assess gastro-oesophageal junction (GOJ) incompetence in patients
with reflux and to evaluate the transit of liquid or solid boluses in motility disorders.
The patient swallows technetium-99m-labelled liquid or solids (e.g. eggs) while the
process of swallowing is recorded by a gamma camera to detect the radioactivity. It
provides useful visualisation of oesophageal function, particularly in the investigation
of achalasia.
Physiological tests
Oesophageal manometry
A soft plastic multilumen tube connected to a pressure transducer system is passed orally
or nasally and positioned at the required point in the stomach or oesophagus. Static
measurements can be made at different positions, or the pressure profile of stomach,
cardio-oesophageal junction and oesophagus can be obtained by recording during a wet
swallow.
The upper oesophageal sphincter can also be assessed, determining the relationship of
pharyngeal and oesophageal relaxation and contraction.
Ambulatory manometry is now available for investigation of infrequent oesophageal
spasm. It is useful for assessment of motility disorders, dysphagia and the complications
of anti-reflux surgery. However, it has low sensitivity for reflux. The technique is not
widely available in most hospitals.
Twenty-four-hour pH monitoring
This is now the preferred method of pH assessment. Patients are assessed when they have
been off all antacid or proton-pump inhibitor medication for 10 days. A twin pH probe
is passed orally or nasally, the oesophageal transducer is positioned 5cm above the high-
pressure zone in the lower oesphagus (as determined by manometry), and the gastric
transducer is positioned in the stomach. The pH in both the oesophagus and the stomach
is monitored for 24 hours. The patient can press an event marker when symptoms are
experienced, and this can be correlated with pH recordings.
The procedure tends to be uncomfortable and requires patient compliance. It is not
widely available in most hospitals.
Hiatus hernia
In this condition, the oesophageal hiatus in the diaphragm is enlarged, allowing part of
the stomach to pass through into the chest.
There are three main types:
✧ type I (70–80%) sliding
✧ type II (8–10%) para-oesophageal
✧ type III mixed.

History
Take a general and oesophageal history.
Type I
✧ Often asymptomatic.
✧ May have symptoms of reflux oesophagitis, chronic blood loss or stricture.
 OESOPHAGUS 61

Type II
✧ Mainly pressure symptoms when distended with gas or food.
✧ Pain, dyspnoea and tightness precipitated by food, bending and stooping.
✧ Pain sharp, beneath lower sternum and radiates to the back, often accompanied by a
bloated sensation, anxiety, palpitations and dyspnoea.
✧ Pain often relieved by belching or vomiting.
✧ Symptoms of anaemia associated with ulcer within the hiatus hernia (Cameron’s
ulcer).
✧ Dysphagia in 20%.

Take a cardiac history to differentiate oesophageal symptoms from atypical angina.

Examination
✧ Perform a general examination.
✧ Examine for anaemia.
✧ Examine the chest for evidence of effusions or infection and examine the supracla-
vicular fossae for evidence of lymph node spread.
✧ Examine the abdomen for epigastric masses or evidence of liver enlargement.

There may be no abnormalities on examination, which makes the diagnosis of hiatus

hernia more likely. Perform a cardiovascular examination if indicated by the history.
Investigations
✧ A CXR may show soft tissue mass or fluid level behind the heart.
✧ Oesophago-gastro-duodenoscopy shows reduced distance from incisors to GOJ, and
the J-manoeuvre in the stomach may show the hernia.
✧ Barium swallow is usually diagnostic in cases not detected by OGD.
✧ Iron deficiency anaemia may be shown by FBC.
✧ Cardiovascular investigations are needed as indicated by atypical chest pain.
Treatment
Symptoms of reflux oesophagitis can be controlled medically with proton-pump
inhibitors (PPI).
If symptoms are severe enough to merit intervention and the patient is a good opera-
tive risk, surgery can be considered.
✧ For type I, reduction and anti-reflux surgery (open or laparoscopic).
✧ For type II, repair of diaphragmatic defect with or without anti-reflux surgery. An
infarcted or strangulated type II may need a thoracotomy or thoraco-abdominal
surgery.
Follow-up
Most patients with oesophageal reflux secondary to hiatus hernia are treated by gastro-
enterologists, who refer patients with uncontrolled or recurrent symptoms on medical
therapy for surgery.
Patients with pressure symptoms in the chest may be referred directly to a surgeon.
Investigations should be completed promptly, especially if a cardiac cause cannot be
excluded on history and examination.
Post-operative follow-up
In routine cases patients are reviewed 4–6 weeks after surgery. Review the operation
notes to determine whether there were any complications during the procedure. Early
complications include wound infection and incisional hernia. Determine whether the
operation has been successful in relieving the original symptoms.
62 GENERAL SURGERY OUTPATIENT DECISIONS

Tight wrap
✧ Patients may complain of dysphagia or gas bloat as if the fundal wrap is too tight.
✧ This is usually mild and will resolve within three months with observation.
✧ Severe or persistent cases beyond three months require further investigation with
barium swallow, OGD or oesophageal manometry.
✧ Treatment options include endoscopic balloon dilatation (often successful) or
remedial surgery.
Slipped Nissen
The Nissen wrap either slips down the stomach, causing an hour-glass deformity and
presenting as dysphagia and abdominal discomfort, or the wrap slips up between the
crura into the chest, with accompanying dysphagia.
✧ Diagnosed by a barium meal.
✧ Requires prompt revision surgery.

Congenital diaphragmatic hernia

This condition is often diagnosed and treated shortly after birth. However, it may be
asymptomatic and present later in life.
✧ Bochdalek hernia. There are persistent pleuroperitoneal canals. It presents in the
neonatal period with respiratory distress.
✧ Morgagni’s hernia. This parasternal hernia presents in adult life with episodes of
pain and tenderness in the subcostal region and intermittent obstructive symptoms.
Complete intestinal obstruction may intervene.
✧ Central tendon defect is associated with a defect in the pericardium. The intestine
herniates into the pericardium.
History
Take a general oesophageal and gastrointestinal history. In particular, note any history of
intermittent subcostal pain or dysphagia.
Examination
Perform a general examination. This is often found to be normal. There may be tenderness
and/or fullness in the subcostal region.
Investigations
✧ Chest X-ray, posterior anterior view (CXR-PA) shows a round, gas-containing shadow
to the right of the cardiac outline. Lateral CXR shows a gas-containing shadow behind
the sternum.
✧ Barium swallow is usually diagnostic.
✧ On the right, ultrasound may be needed to differentiate diaphragmatic neoplasm
(rare) from herniated liver parenchyma.
Treatment
Symptomatic patients are considered for surgical reduction and prosthetic mesh repair.
Right-side abnormalities usually require no treatment, while left-sided and central
hernias require surgical repair.
Follow-up
Follow-up should be at short intervals (1–4 weeks) until the diagnosis is made. Mild cases
can be observed at gradually increasing intervals (1–6 months).
 OESOPHAGUS 63

Post-operative follow-up
Determine if the operation has relieved the symptoms and detect any complications
associated with abdominal and thoracic surgery.
Recurrence of symptoms may indicate recurrence of the hernia – investigate as for
primary cases.
Traumatic diaphragmatic hernia
This hernia may present months or years after the event, e.g. seat-belt injury from a road
traffic accident.
History
Take a general history. Symptoms tend to be related to the size of the herniated contents
and to the onset of mechanical complications such as intestinal obstruction, strangulation,
haemorrhage or progressive cardiorespiratory insufficiency.
Examination
Perform a general examination. Examine the chest for evidence of respiratory insufficiency,
bowel sounds or infection.
Investigations
✧ CXR shows a space-occupying lesion. If spleen or omentum is herniated this appears
solid.
✧ Barium swallow may confirm the diagnosis.
✧ Ultrasound scanning (USS) or CT can be helpful to determine chest contents.
Treatment
✧ If symptomatic, requires surgical repair through abdominal or thoracic approach.
✧ If asymptomatic, mildly symptomatic, or unfit for surgery, manage conservatively.
Follow-up
Severe cases need prompt investigation and treatment. Other cases can be managed
with gradually lengthening follow-up (1–6 months), monitoring for the development of
increasing symptoms and of deteriorating cardiorespiratory function.
Post-operative follow-up
Determine if the operation has relieved the symptoms and detect any complications of
the thoracic and abdominal procedure.
Reflux oesophagitis
Reflux oesophagitis is caused by the abnormal retrograde movement of gastric contents
into the oesophagus. Normal subjects have reflux, but this is harmless because the effect
is short-lived, thanks to an effective oesophageal clearance mechanism. If the oesophageal
clearance mechanism is overwhelmed, inflammation of the lower oesophageal mucosa
occurs.
Oesophagitis may occur not just due to acid reflux but also because of bile salts, trypsin
and lysolecithin, especially after partial gastrectomy.
Complications of reflux oesophagitis include chronic blood loss, deep ulceration with
perioesophagitis, and the formation of strictures and webs.
The presence of columnar mucosal change indicates the development of a Barrett’s
oesophagus. Barrett’s oesophagitis may lead to stricture, ulceration and the development
of adenocarcinoma. Risk of developing cancer is relatively low (approximately 1% per
annum), but is higher in those that develop mucosal dysplasia.
64 GENERAL SURGERY OUTPATIENT DECISIONS

History
Symptoms include heartburn, regurgitation and dysphagia. Symptoms are aggravated
by posture and are worse at night after large meals, bending or stooping. Dysphagia is
intermittent. Persistent dysphagia usually suggests stricture formation.
Other presentations include odynophagia, waterbrash, atypical chest pain or asthma
(due to aspiration).
Examination
✧ Perform a general examination (often normal).
✧ Examine for anaemia and weight loss.
✧ Examine the chest for signs of effusion or infection.
✧ Examine the abdomen for epigastric masses or liver enlargement.
Investigations
✧ Perform oesophago-gastro-duodenoscopy (OGD), and biopsy for histology.
✧ Barium swallow is good for demonstrating hiatus hernia.
✧ Perform 24-hour pH monitoring and manometry.
✧ A FBC may reveal anaemia.
Treatment
Uncomplicated disease
The patient should:
✧ lose weight
✧ avoid spicy foods
✧ raise the head of the bed.
If symptoms do not improve, prescribe antacids, proton-pump inhibitors and prokinetics
(metoclopramide). Prokinetics are particularly useful for relief of nausea, fullness,
regurgitation, belching and odynophagia. A full course of medical therapy lasts for three
months, after which maintenance is continued indefinitely.
An alternative treatment is a proton-pump inhibitors (PPI), e.g. omeprazole, for eight
weeks.
For neutral/alkali reflux in post-operative gastric surgery patients, a bile-salt binding
agent such as cholestyramine is useful.
Complicated disease
If there is Barrett’s with low-grade dysplasia, confirm the diagnosis with two endoscopic
biopsies three months apart, after a course of PPI.
Confirmed cases may require anti-reflux surgery and acid-suppression therapy. This
reverses columnar change in approximately 10%, but all cases need continued OGD
surveillance.
High-grade dysplasia may represent carcinoma in situ and, if confirmed, is an indi-
cation for oesophageal resection. (Once resected, 30 to 40% are found to have invasive
carcinoma in the histological specimen.)
Indications for surgical treatment
The following are indications for surgical treatment.
✧ Failure of medical therapy: persistent symptoms, intractable oesophagitis.
✧ Development of complications, stricture, Barrett’s.
✧ Reflux associated with motility disorders or oesophageal chest pain.
✧ Reflux in children, persisting beyond the age of two.
✧ Reflux after upper abdominal surgery; acid or bile.
 OESOPHAGUS 65

Surgical treatment
This consists of floppy Nissen fundoplication, which is usually laparoscopic.
The thoracic approach is preferred in patients with severe oesophagitis, stricture
formation, perioesophagitis and oesophageal shortening.
Post-operative supercompetence and gas bloat occur in 20%, but with a properly con-
structed loose Nissen fundoplication, dysphagia is rarely encountered.
Follow-up
The majority of patients with oesophageal reflux are treated by gastroenterologists, who
refer patients for surgery if they have uncontrolled or recurrent symptoms on medical
therapy.
Different units have their own policies regarding Barrett’s oesophagitis patients and
whether regular endoscopy monitoring to detect malignant change is performed in all
or just selected patients.
At present there is no conclusive evidence to suggest routine follow up of Barrett’s is
justified in any patient other than those with dysplastic change.
Post-operative follow-up
See hiatus hernia.
Persistent heartburn occurs in approximately 5–8%. It may be due to delayed gastric
emptying because of unrecognised distal peptic ulcer disease, or disruption of the fundal
wrap. Investigate with OGD, barium meal and oesophageal manometry.
Non-reflux oesophagitis
This may occur because of ingestion of corrosive substances; or it may be infective, drug
induced or from radiation.
Specific disorders are Behçet’s syndrome, Crohn’s disease and scleroderma. All produce
a mixture of strictures, motility disorders, hiatus hernias and occasional cancers.
The acute phases are treated as in-patients.
History
Take a general oesophageal history. Usually there will be a history suggestive of the
underlying disorder and progressive dysphagia from liquids to solids.
Examination
✧ Perform a general and systemic examination.
✧ Look for other evidence of an underlying disorder.
✧ Examine hands, face, chest and abdomen.
Investigations
Assess by a combination of OGD, barium swallow, motility and pH studies. If Crohn’s is
suspected, a small bowel follow-through may be helpful.
Treatment
Mild cases are treated medically. More severe cases may be considered for surgery. They
are those with:
✧ extensive persistent stricture
✧ need for frequent dilatations
✧ presence of high strictures or late bronchotracheo-oesophageal fistulas
✧ late oesophageal shortening with reflux oesophagitis
✧ severe dysplasia, carcinoma in situ or invasive carcinoma.
66 GENERAL SURGERY OUTPATIENT DECISIONS

Extensive scarring may require total oesophagectomy and replacement with colon,
isoperistaltic jejunum or stomach.
In some cases there is a frozen mediastinum – leave oesophagus and perform a
bypass.
Follow-up
Follow-up is long term, as complications eventually develop in most cases. If symptoms
are mild and stable, discharge with a plan to return if symptoms increase.
Post-operative follow-up
This is long-term follow-up. Initially, determine the success of the procedure and detect
any complications associated with the abdominal and thoracic procedures.
✧ Monitor nutrition at regular intervals (weight, skin-fold thickness, routine blood
tests). Dietary and vitamin supplements may be necessary.
✧ Monitor function of bypass with regular barium swallows.
✧ Endoscopic dilatation of strictures may be indicated.

Benign oesophageal strictures

All strictures need urgent OGD and multiple biopsies to exclude cancer.
History
Take a general oesophageal history. There may be a history of reflux oesophagitis or
caustic fluid ingestion in the past. Generally dysphagia symptoms will be of slow onset
and progressive from solids to fluids.
Examination
✧ Perform a general oesophageal examination.
✧ Look for evidence of weight loss, anaemia and sepsis.
✧ Examine the chest for respiratory and cardiovascular disease.
✧ Examine the abdomen for other gastrointestinal disease.
✧ Examination may be normal.
Investigations
Strictures are diagnosed by a combination of OGD and biopsies for histological exami-
nation. If surgery is considered, studies of oesophageal motility should be made.
A CT scan to detect scarring in the mediastinum can be performed to help in planning
the procedure.
Treatment
Endoscopic dilatation
✧ An OGD is performed to visualise the stricture and Puestow’s, Celestine tube or
pneumatic guidewire guided dilatation is performed. Some centres prefer to perform
this procedure under fluoroscopic guidance. Severe stenoses require 2–3 dilatation
sessions every 1–2 weeks; each session consists of 3–4 dilator sequences consisting of
a 6–8mm diameter increase. All patients should remain nil-by-mouth for some hours
after dilatation and some centres routinely perform a CXR to exclude perforation
before allowing the patient to eat. Complications include haemorrhage, perforation
and septicaemia.
✧ An equally important aspect of the management of benign stricture is inhibition of
acid reflux, usually with a PPI.
If bile reflux is a problem, revision surgery (Roux-en-Y gastric bypass) is usually
necessary.
 OESOPHAGUS 67

Subsequent treatment
Following a course of dilatation, 20–50% of patients remain symptom-free. Twenty per
cent require frequent dilatation. In these cases surgery should be considered, or consider
insertion of a self-expanding metal stent if unfit. Patients must remain on lifelong treat-
ment if the stricture is not to recur.
Indications for surgery
✧ Young patients with reflux strictures.
✧ Frequent and increasingly difficult dilatations.
✧ Intractable/impassable stricture.
✧ Stricture associated with Barrett’s oesophagus.
Surgery
Perform thoracotomy and intra-operative dilatation, then return to abdomen and
perform Nissen’s. If the oesophagus is too short, perform a Collis gastropexy.
Follow-up
Intervals should be short (1–2 weeks) until cancer is excluded.
If a course of dilatation is indicated, the patient should be reviewed in clinic 2–4 weeks
after completion of the course to detect recurrent symptoms. Thereafter follow up inter-
vals can be lengthened (1–6 months), and if the condition remains stable the patient may
be discharged with advice to reconsult if the symptoms return. Patients are advised they
must remain on lifelong anti-reflux treatment (PPI) if the stricture is not to recur.
Post-operative follow-up
Following surgery, the patient should be reviewed to determine whether the procedure
has relieved the original symptoms and to detect complications. Complications include
wound infection and incisional hernia. Thoracotomy complications include wound
infection and pleural effusion. Patients are advised they must remain on lifelong anti-
reflux treatment if the stricture is not to recur.
Motility disorders
Most motility disorders occur in young adulthood (occasionally children) to late middle
age and can be classified as follows.
✧ Primary (achalasia, vigorous achalasia, diffuse oesophageal spasm, nutcracker
oesophagus).
✧ Secondary
∝ neurological disorders (poliomyelitis, pseudobulbar palsy)
∝ myopathies (dermatomyositis)
∝ systemic disease (scleroderma).
✧ Parasitic infections (Chaga’s disease).

Achalasia
Achalasia is the absence of peristaltic contractions within the oesophageal body and
incomplete relaxation of the high-pressure zone (HPZ) of the lower oesophageal
sphincter.
History
Take a general and oesophageal history. Symptoms include dysphagia, regurgitation and
chest pain.
✧ Typically dysphagia is for solids and liquids, initially intermittent and aggravated by
emotion, and it may be improved by sipping fluids or repeated swallowing and other
manoeuvres, e.g. valsalva.
68 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Odynophagia may be prominent if dilatation is minimal.

✧ As dilatation increases, pain and dysphagia decreases and regurgitation increases –
especially postural regurgitation of foamy, mucoid saliva.
✧ Halitosis and eructation of foul air may be described.

Advanced achalasia leads to massive dilatation of the oesophagus, causing severe dys-
phagia, weight loss, anaemia, respiratory complications due to aspiration; fever, sweating
and breathlessness.
Examination
✧ Perform a general and oesophageal examination (may be normal).
✧ Look for evidence of weight loss, anaemia and sepsis.
✧ Halitosis may be noticed.
✧ Examine the chest for evidence of infection or effusion.
✧ Examine the abdomen for other gastrointestinal pathology.
Investigations
A CXR may show a convex shadow to the right of the vena cava and right atrium,
with or without a fluid level within the shadow. The lungs should also be assessed for
pneumonia.
Barium swallow may show dilatation of the oesophagus and the characteristic rat’s-tail
appearance and absence of the gastric air bubble.
An OGD should be performed to exclude peptic stricture and carcinoma of the
oesophagus.
In early or doubtful cases, oesophageal manometry may demonstrate no relaxation of
the lower oesophageal sphincter with swallowing.
Treatment
In early achalasia, some patients benefit from long-acting nitrates (isosorbide). Endoscopic
pneumatic balloon dilatation up to 90F can be helpful and can be repeated at regular
intervals.
Surgical myotomy (Heller’s procedure) is indicated:
✧ in advanced disease with severe dilatation and oesophagitis
✧ in younger patients
✧ where there is co-existent pathology requiring surgical treatment, e.g. hiatus hernia,
phrenic diverticulum
✧ with failure of dilatation
✧ on recurrence of symptoms.

Severe achalasia with a huge tortuous megaoesophagus may require subtotal oesophagec-
tomy with gastric pull-through and cervical anastomosis.
Follow-up
Severe cases need prompt assessment and treatment within weeks. Mild cases may
respond to nitrates and review at 2–3 monthly intervals to gauge response.
Patients requiring frequent endoscopic dilatation are followed up in the endoscopic
unit or have an open appointment for this treatment when required.
Post-operative follow-up
Patients are reviewed at 4–6 weeks. Early complications include wound infection, pleural
effusion or other respiratory complications if a thoracotomy was performed.
Recurrence of symptoms can be treated with further endoscopic dilatation if persistent.
 OESOPHAGUS 69

Patients treated by oesophagectomy and pull-through procedures can experience

complications of recurrent laryngeal palsy, gastric outlet obstruction, gastro-oesophageal
reflux and dumping (see oesophageal cancer).
Vigorous achalasia
This combines features of achalasia and diffuse oesophageal spasm.
History
Take a general oesophageal history. Symptoms are similar to achalasia, but chest pain is
more prominent. Patients may also present with dysphagia and regurgitation.
Examination
✧ Perform a general examination (which may be normal).
✧ Look for evidence of sepsis, weight loss and anaemia.
✧ Examine the chest for evidence of sepsis or cardiac disease.
✧ Examine the abdomen for evidence of gastrointestinal disease.
Investigations
A barium swallow/meal may show segmental spasm of the lower oesophagus with
dilatation of the proximal half.
Manometry may show repetitive high-amplitude non-peristaltic contraction and
failure of relaxation of lower oesophageal sphincter.
Treatment
✧ Long-acting nitrates may help mild cases.
✧ Endoscopic dilatation does not help.
✧ Surgery may be indicated for severe cases and requires a long myotomy.
Follow-up
Severe cases need prompt assessment and treatment within weeks. Mild cases may
respond to nitrates and review at 2–3 monthly intervals to gauge response. Patients
requiring frequent endoscopic dilatation are followed up in the endoscopic unit or have
an open appointment for this treatment when required.
Post-operative follow-up
This is as for achalasia. Long-term follow-up is recommended, with a barium swallow
performed six months post-operatively.
Chagas disease
Chagas disease is a result of infection by Trypanosoma cruzi, which infects the myenteric
plexus of the oesophagus. It occurs mainly in Latin America and simulates achalasia, both
radiologically and manometrically. Patients are usually in poor medical condition, so they
are treated by endoscopic dilatation.
Diffuse oesophageal spasm
This condition involves hypertrophy of the muscular coats of the oesophagus, Wallerian
degeneration of vagal fibres and sensitivity to cholinergic compounds.
History
✧ Take a general and oesophageal history.
✧ Typical symptoms are substernal midline chest pain (similar to angina pain, it radiates
to back, neck and jaw).
70 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Symptoms include odynophagia and dysphagia, affecting equally solids and liquids.
✧ An emotional personality may be apparent.
✧ It is often diagnosed after normal coronary angiography.
Examination
✧ Perform a general examination (which is often normal).
✧ Look for evidence of weight loss and anaemia.
✧ Examine the chest for any respiratory or cardiovascular abnormalities.
Investigations
✧ Barium swallow shows corkscrew appearance.
✧ Provide OGD to exclude organic disease.
✧ Consider cardiology assessment if cardiac disease is suspected.
✧ Manometry shows simultaneous non-peristaltic repetitive contractions in response to
swallowing; spontaneous contractions not related to swallowing; periods of normal
peristalsis; and normal relaxation of HPZ.
✧ A radionuclide scan shows oscillatory movement of the isotope-labelled bolus and
marked delay in transit time.
Treatment
Conservative treatment is with:
✧ long-acting nitrates and tranquillisers
✧ endoscopic pneumatic dilatation.

Surgery, e.g. thoracoscopic long myotomy, is indicated in fit patients in whom conservative
therapy has failed.
Follow-up
Severe cases are investigated and treated promptly within weeks. Less severe cases can be
assessed at longer intervals (1–2 months) to determine the effect of therapeutic agents.
Assess the need for endoscopic dilatation, or in severe cases in fit patients, the need for
surgery.
Post-operative follow-up
Assess for general complications, wound infection and chest complications. Some centres
recommend a barium swallow at six months to assess the effect of surgery.
Recurrence may respond to further endoscopic balloon dilatation.
Motility disorders secondary to systemic disease
The most common systemic disorder causing oesophageal motility symptoms is systemic
sclerosis (SS). Nearly all patients with SS and oesophageal involvement have symptoms of
oesophageal reflux, often severe. Less common conditions are dermatomyositis, systemic
lupus erythematosus (SLE) and rheumatoid arthritis (RA). Common defects consist of
lower oesophageal sphincter incompetence and complete loss of peristaltic activity in
the lower two-thirds.
History
✧ Take a general oesophageal history.
✧ Patients can present with symptoms of oesophagitis and dysphagia in association with
symptoms of the underlying disorder.
 OESOPHAGUS 71

Examination
Perform a general examination and look for evidence of an underlying disorder, e.g.
Raynaud’s phenomenon or rheumatoid joints.
Investigations
Investigations include barium swallow, OGD, manometry and pH studies.
Treatment
Treatment is mainly medical, using drugs which increase oesophageal motility (dom-
peridone and metoclopramide are used but with inconsistent results). Treat reflux
aggressively with standard medical regimes. Any peptic strictures are treated by endoscopic
dilatation.
Follow-up
Follow-up is long term for treatment of the motility disorder and the underlying con-
dition. Assess for development of strictures and diverticulae. Treat as appropriate with
drugs and regular endoscopic dilatation.
Nutcracker oesophagus
This is symptomatic oesophageal peristalsis.
History
Take a general oesophageal history. The condition typically does not cause dys-
phagia. Instead, there are episodes of chest pain similar to both angina and reflux
oesophagitis.
Examination
✧ Perform a general examination (which may be normal).
✧ Examine the chest for respiratory or cardiovascular disease.
✧ Examine for abdominal pathology.
Investigations
✧ Manometry shows normal peristaltic waves on swallowing, but primary waves of large
amplitude (greater than 150 mmHg) in the distal oesophagus and of long duration
(longer than 5.5 seconds).
✧ Perform 24-hour pH monitoring in all patients to diagnose reflux.
✧ Use OGD to detect oesophagitis.
Treatment
Treatment is medical. If there is reflux, treat with omeprazole, otherwise with long-acting
nitrates or calcium antagonists.
Follow-up
✧ Intervals should be short (1–4 weeks) until cardiac disease is excluded and the
diagnosis is achieved.
✧ Thereafter, follow-up can be at longer intervals to assess the effect of therapeutic
agents.
✧ Discharge the patient once the condition has stabilised.
Pharyngo-oesophageal (Zenker’s) diverticulum – pharyngeal pouch
This is a pulsion diverticulum that occurs through Killian’s dehiscence of the posterior
cricopharyngeus. It usually lies to the left side of the oesophagus and is caused by a
72 GENERAL SURGERY OUTPATIENT DECISIONS

motility defect (failure of relaxation of the cricopharyngeus). The pouch enlarges and
pushes the oesophagus to one side, so food enters the pouch preferentially.
History
✧ Take a general oesophageal history.
✧ Spluttering and coughing with meals is typical.
✧ High dysphagia, progressing to regurgitation, constant throat irritation, gurgling
noises during swallowing, chronic cough and recurrent aspiration pneumonias are
also suggestive.
✧ Compression of the oesophagus causes the dysphagia and attacks of spluttering and
coughing with each meal.
✧ Other symptoms include halitosis, hoarseness and anorexia.
✧ Regurgitated material is non-acid.
Examination
✧ Perform a general examination (which may be normal).
✧ Occasionally, a lump may be palpable in the left side of the neck.
✧ Gurgling may be detected on palpation of the left side of the neck at the level of the
cricoid, performed after the patient is asked to swallow several gulps of air.
✧ Examine the chest for evidence of respiratory or cardiovascular disease.
✧ Examine for abdominal pathology.
Investigations
Investigations comprise:
✧ CXR for chest complications
✧ FBC for anaemia
✧ barium swallow and meal to exclude gross oesophageal motility disorder and hiatus
hernia.

OGD is not necessary initially and carries a risk of perforation.

Treatment
Treatment is surgical. Relief of symptoms is commonly achieved by endoscopic division
of the septum for elderly, unfit patients.
Follow-up
Severe cases should be investigated and treated promptly, within weeks. Less severe cases
can be assessed at longer intervals.
Post-operative follow-up
Determine if operation has relieved the symptoms and assess for general post-operative
complications.
Oesophageal cancer
Ninety-five per cent of cases of oesophageal cancer are either squamous cell or adeno-
carcinomas. In the United Kingdom, adenocarcinomas of the lower third of the oesophagus
predominate. Carcinoma of the gastric cardia that invades the lower oesophagus is a
gastric cancer. Overall the five-year survival for oesophageal cancer is poor (10%).
Risk factors include being male, aged between 30 and 80.
✧ High risk: smoking, excess alcohol intake, tylosis (type A), Plummer-Vinson
syndrome.
✧ Intermediate risk: reflux, Barrett’s, achalasia, ectopic gastric mucosa, previous radio-
 OESOPHAGUS 73

therapy for Hodgkin’s and non-Hodgkin’s disease, previous squamous cell cancer of
head and neck.
✧ Low risk: oesophageal diverticula, corrosive strictures, coeliac disease, scleroderma.
History
✧ Take a general oesophageal history.
✧ The typical history is of progressive dysphagia over a period of months.
✧ There may be symptoms associated with anaemia, caused by bleeding from the
tumour, or there may be symptoms of bleeding.
✧ There may be a history of weight loss.
Examination
✧ Perform a general examination.
✧ Note signs of weight loss, sepsis, anaemia or palpable Virchow’s node in the left
supraclavicular fossa.
✧ Examine the chest for evidence of cardiovascular or respiratory disease.
✧ Examine for abdominal pathology, e.g. epigastric mass or liver metastases.
Investigations
✧ Urgent OGD and biopsy.
✧ Barium swallow may be useful if unable to do an OGD, as lesions longer than 5cm are
associated with deeper invasion levels, irresectability and a worse prognosis.
✧ FBC to detect anaemia.
✧ Assess nutritional status (skin fold, haematological and biochemical indices –
albumin, transferrin, haemoglobin (Hb), iron).
Staging
To establish the presence of inoperable mediastinal or subdiaphragmatic disease.
✧ Staging chest and abdominal CT scan.
✧ Endoscopic ultrasound (EUS) to stage the tumour and nodal status within the chest
and abdomen.
✧ Bronchoscopy, if there is evidence of tracheo-bronchial invasion.
✧ Staging laparoscopy for lower oesophageal cancer, looking for peritoneal disease or
liver metastases.
✧ Vocal cord paralysis (ENT examination) and phrenic nerve paralysis (ultrasound
screening) may indicate mediastinal spread.
Treatment
Treatments include surgical resection, radiotherapy, stenting, laser or electrocoagulation
and combined modality treatment; which treatment depends on stage and operative
fitness, including nutritional state. Malnourished patients may require pre-operative
nutrition.
Surgery
✧ The main objective is restoring the ability to swallow.
✧ Thirty to forty per cent of oesophageal tumours are resectable.
✧ Operative mortality is 5–10%.
✧ Surgical resection is the treatment of choice for tumours of the lower two-thirds,
provided that:
∝ the patient is considered fit for major surgical intervention
∝ pre-operative staging tests indicate the tumour is resectable and there is no
metastatic disease.
74 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Upper-third tumours are treated using either chemo-radiotherapy or pharyngo-

laryngectomy.
✧ Malignant oesophagotracheal fistulas are treated by endoscopic insertion of a covered
oesophageal stent.
✧ Other palliative options include laser or diathermy fulguration.
Follow-up
✧ Intervals are short until the diagnosis and staging are complete.
✧ Curative surgery is performed 4–6 weeks after neoadjuvant therapy.
✧ Palliation requires co-ordination between surgery and oncology.
✧ If symptoms are to be controlled with diathermy or laser fulguration, this treatment
may need to be performed every 1–3 months to keep symptoms under control.
Intubation or stenting may be considered as an alternative.
✧ After intubation, patients need to be reviewed regularly (1–3 monthly) to detect prob-
lems with the stent, e.g. blockage or displacement.
Post-operative follow-up
Long term follow-up will be required. Assess the patient to determine whether the
operation has been a success in relieving the symptoms and completely removing the
tumour.
Review the operation notes and the histology report. Assess for general complications
of abdominal surgery and thoracotomy. More specific early complications include the
following.
✧ Recurrent laryngeal nerve palsy may be caused during resection of the tumour.
Patients may complain of a hoarse voice and a weak cough. If only one vocal cord
is affected, the other side often compensates. The condition may be temporary and
may improve over several months. If the paralysis is permanent, improvement in the
voice can be achieved by referral to the ENT surgeons for teflon injection or a formal
thyroplasty.
✧ Gastric outlet obstruction occurs if the stomach was mobilised and the vagus nerves cut
without an adequate pyloroplasty. Investigate with a barium meal. Remedial surgery
may be necessary in severe cases, but usually endoscopic dilatation is sufficient.
✧ Gastro-oesophageal reflux occurs if the stomach has been moved into the chest to
establish continuity. Treatment is with PPI and prokinetic drugs such as cisapride,
maxalon and erythromycin.

Dumping symptoms are common after oesophageal surgery but usually settle after
12 months with conservative treatment.
Late complications include anastomotic stricture, which can be treated with endoscopic
balloon dilatation.
Evidence of recurrence that is untreatable will require palliation.
Stomach and duodenum
Richard Hardwick

FIVE
Introduction
A general surgical outpatient clinic will commonly have patients who have been sent up
by their GP to discuss a laparoscopic cholecystectomy because an ultrasound scan has
detected gallstones. However, there is a large overlap between biliary and gastroduodenal
symptoms. It is vital that a careful history is taken to avoid inappropriate biliary surgery
when the patient has a duodenal ulcer. More specialist upper gastrointestinal (GI) clinics
will have large numbers of new and follow-up patients with very specific problems,
some of which will be due to the disease process and some due to treatment they have
received. New patients are usually seen by a consultant, but trainees should attend some
of these consultations to learn how to take a rapid and focused history and formulate a
management plan. Gastrointestinal surgeons should be just as competent at diagnosing
and treating GI disease as are their gastroenterology colleagues. Clearly the two specialities
bring their own unique skills and experience to bear on a patient’s problem, but they
should work closely together and refer freely between themselves as appropriate.

Assessment of gastric and duodenal disorders

Gastric and duodenal history
Pain
Pain is generally in the epigastric region and is caused by inflammation, ulceration,
distension or tumour of the stomach.
Characteristics of pain due to peptic ulceration may vary according to the site of the
ulcer.
✧ Gastric ulcer pain may be exacerbated by food and may be relieved by vomiting.
Consequently, the patient is afraid to eat and loses weight.
✧ Duodenal ulcer pain is epigastric but may radiate through to the back. It is typically
relieved by eating and may sometimes wake the patient at night.
✧ Pyloric stenosis: vomiting and weight loss are unusual and may suggest the development
of pyloric stenosis. With the widespread use of acid-suppressing medication this is
now a very rare complication in developed countries. Pain tends to be periodic, lasting
10–14 days every 3–4 months. Pain due to pyloric stenosis may cause abdominal
distension, which is uncomfortable.
✧ Gastric carcinoma: pain due to cancer of the stomach is common and cannot reliably
be distinguished from benign inflammation. Worryingly, patients with gastric cancer
will usually report relief of their burning epigastric pain soon after starting a proton-
pump inhibitor. This falsely reassures both patient and doctor that there is nothing
sinister and delays the diagnostic endoscopy, which then is requested only when the
pain returns or the patient loses weight.
Vomiting
Vomiting may be a feature of gastric ulcer disease with or without gastric outlet
obstruction. Gastric outlet obstruction may also be caused by tumour. Patients report
vomiting undigested food ingested several days before. Always take this symptom
seriously and investigate it.

75
76 GENERAL SURGERY OUTPATIENT DECISIONS

Water brash and heartburn

Water brash is caused by excess secretion of saliva. It tastes salty and is an indicator
of oesophageal reflux. Heartburn is a much commoner symptom. It is often felt after
meals, at night or when bending down. It can radiate into the neck and be very similar
to cardiac chest pain. However, unlike the latter it is quickly relieved by antacids or acid
suppression.
Dysphagia
This is primarily an oesophageal symptom but it may also indicate a gastric problem –
carcinoma of the cardia obstructing the gastro-oesophageal junction. Always investigate
dysphagia urgently.
Fatigue, malaise
These non-specific symptoms may indicate anaemia secondary to chronic blood loss
from a peptic ulcer or tumour.
Drug history
The ingestion of certain medications, e.g. NSAIDs or steroids, may predispose to gastro-
duodenal ulceration, or predispose to complications from ulceration, as, for example,
does warfarin.
Past medical history
Previous peptic ulceration or gastric surgery may be relevant. A social history of smoking
and excess alcohol ingestion is associated with peptic ulceration.
Gastric and duodenal examination
This will usually be entirely normal.
Look for the signs of advanced upper GI malignancy – weight loss, anaemia, an
abdominal mass, ascites and lymphadenopathy. These are signs of incurability and it is sad
that they are still used as ‘alarm features’ to guide GPs to refer patients for investigation.
Curable upper GI malignancy usually presents with mild dyspepsia only, and unless an
endoscopy and biopsy is done then, the chance of cure is often lost.
Distension in the epigastrium and left hypochondrium may represent gastric
distension secondary to gastric outlet obstruction. Auscultation in this region may reveal
a succussion splash in response to rocking the abdomen. Surgical scars may indicate
previous gastric surgery. Always look for the signs of liver disease, such as spider naevi,
liver palms, hepatomegaly, jaundice and tremor.
Investigation of gastric and duodenal disorders
Laboratory investigations
✧ Haematology: routine indications, e.g. full blood count (FBC), may indicate anaemia;
leucocytosis may suggest infection.
✧ Biochemistry: routine indications, e.g. abnormal liver function tests (LFT), may
indicate liver metastases in malignancy. More specialised gastric acid secretion tests
can be made.
✧ Immunology: for example, identification of serum antibodies to Helicobacter pylori
(HP); parietal cell antibodies in pernicious anaemia.
✧ Cytology/histology: cytology of brushings or histology of biopsies taken at
endoscopy.
✧ Urea breath test or faecal antigen test for Helicobacter pylori: patients under the age of
55 (some would argue 45) who present with simple dyspepsia should be tested for HP
and, when positive, undergo triple-therapy eradication treatment with a combination
 STOMACH AND DUODENUM 77

of two antibiotics and a proton-pump inhibitor (clarythromycin, amoxicillin and

omeprazole is one example). Serum antibody testing for HP is possible but will stay
positive for many months after eradication and is less reliable than a urea breath test.
Urea containing radio-labelled carbon is drunk by the patient. If HP is present in
the stomach, the urease enzyme produced by it will split the urea into radio-labelled
carbon dioxide (CO2) and ammonia. The CO2 is exhaled and can be detected. Faecal
antigen testing using HP-specific antibodies is an alternative technique, but it is
not as popular with patients and staff for obvious reasons. A gastric biopsy taken at
endoscopy can also be tested using a test for Campylobacter-like organisms, the CLO
test, which works on the same principle as the urea breath test, except that a colour
change is induced by the urease rather than by CO2.
Imaging techniques
Oesophago-gastro-duodenoscopy (OGD)
This should be the first investigation in all patients with gastroduodenal symptoms.
✧ The request form is usually an endoscopy request form. Include relevant history and
request specific tests, e.g. antral biopsies for Helicobacter.
✧ The report will usually comment on the oesophagus, stomach and duodenum.
Usually measurements will be given for the position of the oesophago-gastric
junction (38–40cm), the presence of the Z-line (squamo-columnar junction) and,
using the J-manoeuvre, the presence of a hiatus hernia. The first (D1) and second
(D2) parts of the duodenum will be described. The site, size and character of any
ulcers or other lesions will be described. If biopsies were taken, look for the histology
report, which may also comment on the presence or absence of Helicobacter pylori.
Recommendations for treatment are sometimes suggested.

The advantages of the procedure are that it allows direct visualisation of gastroduodenal
lesions and enables biopsies to be taken for histological diagnosis. It can visualise
oesophagitis, ulceration, varices etc. Certain therapeutic manoeuvres, e.g. injection of
bleeding ulcers, can be performed.
Disadvantages are that it is an invasive procedure, and it is unable to diagnose early
motility disorders. Some patients may find it unpleasant and are unable to swallow the
scope. Complications include aspiration; or trauma to the oesophagus, stomach and
duodenum that may cause bleeding, pain or occasionally perforation. This is particularly
a risk in an unco-operative patient. Linitis plastica can be difficult to diagnose with OGD.
Patients who are unable to swallow the scope may be offered a general anaesthetic.
CLO test for Helicobacter pylori
✧ Technique: this is often performed in conjunction with OGD. Endoscopic gastric
biopsies are taken under direct vision from the gastric antrum. The tissue is placed
in indicator medium, which detects the presence of urease activity by H. pylori. The
presence of H. pylori results in an indicator colour change within a specified time-
period, e.g. 60 minutes. Colour change after this time period is non-specific.
✧ Request form: write request for CLO test on the endoscopy request form. It is often
performed as routine, even if not specifically requested.

The advantages are that it gives a quick result, enabling eradication therapy to be
immediately prescribed. The disadvantages are that false negatives occur in 5–15%, so a
negative result does not completely exclude the presence of H. pylori. PPI, bismuth and
antibiotic use may interfere with the test and give a false negative result.
78 GENERAL SURGERY OUTPATIENT DECISIONS

Alternative tests for H. pylori

H. pylori can also be detected, using immuno-histochemical stains, from gastric biopsies
sent for histology.
Barium swallow/meal
This technique is used as a second-line investigation if OGD fails to provide a diagnosis.
Indications for its use are:
✧ dysphagia in a frail person not suitable for OGD
✧ dysphagia when patient refuses OGD
✧ to exclude a pharyngeal pouch if there is concern prior to scoping.

An advantage of the technique is that it is useful in the investigation of dysphagia where

endoscopy has not detected a mechanical cause and a motility disorder of the oesophagus
or stomach is suspected. Double contrast (barium-air) barium meals are useful for the
evaluation of suspected gastric cancer. Rigidity and absent peristalsis may occur at the site
of a localised tumour, while linitis plastica produces an abrupt circumferential narrowing
of the stomach lumen.
The disadvantages are that irradiation is used and simultaneous therapeutic procedures
are not possible. Overall, it is not as sensitive as endoscopy for the detection of small
lesions.
Ultrasound
The technique is mainly used non-invasively, with the ultrasound probe applied to the
outside of the body after applying acoustic water-based gel. It often will be needed to
exclude gallstones.
Its advantage is that it is a cheap, quick and safe way of imaging the liver, so it is useful
for screening for liver metastases.
Endoluminal ultrasound (EUS)
This is a technique where a specialised probe is placed in the stomach to provide images
of the stomach wall and adjacent lymph nodes. EUS can:
✧ help with diagnosis of gastric gastrointestinal stromal tumours (GIST)
✧ stage tumour
✧ obtain tissue (using EUS, fine-needle aspiration (FNA) and core biopsy).

Endoluminal ultrasound is good for determining intramural spread and lymph node
involvement.
Combined laparoscopy and laparoscopic ultrasound is good for identifying transcoe-
lomic spread and peritoneal seedlings, which can then be biopsied under direct vision.
Laparoscopic ultrasound gives better images than external ultrasound of intra-abdominal
organs, helping to detect smaller metastases, which can then be biopsied.
The disadvantage is that this is a limited application on its own. Confirmation of
findings is needed by performing a computed tomography (CT) scan, so this tends to be
preferred to ultrasound. Endoluminal ultrasound and laparoscopic ultrasound are not
widely available.
CT scanning
The technique is used in gastric malignancy to demonstrate the extent of mural invasion;
involvement of adjacent structures; and liver and lymph node involvement. Sometimes
CT is used as a ‘diagnostic fishing trip’ when the clinician is worried that the patient has
disseminated cancer but cannot find anything concrete on examination or blood tests.
An advantage is that invasion of the wall of the stomach is demonstrated as wall
 STOMACH AND DUODENUM 79

thickening (greater than 5mm). A thickness greater than 2cm generally correlates with
spread beyond the stomach. Lymph node metastases can be detected in about 70% of
cases. CT is good for detecting liver metastases.
Disadvantages include irradiation and a tendency to underestimate early peritoneal
spread and lymph node metastases. It is not totally reliable in differentiating direct
metastatic spread from reactive inflammation surrounding a tumour. Therefore it tends
to understage tumours.
Barium meal
Barium meal is useful for defining the anatomy of a large hiatus hernia or seeing whether
fluid empties from the stomach. In experienced hands it can be used to diagnose peptic
ulcers and tumour, but it is inferior to endoscopy and should be reserved for specific
cases.
Radioisotope techniques
The only test routinely used is a two-phase gastric emptying study. This is to investigate
patients with suspected functional stomach problems (gastroparesis and gastric hurry).
Technetium-99m-HIDA scan
This scan is used to detect and quantify enterogastric reflux and afferent loop obstruction
after gastrojejunostomy reconstructions.
In this technique, the patient is given an intravenous injection of technetium-99m-
HIDA, which is secreted in the bile and concentrated in the gall bladder. The amount of
radioactivity in the gall bladder is calculated and the gall bladder is stimulated to contract
by administration of a milk meal. This expels the radioactivity into the duodenum. The
passage of the radioactivity along the small bowel can be traced and the obstruction
can be identified. Enterogastric reflux of radioactivity from the small bowel back into
the stomach can be identified and quantified as a percentage of the total abdominal
radioactivity.
Its advantages are that it provides quantitative assessment of the degree of enterogastric
reflux and it can detect afferent loop obstruction in gastrojejunostomy reconstructions.
Disadvantages include the use of radioactivity. It requires a functioning unobstructed
biliary system.
Schilling test
This is a test used to assess the patient’s ability to absorb vitamin B12. Radioactive vitamin
B12 is given by mouth, and urine is collected for 24 hours.
A normal individual will excrete at least 10% of the original dose over 24 hours. A
patient with pernicious anaemia will excrete less than 5%.
The advantage of this test is that it is a quantifiable measure of the ability of the gastro-
intestinal tract to absorb vitamin B12. The disadvantages are that it does not localise the
disease to stomach or terminal ileum and it uses radioactivity.
Laparoscopy
Laparoscopy is being increasingly used for the diagnosis and staging of tumours. The
technique is performed in the operating theatre under general anaesthetic. A laparoscopic
port is inserted under direct vision and CO2 is insufflated to produce a pneumoperito-
neum. It may be combined with intra-operative ultrasound using a special laparoscopic
ultrasound probe. It also enables biopsy of focal lesions under direct vision. Laparoscopy
is performed by a surgeon with a special interest.
The advantages are direct visualisation of abdominal pathology, and in gastric cancer it
may establish irresectability without subjecting the patient to a full laparotomy. It enables
80 GENERAL SURGERY OUTPATIENT DECISIONS

direct biopsy of small lesions, e.g. peritoneal deposits, small liver lesions. Its disadvantage
is that it is an invasive procedure requiring general anaesthetic.

Peptic ulcer disease

Chronic duodenal ulcer
Peak incidence occurs in the 25–50 age range. However, these ulcers are now rare in
developed countries, due to effective treatment in the primary care setting.
History
✧ The patient typically presents with recurrent episodes of epigastric pain.
✧ Exacerbations are associated with stress, dietary/alcoholic overindulgence and
smoking. Symptoms increase during fasting (night pain) and are decreased by food,
especially milk or alkalis.
✧ Pain radiating through to the back is typical of posterior ulceration.
✧ Vomiting is uncommon unless associated with oedema/fibrosis around the ulcer
causing pyloric obstruction.
✧ There may be a history of aspirin or non-steroidal anti-inflammatory drug (NSAID)
ingestion. Often the patient is referred to surgery with a long history of H2-receptor
antagonist (H2RA) or PPI treatment with relapses.
Examination
The patient may be overweight due to constant nibbling and there may be evidence
of anaemia. On abdominal examination there may be diffuse epigastric tenderness. In
cases with a degree of gastric outlet obstruction a succussion splash may be detected.
Examination may otherwise be normal.
Chronic gastric ulcer
This is less common than duodenal ulcer. There are two distinct types.
✧ Type I is in the body of the stomach along the lesser curve. Type I may arise in normal
mucosa or atrophic gastritis. These ulcers are not associated with hyperacidity, and in
fact hypoacidity may be found. Hyperacidity tends to occur in the older age group.
✧ Type II is a pyloric channel ulcer (includes pre-pyloric). The natural history, acid
secretory profile and therapeutic response are the same as for duodenal ulcers.
History
✧ Gastric ulcer patients may describe discomfort and fullness in the stomach.
✧ Eating increases the pain and is relieved by fasting – in fact patients may be afraid to
eat, and they lose weight.
✧ These symptoms are the same as for gastric cancer, but cancer tends to be associated
with more nausea and vomiting, and pain is more constant.
Examination
Examine for evidence of weight loss, anaemia and epigastric tenderness. A palpable
epigastric mass suggests carcinoma of the stomach but may represent an inflammatory
mass.
Investigations
✧ OGD and/or double contrast barium meal are used to investigate all dyspepsia
patients.
✧ OGD combined with CLO testing of gastric antrum biopsies will establish Helicobacter
pylori status.
 STOMACH AND DUODENUM 81

OGD shows duodenal ulcer

✧ Diagnosis and biopsy of gastric antrum are needed to detect H. pylori.
✧ Two more biopsies are needed: one for the instant CLO test, one for histological
examination.

If either is positive, the patient is started on H. pylori-eradication therapy and medical

ulcer-healing therapy. OGD is repeated after medical therapy to check healing.
OGD shows gastric ulcer
Biopsy of the ulcer is mandatory to exclude gastric cancer; and also perform a biopsy
of the antrum looking for H. pylori bacteria. If biopsy is benign, start on medical ulcer-
healing therapy and H. pylori eradication, but repeat the endoscopy after 2–3 months of
medical therapy. If the ulcer is not healed, repeat the biopsy. Failure to heal, even in the
presence of negative biopsies, may be an indication for surgical therapy.
Medical treatment
The first step is to stop any medication such as NSAIDs that might cause ulceration,
and to eradicate H. pylori infection. Thereafter use PPIs. A therapeutic course lasting
2–3 months heals 90%, with symptom relief achieved within 2–3 days.
✧ Resistant ulcers need a double dose of PPI. Only PPIs heal all resistant ulcers. Relapse
is universal unless maintenance therapy is continued indefinitely.
✧ PPIs heal both duodenal and gastric ulcers. Problems of long-term PPI therapy are
achlorhydria and hypergastrinaemia. There is evidence from rat studies of prolifera-
tion of gastric fundal endocrine cells and G-cells with the development of carcinoid
tumours.
✧ Current triple-therapy regimes consist of a PPI, clarithromycin and metronidazole for
1–2 weeks. The PPI is continued for six weeks. Permanent healing rates are achieved
in all patients in whom H. pylori infection is eradicated – approximately 90%. Patients
undergo a urea breath test at 6–8 weeks to confirm eradication. If this fails, the original
regime is tried.
Refractory ulcers
✧ A duodenal ulcer is considered refractory if there is no healing after eight weeks’
therapy.
✧ A gastric ulcer is considered refractory if there is no healing after 12 weeks’ therapy.

Perform an OGD to differentiate patients with a true refractory ulcer from those patients
with persistent symptoms despite ulcer healing, which require investigation of alternative
causes. If a refractory ulcer is present, successful H. pylori eradication should be confirmed
by further biopsy for CLO test and histology. If H. pylori is still present, investigate its
non-compliance with eradication therapy and, if indicated, prescribe another regime. If
no H. pylori is detected, enquire regarding the presence of other ulcerogenic factors, e.g.
smoking (measure urinary nicotine levels) or aspirin ingestion (measure blood salicylate
levels).
True resistant ulcer
A true resistant ulcer fails to heal despite H. pylori eradication. A relapsed ulcer heals
initially but then recurs.
✧ Perform an OGD and take multiple biopsies for evidence of neoplasia, infection or
inflammation.
✧ Measure serum gastrin levels, and, if they are high, investigate for Zollinger-Ellison
syndrome.
82 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Where no cause can be found, the ulcer can be termed an idiopathic refractory ulcer.
Prolonged drug treatment and OGD surveillance, or surgery, is indicated to exclude
undetected malignancy. Indications for surgical treatment of peptic ulcer disease
are:
∝ failure to comply with maintenance
∝ ulcers resistant to H. pylori eradication therapy
∝ gastric ulcers that remain unhealed after three months treatment, irrespective of
the biopsy findings
∝ complications associated with ulcers, e.g. pyloric obstruction, perforation,
bleeding.

Always think: ‘Could this be cancer?’

Follow-up
Follow up with medical therapy and follow-up OGD. Once the ulcer is healed and
H.pylori eradicated, the patient can be discharged.
Post-operative follow-up
This is needed long term to detect complications, which include recurrent ulceration,
dumping, diarrhoea and adverse nutritional consequences. However, remedial surgery
for most chronic conditions is usually delayed for at least 18 months, as most symptoms
improve.
Nutritional consequences of gastric surgery
Nutritional consequences are more common after gastrectomy, which results in:
✧ decreased food intake
✧ malabsorption of fat or nitrogen
✧ decreased small bowel transit time.

Iron deficiency anaemia

Iron deficiency is very common after vagotomy and drainage or gastric resections, espe-
cially in females. The incidence increases with time until it is 60–80% at 10–20 years.
It is caused by altered handling of iron – the failure to reduce it to the ferric form for
absorption. Iron absorption is unpredictable after gastrectomy, and close monitoring of
the FBC is necessary for 1–2 years after surgery.
Macrocytic anaemia
This is caused by vitamin B12 deficiency. It invariably occurs after total gastrectomy
due to loss of the intrinsic factor. After partial gastrectomy, diagnosis is by an abnormal
Schilling test. Treat by three-monthly injections of cyanocobalamin, indefinitely. Partial
gastrectomy and truncal vagotomy and drainage result in lower levels of vitamin B12
due to lack of an acid environment. The Schilling test is normal – treatment is with oral
crystalline vitamin B12.
Bone disease
Bone disease may develop several years after gastric resection with duodenal exclusion; the
duodenum is the major site of calcium absorption. Many females develop osteomalacia
10–20 years after gastrectomy. They may present with symptoms of generalised bone pain,
weakness due to associated myopathy, and stress fractures. Investigations show a raised
serum alkaline phosphatase and calcium, and areas of bone rarefaction on X-rays.
Calcium and alkaline phosphatase levels should be measured annually. After five
years all patients should have a full assessment for metabolic bone disease. Treatment is
 STOMACH AND DUODENUM 83

with oral calcium and vitamin D. Post-menopausal women and all patients aged over 70
should take an oral calcium supplement, twice a day, for life.
Post-gastric surgery dumping and reactive hypoglycaemia
Dumping
This is rapid gastric emptying. Vasomotor symptoms occur within minutes of eating due
to hypovolaemia (decreased cardiac output and peripheral resistance) caused by out-
pouring of fluid into the bowel to dilute hyperosmolar gastric contents.
Treatment of mild or moderate dumping is to advise small dry meals, rich in protein
and fat but low in carbohydrate. Methoxy pectin or bran can be added to the diet to
slow gastric emptying. Dumping rarely has a surgical solution and should be managed
conservatively. Time is usually the best healer, as symptoms will often settle down over
6–12 months.
Reactive hypoglycaemia
Symptoms of sweating and tremor due to hypoglycaemia occur 2–3 hours after a meal.
Diagnosis is made by performing an in-patient extended glucose tolerance test. Following
a meal this shows initial hyperglycaemia, provoking an exaggerated insulin release with
increased plasma insulin and enteroglucagon levels. This results in the subsequent
hypoglycaemia and occurrence of symptoms. Treatment is mainly dietary, with low
carbohydrate-high protein meals. Ingesting fluids at the same time as solids should be
avoided, to help reduce intestinal transit time.
Enterogastric reflux/reflux gastritis
Reflux of bile/pancreatic juice into the stomach causes a reflux erosive gastritis and bilious
vomiting.
History
There is a history of epigastric pain, nausea and vomiting in the early postprandial period.
It is a burning-type pain, aggravated by food and not relieved by antacids. Episodes culmi-
nate in the vomiting of bile-stained fluid 1–2 hours after a meal. Less commonly, vomiting
occurs early in the morning after night pain. Iron deficiency anaemia develops.
Investigations
Diagnosis is confirmed by OGD which reveals gastritis and pooling of bile in the
stomach.
Treatment
✧ Bile-salt binding agents such as cholestyramine, combined with Sulcralfate at night,
are often effective.
✧ If medical therapy fails to control the symptoms, remedial surgery is indicated.
✧ Note that atrophic gastritis and intestinal metaplasia associated with enterogastric
reflux has been implicated in the development of carcinoma and requires long-term
follow-up with regular OGD assessment.
Extrinsic loop obstruction
This is a rare condition. It occurs after truncal vagotomy and gastroenterostomy. It usually
affects the afferent loop and is predisposed to by the formation of antecolic anastomoses
and long loops greater than 20cm.
Causes
Causes include internal herniation; kinking of the anastomosis; volvulus; stenosis;
84 GENERAL SURGERY OUTPATIENT DECISIONS

jejunogastric intussusception; and development of gastric cancer in the stomach remnant.

This operation is no longer performed, so the condition is relevant only to older patients
who have had ulcer surgery in the 1960s and 70s.
History
✧ Usually, intermittent feelings of fullness and cramp-like pain and nausea occur within
one hour of eating.
✧ The attack culminates in vomiting of copious amounts of bile-stained fluid, which
relieves the symptoms.
✧ In acute cases there is no relief. It may be accompanied by development of acute
pancreatitis, jaundice and necrosis with perforation.
Examination
During pain-free episodes examination may be normal. During attacks there may be
upper abdominal distension and tenderness.
Investigations
Liver function tests may be abnormal and there may be a dilated small bowel loop on
abdominal X-ray (AXR). Delayed emptying of the afferent loop may be demonstrated by
99Tcm-diethyl-IDA (EHIDA) scan. There may be failure of barium to enter the afferent
loop during barium meal.
Treatment
Some cases are amenable to endoscopic pneumatic dilatation. Unresponsive cases require
surgical correction.
Acute jejunogastric intussusception
There is severe epigastric pain and haematemesis and a palpable abdominal mass and
high small bowel obstruction. Diagnosis is by AXR, which shows a soft-tissue mass sur-
rounded by air. Treatment is by surgery.
Gastro-oesophageal reflux/oesophagitis
Mobilisation of the oesophagus during surgery may cause cardio-oesophageal incom-
petence. If associated with enterogastric reflux this may lead to a severe neutral/alkaline
oesophagitis and stricture formation.
Post-gastric surgery diarrhoea
Three patterns of diarrhoea occur after gastric surgery:
✧ frequent loose motions
✧ intermittent episodes of short-lived diarrhoea
✧ severe intractable diarrhoea, which occurs in 2% after truncal vagotomy and, unlike
dumping, is often precipitated by small meals.

Diarrhoea may be caused by malabsorption of bile salts and/or fatty acids; accelerated
small bowel transit time; or bacterial overgrowth.
History
Determine the pattern of the diarrhoea and any precipitating or exacerbating factors.
Estimate the severity of the symptoms.
Examination
Examine for anaemia, weight loss and dehydration.
 STOMACH AND DUODENUM 85

Investigations
Investigations are usually delayed until simple treatments have failed to control the
symptoms.
Investigations include faecal fat estimation, butter fat test, small bowel transit time and
C14 glycocholate breath test for bacterial overgrowth.
Treatment
✧ Advise a diet low in animal fat. Intestinal sedatives (codeine phosphate, loperamide)
and bile-salt binding agents (cholestyramine) usually give short-term relief.
✧ If symptoms are severe and fail to settle, consider remedial surgery, e.g. reversed small
bowel segment – but results are poor.
Post-gastric surgery decreased appetite
A small stomach is created by extensive or total gastrectomy and it produces early satiety,
which precludes adequate intake and can cause malnutrition. All patients should be
warned accordingly. For many this symptom reduces with time but it rarely disappears
completely.
History
Determine the average dietary intake and whether this is associated with weight loss.
Examination
Examine for evidence of anaemia and weight loss.
Investigation
Carry out FBC, urea and electrolytes (U&Es) and LFTs to estimate nutrition. Investigate
serum iron, B12 and folate. Take contrast studies to examine the gastric remnant.
Treatment
✧ Mild cases are treated with small, frequent meals. There should be dietician input and
high-calorie supplements.
✧ More severe cases may require elemental diets administered by Clinifeed tube.
Other complications after gastric surgery
Other complications after gastric surgery include the following.
✧ Gallstones.
✧ Bezoars – balls of undigested vegetable/fruit matter in the stomach remnant. There will
be a history of nausea and vomiting; abdominal discomfort; halitosis; and early satiety.
They lead to small bowel obstruction, severe gastritis and ulceration. Investigation is
by OGD or barium meal. Medical treatment is with enzymatic cellulose. Small bezoars
may be removed piecemeal endoscopically, but larger ones will need to be removed
surgically. This may be possible with a laparoscopic approach.
✧ There is an increased risk of carcinoma in the gastric remnant at 15–20 years: OGD
should be performed in any patient with new upper abdominal symptoms after any
previous ulcer surgery. Some clinicians offer all patients who have had old-style gastric
ulcer surgery surveillance endoscopy every 3–5 years, but this is controversial. They
are undoubtedly at high risk of developing stump cancers in their gastric remnants.
Gastric volvulus
Usually a degree of gastric outlet obstruction develops, resulting in a big dilated stomach,
which after a heavy meal is prone to twist.
86 GENERAL SURGERY OUTPATIENT DECISIONS

History
Gastric volvulus can present in the outpatient with chronic symptoms of episodes
of epigastric distress and vomiting; or acutely with severe epigastric pain, ineffectual
retching with distension, tenderness and signs of shock.
Examination
Examination may be normal if performed between episodes, or there may be evidence of
epigastric distension and tenderness with a succussion splash.
Investigations
An AXR may show abnormal gastric shadow. Barium meal may demonstrate an abnormal,
big stomach but endoscopy is the investigation of choice.
Treatment
An acutely volved stomach may untwist if carefully decompressed with a nasogastric tube,
or better, at endoscopy. It is does not, resuscitation and urgent surgery by an experienced
upper GI surgeon will be necessary. A laparoscopic approach is often possible and offers
many advantages to the frail elderly patient.
Follow-up
Follow up at short intervals until diagnosis is established.
Post-operative follow-up
This is as for gastrectomy and gastric ulcer surgery.

Gastritis
Types of gastritis
There are four main types of gastritis.
✧ Type A is an autoimmune condition. Circulating parietal cell antibodies cause perni-
cious anaemia with achlorhydria and absent intrinsic factor. The antrum is spared, so
serum gastrin levels are high due to alkaline conditions. There is significant increased
risk of development of carcinoma, usually of the diffuse type.
✧ Type B begins distally in the pyloric region due to H. pylori infection. Gastrin levels
are normal. It is always present in duodenal ulceration.
✧ Lymphocytic gastritis involves infiltration of the gastric epithelium by T lymphocytes.
OGD shows nodularity, erosions and enlarged mucosal folds.
✧ Erosive gastritis is caused by NSAIDs and alcohol.
✧ Other causes include reflux, stress, granulomatous (TB, Crohn’s) gastritis, cystica
polyposa, AIDS gastritis, eosinophilic gastritis, Ménétrier’s disease, suppurative
gastritis, and emphysematous gastritis.
History
Patients may complain of dyspepsia and abdominal pain. There may be a history of
alcohol or NSAID ingestion.
Examination
Examination may be normal, or there may be evidence of anaemia, weight loss or an
underlying disorder.
Investigations
Carry out OGD and biopsy for detection of dysplasia and H. pylori. Vitamin B12 and
 STOMACH AND DUODENUM 87

folate levels may be low. Perform a Schilling test if atrophic gastritis is suspected. Measure
serum gastrin levels and carry out a FBC for lymphocyte and eosinophil levels.
Treatment
Treatment depends on diagnosis and the effect of symptoms and it should be given in
combination with anti-ulcer therapy if indicated.
✧ Type A: vitamin B12 injection every three months.
✧ Type B: H. pylori eradication.
✧ Erosive gastritis: NSAID or alcohol withdrawal.
✧ Dysplasia: if mild to moderate, can be monitored by regular OGD surveillance. If there
is severe dysplasia, gastric resection is indicated.
Follow-up
If gastritis is accompanied by dysplasia, surveillance by OGD is indicated. If dysplasia is
severe, gastric resection is indicated.
Post-operative follow-up
✧ Review histology.
✧ Refer to oncology if indicated.
✧ Follow-up for complications is the same as for gastrectomy for peptic ulcer disease.
✧ Follow-up is usually long term.

Gastric polyps
Types of polyp
Adenomas and other benign tumours are rare. They account for 5% of benign gastric
polyps. Many are found in the antrum. They may be single or multiple. Progression
to cancer is possible. Adenomatous polyps larger than 4cm are associated with 11%
malignant change over a four-year follow-up period.
The majority (75–95%) of gastric polyps are hyperplastic, which represents regeneration
of the mucosa after mucosal damage. They are benign and have no malignant potential.
The commonest polyps by far are fundic gland polyps, which are frequently seen in
patients taking PPIs. They need surveillance only if large (1cm diameter or greater).
Polyps may also be associated with independent cancer elsewhere in the stomach
(6.5%–25%). Gastrointestinal stromal tumours (GIST) most commonly arise in the
stomach and are frequently polypoid. They are submucosal, may have both an intra-
luminal and extra-luminal component and ulcerate causing haematemesis or anaemia.
History
Polyps are usually asymptomatic unless they are large and situated at the pylorus or cardia
and are causing obstruction.
Examination
Examination is usually completely normal.
Treatment
✧ If polyps are small and found on endoscopy, then endoscopic removal is advisable for
histological diagnosis.
✧ This is combined with multiple biopsies of the stomach with prophylactic anti-ulcer
treatment.
✧ Since endoscopic resection is associated with 40% recurrence of polyps, endoscopic
follow-up is essential.
88 GENERAL SURGERY OUTPATIENT DECISIONS

Follow-up
Intervals should be short until the diagnosis is made and malignancy is excluded. After
treatment, long-term follow-up with OGD surveillance is indicated to detect recurrence
or malignant change.

Post-operative follow-up
Review histology to detect any evidence of malignancy.

Non-neoplastic gastric polyps

Regenerative polyps are inflammatory and associated with gastritis and peptic ulceration.
All should be removed endoscopically for histology. Two per cent have areas of focal
carcinoma, 4% dysplasia. Long-term follow-up with OGD surveillance is indicated.

Other polyps
Inflammatory fibroid polyps are found when eosinophilic gastritis occurs in the pyloric
antrum and duodenum. It is caused by a gastrointestinal allergy.
Others include myoepithelial hamartomas; Peutz-Jeghers syndrome; and heterotopic
pancreatic tissue in the antropyloric region.

Carcinoma of the stomach

Overall, five-year survival for carcinoma of the stomach remains depressingly low in
the United Kingdom, at 5–10%. However, survival is dependent upon cancer stage at
presentation and, to a lesser degree, on the radicality of resection. Early tumours with no
or few involved nodes can be cured by D2 gastrectomy, so early detection is vital.
It is rarely seen before 40 years of age, except in patients with familial hereditary gastric
cancer due to E-cadherin gene mutations. The incidence increases from the age of 55
years onwards and peaks in the sixth and seventh decades. The incidence of distal gastric
cancer in the UK and other post-industrial societies has been falling for 30 years, but at
the same time the incidence of proximal tumours in the gastric cardia, possibly due to
gastrointestinal reflux, has been rising.
The male–female ratio is 2:1.
The aetiology of distal tumours includes H. pylori infection, spicy food, polycyclic
hydrocarbons, high salt intake and tobacco smoking. For proximal tumours it is gastro-
oesophageal reflux disease (GORD).
Risk factors are atrophic gastritis; pernicious anaemia; previous partial gastrectomy;
adenomatous and regenerative polyps; familial polyposis; hypogammaglobulinaemia;
blood group A; type III intestinal metaplasia; and severe dysplasia.

Dysplasia
Dysplasia can be a marker of gastric cancer.
✧ Type A affects the metaplastic gastric epithelium and can lead to the development of
the intestinal type of gastric cancer.
✧ Type B arises in the non-metaplastic gastric epithelium and predisposes to diffuse or
intermediate gastric cancers.
History
Most patients present with dyspepsia, and dysplasia is detected during routine investiga-
tion. Some cases are detected by screening.
 STOMACH AND DUODENUM 89

Examination
A normal examination is a good sign. Look for evidence of malignancy such as epigastric
mass and weight loss.
Investigations
✧ Diagnose by OGD and biopsy for histology.
✧ Dysplasia is graded into mild, moderate and severe (carcinoma in situ).
Treatment
✧ Mild to moderate dysplasia requires regular OGD surveillance.
✧ For severe dysplasia a second OGD and biopsy is mandatory within a few weeks. If
severe dysplasia is confirmed, gastrectomy is advised.
✧ The histology of gastrectomy specimens shows that 40–50% have early invasive gastric
cancer.

Follow-up is at short intervals initially, until neoplasia is excluded. Regular OGD surveil-
lance to detect development of neoplasia and grade it is required.
Pathology of gastric cancer
The main classification of gastric cancers is into:
✧ intestinal type
✧ diffuse type.

Each is then classified into ‘well differentiated’, ‘poorly differentiated’ or ‘undifferentiated’.

The undifferentiated diffuse type is equivalent to linitis plastica.
There are no reliable serum markers of gastric cancer.
Early gastric cancer
Cancer limited to the mucosa and submucosa, regardless of nodal status, if completely
resected by gastrectomy has a five-year survival of 80%.
Endoscopic appearance may be protruding, superficial or excavated. At the time of
diagnosis, 10–15% of early gastric cancers have already spread to the lymph nodes.
Advanced gastric cancer
The tumour involves the muscularis propria. Advanced gastric cancer represents 95% of
gastric cancer diagnosed in the UK. Most have lymph node spread as well as peritoneal
and liver spread.
Staging of gastric cancer
This involves the TNM system. It describes: (T) the depth of the tumour’s penetration
into the stomach wall, (N) the involvement of local or distant lymph nodes and (M)
distant metastases.
Measurements are T1–4, N0–3 and M0–1 where N1 = 1–6 positive nodes, N2 = 7–15
positive nodes and N3 = more than 15 positive nodes.
Stage for stage, intestinal tumours have a better prognosis than diffuse tumours; well
differentiated tumours do better than poorly differentiated ones; and distally located
cancers do better than proximal ones.
Spread
Nodal spread to lymph nodes on the lesser and greater curves, the so-called D1 tier of
nodes, is common (stations 1–6). The second tier of nodes, the D2 group, includes those
along the left gastric artery, the coeliac trunk, the common hepatic artery and the splenic
90 GENERAL SURGERY OUTPATIENT DECISIONS

artery (stations 7–12a). Involved nodes beyond these locations are classified D3 and imply
incurability.
Para-aortic nodal disease, peritoneal metastases and spread to the liver or lungs are
incurable. Para-oesophageal nodes, if positive, usually count as distant metastases unless
the tumour is located in the gastric cardia, in which case they are counted as regional D1
nodes and cure is still achievable if all the disease is resected (an R0 resection).
History
Early disease is often asymptomatic, or presents with mild dyspepsia which responds
to acid suppression. Symptoms of malaise, early satiety, postprandial fullness, loss of
appetite and weight loss usually indicate advanced disease.
Cardia lesions may present with dysphagia; middle and pyloric tumours may
present with vomiting after meals. Advanced cases may present with haematemesis and
melaena.
The most common presentation is recent onset dyspepsia in someone over the age of 55.
Therefore all patients in this age group should have an urgent OGD before starting ulcer
treatment. Younger patients should also be scoped if they have unexplained symptoms
or persistent symptoms despite treatment. All patients with ‘alarm symptoms’ such as
anaemia or weight loss should undergo urgent upper GI endoscopy (see NICE Guidance
on Dyspepsia).
Examination
✧ No abnormal findings is a good sign.
✧ Anaemia often presents at diagnosis.
✧ Signs of weight loss, an epigastric mass and an enlarged left supraclavicular lymph
node indicate late disease.
✧ Jaundice, hepatomegaly or ascites indicate incurable disease.
Investigations
✧ OGD and multiple biopsies and brush cytology.
✧ CT of chest and abdomen.
✧ EUS for local staging of proximal tumours involving the cardia.
✧ Staging laparoscopy to exclude peritoneal and small liver metastases.
✧ PET-CT can be useful to help determine the nature of distant lesions seen on CT if
this is likely to radically change management (i.e. an adrenal metastasis).
Treatment
Treatment takes place in the setting of a multidisciplinary team.
Curative surgery
This should be performed in a high volume centre by a surgeon with appropriate training
who does this type of surgery frequently and who works as part of a multidisciplinary
team that can provide all aspects of specialist care 24 hours a day, 365 days of the year.
The aim of surgery should be to obtain a complete resection of the primary tumour
(R0); an adequate resection of regional lymph nodes (a minimum of 15 nodes for TNM
staging by D1 or D2 resection); and to provide patients with the best possible quality of
life. Open and close rates (failure of staging) and peri-operative mortality should both be
less than 5%. Patients with locally advanced disease should be considered for neoadjuvant
chemotherapy prior to resection.
Palliative treatment
Gastrectomy with palliative intent is rarely indicated. Incurable distal tumours causing
 STOMACH AND DUODENUM 91

outlet obstruction can be palliated by laparoscopic gastric bypass or endoscopic duodenal

stenting. Cardia tumours can usually be stented, and tumours of the gastric body may be
palliated by chemotherapy.
Chemotherapy
Cisplatin-based regimens can be used to shrink tumours prior to resection, increasing
the chance of an R0 resection, or as palliative therapy for patients with incurable disease.
Randomised controlled trials of palliative chemotherapy have shown a doubling of
survival from three to six months and improved quality of life.
Radiotherapy
Radiotherapy can be useful for palliation to reduce bleeding from an incurable tumour.
It is occasionally used as part of an adjuvant regimen of chemo-radiation post resection,
but it is poorly tolerated and is not routine in the UK.
Follow-up
Make a baseline CT scan at three months and again at one year. There should be further
CTs if there is any deterioration in clinical status. Perform examination and bloods three
times in the first year, twice in the second year and annually thereafter for five years, then
discharge. All total gastrectomy patients need B12 injections every three months.
Post-operative follow-up
Check histology to confirm complete excision and correct resection level. Arrange
oncology referral if appropriate. Follow up for complications of gastric surgery as
previously described.
Other tumours
✧ Other tumours include leiomyoma (benign) and leiomyosarcoma (malignant).
✧ Submucosal and intramuscular tumours occur in the upper and middle third of the
stomach.
✧ Ulceration and/or bleeding is a common presentation.
✧ They are treated by wedge resection if small or partial gastrectomy if large.

Gastric lymphomas (2–5%)

These are mainly B-cell non-Hodgkin’s lymphomas arising in the mucosa-associated
lymphoid tissue (MALT), or extra-nodal marginal zone B-cell lymphomas according to
the WHO classification. They are slow growing, remain localised until late and are less
aggressive than non-Hodgkin’s. They infiltrate the wall, producing mucosal thickening,
and may present with ulceration and bleeding. Lymph node spread occurs late and tends
to remain in regional lymph nodes.
History
✧ There are the usual dyspeptic symptoms, but nausea, vomiting and weight loss are
more common. Diarrhoea is often present.
✧ Some patients will present as emergencies with perforation or haematemesis.
✧ Pain, fever and anorexia may also be features.
Examination
A palpable epigastric mass may be present in 20% of patients and does not indicate
inoperability. However, hepatomegaly and/or splenomegaly suggest a diffuse process with
a worse prognosis, as does general lymphadenopathy.
92 GENERAL SURGERY OUTPATIENT DECISIONS

Investigations
✧ Faecal occult blood tests are positive in 50%.
✧ Erythrocyte sedimentation rate (ESR) is usually grossly elevated.
✧ Diagnosis is by OGD with cobblestone mucosal appearance and rugal hypertrophy,
multiple tumour nodules.
✧ Biopsies for histology are taken but may be negative in a large proportion of cases
due to the submucosal location of the tumour. Therefore, in the presence of a typical
appearance a negative histology result does not rule out the diagnosis. Repeat.
✧ OGD and deeper biopsies may be indicated.
✧ Endoscopic ultrasound is useful.
Staging
✧ Ann Arbor or TNM for gastric lymphoma.
✧ CT scan of the chest and abdomen is performed to detect spread.
✧ Bone marrow aspirate and biopsy may demonstrate diffuse disease.
✧ Laparoscopy is useful for stage III and IV and distinction between primary gastric
lymphoma and advanced primary nodal disease.
Treatment
Low-grade MALT lymphoma
If associated with H. pylori infection, this should be eradicated with triple therapy,
as many tumours will regress. If this fails, chemotherapy with cyclophosphamide,
doxorubicin, vincristine and prednisone (CHOP) regimen, with or without rituximab,
is indicated. Surgery is not indicated.
High-grade MALT lymphoma or diffuse B-cell lymphoma
This is also treated with chemotherapy. Surgical resection is reserved for treatment fail-
ures. Survival rates of greater than 90% can be expected with this approach.
Follow-up
There should be regular OGD review and follow-up by haematologists.
Gastric carcinoids
These tumours are associated with atrophic gastritis (type A) and chronic hypergastri-
naemia of pernicious anaemia. The incidence in pernicious anaemia patients is 2–9%.
More recently, fundal enterochromaffin tumours in Zollinger-Ellison patients have
been treated with omeprazole. The tumours produce gastrin, somatostatin, serotonin
and vasoactive invasive peptide. They are generally slow growing and indolent but can
metastasise if they exhibit abnormal cytology and are larger than 2cm.
History
✧ Rarely symptomatic.
✧ Usually diagnosed on endoscopy in investigation for dyspepsia.
✧ Other presentations include abdominal pain or evidence of gastrointestinal bleeding.
✧ The carcinoid syndrome can be produced by gastric carcinoids, but this is usually
endocrinologically silent unless associated with liver metastases. Typically, gastric
carcinoid produces bright red geographical flushing.
Examination
Examination may be normal, but examine for evidence of tumour and spread. Epigastric
mass and liver enlargement are late signs.
 STOMACH AND DUODENUM 93

Investigations
OGD with biopsy is usually diagnostic. Investigate for carcinoid syndrome if suspected.
Treatment
Treat with local resection (or endoscopic) followed by endoscopic surveillance.
Larger tumours require surgical excision, which may be possible laparoscopically.
Resection of the gastric antrum reduces the gastrin drive to the remainder of the
stomach.
Follow-up
Follow up at short intervals until diagnosis and treatment is performed. Tumours treated
by endoscopic resection require long-term endoscopic follow-up to detect recurrence.
Irresectable lesions require oncology referral for chemotherapy and, if necessary, treat-
ment of the carcinoid syndrome.
Post-operative follow-up
Check histology for resection. There may be complications of gastrectomy, as previously
described.
 The small intestine and vermiform appendix
Alastair Windsor
SIX

Introduction
The basic functions of the small bowel are digestion and assimilation. Most chronic
disorders of the small bowel tend to be managed by gastroenterologists with referral to
surgeons if surgery is indicated. However, some knowledge of these disorders is necessary
for the surgeon, especially in the case of small bowel inflammatory conditions such as
Crohn’s, small bowel tumours, and in the investigation of weight loss and diarrhoea,
which may be referred to the surgical clinic.

Assessment of small bowel disorders

Small bowel history
Take a general gastrointestinal history. There are no symptoms which exclusively indi-
cate small bowel disease, but small bowel disorders should be considered in patients
presenting with intermittent, colicky central abdominal pain. These symptoms may be
accompanied by diarrhoea, stool that are difficult to flush away and weight loss. Patients
may also complain of symptoms typical of anaemia. Intermittent small bowel obstruction
secondary to adhesions is very common after any abdominal surgery, so an enquiry about
previous operations is important. Patients may complain of regular vomiting 1–2 hours
after meals.
Small bowel examination
Perform a general examination. Examine for anaemia and weight loss. Examine the
mouth and pharynx for ulcers. Abdominal examination may reveal distension, scars from
previous surgery, tenderness or a mass. Rectal examination, sigmoidoscopy and biopsy if
indicated complete the examination.
Laboratory investigations
Full blood count (FBC) may reveal anaemia due to gastrointestinal (GI) bleeding or
chronic disease. Abnormal white cell count (WCC) may indicate infection or lymphoma.
Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may indicate
active inflammatory bowel disease.
Biochemistry
✧ Urinalysis: raised urinary levels of 5-hydroxyindoleacetic acid (5-HIAA) may indicate
carcinoid syndrome.
✧ Serum biochemistry: routine indications. Abnormalities of serum albumin, transferrin,
urea and electrolytes, including calcium, may occur in small bowel disease.
✧ Liver function tests (LFT): abnormal LFTs may be associated with inflammatory
bowel disease.
✧ Blood sugar tests: may reveal diabetes mellitus.
✧ Estimation of faecal fat: from a 3–5 day collection on a standard diet containing
80–100 g of fat. Normal excretion is less than 6.0 g/day (18 mmol triglyceride). This is
a non-invasive screening test for malabsorption.
Microbiology
Stool cultures are useful in various small bowel infections, e.g. Yersinia.

94
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 95

Cytology/histology – jejunal mucosal biopsy

The Crosby suction capsule is at the end of a fine-bore catheter. The patient swallows the
capsule and time is allowed for the capsule to be propelled into the jejunum, which is
confirmed by plain abdominal X-ray (AXR). The capsule is opened and suction applied
via the catheter. The capsule is then closed, taking a jejunal mucosa biopsy, and the
capsule is removed. The tissue is sent for histology.
This method is used for diagnosis of coeliac disease, Whipple’s, parasites and amyloid.
It is a random biopsy of jejunal tissue, not performed under direct vision. This technique
has largely been replaced by endoscopy and biopsy of the second part of the duodenum,
under direct vision.
Imaging techniques
AXR plain
An X-ray may identify dilated small bowel loops in obstruction, or thickened bowel loops
in inflammatory disorders.
Small bowel follow-through (SBFT)
The patient drinks radiological contrast. The path of the contrast through the stomach
and small bowel is followed at regular intervals by repeated X-rays. It is easier to perform
than small bowel enema but provides less detail of the small bowel due to dilution of
contrast, the time taken to empty from the stomach and overlapping bowel loops.
Small bowel enema (SBE)
Contrast medium is instilled through a Bilbao-Dotter tube directly into the upper
jejunum. It has a high diagnostic yield for small bowel tumours, Crohn’s, occult GI
bleeding and malabsorption. Malabsorption shows flocculation and segmentation of
barium, thickening of mucosal folds and dilatation of intestinal loops. There may be
difficulty swallowing the tube and passing the tube through the pylorus.
Small bowel magnetic resonance imaging (MRI)
MRI is performed with small bowel contrast using water or locust bean gum. Although
currently not universally used, the technique is increasingly being shown to be very
accurate at imaging the small bowel. Most of the work has been done in Crohn’s disease.
Its ability to indicate areas of inflammation may allow differentiation between fibro-
stenotic and inflammatory strictures.
Selective splanchnic angiography
An angiography catheter is passed, using the Seldinger technique, through the femoral
artery, and the catheter is manipulated through the aorta into the visceral arteries (coeliac,
superior mesenteric artery (SMA), inferior mesenteric artery (IMA). Radiological contrast
is injected. Certain appearances are characteristic of certain lesions, e.g. intraluminal
bleeding, tumour or stenoses/occlusions of the coeliac, or mesenteric arteries indicating
mesenteric ischaemia.
The technique allows identification of obscure GI bleeding not identified by oesophago-
gastro-duodenoscopy (OGD) or colonoscopy. It is diagnostic for angiodysplastic lesions
during active bleeding and may be useful for diagnosis of mesenteric ischaemia. It is an
invasive technique that can have complications associated with arterial puncture, e.g.
haemorrhage, haematoma, false aneurysm; and with the use of radiological contrast,
e.g. allergic reactions, renal failure.
Contrast CT
The patient drinks, or has instilled through a nasogastric tube, a special radiological
96 GENERAL SURGERY OUTPATIENT DECISIONS

contrast solution (E-Z-CAT®) to opacify the intestine. The patient is then passed through
the CT body scanner. The scan is useful for detecting thickening of the bowel wall and the
presence of enterocolic and enterovesical fistulas. It provides detailed information about
the small and large bowel, but it is expensive and time-consuming and it uses ionising
radiation.
Ultrasound scan
An ultrasound probe is passed over the abdomen using aqueous gel as a coupling
medium. Images of the underlying organs are formed from the differential amount of
ultrasound reflected from different organs. Using the Doppler Effect and colour coding,
blood flow can be imaged in major arterial and venous vessels. It is useful for detecting
fluid-filled loops of small bowel, detecting peristalsis, estimating bowel wall thickness,
detecting intra-abdominal fluid and detecting blood flow in major vessels.
Visualisation of the small bowel
Small bowel enteroscopy
A long endoscope is inserted into the duodenum, a balloon is inflated, and gut peristalsis
carries the scope to the caecum, as confirmed by X-ray screening. Inspection is made as
the instrument is withdrawn. It may be useful to visualise obscure bleeding but is not
widely available.
Capsule endoscopy (CE)
The PillCam video capsule contains a miniaturised camera, a light source and a wireless
circuit for acquisition and transmission of signals. The patient swallows a capsule and
the device is passively propelled through the gastrointestinal tract by peristalsis. Images
are transmitted to a data recorder and then downloaded to be reviewed on a monitor.
The capsule is passed in the patient’s stool usually in 24–48 hours. Currently, best
evidence for its use includes evaluation of patients with obscure bleeding, inflammatory
bowel diseases, suspected small bowel tumours, hereditary polyposis syndromes and
complicated coeliac disease. It cannot be used in patients with motility disorders or
mechanical obstruction.
Radioisotope techniques
Isotope scintigraphy
Isotope scintigraphy involves intravenous administration of a radio-labelled compound
or autologous cells. It may be useful to show occult GI bleeding, suspected intra-
abdominal localised inflammation/abscess, inflamed Crohn’s and intestinal transit time,
and also for evaluation of bilioenteric anastomoses. However, it requires radioactivity
and it poorly localises bleeding points or abscesses in the abdomen.
Small bowel transit time
This is shown by external scintigraphy after administration of isotope-labelled meals or
by breath tests. For meals the detection of caecal radioactivity is used as the end-point
for the estimation of small bowel transit time (includes gastric emptying time as well).
Breath tests are a simpler way of obtaining similar information.
White cell scan
Indium 111-labelled autologous leucocytes are injected intravenously and settle in areas
of abscess/inflammation. An abdominal scintiscan is performed at 2, 6, 20 and 24 hours.
The scan can be used to detect the extent and severity of inflammatory bowel disease.
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 97

Tests of small bowel function

Breath tests
Breath tests are used in the detection of bacterial overgrowth, the demonstration of
carbohydrate malabsorption and the assessment of small bowel transit time.
Bacterial overgrowth
The 14C-glycocholate breath test can show bacterial overgrowth in the small intestine.
Bacteria deconjugate the compound, which is absorbed into the bloodstream and
exhaled. It can also be positive in the presence of ileal disease, and in this circumstance
14C-D-xylose is more reliable.
Carbohydrate malabsorption
Ingestion of 14C-lactose is the conventional test for lactose intolerance, i.e. brush-border
lactase deficiency.
Hydrogen breath test for small bowel transit time and bacterial overgrowth
The hydrogen (H2) breath test is supplanting other tests for small bowel transit time.
Repeated measurements of H2O in end-expiratory air are taken after a drink of lactulose
or a meal of mashed potato and beans. When the meal reaches the caecum bacterial
fermentation occurs, resulting in increased breath H2.
The test includes gastric emptying time. If the meal is radio-labelled with technetium-
99m (99mTc), both gastric emptying and small bowel transit times can be calculated from
the one investigation.
Tests of intestinal permeability
51Cr-labelled EDTA is given orally. It is not absorbed in a healthy person. Urinary
estimation is performed and if EDTA is detected this indicates abnormal intestinal
permeability. It may be useful in the diagnosis of obscure cases of Crohn’s, but it is not
widely available.
Ileal malabsorption
The Schilling test shows the ability of the ileum to absorb vitamin B12.
The SeHCAT test assesses the ileal absorptive capacity for bile salts.
Investigation of specific small bowel abnormalities
Investigation of intestinal bleeding
Causes may be Meckel’s diverticulum, polyps and tumours – especially smooth muscle
neoplasms and vascular malformations.
Tests
OGD and SBE are usually negative. The use of radio-labelled red cells is suitable for
intermittent bleeding, but not for active rapid bleeding. For rapid bleeding, it is best to
use angiography and embolisation.
Investigation of suspected malabsorption
Malabsorption is either due to small bowel disease, bacterial overgrowth or pancreatic
exocrine insufficiency.
Tests
✧ The first test is for abnormal faecal fat excretion (greater than 6.0 g/day).
✧ For the second test give SBE. If it is normal, perform a mucosal biopsy, and if this is
98 GENERAL SURGERY OUTPATIENT DECISIONS

normal perform pancreatic function tests. If the small bowel enema is abnormal, a
mucosal biopsy can be performed, or proceed directly to the Schilling test and follow
with tests for bacterial overgrowth.

Syndromes resulting from disease or surgery on the gastrointestinal

tract
These syndromes include bacterial overgrowth (stagnant loop syndrome), short gut
syndrome and protein-losing enteropathy.
Bacterial overgrowth
The causes of bacterial overgrowth fall into two groups.
✧ Excessive entry of bacteria into the small intestine, caused by achlorhydria,
gastrojejunostomy, partial/total gastrectomy, enterocolic fistulas, cholangitis or loss
of ileocaecal valve following right hemicolectomy.
✧ Intestinal stasis, caused by Crohn’s disease (stenosis), TB (stenosis), small bowel
diverticulosis, afferent loop stasis, entero-enteric anastomosis and other intestinal
bypass procedures, subacute obstruction or blind loops. Also diabetes mellitus,
radiation enteritis, scleroderma and amyloidosis.
History
There may be asthenia, nausea and vomiting, excessive borborygmi or weight loss.
Diarrhoea is frequent and watery. Less common is steatorrhoea.
Examination
Look for glossitis, stomatitis, anaemia, hypoproteinaemia with peripheral oedema, tetany,
osteomalacia and rickets.
Investigation
Carry out 14C-glycocholate or 14C-D-xylose breath tests.
Treatment
Treatment is of the underlying condition. Surgery is not indicated because there
is widespread disease. Treat with intermittent courses of antibiotics. Neomycin or
metronidazole for 10–14 days may give symptomatic improvement for several months.
Fresh unpasteurised yoghurt or lactobacillus preparations should be given with and after
antibiotics to inhibit recolonisation.
Follow-up
Follow up long term at regular intervals, depending on the clinical condition.
Short gut syndrome
The causes of short gut syndrome include operations requiring extensive small bowel
resection, Crohn’s, mesenteric infarction, radiation enteritis, midgut volvulus, multiple
fistulas and small bowel tumours.
A small bowel that is less than 2 m long has a diminished work capacity and those with
less than 100cm require parenteral nutrition for life. Those with borderline length may
benefit from enteral feeding and/or additional intravenous fluids. Ileal resections are
less well tolerated than jejunal resections, largely because active transport sites for bile
salts and vitamin B12 are localised in the ileum. Efforts should be made to try to retain
a portion of the terminal ileum and the ileocaecal valve if possible.
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 99

Consequences of short gut syndrome

Short gut syndrome has a number of consequences.
✧ Malabsorption and malnutrition (also gastric hypersecretion – transient).
✧ Gallstone formation, mainly cholesterol stones due to decreased bile salts.
✧ Hepatic disease: fatty liver, onset of liver failure after jejunoileal bypass. If there is a
history, up to six months post-operatively, of flu-like illness, anorexia, nausea and
vomiting, weight loss and decreased serum albumin, it is an indication to restore
intestinal continuity.
✧ Impaired renal function and stone formation: diarrhoea and loss of electrolyte-rich
fluid leading principally to hyponatraemia. There may be metabolic acidosis and
formation of urinary calculi. Increased aldosterone leads to chronic hypokalaemia
causing muscle weakness, anorexia and cardiac arrythmias.
✧ Metabolic bone disease: hypocalcaemia and hypomagnesaemia are common. Treat
with 1-alpha-hydroxy-cholecalciferol.

History
Take a general small bowel history. Enquire about the causes of short bowel syndrome
and the consequences of it (see above).

Examination
Perform a general examination. Look for evidence of anaemia and weight loss. Examine
for evidence of the consequences of short gut syndrome.

Treatment
Support the patient until adaptation occurs – up to six months post-operatively. Give
parenteral nutrition in the immediate stage of 3–6 weeks’ transition to an oral diet. If one
metre of small bowel remains, a normal diet may be achieved. However, these patients
may require long-term enteral feed with polymeric or elemental formula diets and, on
occasion, additional intravenous fluid (saline). Supplements of calcium, magnesium and
vitamin C are needed, and in cases of ileal resection, Vitamin B12 injections are needed
every three months for life.

Follow-up
Follow-up is long term at regular intervals determined by the clinical condition. There
are the following possible complications.
✧ High output states: sodium and water can be lost in significant amounts. A combination
of oral fluid restriction, loperamide and, on rare occasions, infusion/subcutaneous
injection of long-acting somatostatin may be needed.
✧ Steatorrhoea: the cause is excess fat in the diet. Treat by substituting fat with medium
chain triglycerides which do not require the presence of bile salts for digestion.

Long-term treatments include combined hepatic and small bowel transplant or techniques
such as reversed antiperistaltic small bowel segment to decrease the diarrhoea. If the
patient is young and symptoms are not improving, transplantation may be considered.

Protein-losing enteropathy
The causes of protein-losing enteropathy include coeliac disease, Whipple’s disease,
bacterial overgrowth and inflammatory bowel disease (IBD).

History/examination
Usually the clinical picture is dominated by the underlying condition, but the loss of
100 GENERAL SURGERY OUTPATIENT DECISIONS

protein leads to hypoproteinaemia with secondary water and salt retention. Albumin and
immunoglobulin A (IgA) are depleted more than other larger proteins.
Investigation
Albumin labelled with iodine-131 or chromium-52 is injected intravenously and levels
are monitored for two weeks. A plasma die-away curve is plotted and faecal radioactivity
is measured. Daily enteric losses are calculated and excessive loss can be detected.
Treatment
Treatment is with albumin infusions or surgery of the underlying condition. A high-
calorie, high-protein diet is needed.
Follow-up
Follow-up is long term, at regular intervals determined by the clinical condition.

Vascular anomalies, hamartomatous lesions and vasculitic/connective

tissue disease (CTD) of gastrointestinal tract
Bleeding into the small intestine may be part of systemic vasculitic and connective tissue
disorders. The conditions in which intestinal involvement is common are polyarteritis,
Henoch-Schönlein purpura, pseudoxanthoma elasticum and Ehlers-Danlos syndrome.
Angiodysplasia
Angiodysplasia consists of clusters of arteriolar, venular and capillary vessels in the
mucosa and submucosa of the gastrointestinal tract, so it is not visible or palpable from
the outside. Rupture of the mucosal component causes bleeding. It commonly occurs in
the right colon but also occurs in the stomach and small intestine.
History
There is increased incidence in patients suffering from aortic valve disease and chronic
lung disease. Colonic lesions are commonest between ages 50–55, small bowel lesions
between ages 30–35. There is episodic or chronic occult GI bleeding over the years. It may
present as iron deficiency anaemia, overt melaena or acute haemorrhage.
Examination
Perform a general examination. Examine for signs of weight loss and anaemia. Examine
for general features of connective tissue disease. Abdominal examination may be normal
but rectal examination may reveal melaena.
Investigation
Use OGD and colonoscopy to locate or exclude these sites as the source of bleeding.
Colonic angiodysplasia is well visualised by colonoscopy as cherry red lesions similar to a
spider naevus. If the small bowel is suspected as the source, options include radionuclide
scan using 99mTc, Sc or 99mT-labelled red cells. Selective mesenteric angiography is useful
to demonstrate abnormal vessel patterns, even in the absence of active bleeding.
Treatment
Treatment is conservative, as blood vessels are involved. Endoscopy and diathermy are
especially useful in colonic lesions. Laparotomy with peroperative endoscopy can be used
to transilluminate the bowel and localise the lesion for excision.
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 101

Follow-up
Intervals should be short or the patient should be admitted for investigation until the
source of bleeding is identified. One this has been treated, follow up at regular intervals
(1–6 months) until further episodes are excluded.
Other causes of small bowel bleeding
Other causes of small bowel bleeding include the following.
✧ Phlebectasia: a meshwork of dilated veins in the submucosa frequently occurs in the
oesophagus, mid-small bowel and rectum, but they are a rare cause of bleeding.
✧ Haemangiomas (vascular malformations) occur in the small and large intestine.
Treatment is by either surgical excision or selective embolisation.
✧ Hereditary haemorrhagic telangiectasia – Peutz-Jeghers syndrome – causes bleeding
from polyps in the bowel. There is a risk of malignancy, so all polyps larger than 2cm
should be removed.
✧ Polyarteritis: systemic necrotising vasculitis with fibrinoid necrosis affecting blood
vessels of several organs including the gut. Weakened vessels lead to aneurysm
formation. They rupture, bleed and thrombose.
Inflammatory bowel disease (IBD)
Crohn’s disease
Crohn’s disease most commonly affects the terminal ileum, colon and rectum, stomach
and duodenum, and oesophagus, in that order.
A chronic granulomatous disease, it is a segmental condition with areas of involvement
strongly demarcated from the contiguous normal bowel. Oedema, sloughing and linear
ulceration lead to the formation of pseudopolyps and mucosa bridges. Ulcers are typically
deep, penetrate into the muscle layers (fissuring) and account for the tendency to localised
perforation, adhesions and fistula formation.
History
Crohn’s may present in a variety of ways and variable presentation often delays diagnosis.
It is commonest in the third decade of life, with abdominal pain that varies from dis-
comfort to severe and colicky. It is often associated with diarrhoea and weight loss.
There is early satiety or a sense of fullness. Abdominal distension occurs during bouts of
abdominal pain. Colonic rectal bleeding may present.
✧ Pseudoappendicitis syndrome shows acute abdominal pain. Remove the appendix if
caecum appears normal. Only one in eight cases of acute terminal ileitis are due to
Crohn’s. Always review the histology.
✧ Small bowel obstruction is usually partial or subacute. It is more commonly due to
adhesions or stricture. Early operation is advisable. Intermittent self-limiting episodes
invariably have gross bacterial overgrowth which may cause malabsorption.
✧ Abscess results from localised perforation or lymph node mass. It presents with local
signs and increased catabolism, weight loss, fever and anorexia. It is commonest
in the right iliac fossa. The abscess may track through to the pelvis and under the
inguinal ligament to the anterior compartment of the thigh. Free perforation causing
peritonitis is rare.
✧ A perianal fistula may present before intestinal disease. An enterocutaneous fistula
is classified as high or low output. Spontaneous closure with parenteral nutrition is
usually only possible with low-output fistulas.
✧ Diarrhoea is present in 70–80%. It is colonic, associated with mucus and blood. The
small bowel is associated, with protein-losing enteropathy and/or steatorrhoea due to
bacterial overgrowth or bile salt malabsorption.
102 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
Perform a general examination. Examine for evidence of anaemia and weight loss and
other systemic features of Crohn’s such as clubbing, proximal myopathy, easy bruising,
and, in toxic cases, raised temperature, tachycardia and oedema. Abdominal examination
may be normal or there may be evidence of a mass, particularly in the right side of the
abdomen. Examine the anus for fissures, fleshy skin tags and sinuses.
Investigations
These should be a combination of luminal investigation (usually endoscopic) with
appropriate histology, in association with raised inflammatory markers (CRP, ESR and
white cell count). In addition, a number of serological markers such as anti-Saccharomyces
cerevisiae antibodies (ASCA), antineutrophil cytoplasmic antibody (ANCA) and OMP-C
may provide additional information about disease severity. Demonstration of diseased
segments can be made by contrast radiology and/or MRI, showing narrowing of lumen,
nodularity of mucosal pattern, irregularity and deep ulcers or fistulas. The string sign may
be seen. Fistulas and sinuses are shown by injection of contrast +/– CT scans.
Treatment
The management of Crohn’s disease is dependent on the assessment of the disease loca-
tion and its severity. The therapeutic goals are to induce a clinical remission, to maintain
that remission and to prevent post-operative relapse.
Mild to moderate disease
The initial choice is 5-aminosalicylate (5-ASA), although there is little evidence to
support its efficacy. Budesonide seems to be as effective as prednisolone, with a reduction
in adverse effects. Metronidazole and ciprofloxacin regimens can give similar results to
5-ASA, particularly in Crohn’s ileocolitis and in perianal disease.
Moderate to severe disease
Steroids provide rapid remission but their use should be short and sharp to prevent
side effects. There is no role for steroids in maintenance of remission. Introduction of
immunosupression such as Azathioprine or Methotrexate will allow long-term control
of the disease.
Severe Crohn’s disease
Patients are admitted into the hospital. They require standard resuscitation and then
are treated with intravenous medication. Options include steroids, cyclosporine and
biological therapy such as infliximab.
Dietary manipulations
Evidence exists to support the use of an exclusive enteral diet in the management of mild
to moderate disease. This provides an equivalent, if slower, remission rate to that of oral
steroids. Compliance may be a problem.
Surgery
Common indications for surgery include:
✧ intestinal obstruction
✧ abscess formation
✧ fistula formation
✧ failure of medical treatment for limited disease
✧ need to raise an ileostomy to defunction diseased bowel
✧ nutritional failure
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 103

✧ small bowel perforation (rare)

✧ acute severe haemorrhage (rare).

Procedures are small bowel resection, strictureplasty and ileostomy.

Post-operative follow-up
Review with histology to confirm diagnosis and exclude other diagnoses, e.g. small
bowel lymphoma. Examine for any post-operative complications, including anastomotic
leakage resulting in fistula formation or intra-abdominal abscess. Long-term follow-up
is indicated to continue medical management in an attempt to reduce post-operative
recurrence.
Complications of surgical treatment in Crohn’s disease
The incidence of post-operative complications is 10–15%.
✧ Acute complications include anastomotic leakage, fistula formation, intra-abdominal
abscess and haemorrhage.
✧ Late complications are short bowel syndrome, urinary lithiasis, cholelithiasis, gastric
hypersecretion and peptic ulcer disease.

Recurrence after resection for small bowel resection is 30% at five years. Medical
treatment may influence the recurrence rate.
Short gut syndrome treatment options include home parenteral nutrition, small bowel
transplant or small bowel and hepatic transplantation.
Ileostomy care
Patients require adequate salt and water intake, as they typically lose 500 to 600 mls of
fluid and 40–50 mmols Na+ each day via the ileostomy.
Local complications of terminal ileostomies – stenosis, prolapse – may require revision
surgery.
✧ Peristomal irritation occurs in 20–40% but responds to regular cleaning and use of
skin barriers like Stomahesive or Comfeel.
✧ Para-ileostomy hernia in 5% leads to ill-fitting of appliance and leakage, and it may
cause internal strangulation. It may require surgical re-siting, but it tends to recur so
reserve this for the severe cases.
✧ Ileostomy diarrhoea: the causes include proximal stoma, partial obstruction, internal
abscess formation and recurrence of Crohn’s. Investigations include AXR, small bowel
enema (through stoma) and endoscopic examination through the stoma.
✧ Treatment of high output ileostomy (see short bowel syndrome).

Tumours of the small intestine

These are rare – fewer than 10% of all GI neoplasms.
Benign tumours
Most are detected as incidental findings at post-mortem. They include tubular and villous
adenomas, lipomas, haemangiomas and neurogenic tumours. Adenomas may also occur
in association with familial polyposis coli, Gardner’s syndrome (intestinal polyps and
epidermoid cysts), and Turcot’s syndrome (intestinal polyps and brain tumours). In
addition to the known risk of colonic carcinoma, these patients are liable to develop car-
cinoma of the duodenum and biliary tract. In the non-familial group, villous adenomas
are prone to malignant change.
104 GENERAL SURGERY OUTPATIENT DECISIONS

History
May present acutely as intussusception, or chronic bleeding causing iron deficiency
anaemia, or occasionally overt haemorrhage. Most are asymptomatic. Take a general
small bowel history. Enquire regarding the symptoms of anaemia, family history or
history relating to the rare causes outlined above.
Examination
Perform a general examination. Depending on the mode of presentation the examination
may be normal or there may be signs of anaemia and an abdominal mass. Rectal
examination may reveal melaena.
Investigations
Faecal occult blood test (FOB) may be positive for blood. Make OGD to exclude other
causes of GI bleeding and to diagnose duodenal tumours. SBE may demonstrate lesions
further down the small bowel. Use an ultrasound scan (USS) to detect lesions and
examine the liver to exclude metastases.
Treatment and follow-up
Treatment is by surgical resection. Follow-up is at short intervals until diagnosis is
obtained and malignant tumours are excluded.
Post-operative follow-up
Review the histology to confirm the benign nature of the tumour and ensure complete
excision. Detect complications related to laparotomy and small bowel resection.
Discharge once asymptomatic. Long-term follow-up is needed for Gardner’s and Turcot’s
syndromes.

Polyposis and duodenal tumours

Peutz-Jeghers syndrome
Background
Peutz-Jeghers syndrome is an inherited autosomal dominant polyposis syndrome.
Multiple hamartomatous polyps develop throughout the stomach and the small and
large bowel. Patients usually have speckled pigmentation around the oral and buccal
mucosa.
History
The polyps eventually produce symptoms such as obstruction or anaemia secondary to
chronic bleeding. Malignant change may occur in the polyps.
Investigation
Investigate with contrast radiology, endoscopy and capsule endoscopy.
Treatment
Surgery for small bowel polyps is indicated if the patient becomes symptomatic or the
polyps exceed 1.5cm in diameter. On-table enteroscopy with endoscopic snare resection
is the intervention of choice for small bowel polyps, as endoscopy can control colonic,
gastric and duodenal polyps.
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 105

Duodenal tumours
Background
Duodenal neoplasms are rare. They are most common in the first part of the duodenum.
The risk of malignancy increases as they become more distal.
History
Presentation is most commonly with gastrointestinal haemorrhage. Adenomas are
the most common tumours. Presentation may be with obstructive symptoms or an
abdominal mass.
Investigation
Investigate with endoscopy and cross-sectional imaging.
Treatment
If the lesion is resectable, pancreaticoduodenectomy is the procedure of choice. More
commonly, however, radical resection is contraindicated due to local invasion or meta-
static disease, and then palliation only is appropriate. This may involve biliary stenting
or surgical bypass if there is biliary obstruction, or a surgical gastrojejunostomy for
duodenal obstruction.
Duodenal disease in familial adenomatous polyposis
Background
Familial adenomatous polyposis (FAP) was previously known as familial polyposis coli, the
change in name reflecting the recognition of extracolonic polyps and cancers. Adenomas
tend to be noted in the duodenum approximately 15 years after colonic polyps occur.
Investigation
Investigate with regular endoscopy and biopsy. The severity of duodenal polyposis can
be quantified using a staging system developed by Spigelman and colleagues, which relies
on clinical and histological assessment of the duodenum to provide a four-stage scoring
system.
Natural history
Polyposis is associated with a high frequency of duodenal or periampullary cancer with
estimates of between 1 and 12%. These cancers are the commonest cause of death in
polyposis.
Treatment
Treatment is endoscopic surveillance with therapeutic options such as mucosal resection
and argon beam coagulation. Duodenectomy or pancreaticoduodenectomy is needed for
more advanced polyps and/or cancer.
Malignant small bowel tumours
These are rare and present late. They are adenocarcinoma (40%), carcinoid tumours
(30%), lymphoma (25%) and smooth muscle tumours (5%). Of the adenocarcinomas,
40% are duodenal, 40% jejunal and 20% ileal. Most duodenal carcinomas are found in
the periampullary region and in the third part of the duodenum. They spread to regional
lymph nodes, the liver and the peritoneal cavity.
Carcinoma in Crohn’s disease has a particularly poor prognosis. It occurs in the
40–50 year age-group. It is more common in males (3:1) and affects the ileum in 75%
of cases.
106 GENERAL SURGERY OUTPATIENT DECISIONS

History
They mainly occur in the over-60 age group. They present with epigastric or periumbilical
discomfort or pain. Pain is usually postprandial and colicky. There may be nausea and
vomiting and weight loss; GI bleeding; and intestinal obstruction or intussusception.
Duodenal carcinoma presents with obstructive jaundice.
Examination
Perform a general examination. Examine for evidence of anaemia or jaundice. The
abdominal examination may be normal, or there may be a mass or evidence of small
bowel obstruction. The liver may be enlarged due to metastases.
Investigations
Malignant tumours are diagnosed by OGD for the duodenum and by small bowel enema
for jejunal and ileal lesions.
Treatment
Treatment is by surgical resection. Small intestine adenocarcinomas do not respond to
chemotherapy or radiotherapy.
Follow-up
Intervals should be short (1–4 weeks) until diagnosis is obtained.
Post-operative follow-up
This should be long term, looking for signs of recurrence. Five year survival is 20–45%,
but better for duodenal tumours.
Carcinoid tumours
Classification
Carcinoid tumours are classified into three groups.
✧ Foregut – stomach, duodenum, pancreas, biliary tract and bronchus.
✧ Midgut – jejunum, ileum and right colon.
✧ Hindgut – left colon and rectum (do not secrete active peptides).

Foregut and midgut tumours may secrete almost any gut hormones and serotonin.
Tumours smaller than 1.0cm are rarely malignant; those 1.0–1.9cm may be malignant;
those greater than 2.0cm are invariably invasive and metastasise. Invasion occurs into the
bowel wall, mesentery and parietal peritoneum and adjacent organs. There is spread to
lymph nodes and the liver and less frequently to lungs and bones.
The commonest sites for tumours are the appendix, jejunoilium and rectum, in that
order.
History
The commonest age group is 45–55 years. Duodenal carcinoids present with vomiting or
bizarre endocrine syndrome. Jejunoileal carcinoids present with diarrhoea or intestinal
obstruction and/or a palpable abdominal mass. Appendix tumours present usually as
acute appendicitis. The presence of symptoms of the carcinoid syndrome indicates
advanced disease with extensive hepatic involvement.
Examination
Perform a general examination. Examine for presence of a tumour and metastases, e.g.
enlarged liver. Examine for carcinoid syndrome (see below).
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 107

Investigations
Carry out OGD, SBE and USS of the abdomen and liver. Measure urinary levels of
5-hydroxytryptamine (5-HT) (see below).
Treatment
Treatment by resection of the tumour, with wide margins of healthy tissue, regional
lymph nodes and associated mesentery is standard. External beam radiotherapy for
inoperable tumours has given disappointing results. Resectable hepatic deposits can be
treated by surgical resection. Debulking of the tumour may help distressing symptoms.
Follow-up
Follow-up is at short intervals (1–4 weeks) until diagnosis is obtained.
Post-operative follow-up
This should be long term to detect recurrence or onset of carcinoid syndrome. Many
patients survive long periods despite the presence of residual or metastatic disease. There
is 60% five-year survival.
Carcinoid syndrome
Carcinoid syndrome is rare, affecting 10% of carcinoid tumours. It indicates advanced
disease with extensive hepatic involvement. Inappropriate secretion of 5-HT and other
vasoactive substances is responsible for the symptoms.
History
Patients may describe several types of flushing syndromes – cutaneous flushing affecting
the upper part of the body and accompanied by sweating, itching, oedema, palpitations
and hypotension. Patients may also complain of intestinal colic and diarrhoea, broncho-
spasm and hypoproteinaemia and oedema. Other presentations include cardiac lesions,
tricuspid insufficiency or pulmonary stenosis, photosensitive dermatitis, neurological
signs, peptic ulceration and arthralgia.
Examination
Perform a general examination. Examine for evidence of flushing and/or dermatitis and
oedema. Examine the chest for presence of cardiac lesions and bronchospasm. Examine
the abdomen for evidence of a tumour and/or metastases or an enlarged liver. Perform
a neurological examination.
Investigations
Look at urinary levels of the metabolite 5-hydroxyindole acetic acid (5-HIAA). Take a
USS of the liver and perform investigations for a carcinoid tumour as described above.
Treatment
Carry out surgical resection/debulking covered by antiserotonin therapy with cyprohep-
tadine and parachlorophenylalanine. Also use selective arterial embolisation (cover with
antibiotics and methylprednisolone).
Chemotherapy uses cyclophosphamide, Adriamycin and 5FU, which are given
intravenously or by infusion into the hepatic artery using implantable reservoirs. Use
somatostatin and antiserotonin drugs.
Follow-up
Follow-up is long term at regular intervals determined by the clinical condition.
108 GENERAL SURGERY OUTPATIENT DECISIONS

Primary gut lymphomas

Characteristically, primary gut lymphomas of the small bowel are seldom diagnosed pre-
operatively and at operation may be confused with Crohn’s disease. When gut lymphoma
is diagnosed, one of the first tasks is to determine the type of lymphoma and whether
this primarily affects the bowel or whether the bowel is involved as part of a systemic
lymphoma.
Criteria for diagnosis of primary gut lymphomas
✧ No palpable superficial lymphadenopathy.
✧ No mediastinal lymph nodes on CT or CXR.
✧ Normal white cell count, normal bone marrow.
✧ Patients present with GI symptoms.
✧ Bowel lesions predominate at laparotomy and only regional lymph nodes (LN) are
involved.
✧ Liver and spleen are not involved.

Primary gut lymphoma is rare. Predisposing conditions include immunoproliferative

small intestine disease (IPSID), ulcerative colitis, Crohn’s disease, AIDS and other
immunodeficiency states.
Site
Primary gut lymphoma arises in the following sites: duodenum 8%, jejunum 33%, ileum
59%, more than one site 32%.
Type of lymphoma
Hodgkin’s lymphoma accounts for less than 1% of gut lymphomas. Non-Hodgkin’s
lymphoma accounts for the vast majority – mostly B-cell lymphoma (mucosa-associated
lymphoid tissue (MALT) lymphomas).
Histological grading
Polymorphic B-cell lymphomas stay localised. They are classified into high grade and low
grade and they metastasise late. There are many different types. Centrocytic lymphomas
are characterised by wide and extensive mucosal involvement and are therefore not
controlled by surgery – treatment is by chemotherapy. T-cell lymphomas also occur.
There are many types, differentiated into high grade and low grade.
Staging
This is modified Ann Arbor.
✧ Stage I: disease confined to one extralymphatic site.
✧ Stage II: localised involvement of one organ site and involvement of a group of
regional lymph nodes on one side of diaphragm.
∝ II1 – regional adjacent lymph node involvement.
∝ II2 – regional but non-confluent lymph node involvement
✧ Stage III: localised involvement of organ or site plus involvement of lymph node.
✧ Stage IV: diffuse disseminated disease with involvement of more than one organ and
lymph node enlargement.
History
Lymphomas occur at any age except infancy. There is a peak in the sixth decade and a
small peak in the first to third decades. They often present as an emergency with intestinal
obstruction, haemorrhage or perforation. Chronic symptoms are malaise, abdominal
pain, weight loss, diarrhoea/steatorrhoea and anaemia (may be normochromic). There
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 109

may be a previous history of coeliac disease, previously controlled, with symptoms

returning usually in the fifth to seventh decade.
Examination
Perform a general examination. Examination may be normal or there may be evidence
of weight loss and anaemia. Examine all lymph node sites and examine the abdomen for
hepatosplenomegaly. An abdominal mass may be present.
Investigations
Look for ESR increase and hypoproteinaemia. Take a FBC to detect raised WCC. Most
cases are diagnosed on SBE, USS or CT. Occasionally laparoscopy and biopsy provides
the diagnosis. IPSID abnormal alpha chain is diagnosed by immunohistochemistry of
tumour sections.
Treatment
✧ For the acute, disease treatment is by resection of disease with post-operative
chemotherapy.
✧ Elective surgery is followed by chemotherapy/radiotherapy for stage I and stage II.
Chemotherapy alone is used for more advanced disease.
Follow-up
Follow-up is at short intervals until diagnosis is obtained (1–4 weeks).
Post-operative follow-up
Review with histology and liaise with oncologists. Complete the grading and staging
procedure. Detect early complications related to laparotomy and small bowel resection.
Gastrointestinal stromal tumours
Background
These were previously known as leiomyoma and leiomyosarcoma.
History
In the 60–70 age group, with a long history of bleeding, abdominal pain, anaemia and
weight loss. Repeated episodes of melaena (or haematemesis). They are 60% gastric, 40%
small bowel, rare elsewhere.
Examination
There is a palpable mass in one-third of patients.
Investigations
Use cross sectional imaging, such as CT or MRI.
Treatment
Treat with surgical excision for local disease. Non-resectable or metastatic disease
responds to tyrosine kinase inhibitors.
Post-operative follow-up
Review with histology to confirm diagnosis and that there is adequate resection.
Thereafter follow up long term to detect recurrence.
110 GENERAL SURGERY OUTPATIENT DECISIONS

Chronic infective/inflammatory conditions of the small bowel

Yersinia
Yersinia is one of the most common and clinically important infections. In the acute
phase the differential diagnosis includes Salmonella and Campylobacter, which also may
become chronic infections.
History/examination
The acute condition is self-limiting. The chronic disease in children may simulate Crohn’s
disease. There is a swollen terminal ileum and colon exhibiting ulcerated, nodular and
cobblestone change.
Investigations
It is diagnosed by recovery of the organism from stool. It also causes a pseudoappendicitis
syndrome in older children and adults. SBE may exhibit typical Crohn’s type changes.
At operation the terminal ileum and lymph nodes are inflamed and oedematous. Send
lymph nodes for culture.
Treatment
Yersinia usually resolves and never progresses to Crohn’s.
Intestinal tuberculosis (TB)
There are four macroscopic forms: hypertrophic, ulcerative, fibrotic and ulcerofibrotic.
✧ Hypertrophic shows thickening of the terminal ileum and colon. There is recent
subacute obstruction, pain and vomiting.
✧ Ulcerative affects the terminal ileum: there are deep ulcers which may reach serosa and
perforate. There is subacute obstruction and pain, vomiting and constipation.
✧ Fibrotic is in the terminal ileum, caecum and ascending colon. There is shortening
and narrowing of segments.
✧ Ulcerofibrotic is a combination of ulcerative and fibrotic subtypes.

History
Take a general small bowel history. It mainly occurs in children and young adults – 25%
have co-existing pulmonary disease and give a history of chronic ill health, malaise,
anorexia, fever, night-sweats, dyspepsia and weight loss.
Examination
Perform a general examination. Examine for evidence of weight loss and general debility.
Examine lymph node fields and the chest for evidence of systemic TB. Examine the
abdomen for abdominal masses or intestinal obstruction (may be normal).
Investigations
Mantoux test may be negative. Try to culture TB from gastric washing, faeces and peri-
toneal fluid and lymph node biopsy. AXR may show extensive calcification. Barium
studies have the above changes according to the type of intestinal TB, but the changes
may be indistinguishable from Crohn’s. Laparoscopy and sampling of peritoneal fluid
may be required for diagnosis.
Treatment
In the absence of obstruction or perforation give chemotherapy for 12 months.
Surgery (e.g. right hemicolectomy) is needed for complications and failure of medical
therapy.
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 111

Follow-up
Follow up at regular intervals, e.g. three-monthly during the first eighteen months, to
detect obstruction, perforation or intra-abdominal abscess formation. Discharge when
the patient has finished chemotherapy and remains asymptomatic.
Actinomycosis
Actinomycosis is rare – diagnosis usually follows perforated appendix.
History/examination
The patient presents some weeks after appendicectomy with abscess and sinus formation
and fixed indurated mass in the right iliac fossa. It may progress to abscesses in the
liver.
Investigations
Do a FBC; microbiology of pus; and a USS of mass and liver.
Treatment
Treatment is prolonged therapy with penicillin and lincomycin.
Follow-up
Follow up at regular intervals until the patient is off all treatment and asymptomatic.
AIDS, opportunistic small bowel infection and HIV-1 enteropathy
Small bowel infections are extremely common in AIDS. They are mostly due to
opportunistic ulceration with protozoa, bacteria, viruses and fungi. In some 30% no
pathogen is identified – this is AIDS enteropathy.
History/examination
There is diarrhoea, weight loss and abdominal pain.
Investigations
Investigate with sigmoidoscopy and stool cultures.
Treatment
For bacterial infection, treat with antibiotics. Otherwise give symptomatic treatment
with loperamide.
Follow-up
Follow up in conjunction with a specialist AIDS clinic. Make regular stool cultures and
sigmoidoscopy until asymptomatic then discharge to a specialist AIDS clinic.
Radiation-induced bowel disease
Symptoms are encountered in most patients during the first few weeks of radiotherapy
– they include anorexia, nausea and vomiting and central nervous system (CNS) effects
and they should settle.
In true radiation-induced disease the interval may be from two months to two years
after radiotherapy.
History/examination
There is vague abdominal discomfort, diarrhoea, mild rectal bleeding and passage of
mucus. Intestinal obstruction may be acute, subacute or recurrent.
112 GENERAL SURGERY OUTPATIENT DECISIONS

Investigations
Investigations include SBE, barium enema, malabsorption studies, flexible sigmoidoscopy
and colonoscopy.
Treatment
Treatment should be conservative whenever possible, including correction of nutritional
deficiencies. Use Lomotil, Salazopyrin and steroids. Give Predsol enemas for radiation
proctitis; antibiotics for bacterial overgrowth; and bile-salt binding agents for ileal disease.
Dietary management includes elemental diets. If there is extensive disease it requires
intermittent or indefinite total parenteral nutrition (TPN).
Surgical resection is used in localised disease. Protect anastomoses with a stoma. For
fistulas and extensive disease carry out a complete bypass and exclusion of the diseased
segment – these procedures can be safer than resection.
Follow-up
Follow-up is long term at regular intervals until the patient is asymptomatic or symptoms
are well controlled.
Appendicitis follow-up
Objectives
The main objectives of the follow-up visit after surgery are the detection of post-operative
complications and the exclusion of underlying pathology such as inflammatory bowel
disease or tumours of the appendix. Always ensure that you have read the histology report
before you see the patient. Complications include:
✧ chronic wound infection
✧ abscess/mass in right iliac fossa (RIF)
✧ faecal fistula
✧ intraperitoneal abscess formation – solitary (pelvic/subphrenic) or multiple small
loop abscesses
✧ recurrent intestinal obstruction – late complication secondary to adhesions
✧ pylephlebitis (portal pyaemia).

Superficial chronic wound infection that has not responded to antibiotics may indicate a
stitch sinus, which can be treated by exploration of the wound either in the clinic or as a
day-case. It is a local anaesthetic procedure and the residual stitch material is removed.
Deeper chronic wound infection, or the presence of a mass or faecal fistula, may
indicate the presence of an underlying condition such as Crohn’s, a tumour or chronic
infective inflammatory conditions.
Inflammatory bowel disease
The histology report may describe changes suggestive of Crohn’s disease. In this situation
a full assessment for Crohn’s is required, including SBE (see Crohn’s section).
Tumours of the appendix
This includes carcinoids, adenocarcinoma, mucinous neoplasm and lymphoma. Assess
according to the relevant section.
Carcinoid
Carcinoid usually occurs at the tip. There is invasion of muscularis mucosa in 30% but
nodal and distal metastases are rare. Appendicectomy is usually curative but assess as
described in the section on carcinoid.
 THE SMALL INTESTINE AND VERMIFORM APPENDIX 113

Adenocarcinoma
Adenocarcinoma is rare. It may present as acute appendicitis or intestinal obstruction.
The correct treatment is right hemicolectomy.
Mucinous neoplasm
This is a simple mucocele where there is obstruction but no infection. The lesion may
calcify.
Chronic appendicitis
There is some controversy as to whether this condition exists, but removal of the appendix
appears to be gaining in popularity when combined with a diagnostic laparoscopy and is
successful in relieving the symptoms in a number of patients.
History
There are episodes of recurrent right iliac fossa pain. They may be severe and debilitating.
Pain is often colicky in nature but the patient appears otherwise well. Take a full gastro-
intestinal and gynaecological history. In particular, enquire about bowel habits. Consider
irritable bowel syndrome – ask regarding symptoms in other body systems suggestive of
this, e.g. intermittent dysphagia.
Examination
Perform a general examination. This is usually normal. Examine for abdominal
masses and tenderness. Perform a rectal examination and arrange for a gynaecological
examination.
Investigations
Carry out routine biochemistry and haematology plus investigations to exclude
inflammatory bowel disease and gynaecological disease in females. The main finding in
chronic appendicitis may be that a barium enema is normal but the appendix does not
fill because the appendix is often long fibrotic and contains faecoliths.
Diagnostic laparoscopy combined with appendicectomy is an alternative to invasive
radiological investigations.
Treatment
Give conservative treatment; or laparoscopic appendicectomy if other pathology has
been excluded.
Follow-up
Follow up at regular intervals as determined by the severity and effect of the symptoms,
until serious causes are excluded. Then either provide treatment for the specific disorder;
discharge with advice; or proceed to laparoscopic appendicectomy.
Post-operative follow-up
Review with histology. If it is normal, discharge with advice and reassurance.
Meckel’s diverticulum
Meckel’s diverticulum arises from the antimesenteric border of the ileum, within 90cm
of the ileocaecal valve. It is a true diverticulum, i.e. it contains all three layers of bowel
wall. There is ectopic tissue (gastric, pancreatic, duodenal, colonic) in 50–70% of cases.
Ulceration of ectopic gastric mucosa may cause copious rectal bleeding.
114 GENERAL SURGERY OUTPATIENT DECISIONS

History
Take a general small bowel history. Most are asymptomatic. However, the patient may
complain of symptoms similar to peptic ulceration but in a different abdominal site;
intestinal colic; or intermittent GI bleeding or melaena. Unexplained anaemia may be
another presentation. It may present acutely as acute appendicitis or perforation.
Examination
Perform a general examination. Examine for evidence of anaemia and abdominal
tenderness. Occasionally there may be an inflammatory mass to palpate but examination
is often normal.
Investigations
Ectopic gastric mucosa can be identified by 99mTc scan.
Treatment
If there is an uninflamed Meckel’s at laparotomy with a wide base and normal to
palpation – leave it. If there is a narrow neck, or it is nodular, chronically inflamed or has
faecoliths – excise. Symptomatic Meckel’s require excision.
Follow-up
This should be at short intervals until diagnosis is obtained and other causes excluded.
Post-operative follow-up
Review with histology and ensure that all ectopic mucosa has been excised. Check for
post-operative complications associated with laparotomy and small bowel resection.
Discharge the patient once they are recovered and asymptomatic.
The spleen and lymph nodes
Neville Jamieson

SEVEN
The spleen
The spleen has important haematological and immunological functions. However,
the main involvement of the surgeon is to remove the spleen. One of the commonest
indications for removal of the spleen is trauma, which seldom presents to the outpatient
department. However, patients return to the surgical clinic following splenectomy and it
is important to have an appreciation of the implications of the long-term management
of the asplenic patient. In particular, trauma patients are young, fit individuals who had
an otherwise healthy spleen removed, so no other clinical specialities (e.g. haematology)
will have been involved. Splenectomy is also performed as an intentional part of resection
for other pathologies, e.g. carcinoma of the stomach. In this instance, as well as managing
the primary condition the effects of splenectomy must also be considered. The spleen
may also be removed during operations on the pancreas or, less commonly, as part of the
treatment of portal hypertension.
In other situations the patient will be referred from another speciality for consideration
of splenectomy because the spleen itself is diseased or involved in a disease process, or
because it is adversely affecting haematological function.
In the commonest diseases to affect the spleen, enlargement occurs (splenomegaly)
and a common result of this enlargement is that the spleen becomes overactive (hyper-
splenism). The commonest clinical features of a diseased spleen are splenomegaly and an
abnormal blood film result. Key to understanding these disease processes and the effects
of splenectomy is an understanding of the normal function of the spleen and the effect
of an overactive or underactive spleen.
Haematological function
The spleen removes fragmented, damaged or senescent red blood cells (culling). It removes
mature red blood cells (target cells – high membrane to intracellular haemoglobin).
It removes intra-erythrocytic inclusions (pitting), e.g. Howell-Jolly bodies (nuclear
remnants), siderotic granules (haemosiderin) and Heinz bodies (aggregates of denatured
haemoglobin (Hb)). It removes irregular-shaped red blood cells (acanthocytes, irregular
crenated cells and target forms). All of these appear in the bloodstream after splenectomy.
Within its volume is a large number of sequestered platelets.
Following splenectomy there is a transient thrombocytosis. There is no haemopoiesis
after foetal life unless the bone marrow becomes diseased, e.g. myelofibrosis.
There is storage of iron and factor VIII.
Immunological function
The spleen is involved in antibody production and cell-mediated responses. It is
important for phagocytosis and the maturation of lymphoid cells, and it is significant in
lymphopoiesis.

Clinical manifestations of splenic disorders

Most common splenic disorders cause pathological destruction or pooling of blood
elements. Splenic enlargement, as occurs with venous thrombosis and congestion, causes
entrapment and pooling resulting in destruction of normal cells.

115
116 GENERAL SURGERY OUTPATIENT DECISIONS

Hypersplenism
Hypersplenism is splenomegaly plus decreased numbers of circulating blood elements
(anaemia, leucopenia and/or thrombocytopenia). This is different from ‘work hypertrophy’,
where the spleen enlarges due to constant exposure of the spleen’s phagocytic mechanism
to abnormal cells. Hypersplenism leads to a decreased number of normal cells. If the bone
marrow cannot compensate, the patient becomes anaemic.
Splenomegaly
Causes of splenomegaly include the following.
✧ Infections:
∝ acute (mononucleosis, septicaemia)
∝ subacute (bacterial endocarditis, tuberculosis (TB), brucellosis)
∝ chronic (fungal diseases, syphilis, bacterial endocarditis).
✧ Congestive in a setting of portal hypertension due to:
∝ cirrhosis of all causes
∝ prehepatic portal hypertension
∝ posthepatic
∝ segmental portal hypertension usually due to splenic vein occlusion as a result of
inflammation (post severe pancreatitis) or tumour.
✧ Haematological:
∝ haemolytic disorders
∝ myeloproliferative (myeloid metaplasia, essential thrombocythaemia)
∝ miscellaneous (megaloblastic anaemia).
✧ Malignant:
∝ haematological (acute or chronic leukaemias, lymphomas)
∝ intrinsic malignancies (primary – lymphosarcoma, plasmacytoma, fibrosarcoma;
secondary – carcinoma, melanoma; benign – hamartoma).
✧ Inflammatory or granulomatous: Felty’s, systemic lupus erythematosus (SLE),
rheumatoid arthritis.
✧ Storage: Gaucher’s, Wilson’s.
✧ Miscellaneous: cysts, parasitic and non-parasitic. Other causes, e.g. amyloid,
hyperthyroidism.
Hyposplenism
The causes of hyposplenism include the following.
✧ Splenectomy.
✧ Splenic agenesis.
✧ Atrophy: coeliac disease, dermatitis herpetiformis, sickle cell anaemia, thrombo-
cytopenia, SLE.

Assessment of splenic disorders

The main purpose of the assessment is to determine whether the spleen is enlarged
because of a primary disorder or because it is involved in a generalised disease process.
Therefore, assessment may also involve a haematological investigation, investigation
of hepatobiliary disease and portal hypertension (ultrasound and oesophago-gastro-
duodenoscopy (OGD)) and investigation of the causes of lymphadenopathy (lymph
node biopsy).
Splenic history
The patient may be asymptomatic with regard to the spleen; or be referred from another
speciality with the diagnosis already made; or be referred from the GP because of
 THE SPLEEN AND LYMPH NODES 117

detection of an abdominal mass. Occasionally if the spleen is very large the patient may
complain of a heaviness in the left subcostal region, especially on exercise. The patient
may complain of weakness, tiredness or lethargy due to anaemia or may complain
of haemorrhage or the appearance of skin purpura or ecchymoses related to other
haematological abnormalities.
Further questioning is directed at differentiating the common causes of splenomegaly
as outlined above. Remember to ask about other diseases, family history, drug history
and travel abroad.
Splenic examination
Perform a general examination looking for any of the causes of splenic enlargement.
Look for evidence of haematological abnormalities, e.g. purpura, ecchymosis, lym-
phadenopathy, signs of liver disease and portal hypertension. Examine the abdomen.
Differentiate splenic from renal enlargement and other abdominal masses, e.g. stomach,
colon. Features of an enlarged spleen are that the examining hand cannot get above it;
there is a notched anterior border; it enlarges towards the right iliac fossa; and there is
usually an absence of bowel gas in front of it (unlike the kidney). With a renal mass the
kidney moves downwards on respiration and organ shapes are different. Examine for
liver enlargement and the presence of ascites. Rarely, auscultation may reveal a rub when
there is a splenic infarct.

Investigation of splenic disorders

Laboratory investigations
Haematology
Full blood count and blood film provide information on the number of blood cells
circulating and the presence of abnormal cell types (as described above).
✧ Hypersplenism results in anaemia, leucopenia and/or thrombocytopenia.
✧ Hyposplenism results in abnormal red blood cells (Burr cells, target cells, pitted
cells); red cell inclusions (Howell-Jolly bodies, siderotic granules); abnormal platelet
morphology; thrombocytosis; and leucocytosis (neutrophilia, lymphocytosis,
monocytosis).

Tests of clotting, haemolysis and bone marrow aspiration/biopsy are part of the haematol-
ogy work-up. Refer if initial blood results indicate a possible haematological disorder.
Biochemistry
Liver function tests (which include a clotting profile) may indicate underlying liver
disease.
Immunology
Look at autoantibodies as a cause of haemolytic anaemia. Investigate rheumatoid
arthritis, Felty’s syndrome and SLE.
Lymph node biopsy
Investigation of lymphadenopathy associated with splenomegaly.
Imaging techniques
Abdominal X-ray (AXR)
AXR may show an enlarged soft-tissue shadow or calcification in the spleen, which may
represent old infarcts, hydatid cyst or TB.
118 GENERAL SURGERY OUTPATIENT DECISIONS

Ultrasound scan (USS)

This is the first-line investigation for differentiating splenic from renal enlargement. It is
good for detecting all forms or splenic enlargement, e.g. splenic cysts. It can also detect
other disease processes, e.g. portal hypertension, ascites, liver enlargement.
Computed tomography (CT) scan
This may give better visualisation of the spleen than USS, especially in the presence of
ascites or obesity. It is particularly useful for the detection of intra-abdominal lympha-
denopathy. However, it is expensive and involves the use of radiation.
Magnetic resonance imaging (MRI) scan
MRI may give better visualisation of the spleen and additional definition of tissues, but
it is expensive and time-consuming, with limited availability.
Radioisotopes
Technetium-99m-labelled colloid can be injected into the patient and scanned by a gamma
camera to detect the position and size of the spleen or to detect accessory spleens. Some of
the patient’s own red blood cells are heat damaged and then labelled with 51Cr; or platelets
are labelled with indium-111; and they are reinjected. Scans with a gamma camera are
performed after hours or days to provide information about the sequestration of these
elements in the spleen. The method provides quantifiable information on the activity of
the spleen. It uses radioactivity, albeit in small doses, and is becoming less common.
Indications for splenectomy
Definite indications for splenectomy
These include the following.
✧ Neoplasms of spleen (primary, lymphomas, benign).
✧ Splenic abscess (not small septic emboli).
✧ Echinococcal cysts.
✧ Splenic vein thrombosis with segmental portal hypertension and resulting gastric
varices.
✧ Splenic artery aneurysm (asymptomatic splenic artery aneurysm less than 1.5cm
diameter can be observed – rupture is common during pregnancy).
✧ En bloc resection of adjacent neoplasm.
✧ Non-salvageable splenic injury.

Splenectomy is desirable
Indications include the following.
✧ Hereditary spherocytosis.
✧ Idiopathic thrombocytopenia purpura.
✧ Autoimmune haemolytic anaemia, genetic defects of red cells, e.g. pyruvate kinase
deficiency.
✧ Gastro-oesophageal devascularisation procedures for oesophageal varices.

Splenectomy is debatable
The necessity for splenectomy is debatable for the following.
✧ Small splenic cyst – may be observed if less than 5cm diameter.
✧ Small pseudocyst.
✧ Thalassaemia syndromes.
✧ Lymphoma and specific cytopenia or pancytopenia.
✧ Thrombotic thrombocytopenia purpura.
✧ Myeloproliferative disorders.
 THE SPLEEN AND LYMPH NODES 119

Pre-operative preparation
Check full blood count (FBC), clotting and liver enzymes. Platelet transfusion may be
needed intra-operatively to correct thrombocytopenia (platelets are not usually given
until the spleen has been devascularised, as otherwise they will simply disappear into the
spleen and be ineffective – discuss with haematology).
If thrombocytopenia is due to immune disease, do not give platelet infusion. Give
human immunoglobulin (IgG) to increase platelets. Correct coagulopathies with fresh
frozen plasma or cryoprecipitate.
Post-operative follow-up
Following splenectomy, patients are reviewed six weeks after leaving hospital. They are at
specific risk of sepsis due to capsulated bacteria and they require appropriate prophylaxis.
Ideally, Haemophilus influenzae type b (HIB), Meningovax and Pneumovax vaccinations
should be given prior to surgery, but if not given pre-operatively they may be given post-
splenectomy once the patient is stable. Patients should also receive long-term low-dose
antibiotic prohylaxis (usually with penicillin/amoxycillin or erythromycin in sensitive
patients); be advised to have annual flu vaccinations; and take advice about additional
prophylaxis if travelling to malarial areas. They should be advised to seek early medical
advice should they become unwell. Most hospitals will now have a written protocol and
patient advice sheet.
Early complications
Early complications include bleeding and left subphrenic collection. Immediately follow-
ing splenectomy, thrombocytosis is common, with an increased risk of thrombotic
events. The platelet count should be monitored daily and will usually rise for a number
of days before falling back to normal values. In addition to standard thrombo-embolic
prohylaxis, if the platelet count increases to more than 1000 × 109/dl give an anti-platelet
agent such as low-dose aspirin or an alternative (Persantin, clopidogrel).
Necrosis of the greater curve of the stomach due to poor surgical technique is a rare
complication that may lead to subphrenic abscess and/or fistula.
Trauma to the tail of the pancreas leads to subphrenic fluid collections, abscess or
pancreatic fistula. Diagnose by USS or CT scan and treat by percutaneous drainage under
imaging.
Late complications
Late complications include migrating thrombophlebitis or deep-venous thrombosis
(DVT) caused by thrombocytosis. It needs long-term anticoagulant therapy. Recurrence
of presenting symptoms may mean retained accessory spleen. Image with radio-labelled
nuclear scan and plan curative surgical resection.
Remember to educate the patient regarding overwhelming post-splenectomy infection
(OPSI) and meningococcal, pneumococcal and H. influenzae vaccination. Make sure they
have an advice sheet. Consider the possibility of a MedicAlert® bracelet.
Postsplenectomy sepsis
Increased risk and incidence is related to the indication for splenectomy. Trauma has
a low risk with an incidence of 1–2%; thalassaemia has an incidence of 25%. Strep
pneumonia is responsible for over half of all septic episodes, Escherichia coli, H.influenzae
and Neisseria meningitidis for most of the rest. The mechanism responsible is thought
to be impaired filtration, decreased phagocytosis, decreased immunoglobulin M (IgM)
levels and loss of the opsonic tetrapeptide, tuftsin.
120 GENERAL SURGERY OUTPATIENT DECISIONS

Overwhelming post-splenectomy infection (OPSI)

This life-threatening disorder is a constant threat in patients who have a splenectomy.
Constant vigilance on the part of the patient and the surgeon is required if effective
treatment is to be started in time.
History/examination
It is an insidious viral-like illness leading to high fevers, nausea and vomiting, dehydration,
hypotension and collapse.
Investigation
Investiage with gram stain of peripheral blood smears.
Treatment
Admit the patient for intravenous antibiotics and fluids.
✧ Prognosis: mortality is 50–80%. Often a post-mortem shows bilateral adrenal
haemorrhage.
✧ Prevention: the pneumococcal vaccine covers 90% of pneumococcal variants but
leaves 10% uncovered. Vaccination should precede splenectomy by 10–14 days. Not
all patients convert, but those who do should have elevated pneumococcal antibodies
for 42 months. However, no form of prophylaxis is completely effective, so close
surveillance is necessary with specific patient education to seek medical attention at
the first signs of infection. The key to successful management is aggressive treatment
and awareness of the risk of OPSI.

Specific disorders of the spleen

Splenic infarction
Apart from sickle cell, splenic infarction most commonly occurs with congestive disease,
chronic myeloid leukaemia (CML) and myelosclerosis, but it can also occur as a result of
arterial emboli (rare) or as a complication of severe acute pancreatitis.
History
Take a general splenic history. There may be sudden-onset left-sided abdominal and loin
pain. Infarction causes a capsular reaction, irritating the left hemidiaphragm and leading
to left basal pleurisy with or without rub and pain to the left shoulder. Pain may be worse
on inspiration.
Examination
Perform a general examination. The patient may be in pain. Examine the chest for signs
of a left basal rub or effusion. There may be tenderness in the left side of the abdomen
and loin.
Investigations
USS may be useful to exclude other pathologies. CT scan with contrast is diagnostic.
Treatment
Give appropriate analgesia. Splenectomy is reserved for severe cases or diagnostic
confusion.
Follow-up
Monitor for development of hyposplenism, but management of the underlying condition
will usually take precedence. Discharge if stable after follow-up and when the underlying
condition resolves.
 THE SPLEEN AND LYMPH NODES 121

Post-operative follow-up
As for splenectomy.
Splenic abscess
A splenic abscess is a complication of severe sepsis, bacterial endocarditis, leukaemia,
diabetes or prematurity. Multiple abscesses are often fatal.
History
Take a general splenic history. It may be non-specific with fever, pain and possibly left
upper quadrant (LUQ) tenderness.
Examination
Perform a general examination. Splenomegaly occurs in less than 50%.
Investigations
Chest X-ray (CXR) shows left pleural effusion and USS shows immobile diaphragm.
Treatment
Treat with USS percutaneous drainage or splenectomy. A rupture is fatal.
Follow-up
If the patient recovers from the acute episode, monitor for development of hyposplenism.
Discharge when stable.
Post-operative follow-up
As for splenectomy.
Splenic cysts
Most splenic cysts are post-traumatic. True cysts are rare. They include haemangioma,
lymphangioma, parasitic, epidermoid and dermoid. They may occasionally rupture or
become infected.
History
The history is mostly size-related, but they are usually asymptomatic.
Examination
There is a mass in the LUQ.
Investigation
USS can identify cysts. Use CT scan with contrast if doubts exist.
Treatment
If cysts are small and asymptomatic, observe or treat with laparoscopic deroofing.
Splenectomy is advised for large or symptomatic cysts or any complications.
Follow-up
Monitor for development of complications or enlargement. Discharge when stable.
Post-operative follow-up
As for splenectomy.
122 GENERAL SURGERY OUTPATIENT DECISIONS

Splenic vein thrombosis

Splenic vein thrombosis follows acute pancreatitis or may arise in chronic pancreatitis or
a pancreatic tumour. Isolated splenic vein thrombosis (without portal vein thrombosis)
results in splenomegaly and segmental portal hypertension (predominantly gastric
varices – oesophageal varices are present but are less prominent). Portal venous pressure
is normal. Varices are often missed on endoscopy.
History/examination
It may present with massive gastrointestinal (GI) haemorrhage. Splenic vein thrombosis
should be suspected in cases of GI bleeding with a history of previous pancreatitis.
Investigations
Carry out endoscopy, Duplex USS and selective visceral angiography. MRI is better.
Treatment
The condition is cured by splenectomy.
Post-operative follow-up
As for splenectomy.
Splenosis
There is a need to differentiate between splenosis and accessory spleens. Accessory spleens
are found at the hilum of the spleen and omentum; number fewer than 10; and have hilar
vessels with normal splenic architecture. Implantation splenosis tends to number more
than 20; there is a history of trauma; they are scattered over the peritoneum; and do not
have a co-ordinated circulation.
Treatment
Neither condition needs therapy unless it is causing recurrent disease.
Gaucher’s disease
Gaucher’s is a hereditary lipid storage disease.
Clinical
There is hypersplenism and massive splenomegaly.
Treatment
Splenectomy is needed for the symptoms and complications of hypersplenism.
Disorders affecting the spleen and lymph nodes
Disorders affecting both the spleen and the lymph nodes can be considered in three main
groups.
✧ Immunological reactivity: non-specific, granulomatous (caseating, non-caseating).
✧ Neoplasia (mainly non-Hodgkin’s and Hodgkin’s lymphoma).
✧ Primary haematological disorders: myeloid leukaemia, myelosclerosis and
polycythaemia rubra vera (PRV).
History
Take a general splenic history. Ask questions regarding each of the causes of splenomegaly.
Ask about foreign travel. If there is a history of prior pancreatitis or abdominal
pain, exclude a splenic vein thrombosis. If there is pruritus, exclude PRV and other
myeloproliferative disorders.
 THE SPLEEN AND LYMPH NODES 123

Examination
Perform a general examination. A left upper quadrant mass with a spleen auscultation
may reveal a rub. With a renal mass the kidney moves downwards on respiration, organ
shapes are different and there is usually colonic resonance in front of the kidney. Search
for lymphadenopathy, including posterior pharynx. Look for the stigmata of chronic liver
disease. Look for purpura or bruising.
Investigations
✧ Take peripheral blood film and bone marrow.
✧ Take FBC and serology to investigate infective causes. Mononucleosis shows atypical
lymphocytes on blood film, positive Paul Bunnell test and raised Epstein-Barr virus
titre.
✧ If there is a positive history for travel, perform blood smears for malaria or bone
marrow tests for Leishman-Donovan bodies.
✧ If the patient is an immigrant, test for TB.
✧ Ultrasound scan or CT.
✧ Splenic vessels: Duplex, dynamic CT or selective angiography.
✧ Splenic function: injection of labelled platelets.

Disorders of the lymph nodes

Palpable lymph nodes should be considered diseased until proven otherwise. Always
remember that in addition to haematological disorders and infection, a lymph node may
be the first sign of metastatic carcinoma at a yet undetermined site. This is particularly
important in the neck, where node biopsy should not be performed without an
appropriate ENT examination, as such a biopsy may preclude potentially curative ENT
surgical excision and block dissection of diseased lymph nodes.
Localised lymphadenopathy
Acute infections usually subside.
✧ Chronic infections:
∝ lymphadenopathy without signs of inflammation may be cat scratch fever
∝ single tender node: primary bovine TB
∝ chronically enlarged lymph nodes matted together: syphilis, leprosy, fungal
infection, lymphogranuloma venereum.
✧ Occipital: chronic scalp infection.
✧ Posterior auricular: rubella.
✧ Anterior auricular: bacterial infection of eyelids or conjunctiva.
✧ Axillary: distal upper limb infection, occasionally lymphoma or Hodgkin’s.
✧ Neck: most common site for lymphomas.
✧ Painless epitrochlear: childhood viral illnesses, secondary syphilis or TB.
✧ Mediastinal hilar: not noticeably enlarged with bacterial pneumonia, mainly TB
(unilateral hilar lymphadenopathy). Infectious mononucleosis may cause mediastinal
lymphadenopathy for several months. Most common cause of persistent mediastinal
lymphadenopathy is malignant disease and sarcoidosis.
✧ Intra-abdominal or retro-peritoneal: lymphadenopathy is not commonly inflammatory.

Generalised lymphadenopathy
Noticeable lymph node enlargement in more than one drainage site is most commonly
viral, e.g. mononucleosis, viral hepatitis, influenza, cytomegalovirus, rubella and also has
other causes such as syphilis, TB, salmonella and toxoplasmosis. But malignant causes
should always be excluded.
124 GENERAL SURGERY OUTPATIENT DECISIONS

Malignant conditions of lymph nodes

Metastatic carcinomas rarely produce a generalised lymphadenopathy – they present
more often as a group of nodes adjacent to the primary tumour site. Hodgkin’s and non-
Hodgkin’s lymphomas commonly present with superficial lymph node enlargement.
Hodgkin’s lymphoma
Hodgkin’s is found mostly in men, presenting with a group of painlessly enlarged anterior
cervical lymph nodes. Axillary is the first site in 20%, mediastinal or inguinal in 15%.
History
There will be a history of fevers, pruritus, malaise, weight loss, anorexia and sweats.
The absence of systemic symptoms is signified by adding ‘A’ to the stage; the presence of
systemic symptoms is signified by adding ‘B’ to the stage.
Examination
Examination reveals painless enlarged lymph nodes. Hepatosplenomegaly appears late.
Investigation
Investigation is by lymph node biopsy (excisional) and bone marrow aspirate. A team
approach is essential. Staging laparotomy has now been replaced by high-quality cross-
sectional imaging.
Staging
Classification is for stages I-IV. Staging depends on the history and examination findings;
CXR and AXR; and CT chest, abdomen.
Treatment
Treatment depends on the Hodgkin’s stage:
✧ Hodgkin’s I and II: wide field radiotherapy
✧ IIIA: radiotherapy and/or chemotherapy
✧ IIIB and IV: multiagent chemotherapy.
Follow-up
Follow-up is under a haematologist/oncologist.
Non-Hodgkin’s lymphoma
This may present with painless enlargement of one or more superficial lymph nodes.
Extranodal disease may be present.
Biopsy is now assessed with multiple immuno stains to accurately define cellular type
and direct treatment.
Staging
Staging depends on results of node biopsy, bone marrow biopsy, and cross-sectional
imaging.
Treatment
Localised disease is commonly still managed with radiotherapy. More advanced disease
is managed with various chemotherapy regimes including monoclonal antilymphocyte
preparations such as rituximab.
 THE SPLEEN AND LYMPH NODES 125

Tumours of the peritoneum

Tumours of the peritoneum are mainly secondary, including pseudomyxoma peritonei.
Primary methothelioma may occur, but is rare.
Pseudomyxoma peritonei
The peritoneum is filled with yellow-brown mucoid substances caused by the presence
of a well-differentiated pseudomucinous cystadenoma/carcinoma. The most common
primary is the ovary; then the appendix, uterus, bowel and urachus. The primary tumour
is often slow growing and rarely metastasises or invades adjacent viscera.
History
Patients complain of increasing abdominal distension or present acutely with abdominal
pain, peritonitis or intestinal obstruction.
Examination
Perform a general examination. The main finding is abdominal distension.
Investigations
Perform a diagnostic peritoneal tap and biopsy.
Treatment
Treatment is by aggressive surgical evacuation and resection of the primary tumour. This
is followed by systemic chemotherapy including cisplatin. Radiotherapy is ineffective.
Prognosis is guarded but long-term survival can occur. One useful prognostic factor
appears to be the number of cells in the mucus. There is poor correlation between
histology of the primary and survival. Management following diagnosis is usually in a
regional or supra-regional specialist centre.
Follow-up
Follow-up is long term to detect deterioration and provide symptomatic support.
Peritoneal mesothelioma
Peritoneal mesotheliomas carry a poor prognosis of 8–12 months. There are two main
types: diffuse malignant (the majority) and fibrotic benign (rare, and can be cured by
surgical excision). Among the malignant tumours the only treatable lesions are the stage I
tumours that are confined to one hemithorax or to the peritoneum.
History
Peritoneal mesothelioma presents with anorexia, ascites and intestinal obstruction. There
is fever and weight loss.
Investigations
Perform paracentesis and laparoscopy and peritoneal biopsy.
Treatment
Treatment for stage I is surgical resection, radiotherapy and chemotherapy (systemic and
intraperitoneal).
Follow-up
Follow-up is long term to detect deterioration and provide symptomatic support.
126 GENERAL SURGERY OUTPATIENT DECISIONS

Desmoid tumours (of abdominal wall)

These are slow-growing well-circumscribed hard tumours that involve fascial and muscle
layers. They recur after local excision (10–20%). They may be associated with Gardner’s
syndrome.
Treatment
Treatment is surgical, by wide local excision.
Follow-up
Follow-up is long term to detect recurrence, or discharge with advice to GP to continue
follow-up.
Liver, biliary system and pancreas
Satyajit Bhattacharya and Adrian O’Sullivan

EIGHT
Introduction
In this chapter, disorders of the liver, pancreas, biliary system and spleen are considered
separately. However, it is important to appreciate that these systems are closely inter-
related and may present with similar clinical features. For example, a patient may be
jaundiced due to a primary liver disorder such as cirrhosis, due to a biliary problem such
as choledocholithiasis, or due to obstruction of the extrahepatic bile duct by a pancreatic
neoplasm. Conversely, each of these conditions can in turn, if not corrected, eventually
cause secondary biliary cirrhosis. When a patient presents with jaundice, one of the main
tasks is to determine what the primary disorder is and then determine the effect this has
had on the function of the liver, pancreatic and biliary systems.

Assessment of liver disorders

Liver disease
The main clinical features of liver disease are jaundice and signs of liver failure. As the
assessment and management of liver disease is complex, it is useful to have an initial
overview of the consultation objectives.
Objectives
Confirm that the symptoms and signs of liver disease are present.
1. Determine the cause through history, examination, urine and blood tests, imaging
and histology.
2. Detect the clinical consequences of liver disease through history, examination, urine
and blood tests (Child score (see later)), imaging and endoscopy:
✧ encephalopathy
✧ ascites
✧ portal hypertension
∝ hypersplenism
∝ gastrointestinal bleeding – varices (oesophageal, gastric or rectal)
∝ ascites
✧ jaundice
✧ clotting abnormalities
✧ hepatorenal failure.
3. Treat the underlying cause of the liver disease, which may lead to improvement in the
clinical consequences of liver disease.
4. Treat the clinical consequences:
✧ measures to reduce encephalopathy
✧ treat ascites
✧ treat the consequences of portal hypertension
∝ hypersplenism: splenectomy if surgery for portal shunt considered
∝ varices: Sengstaken tube, vasoactive drugs, injection sclerotherapy or fibrin
glue, transjugular intrahepatic portosystemic shunt (TIPS), surgery
∝ ascites: medical, tap ascites, peritoneovenous shunt
✧ jaundice: symptomatic, or relieve obstruction if present
✧ clotting abnormalities: correct with vitamin K or fresh frozen plasma
✧ hepatorenal failure: treat underlying liver condition, provide renal support.

127
128 GENERAL SURGERY OUTPATIENT DECISIONS

Liver history
Start with a general gastrointestinal history. When responses indicate a possible liver
problem, a more detailed liver history is required. This includes questions about general
symptoms, aetiological factors and symptoms related to the clinical consequences of
liver disease.
General symptoms that may indicate liver disease include jaundice, fatigue, malaise,
headache, myalgia, arthralgia and fever. To determine the aetiology of the liver disease
ask about excessive or chronic alcohol ingestion, the ingestion of drugs (therapeutic or
recreational), occupation, pets, foreign travel, contact with jaundiced individuals, family
history of jaundice or liver problems, recent anaesthetics, surgery or blood transfusions,
sexual contacts and ingestion of raw shellfish or wild mushrooms.
The clinical consequences of liver disease include:
✧ encephalopathy – a range of reversible neuropsychiatric states ranging from confusion
and forgetfulness to coma
✧ ascites – the presence of intra-abdominal fluid
✧ portal hypertension (varices) – which may be asymptomatic or may present with
haematemesis (vomiting of bright red blood) or melaena
✧ jaundice – patients may simply report that they have turned yellow. Enquire about
pale stools, dark urine and pruritus. Determine if the jaundice is painless or associated
with right upper quadrant or epigastric abdominal pain
✧ clotting abnormalities – spontaneous bleeds, easily bruised
✧ hepatorenal failure – increasing lethargy, nausea, oedema.

Liver examination
Perform a general examination and once again look for general signs of liver disease,
aetiological signs and signs of clinical consequences. Liver disease commonly presents
with jaundice. However, other signs may also be present: palmar erythema, finger
clubbing, leuconychia, bruising, asterixis, spider naevi, gynaecomastia, muscle wasting,
scratch marks, ascites, caput medusae, hepatosplenomegaly, testicular atrophy and loss
of axillary and pubic hair. Hepatomegaly may be real or apparent (pushed down by over-
inflated lung) and enlargement may be focal or generalised, smooth or irregular. Liver
tenderness may be elicited by palpation or percussion through the rib cage. Auscultation
over the liver may reveal a friction rub (tumour, abscess) or a systolic bruit.
Aetiology may be indicated by the smell of alcohol, tattoos or evidence of drug injec-
tions (e.g. antecubital fossa).
The following are signs of clinical consequences.
✧ Encephalopathy: poor scores on cognitive function tests, inability to draw a star, liver
flap, decreased consciousness level.
✧ Peripheral neuropathy may indicate the effect of liver failure on the nervous system.
✧ Ascites: abdominal distension, eversion of umbilicus, flank dullness, shifting
dullness.
✧ Portal hypertension: dilated periumbilical veins (late), anaemia, ascites, splenomegaly,
hepatosplenomegaly.
✧ Jaundice: yellow conjunctiva, pale stool on rectal examination, dark urine.
✧ Clotting abnormalities: evidence of bruising.
✧ Hepatorenal failure: oedema, decreased urine output, uraemia.
 LIVER, BILIARY SYSTEM AND PANCREAS 129

Investigation of liver disorders

Laboratory investigations
Urinalysis
✧ The technique is dipstick urinalysis. A variety of dipsticks can test for a number of
substances in a fresh specimen of urine, including conjugated bilirubin. Generally the
presence of conjugated bilirubin indicates obstructive jaundice, although some other
conditions associated with excess bilirubin production also result in some bilirubin
in the urine.
✧ There is no request form.
✧ The results are sticks that are compared to a reference chart.
✧ The advantage is it is a quick and easy method that can be performed in the clinic.
✧ The disadvantage is that limited information is available.

Blood tests
Blood tests form an integral part of the diagnosis of liver disorders. The commonest tests
are described under the department that analyses the samples.
Biochemistry
Release of integral membrane enzymes
Minor increases of alanine transaminase (ALT) or serum glutamic pyruvic transaminase
(SGPT), and aspartate aminotransferase (AST) or serum glutamic oxaloacetic transami-
nase (SGOT) occur in cholestasis and chronic liver disease. Major increases are associated
with acute hepatitis or with liver cell necrosis of any cause.
Alkaline phosphatase (ALP) from the liver, biliary tract, bone, intestine, kidney and
placenta can be differentiated by immunoassay. Cholestasis and obstructive jaundice are
associated with an increased alkaline phosphatase.
Gamma-glutamyl-transpeptidase (gamma GT) is particularly raised in alcoholic liver
disease and obstructive jaundice from any cause. Secondary tumour deposits cause a
rise in alkaline phosphatase and gamma GT and a small rise in bilirubin. These can vary
depending on the burden of underlying disease.
Serum markers of liver disease
✧ Serum protein changes: hypoalbuminaemia often occurs in liver disease. An altered
albumin/globulin ratio may occur in the presence of a normal albumin, e.g. increased
immunoglobulin (IgG) in cirrhosis and chronic active hepatitis. Primary biliary
cirrhosis is associated with increased immunoglobulin M (IgM) and antimitochondrial
antibody.
✧ Marker proteins: alpha-foetoprotein (AFP) is the most commonly used tumour
marker for hepatocellular carcinoma. It may also be raised in pregnancy, germ cell
tumours, and chronic liver disease. Abnormal prothrombin antigen (APT) is increased
in 90% of primary hepatocellular carcinoma (greater than 300 ng/ml indicates
primary hepatocellular carcinoma). There are small increases in other disorders.
Levels decrease or are eliminated after curative resection or chemotherapy. There is
little correlation between APT and AFP. Human chorionic gonadotropin (beta-hCG)
and carcinoembryonic antigen (CEA) are also useful liver tumour markers.
✧ Urea and electrolytes may indicate electrolyte abnormalities, particularly hypona-
traemia and hypoglycaemia. Evidence of raised urea and creatinine levels may indicate
impaired renal function associated with liver disease (hepatorenal syndrome).
Haematology
✧ Full blood count (FBC) may reveal anaemia of chronic disease or indicate blood loss
from gastrointestinal (GI) bleeding. Other abnormalities of the blood cells may be
130 GENERAL SURGERY OUTPATIENT DECISIONS

detected, such as haemolytic anaemia, leukaemia and lymphoma. Thromocytopenia

may suggest hypersplenism.
✧ Clotting tests: clotting, in particular the international normalised ratio (INR), may be
abnormal in liver disease due to the defective production of clotting factors.
Immunology
Hepatitis serology is routine screening in liver disease, for hepatitis A, B and C.
There is also screening for autoimmune disease and primary biliary cirrhosis (anti-
mitochondrial antibody).
Imaging techniques
Ultrasound scanning (USS)
Ultrasound uses high-frequency sound waves that enter the tissues and are reflected
in different amounts from structures of different compositions. The reflected waves
are detected and used to construct representative images of the underlying insonated
tissues. Acoustic water-based gel is applied and an ultrasound probe manipulated over
the abdomen by the sonographer.
✧ The request form is from radiology/ultrasound (check if your department uses the
same or different forms).
✧ Results are in a written report compiled by the radiologist or sonographer, with a
selection of ultrasound photographs.
✧ USS is a very good non-invasive technique for visualising the liver parenchyma. It
can detect small (1cm) focal lesions, including liver cysts and abscesses, and primary
and secondary liver tumours. Liver cirrhosis is suggested by areas of increased and
irregular attenuation. The intrahepatic and extrahepatic bile ducts and the gall
bladder are well visualised, and dilatation and stones can be detected. Using colour
Duplex, blood flow in the portal vein can be identified and the diameter can be
measured, giving an estimation of the presence of portal hypertension. Ultrasound-
guided biopsy can be performed.
✧ The disadvantages are that accuracy is dependent on the experience of the operator;
it is less reliable in fat or gaseous patients; and it is less reliable than computed
tomography (CT) for defining lesions such as haemangiomas, but it can be used to
follow these lesions once CT has established the diagnosis.
CT scan
In this technique X-rays are used to obtain multiple cross-sectional slices of the patient,
which are then reconstructed by a computer to produce the images. Intravenous contrast
to outline the vessels and focal lesions within the liver can also be given, and multiple
scans can be performed to give non-contrast, arterial, venous and delayed phases of
scanning. Oral contrast agents can be given to outline the stomach and duodenum.
Modern multi-slice spiral CT scans can be performed quickly (15–30 seconds) using
5mm cuts, giving more detail and allowing sophisticated reconstructions. See also CT
angioportography and lipiodol CT.
✧ The request form is from radiology or use a specific CT request form.
✧ Results are in a report written by the radiologist and a selection of still CT images.
✧ When used with contrast, CT is more sensitive than USS at determining the nature
of lesions within the liver, especially differentiating between small tumours, cysts or
abscesses. CT-guided biopsies can be performed. It is invaluable in planning liver
resection surgery.
✧ Disadvantages are that it is expensive and time-consuming; it uses ionising radiation;
and certain lesions such as hepatic adenomas or focal nodular hyperplasia may be
difficult to differentiate on CT.
 LIVER, BILIARY SYSTEM AND PANCREAS 131

Liver scintiscan
A liver scintiscan uses isotopes technetium-99m, gallium-67 citrate or indium-113. The
isotopes are injected intravenously and concentrated in liver lesions. Excess uptake is
detected by a gamma camera.
✧ The radioisotopes request form is usually in the medical physics department.
✧ The results are as a written report and selection of images.
✧ The advantages are that technetium-99m is taken up by the reticuloendothelium
system and can detect lesions larger than 2cm in about 66% of cases; gallium-67
citrate is concentrated in neoplastic lesions and abscesses; indium-113 is concentrated
in haemangiomas.
✧ The disadvantage is that it uses radioactivity. Other techniques usually provide the
same information.
Magnetic resonance imaging (MRI)
MRI detects minute quantities of energy released by hydrogen ions when they are forced
to change direction by a strong magnetic field. The patient passes through the scanner,
which is quite claustrophobic and noisy.
✧ There is a specialised MRI request form.
✧ The advantages are that it provides detailed information regarding liver parenchymatous
disease, especially certain types of cirrhosis, e.g. haemochromatosis, Wilson’s and
primary biliary cirrhosis; MR cholangiopancreatography (MRCP) is very useful for
non-invasive imaging of the biliary tree; MRI is very useful as an adjunct to other
imaging modalities to further characterise liver lesions; and recent advances include
liver-specific MRI constrast agents.
✧ The disadvantages are that it is expensive and time-consuming; and patients may find
the experience unpleasant.
Angiography/venography; hepatic wedge pressure and venography; portography
techniques
These invasive techniques to visualise the hepatic vasculature are being less commonly
used.
Portography
This involves puncture of the spleen percutaneously through an intercostal space and the
injection of contrast to outline the splenic and portal vein and enable the measurement
of portal venous pressure. A transhepatic route may also be used.
Hepatic wedge pressure and venography
A catheter is passed from the brachial vein or internal jugular vein through the superior
vena cava into the hepatic veins as far as possible, and the wedge pressure is measured.
Under certain circumstances this is representative of the portal venous pressure. Injection
of contrast can demonstrate the presence of thrombus or occlusion, e.g. in Budd-Chiari
syndrome.
Angiography/venography
The coeliac and superior mesenteric arteries are selectively catheterised. The arterial
supply of the liver can be visualised and the venous phase can demonstrate the portal
system. Selective angiography can be combined with CT scanning for the technique – CT
angioportography. Contrast is delivered into the splenic artery or SMA and enhances the
liver via the portal venous blood. Liver tumours are supplied almost exclusively by hepatic
artery blood and are therefore visualised as non-enhancing lesions. Another variation
is lipiodol CT. Iodised poppy-seed oil, injected via angiography of the hepatic artery, is
132 GENERAL SURGERY OUTPATIENT DECISIONS

retained for long periods by hepatocellular carcinoma, causing dense enhancement of

these lesions on subsequent CT scan (two weeks later).
✧ The request form is from radiology, but these are specialised investigations. Contacting
a radiologist directly to discuss the indications is recommended.
✧ Results are a written report by the radiologist and a selection of images.
✧ The advantages are that the methods provide direct measurements and images of
the portal system; and selective arteriography is useful in planning resection of liver
tumours.
✧ The disadvantages are that the procedures are invasive and associated with complica-
tions; much of this information can be obtained by less invasive means, e.g. Duplex
ultrasound, MRI angiography, spiral CT.
Liver needle biopsy
This is usually performed as an in-patient procedure (or as an outpatient/day-case proce-
dure in selected patients) as the patient requires strict bed rest and frequent observation
after the procedure.
Indications for liver biopsy include alcoholic liver disease, cholestatic jaundice without
dilatation of the bile ducts on ultrasound, unexplained hepatomegaly, drug-induced liver
disease and unexplained focal lesions of the liver (after consultation with a liver surgeon).
The procedure is only performed when the INR is normal and the platelet count exceeds
60 000/ml.
Usually a Tru-cut needle is preferred. The patient is placed supine with the right arm
abducted. A lateral intercostal approach is used, or if a focal mass is apparent this is
approached directly (better performed under ultrasound control). The liver dullness is
percussed and marked. Local anaesthetic is infiltrated and a small incision is made in the
skin. The patient is instructed to cease breathing in expiration and the needle is inserted,
the sample is taken and the needle is removed. The patient resumes respiration and the
sample is placed whole into fixation fluid. The patient remains in bed with frequent
observations of pulse and blood pressure.
✧ The procedure requires admission to hospital as an in-patient or a day-case. Determine
the exact arrangements for request forms in your hospital. The sample is sent for
histology.
✧ Results are as a written report from the histopathologist.
✧ The advantage is that it provides a core of tissue for histological diagnosis.
✧ The disadvantages are complications, including haemorrhage, intrahepatic haema-
toma, pleurisy, arteriovenous fistulae and biliary peritonitis. If there is any suspicion
of a pnemothorax, an urgent chest X-ray is obtained and a chest drain is placed.
Laparoscopy
This operation is being increasingly used for the assessment of a number of disorders
such as jaundice, chronic liver disease, ascites of unknown origin and the staging of
primary and secondary hepatic and pancreaticobiliary tumours. A general anaesthetic is
required. The laparoscope is inserted using an open technique through an infraumbilical
approach. Further ports may be inserted if necessary. The technique can be combined
with intra-operative liver biopsy, ultrasound and cholangiography.
✧ There is no request form. It is usually performed as an in-patient procedure.
✧ The results are a written or printed operation note recording the main intra-operative
findings, and a histology report if any biopsies were taken.
✧ The advantages are direct visualisation of lesions, enabling accurate characterisation
and biopsy. After biopsy haemostasis can be confirmed. In experienced hands, ultra-
sound applied directly to the liver is more sensitive at detecting abnormalities.
✧ The disadvantages are that it requires a general anaesthetic and is an invasive
 LIVER, BILIARY SYSTEM AND PANCREAS 133

procedure that is expensive and time-consuming. Risks and benefits must be carefully
balanced.

The clinical consequences of liver disease

Assessment of hepatic dysfunction
Certain management options depend on an objective assessment of the degree of liver
impairment. One such assessment is Pugh’s modification of Child’s scoring for hepatic
dysfunction (Table 8.1). A worse prognosis is associated with a higher score.
TABLE 8.1 Pugh’s modification of Child’s score for hepatic dysfunction.
1 2 3
Encephalopathy None 1–2 3–4
Ascites Absent Slight Moderate
Albumin g/l 35 28–35 <28
Prothrombin time (sec prolonged) <3 4–10 >10
Bilirubin (micromol/l) <34 35–51 >51
Grade A (good) = 5–6, Grade B (moderate) = 7–9, Grade C (poor) = 10+

Hepatic encephalopathy
A spectrum of syndromes exists:
✧ acute (fulminant) liver failure
✧ cirrhotic patients with a precipitant
✧ chronic portal-systemic encephalopathy.

Grades are from I to IV, ranging from mild confusion, to drowsiness, to somnolent-but-
rousable, to coma.
Causes are acute liver failure from any cause and exacerbation of chronic disease by
precipitants such as GI haemorrhage, infection, drugs, hypokalaemic alkalosis, diuretic
therapy, sedation, sepsis and portosystemic surgical shunting.
History
There may be a history of chronic liver disease and symptoms of intellectual impairment.
There may also be a history of recent GI haemorrhage, diuretic therapy or other causes
of encephalopathy.
Examination
Examination shows a decreased level of consciousness and abnormalities on cognitive
testing – apraxia, hyperactive stretch reflexes.
Treatment
Withdraw the underlying cause (e.g. sedatives), stop haemorrhage and give phosphate
enema to treat infection. The effect of GI haemorrhage is reduced by purgation with mag-
nesium sulphate. Bacterial production of protein metabolites within the bowel is reduced
using neomycin, metronidazole and lactulose. Ensure a protein-restricted diet.
For chronic treatment, decrease protein diet, but not less than 40 g. Severe encephalo-
pathy after insertion of surgical shunts is treated by radiological blocking of the shunt.
Follow-up
Follow-up is long term at regular intervals (1–3 months) with frequent assessment for
the presence of subclinical encephalopathy.
134 GENERAL SURGERY OUTPATIENT DECISIONS

Portal hypertension
Obstruction to portal venous flow results in increased pressure in the splanchnic venous
circulation. Normal portal pressure is 5–10 mmHg with a portal flow in the region of
1.5 l/min. Portal hypertension occurs if the pressure in the portal venous system exceeds
20cm of saline or 12 mmHg.
Causes of obstruction include the following.
✧ Extrahepatic compression of the portal vein, or thrombosis of portal, mesenteric
or splenic veins. Twenty five per cent of patients with portal hypertension will have
an extrahepatic block, and a proportion of these will have underlying liver disease
or polycythaemia. Chronic pancreaticobiliary disease or pancreatic neoplasm may
precipitate portal vein thrombosis.
✧ Compression of portal venous radicles within the liver, by disease. Most commonly
this obstruction is sinusoidal and results from cirrhosis of the liver. In cirrhosis,
portal hypertension is due to both obstruction and increased splanchnic blood flow
secondary to elevated levels of vasodilators, e.g. glucagon, and decreased sensitivity to
vasoconstrictors. Pre-sinusoidal obstruction can develop in schistosomiasis.
✧ Obstruction to venous outflow from the liver, usually due to thrombosis of the hepatic
veins. Causes of thrombosis include the contraceptive pill, ingestion of Bush teas,
congenital diaphragm of the vena cava or congestive right heart failure. These patients
rarely present with bleeding but have intractable ascites, painful hepatomegaly and
rapidly deteriorating liver function.

Obstruction of portal venous flow results in enlargement of portosystemic communica-

tions and a risk of bleeding from oesophageal and gastric varices. Bleeding from varices
usually occurs when the portal hypertension exceeds 30cm saline. However, only 50% of
varices ever bleed and only 15–40% of patients with chronic liver disease develop portal
hypertension.
Clinical features of portal hypertension
Three clinical syndromes can be attributed to portal hypertension: hypersplenism,
gastrointestinal bleeding and ascites.
Objectives
Detect portal hypertension, determine the cause, detect the syndromes associated with
it, treat portal hypertension and its effects.
Hypersplenism (an overactive spleen)
Portal hypertension causes the spleen to enlarge (splenomegaly). Enlargement of the
spleen causes increased sequestration of blood elements, enough to result in haemolytic
anaemia, leucopenia and thrombocytopenia. These seldom cause major symptoms
but may debilitate. After portal decompression, hypersplenism may remain. Therefore,
pancytopenia in patients requiring portal decompression may be an indication for
incorporating splenectomy as part of the procedure.
Gastrointestinal haemorrhage
The main causes of haemorrhage are oesophageal varices and gastric fundal varices.
Colonic and rectal varices are detectable but seldom cause haemorrhage. After diagnosis
of varices, 30% of patients bleed within two years – then a smaller proportion bleed each
year after that. Increased risk of bleeding is associated with the following endoscopic
characteristics: size graded from I (small) up to III, cherry-red spots, overlying varices, red
whale markings and blue varices (as opposed to white). Grade I varices may be reversible
with improvement of the liver condition. Other grades do not regress.
 LIVER, BILIARY SYSTEM AND PANCREAS 135

History
The patient may present with symptoms and signs of anaemia, massive haematemesis, a
herald bleed (a mouthful of bright red blood) or melaena.
Examination
There may be stigmata of chronic liver disease.
Investigations
The primary investigation is endoscopy, performed by an operator experienced in dealing
with variceal haemorrhage. FBC may reveal anaemia; clotting screen may detect a raised
INR. Liver function tests (LFT) may be abnormal. Blood urea may be raised.
Treatment
The initial management of acute variceal bleeding is resuscitation and institution of
measures to stop encephalopathy. Treatment to stop the bleeding may consist of drug
therapy such as somatostatin to lower transhepatic venous gradient or of other vasoactive
drugs such as terlipressin. Pentagastrin induces contraction of the lower oesophageal
sphincter, as does metaclopramide.
Use balloon tamponade followed by endoscopy and sclerotherapy, banding or fibrin
glue. If these measures fail to arrest the bleeding, a transjugular intrahepatic porto-
systemic shunt (TIPS) procedure should be considered. Surgery can be an option, but
the procedure carries a significant mortality in the acute setting. After the bleeding has
stopped, management is aimed at preventing recurrent bleeding by treating the under-
lying liver condition, treating the varices and reducing the portal hypertension. This is
co-ordinated from the OPD.
Endoscopic sclerotherapy
Sclerotherapy (using ethanolamine oleate, 3% tetradecyl sulphate or absolute alcohol) is
repeated at three-weekly intervals until all the varices are obliterated.
Complications of sclerotherapy
There may be oesophageal ulceration, perforation, stricture, acute respiratory distress
syndrome (ARDS), mediastinitis, bacteraemia (10%), anaphylaxis (especially with
ethanolamine), pneumatosis intestinalis, pneumoperitoneum and portal vein thrombosis
(36% – therefore use with caution in good-risk Child’s A patients who may later require
a shunt operation or liver transplant).
Recurrence of oesophageal varices after initial obliteration by sclerotherapy occurs in
about 60% of patients. Failed sclerotherapy is managed by oesophageal transection or
shunt procedure.
Endoscopic banding
Using rubber band treatment to ensnare the varices is producing results as effective as
sclerotherapy.
TIPS can be considered in persistent bleeding for suitable patients (without extrahepatic
venous thrombosis). Access is obtained by cannulating the internal jugular and then the
middle hepatic vein. A needle is then passed from the hepatic venous system to the portal
venous system, which is then replaced by a wire and subsequently an expanding metal
stent.
Complications of TIPS include haemorrhage, stent dislodgement or occlusion, infec-
tion and shunt encephalopathy.
136 GENERAL SURGERY OUTPATIENT DECISIONS

Surgical treatment
Indications include patients who continue to bleed or have recurrent bleeding. Bleeding
often downgrades a patient from Child’s A/B to C. Portosystemic shunting in the emer-
gency carries a prohibitive mortality, and oesphageal transection is performed instead.
In the elective situation two groups of patients are considered for surgery.
✧ Bleeding arrested and good liver function (Child’s A/good B). Since there is no effective
method for prevention of further bleeding, portosystemic shunting or oesophageal
transection with devascularisation (Sugiura procedure) should be considered.
✧ End-stage liver disease (Child’s C) controlled by sclerotherapy – consider for
transplantation. For patients considered for hepatic transplantation, surgery should
be avoided but TIPS has been successfully employed to achieve portal decompression
and avoid further bleeding.

Liver transplant should be considered in all patients with variceal bleeding and good liver
function but with poor quality of life.
Follow-up
Review at three-weekly intervals until all the varices are obliterated. Look for other
signs of liver dysfunction and syndromes associated with portal hypertension. Detect
complications of sclerotherapy. Estimate the Child score and formulate a plan for
definitive management. Follow-up endoscopy every 6–12 months is recommended.
Beta blockade should be considered. If rebleeding occurs after successful obliteration of
varices, a shunt procedure or oesophageal transection procedure should be considered.
Consider liver transplantation for suitable candidates.
Ascites
Ascites is clinically detectable when volume exceeds one litre.
Causes of ascites include:
✧ infection – TB, peritonitis
✧ inflammation – Crohn’s, starch peritonitis
✧ hypoproteinaemia – nephrotic syndrome, liver disease, protein-losing enteropathy
✧ lymphatic obstruction – TB, filariasis, lymphoma, metastatic carcinoma, Milroy’s
disease, rupture/damage of abdominal lymphatics
✧ increased lymph flow/pressure – cirrhosis, congestive cardiac failure, constrictive
pericarditis, Budd-Chiari syndrome
✧ neoplasms – primary and secondary tumours of the peritoneal cavity
✧ chronic pancreatitis – pancreatic ascites (caused by disruption of the pancreatic
duct).

Intractable ascites is seen in advanced chronic liver disease, Budd-Chiari and peritoneal
carcinomatosis. These patients cease to respond to diuretic therapy and develop pre-renal
azotaemia. Pericardial effusions occur in 60% of alcoholic cirrhotics.
Differential diagnosis
This includes large ovarian cysts, pancreatic pseudocysts, mesenteric cysts, hydramnios
and acute gastric dilatation.
Objectives
Diagnose the cause, treat the underlying disorder, treat ascites.
History
Take a general liver history. Patients may report increasing abdominal girth and fullness.
 LIVER, BILIARY SYSTEM AND PANCREAS 137

They may also complain of leg swelling or difficulty breathing due to splinting of the
diaphragm. Ask about symptoms associated with each of the causes outlined above.

Examination
Perform a general examination. Early signs include dullness in the flanks. Shifting dull-
ness and a fluid thrill may be elicited. Later, ascites may produce a tense, distended
abdomen with grossly elevated intra-abdominal pressure, causing venous congestion and
lower limb oedema. Respiratory distress may occur due to splinting of the diaphragm.
Umbilical hernias are not uncommon. Look for signs associated with each of the causes
outlined above.

Investigations
Use ultrasound to confirm presence of ascites.
Carry out diagnostic paracentesis – take off 20–50 ml and send samples of fluid for
biochemistry, cytology, culture and sensitivity, and TB culture.
Determine serum/ascitic fluid albumin ratio. Gradients less than 11 g/litre are present in
patients without portal hypertension. Gradients greater than 11 g/litre are associated with
portal hypertension. This ratio helps to distinguish high-protein transudates in patients
with portal hypertension from true exudates (e.g. TB and peritoneal carcinomatosis).
Laparoscopy is useful for uncertain cases, for inflammatory cases and for performing
a peritoneal biopsy. Ascitic fluid can be described as serous, pseudochylous, bloodstained
(often malignant) and myxomatous. Chylous ascites has a milky appearance and a high
fat content on analysis. When chylous ascites arises spontaneously, it can indicate lym-
phatic obstruction by lymphoma or nodal deposits from carcinoma.

Treatment
Restrict sodium. Give spironolactone diuretic – loop diuretics increase the risk of
encephalopathy, especially in the presence of subclinical renal impairment. The aim is
for gradual loss of fluid of about 3 kg/week.
If this fails or patients become oliguric, other treatments apply.
✧ Therapeutic paracentesis with intravenous 5% albumin infused over two hours with
50 mg of frusemide and 250 ml of 20% mannitol over 20–30 minutes. If diuresis is
not established, peritoneovenous shunting is indicated.
✧ Peritoneovenous shunting is effective in decreasing hospital stay; increasing muscle
mass; and providing adequate long-term control on patients with ascites and good
liver function (Child’s A and B). It is ineffective and increases mortality in patients
with advanced disease. Contraindications to peritoneovenous shunting include
encephalopathy, uncorrectable bleeding diathesis, renal failure due to primary renal
disease, recent variceal haemorrhage and cardiac failure. There have been reports
of the successful use of the long saphenous vein as a saphenoperitoneal shunt. This
avoids the cost and foreign body complications of an artificial shunt.

Follow-up
Follow-up is long term at regular intervals (1–3 months) to detect complications, which
include blockage of the shunt and the development of disseminated intravascular
coagulation (most commonly occurs just after shunt insertion).

Renal disease and hepatorenal failure

Hepatorenal syndrome is characterised by the development of renal failure in patients
with severe liver disease without underlying renal disease. Diagnosis is dependent on a low
glomerular filtration rate; absence of shock; ongoing sepsis; fluid loss or haemorrhage;
138 GENERAL SURGERY OUTPATIENT DECISIONS

no improvement despite adequate plasma volume and diuretic withdrawal; proteinuria

less than 500 mg/day; and no evidence of renal tract obstruction.
There are two types. Type 1 is rapidly progressive, of less than two weeks’ duration and
doubling of the initial creatinine, with a mortality of 80% at two weeks. Type 2 satisfies
the criteria for diagnosis but is not rapidly progressive. It does not usually respond to
dialysis. Best treatment is to improve underlying liver function.
Jaundice
Jaundice is recognised when serum bilirubin exceeds 40 umol/l. Mechanisms include
excess bilirubin production, impaired uptake by the hepatocyte, failure of conjugation,
impaired secretion of conjugated bilirubin into bile canaliculi, and impairment of bile
flow subsequent to the secretion by the hepatocytes (cholestatic or obstructive). Causes
include haemolysis, liver disease, adverse drug reactions and biliary tract obstruction
(intrahepatic or extrahepatic). Table 8.2 shows types of jaundice.
TABLE 8.2 Types of jaundice.
TYPE MECHANISM
Hepatocellular Defective secretion of conjugated bilirubin into the bile canaliculi
Cholestatic intrahepatic/extrahepatic Impairment of bile flow subsequent to the above secretory step
Haemolytic Excess bilirubin production
Benign congenital hyperbilirubinaemia Defective bilirubin uptake, conjugation or secretory defect

Hepatocellular jaundice
✧ The acute form is seen in viral hepatitis, liver cell necrosis and acute alcoholic
hepatitis.
✧ The chronic form is seen in chronic active hepatitis, cirrhosis–alcoholic, cryptogenic,
primary biliary. It is characterised by increased transaminases on the LFTs. If alcoholic,
gamma-glutamyl-transpeptidase (gamma GT) is also raised.
Cholestatic jaundice
✧ Intrahepatic is functional (drugs, hepatitis) or organic (obstruction of intrahepatic
biliary tree).
✧ Extrahepatic examples are duct stones and pancreaticobiliary cancer. It is characterised
by:
∝ conjugated hyperbilirubinaemia
∝ increased alkaline phosphatase, gamma GT and 5-nucleotidase (5-nucleotidase
is the most reliable, as it is not influenced by bone disease and not induced by
alcohol)
∝ minor or no elevation of transaminases
∝ bilirubin in the urine
∝ elevation of serum cholesterol and bile acid levels.

Haemolytic jaundice
Unconjugated hyperbilirubinaemia results from haemolysis. Unconjugated bilirubin
is not water soluble and is therefore carried in the blood bound to albumin. Increased
unconjugated bilirubin leads to increased production of conjugated bilirubin and this
leads eventually to increased urobilinogen and urobilin in urine. Therefore prolonged
and recurrent haemolysis may produce a cholestatic component. Causes of haemolysis
include abnormalities of red cells or increased red-cell destruction.
 LIVER, BILIARY SYSTEM AND PANCREAS 139

Assessment of the jaundiced patient

Objectives
Diagnose jaundice, diagnose the underlying cause, treat jaundice, treat the complications
of jaundice, treat the underlying cause.
History
Take a general liver history. Enquire regarding drug intake (legal and illicit), injection with
hypodermic needles (legal and illicit), alcohol abuse, anaesthetics, transfusion of blood
and blood products, contact with jaundiced individuals, family history, sexual contacts,
travel to hepatitis-endemic areas and ingestion of raw shellfish and wild mushrooms. Ask
about the colour of urine, stools, itching and previous surgical procedures.
Examination
Perform a general examination. Is the patient jaundiced and has the patient any evi-
dence of parenchymatous liver disease? Look for evidence of jaundice, e.g. yellow sclera.
Examine for palmar erythema, spider naevi, bruising, splenomegaly, hepatomegaly or
decreased liver size, fluid retention (ascites and oedema), muscle wasting, finger clubbing,
white nails, enlargement of parotid gland, gynaecomastia and testicular atrophy. Scratch
marks are commonly seen. Look for inco-ordination; neurological signs including hyper-
reflexia and apraxia; altered sleep rhythm; confusion; flapping tremor; stupor; and foetor
hepaticus.
Is there any evidence of malignancy, such as recent weight loss, enlarged left-sided
supraclavicular lymph nodes, enlarged nodular liver, palpable gall bladder (Courvoisier’s
sign), palpable intra-abdominal mass (epigastric, iliac fossae) rapidly arising ascites or
rectal neoplasm on rectal examination.
Investigations
Is the jaundice cholestatic? Cholestatic jaundice is characterised by dark and frothy urine
and pale stools. There is bilirubin in urine. Serum alkaline phosphatase and gamma GT
are elevated. There are slightly increased transaminases, usually less than 400 IU/ml (this
amount virtually excludes significant hepatocellular damage). Check hepatitis A, B and
C status in all jaundiced patients.
Is there dilatation of the biliary tree? Ultrasound is good at differentiating intrahepatic
and extrahepatic jaundice, identifying stones and demonstrating the level of obstruction.
Further investigation of the nature of the obstruction involves cross-sectional imaging (CT
or MRI) and a cholangiogram (MRCP, endoscopic retrograde cholangiopancreatography
(ERCP) or percutaneous transhepatic cholangiography (PTC)).
Intrahepatic cholestasis requires further investigation with liver biopsy for histology
and serum autoantibody screen (antimitochondrial, anti-smooth muscle and immuno-
globulin titres).
Liver biopsy can be performed (if clotting is normal) as a day-case or in-patient
under USS guidance, or during diagnostic laparoscopy. If liver biopsy suggests bile duct
obstruction despite a non-dilated duct, visualisation of the biliary tract is best achieved
by ERCP.
Treatment
For the surgeon this consists of:
✧ treating the specific cause of the jaundice
✧ treating the general effects of jaundice prior to any radiological/surgical
intervention.
140 GENERAL SURGERY OUTPATIENT DECISIONS

General management of jaundice

Pre-operative management aims to minimise the incidence of complications associated
with prolonged or severe cholestasis, which include infection (cholangitis, septicaemia,
wound infections), disorders of the clotting mechanism, renal failure, liver failure and
fluid and electrolyte abnormalities. Delayed wound healing is more associated with
malignancy than jaundice alone.
Correct disorders of nutrition
Oral dietary supplements are preferred to intravenous supplements to control gut
bacteria. Some centres advocate the oral administration of bile salts, and more recently
lactulose, to reduce the intestinal absorption of endotoxins for the intestinal microflora
and thus minimise the incidence of renal failure following surgical intervention. There
are suggestions that probiotics may help modulate intestinal microflora. Hypokalaemia
is frequent and should be corrected.
Prevention of infective complications
Prophylactic antibiotics are given to cover high-risk patients: all jaundiced patients,
patients with rigors and pyrexia, patients undergoing emergency biliary procedures/
operations, elderly patients, and patients with common bile duct stones or secondary
biliary interventions.
Correct disorders of coagulation
When prolonged prothrombin time secondary to vitamin K deficiency (give intravenous
injections of 10 mg vitamin K until deficit is corrected). Poor prognosis is associated with
poor response, therefore give FFP just prior to surgery. Severely jaundiced patients need
careful monitoring of fibrinogen levels, fibrin degradation products and platelet counts
to rule out disseminated intravascular coagulopathy DIC.
Prevention of renal failure
The patient should be well hydrated. Administer intravenous fluids, e.g. 12–24 hours
prior to surgery infuse 5% dextrose intravenously, then give mannitol at induction of
anaesthesia.
Prevention of hepatic encephalopathy
Particularly consider this in patients with prolonged bile duct obstruction and those with
pre-existing hepatocellular disease such as cirrhosis or chronic active hepatitis.
Stenting
If jaundice is severe (serum bilirubin greater than 150 umol/l); the patient is very
distressed with pruritus; there are signs of cholangitis; there is going to be an undue
delay in getting to surgery; or there are signs of impending liver failure; then a period of
decompression is indicated by insertion of a biliary stent via ERCP. PTC can be performed
if ERCP fails, and it is more likely to be needed in obstruction at the hilum.
Hepatomegaly
A patient may be referred to the surgical clinic with an enlarged liver, or hepatomegaly
may be discovered on routine abdominal examination. Generally a liver that is palpable
below the costal margin is thought to be enlarged, but this is not always the case.
Determine the following features.
✧ Is the liver truly enlarged? True enlargement is suggested by liver dullness extending
from the fifth intercostal space to a point below the costal margin. Apparent enlarge-
ment may occur when a liver is pushed down by a hyperexpanded lung, as occurs in
 LIVER, BILIARY SYSTEM AND PANCREAS 141

chronic obstructive airways disease, and is suggested by lower level of liver dullness.
✧ Is the enlargement focal or generalised? Localised swellings are caused by conditions
such as Riedel’s lobe, hydatid cyst, amoebic abscess and primary carcinoma.
✧ Is generalised enlargement smooth or irregular? Causes of smooth enlargement include
congestive cardiac failure, cirrhosis, reticuloses, Budd-Chiari and storage diseases.
Irregular enlargement is associated with metastatic liver tumours, macronodular
cirrhosis, primary liver tumours and polycystic disease.
✧ Is jaundice present? Smooth enlargement associated with jaundice includes viral
hepatitis, biliary-tract obstruction and cholangitis. Irregular enlargement associated
with jaundice occurs with macronodular cirrhosis and multiple metastases.
Objectives
Identify the cause, identify treatable causes, treat the cause.
History
Take a general hepatobiliary history. If jaundice is present take a general jaundice history.
Establish whether there has been previous treatment for malignancy. If not, are there
symptoms in other systems to suggest malignancy?
Examination
Determine whether true liver enlargement exists. Determine whether this is localised
or generalised, smooth or irregular. Determine whether jaundice is present. Perform
a general examination looking for causes of liver enlargement and evidence of liver
impairment.
Investigations
Carry out urinalysis, liver function tests, FBC and clotting studies. Ultrasound is often
diagnostic and answers the above questions in more detail. Liver biopsy may be indicated
in cirrhosis and tumours (after consultation with a liver surgeon).
Treatment
Treat according to the specific condition diagnosed.
Follow-up
Intervals should be short until diagnosis is established and malignancy excluded:
1–2 weeks.
Liver cirrhosis
Cirrhosis is the end result of liver cell death by whatever cause – alcoholic, metabolic or
cholestatic. Three morphological types are described: micronodular (alcoholic, malnutri-
tion); macronodular; and mixed. Cirrhosis has two major consequences: hepatocellular
failure and portal hypertension.
Objectives
Diagnose cirrhosis, detect the underlying cause, detect major consequences, treat
cirrhosis, treat the underlying cause, treat consequences.
History
Take a general liver history. Uncomplicated cirrhosis is often asymptomatic. Ask about the
complications of cirrhosis, e.g. gastrointestinal haemorrhage (varices) or hepatocellular
failure. Ask about possible underlying causes, e.g. alcohol, drugs, hepatitis, previous
biliary disorders, metabolic disorders or autoimmune disorders.
142 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
Perform a general examination. Examine for palmar erythema or unexplained peripheral
oedema, muscle wasting, ascites, jaundice or hepatic encephalopathy.
Prior to any surgical procedure in the presence of liver disease, assess the risk using a
Child score.
Investigations
LFTs, USS and liver biopsy are usually diagnostic. Other useful investigations include
FBC, clotting and serology for hepatitis A, B and C, autoimmune disease and primary
biliary cirrhosis (antimitochondrial antibody). OGD to detect varices is performed if
indicated.
Treatment
Treatment is mainly medical but is important to the surgeon if a patient with cirrhosis
is to undergo a surgical procedure or requires surgical intervention for the consequences
of cirrhosis, e.g. bleeding varices. Note that cirrhotic liver does not regenerate as normal
liver does. There is no specific medical treatment for cirrhosis. Treatment is aimed
at the underlying cause and at detecting and treating the consequences of cirrhosis,
such as hepatocellular failure and portal hypertension (see relevant sections). Liver
transplantation should be considered in patients heading towards end-stage liver failure,
provided they meet the eligibility criteria.
Follow-up
Follow-up is long term for detection of hepatocellular failure and portal hypertension.
There should be periodic (six-monthly) estimations of AFP and liver USS to detect the
development of primary liver tumours in Child’s A/B cirrhotics.
Alcoholic liver disease
Damage varies, from fatty infiltration to alcoholic hepatitis, hepatic fibrosis and
cirrhosis.
Objectives
Diagnose alcoholic liver disease, assess the severity, treat the alcoholic liver disease, treat
the underlying cause.
History
Take a general liver history. There may be general symptoms of liver disease and a history
of high and/or prolonged alcohol ingestion. Enquire for symptoms suggesting the
development of liver failure or portal hypertension. There may be associated symptoms
of alcohol damage to other organs, chronic pancreatitis, cardiomyopathy, myopathy,
peripheral neuropathy and neurological effects.
Examination
Perform a general examination. The commonest and earliest sign of liver disease is
hepatomegaly, which may progress to a tender liver from fatty infiltration of the paren-
chyma and from jaundice. Examine for evidence of liver failure or portal hypertension.
Investigations
LFTs may show raised transaminases, FBC may indicate anaemia and there may be a
leucocytosis indicating hepatitis. An elevated mean corpuscular volume (MCV) may be
indicative, but can also be elevated in other conditions such as B12 and folate deficiency.
Clotting abnormalities may be present. Liver biopsy is performed – early disease shows
 LIVER, BILIARY SYSTEM AND PANCREAS 143

fatty infiltration, later cases show the classic features of micronodular cirrhosis.
Raised gamma GT is suggestive of diagnosis.
Treatment
Abstinence from alcohol and psychiatric help may be necessary. Corticosteroids may be
prescribed in alcoholic hepatitis. Liver transplant can be an option for synthetic failure
or the complications of liver failure if six months abstinence is documented. Otherwise
treatment is as for cirrhosis.
Follow-up
Follow-up is generally managed by a gastroenterologist with a liver interest with involve-
ment of the surgeon if the patient is referred for treatment of co-existing disorders or being
considered for transplant. If cirrhosis is present, follow-up is the same as for cirrhosis.
Cholestatic liver disease
This consists of impaired bile secretion/excretion leading to conjugated hyperbilirubi-
naemia and raised ductular enzymes.
The causes include excess alcohol ingestion, viral hepatitis and obstructive lesions of
biliary tract, both intrahepatic and extrahepatic.
Primary biliary cirrhosis
Intrahepatic bile ducts are progressively destroyed by an immunological process. It is
often asymptomatic for long periods, and it is diagnosed on abnormal liver function
tests.
History
Take a general liver history. The patient may be asymptomatic or complain of itching,
weight loss, malaise and icterus.
Examination
Perform a general examination. Examination may be normal in early disease but later the
liver becomes enlarged and the development of portal hypertension leads to splenomegaly.
Deposition of cholesterol in the tissue around the orbits and extensor surface of the large
joints may be detected. In advanced disease, intrapulmonary shunting leads to finger
clubbing. Malabsorption of fat-soluble vitamins may lead to osteoporosis.
Investigations
Test urea and electrolytes (U&E) to detect hyponatraemia. LFTs are abnormal with a
raised alkaline phosphatase. Antimitochondrial antibodies are found in all patients. IgM
and smooth muscle antibody is also elevated. Clotting may be abnormal. USS may not
be diagnostic but it helps to exclude other causes such as extrahepatic biliary obstruction,
and it may detect portal hypertension.
Treatment
There is no effective medical treatment. Treat symptoms with cholestyramine for itch-
ing and ursodeoxycholate for other symptoms, and this may improve the liver function
tests. If there is no improvement, prednisolone may be effective in decreasing fatigue and
itching and in causing an improvement in LFTs. Give a monthly injection of fat-soluble
vitamins.
Surgical intervention is liver transplantation before the onset of hyponatraemia or
significant osteoporosis. Indications for surgery include decreased quality of life or
bilirubin greater than 100 mmol/l and/or portal hypertension.
144 GENERAL SURGERY OUTPATIENT DECISIONS

Follow-up
Follow-up is long term, for life.
Metabolic liver disease
Metabolic liver disease can be classified into two main types:
✧ disorders of mineral deposition
✧ disorders associated with defective enzyme production or release.

Objectives
Diagnose metabolic liver disease, diagnose the underlying cause, treat cirrhosis, treat
underlying cause, treat the complications of cirrhosis.
Haemochromatosis
Primary is genetic, autosomal recessive; secondary is acquired due to multiple blood
transfusions and polycythaemia.
Primary haemochromatosis leads to progressive iron deposition in the liver, heart,
pancreas, joints and endocrine glands, with sparing of the spleen, lymph nodes and bone
marrow. Hepatic accumulation leads to cirrhosis with increased risk of hepatocellular
carcinoma.
History
History of diabetes (75%) and increasing pigmentation (‘brown diabetes’).
Examination
There is dusky brown pigmentation of skin, buccal mucosa and conjunctiva; and
cirrhosis. Also look for polyarthropathy, hypopituitarism and hypogonadism.
Investigations
Investigate with liver biopsy. There is excessive iron in the hepatocytes and Kupffer cells,
with fibrosis or macronodular cirrhosis. Serum ferritin and transferrin saturation exceeds
55%.
Treatment
Treatment is by phlebotomy, decreasing dietary intake of iron, giving iron chelating
agents and long-term follow-up.
Follow-up
Follow-up is long term. Monitor for development of hepatocellular carcinoma.
Wilson’s disease
There is copper deposition in the liver, cornea, kidneys and central nervous system (CNS)
(basal ganglia). Liver fibrosis and cirrhosis occurs at an early age.
History
Symptoms are similar to cirrhosis. Enquire about symptoms of liver failure and portal
hypertension.
Examination
Look for Kayser-Fleischer rings of pigment in the cornea. Examine for evidence of
cirrhosis liver failure and portal hypertension.
 LIVER, BILIARY SYSTEM AND PANCREAS 145

Investigations
Perform routine liver investigations: FBC, clotting, LFTs, USS liver biopsy. Copper
studies show serum copper and serum caeruloplasmin are reduced and urinary copper
levels are elevated in all young patients with chronic liver disease. There is low serum
caeruloplasmin and aminoaciduria.
Treatment
Treatment is by chelation with penicillamine or tientine; avoid copper and zinc
supplements. Liver transplant can be considered for end-stage liver disease.
Follow-up
Follow up long term for the treatment of copper storage and the consequences of
cirrhosis.
Cystic fibrosis
Of cystic fibrosis patients, 25% have clinical and biochemical evidence of liver disease,
including fatty change, focal biliary cirrhosis and portal fibrosis followed by multilobar
biliary cirrhosis. They may develop intrahepatic and extrahepatic strictures. Prognosis
is determined by the pulmonary disease rather than the liver disease, and as patients are
living longer features of liver disease may become more common.
Treatment
Treatment is long term for the development of cirrhosis. Ursodeoxycholic acid alters bile
flow and composition, leading to an increase in less toxic hydrophilic bile acids. Liver
transplant either alone or in combination with lung transplantation can be considered
for end-stage liver disease.
Alpha-1-antitrypsin deficiency
Lack of inhibition of neutrophil elastase leads to pulmonary and liver damage.
Treatment
There is no effective medical treatment. Plasma derived or synthetic α1-antitrypsin has
been used to treat pulmonary disease. Surgical treatment is liver transplantation and is
the second commonest indication for liver transplant in childhood.
Hereditary tyrosinaemia type 1
This is an autosomal recessive disorder resulting in the lack of the enzyme fumaryl
acetoacetate hydrolase and leading to the accumulation of the toxic products of amino
acid degradation in the kidney, liver and nervous tissues.
The acute form leads to liver failure in infancy and death in the first year of life.
In the chronic form there is renal tubular dysfunction, rickets, progressive liver disease
and development of hepatocellular carcinoma (40%).
Treatment
Treatment is by hepatic transplantation.
Hepatic abscess
There are two main types: pyogenic and amoebic. All abscesses are more common in
the right lobe and both types have a high incidence of right lower lung abnormalities
(50%). Mortality is increased by multiple abscesses, hyperbilirubinaemia and co-morbid
disease.
146 GENERAL SURGERY OUTPATIENT DECISIONS

Objectives
Diagnose abscess, diagnose the cause, treat abscess.
Pyogenic abscess
The main aetiology is from bile duct-ascending cholangitis, caused by Escherichia coli
and anaerobic organisms. Other causes include portal pyaemia, e.g. from complicated
diverticular disease; septicaemia; direct extension from suppurating cholecystitis;
penetrating peptic ulcer disease or devitalised liver from trauma. In the frail geriatric
population, liver abscesses may be insidious and non-specific, caused by Strep. milleri.
Pyogenic abscesses can be either pus, surrounded by a fibrous capsule or, if antibiotics are
used early in the course, a solid abscess containing inflammatory cells, dying liver cells
and fibrotic tissue, mimicking a neoplastic lesion.
Amoebic abscess
This spreads to the liver via the portal vein from the bowel. It tends to affect younger
patients.
Hepatic candidiasis
This occurs in immuno-compromised patients and complicates systemic candidiasis.
There is often combined hepatic and splenic involvement. It forms target lesions – a
central mass of fungus surrounded by necrotic liver cells, detected by CT or USS. Needle
biopsy is not performed. These lesions need open or laparoscopic wedge excision for
diagnosis and treatment.
History
Pyogenic abscesses tend to present as a primary disorder with fever, rigors, profuse
sweating, anorexia and vomiting – pain is a late symptom. Amoebic abscesses present
with a low-grade fever but with more pain, which is aggravated by movement and
coughing.
Examination
Hepatomegaly may be a feature and 50% will have diarrhoea. In right lobe disease the
patient may exhibit bulging and pitting of the intercostal spaces.
Investigations
FBC may show anaemia and leucocytosis. LFTs usually show an abnormal alkaline
phosphatase, and alanine transaminase may also be raised. The ESR is raised. Amoebic
abscess is diagnosed by positive serological tests (serum complement fixation test),
amoebic trophozoites in abscess fluid and a rapid response to anti-amoebics. USS and
CT scan are performed and diagnostic aspiration under imaging control is performed
if indicated. CXR may detect lung involvement. In pyogenic abscesses with no obvious
source of sepsis in the gut or biliary tree, look for an occult focus of infection elsewhere
(e.g. endocarditis, dental sepsis); do blood cultures before starting antibiotic therapy.
Treatment
Treat pyogenic abscess with aspiration or drainage under radiological control and
appropriate antibiotics based on microbiological samples. Treat amoebic abscess with
metronidazole. If there is no improvement and the cyst is single and unilocular, provide
percutaneous drainage. Otherwise surgical drainage is indicated.
Follow-up
Treatment is mainly as an in-patient. After percutaneous or surgical drainage, monitor by
 LIVER, BILIARY SYSTEM AND PANCREAS 147

frequent USS until there is evidence of resolution, then discharge with advice to return if
symptoms recur. Very occasionally a neoplasm may mimic an abscess.
Liver cysts
There are two main types: non-parasitic or parasitic.
Non-parasitic liver cysts
These may be developmental, traumatic, dermoid or associated with other disorders such
as congenital hepatic fibrosis, hamartoma, Caroli’s disease, choledochal cyst or polycystic
disease (liver, kidneys). Non-parasitic cysts are usually detected in middle-aged females.
Objectives
Diagnose the cause, treat the cause.
History
Most are asymptomatic until large enough to press on other structures. They are often
present with non-specific symptoms of vomiting, upper abdominal pain and occasionally
diarrhoea. Torsion, rupture or haemorrhage into a cyst produces sudden-onset pain.
Examination
Most have a non-tender liver swelling. Jaundice is rare.
Investigations
Liver function tests are usually normal. USS is usually diagnostic, although CT can also be
used. It is important to identify cystic neoplasms (e.g. biliary cystadenoma). If in doubt,
do fine-needle aspiration of the cyst fluid under ultrasound guidance and send the fluid
for cytology and CEA level (high levels suggest a mucinous neoplasm). Ultrasound is
useful in detecting cysts in the kidneys, which develop before liver cysts in polycystic
disease. Occasionally multiple cysts can be confused with metastases.
Treatment
Small asyptomatic cysts do not require treatment unless complications occur. Treatment
is confined to single large cysts, which are treated by laparoscopic surgical deroofing.
Polycystic liver disease treatment is confined to those patients who develop local
symptoms or portal hypertension due to compression of the portal vein. Aspiration of
cysts with instillation of fibrosing agents is almost never effective. Laparoscopic deroofing
and liver resection have been advocated in specialised centres.
Follow-up
Intervals are short until diagnosis is achieved and neoplastic lesions excluded. Thereafter
small asymptomatic cysts can be followed up yearly with an USS to detect enlargement.
Post-operative follow-up
Review histology. Detect general complications of surgery like wound healing. Give
regular USS to detect recurrence, or reserve until symptoms recur.
Parasitic cysts – Hydatid cysts
These are caused by ingestion of vegetables and water contaminated (usually by dogs)
with the eggs of the parasite Echinococcus granulosus (unilocular cyst, good prognosis)
or E. multilocularis (multiple cysts, poor prognosis).
148 GENERAL SURGERY OUTPATIENT DECISIONS

History
General health is good. In all ages pain, jaundice, and ascites are uncommon. Patients
usually present with a painless liver mass or complications. A history of contact with dogs
or sheep is usual. Patients occasionally complain of right upper quadrant (RUQ) pain.
Examination
There is a smooth, rounded tense mass. If there is secondary infection there may be hepa-
tomegaly, rigors and pyrexia and deep-rooted continuous pain. Jaundice is infrequent.
Complications
Intrabiliary rupture of the cyst produces biliary colic, jaundice and fever. Vomitus may
contain hydatid cysts and membranes.
Intraperitoneal rupture leads to severe pain and shock with urticaria and pruritus.
Intrathoracic rupture produces bile-stained sputum.
Investigations
AXR shows calcified reticular shadow. Following intrabiliary rupture there may be gas in
the cyst. Ultrasound shows an echogenic cyst.
FBC shows eosinophilia in 25%. Complement fixation test for hydatids is positive in
93%. Enzyme-linked immunosorbent assay (ELISA) gives positive results in 90% of cases
(so 10% of patients can be false negative). Casoni’s test has been largely abandoned. LFTs
are usually abnormal and may demonstrate an obstructive picture.
Treatment
Cysts with extensive calcification are usually sterile and best left alone.
✧ Medical treatment consists of albendazole: 30% of cysts disappear, 30–50% show
reduction and 20–40% remain unchanged.
✧ Radiological teatment consists of the PAIR routine: percutaneous fine-needle
puncture, aspiration, injection of hypertonic saline and reaspiration. There is a small
but definite risk of anaphylaxis and a theoretical risk of peritoneal seeding.
✧ Surgical treatment consists of removing the cyst entirely, cystectomy with removal
of the germinal and laminated layers and preservation of the host-derived ectocyst.
Alternatively it may be possible to enucleate the cyst. Cysts complicated by secondary
infection require surgical drainage. Treatment by partial liver resection may be
required, especially if the cysts are large and/or multiple. Remember to administer a
course of albendazole before PAIR or surgery.
Follow-up
Follow up at short intervals until diagnosis is achieved. Then treatment is arranged.
Post-operative follow-up
Check pathology results. Detect general complications of surgery. Ascites may complicate
this surgery and may indicate disseminated disease. Repeat USS until resolution of the
cyst is confirmed, then discharge with advice.

Benign solid tumours

Haemangioma (vascular malformation)
These are blood-filled endothelial lesions with fibrous tissue. If big enough they produce
size effects of pain, vomiting and elevation of diaphragm. There may be a palpable
abdominal mass, which, if large, may produce heart failure in children and be associated
with skin lesions in 85%. A bruit is audible in 15%. Rupture is rare. Lesions are hyperechoic
 LIVER, BILIARY SYSTEM AND PANCREAS 149

on USS. CT scans with intravenous (IV) contrast are usually diagnostic. If doubt still
exists, a labelled red cell scan is performed.
MRI can be useful in confirming the disease when it is equivocal on other imaging
modalities. Where the diagnosis is certain and the risk of bleeding minimal, lesions can
be observed. If large and peripherally placed, it may be suitable for surgical resection. If
it is difficult to differentiate from neoplastic lesions, surgical resection is indicated.
Hamartoma
This is a congenital condition of normal tissues with disorderly arrangement. It presents
as large liver masses in children, which produce pressure effects (pain, vomiting). Patients
complain of an expanding abdomen with a mass. CT scan is diagnostic. Treatment is by
surgical excision if the diagnosis is clear. Occasionally these are sarcomatous.
Adenomas and focal nodular hyperplasia
These are very similar in pathological terms.
✧ Adenomas are variable in size (4–30cm) and 90% occur in women between the ages
of 30–60.There is an association with long-term use of oestrogen contraceptive pills.
Thirty per cent rupture or haemorrhage and can be difficult to distinguish from low-
grade hepatoma. There is an increased risk of rupture in pregnancy. Adenomas are
pre-malignant.
✧ Focal nodular hyperplasia (FNH) occurs in the same patients, is not pre-malignant and
may be observed without serious risk. If haemorrhage occurs, successful management
can be ligation of the feeding vessel or wedge resection.
History
Take a general liver history. Most patients will be women aged from 30–60 with a history
of oral contraceptive use. A third present with an abdominal mass, a third with rupture
and a third are incidental findings. Symptoms are commonly vague – upper abdominal
pain and discomfort.
Examination
Perform a general examination. Evidence of jaundice and anaemia may be present. The
liver may be focally enlarged.
Investigations
LFTs are usually normal. FBC may reveal anaemia due to bleeding. Adenomas appear
solid on ultrasound and have a characteristic arteriographic appearance. FNH also has a
characteristic CT appearance with the presence of a central scar. Open/laparoscopic liver
biopsy for histology can be performed where the diagnosis is unclear, but adenomas can
be difficult to distinguish from well-differentiated hepatocellular carcinoma.
Treatment
Ruptured and bleeding lesions are excised as emergencies. Hepatic arterial embolisation
can be useful in stopping bleeding. Intracapsular haemorrhage presents as an expanding
tumour and requires partial liver resection. FNH does not need any treatment once
confirmed on imaging, whereas adenomas should be excised as they are pre-malignant.
Follow-up
Patients with multiple adenomas need prolonged follow-up with repeated imaging. In
females, stop the oral contraceptive pill. If diagnosis is certain then it is acceptable to
monitor lesions every 6–12 months with ultrasound scans. If static or diminishing in size
then operation may be deferred.
150 GENERAL SURGERY OUTPATIENT DECISIONS

Post-operative follow-up
Enlargement of residual adenomas requires elective excision.
Adenomatous hyperplasia
This refers to sizeable nodules which develop in chronic liver disease. They may have
pre-malignant potential and require long-term follow-up. Cholangioma and biliary
cystadenoma are rare lesions.

Primary malignant tumours of the liver

The commonest tumour is primary hepatocellular carcinoma. Its incidence and geo-
graphical distribution parallels that of hepatitis B infection. It usually develops on a
background of cirrhosis, but can also develop in a normal liver. Other rarer tumours
include hepatocellular cholangiocarcinoma. This rare tumour shows features of both
hepatocellular and cholangiocarcinoma and is thought to represent a coincidental
occurrence of both. Cystadenocarcinoma tends to present as a large cystic tumour in
adults. Sarcoma arises from the connective tissue elements of the liver and presents as a
rapidly enlarging lesion associated with hypoglycaemia. Angiosarcoma is associated with
the occupations linked to vinyl chloride production or ingestion of arsenic or anabolic
steroids. It is an aggressive tumour.
In children the main tumours are hepatocellular carcinoma and hepatoblastoma.
Hepatoblastoma tends to occur by the third year and produces increased levels of alpha-
foetoprotein and gonadotropins, occasionally causing sexual precocity. Liver resection
produces long-term survivors in 30%.
Hepatocellular carcinoma
Objectives
Diagnose hepatocellular carcinoma (HCC), differentiate from other causes of liver
tumours, localise and stage the tumour, determine resectability, treat the tumour.
History
Take a general liver history. In areas of the world that screen for hepatocellular cancer
the tumour may be detected when it is asymptomatic. In patients with the onset of liver
cirrhosis, HCC is heralded by a worsening of liver function, producing ascites, jaundice,
encephalopathy, and variceal bleeding. Patients may describe a feeling of a heavy mass
within the abdomen dragging down, especially during exercise. General symptoms
include anorexia, weight loss, abdominal or chest pain, vomiting, fever and weakness.
Examination
There is occasionally jaundice. There is abdominal distension and a liver mass. There
is a bruit over the liver in 10% or friction rub is audible. Ascites is common and some-
times bloodstained. Additional infrequent clinical features include hypoglycaemia,
hypercalcaemia, hyperlipidaemia and hyperthyroidism. Examine for features of liver
failure and portal hypertension.
Investigations
LFTs are frequently abnormal. FBC may show either anaemia due to haemorrhage or
polycythaemia from anomalous erythropoietin production. AFP is raised in one-third
of cases. It is often high in undifferentiated disease and if it falls after resection it is useful
as a marker for recurrence. Hepatitis B and C serology needs to be done in all patients.
Clotting may be abnormal.
✧ Tumour markers are AFP and abnormal APT. Also measure CEA and carbohydrate
 LIVER, BILIARY SYSTEM AND PANCREAS 151

antigen 19–9 (CA 19–9) (markers for biliary-tract malignancies). Very high levels
are associated with undifferentiated disease and a poor prognosis. This is a variable
predictor for detection of hepatocellular carcinoma but any patient with chronic
active hepatitis or cirrhosis who develops a rising level of AFP or a level exceeding
500 ng/ml should have investigations for the detection of hepatocellular carcinoma,
e.g. USS.
✧ Tumour localisation: USS or CT scan are used to demonstrate size and position,
multiple deposits and extrahepatic spread, e.g. porta hepatis. CXR may show direct
diaphragmatic involvement or pulmonary metastases. Occasionally neither CT nor
USS show a lesion in a cirrhotic patient who has a rising level of AFP. In these cases
MRI may be useful or alternatively use a lipiodol-CT scan. Fine-needle aspiration
cytology under USS or CT guidance has been advocated to differentiate HCC from
other benign lesions in both cirrhotic and non-cirrhotic livers. However, there is a
proven risk of seeding tumour along the needle track and it is only necessary if the
diagnosis is in doubt.

Multi-slice helical CT scanners have reduced the need for arterioportography. For large
posterior tumours consider imaging of the vena cava (cavography) to exclude caval
involvement.
MRI scans carry a high diagnostic yield and can distinguish between benign and
malignant lesions.
Pre-operative preparation
Correct fluid, electrolyte and clotting abnormalities. Determine the operative risk.
Important considerations are that patients in Child’s grades B and C have lost 50–60%
of liver parenchyma already and patients with cirrhosis may not be able to regenerate
liver tissue.
Treatment – surgical
Surgical resection is the optimal treatment and small tumours (smaller than 5cm) carry the
best prognosis. Favourable results have also been obtained with local ablative techniques
such as alcohol injection and radiofrequency ablation (RFA). Recently investigated
modalities, e.g. radio-labelled ablation, laser photocoagulation and electrolysis, may
become important.
Liver transplantation is a recognised treatment of HCC arising in a cirrhotic liver.
Consideration is based on the Milan criteria: a single lesion less than 5cm or no more than
three lesions less than 3cm. The University of California, San Francisco (UCSF) expanded
criteria have included patients not meeting the Milan criteria.
Unresectable lesions
✧ Chemotherapy: both systemic and regional hepatic artery infusions give poor results,
with response rates as low as 10–15%, but sorafenib has been recently associated with
a small survival benefit. Immunotherapy, e.g. interferon or cytokines, has not proved
helpful.
✧ Chemoembolisation: transarterial embolisation of tumours with gelatin sponge
with or without added transarterial chemotherapeutic agents may give symptomatic
benefit, with slight improvement in overall survival in some studies. Microspheres
containing cytotoxic drugs can be given via the hepatic artery.
✧ Radiotherapy: external beam radiation causes radiation-induced hepatitis and is
rarely used. Microspheres containing radioisotopes like yttrium-90 can be injected
via the hepatic artery.
152 GENERAL SURGERY OUTPATIENT DECISIONS

Follow-up
Intervals should be short (1–4 weeks) until the diagnosis and treatment plan have been
decided. Many of these patients will have been followed up for cirrhosis.
Post-operative follow-up
Check the histology for the pathology and adequate resection margins. Common post-
operative complications include the development of liver failure and intra-abdominal
fluid collections. Investigate as indicated. The most common serious complication is
tumour recurrence. Monitor serum AFP levels and perform serial USS of the liver every
4–6 months. Further resection, if recurrence is localised, can be performed and has been
associated with extended survival. Median survival for these patients is in the region of
one year.
Metastatic disease of the liver
Direct invasion can occur from adjacent organs such as the stomach, pancreas and hepatic
flexure of colon. Most common tumours are metastatic from distant organs.
Objectives
Diagnose metastatic lesions, differentiate suitable lesions for resection, stage the tumours,
treat the tumours.
History
Take a general liver history. Many are asymptomatic. There may be a history of previ-
ous malignancy. If large, expansion of the liver may cause pain in the abdomen and
back. Flatulence and nausea may be features and lead to decreased appetite and weight
loss. Eventually malnutrition and cachexia develops. Symptoms of cirrhosis may be
present.
Examination
Perform a general examination. There may be evidence of weight loss. Hepatomegaly may
be present. Examine for underlying features of cirrhosis.
Investigations
USS will detect metastases larger than 1cm diameter and, combined with CT scan, will
reduce the false negative rate. LFTs may be normal. Serial CEA detects 30% of metastatic
livers with normal USS (false positive rate is 15%). Laparoscopy should ideally be
combined with intra-operative laparoscopic USS and liver biopsy.
Treatment – surgical
Fewer than 5% of liver metastases are suitable for resection. Surgical resection of the
liver is usually confined to metastatic colorectal, neuroendocrine or congenital tumours.
Rarely, other metastases may be considered for resection. Resection is contraindicated if
less than 25% (fewer than two segments) of the liver can be left. Likely residual volumes
can be calculated from CT images. Liver resection for colorectal metastases carries less
than 5% peri-operative mortality and a five-year survival of 35–45%.
Other treatments
✧ Chemotherapy: regional hepatic artery infusion or systemic chemotherapy produces
the same poor two-year survival. Intraperitoneal infusion has also been used.
✧ Chemoembolisation: transarterial chemoembolisation (TACE) using gelatin sponge
with 5FU, doxorubicin and cisplatin is beneficial in ocular melanoma, advanced
carcinoid syndrome and islet cell tumours. Complications include postembolisation
 LIVER, BILIARY SYSTEM AND PANCREAS 153

syndrome (nausea and vomiting, fever, abdominal pain and ileus), infarction of gall
bladder, pancreatitis and bleeding.
✧ In-situ ablative techniques are receiving much interest in the literature. These
techniques of cryotherapy (to produce an ice ball), radio-frequency, microwave and
laser therapy (to produce thermal necrosis) and electrolytic destruction have yet to
be tested in prospective randomised trials but are now commonly used as adjuncts to
surgical treatments or in patients deemed unresectable.
Follow-up
Follow up at short intervals until suitability for resection is determined. Arrange operative
or non-operative treatment as appropriate.
Post-operative follow-up
Check the histology for the pathology and adequate resection margins. Common post-
operative complications include the development of liver failure and intra-abdominal
fluid collections. Investigate as indicated. Monitor for recurrences with regular USS every
3–6 months, checking CEA levels. Occasionally re-resection is indicated.

The biliary tract

Liver, pancreatic and biliary disorders are closely related and should be considered
together. For instance, a lesion in the head of the pancreas may cause obstruction of
the biliary tract, which affects the function of the liver. One of the first objectives of the
assessment is to determine which system contains the primary disorder and then deter-
mine what effect this has had on the function of the others.
Assessment of biliary tract disorders
Biliary history
Start with a general gastrointestinal history. When responses indicate a possible biliary
problem, a more detailed biliary history is required. This may also mean a liver and
pancreatic history. The two main indicators of biliary disease are pain and jaundice, and
gallstones are the commonest cause.
✧ Biliary pain is colicky, severe and occurs in the right upper quadrant. It may radiate
around to the back. Colicky pain is caused by the gall bladder contracting to try and
overcome an obstruction. Eventually the contraction relaxes and the acute pain is
relieved, leaving a dull ache until the next contraction starts. If the obstruction is
caused by a gallstone, the stone may be expelled and the bout of biliary colic resolves
until the next stone produces another episode. If the stone becomes impacted,
inflammation and infection of the biliary tract can ensue. In the gall bladder the result
is cholecystitis and the pain becomes constant. If the bile ducts are affected, jaundice
and cholangitis may be produced.
✧ Jaundice: obstructive jaundice typically causes pale stools and dark urine and often
causes pruritus. An enquiry into possible liver and pancreatic disease is indicated.
Usually, jaundice caused by gallstone disease is associated with episodes of biliary
colic. The onset of painless jaundice may indicate a neoplastic cause.
✧ Rigours: a history of fever with rigours indicates infection of the biliary tree, and
when combined with pain and jaundice (Charcot’s triad) indicates an infected, ob-
structed biliary tree that requires urgent treatment (decompression) to prevent septic
shock.
✧ Risk factors: ask about previous biliary interventions or surgery. Recurrent biliary
symptoms may be due to complications of these original treatments. There may be a
family history of gallstones or there may be some inherited disorder that predisposes
154 GENERAL SURGERY OUTPATIENT DECISIONS

to the formation of gallstones, e.g. haemolytic anaemia, hyperlipidaemia, ileal disease

or surgical resection, cirrhosis or cystic fibrosis.
Biliary examination
Perform a general and gastrointestinal examination, but in particular look for signs of
jaundice and liver disease. Between episodes, abdominal examination may be normal.
An enlarged palpable gall bladder in the presence of jaundice is indicative of a neoplastic
cause rather than stone disease (Courvoisier’s law). Severe inflammation of the gall
bladder with adherent omentum may also produce a mass in the right upper quadrant;
however, all masses should be considered to be malignant until proven otherwise.
Rectal examination revealing the typical pale, toothpaste-consistency stools is typical of
obstructive jaundice.
Investigation of biliary tract disorders
Laboratory investigations
Urinalysis
The presence of conjugated bilirubin indicates obstructive jaundice, although in some
conditions associated with excess bilirubin production this will result in some bilirubin
in the urine.
Biochemistry
✧ Release of integral membrane enzymes: cholestasis and obstructive jaundice are
associated with an increased alkaline phosphatase. Gamma GT is particularly raised
in alcoholic liver disease. Minor increases in ALT and AST occur in cholestasis and
chronic liver disease. Significant increases are associated with acute hepatitis or with
liver cell necrosis of any cause. Secondary tumour deposits cause a rise in alkaline
phosphatase and gamma GT and a small rise in bilirubin.
✧ Tests for urea and electrolytes may indicate electrolyte abnormalities, particularly
hyponatraemia and hypoglycaemia. Evidence of raised urea and creatinine levels may
indicate impaired renal function associated with liver disease.
Haematology
FBC may reveal anaemia of chronic disease or indicate blood loss from the biliary system
into the gastrointestinal tract. Other abnormalities of the blood cells may be detected,
such as haemolytic anaemia, leukaemia and lymphoma. Clotting, particularly the INR,
may be abnormal in liver and biliary disease.
Immunology
Hepatitis serology: screen for hepatitis B and C. Also screen for autoimmune disease and
primary biliary cirrhosis.
Imaging techniques
Ultrasound
For technique, request form, results.
✧ The advantage of USS is that, as the first-line investigation, it is a very good non-
invasive technique for visualising the presence of stones, gall bladder disease, dilatation
of biliary tract and hepatic parenchymal disease. Also possible is ultrasound-guided
biopsy of the liver and pancreas. A common hepatic duct with a diameter over 10mm
is deemed dilated. A diameter above 15mm indicates significant organic disease.
However, there is a 5–10% incidence of ductal stones in a common bile duct (CBD)
of 5mm diameter. Other causes of duct dilatation include pancreaticobiliary cancer,
chronic pancreatitis, congenital cystic disease and parasitic infestation.
 LIVER, BILIARY SYSTEM AND PANCREAS 155

✧ The disadvantages are that accuracy is dependent on the experience of the operator;
and it may be unsatisfactory in obese patients, following previous surgery, or in the
presence of ascites or gaseous distension of upper abdominal viscera. In these cases
do a CT scan.
CT scan
For technique, request form, results.
✧ The advantages are that intravenous contrast can be given to outline the vessels
and focal lesions within the liver and multiple scans can be performed to give non-
contrast, arterial, venous and delayed phases of scanning; modern multi-slice spiral
CT scans can be performed quickly (15–30 seconds) using 5mm cuts, giving more
detail and allowing more sophisticated reconstruction; when used with contrast, CT
is more sensitive than ultrasound at determining the nature of lesions within the liver,
especially differentiating between small tumours cysts or abscesses; and CT is better
for detection of solid lesions in the extrahepatic bile ducts (cholangiocarcinoma),
pancreas and liver. MRI is useful in hilar carcinoma and primary carcinoma of the
gall bladder, where it is superior to CT in assessing the presence and extent of extra-
mural invasion.
✧ The disadvantages are that it is expensive and it uses ionising radiation.

MRI
For technique, request form, results.
✧ MRI is useful in hilar cholangiocarcinoma and primary carcinoma of the gall bladder,
where it is superior to CT in assessing the presence and extent of extramural invasion.
Newer techniques include MRCP, which may supersede diagnostic ERCP.
✧ The disadvantages are that it is expensive and time-consuming; and many patients
find the experience unpleasantly claustrophobic.
PTC
Ultrasound is used to identify the dilated biliary system. Under local anaesthetic a needle
is inserted through the liver parenchyma into the dilated bile duct and contrast agent is
injected under X-ray screening to visualise the biliary system. Where an obstruction is
detected a percutaneous drain can be inserted to continue drainage after the procedure.
Prior to procedure cover with antibiotics and correct any clotting abnormalities.
✧ The request form is the radiology/ultrasonography request form.
✧ Results are as a written report and selection of X-ray images.
✧ The advantages are that it is used for visualisation of the biliary tract in the jaundiced
patient, transhepatic drainage and insertion of endoprosthesis. In practice PTC is
used when ERCP has failed, or for insertion of stents for palliation of large bile duct
obstruction due to inoperable/incurable malignancy. It can be better at biliary drainage
and visualisation of the biliary tree than ERCP for hilar cholangiocarcinoma.
✧ The disadvantages are complications including septicaemia, haemorrhage into
peritoneal cavity and haemobilia, biliary peritonitis, intrahepatic arterioportal fistula,
pneumothorax and contrast reactions.
ERCP
ERCP is performed using a large-bore side-viewing endoscope. The scope is passed
through the stomach into the second part of the duodenum. The duodenal papilla is
cannulated and contrast is injected under X-ray screening. The pancreatic and biliary
duct system is visualised.
✧ The request form is the endoscopy/radiology form. It is a joint procedure between the
radiology department and the endoscopy service.
156 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Results are as a written report and selection of ERCP images.

✧ The advantages are that it can be performed in all cholestatic jaundice patients irre-
spective of whether the ducts are dilated or not; it also gives views of the stomach and
duodenum; the pancreaticogram can be performed; certain lesions can be treated or
palliated during the procedure – stone removal, endoscopic nasobiliary drainage, stent
insertion for inoperable malignant large bile duct obstruction; and ERCP is good for
diagnosis of ductal calculi, tumours of bile duct and pancreas and sclerosing cholan-
gitis. In patients with complete biliary obstruction the proximal biliary tree may not
be visualised and PTC is then indicated.
✧ The disadvantages are complications, which include pancreatitis (1–2%). If sphinc-
terotomy is also performed complications rise to 6–10% and include haemorrhage,
acute pancreatitis, cholangitis, retroperitoneal perforation, impacted Dormia basket,
acute cholecystitis and gallstone ileus. Technical failure may result in patients with
duodenal stenosis, previous Billroth II and duodenal diverticula and in an unco-
operative patient.
Biliary manometry
This technique is performed at ERCP. The common bile duct is cannulated and the
pressure in the bile duct is measured.
Request form and results are as for ERCP.
✧ The advantage is that it is good for investigation of patients with biliary dyskinesia
(persistent pain after cholecystectomy) to characterise abnormalities of the sphincter
(stenosis, dyskinesia). Measures are basal sphincter pressure, rate and progression of
sphincter contractions and response to morphine and cholecystokinin. Dyskinesia
is diagnosed by increased basal pressure, altered frequency and amplitude of phasic
contractions and reversal of normal peristaltic direction.
✧ The disadvantages are as for ERCP. Results can be difficult to interpret.

Laparoscopy
Under general anaesthetic a laparoscope is inserted through a small sub-umbilical incision.
It can be used as an investigative technique and can be combined with laparoscopic
ultrasonography, cholangiography, biopsy or cytology.
✧ No request form. It is a surgical operation.
✧ The results is a written operation note, sometimes with photographic images.
✧ The advantages are that it allows visualisation of the liver, gall bladder, extrahepatic
biliary system and pancreas and peritoneal lining; it can diagnose hepatic disease,
primary neoplasms, secondary tumour deposits in the liver and peritoneum, and it
enables biopsy of these lesions for histology; it also enables staging of hepatobiliary
and pancreatic tumours; and it is useful for liver biopsy in chronic liver disease with
a high risk of bleeding – haemostasis can be achieved and observed.
✧ The disadvantage is that it requires a general anaesthetic and is therefore associated
with GA complications.
Biliary scintiscanning
The technique uses 99mTc-labelled compounds of iminodiacetic acid (HIDA, DISIDA,
PIPIDA). HIDA is injected intravenously, taken up by hepatocytes, and then secreted into
bile ducts and concentrated in a functioning gall bladder.
✧ Request form is for radioisotopes (medical physics department).
✧ Results are as a written report and selection of images.
✧ The advantages are that if the compounds are not taken up by the gall bladder, the
most likely diagnosis is cholecystitis (false positives – chronic cholecystitis, gallstone
pancreatitis, patients with alcoholic liver disease, patients receiving parenteral
 LIVER, BILIARY SYSTEM AND PANCREAS 157

nutrition); if the gall bladder is visualised, then it is 100% certain that it is not
cholecystitis; it is routinely used in the jaundiced neonate for diagnosis of biliary
atresia; and it is also useful for the functional evaluation of surgically constructed
bilioenteric anastomoses.
✧ The disadvantage is the use of radioactivity. It is not used routinely – only for specific
indications.
Intra-operative cholangiography and choledochoscopy
These techniques are used intra-operatively to assess the biliary system to identify abnormal
anatomy or the presence of stones and to confirm their absence or complete removal.
Disorders of the biliary tract
Cystic disease of the biliary tract
Choledochal cysts include bile duct dilatation, choledochocele, bile duct diverticulae and/
or liver cysts. There is increased incidence in the Japanese and 60% of cases occur in the
first 10 years. Complications include cholangitis, pancreatitis, hepatic abscess formation
and cholangiocarcinoma.
History
Symptoms of increasing jaundice, right upper quadrant pain and complications.
Examination
Cholestatic jaundice, abdominal mass and tenderness.
Investigations
USS and CT gives the diagnosis. MRCP or ERCP defines the anatomy.
Treatment
Treatment is surgical excision of extrahepatic biliary tree and reconstruction in the form
of a hepatico-jejunostomy, with or without liver resection, and drainage of simple liver
cysts. Surgery is recommended even in asymptomatic patients to reduce long-term risk
of cholangiocarcinoma.
Gallstones
Gallstones are very common (18.5% in autopsy studies). There are three types:
✧ cholesterol: often radiolucent, multiple or large and single
✧ pigment: associated with infection or with haemolytic disease
✧ mixed.

Risk factors
Gallstones are more common in females and are associated with obesity, increasing age,
genetic and ethnic factors, refined diet high in animal fat, diabetes mellitus, ileal disease
and resection, haemolytic states, infection of biliary tract, parasitic infection, cirrhosis
and cystic fibrosis.
Differential diagnosis
Most gallstones are clinically silent. Common co-existing causes of abdominal pain
include colonic motility disorders and diverticular disease, gastritis and peptic ulcera-
tion, reflux oesophagitis and hiatus hernia, pancreatitis, colonic cancer, renal disease and
ischaemic heart disease. In addition to gall bladder imaging, an OGD (or barium series)
and barium enema may be necessary in patients undergoing elective cholecystectomy
for chronic symptoms.
158 GENERAL SURGERY OUTPATIENT DECISIONS

Silent gallstones
The vast majority will not cause symptoms or complications during life. Therefore there
is no indication for cholecystectomy in the management of asymptomatic gallstones,
except in acromegalic patients on long-term somatostatin analogue where gallstones can
get very large; and in diabetic patients with gallstones.
Symptomatic gallstones – acute cholecystitis
This often presents with admission to hospital with acute abdominal pain, where the
relevant investigations are performed and treatment is arranged.
Chronic cholecystitis
Cholecystectomy for gallstones is one of the commonest operations performed in the
Western world. Partly this is because ultrasound is widely used for the investigation of
abdominal pain and is very sensitive at detecting gallstones. Once detected, gallstones can
be difficult to exclude as the cause of the pain until they are removed.
Objectives
Diagnose gallstones, differentiate from other causes of abdominal pain, treat gallstones.
History
Take a general biliary history. Typically, patients report recurrent attacks of epigastric
or right hypochondrial pain, often radiating to the right side of the back or shoulder
blade. Bouts of pain last several minutes to hours; they may subside or progress to acute
cholecystitis. Nausea and vomiting may accompany each episode. Jaundice and dark
urine may follow an acute attack and indicate a CBD stone. Intolerance to fatty foods,
abdominal distension and belching can occur with the same frequency in the general
population as they do in patients with gallstones.
Examination
Perform a general examination. Look for jaundice and signs of liver disease. Examination
may be normal or there may be tenderness in the right upper quadrant. Occasionally
adherent omentum to a previously inflamed gall bladder may produce a right upper
quadrant mass.
Investigations
LFTs may be normal or demonstrate obstructive jaundice. USS detects gallstones and
the presence of a dilated CBD. OGD and/or barium enema is used in selected patients to
exclude co-existing disorders.
Treatment
Treatment is usually surgical. The current surgical standard is laparoscopic cholecys-
tectomy. Advantages claimed for the laparoscopic approach include less pain, absence
of ileus, day-case surgery, back to work in 10–14 days, less wound infection, less chest
infection and less wound dehiscence. Warn the patient that the operation may be
converted to an open procedure if there is dense fibrosis in Calot’s triangle, severe
adhesions from previous surgery, Mirizzi’s syndrome or severe acute disease with
inflammatory oedema. Conversion rate is widely reported as 5%.
Mini-cholecystectomy is an open cholecystectomy via a 5cm subcostal incision with
use of a circular retractor. There is little evidence now to support its routine use.
Follow-up
Straightforward cases can be reviewed in 4–6 weeks with the results of investigations. If
there are atypical features to the history or examination, review sooner.
 LIVER, BILIARY SYSTEM AND PANCREAS 159

Post-operative follow-up
Review uncomplicated cases in 4–6 weeks after surgery with histology. If histology
confirms chronic cholecystitis and the patient is symptom-free, discharge. Complications
include wound infection, incisional hernia and wound pain. Long-term complications
include duct injury (which may present as progressive jaundice); damage to duodenum,
jejunum and colon; and abscess formation around lost stones.
Persistence of original symptoms may be due to residual stones or alternative causes
of abdominal pain and is known as post-cholecystectomy syndrome.
Other treatments for gallstones
Remember, cholecystectomy is the treatment of choice.
Cholecystolithotomy
This procedure is indicated in patients with a previous vagotomy for ulcer disease in the
presence of a functioning gall bladder (demonstrated on biliary scintiscan). Vagotomised
patients frequently develop symptomatic gallstones, but if a functioning gall bladder
is removed a high percentage develop debilitating explosive diarrhoea. Therefore
cholecystectomy is not performed and removal of the stones followed by oral bile salt
therapy is the appropriate treatment. However, cholecystectomy is the right treatment if
the gall bladder is non-functioning.
Dissolution by methyl tert-butyl ether (MTBE)
This dissolves cholesterol stones in hours via a pigtail catheter inserted radiologically
in the gall bladder. It is left in the gall bladder a few hours then aspirated. It may cause
damage if it escapes into the CBD or duodenum – it is best used in a non-functioning
gall bladder. The main indication for use is in poor-risk patients or those who have had
a previous vagotomy.
Extracorporeal shock wave lithotripsy
There is successful stone fragmentation in 80% of patients with solitary small gallstones.
It fails if stones are larger than 3cm, multiple or calcified. Repeat treatments are frequently
required. Maintenance therapy with bile salts is required. Recurrence rates are 50% at five
years. Therefore the current role is restricted to fragmentation of occluding ductal calculi
in jaundiced patients. It is not routine – 50% of patients require additional procedures
to achieve stone removal.
Oral dissolution
This is only applicable to patients with a functioning gall bladder (on biliary scintiscan).
Chenodeoxycholic and ursodeoxycholic oral bile salts result in dissolution after several
weeks or months. Maintenance with ursodeoxycholate is then required. Recurrence is
12.5% after the first year, 61% by the eleventh year. The technique fails if the gallstone
load is large (larger than 3cm or multiple) and/or stones are calcified. Bile salt therapy
is restricted to patients in whom cholecystectomy is contraindicated, either as a primary
treatment or after gallstone extraction, fragmentation or dissolution by MTBE.
Acalculous chronic gall bladder disease
There are two variations:
✧ adenomyomatosis of the gall bladder: diverticular formation of the epithelial lining
✧ cholesterolosis of the gall bladder: epithelial cells and macrophages in the gall
bladder mucosa become laden with cholesterol, inducing chronic inflammation – the
strawberry gall bladder.
160 GENERAL SURGERY OUTPATIENT DECISIONS

Objectives
Diagnose the cause, differentiate from other causes of abdominal pain including gallstone
disease, differentiate from cancer of the gall bladder, treat the cause.
History
Vague symptoms similar to chronic cholecystitis, but no gallstones.
Examination
This may be normal or there may be tenderness in right upper quadrant.
Investigations
USS normal or thickening of the gall bladder wall.
Treatment
Treat with cholecystectomy.
Follow-up
Straightforward cases can be reviewed in 4–6 weeks with results of investigations. If there
are atypical features to the history or examination, review sooner.
Post-operative follow-up
Review uncomplicated cases in 4–6 weeks after surgery with histology. If histology
confirms chronic cholecystitis, and the patient is symptom-free, discharge.
Mucocele of the gall bladder
There is a grossly distended gall bladder associated with cystic duct obstruction, usually
by a stone, but it does not result in inflammation or infection. The gall bladder is filled
with mucoid material.
Objectives
Diagnose mucocele, differentiate from other causes of abdominal pain and from cancer
of the biliary tract, treat mucocele.
History
Take a biliary history. Patients are usually elderly and present with a painless mass in the
right hypochondrium. There may be a history of acute pain in the right upper quadrant,
like biliary colic or acute cholecystitis.
Examination
Patients are usually not jaundiced. Look for a painless mass in the right upper
quadrant.
Investigations
LFTs are usually normal. USS shows distended gall bladder but normal CBD diameter.
Treatment
Treat with cholecystectomy.
Follow-up
Follow up at short intervals of 2–4 weeks until malignant obstruction of the biliary
system is excluded.
 LIVER, BILIARY SYSTEM AND PANCREAS 161

Post-operative follow-up
Review in 4–6 weeks after surgery with histology. If histology confirms chronic cholecystitis
and the patient is symptom-free, discharge.
Ductal calculi
These are mostly in the CBD; 5% are in intrahepatic ducts, more commonly in the left
system of ducts. They arise as either secondary calculi from migration of gallstones or
as primary calculi arising de novo within bile ducts. The predisposing factors to primary
duct stones include stasis in the biliary tract caused by strictures, parasitic infestations,
recurrent pyogenic cholangitis and indwelling stent. Stone impaction may result in
progressive jaundice, cholangitis, gallstone pancreatitis, secondary biliary cirrhosis and
portal hypertension.
Objectives
Diagnose the cause, differentiate from other causes of pain/jaundice, treat the cause.
History
Take a general biliary history; 15–20% of duct stones are asymptomatic. Symptoms
include recurrent bouts of biliary colic (with or without jaundice), episodic upper
abdominal pain and dyspepsia.
Examination
Perform a general examination. Examination may be normal. The patient may or may
not be jaundiced. Examine for scars from previous biliary surgery, tenderness in the RUQ
and evidence of liver disease.
Investigations
LFTs reveal obstructive jaundice. USS detects a dilated bile duct system. MRCP defines
the anatomy and the obstruction, whereas ERCP does the same but can be combined with
sphincterotomy or endoscopic stent placement.
Treatment
Ductal calculi found incidentally during intra-operative cholangiography
Stones less than 2mm diameter can be left alone, as more than 95% pass spontaneously.
If they become symptomatic, remove them at ERCP. Stones larger than 2mm and smaller
than 10mm can be removed by intra-operative duct exploration (laparoscopic or open)
or by post-operative ERCP. Post-operative ERCP stone extraction is likely to fail for stones
larger than 10mm diameter, and these are best removed surgically.
Ductal calculi without previous cholecystectomy
A cholecystectomy and common bile duct exploration can be performed either open
or laparoscopically. In young patients with small CBD, explore and clear the duct and
insert a T-tube. If there are multiple ductal calculi and/or a grossly dilated duct, some
form of drainage may be required, e.g. hepatico-jejunostomy Roux-en-Y. If the patient
is elderly or a poor operative risk, then perform ERCP and stone extraction, and reserve
cholecystectomy for those who develop symptoms.
Patients with ductal calculi prior to laparoscopic cholecystectomy
Two procedures are possible.
✧ Pre-operative ERCP and sphincterotomy – but this carries the risk of combined
morbidity of two procedures and the unknown risk of sphincterotomy in the under-
50 age group.
162 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Combined open or laparoscopic cholecystectomy and exploration of common bile

duct.
Ductal calculi discovered after cholecystectomy and exploration of CBD
Missed stones are rare where intra-operative choledochoscopy is used, but the incidence
increases to 8% for completion T-tube cholangiography.
Treat by post-operative ERCP and sphincterotomy utilising flushing and drug-induced
relaxation of the sphincter of Oddi. Other alternatives include dissolution with MTBE
or percutaneous stone extraction via the T-tube tract, performed after 4–6 weeks of tract
maturation. If stones are not detected during or soon after surgery (if cholangiogram
was not performed or a T-tube was not inserted at operation), recurrent symptoms from
missed stones usually occur within two years of cholecystectomy. Ductal stones present-
ing beyond this period are generally considered to be primary.
Recurrent ductal calculi
These are often multiple and associated with gross dilatation of the bile duct with or
without duct stenosis. Duct stenosis may be primary (papillary stenosis) or secondary to
previous bile duct exploration. Treat by either ERCP and sphincterotomy or surgically
with hepatico-jejunostomy Roux-en-Y.
Multiple intrahepatic calculi
These are common in the east, associated with strictures of the hepatic ducts. Treatment
is standard operative choledochotomy and stone extraction, transhepatic lithotomy and
resection of the involved lobe.
Follow-up
Follow up at short intervals of 1–4 weeks until cancer is excluded and to prevent deterio-
ration from jaundice. Consider admission and further investigation as an in-patient if
the patient is frail or shows evidence of liver dysfunction.
Post-operative follow-up
Follow up until the patient is symptom-free and LFTs return to normal. When stable,
discharge with advice regarding late development of bile duct strictures.
Cholangitis
Cholangitis is infection of an obstructed biliary tract. Systemic symptoms result from
bacteraemia secondary to cholangiovenous reflux induced by biliary hypertension. Most
commonly the obstruction is due to a stone; bile duct strictures; tumours of the bile duct
and pancreatic head; and periampullary lesions. Less commonly it is due to bilioenteric
anastomoses, spontaneous bilioenteric fistulas, cystic disease of the biliary tract and
duodenal diverticula.
History
Take a general biliary history. The classical Charcot’s triad of symptoms are pain in RUQ,
intermittent fever/rigours and jaundice. Rigours are severe and nausea and vomiting are
frequent.
Examination
Perform a general examination. Commonly there is tenderness in the right upper
quadrant. Clinically apparent jaundice may not be present in the early stages.
 LIVER, BILIARY SYSTEM AND PANCREAS 163

Investigations
Treatment should not wait for the results of investigations. LFTs and USS confirm the
diagnosis. Perform blood cultures, FBC, coagulation screen and U&E to detect renal
impairment.
Treatment
Treatment is admission to hospital and resuscitation with oxygen, intravenous fluids
and antibiotics; and urgent biliary decompression, e.g. ERCP and sphincterotomy/stent
or percutaneous transhepatic biliary drainage. Specific treatment is then directed at the
underlying cause. Watch out for concomitant renal failure.
Follow-up
Depends on the underlying condition and the treatment performed.
Post-operative follow-up
If a cholecystectomy and exploration of common bile duct was performed, this is
followed up in the usual way: review histology, determine the presence of complications.
Discharge once the patient is symptom-free and no other treatment is indicated. Advise
regarding the late development of strictures.
Bilioenteric fistulas
Bilioenteric fistulas are an abnormal connection between the biliary system and other
viscera. Bilioenteric fistulas can be classified as either internal or external.
✧ External fistulas communicate with the skin and are caused either by trauma
or as a complication of surgery or therapeutic intervention, e.g. T-tube, stents,
cholecystectomy.
✧ Internal fistulas occur between a variety of organs and are caused by a variety of
pathologies (see Table 8.3)
TABLE 8.3 Causes of internal biliary fistulas.
INTERNAL BILIARY FISTULAS PATHOLOGY
Bilioenteric
Cholecystoduodenal Gallstones
Cholecystocolic Gallstones, carcinoma
Cholecystogastric Gallstones, carcinoma, peptic ulceration
Choledochoduodenal Ductal calculi, iatrogenic, duodenal ulcer, carcinoma
Bilio-bilial
Cholecystocholedochal Gallstones (Mirizzi’s syndrome)
Others
Broncho/pleuro-bilial Trauma, operative injuries, liver abscesses/hydatid, subphrenic abscess
Cholecystorenal Gallstones

Objectives
Diagnose fistula, determine underlying pathology, treat fistula, treat the underlying cause.
History
Take a general biliary history. Symptoms of non-malignant internal fistulas involving the
gall bladder are similar to chronic cholecystitis, but jaundice and cholangitis are more
common.
164 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
Perform a general examination. Examine for jaundice or evidence of underlying sepsis.
Examine the chest. Examine for abdominal masses or tenderness.
Investigations
LFTs show general derangement, USS and AXR may show gas in the biliary tree. FBC
may reveal anaemia and a raised WCC. U&Es may reveal renal impairment and blood
cultures.
Treatment
Treat the underlying gallstone disease with cholecystectomy and closure of the fistula.
For Mirizzi’s syndrome, leave a cuff of gall bladder to close the fistulous opening. CBD is
explored through a choledochotomy lower down. Management of bronchobiliary fistulas
consists of adequate drainage of the hepatic/subphrenic abscess and decompression of
the biliary tract.
Follow-up
Follow up at short intervals of 1–2 weeks to confirm the diagnosis, to prevent deteriora-
tion from the underlying condition and to exclude neoplastic causes. Consider admission
for investigation and treatment.
Post-operative follow-up
This depends on the treatment and procedure performed. Review with regard to the
histology and post-operative complications related to cholecystectomy and exploration
of bile ducts. Monitor for the detection of bile duct stenoses with regular estimation of
LFTs, USS and MRCP if necessary. Discharge once the patient is symptom-free and LFTs
are normal, with advice regarding the late development of bile duct stenoses.
Gallstone ileus
This rare condition is caused by an intraluminal intestinal obstruction by a large
gallstone subsequent to the establishment of a fistula, usually between gall bladder and
duodenum.
History/examination
There is a history of gall bladder disease and it presents with small bowel obstruction.
Elderly patients present with small bowel obstruction and air in the biliary tree.
Investigations
LFTs, USS, AXR shows air in the biliary tree. CT scan for anatomical information.
Treatment
Treat with surgery – enterolithotomy, check for other gallstones in the gut. The cholecysto-
duodenal fistula should be left intact unless at a specialist centre.
Follow-up/post-operative follow-up
Follow up as for bilioenteric fistula.
Post-cholecystectomy syndrome
This syndrome is the persistence of symptoms referable to the biliary tract after
cholecystectomy (excludes diseases outside the biliary tract). A careful history and
investigation with laboratory tests, MRCP and/or ERCP is advised in all patients.
Common causes are the following.
 LIVER, BILIARY SYSTEM AND PANCREAS 165

✧ Retained or recurrent calculi: diagnose and treat by ERCP.

✧ Gall bladder or cystic duct remnants: diagnosed if operative note indicates leaving gall
bladder remnants behind or cholecystotomy was performed. USS and ERCP are useful
to confirm diagnosis and exclude other causes. Treat by cholecystectomy.
✧ Bile duct strictures and other unrecognised iatrogenic injuries (choledochoduodenal
fistula).
✧ Papillary stenosis, sphincter of Oddi dysfunction (SOD) syndrome and biliary
dyskinesia.
Papillary stenosis
Fibrosis or fibromuscular hyperplasia of the sphincter of Oddi.
History
Pain similar to chronic cholecystitis.
Examination
Normal, or slight tenderness in right upper quadrant.
Investigations
LFTs show a slight derangement, including hyperbilirubinaemia and raised alkaline
phosphatase. USS may demonstrate duct dilatation. ERCP shows the transduodenal
segment of duct wider than the intrapancreatic segment. Biliary sludge and small calculi
are often present. The resting sphincter pressure is raised and the normal phasic sphincter
activity is lost.
Treatment
Treat with ERCP and sphincterotomy or with operative transduodenal sphincteroplasty.
Biliary dyskinesia
There is persistent pain after cholecystectomy but no abnormality on examination and
routine investigations. The following abnormalities are demonstrated during ERCP
manometry:
✧ elevated resting pressure
✧ tachyarrhythmia (increased phasic activity of the sphincter)
✧ retrograde contractions of the sphincter
✧ paradoxical response to cholecystokinin.

Treatment
Treat with ERCP and sphincterotomy.
Benign bile duct strictures
Most common causes are secondary to operative trauma. Untreated, the late consequences
are liver fibrosis, secondary biliary cirrhosis and development of portal hypertension.
Strictures may develop many years after cholecystectomy. Alternatively, damage to the
CBD or CHD may present in the immediate post-operative period with development
of an external biliary fistula associated with sepsis and development of subphrenic/
subhepatic abscess. Peritonitis may occur and jaundice is often present but may not be
severe or progressive. Other causes of bile duct strictures include: penetrating and non-
penetrating abdominal injuries, chronic duodenal ulcer, chronic pancreatitis, recurrent
pyogenic cholecystitis and parasitic infestations, sclerosing cholangitis.
166 GENERAL SURGERY OUTPATIENT DECISIONS

Objectives
Diagnose stricture, detect the underlying cause, differentiate from neoplastic causes, detect
liver dysfunction, treat stricture, treat the underlying cause, correct liver dysfunction.
History
Take a general biliary history. Commonly there is a history of previous biliary surgery.
Determine the details of this: ask about length of stay and whether there were any
complications at the time. The patient may complain of colicky RUQ pain similar to
chronic cholecystitis or may present with mild painless jaundice. Ask about symptoms
which would suggest any of the other causes.
Examination
Perform a general examination. May be normal or mildly jaundiced. Tenderness may be
present in the RUQ.
Investigations
LFTs show raised bilirubin and alkaline phosphatase. USS may show a dilated intrahepatic
duct system and evidence of portal hypertension. In stable patients MRCP is an excellent
non-invasive method of visualising the biliary tree. ERCP or PTC or both can be further
used to determine the relevant anatomy of the abnormality and provide information to
assist reconstruction and treat the underlying condition. Liver biopsy may be indicated
if cirrhosis is suspected.
Treatment
Treat with ERCP – balloon dilatation and indwelling stent for several months. But the
majority of injuries require surgical repair in a specialist centre, as the correct treatment
depends on accurate classification of the injury (e.g. Bismuth classification I –V).
Numerous surgical procedures are possible depending on the exact injury, but most
involve the use of a Roux-en-Y hepatico-jejunostomy. Best results are obtained with the
first surgical repair and so should be performed in a specialist centre.
Follow-up
Follow up at short intervals of 1–4 weeks until diagnosis is confirmed and malignant
causes excluded. Following repair of bile duct injuries there is a high incidence of further
stricture formation and the development of biliary cirrhosis and portal hypertension.
Therefore, these patients require long-term follow-up with USS and LFTs at regular
intervals.
Sclerosing cholangitis
This is an obscure disorder of uncertain aetiology that results in progressive fibrous
obliteration of the biliary tract. It is currently considered to be an autoimmune disorder.
There were previously two categories: ‘primary’ where there was no previous biliary
surgery or biliary tract disease; and ‘secondary’ where there was previous biliary surgery
or biliary tract disease. However, both categories are often associated with inflammatory
bowel disease (usually ulcerative colitis, occasionally Crohn’s). Classification is based
on the extent of involvement of the biliary tree: total diffuse, localised hilar, diffuse
intrahepatic, diffuse extrahepatic and localised extrahepatic distal.
The disease progresses inevitably to cirrhosis and development of portal hypertension.
Patients have a high risk of developing cholangiocarcinoma.
Objectives
Diagnose sclerosing cholangitis (especially in patients with UC or Crohn’s), exclude
 LIVER, BILIARY SYSTEM AND PANCREAS 167

cholangiocarcinoma, classify the disease, detect the degree of liver impairment, treat
sclerosing cholangitis, treat the liver impairment.
History
Take a general biliary history. Look for vague ill health, asthenia, pain in the RUQ,
jaundice, itching, pyrexia and attacks of rigours.
Examination
Perform a general examination. Examine for jaundice, anaemia and signs of liver disease.
Examination may be normal but the liver is palpable and tender, the spleen is enlarged
and jaundice is present in approximately 50%.
Investigations
LFTs show a cholestatic pattern but the alkaline phosphatase is often elevated out of pro-
portion to the bilirubin. Most patients are hepatitis B surface antigen (HBsAg) negative.
Antimitochondrial, anti-smooth muscle and antinuclear antibodies are absent – if
present, suspect primary biliary cirrhosis. MRCP/ERCP/PTC show ducts are smaller in
number and size with stricture formation. Saccular dilated areas between strictures are
seen in diffuse disease. Differentiation from hilar and diffuse cholangiocarcinoma is dif-
ficult even with histology obtained from biopsies, or cytology from brushings at ERCP.
Treatment
Pruritus is controlled by cholestyramine and ursodeoxycholate. Cholangitis episodes
are managed by intravenous antibiotics with or without stenting. Progressive jaundice
and recurrent cholangitis are indications for surgical intervention. The aim of surgical
treatment is to treat dominant strictures.
In the absence of cirrhosis, occasionally good results in localised disease have been
obtained by ERCP or percutaneous balloon dilatation and stent insertion. Surgical
options include Roux-en-Y hepatico-jejunostomy or intra-operative dilatation and
external stent insertion. The stent is left in for 12 months and progress assessed by
cholangiograms performed through the stent.
Diffuse disease or the presence of cirrhosis requires hepatic transplantation.
Unexpected cholangiocarcinomas have been reported in 8% of livers removed during
liver transplantation.
Follow-up
Follow up at short intervals until diagnosis is confirmed and cholangiocarcinoma
excluded. Then follow up long term. Treat mild cases expectantly and monitor for the
development of complications.
Post-operative follow-up
This depends on the operation and procedures performed. Review with histology and for
the detection of complications of biliary surgery. Then provide long-term monitoring
for the recurrence of symptoms or development of stenoses, using LFTs and USS, ERCP.
Take a HIDA scan if stenoses of bilioenteric anastomoses are suspected.
Biliary disorders in AIDS
AIDS patients are prone to developing acute acalculous cholecystitis, papillary stenosis
and abnormalities of the bile ducts similar to sclerosing cholangitis. Papillary stenosis and
cholangiopathy produce symptoms of pain and raised bilirubin and alkaline phosphatase,
and are diagnosed by ERCP and treated appropriately. The treatment for acalculous
cholecystitis is cholecystectomy.
168 GENERAL SURGERY OUTPATIENT DECISIONS

Recurrent pyogenic cholangitis

Recurrent pyogenic cholangitis is prevalent in Southeast Asia. It may occur in immuno-
compromised people. There are recurrent bouts of bacterial cholangitis leading to
formation of pigment stones and strictures. It affects intra- and extrahepatic ducts with
a predilection for the left lobe of the liver.
History
Attacks of RUQ pain and rigours. May develop jaundice.
Examination
May be normal or tender RUQ. Mild jaundice.
Investigations
Investigate with obstructive LFTs and duct dilatation on USS. Diagnosed by ERCP.
Treatment
Treatment is surgery (of strictures and stones).
Duodenal diverticula
Duodenal diverticula are present in 12.5% of patients undergoing ERCP. They are
usually asymptomatic but their significance in this situation is that they are associated
with an increased incidence of post-procedural bacterial infection and can make ERCP
technically difficult to perform.
Haemobilia
This is rare upper gastrointestinal bleeding originating from the biliary system. Causes
include iatrogenic percutaneous radiological intervention; liver biopsy; blunt or
penetrating trauma; extrahepatic bile duct tumours. Diagnosis and treatment is by
selective mesenteric angiography and embolisation.

Tumours of the gall bladder

Benign tumours
Benign tumours are adenomas and papillomas. They are usually an incidental finding
on USS during investigation of RUQ pain. Treatment is by cholecystectomy to exclude
carcinoma. At post-operative follow-up determine that no malignant focus was detected
and that excision was complete.
Carcinoma of gall bladder
This is often incidental on the histology report after cholecystectomy. Female to male
ratio is 3:1 and it is more common in the over-65 age group. Gallstones are present in
75–90% of cases. The majority are adenocarcinomas. Rare types are neuroendocrine
tumours and melanoma. If detected pre-operatively these tumours can be difficult to
differentiate from Klatskin tumours or even Mirizzi’s syndrome.
History
Often presents as chronic cholecystitis. Additional non-specific symptoms may be
anorexia, nausea and vomiting and weight loss.
Examination
Normal or inflammatory mass in the RUQ or acute cholecystitis. In advanced cases there
may be jaundice, enlarged liver and a palpable gall bladder. In very advanced cases there
may be ascites. Anaemia is present in 50% due to haemobilia.
 LIVER, BILIARY SYSTEM AND PANCREAS 169

Investigations
LFTs may have raised alkaline phosphatase even if bilirubin is normal. FBC may show
iron-deficiency anaemia. USS tends to identify only advanced cases. CT scan is more
informative. AXR occasionally identifies the intramural calcification of a ‘porcelain’
gall bladder. Porcelain gall bladder is a pre-malignant condition. ERCP/PTC are usually
needed to define these lesions. Also, the involvement of segment V duct by a gall bladder
mass is indicative of cancer.
Staging
Staging is as follows.
✧ I: confined to mucosa/submucosa.
✧ II: involvement of the muscle layer.
✧ III: serosal involvement.
✧ IV: spread to cystic node.
✧ V: invasion of liver and adjacent organs.
Treatment
Stage I–II disease is treated by cholecystectomy. Porcelain gall bladders require resection.
Stage III-IV needs extended right hepatectomy with excision of the biliary tree and
lymphadenectomy. Response to radiotherapy and chemotherapy is poor.
Follow-up
Follow up at short intervals until diagnosis is confirmed and treatment is instituted.
Post-operative follow-up
Review within 2–4 weeks with histology and complete the staging process. Detect any
post-operative complications. Thereafter follow-up is long term to detect recurrence and
institute palliative therapy. Overall five-year survival is 5%. For surgically resectable cases
it is 25%. Prolonged survival has been recorded for types I and II.

Tumours of the bile ducts

Benign tumours
These are adenomas and papillomas – rarer than carcinomas. They have a tendency to
recur after excision. They present with jaundice and haemobilia (anaemia).
Malignant tumours (cholangiocarcinoma)
The tumours are classified according to position.
✧ Intrahepatic: minor hepatic ducts.
✧ Proximal: right and left hepatic ducts, hilar confluence and proximal common hepatic
duct (Klatskin tumours).
✧ Middle: from distal common hepatic duct, cystic duct and confluence with common
bile duct.
✧ Distal: from common bile duct to periampullary region.

There are three forms.

✧ Stricture: difficult to differentiate from sclerosing cholangitis.
✧ Nodular: form extraductal nodules.
✧ Papillary: friable tumour in the distal duct tends to produce haemobilia.

Cholangiocarcinomas grow slowly, infiltrate locally and metastasise late. They have a
special predilection for perineural spread and rarely metastasise beyond the liver.
170 GENERAL SURGERY OUTPATIENT DECISIONS

Objectives
Diagnose tumour, differentiate from other lesions, classify tumour, determine resectability,
treat tumour, follow up to detect recurrence.
History
Take a general biliary history. The main presentation (90%) is with progressive, obstruc-
tive jaundice accompanied by itching and anorexia. They may also complain of a dull
upper abdominal pain. Alternatively, presentation may be acute, with cholangitis or
cholecystitis. Duration of symptoms is usually short and measured in months.
Examination
Perform a general examination. Anaemia may be due to haemobilia, especially with
periampullary lesions. Stools may have a silvery appearance due to steatorrhoea and blood.
Hepatomegaly may be present or there may be a palpable gall bladder in distal tumours.
There may be a scar from previous cholecystectomy (an operative cholangiogram should
never be passed as normal unless there is adequate and complete filling of the intrahepatic
biliary tree).
Investigations
LFTs may show an obstructive pattern with a raised alkaline phosphatase and bilirubin
and low albumin indicating impaired nutritional status. FBC may reveal an iron-
deficiency anaemia. Clotting may be abnormal. CEA and CA19 are often elevated. USS
identifies dilatation of biliary tree.
A triple-phase CT scan gives more detailed information about anatomy and the extent
of arterial and venous involvement. CT can also be used for needle biopsy to confirm the
diagnosis. MRCP can now give a detailed pre-operative road map of the biliary system.
ERCP/PTC are needed for decompression of the biliary tree and transbiliary biopsy
can be performed. Coeliac axis angiography is sometimes performed to delineate vascular
anatomy and tumour involvement at the hilum, although colour Duplex is a less invasive
alternative.
Treatment
Surgical resection gives the best chance of cure and also offers the best means of pallia-
tion. Hilar lesions are treated by an extended right or left hepatectomy with resection of
the caudate lobe and by resection of tumour and extrahepatic biliary tree with hepatico-
jejunostomy.
Mid-duct tumours can be treated by extrahepatic biliary tree excision alone, provided
the proximal resection margins are negative.
Periampullary tumours need a pancreatico-duodenectomy. Approximately 20% of
lesions are resectable.
Irresectable lesions are treated by a surgical biliary bypass (Roux loop to segment III
duct) or by percutaneous transhepatic or endoscopic stenting. Intracavity irradiation
through stents is possible.
Photodynamic therapy can be used to treat unresectable tumours. This involves the
administration of a photosensitising drug that accumulates in cancer cells, followed by
exposure of the tumour to the appropriate wavelength of light. This results in tumour
destruction by the activation of the photosensitiser. These tumours have a poor response
to chemotherapy.
Follow-up
Follow up at short intervals (2–4 weeks) until diagnosis is established and treatment is
instituted.
 LIVER, BILIARY SYSTEM AND PANCREAS 171

Post-operative follow-up
Follow-up is long term at regular 3–6 monthly intervals. Five-year survival is 30% for
distal and periampullary tumours. If there is diffuse intrahepatic disease, most patietns
die within one year. Five-year survival for proximal lesions is 5–15%. Recurrence of
jaundice may indicate anastomotic stenosis or tumour recurrence, which can be treated
by stenting.

Biliary parasites
Ascaris lumbricoides
Presentation is with biliary colic, pancreatitis, cholangitis, cholecystitis and eosinophilia.
Plain radiography may show calcified worms and ultrasound can show linear filling
defects that move. Treatment is ERCP, and removal of worms with laparotomy is only
performed following endoscopic failure. Antihelminthic therapy kills the worms but they
still need to be removed.
Clonorchis sinensis
This causes cholangitis and septicaemia. It is associated with development of bile duct
carcinoma. It is diagnosed by finding typical ova in the faeces. It can be treated by
chloroquine 300 mg for 2–6 months but relapse is common. The bile ducts must be
cleared of worms and stones (surgically if endoscopic methods fail).

The pancreas
The pancreas serves endocrine and exocrine functions. The common bile duct runs
through it. It is in close proximity to the stomach, duodenum, small bowel, large bowel,
spleen, kidneys, portal vein and vena cava, while being tucked away in the retroperitoneum.
Unfortunately the gland is prone to inflammation and tumour formation.
Tumours in the head of the pancreas and lesions of the body and tail of the pancreas
present with very different symptoms and signs. Lesions in the head of the pancreas tend
to obstruct the common bile duct and present with obstructive jaundice, while lesions
affecting the body and tail of the gland have a more insidious presentation with weight
loss and pain as their primary symptoms.
Lesions of the exocrine pancreas produce symptoms and signs of malabsorption,
while lesions of the endocrine pancreas produce a variety of endocrine syndromes, e.g.
diabetes mellitus and a wide range of syndromes associated with autonomous secretion
of pancreatic and enteric hormones, e.g. insulinoma, gastrinoma, glucaconoma.
Inflammation of the gland is known as pancreatitis. Acute pancreatitis may be severe
and life-threatening. Chronic pancreatitis can run a relapsing course with gradual
destruction of the whole gland.
Assessment of pancreatic disorders
Pancreatic history
Start with a general gastrointestinal history. When responses indicate a possible pancreatic
problem, a more detailed pancreatic history is required.
✧ Pain: site, severity, radiation, exacerbating and relieving factors.
✧ Jaundice: general questions regarding the aetiology of jaundice. Is the jaundice
painless?
✧ Endocrine function: symptoms attributable to diabetes mellitus or, if indicated,
symptoms associated with rare disorders, e.g. insulinoma, Zollinger-Ellison.
✧ Exocrine function: symptoms of weight loss and malabsorption, fat intolerance,
frequent greasy stools that are difficult to flush away and foul smelling.
172 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Aetiological factors for pancreatitis: gallstones, previous biliary surgery or interventions,

alcohol intake, hyperlipidaemia, hypercalcaemia, medications.
✧ Effect on other organs: symptoms attributable to liver failure, biliary obstruction,
portal hypertension and hypersplenism, gastric outlet obstruction.
Pancreatic examination
Perform a general examination and in particular look for signs of weight loss, anaemia and
jaundice; evidence of liver disease; upper abdominal mass; liver and spleen enlargement;
portal hypertension; palpable gall bladder.

Investigation of pancreatic disorders

The methods of investigation include imaging, assessments of endocrine and exocrine
function, analysis of serum markers of pancreatic disease and pancreatic biopsy for
cytology/histology.

Laboratory investigations
Haematology
FBC may reveal anaemia due to a haemobilia or chronic disease. Leucopenia and
thrombocytopenia may indicate hypersplenism secondary to splenic vein thrombosis.
Clotting may be impaired in the presence of liver disease.

Biochemistry
✧ Liver function tests may reveal a cholestatic picture with a raised alkaline phosphatase.
Raised bilirubin may indicate bile duct obstruction, while a raised gamma GT may
indicate alcohol abuse.
✧ Blood sugar may reveal diabetes mellitus.
✧ Serum amylase is particularly useful in the acute setting for the diagnosis of acute
pancreatitis but is not elevated in chronic pancreatitis. A raised serum amylase may
be a marker of pancreatic trauma. Serum lipase is more sensitive and specific in the
diagnosis of acute pancreatitis, but not routinely available.

Exocrine Function
Faecal fat excretion
A stool examination for fat is useful only for malabsorption. However, 80% of pancreatic
secreting capacity may be lost without detection by the test.

Direct measurement
Direct measurement of pancreatic, digestive and secretory function is mainly used as a
research tool, but these are the best tests for diagnosis of pancreatic exocrine insufficiency.
The concentrations of bicarbonate and pancreatic enzymes are measured in duodenal
juice after stimulation by a meal (Lundh test) or injection of secretin/cholecystokinin
(secretin-pancreozymin test).
The faecal elastase test is easy to perform. Absence of elastase in faeces indicates
exocrine insufficiency.
✧ No request forms are available. Specialised tests are not routinely available.
✧ Results are given as a written report.
✧ The advantage is that it provides a direct measurement of pancreatic exocrine
function.
✧ The disadvantages are that the tests are invasive, expensive and only available in
specialised centres.
 LIVER, BILIARY SYSTEM AND PANCREAS 173

Endocrine function
Fasting levels of glucose and/or hormones secreted by islets – insulin, proinsulin,
C-peptide, glucagon, somatostatin and gastrin – are measured.
Provocative tests are used to measure serum level if fasting levels are not conclusive. For
example, calcium perfusion of insulinomas and gastrinomas at angiography can cause a
spurt of hormone release.
✧ There is no request form. Specialised tests are arranged by a clinician with a special
interest or direct contact with a clinical biochemist to discuss the conditions for
performing the tests.
✧ Results are given as a written report.
✧ The advantage is that direct information regarding the level of hormones often
provides the diagnosis.
✧ The disadvantage is that specialised tests are not routinely available. They often
require specialised biochemical analysis.
✧ Tumour markers include CEA and CA19-9.

Imaging techniques
Indirect imaging
Abdominal X-ray
An AXR may visualise the effect of the pancreas on adjacent organs, e.g. the colon cut-off
sign may indicate displacement, stricture or fistula of the transverse colon. Calcification
usually indicates chronic pancreatitis (though occasionally radiating sunburst calcifica-
tion may be seen in cystadenoma or cystadenocarcinoma). A CXR may occasionally
demonstrate a pancreatic pseudocyst in the posterior mediastinum.
Small bowel contrast series
This may show effacement or hypertrophy of folds in malabsorption secondary to chronic
pancreatitis. Enlargement of the pancreatic head may cause widening of the C-loop of
the duodenum and/or displacement of the angle of Treitz, e.g. advanced pancreatic
carcinoma. Contrast studies may also reveal post-bulbar duodenal ulceration, which is
characteristic of Zollinger-Ellison syndrome.
Direct imaging
Direct imaging of pancreatic parenchyma is provided by USS, CT and MRI. ERCP images
the pancreatic duct system. Angiography images the pancreatic and peripancreatic
vasculature. The newer techniques of MRCP and endoscopic ultrasound (EUS) are being
increasingly used.
Ultrasound
Acoustic water-based gel is applied and an ultrasound probe manipulated over the
abdomen by the sonographer.
✧ The request form is from radiology/ultrasound (check if your department uses the
same or different forms).
✧ Results are in a written report compiled by the radiologist or sonographer and a selec-
tion of ultrasound photographs.
✧ The advantages are that it is a non-invasive technique. Indicators of pancreatic
disease include diffuse or localised atrophy, alteration of texture and dilated bile duct.
Abnormal dilatation of the pancreatic duct may be a result of cancer or chronic pan-
creatitis. EUS is excellent for chronic pancreatitis and endocrine tumours.
✧ The disadvantages are that it is operator dependent; the non-visualisation rate is
10–15%; only 50% of changes caused by chronic pancreatitis are detected by USS; and
174 GENERAL SURGERY OUTPATIENT DECISIONS

there is poor visualisation in the obese and when gaseous distension of the bowel is
present.
CT scan
Multislice helical CT scanners can now examine the pancreas with 5mm slices and when
combined with contrast, arterial and venous phase images can give detailed pancreatic
anatomy.
✧ The request form is from radiology or is a specific CT request form.
✧ Results are as a written report by the radiologist and a selection of still CT images.
✧ The advantages are that it gives better visualisation of the gland than USS, especially
in the presence of ascites or obesity and it is better at detection of calcification, gas,
dilatation, small intrapancreatic pseudocysts and thicker walls of pancreatic abscess.
The most valuable sign is localised or diffuse enlargement of the gland.
✧ The disadvantages are the use of radiation and that the procedure is expensive.

ERCP
A large-bore side-viewing endoscope is passed into the second part of the duodenum.
The duodenal papilla is cannulated and contrast injected under X-ray screening. The
pancreatic and biliary duct system is visualised. Brushings or biopsy can be performed
to provide a tissue diagnosis. A stent can be placed.
✧ The request form is an endoscopy/radiology form. This is a joint procedure between
the radiology department and the endoscopy service.
✧ Results are in a written report and selection of ERCP images.
✧ The advantages are that it allows diagnosis of a wide range of pancreatic conditions;
the obtaining direct tissue samples; and the placing of a stent to relieve obstruction.
It is good for diagnosis of ductal calculi, tumours of the bile duct and pancreas and
sclerosing cholangitis.
✧ The disadvantages are complications, including pancreatitis(1%) – if sphincterotomy
is also performed complications rise to 6–10% and include haemorrhage, acute
pancreatitis, cholangitis, retroperitoneal perforation, impacted Dormia basket, acute
cholecystitis and gallstone ileus; technical failure may result in patients with duodenal
stenosis, previous Billroth II and duodenal diverticula – and in an unco-operative
patient. In patients with complete biliary obstruction the proximal biliary tree may
not be visualised and PTC is then indicated.
Angiography
Angiography generally requires admission to hospital, although some centres do this
as a day-case. Under local anaesthetic, the femoral artery is cannulated and a catheter
manipulated into the coeliac and superior mesenteric arteries. Contrast is injected and
X-rays taken.
✧ The request form is from radiology.
✧ Results are in a written report from the radiologist and a selection of angiography
images.
✧ Useful signs include arterial encasement – narrowing or irregularity of a vessel
caused by invasion of tumour. Smooth encasement may be caused by chronic
pancreatitis. Major venous involvement may indicate similar disease but is not as
reliable. Angiography defines arterial variability for resection purposes.
✧ The disadvantages are that it is an invasive technique; and risks include haematoma
at the puncture site. It is being replaced by reconstruction of vascular anatomy from
CT or MR images, and by Duplex ultrasound. Angiography still has a role in localising
pancreatic neuroendocrine tumours such as insulinomas, using selective calcium
stimulation.
 LIVER, BILIARY SYSTEM AND PANCREAS 175

Diagnostic laparoscopy and intra-operative ultrasound

Under general anaesthetic a laparoscopy is performed, which enables direct visualisation
of the intra-abdominal structures, in particular the liver and biliary system. Through a
second port a special intra-operative ultrasound probe is inserted, which enables ultra-
sound images of the pancreas to be obtained. Biopsy of lesions can be performed under
direct vision. The yield is higher the greater the extent of the exploration done by the
surgeon.
✧ There is no request form.
✧ Results are an operation note and a selection of printed ultrasound images.
✧ The advantages are that direct visualisation of the liver can be obtained, which may
reveal multiple small metastases; and better ultrasound images of the pancreas can be
obtained. This can give valuable information regarding resectability before resorting
to a full laparotomy.
✧ The disadvantage is that it is an invasive operative procedure.

Disorders of the pancreas

Congenital anomalies of the pancreas
✧ Ectopic pancreas presents with abdominal pain similar to peptic ulceration. It
occasionally causes interference with gastric emptying.
✧ Annular pancreas may present with vomiting, with or without bile. Fifty percent
of cases present in the newborn, where urgent operation is needed. The other 50%
present between the ages of 20 to 70, when inflammation of the pancreas leads to
constrictive symptoms.
✧ Accessory main pancreatic duct (pancreas divisum) is the result of the non-union
of the dorsal and ventral portions of the pancreas. Patients most commonly present
with recurrent pancreatitis or a single episode of pancreatitis, which is initially
thought to be idiopathic. Diagnosis is by MRCP, where separation of the main and
accessory pancreatic ducts is seen. ERCP can also be diagnostic, and therapeutic by
endoscopic accessory duct sphincteroplasty. Open accessory duct sphincteroplasty
can be performed.
Pancreatitis
Acute pancreatitis usually presents as an emergency admission with the typical abdominal
pain and enzyme changes.
Although pain is a common feature of chronic pancreatitis, it can present in the out-
patient department with signs of pancreatic endocrine and exocrine insufficiency and
little in the way of serum enzyme changes. Chronic relapsing pancreatitis describes a
condition of repeated attacks of acute pancreatitis, usually resulting in gradual destruc-
tion of the gland.
Risk factors are alcoholism, biliary tract disease, trauma (surgical, blunt, penetrating,
ERCP), drugs (thiazides, steroids), metabolic disorders (hyperparathyroidism, hyperli-
pidaemia), infections (mumps, coxsackie B virus, mycoplasma pneumoniae, infectious
mononucleosis, septicaemia), congenital mechanical obstruction of pancreatic duct
(pancreas divisum), periampullary carcinoma, hereditary pancreatitis and vascular disease.
Acute pancreatitis
Patients with acute attacks are treated as an in-patients. Once the symptoms subside,
patients are reviewed in the outpatient clinic.
Objectives
The outpatient consultation has three main objectives.
176 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Determine the underlying cause of the pancreatitis.

✧ Arrange treatment of the underlying cause to prevent further attacks.
✧ Detect any complications of pancreatitis, e.g. pseudocyst, pancreatic abscess.
Determine the underlying cause
Often this will have been identified during the in-patient episode, but the outpatient
visit gives an opportunity to review the history now the patient is under less stress in
order to identify any other significant factors: e.g. gallstones and alcohol consumption
may co-exist.
Treatment of the cause
Each of the causes of pancreatitis can be dealt with as follows.
✧ Alcoholism: estimation of weekly alcohol consumption (truthful or untruthful); smell
of alcohol on breath (or alternatively smell of strong mints); gamma GT levels, urine
or serum ethanol levels. May respond to explanation, but usually need referral to a
psychiatrist with an interest in alcohol abuse.
✧ Biliary tract disease: has the in-patient ultrasound scan given all the information
necessary to arrange treatment, e.g. laparoscopic cholecystectomy? In cases of previ-
ous pancreatitis some assessment of the common bile duct is mandatory to exclude
ductal stones, even in the face of normal common bile duct diameter and LFTs. For
example, MRCP or pre-operative ERCP with or without sphincterotomy, intra-
operative cholangiography or both.
✧ Trauma: it would be wise to repeat imaging, USS and/or CT, now the acute inflamma-
tion has settled, to determine whether trauma has resulted in distortion of the biliary
system that will lead to long-term problems or require long-term follow-up. LFTs
should also be monitored. MRCP with or without secretin will determine if there is
duct disruption. ERCP may give similar information; however it is invasive (and may
have been the cause of the trauma in the first place).
✧ Drugs: once again review the history, examination and investigation findings to
confirm that pancreatitis can be ascribed to this cause. Repeat the investigations if in
any doubt. Arrange for these drugs to be avoided or administered under close medical
supervision in future.
✧ Metabolic disorders: perform serum calcium levels, serum parathormone levels and
fasting serum lipids. Treat as appropriate.
✧ Infections: review the history, examination and investigation findings. Viral titres
often need repeating 4–6 weeks after the acute episode to provide a diagnosis.
✧ Have the remaining causes been excluded, especially pancreas divisum and periam-
pullary carcinoma, by ERCP? At ERCP, biliary manometry can also be performed
to exclude sphincter of Oddi dysfunction and to sample bile to exclude bile crystals
(microlithiasis) as a cause of pancreatitis.
Complications of acute pancreatitis
Any patient who has a persistence or reappearance of the inflammatory manifestations
of acute pancreatitis must be suspected of developing a pancreatic pseudocyst or a pan-
creatic abscess. Other local complications of pancreatitis include haemorrhage, peptic
ulceration and erosions, left-sided portal hypertension and variceal haemorrhage and
vascular complications.
Pancreatic pseudocyst
Pseudocysts are thought to arise secondary to pancreatic duct disruption and leakage.
These are not true cysts because they lack an endothelial lining.
 LIVER, BILIARY SYSTEM AND PANCREAS 177

Objectives
Diagnose pseudocyst, differentiate those suitable for conservative therapy, monitor for
the development of complications, treat pseudocyst.
History
Recurrence of pain, nausea and vomiting, anorexia, weight loss.
Examination
Tender upper abdomen. Sometimes a tender mass.
Investigations
Leucocytosis, hyperamylasaemia may be present. USS or CT scan is diagnostic. Air within
a pseudocyst suggests an abscess. USS may also detect a splenic artery aneurysm and
portal hypertension. In chronic or recurrent pseudocysts an ERCP will exclude pancreatic
duct stenosis as an aetiological factor.
Treatment
✧ Acute pseudocysts should be managed expectantly for 4–6 weeks, as spontaneous
resolution sometimes occurs and surgical therapy is more effective if the cyst wall has
been given time to mature.
✧ Chronic pseudocysts are usually asymptomatic and no recent attack of pancreatitis
can be identified, but there may be a history of blunt abdominal trauma. Spontaneous
resolution is rare and there is a high risk of complications (e.g. haemorrhage –
erosion of major vessels, rupture, infection and local pressure effects) if treatment is
delayed.
✧ Other factors for consideration in the treatment of pseudocysts are the following.
∝ Size: those smaller than 6cm may be observed and expected to resolve. Larger ones
will probably need surgical drainage.
∝ Development of symptoms: compression of adjacent organs or indicative of an
impending complication such as rupture, haemorrhage and infection.
∝ Maturity: acute 4–6 weeks.
∝ Vascular complications: CT angiography or intra-arterial angiography identifies a
subgroup of patients with vascular complications associated with acute pancreatitis,
including pseudoaneurysms and left-sided portal hypertension from splenic vein
thrombosis. Presence of a pseudoaneurysm is rare. Treatment is angiography and
embolisation or, if this fails, open exploration and exclusion of the aneurysm or
pancreatic resection, as opposed to internal drainage of a pseudocyst. Presence of
portal hypertension may be an indication for splenectomy with or without gastric
devascularisation if there have been repeated gastric fundal variceal bleeds that
have failed endoscopic treatment.
∝ Site of pseudocyst: retrograde enlarging anteriorly responds to a posterior cysto-
gastrostomy. A cyst around the head of the pancreas close to the duodenum can
easily be drained by cyst duodenostomy. Large cysts bulging into the transverse
mesocolon can be drained using a Roux-en-Y loop for a cystjejunostomy. Cysts
in the tail or body of the pancreas require a distal pancreatectomy or longitudinal
pancreatico-jejunostomy. Infected or ruptured cysts or acute cysts with thin
friable walls are best drained externally with wide-bore drains. In many instances
the resulting pancreatic fistula will gradually close spontaneously. Occasionally a
second procedure is needed to implant the fistulous tract into a Roux-en-Y loop
of jejunum.
178 GENERAL SURGERY OUTPATIENT DECISIONS

Percutaneous drainage of a pseudocyst

Indications for this procedure include the following.
✧ Patient is unfit for, or refuses, an operation.
✧ Acute fluid collection that is rapidly enlarging and needs external drainage.
✧ Infected pseudocyst that needs external drainage in a very sick patient.
✧ A pseudocyst that is in an unusual location (e.g. mediastinum, pelvis) and is not
readily amenable to internal drainage.

Prior to drainage an MRCP or ERCP is required to delineate pancreatic duct anatomy.

If the pseudocyst does not connect with the pancreatic duct, external drainage can
be considered. If the pseudocyst connects with the pancreatic duct, drainage must be
internal. Pseudocysts can also be drained by percutaneous cyst gastrostomy or via EUS-
guided stenting of the pseudocyst into the stomach or duodenum.
Surgical drainage of a pseudocyst
This should also deal with the gall bladder if it has been identified as the original cause
of pancreatitis.
Open: via an upper abdominal incision, lesser sac pseudocysts can be drained by
a posterior cyst gastrostomy; pancreatic head or uncinate process pseudocysts can be
drained into the duodenum; pseudocysts bulging through the transverse mesocolon can
be drained by a cystjejunostomy.
Follow-up
Review with ultrasound scans to ensure those pseudocysts being managed conservatively
are resolving. If there is no resolution after six weeks, consider surgical or radiological
intervention if they are large or symptomatic.
Post-operative follow-up
Review within four weeks after surgery and at regular intervals (3–6 monthly) thereafter.
Determine the success of the operation and detect any complications. Review histology
of the pseudocyst wall to exclude a neoplastic cyst. Repeat abdominal USS to confirm
that the pseudocyst is resolving if there are persistent symptoms (cysts can still recur
despite surgery).
Complications include those of laparotomy and general anaesthesia. More specific
complications depend on the procedure performed. Persistent leakage of fluid from a
wound or drain site may indicate a pancreatic fistula. Send fluid for amylase concentration
analysis. It is very high if from a pancreatic fistula. Pancreatic fistulas require admission
for further assessment and treatment. Other complications include gastric outlet or small
bowel obstruction related to the surgical procedure.
Pancreatic abscess
Pancreatic abscess is caused by extensive pancreatic and peripancreatic necrosis with
formation of a peripancreatic fluid collection that gets secondarily infected (usually by
E. coli, enterococci or fungi). It develops after the second week of acute pancreatitis and
carries a high mortality/morbidity. Occasionally an infected pseudocyst may lead to an
abscess.
Objectives
Diagnose pancreatic abscess, differentiate from pseudocyst, treat.
History
Take a general pancreatic history. Pancreatic abscess usually becomes apparent 2–5 weeks
 LIVER, BILIARY SYSTEM AND PANCREAS 179

after an attack of pancreatitis as the attack appears to be resolving. The patient complains
of increasing fever, pain and tenderness.
Examination
Perform a general examination. Patients with pancreatic abscess will look unwell, with
evidence of sepsis. An abdominal mass may be palpable.
Investigations
Investigate with FBC, looking for leucocytosis or hyperamylasaemia; blood cultures are
usually negative in the early stages. AXR shows soap-bubble appearance of a retroperi-
toneal abscess in less than 20% of cases. USS or CT scan is usually diagnostic. CT scan
detection of air in the pancreas is diagnostic, or it may detect areas of low attenuation
with contrast, which suggests necrosis.
Treatment
✧ Radiological: percutaneous drainage with wide-bore drains. Two drains can be placed
side by side for irrigation and drainage. A sample should be sent for amylase and
microbiology and appropriate antibiotics started. Will require follow-up scans and
drain adjustment with or without further drainage.
✧ Surgical: retroperitoneal debridement and drainage.
Follow-up
Investigation of these patients is usually performed as an in-patient investigation.
Post-operative follow-up
Patients are usually in hospital for long periods until they recover from the acute episode.
Possible long-term consequences of pancreatic debridement are endocrine and exocrine
deficiency, for which insulin and pancreatic enzyme supplements may be necessary, and
pancreatic fistulae.
Recurrent pancreatitis
More than one attack of acute pancreatitis needs further investigation for aetiology. If the
cause is unclear, think of rarer causes of recurrent pancreatitis such as the following.
✧ Stenosis of the sphincter of Oddi, e.g. fibrosis after passage of a stone. This is
diagnosed by ERCP and treated by ERCP sphincterotomy. If this fails or the problem
recurs, open sphincteroplasty can be performed.
✧ Pancreas divisum: the duct of Wirsung is very small, therefore the duct of Santorini
becomes the major ductal system, but it has a small papilla, therefore there is
relative stenosis. This predisposes to pancreatitis. Divisum is found in 3–4% of the
population, but in approximately 12% of patients with idiopathic pancreatitis. Thus
the relationship between pancreas divisum and pancreatitis is unclear and surgical
treatment carries a poor prognosis. Diagnosis is made at ERCP when pancreatic
stenting may alleviate symptoms. Acessory duct sphincteroplasty can be performed at
ERCP or at open surgery if relief has been obtained after a trial of a pancreatic stent.
✧ Biliary microlithiasis: biliary crystals can be seen at EUS or on microscopy of a
bile sample taken at ERCP. Treatment involves cholecystectomy and/or endoscopic
sphincterotomy.
Chronic pancreatitis and chronic relapsing pancreatitis
This condition may present with frequent attacks of pancreatitis requiring admission
to hospital, or it may be insidious in onset with increasing pancreatic insufficiency.
Unlike acute pancreatitis, gallstones are thought to be an uncommon aetiological factor.
180 GENERAL SURGERY OUTPATIENT DECISIONS

Instead alcohol is the prime aetiological factor in 60–70% of cases, with no cause found
in 30–40%. Rare causes such as pancreas divisum, neoplasia, trauma, cystic fibrosis and
radiotherapy are responsible for the rest. Family history is very important: in younger
patients with a strong family history, suspect familial pancreatitis.
Objectives
Diagnose chronic pancreatitis, exclude pancreatic cancer, identify underlying aetiological
factor, detect pancreatic insufficiency, treat pancreatitis, treat aetiological factor, treat
pancreatic insufficiency.
History
Take a general pancreatic history. Patients may complain of repeated bouts of upper
abdominal pain which may or may not be related to alcohol ingestion. The pain may
radiate to the back or shoulder tip and is constant and dull. Patients avoid lying on their
backs, as this makes the pain worse. Initially pain is intermittent and episodic, progressing
to constant pain. On questioning, the patient may admit to stools which are pale, bulky,
oily or difficult to flush away. Symptoms due to the onset of diabetes mellitus are unusual
in the early stages.
Patients may give a history of weight loss due to exocrine insufficiency and/or anorexia
and nausea. Jaundice may be caused by biliary duct obstruction due to inflamma-
tion and fibrosis in the head of the pancreas. Similarly, signs and symptoms of gastric
outlet obstruction may result from an inflammatory mass in the head of the pancreas.
Haematemesis may be due to oesophageal varices. Take a detailed history of alcohol con-
sumption. Take a detailed family history.
Examination
Perform a general examination. Look for evidence of weight loss, malnutrition, jaundice
and/or stigmata of liver disease. Erythema ab igne from frequent application of a hot
water bottle is often seen. Examination may be normal, but examine for a palpable epi-
gastric mass representing an inflamed or fibrosed pancreas or a pseudocyst. Rupture
of a pseudocyst may produce ascites. Splenomegaly usually indicates splenic vein
thrombosis.
Investigations
Serum amylase may be normal and LFTs may indicate cholestasis. Blood sugar may be
abnormal, as may clotting. FBC may reveal leucopenia and thrombocytopenia indicating
hypersplenism. Faecal elastase will identify exocrine insufficiency. USS and CT scan
can identify features suggestive of chronic pancreatitis and detect complications such
as a dilated biliary tract and splenic vein thrombosis. MRCP can delineate biliary and
pancreatic duct anatomy. EUS can be used to exclude a neoplasm as well as obtaining
tissue for histology to exclude neoplasia or autoimmune disease.
Treatment – medical
Control pain and treat endocrine and exocrine insufficiencies. Treat any drug or alcohol
addiction.
✧ Pain: usually requires opiates starting with dihydrocodeine (DF118) or codeine for
mild to moderate pain, increasing to buprenorphine (sublingual), pethidine or mor-
phine sulphate (MST). NSAIDs may increase the risk of gastrointestinal haemorrhage.
Coeliac plexus blocks can be performed via EUS and can reduce opiate requirements,
but recurrence of symptoms may occur in time.
✧ Exocrine insufficiency: Creon® and pancreatin contain enteric-coated microspheres
that prevent deactivation in the stomach and allow a normal fat intake, which is
 LIVER, BILIARY SYSTEM AND PANCREAS 181

important for maintenance of weight and correction of malnutrition. Fat-soluble

vitamin supplements are necessary.
✧ Endocrine insufficiency: diabetic control is usually obtained with oral hypoglycaemics
but sometimes insulin is necessary. Blood-sugar control can be difficult in the
presence of variable food intake due to the pain induced by eating. Therefore careful
monitoring is required.
Treatment – surgical
Operations are considered mainly for the relief of pain, but no surgical procedure can
restore endocrine or exocrine function. Rehabilitation must be planned in advance and
there must be absolute avoidance of alcohol.
Indications for surgery
✧ Intractable pain (consider disruption to patient’s life, narcotics needed to control the
pain, control of alcoholism, age and general condition of patient).
✧ Development of complications, including the following.
∝ Lower bile duct obstruction: ERCP to exclude other causes and cancer. Relief of
obstruction may relieve the pain.
∝ Duodenal obstruction: rare in chronic pancreatitis. Exclude cancer by biopsy. Treat
non-cancerous cases by gastrojejunostomy.
∝ Vascular involvement: pseudoaneurysms and portal hypertension.
∝ Pancreatic cysts, pseudocysts, abscess, pancreatic ascites and pleural effusions.
∝ Presence of a dominant mass leading to suspicion or fear of cancer.
∝ Portal vein compression/mesenteric vein thrombosis.
∝ Pancreatic duct stricture with upstream dilatation with or without pancreatic
duct stones.
∝ Colonic stricture.

Surgery/intervention
Isolated pancreatic stricture can be treated at ERCP, or if this fails and there is upstream
duct dilatation, perform longitudinal pancreatico-jejunostomy.
For a mass in the head of the gland, perform pylorus-preserving pancreatoduodenec-
tomy (PPPD) or standard Whipple’s or Beger’s operation (duodenum-sparing pancreatic
head resection to be considered only if absolutely sure it is not malignant).
Inflammation restricted to the body and tail of the gland may be treated by distal
pancreatectomy.
Whole gland disease may very, very rarely be treated by total pancreatectomy with or
without islet cell autotransplantation (depending on pre-operative endocrine testing).
Open coeliac plexus block can be combined with open procedures.
Other procedures like cholecystectomy and parathyroidectomy should be performed
for their own indications. These procedures will not affect the natural history of chronic
pancreatitis.
Thoracoscopic splanchnicectomy for pain relief is effective, although the results may
only last 12–18 months.
Follow-up
Follow up at short intervals of 2–4 weeks until pancreatic neoplasia is excluded. Then
follow up long term at regular intervals to monitor pain control, endocrine and exocrine
insufficiency and abstinence from alcohol. Monitor weight and nutritional status,
including vitamin deficiencies.
182 GENERAL SURGERY OUTPATIENT DECISIONS

Post-operative follow-up
Assess the patient for success of the operation in relieving pain (approximately 70%
of patients) and for the development of complications, both expected (endocrine and
exocrine insufficiency) and unexpected (pancreatic fistula, small bowel obstruction).
Follow-up is long term for detecting and managing endocrine and exocrine insufficiency.
Gradually increase the intervals as the patient stabilises (1–6 months).

Neoplasms of the exocrine pancreas

Benign neoplasms are rare and seldom of clinical significance unless they become very
large and impinge on adjacent structures (CBD, duodenum, stomach or main pancreatic
duct). They include adenoma, cystadenoma, lipoma, fibroma, leiomyofibroma, myoma,
haemangioma, lymphangioma, haemangioendothelioma and neuroma. They usually
need resection to confirm their benign nature.
Pancreatic cancer
Pancreatic ductal adenocarcinoma constitutes 80–90% of all primary malignant tumours
arising from the gland and accounts for 10% of all cancers of the digestive tract. When
cancer arises in the head (70%) it must also be differentiated from cancer arising in the
ampulla, duodenum or lower common bile duct, which has a much better prognosis
than true pancreatic adenocarcinoma. The rare mucinous cystic neoplasms (mucinous
cystadenoma/adenocarcinoma) have a good prognosis if completely resected.
Pancreatic cancer is more common in older people. It has an increased incidence in
smokers, diabetics (pancreatic cancer can cause diabetes mellitus), alcoholics and in those
with hereditary pancreatitis.
Carcinoma of the head of the pancreas
History
The term ‘periampullary’ does not differentiate between carcinomas of the duodenum,
pancreas, common bile duct or ampulla, but all these tumours present with similar
symptoms. Jaundice is present in 90% and is classically described as painless, although
pain can be present in up to 70% of patients. Severe pain radiating to the back is a sinister
symptom suggestive of retroperitoneal tumour infiltration. Weight loss and anorexia are
common even in the early stages. Nausea and vomiting, epigastric bloating and change
of bowel habit can be reported. Haematemesis and melaena occur in late cases due to
direct invasion of mucosa or portal hypertension secondary to portal vein compression
by the tumour. Chills and fever due to cholangitis can occur.
Duodenal cancer can present with iron deficiency anaemia caused by occult GI bleeding
or with symptoms of gastric outlet obstruction. Fluctuating jaundice is a characteristic of
ampullary tumours, as are silver stools – steatorrhoea combined with GI blood loss.
Examination
Perform a general examination. Examination may be normal or jaundice and a palpable
gall bladder (Courvoisier’s sign) may be present in 25%. The liver is enlarged on palpation
in up to 80% of patients at presentation.
Carcinoma of the body and tail of the pancreas
History
There is pain and weight loss. Jaundice is uncommon and may indicate involvement of
the porta hepatis. Pain is usually dull, vague in the epigastrium or back. Can be episodic
and related to meals, or constant and severe. Partial relief may be obtained by flexing
 LIVER, BILIARY SYSTEM AND PANCREAS 183

the trunk forward. Severe pain may indicate extension of the tumour into perineural
tissues, lymphatics and posterior retroperitoneum. Weight loss may be severe and rapid.
Haemetemesis and melaena may occur.
Examination
Perform a general examination. There may be evidence of weight loss, but otherwise
examination may be normal. Occasionally there may be migratory thrombophlebitis
(Trousseau’s sign), indicating advanced cancer. Early cases have few signs. Late signs are
an abdominal mass or liver metastases. A rectal shelf may be evident on rectal exami-
nation in the rectovesical/vaginal pouch. Other late signs are ascites and an enlarged
lymph node in the supraclavicular fossa.
Investigations
Ninety per cent of patients are diagnosed too late. Always suspect pancreatic cancer in
patients with seemingly recent symptoms, absent physical signs and negative routine
X-ray investigations.
FBC may reveal iron-deficiency anaemia. Blood sugar testing may detect diabetes
mellitus or impaired glucose tolerance in 15% of patients. LFTs may indicate a cholestatic
picture. Faecal elastase test may be abnormal.
USS is a good initial imaging technique and can usually identify a pancreatic
mass, bile duct dilatation, liver metastases, ascites, extrapancreatic spread and portal
hypertension.
Contrast enhanced CT scan is the gold standard for diagnosis and accurate staging
of the disease. ERCP may be necessary to decompress the biliary tree, and it enables
cytology. Alternatively, percutaneous needle biopsy under USS/CT control for diagnosis
in potentially incurable cases avoids a diagnostic laparotomy. In cases where this is not
possible a laparoscopic biopsy is less invasive than open operation.
Markers for pancreatic cancer, e.g. CA-19-9 and CEA, may be raised and may fall
to normal after resection, providing a means of monitoring recurrence if levels rise
again.
Pancreatitis can co-exist with all cancers and there may be gallstones – the presence
of one does not exclude the other. Truly representative needle biopsies of the pancreas
are often hard to obtain because of sampling error and confusion between tumour and
associated pancreatitis.
Staging
The main objective is to detect irresectable disease – vascular invasion (portal vein, SMA,
coeliac or hepatic artery) and metastases to the liver, peritoneal cavity, coeliac nodes or
beyond. These can usually be detected by CT.
Tumour size greater than 3cm, invasion of contiguous organs like the duodenum or
colon, and enlarged lymph nodes within the resection field are not contraindications
to surgery. EUS can provide detailed assessment of vascular involvement and when
combined with biopsy can give histological diagnosis. Staging laparoscopy can exclude
liver and peritoneal metastases and when combined with intra-operative ultrasound can
give further accurate staging.
Treatment – surgical
Pre-operative preparation
A good state of nutrition and hydration supplemented with intravenous fluids, elemental
diet and multivitamins is required. Correct any clotting deficiency with vitamin K or
FFP. If the serum bilirubin is high (greater than 200 umol/l), or in the presence of sepsis,
hepatorenal failure, severe cardiopulmonary disease expected to respond to medical
184 GENERAL SURGERY OUTPATIENT DECISIONS

management and severe malnutrition, a temporary percutaneous or transhepatic biliary

decompression should be considered.
Exclusions for surgery
Apart from irresectable disease, exclusions are very elderly or frail patients with multiple
systemic disorders or a life expectancy of less than five years.
Surgery
Surgery is Whipple’s pancreaticoduodenectomy or PPPD or total pancreatectomy.
Whipple’s operation is indicated for tumour confined to the duodenum, ampulla of
Vater or lower CBD. However, if the rest of the gland is severely affected by pancreatitis,
total pancreatectomy may be the better option. If frozen section confirms cancer at the
resection margin a total pancreatectomy may occasionally be necessary. A suspected
cancer of the body and tail is treated by a distal pancreatectomy. If unresectable or
metastatic, a palliative biliary and gastric bypass is performed.
Follow-up
Follow up at short intervals (1–4 weeks) in cases where cancer is suspected.
Palliation
✧ Relief of jaundice, pruritus or impending cholangitis: ERCP/PTC and biliary stenting
or hepatico-jejunostomy.
✧ Relief of duodenal obstruction: endoscopic or radiological stenting or open/laparo-
scopic gastrojejunostomy.
✧ Relief of pain: coeliac plexus block (50 ml of 50% alcohol plus 20 ml of 6% phenol).
External beam radiotherapy.
✧ Unfit for surgery: ERCP sphincterotomy and biliary stent.
✧ Stent blockage: indicated by recurrent jaundice and cholangitis. ERCP and change
of stent.
Post-operative follow-up
Review to determine the success of the operation and to detect any complications. Review
the histology to determine whether resection margins are clear of tumour. Examine for the
general complications of a laparotomy and general anaesthesia. Small bowel obstruction
may be due to recurrent tumour or adhesions – laparotomy is indicated to establish the
diagnosis and relieve obstruction. Biliary obstruction may be due to tumour recurrence
or anastomotic stricture. Exclude endocrine and exocrine pancreatic insufficiency.
Monitoring of recurrence
All patients should be referred for adjuvant chemotherapy following surgery. Single agent
gemcitabine has a survival benefit versus no chemotherapy. Patients with locally advanced
disease may have a response to combination chemoradiotherapy, whereas patients with
metastatic disease should be offered palliative chemotherapy. A small number of patients
have increased levels of tumour marker such as CA 19-9 or CEA levels pre-operatively
and serial monitoring post-operatively is useful.
✧ Management of pancreatic endocrine insufficiency: insulin.
✧ Management of pancreatic exocrine insufficiency: Creon®/pancreatin tablets, vitamins
and antibiotics.
Prognosis
Operative mortality is 1–5% in high-volume centres. Five-year survival is 10–25% for
pancreatic ductal adenocarcinoma, 40–50% for ampullary carcinoma and distal cholan-
 LIVER, BILIARY SYSTEM AND PANCREAS 185

giocarcinoma, higher for mucinous cystic neoplasms and neuroendocrine tumours. Most
mortality occurs from two months to two years.

Lesions of the endocrine pancreas

Endocrine cancers are relatively slow growing and many apparently metastasise only to
regional lymph nodes. This allows surgical cure in a sizeable proportion of patients.
Insulinoma
Hyperinsulinaemia causes symptomatic hypoglycaemia. It is caused by B-cell neoplasia
(insulinoma) or rarely, B-cell hyperplasia/microadenomatosis. In adults 80% of insuli-
nomas are benign solitary tumours, 10% are multiple and are part of MEN I and 10%
are malignant. There is an even distribution of tumours in the head, body and tail of the
pancreas.
Differential diagnosis
Includes brain tumour, epilepsy, alcoholism and drug abuse, fibrosarcoma and non-
pancreatic tumours, glucocorticoid deficiency, diffuse liver disease and factitious
hyperinsulinaemia due to insulin abuse.
Objectives
Diagnose the cause, differentiate from other causes, localise tumour, treat hypoglycaemia,
treat tumour.
History/examination
Take a general pancreatic history and perform a general examination. There are symptoms
of weakness, sweating, hunger, palpitations and trembling. The median time of onset
of symptoms to diagnosis is two years, because of the rare diagnosis and non-specific
nature of the symptoms. Determine the relationship of symptoms to exercise and food.
Hypoglycaemia may occur after fasting or soon after eating (reactive hypoglycaemia).
Fasting hypoglycaemia is more typical of an insulinoma, reactive hypoglycaemia occur-
ring after meals is seen more commonly in alimentary disorders, e.g. post-gastrectomy.
Examination may be normal.
Investigations
For definitive diagnosis, measure simultaneous insulin and glucose levels at the time of
hypoglycaemia. A diagnostic 72-hour fast in hospital will detect all cases. Other causes
of hypoglycaemia such as fibrosarcoma and non-pancreatic tumours, glucocorticoid
deficiency or diffuse liver disease will not be associated with a raised insulin level.
Occasionally provocative tests to induce hypoglycaemia are needed, but these are second-
line investigations.
Diagnosis
A positive diagnosis is based on three elements:
✧ recognition of probable nature of patient’s symptoms
✧ presence of Whipple’s triad:
∝ hypoglycaemic symptoms produced by fasting
∝ hypoglycaemia documented during symptomatic episodes
∝ symptoms relieved by glucose intake
✧ demonstration that plasma insulin concentration is inappropriately high for the
existing levels of plasma glucose. An insulin (IU/ml) to glucose (mg/dl) ratio of
greater than 0.3 indicates insulinoma.
186 GENERAL SURGERY OUTPATIENT DECISIONS

Pre-operative localisation
Seventy-five per cent of tumours are less than 1.5cm and are not visible or palpable. EUS
is particularly useful for endocrine tumours of the pancreas.
Angiography is the most reliable localising investigation, especially when combined
with a calcium stimulation test. CT can detect less than 60% of tumours. MRI may be
more reliable. If imaging is negative, selective venous sampling for insulin is necessary.
However, at laparotomy a complete examination of the whole gland is needed, including
the use of intra-operative ultrasound to exclude multiple tumours.
Treatment
Benign disease
Treat with the simple enucleation, or with Whipple’s operation or distal pancreatectomy,
depending on the size and location of the lesion. Beware of enucleating lesions close to
the main pancreatic duct – a pancreatic leak or fistula may develop.
Multifocal malignant disease
This may require a total pancreatectomy. Ninety-five percent of patients are cured, 5–10%
experience recurrent hypoglycaemia requiring re-operation. Surgical mortality is less
than 5%.
✧ Diazoxide for control of pre-operative hypoglycaemia – needs careful monitoring.
✧ Octreotide – infusion or long-acting depot preparation. Streptozotocin for metastatic
insulinoma.
Follow-up
Follow up at short intervals(1–4 weeks) until diagnosis is achieved. Consider admission
to hospital, and monitor and treat hypoglycaemia.
Post-operative follow-up
Determine the success of the operation by the relief of symptoms. Check histology to
confirm complete excision. Long-term follow-up is required for management of pan-
creatic insufficiency.
Gastrinoma (Zollinger-Ellison syndrome (ZE))
This consists of intractable peptic ulceration caused by excess gastrin secretion. Twenty-
five per cent have MEN I (also parathyroid hyperplasia and pituitary prolactinoma). Of
gastrinomas, 60–90% are malignant and 50–80% will have lymph node metastases at
presentation. They arise in the pancreas in 75% of cases. Other sites are the duodenum,
omental lymph nodes, liver and gastric antrum. These tumours are more often multiple
than solitary.
Objectives
Diagnose gastrinoma, differentiate from other causes of recurrent ulceration, localise
gastrinoma, treat gastrinoma, screen for MEN I.
History/examination
Take a general pancreatic history and perform a general examination. Patients may
present with symptoms of dyspepsia and/or severe diarrhoea in 5–7%, usually over
several years. Examination is frequently normal.
Suspect in any patient with:
✧ peptic ulcer disease refractory to treatment
✧ multiple ulcers or ulcers in unusual places (distal duodenum or jejunum)
✧ peptic ulcer disease with diarrhoea
 LIVER, BILIARY SYSTEM AND PANCREAS 187

✧ recurrence after operation

✧ strong family history of MEN I or other feature of MEN, e.g. hypercalcaemia.
Investigations
Perform an OGD to document the ulceration. Determine gastric basal acid output –
evidence of acid hypersecretion such as a basal level of more than 15 mmol/l suggests
gastrinoma.
A normal basal acid level makes ZE unlikely. In patients with high basal acid levels,
measure fasting serum gastrin levels. Gastrinoma is characterised by a basal gastrin level
greater than 100 pg/l in the presence of acid hypersecretion (must be measured without
proton-pump inhibitor (PPI) medication, which increases gastrin levels). Levels greater
than 500 pg/ml are almost diagnostic of gastrinoma and levels from 100–500 pg/ml are
highly suggestive.
Basal gastrin levels are also raised in pernicious anaemia, atrophic gastritis and gastric
cancer, but these conditions do not have acid hypersecretion. Conditions which have
raised gastrin levels and acid hypersecretion include gastrinoma, retained gastric antrum
after Billroth II, antral G-cell hyperplasia and gastric outlet obstruction. Gastrinoma can
be differentiated from these conditions by the secretin stimulation test. After injection of
secretin gastrin, levels rise to over 200 pg/ml in gastrinoma patients only.
Once gastrinoma is diagnosed MEN syndrome needs to be excluded – serum calcium,
phosphate and plasma prolactin levels need to be measured.
Tumour localisation
Most can be localised by CT scan. However, tumours less than 7mm are not detected. MRI
may improve visualisation. Angiography is not used, as gastrinomas are hypovascular.
EUS is useful where available. Somatostatin receptor scintigraphy (octreotide scan) can
be positive in up to 80% of patients.
Laparotomy and operative search with intra-operative ultrasound and OGD to detect
duodenal wall tumours by transillumination.
Treatment
Patients with pre-operatively identified liver metastases or MEN I are treated medically
with control of ulceration by omeprazole. In the absence of liver metastases or MEN I,
medical therapy is used for 6–12 months. Young and fit patients undergo surgical
exploration, after initial stabilisation on medical therapy. At operation, if complete tumour
resection is possible this is performed. However, if complete removal is impossible, as
much tumour as possible is removed. Post-operatively, medical therapy is reintroduced
and continued for as long as symptoms are controlled. If medical therapy fails again,
rarely a total gastrectomy may be considered. Similarly for patients where total tumour
removal was performed, basal and stimulated gastrin levels are measured at intervals
post-operatively. If gastrin levels are still raised, medical therapy is reintroduced and
gastrectomy is considered for poorly controlled patients.
Old or poor-risk patients are continued on medical therapy for as long as symptoms
are controlled. If at any stage medical treatment ceases to be effective the patients are
explored surgically for the tumour. The tumour is resected if possible, otherwise a total
gastrectomy is performed.
Palliation
Liver metastases and advanced disease: streptozoticin and 5FU chemotherapy. Octreotide
for symptoms. Liver resection in selected cases.
188 GENERAL SURGERY OUTPATIENT DECISIONS

MEN I
Perform parathyroid surgery first, which may relieve symptoms completely. However, this
is often only temporary, so continue to follow up in the clinic and proceed to gastrinoma
treatment if symptoms recur.
Follow-up
See treatment section.
Post-operative follow-up
See treatment section. Long-term surveillance is needed, as recurrences may be late.
Successful removal of all gastrin-secreting tumours needs to be confirmed by serially
negative plasma gastrin responses to secretin stimulation.
VIPoma
Rare primary lesion is in the pancreas in 80%, 20% are ganglioneuromas and
neuroblastomas.
History/examination
The condition is characterised by watery diarrhoea.
Investigations
Diagnosed by increased VIP levels, hypokalaemia, achlorhydria and acidosis.
Localisation
Usually solitary and large, and can be detected by USS, CT or angiogram.
Treatment
Initially medical, by intravenous fluids and octreotide. Therapeutic options include
surgical excision, debulking and medical treatment. Metastatic disease is treated by
streptozotocin.
Follow-up
Long term to detect recurrence and deterioration in condition.
Glucagonoma
This is a rare condition arising in the A cells of islets. Seventy to eighty per cent are
malignant, with 50% having metastases at the time of presentation.
History/examination
There is a characteristic skin rash, necrolytic migrating erythema, weight loss, diabetes
mellitus, DVT, anaemia, hypoaminoacidaemia, glossitis and cheilitis. Diagnosis is based
on a recognition of skin rash in combination with diabetes mellitus in a setting of a
chronic wasting disorder.
Investigations
Glucagon levels exceed 1000 pg/ml. Other conditions associated with increased glucagon
levels are diabetes, chronic renal failure, shock states (myocardial infarction (MI),
septicaemia, burns) acute pancreatitis, cirrhosis, familial hyperglucagonaemia and
exercise.
Localisation
Usually large, therefore USS or CT is reliable.
 LIVER, BILIARY SYSTEM AND PANCREAS 189

Treatment
Treat with topical steroids and intravenous amino acids. Octreotide is good at controlling
symptoms in the pre-operative period and as palliation. Perform surgical excision or
debulking (effective in symptom relief). If surgery is not an option then perform selective
arterial embolisation and chemotherapy with streptozocin and 5FU.
Follow-up
Long term to detect recurrence or deterioration in clinical condition.
Multiple endocrine neoplasia I
This is an autosomal dominant familial disorder characterised by the development
of synchronous and metachronous endocrine and non-endocrine tumours, but with
considerable phenotypic variability.
Parathyroids are involved in 85% and the majority of lesions consist of hyperplasia.
Pancreatic islets (30–80%) are inevitably involved and the commonest pancreatic tumour
is the gastrinoma. Pancreatic tumours are usually multiple. Pituitary tumours are
most commonly prolactinomas with growth-hormone tumours next (10–60%). Other
occasional tumours are adrenocortical lesions (25%), thyroid nodules, bronchial and
intestinal carcinoids and lipomas.
Investigations
All patients with endocrine pancreatic tumours should be investigated by testing of serum
calcium and phosphate levels, plasma assays of parathormone, insulin, gastrin, glucagon,
somatostatin, pancreatic polypeptide, prolactin, growth hormone, ACTH and cortisol,
chromogranin A and MRI scan of pancreas, pituitary and abdomen. All family members
should be screened.
Multiple endocrine neoplasia II
An autosomal dominant familial cancer syndrome characterised by the development of
medullary thyroid cancer (90%), phaeochromocytoma (50%) and hyperparathyroidism
(20–30%) with variable expression. Type A consists of hyperparathyroidism, medullary
carcinoma of the thyroid and phaeochromocytoma.
Type A can be associated with cutaneous lichen planus and Hirschsprung’s disease.
Type B has a low incidence of parathyroid diseases but multiple mucosal neuromas,
intestinal ganglioneuromas leading to megacolon and constipation, a Marfanoid habitus
and characteristic facies with thickened lips and alae nasi along with medullary carcinoma
of the thyroid and phaeochromocytoma.
Investigations and screening
Calcitonin, CEA, metanephrine and normetanephrine both urinary and serum, ionised
calcium, parathyroid hormone.
 Colon, rectum and anus
Henry Tilney and Paris Tekkis
NINE

Introduction
Conditions affecting the colon, rectum and anus range from the trivial to the life-
threatening. The knowledge of these conditions among the public is complicated by
embarrassment and folklore. Many patients attending the surgical outpatients are
concerned about the intimate nature of the examinations that they are likely to undergo
and require careful reassurance. Certain groups of patients become very preoccupied
with the maintenance of a ‘regular bowel habit’ and consult if there is any variation in
what is perceived as normal, while reluctance to attend can result in others consulting
only when symptoms are severe and tumours may be advanced. In addition to these
difficulties colorectal cancer is one of the commonest malignancies and can mimic the
presentation of nearly all other colorectal and anal disorders. The priority of investigation
for many patients is to exclude colorectal malignancy, but the necessary tests are often
unpleasant and invasive and their application to all patients with colorectal symptoms
would be impractical. However, the diagnosis must always be kept in mind, especially
if minor conditions do not respond to treatment. It is this combination of factors that
makes the assessment of colorectal disorders particularly difficult. After introductions
and putting the patient at ease it is important to ascertain what they are hoping for from
their consultation, as investigations to exclude malignancy are sufficient to satisfy many
patients, who are then content to manage their own symptoms with simple advice.

Assessment of colorectal disorders

Colorectal history
The history should include a basic history of the whole gastrointestinal (GI) tract, includ-
ing questions about non-specific features such as malaise, weight loss and vomiting. When
the responses indicate a possible colorectal problem a more detailed colorectal history
is required. Abdominal symptoms include pain (ask about site, periodicity, aggravating
factors and nature: constant or colicky), distension or borborygmi (noisy bowels). Ask
about any medications, in particular the long-term use of laxatives or antidiarrhoeal
drugs. Ask about urgency, tenesmus, wet-wind, incomplete evacuation and weight loss. A
history of recent exotic travel may be relevant, and a careful family history with particular
attention to colitis, polyposis syndromes and colorectal cancer is essential.
Abdominal pain
Typically, abdominal pain in colonic disorders is colicky. Visceral midgut pain is
generally felt in the periumbilical region, while hindgut pain tends to lead to suprapubic
discomfort. The left iliac fossa is a common site for pain and this may be associated with
diverticular disease, although other diagnoses are not excluded. Colicky colonic pain may
equally be a feature of benign irritable bowel syndrome or a stenosing carcinoma of the
colon. Constant pain may indicate a complication of diverticular disease (e.g. localised
or free perforation, abscess) or advanced bowel cancer with nerve involvement.
Alteration in bowel habit
There are a wide variety of bowel habits that may be considered normal, but a change may
be an important symptom of colorectal disease, which can suggest bowel cancer. Time
should be taken to identify the previous bowel habit, the new bowel habit, the timing of

190
 COLON, RECTUM AND ANUS 191

the change and the presence of constipation or diarrhoea. Enquire about the consistency
and frequency of stool and whether this is associated with the passage of blood or slime
(mucus).
Rectal bleeding
If rectal bleeding is part of the history ask about the timing of this and whether there
have been any previous episodes of rectal bleeding. Is the bleeding bright red, dripping
into the toilet as in haemorrhoids or mixed in the motion as with inflammatory bowel
disease or malignancy? Is the bleeding painful, as with an anal fissure, or painless? Does
bleeding only occur at defaecation or at times in between? Ask about the amount of
blood, although patients commonly overestimate this. Does it drip into the toilet, are
there dark clots (suggests bleeding higher in the colon) or is there just a smear on the
toilet paper? Note that the history is not totally reliable in excluding a cancer of the bowel,
which can present with any type of rectal bleeding.
Anal and perineal symptoms
These include pruritus (itching), pain and its relation to defaecation, discharge and
bleeding.
Prolapse
Something ‘comes down’ at defaecation or on straining or coughing. These lumps may
reduce spontaneously or require manual reduction.
Incontinence
Ask about timing and severity; incontinence to flatus, liquid stool, solid stool. Enquire
regarding urgency, tenesmus, wet-wind and incomplete evacuation. A history of previous
anal surgery or trauma is important, and in female patients a careful obstetric history is
essential, noting the number and nature of previous deliveries, obstructed and prolonged
labour, instrumental delivery and obstetric tears or the need for episiotomy.
Colorectal examination
General examination may reveal anaemia associated with neoplasia or inflammatory
bowel disease. Dermoid cysts are associated with Gardner’s syndrome; acanthosis
nigricans and dermatomyositis with neoplasia; and pyoderma gangrenosum, arthropathy,
uveitis and finger clubbing with inflammatory bowel disease. Examination of the
gastrointestinal tract begins with the mouth, which may reveal oral Crohn’s or the
perioral pigmentation associated with Peutz-Jeghers syndrome.
Abdominal examination
Inspect the supine abdomen for stomas; the scars associated with previous colorectal
surgery; evidence of distension; visible peristalsis; and a mass or other organomegaly.
Palpation may reveal tenderness or a palpable sigmoid colon, which is common and
a normal finding, especially in constipation. Neoplasm or diverticular disease may be
associated with a bowel mass. The liver may be enlarged due to secondary spread from
a bowel neoplasm.
Rectal examination
Explain the procedure to the patient, explain the justification for it and obtain verbal
consent. Place the patient in the left lateral position with the knees flexed as far as pos-
sible into the abdomen. Cover the patient’s legs with a blanket to minimise exposure. On
inspection look for evidence of pruritus ani, perianal warts, perianal abscess, perianal
haematoma, prolapsing haemorrhoids, thrombosed haemorrhoids, skin tags, anal
192 GENERAL SURGERY OUTPATIENT DECISIONS

fistulas, anal fissures (and the frequently associated ‘sentinel tag’), anal cancer, rectal
prolapse and faecal soiling of the perineum.
Ask the patient to bear down as if defaecating. Look for abnormal perineal descent,
eversion of the anus, prolapsing haemorrhoids and other protruding lesions such as rectal
prolapse or neoplasm. The pulp of a gloved lubricated index finger is used to palpate for
the thickened cord of a fistula track or other abnormalities around the anus. The pulp of
the finger is then pressed onto the anus until the sphincter relaxes and the finger is them
slid into the rectum. Significant pain at this point may indicate an anal fissure and the
examination may have to be deferred until it is less painful following treatment of the
fissure, or if diagnostic concern is present then examination should be performed under
anaesthetic. Note the state of the resting anal tone, which largely reflects the condition of
the internal anal sphincter. Ask the patient to contract the anus (examining the ‘squeeze
pressure’ provided by the external sphincter) and hook the finger over the puborectalis
muscle. This indicates the uppermost limit of the external sphincters and can be used as a
landmark to determine the position of lesions, e.g. lesions above this indicate supralevator
disease.
The rectum should be assessed in relation to three parts: the lumen and its contents,
the rectal wall and structures outside the rectum. Note the contents of the rectum and the
consistency of the faeces. Consider the rectum in quadrants (front, back, left, right) and
palpate each one in turn. Note the position of any abnormality in relation to a notional
clock-face where the anterior wall is considered 12 o’clock and posterior 6 o’clock (as if
the patient is viewed in the lithotomy position). Withdraw the finger and inspect it for
blood, mucus, pus and the nature of the faeces.
Extra-intestinal signs of inflammatory bowel disease (IBD)
There are various eye and skin signs, which should be identified on examination in
relation to Crohn’s disease and ulcerative colitis.
Ophthalmic signs
There are generally seen in active disease and are more common in Crohn’s than in
ulcerative colitis.
✧ Episderitis: redness and soreness of the eye similar to conjunctivitis. This is the most
common ophthalmic manifestation of IBD.
✧ Iritis and uveitis: this is less common. It is associated with reduced visual acuity and
a painful red eye.
Cutaneous signs
✧ Erythema nodosum: painful, raised red lesions, often on the shins, most frequently
associated with Crohn’s disease, affecting 15% of sufferers. Mirrors disease activity
and biopsy shows subcutaneous septal panniculitis with neutrophil infiltrate.
✧ Pyoderma gangrenosum: affects around 2% of those with IBD, especially Crohn’s coli-
tis. Lesions are deep ulcers with a necrotic base and an undermined purple edge. They
characteristically occur on the lower limbs and can be single or multiple, but are also
seen around stomas and surgical scars. Histology reveals a neutrophilic dermatitis.

Investigation of colorectal disorders

Laboratory investigations
Blood tests
Haematology
Full blood count (FBC) for iron-deficiency anaemia and white cell count and differential.
Plasma viscosity, erythrocyte sedimentation rate.
 COLON, RECTUM AND ANUS 193

Biochemistry
Liver function tests (LFT) for indicating metastases. Thyroid function tests may be
useful in the assessment of constipation and diarrhoea. C-reactive protein (CRP) for
inflammatory conditions including colitis.
Immunology
Alpha-foetoprotein (AFP) and carcinoembryonic antigen (CEA) may be raised in colonic
neoplasms.
Faecal tests
Faecal occult blood
This guaiac-based test for peroxidase activity can be performed at home by the patient.
The patient smears a faecal sample onto a pre-prepared card which is then returned
to the laboratory, where the presence of blood can be detected. The presence of blood
can occur in normal individuals but may be an indicator of gastrointestinal pathology,
and a consistent finding requires further investigation. This test forms the first-line
investigation in the UK National Bowel Cancer Screening Programme. It is a simple and
quick screening test, sensitivity is 50–70% and about two-thirds of tumours are thought
to bleed in the course of a week. There are false positives caused by ingestion of animal
haemoglobin, nosebleeds and so on, and dietary restrictions are required for two days
prior to testing. False negatives occur due to intermittent bleeding of the tumour. The
test is of no use in patients with obvious rectal bleeding.
Microbiology
In patients with diarrhoea, potential infective causes should be excluded by a stool
culture. Fresh faecal samples are required and if parasites are suspected these samples
should be transported immediately to the laboratory for examination. Toxins produced
by Clostridium difficile may be identified in patients with pseudomembranous colitis.
Imaging techniques
Proctoscopy
A rectal examination is performed prior to insertion of the proctoscope. The technique
consists of insertion of either a metal or disposable plastic rigid tube fitted with a fibre-
optic light source for inspection of the distal rectum and anus. The proctoscope is
lubricated with water-soluble gel and inserted with the central obturator in place until
the rectum has been entered, and then it is removed. The rectal mucosa is inspected as the
instrument is slowly withdrawn. The patient can be asked to bear down to demonstrate
prolapsing mucosa and haemorrhoids. This short instrument gives a good view of the
distal rectum and anal canal and is particularly useful for the diagnosis of haemorrhoids.
Injection or banding of the haemorrhoids can be performed through the proctoscope.
The procedure may be unpleasant for the patient. Only the distal rectum can be
observed.
Rigid sigmoidoscopy
A rectal examination is performed prior to insertion. The sigmoidoscope is a rigid tube,
made of metal or disposable plastic, with a removable central obturator. The longer
length of the sigmoidoscope enables more of the rectum and lower sigmoid colon to be
inspected, although in practice only the distal two-thirds of the rectum can frequently
be assessed.
In addition to the fibre-optic light source there is a connection for air insufflation
using a rubber bulb. The sigmoidoscope is inserted for a few centimetres through the
194 GENERAL SURGERY OUTPATIENT DECISIONS

anus, with anterior angulation of the scope being required to negotiate the 90-degree
anorectal junction. The obturator is removed and the scope window secured to provide
an air-tight seal. The rectal ampulla is inspected and the lumen of the bowel identified. Air
is introduced via the instrument to open up the lumen ahead. Patients should be warned
that air is being introduced and they may feel the need to pass flatus but ask them to try
and retain the air if they can.
The instrument is advanced only when the lumen ahead is visible. More of the rectum
and lower sigmoid can be inspected. The procedure can usually be performed in the
outpatient department without bowel preparation (although a phosphate enema can be
administered if necessary).
Biopsies can be taken from abnormal lesions. However, care should be taken when
sampling mucosal lesions above 10cm because of the risk of perforation, especially if
the bowel is inflamed. There is a risk of bowel perforation if not performed gently. It is
uncomfortable for the patient, especially if too much air is introduced.
Flexible sigmoidoscopy
This involves insertion of a 60cm flexible fibre-optic sigmoidoscope via the anus, and it
is frequently capable of evaluating the colonic mucosa as far as the splenic flexure. It is
usually performed as a day-case procedure involving bowel preparation with phosphate
enema just prior to the procedure. In some units flexible sigmoidoscopes are available
for use in the clinic rooms or in a designated ‘rapid access’ endoscopy list running con-
currently with the colorectal outpatient clinic. Patients who can be selectively asked to
self-administer enemas at home on the basis of their referral letters can be investigated
immediately. The steerable nature of the scopes enables the turns of the sigmoid colon to
be negotiated. Once again air insufflation is used to open up the lumen ahead. The scope
is advanced when the lumen ahead is visible.
Approximately 70% of colorectal carcinomas are within reach of the flexible scope.
Biopsies can be performed and polyps excised. Bowel preparation (with an enema) is
necessary; equipment is expensive and needs careful cleaning and maintenance. Not all
of the colon is inspected.
Colonoscopy
Colonoscopy involves using a flexible fibre-optic scope that is longer than the flexible
sigmoidoscope and allows the whole of the colon to be inspected successfully by experi-
enced operators in 90% of cases. Formal bowel preparation is required in the days prior
to the procedure through the use of purgatives, and intravenous sedation (usually with
benzodiazepines and opiates) is used for the procedure itself. Patients who are sedated
should be warned not to drive or operate machinery for 24 hours after the procedure.
The scope is steerable and air insufflation is used.
The whole colon can be visualised and biopsies can be taken for tissue diagnosis.
However, the technique is very much operator dependent and one must trust the opinion
of the operator who makes the report. Therapeutic procedures such as polypectomy can
be performed.
Being operator dependent, it requires training and an experienced practitioner. It is
uncomfortable for the patient. Major risks, of which patients should be warned, include
colonic perforation in 0.1% (rising to 0.3–4% following biopsy/polypectomy), and
haemorrhage rates are quoted at 0.03% following diagnostic colonoscopy and 1.9% after
polypectomy.
Double contrast barium enema
The procedure involves infusing barium contrast through a catheter into the rectum. The
balloon on the catheter is inflated to prevent leakage. The patient is placed on a tilt table
 COLON, RECTUM AND ANUS 195

which is manoeuvred through different positions to coat the whole bowel in barium. Air
is insufflated after evacuation of most of the barium to finely coat the bowel wall with
barium and provide mucosal detail.
It provides fine mucosal detail as well as gross anatomy and shows fistulas not easily
visible on colonoscopy. It involves a significant dose of X-rays; bowel preparation is
required; and rates of colonic perforation between 0.01 and 0.04% are reported.
Abdominal ultrasound technique
This is a useful non-invasive technique for the investigation of abdominal pain in order
to detect pathology in other organs, e.g. the gall bladder, although its ability to detect
colonic pathology is somewhat limited.
Pre-operatively it can be used to detect liver metastases in patients with colorectal
cancer, although its accuracy in this respect is considered inferior to that afforded by CT
scans. Ultrasound can also be used intra-operatively for the same purpose. It is operator
dependent and, therefore, may be poor at defining bowel pathology.
Endoanal/transrectal ultrasound
A specially designed lubricated rotating probe, confined within a fluid-filled sheath to
maintain tissue contact, is inserted into the rectum. Alternating bright and dark rings
represent the anal sphincters and layers of the bowel wall, and sphincter defects and the
relation of tumours or fistula tracks to the muscles can be assessed.
Transrectal ultrasound is a specialised technique, but in the centres where it is used it
has proved useful in determining the local spread of rectal cancers and in the assessment
of perianal fistulas and anal sphincters. It is an uncomfortable technique for the patient,
which occasionally needs to be performed under anaesthetic. It is operator dependent.
Computed tomography (CT) scan
The scan gives an accurate definition of anatomy. It is useful for defining the extent of
local spread of tumours and for investigating potential metastatic deposits. It is com-
monly used to assess for complications of diverticular disease.
It is expensive and associated with high doses of radiation. Equivalent information can
often be obtained by other means with lower radiation exposure.
Magnetic resonance imaging (MRI)
MRI detects minute quantities of energy released by hydrogen ions when they are forced
to change direction by a strong magnetic field. The patient passes through the scanner,
which is quite claustrophobic and noisy. The scan does not require exposure to ionising
radiation. It provides detailed information, which is useful in assessing the nature and
extent of complicated perianal and other fistulas. Reconstructions in multiple planes
are possible, allowing excellent anatomical detail. It can be particularly useful in the
assessment of rectal tumour encroachment on the mesorectal fascia (the circumferential
resection margin), which can help to select those who would benefit from pre-operative
radiotherapy, and in the investigation of complicated anorectal sepsis. It is expensive and
time-consuming. Some patients find the experience intolerable.
Examination under anaesthetic
This may be useful for patients with very painful anal conditions preventing adequate
exami na tion and diagnosis in the outpatient clinic, or in cancer to assess rectal
resectability.
Diagnostic laparoscopy
This can potentially be used for assessment of a number of pathologies including the
196 GENERAL SURGERY OUTPATIENT DECISIONS

assessment of liver metastases when combined with intra-operative ultrasound, although

the technique is not as widespread as the practice of the ‘staging laparoscopy’ in the
assessment of upper GI malignancies.
Physiological techniques
Anal manometry
This involves the insertion of air/water-filled balloon pressure measuring systems into
the rectum. The pressure inside the rectum is recorded during different conditions. The
maximum resting pressure reflects function of the internal sphincter while the maximum
squeeze pressure indicates function of the external sphincter. Pressures decrease with age
and are commonly reduced in incontinence.
Rectal compliance
A balloon is inflated in the rectum and the volume and pressure is recorded at first
sensation and the maximum amounts tolerated. Compliance is decreased in inflammatory
bowel disease but increased in patients with chronic constipation, who are used to
harbouring large volumes of stool in the rectum.
Electromyography
This involves the insertion of fine electrodes into the anal sphincter muscles and is useful
in identifying damage to the sphincters, although this is generally now regarded as a
research tool.
Pudendal nerve latency
This is measured by the use of a disposable electrode attached to a gloved finger. The nerve
is stimulated as it crosses the ischial spine, and the time taken for the impulse to travel to
the sphincter is recorded. Prolonged latency is associated with faecal incontinence, rectal
prolapse, solitary rectal ulcer syndrome, severe constipation and sphincter defects.
The rectoanal reflex
Normal reflex consists of an inhibition of sphincter contraction in response to inflation
of a balloon in the rectum. The loss of this reflex is almost diagnostic of Hirschsprung’s
disease, but may also be absent in patients with rectal prolapse and incontinence if resting
pressures are already low.
Anal sensation can be assessed in relation to a thermal or electrical stimulus applied
to the anal mucosa. Reduced sensation may be an important factor in patients with
incontinence, especially if they have had previous anal surgery.
Defaecating proctogram
Barium suspension is infused into the rectum, and the patients are recorded as they void
this suspension. This simulates defaecation and is useful for demonstrating abnormal
anorectal angles in patients with pelvic floor weakness or prolapse, rectoceles, or the
function of ileoanal pouches. In patients with anismus or obstructed defaecation,
the acute anorectal angle may be maintained during attempted defaecation due to
paradoxical contraction of the external sphincter complex, and this can be demonstrated
by the defaecating proctogram.
Colonic transit time
The patient ingests special radio-opaque markers that can be followed by plain abdominal
X-rays. This technique may be used to diagnose slow transit constipation.
 COLON, RECTUM AND ANUS 197

Disorders of the colon and rectum

Rectal bleeding
Most cases of rectal bleeding presenting to the surgical clinic are due to minor anorectal
conditions that are easily diagnosed and treated. However, sometimes these minor
conditions co-exist with other more serious pathology, such as colorectal cancer.
Therefore, the more serious causes of rectal bleeding should be excluded in the middle-
aged or older patient initially and in any age group where the symptoms fail to settle
despite apparently adequate treatment, rather than attributing the symptoms to minor
anal conditions. Causes of rectal bleeding, in decreasing order of incidence, include the
following.
✧ Diverticular disease.
✧ Inflammatory bowel disease:
∝ Crohn’s disease
∝ ulcerative colitis
∝ infective colitis
∝ ischaemic colitis.
✧ Neoplasia:
∝ benign polyps
∝ adenocarcinoma.
✧ Coagulopathy.
✧ Benign anorectal disease:
∝ haemorrhoids
∝ anal fissure
∝ fistula-in-ano
∝ rectal prolapse
∝ rectal varices
∝ solitary rectal ulcer.
✧ Arteriovenous malformation.
✧ Radiation proctitis/enteritis.
✧ Profuse upper gastrointestinal bleeding/small bowel bleeding including gastroduo-
denal ulceration, jejunoileal diverticula and Meckel’s diverticulum.
History
Take a general colorectal history and anorectal history. Determine the type of bleeding,
the timing and the amount. Determine whether the blood is separate from the stool or
mixed in. Is the blood bright red or dark? Is there pain associated with the passage of
blood?
✧ Haemorrhoids are associated with bright red rectal bleeding separate from the stool
or coating it, on the paper or dripping into the toilet. Bleeding is usually painless and
may be associated with prolapsing haemorrhoids.
✧ Anal fissure is associated with a smear of bright red blood on the paper and pain on
defaecation.
✧ Rectal prolapse is associated with a serosanguinous discharge and the prolapse.
✧ Inflammatory bowel disease is usually associated with blood mixed in with stool,
which may be loose or diarrhoea. It is associated with frequent, loose, bloody stools
and the presence of mucopus in more severe cases. Systemic disturbance, abdominal
pain, malaise and weight loss may also be features.
✧ Tumours vary in their presentation, depending on the site of the tumour and the rate
of bleeding. Tumours near the anus tend to present with bright red bleeding similar
to haemorrhoids. More proximal tumours may present with dark red bleeding, while
caecal tumours may be insidious and only present with iron-deficiency anaemia.
✧ Diverticular disease or angiodysplasia may present with a history or episodes of brisk
198 GENERAL SURGERY OUTPATIENT DECISIONS

rectal bleeding of large amounts or with the passage of a large dark red stool. This
bleeding usually stops and stools return to normal before the next episode.
✧ Ischaemic colitis is associated with left-sided abdominal pain and blood-stained
diarrhoea in elderly patients with evidence of atherosclerosis or previous aortic
aneurysm repair.
✧ Radiation proctitis patients have a history of radiotherapy, possibly following
resection of a rectal carcinoma.
Examination
Perform a general colorectal and anorectal examination. Examine for the presence of
anaemia and all causes outlined above.
Investigations
Investigations are FBC to detect anaemia; inflammatory markers including erythrocyte
sedimentation rate (ESR) and CRP; and stool cultures in the case of bloody diarrhoea.
Perform proctoscopy and rigid sigmoidoscopy in all patients. If indicated to
exclude carcinoma or other underlying pathology, proceed to colonoscopy or flexible
sigmoidoscopy and barium enema to look for more proximal colonic lesions.
Selective mesenteric angiography may be useful in identifying abnormal blood vessels
associated with angiodysplasia, but is more useful in identifying actively bleeding lesions
in the acute situation where rates of bleeding of 0.5–1.0 ml per minute can be detected.
Bleeding as slow as 0.1 ml per minute can be detected by using radio-labelled red-cell
scans.
Treatment
In young patients with haemorrhoids and no other suspicious features in the history it
may be justified to treat the minor anorectal condition and review at 4–6 weeks to assess
whether the bleeding stops. If the symptoms are persistent, or there are any features in
the history that might suggest a malignancy is possible, direct visualisation of the colon
should be performed early. Treat underlying causes as appropriate.
Follow-up
Following exclusion of serious underlying pathology, patients can be followed at six-
weekly intervals until the cause of the bleeding has been successfully treated.
Diarrhoea
Diarrhoea can be defined as the passage of more than three loose stools a day or of a
stool mass greater than 200 g/day. Diarrhoea can be classified as acute or chronic and the
causes fall into several groups.
Acute diarrhoea is classified into the following groups.
✧ Infective or toxin diarrhoea:
∝ viral: adenovirus, Norwalk, rotavirus
∝ bacterial: Campylobacter, Escherischia coli, Shigella
∝ toxins: Clostridium difficile, Staphylococcus spp.
∝ parasites: Entamoeba, Giardia.
✧ Drugs: angiotensin-converting enzyme (ACE) inhibitors, antibiotics, digoxin,
fluoxetine, lithium, metformin, non-steroidal anti-inflammatory drugs (NSAIDs),
proton-pump inhibitors (PPI), ranitidine, statins, 5-aminosalicylates (5-ASA),
alcohol, cocaine.
✧ Ischaemic colitis.
✧ Inflammatory bowel disease.
 COLON, RECTUM AND ANUS 199

Chronic diarrhoea is classified as follows.

✧ Infection: Giardia, Campylobacter, Salmonella.
✧ Drugs (see above).
✧ Malabsorption: lactose intolerance, chronic pancreatitis, bacterial overgrowth, short
gut, coeliac disease.
✧ Inflammatory bowel disease: Crohn’s disease, ulcerative colitis.
✧ Metabolic disease: diabetes mellitus, hyperthyroidism.
✧ Neoplasia: bowel cancer, pancreatic cancer, carcinoid, VIPoma, medullary thyroid
cancer, Zollinger-Ellison syndrome.
✧ Functional.
✧ Irritable bowel syndrome.
✧ Faecal impaction.
✧ Anal sphincter damage.
✧ Purgative abuse.

History
Take a general colorectal history. Ask about stool frequency and consistency. Ask about the
duration of symptoms and associated blood or mucus. Differentiate from incontinence
and the passage of frequent small hard stool with irritable bowel syndrome. How has the
bowel habit changed, and over what period?
A short history may suggest an infective cause, but may also be the first presentation
of inflammatory bowel conditions such as Crohn’s. Evidence should be sought regarding
travel abroad, food poisoning and diarrhoea among other family members or close
acquaintances.
Food poisoning
Food poisoning is usually obvious from the history. Onset within 12 hours suggests a
toxin cause, e.g. Staphylococcus aureus toxin or Bacillus cereus. Vibrio parahaemolyticus
is responsible for most seafood poisoning and may be associated with vomiting and
severe abdominal pain. After this time, and up to three days, Salmonella enteritis is the
commonest cause.
Viral gastroenteritis
This is one of the commonest infections of the small bowel and causes vomiting,
abdominal pain and diarrhoea. Characteristically the diarrhoea is profuse and watery.
Bloody diarrhoea
Bloody diarrhoea usually indicates large bowel infection, e.g. Shigella or Entamoeba
histolytica.
Crohn’s or ulcerative colitis (UC)
These conditions may be suggested by a positive family history, or symptoms of longer
than 1–2 weeks’ duration or frequent bouts of diarrhoea over time. Ask about other
symptoms associated with these conditions: skin rashes, arthritis, iritis.
Previous surgery
Surgery on the stomach or small bowel such as partial gastrectomy or small bowel resec-
tion predisposes to conditions associated with diarrhoea such as dumping or short gut
syndrome.
Malabsorption
This is suggested by chronic diarrhoea not associated with fever or blood in the stools,
200 GENERAL SURGERY OUTPATIENT DECISIONS

but with weight loss and signs of nutritional deficiencies. Stools are often described as
pale and offensive, and oily droplets within the stool may have been noticed. Could the
patient have exocrine pancreatic failure?
Ask about change of bowel habit and alternating constipation and diarrhoea, which
suggests a possible colonic cancer. A long-standing history of alternating constipation and
diarrhoea associated with left iliac fossa pain in older patients is suggestive of diverticular
disease.
Ask about symptoms of hyperthyroidism. Ask about diabetes mellitus – autonomic
neuropathy can be associated with diarrhoea.
Tuberculosis is a rarer cause of diarrhoea and may be associated with ethnicity or travel
to or from areas where TB is common. Lymphoma may be suggested by a chronic history
of weight loss and night sweats.
A drug history is important. In particular ask about antibiotic therapy and other drugs
associated with diarrhoea.
Rare causes such as carcinoid tumours may be associated with other symptoms such
as severe flushing and recent-onset asthma. Zollinger-Ellison usually presents with severe
peptic ulceration resistant to treatment.
Examination
Perform a general colorectal examination. Assess hydration and examine for pyrexia.
Perform a rectal examination and proctoscopy/sigmoidoscopy to identify inflammatory
mucosa or other lesions, and obtain a stool sample for microbiology. Perform a rectal
biopsy for a diagnosis of inflammatory mucosa.
Investigations
Exclude infection and inflammatory bowel disease.
Food poisoning can be confirmed by sending stool and food samples for
microbiology.
If parasites are suspected, the stool sample should be transported to the laboratory
immediately for inspection – ask for ova, cysts and parasites.
Perform a rectal biopsy for histology to differentiate inflammatory bowel disease from
infective causes of bloody diarrhoea (Shigella, Entamoeba histolytica) and to differentiate
between Crohn’s and ulcerative colitis.
Use abdominal X-ray (AXR) to exclude dilated colon, e.g. toxic megacolon in severe
ulcerative colitis.
Colonoscopy/barium enema is used to exclude carcinoma if indicated. Care should
be taken in the colonoscopy of acute colitics due to the risk of perforation, but in those
over the age of 45 with chronic diarrhoea, imaging of the entire colon is mandatory to
exclude malignancy.
If malabsorption is suspected, perform a faecal fat estimation and if confirmed
investigate further to identify the underlying cause.
Routine blood tests include Salmonella titres and amoebic serology if suspected; blood
cultures if pyrexial; FBC; ESR/CRP; thyroid function tests; blood sugar; antiendomysial
or anti-tissue transglutaminase antibodies (for coeliac disease); serum albumin; iron
studies; folate and B12 levels.
Treatment
Food poisoning and infective diarrhoea can be managed with isolation, fluid resusci-
tation and other supportive measures until the episode subsides. Antibiotics are
prescribed where indicated for severe infection with Shigella or Campylobacter. Travellers’
diarrhoea is most commonly caused by E. coli and can be treated with trimethoprim or
ciprofloxacin.
 COLON, RECTUM AND ANUS 201

The management of Crohn’s and ulcerative colitis, irritable bowel syndrome, colorectal
carcinoma, diverticular disease, malabsorption, hyperthyroidism, carcinoid syndrome
and Zollinger Ellison syndrome will be described under the relevant sections.
Follow-up
Follow up at short intervals until the cause is identified and serious causes are excluded.
There may be an indication for in-patient management in severe cases to avoid dehydration
and facilitate prompt investigation.
Constipation
There is a wide range of normal bowel frequency, from two to three times a day to once a
week. However, defaecation less than twice a week or straining at stool for more than 25%
of bowel movements merits consideration, as do a sensation of incomplete defaecation
and excessive time spent attempting to open the bowels. Symptoms are said to have a
prevalence of 2–28%. Most cases (50–60%) are simple/functional constipation with
normal transit times and need no investigation as they respond to dietary manipulation
and laxatives. In 10–15% there is slow transit constipation, which often requires long-
term laxative use.
Causes of chronic constipation include the following.
✧ Idiopathic slow transit constipation: the colon may be normal or have a variety of
physiological derangements.
✧ Colorectal disease: underlying bowel disorder, the most important of which is cancer.
Other conditions that can cause constipation are irritable bowel disease, diverticular
disease, Crohn’s ulcerative colitis, ischaemic colitis, hernias and volvulus.
✧ Anal pathology: anal fissure, anal stenosis, anterior mucosal prolapse, haemorrhoids,
descending perineum syndrome, perianal abscess, rectocoele, anal cancer.
✧ Neurological disease or injury:
∝ peripheral: Hirschsprung’s, autonomic neuropathy, Chagas disease
∝ central: cerebrovascular accident, cerebral tumours, Parkinson’s disease, menin-
gocele, multiple sclerosis, paraplegia
∝ muscular: dermatomyositis, systemic sclerosis.
✧ Metabolic disease, e.g. diabetes mellitus, hypothyroidism, hypercalcaemia.
✧ Psychiatric illness, depression or debility.
✧ Gynaecological pathology: large fibroids, ovarian cysts.
✧ Drugs, e.g. codeine preparations, morphine, antidepressants, iron, anticholinergics.

History
Take a general colorectal history. Determine what the patient means by constipation.
Determine the time-course of the symptoms – sudden onset, especially in patients over
50, is more indicative of a serious underlying cause, as are other alarm symptoms includ-
ing rectal bleeding and weight loss. Ask about the frequency of stool, the amount and the
consistency. The passage of small amounts of hard faeces suggests constipation. Pain on
passing faeces suggests anal pathology.
Ask about change in bowel habit – is this a recent problem or has it been going on
for years? Ask about abdominal pain and bloating or alternating bouts of diarrhoea. Ask
about medications. Ask about lifestyle – some work conditions or poor toilet facilities
may lead to prolonged avoidance of defaecation, which predisposes to constipation.
Ask about obstetric and gynaecological history to identify possible birth injury from
instrumentation or gynaecological pathology associated with constipation, e.g. ovarian
cysts. Ask about the other causes of constipation.
202 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
Perform a general examination. Examine for anaemia, jaundice, hypothyroidism and
weight loss. Perform an abdominal examination: palpable masses may be faecal, diverticu-
lar, neoplastic or gynaecological in origin. Perform a rectal examination and remember to
examine for conditions such as faecal impaction, perianal scars, fissures, haemorrhoids,
prolapse or neoplasm. Assess perianal descent (the extent to which the anus descends on
bearing down – normally 1–3.5cm). Excessive descent (greater than 3.5cm or below the
plane of the ischial tuberosities) suggests perineal laxity and can lead to a sensation of
incomplete evacuation and/or mucosal prolapse.
Investigations
Proctoscopy, sigmoidoscopy and AXR (dilated colon and faecal masses) should be
performed on everybody. Patients with loss of haustral pattern or megacolon/rectum on
X-ray are unlikely to respond to simple laxatives and further investigation is indicated.
Gross structural abnormalities and colonic strictures can be excluded using a double
contrast barium enema. Colonoscopy should be reserved for those in whom colorectal
cancer or inflammatory bowel disease need exclusion (alarm symptoms are sudden onset
after 50 years of age or a significant family history of colorectal neoplasia or inflammatory
bowel disease).
Urea and electrolytes including calcium, blood sugar and if indicated thyroid function
tests, parathormone and serum porphyrins for metabolic and endocrine causes are
performed.
Colonic transit time studies are useful for those with normal diameter colons and
persistent symptoms.
Anorectal physiology and electromyography of puborectalis and external anal sphincter
are useful for suspected abnormalities of the defaecation mechanism.
Full thickness rectal biopsy under general anaesthetic is used to exclude adult
Hirschsprung’s disease (absent anorectal reflex on anal physiology). Samples are sent
fresh for immediate acetylcholine analysis.
Treatment
Older patients or patients who present with sudden-onset constipation need urgent
investigations including barium enema/colonoscopy to exclude underlying cancer or
other serious pathology. In younger patients with no other suspicious clinical features or
older patients in whom serious underlying pathology has been excluded, more time is
available for assessment and trial of therapies. Education regarding diet and exercise and
what constitutes a normal bowel habit should be given.
If the problem is simply straining at hard stool without abdominal or anal pain,
simple advice regarding fibre in the diet removes the need for further assessment unless
the condition fails to respond. Increase the amount of fibre in the diet – give a dietitian
referral or high-fibre diet sheet. Prescribe ispaghula husk. Lactulose softens a hard stool.
Senna increases bowel contractility to expel the stool (care is needed in long-term use).
Glycerin suppositories and arachis oil enemas are useful to soften hard stool impacted
in the rectum. Phosphate enemas can be useful to clear more stubborn stool extending
into the sigmoid colon.
In those with established defaecatory disorders, biofeedback may be useful, but when
there is established intractable constipation, an initial purge with potent osmotic laxatives
may be required, followed by regular high doses of more gentle osmotic laxatives with or
without stimulant laxatives. However, care should be exercised, especially in the elderly,
who may require in-patient treatment and an intravenous drip.
Laxatives are unlikely to be effective if the haustral pattern of the colon has been
lost or there is megacolon or megarectum. In these patients anorectal manometry is
 COLON, RECTUM AND ANUS 203

useful to identify underlying disorders such as Hirschsprung’s. Patients who have an

absent rectosphincteric reflex and evidence of megacolon/rectum should undergo a full
thickness rectal biopsy to exclude Hirschsprung’s.
Patients with severe idiopathic constipation should undergo colonic transit studies
and anorectal physiology studies, as there are a number of abnormalities of defaecation
that can be diagnosed, such as an increased anorectal angle caused by abnormal con-
traction of the puborectalis muscle at defaecation; failure of the pelvic floor to relax on
attempted defaecation – the outlet syndrome; abnormal perineal descent; and pudendal
nerve neuropathy.
Surgery
Hirschsprung’s short segment disease can be treated with an anorectal myectomy, rectal
myectomy or anal sphincterotomy. Distal disease can be treated by a ‘pull-through’
operation.
Anorectal myectomy may be effective in the ‘outlet syndrome’ (contraindicated if
marker studies indicate severe colonic inertia).
Surgery is rarely used in severe idiopathic constipation except in the most serious
and persistent cases, e.g. ileostomy, irrigating caecostomy, percutaneous endoscopic
colostomy (PEC) with anterograde irrigation.
In those with refractory slow transit constipation and no defaecatory disorder,
colectomy and ileorectal anastomosis is occasionally indicated, but only after more than
one expert opinion has been obtained.
Follow-up
After the exclusion of serious underlying pathology, most patients can be discharged to
the care of the GP, following simple advice on diet and laxatives. In those with refrac-
tory constipation, further follow-up should be guided according to the results of special
investigations.
Post-operative follow-up
Review with histology to confirm the diagnosis and determine the success of the operation.
Detect any complications of general anaesthesia and of the specific procedure. For ‘pull-
through’ operations, check the histology to confirm that normally innervated bowel had
been reached. Residual Hirschsprung’s can be a cause of residual constipation.
Chronic megacolon
Chronic megacolon is an abnormally dilated colon or rectum with loss of haustral
pattern. It may affect the total colon or segments. Causes are congenital (Hirschsprung’s)
or acquired.
Acquired causes include the following.
✧ Obstruction: chronic anal stenosis, strictures (ischaemic), annular neoplasms.
✧ Chagas disease.
✧ Hypothyroidism.
✧ Neurological disorders: spina bifida, cauda equina, paraplegia, Parkinson’s.
✧ Psychological disturbances.
✧ Idiopathic: no underlying cause. Adynamic bowel syndrome may affect the colon
only, with normal rectum, or it may present as megarectum with variable colon in
continuity. Rectal capacity and sensation are diminished but sphincteric responses
and rectal biopsy are normal.
History
Take a general colorectal history. Patients may present with similar symptoms to chronic
204 GENERAL SURGERY OUTPATIENT DECISIONS

constipation or faecal incontinence due to overflow secondary to faecal impaction. Those

with idiopathic megacolon may describe abdominal pain and distension in the context
of chronic constipation.
Examination
Perform a general colorectal examination, looking for the same abdominal and perianal
conditions as are associated with chronic constipation.
Investigations
Investigate with proctoscopy, sigmoidoscopy and AXR. X-ray reveals abnormally dilated
large bowel and loss of haustral pattern. Give colonoscopy/barium enema to exclude
underlying organic disease in older patients and other age groups where indicated.
Perform anal physiology studies. Exclude Hirschsprung’s with full thickness rectal biopsy
in selected patients.
Treatment
Treat underlying conditions. Otherwise treat medically with colonic washouts, disimpac-
tion of faeces and, in severely symptomatic patients, surgical treatment bowel resection.
Generally the longer the history, the worse the outcome, but procedures including
colectomy with ileorectal anastomosis and restorative proctocolectomy have good
reported outcomes, with permanent stomas affording a generally good quality of life in
those in whom initial surgery has failed.
Follow-up
Following the initial consultation, serious underlying causes, suggested by the history and
clinical examination, should be excluded. Chronic and idiopathic causes can be reviewed
at 3–4 monthly intervals to assess the efficacy of conservative treatments. Discharge with
advice to the GP on future management and discharge once organic causes have been
excluded and the condition stabilised, or offer surgery in an appropriately counselled
patient when all other avenues of treatment have failed.
Rectal inertia
Mainly seen in children where the rectum is over-stretched by repeatedly inadequate
evacuation.
History
There is chronic constipation in apparently healthy individuals, with mild abdominal dis-
tension and occasional perianal soiling. Older children and adults may have psychological
problems. Differentiation from Hirschsprung’s may be difficult, but Hirschsprung’s
normally presents with problems from birth, while rectal inertia presents only after toilet
training.
Examination
Abdomen is flat but faecal masses are palpable in left colon. Make rectal examination
to exclude underlying physical problems like anal fissure or anal stenosis. There may be
evidence of soiling, poor anal tone and hard faecal masses.
Investigations
In cases that do not respond to medical treatment examine under anaesthetic and take
full thickness rectal biopsy.
 COLON, RECTUM AND ANUS 205

Treatment
Empty the bowel by saline rectal washouts (in-patient if necessary for 2–3 weeks).
If indicated perform manual evacuation, then recommence toilet training at regular
intervals. For adults, continue the use of phosphate enemas or suppositories. Do not
stimulate the proximal colon with laxatives as it may aggravate the condition.
Follow-up
There is usually a chronic history so there is no urgency for investigation unless the history
and examination suggest suspicious features. Investigations and trials of treatment can
be performed at 1–3 monthly intervals until symptoms are controlled. Discharge once
stable on medication.
Diverticular disease
Colonic diverticula are false, pulsion diverticula consisting of mucosa and serosa, which
form at areas of structural weakness of the colonic wall where the vasa rectae penetrate the
muscularis propria to supply the mucosa. The condition is thought to be a consequence
of the Western diet, with a relative lack of vegetable fibre, although structural changes in
the colonic wall associated with aging and disordered motility (hyperelastosis and altered
collagen structure) are thought to contribute.
Diverticulosis describes the presence of diverticula, and is very common, affecting more
than 60% of those over 70 years. Around 90% of people are said to be asymptomatic,
perhaps explaining how relatively infrequently people are admitted with symptomatic
diverticula (diverticular disease), given the high prevalence.
The term ‘diverticulitis’ implies infection and inflammation in association with
diverticula. Right-sided diverticula are common in the Orient, while in the West left-
sided diverticulosis is more typical. The condition typically starts after age 30 and
peaks in 60s–70s, but younger patients do present acutely with complicated diverticular
disease. Severity ranges from episodes of mild discomfort to the onset of complications
which include perforation, abscess formation, intestinal obstruction, fistulation into
neighbouring organs and haemorrhage. Carcinoma of the colon can co-exist with
diverticular disease.
History
Take a general colorectal history. Symptoms may be episodic and recurrent and include
mild to severe left iliac fossa (LIF) or lower abdominal pain, dull and constant, lasting
hours to days and precipitated by diet or stress. There are sheep-dropping faeces, with
occasional mucus and diarrhoea.
The following symptoms may suggest the onset of complications.
✧ Perforation: severe constant pain in the lower abdomen and feeling systemically
unwell.
✧ Intestinal obstruction: history of increasing constipation and abdominal distension
associated with colicky abdominal pain. Diverticular strictures are related to scarring
following previous episodes of diverticulitis, and distinction from malignant stric-
tures can often only be finally made after histological examination of the resected
specimen.
✧ Fistulation can occur into the colon, small intestine, uterus, vagina, abdominal wall
and bladder. Fistulae form when an inflamed diverticulum adheres to an adjacent
organ and a pericolic abscess ruptures into it. May present with symptoms of chronic
ill-health, low abdominal tenderness, intermittent diarrhoea, pneumaturia and faecal
vaginal discharge.
∝ Colovesical: urgency and dysuria (recurrent urinary tract infections (UTI)),
pneumaturia and faecaluria.
206 GENERAL SURGERY OUTPATIENT DECISIONS

∝ Colovaginal: air and faeces per vagina, much more common following a previous
hysterectomy.
✧ Haemorrhage: there may be a history of episodes or brisk bright-red bleeding per-
rectum.
✧ Caecal or right-sided diverticula is found in one-third of diverticular patients: shows
appendicitis-type symptoms.
Examination
Perform a general examination. In acute attacks there may be low-grade fever, tenderness
and rigidity and occasionally a mass in the lower abdomen. Localised perforation
and abscess formation may be suspected if examination reveals a localised mass,
while free perforation into the abdominal cavity generally presents as an emergency
with generalised peritonitis. Vaginal examination may reveal a foul, brown discharge.
Abdominal distension and active bowel sounds may suggest intestinal obstruction. Rectal
examination may reveal blood or pus.
Investigations
Flexible sigmoidoscopy shows the multiple openings of the diverticula, and in acute
attacks may reveal an inflamed mucosa and oedema. Barium enema is not advisable in
the acute phase, due to the risk of perforation, but is useful for investigation of chronic
symptoms. Barium shows the typical out-pouchings and long constricted segments
of bowel. Perform flexible sigmoidoscopy to exclude carcinoma within segments of
diverticulosis. Take a mid-stream urine specimen for microscopy and culture to detect
subclinical fistulation.
CT is useful for assessment of adjoining organs for fistula and involvement of tissue
planes, and the presence of an inflammatory phlegmon or abscess.
✧ Perforation: the presence of a localised mass or abscess can be confirmed on USS, but
CT is increasingly used in the acute setting as it provides more information.
✧ Intestinal obstruction is usually diagnosed by plain AXR. Gastrograffin enema can
confirm the diagnosis and identify the level of obstruction.
✧ Fistula: barium enema can define the tract, but such connections are commonly not
seen even when they exist. Cystography and cystoscopy can be used to confirm and
define colovesical fistulas and exclude primary bladder neoplasms.
✧ Haemorrhage: differentiate from vascular ectatic lesions. Use sigmoidoscopy to
exclude bleeding from piles and use arteriography to exclude vascular ectatic lesions
and potentially arrest bleeding in the case of massive diverticular bleeds.
Treatment
Diverticular pain
Colonic spasm rather than inflammation is relieved by faecal bulk-forming agents –
Isogel, Fybogel, antispasmodics. Colonic resection only for severe cases requiring repeated
admissions, or those with complicated disease (local or free perforation, stricture,
fistulation). Elective resections are increasingly being performed laparoscopically.
Uncomplicated disease
Acute attack settles over 4–5 days and only 30% have recurrent symptoms. However,
5–10% become severe and need sigmoid colectomy.
Diverticular abscess
CT-guided percutaneous drainage and intravenous antibiotics should be the first-line
treatment in those with localised signs and a confirmed abscess, with emergency surgery
reserved for those with generalised peritonitis.
 COLON, RECTUM AND ANUS 207

Complicated disease and peritonitis

Treat with Hartmann’s procedure (resection and end colostomy) or colonic lavage,
primary anastomosis and defunctioning ileostomy, depending on the extent of peritoneal
contamination. If soiling is minimal then consideration can be given to omission of the
defunctioning stoma.
Fistulation
Treat with elective sigmoid resection with primary anastomosis and repair of fistulous
opening in the affected organ. In the case of colovesical fistula, no attempt is made to
close the bladder but the urethral catheter is left for 10 days and many surgeons request
a cystogram to ensure closure of the defect prior to catheter removal. However, in the
elderly patient, or one unfit for surgery, a trial of conservative therapy with prolonged
antibiotics may be justified.
Follow-up
Initial investigation should be tailored to exclude serious underlying pathology, and
colonoscopy should be performed if concerning symptoms are present in patients over
the age of 50 or who have a strong family history of colorectal cancer or inflammatory
bowel disease.
In most patients the diagnosis can be confirmed by barium enema, and patients are
seen once following this investigation to give simple dietary advice.
For those with complications, or two episodes of significant diverticulitis, surgical
resection should be considered on an elective basis to prevent future emergency admissions
and to reduce the likelihood of a Hartmann’s procedure being required.
Post-operative follow-up
Review with the histology to exclude co-existent carcinoma. Examine for complications
of laparotomy and general anaesthetic. If a Hartmann’s was performed, determine the
timetable for reversal or whether reversal is to be performed. Symptoms continue in
25% of patients after surgery and are thought to be caused by the underlying disordered
bowel motility.
Polyps in the colon and rectum
A polyp is an abnormal overgrowth of the colonic mucosa and can be sessile (flat) or
pedunculated (on a stalk). Polyps fall into the following categories.
✧ Inflammatory: occur in UC, Crohn’s, diverticulitis, chronic dysentery and, rarely,
benign lymphoid hyperplasia.
✧ Hamartomatous polyps: juvenile and Peutz-Jeghers (P-J) have significant malignant
potential.
✧ Metaplastic polyps: size 1–2mm, rarely larger than 5mm; biopsy confirms the
diagnosis and they need no ongoing observation.
✧ Adenomatous polyps: benign tumours composed of abnormal colonic glands.
Classified according to the growth pattern of the glands: 75% are tubular adenomas,
10% villous and 15% tubulovillous adenomas. All have malignant potential.
Relationship of polyps to cancer
There is a strong relationship. Approximately 40% of patients treated for a polyp develop
further polyps. Only 3% of adenomatous polyps are malignant, but a third of villous
papillomas are malignant. The risk of malignancy increases with size, from 1% for polyps
less than 5mm to 40% for polyps larger than 2cm and 60% for those greater than 3cm.
208 GENERAL SURGERY OUTPATIENT DECISIONS

Familial polyposis – hereditary

Familial adenomatous polyposis (FAP)
FAP is characterised by hundreds of adenomatous colorectal polyps by the second or
third decade of life. It is an autosomal dominant mutation of the APC gene at position
21 on chromosome 5q.
Screening should begin in the early teens for patients from affected families, whose
information is collected in polyposis registries. To prevent the almost inevitable
development of colorectal cancer, resection (restorative proctocolectomy or colectomy
and ileorectal anastomosis, which necessitates ongoing rectal surveillance) should be
performed as soon as practically possible following diagnosis.

Hereditary non-polyposis colorectal cancer (HNPCC)

HNPCC is responsible for 2% of colorectal cancer. It is characterised by early diagnosis
of colorectal cancer (approximate age 45, compared with 65 for the general population).
HNPCC is diagnosed according to the Amsterdam Criteria II, as follows.
✧ At least three relatives should have an HNPCC-associated cancer (colorectal,
endometrial, small bowel, ureter, renal pelvis), of whom one should be a first-degree
relative of the other two.
✧ At least two successive generations should be affected.
✧ At least one colorectal cancer should be diagnosed before the age of 50.
✧ FAP should be excluded.
✧ Tumours should be verified pathologically.

History
Take a general colorectal history and a careful family history. Polyps are usually asympto-
matic and may present as anaemia due to occult bleeding. Retrograde propulsion of large
pedunculated polyps may produce abdominal pain, spasm and colic and cause colocolic
intussusception. Rectal lesions can cause tenesmus or change in bowel habit to diarrhoea.
Mucous discharge may occur, especially with villous papilloma, which may lead to
dehydration and electrolyte imbalance. Large papillomas may produce hypokalaemia,
metabolic acidosis leading to symptoms of lethargy, muscle weakness, mental confusion
and renal failure.

Examination
Perform a general examination. Examination may range from normal to signs of
dehydration, anaemia, mental confusion and muscle weakness.

Investigations
FBC may reveal anaemia. Urea and electrolytes (U&E) may indicate dehydration or
hypokalaemia. Rigid sigmoidoscopy may reveal the presence of rectal adenomas, which
should prompt colonoscopy examination and polypectomy.

Treatment
Treatment of colorectal polyps and villous papillomas is by regular colonoscopy with
intervals as specified by British Society of Gastroenterology guidelines. CT colonography
or barium enema are alternatives for patients in whom colonoscopy is technically
challenging.

Malignant polyps
Following colonoscopic excision of a malignant polyp, a decision must be made as
to whether radical resection of the excision site is required. Considerations include
 COLON, RECTUM AND ANUS 209

the likelihood of the cancer being completely excised and the chance of lymph node
metastases being present.
Favourable characteristics include:
✧ complete endoscopic resection with a margin of normal tissue
✧ cancers confined to the head of a polyp
✧ well or moderately differentiated tumours
✧ absence of lymphovascular invasion.

If doubt exists in patients fit for major surgery then radical resection of the site is
indicated. This is technically easier if the site of the polyp is ‘tattooed’ with ink at the time
of polypectomy, to ensure that it is removed and examined histologically.
Follow-up
All patients are followed up by regular colonoscopy, according to British Society of
Gastroenterology guidelines.
Carcinoma of colon and rectum
The UK lifetime risk of colorectal cancer is around 5%, with nearly 35 000 new cases
diagnosed in 2002, and it is responsible for 19 000 deaths annually. Seventy per cent of
cases occur within reach of the 60cm flexible sigmoidoscope (i.e. distal to the splenic
flexure). Rectal cancers, by definition, occur within 15cm of the anal verge. Overall five-
year survival has improved from 22% to 50% over the last 10 years.
Predisposing conditions are genetic; dietary factors (increased animal fat and
proteins); colorectal polyps; familial polyposis coli; radiation proctocolitis; previous
ureterosigmoidostomy, ulcerative colitis (especially total colon involvement longer than
10 years – consider for prophylactic bowel excision); and schistosomiasis.
Staging of colorectal carcinoma
Dukes’ staging (modified by Astler and Coller) is shown in Table 9.1.
TABLE 9.1 Staging of colorectal carcinoma.

UICC/TNM DUKES’ STAGE

Stage 0 Carcinoma in situ

Stage I No nodal involvement, no distant metastasis A

Tumour invades submucosa (T1, N0, M0)

Tumour invades muscularis propria (T2, N0, M0)

Stage II No nodal involvement, no distant metastasis B

Tumour invades into subserosa (T3, N0, M0)

Tumour invades into other organs (T4, N0, M0)

Stage III Nodal involvement, no distant metastasis C

1 to 3 regional lymph nodes involved (any T, N1, M0)

4 or more regional lymph nodes involved (Any T, N2, M0)

Stage IV Distant metastasis (any T, any N, M1) D

210 GENERAL SURGERY OUTPATIENT DECISIONS

Note: in the commonly used Astler-Coller modification of the Dukes’ stage, C1 implies
any lymph-node involvement, while if the apical lymph node removed (closest to the tie
on the arterial pedicle) is involved it is classified as C2.
Modes of spread
Intramural spread may be transverse, lateral and radial. Most consider a longitudinal
clearance of 2cm to be adequate. In rectal cancer, where ‘total mesorectal excision’ is
the recommended method of excision, a circumferential resection margin (distance
from the tumour to the nearest radial cut edge) of greater than 1mm is considered to be
uninvolved.
Extension to adjacent structures
This applies more to the rectum than the colon.
✧ Anterior spread is to seminal vesicles and prostate in the male and to the posterior
vaginal wall in the female.
✧ Lymphatic spread: rectal cancer occurs in 50% of pararectal nodes, to lower colic
nodes, to inferior mesenteric nodes. Lateral lymph node spread is more common to
the hypogastric lymph nodes (internal iliac nodes).
✧ Haematogenous spread is to the liver in 18–20% at presentation, the lung in 5%.
✧ Perineal spread, transperitoneal spread.

History
Take a general colorectal history. The onset is often insidious, but after that the develop-
ment of symptoms depends on the site of the tumour. Enquire regarding predisposing
conditions, e.g. ulcerative colitis, Crohn’s, previous gastric surgery (which doubles the
risk of colorectal cancer).
In addition to the polyposis syndromes, a positive family history is an important risk
factor for the development of colorectal cancer. In one study with a baseline population
risk of 1/50, the risk rose to 1/17 for any positive family history, 1/10 if one relative was
affected below the age of 45 and 1/6 if two or more relatives were affected.
Caecal, ascending colon and hepatic flexure
Symptoms are insidious for a long time, with vague upper abdominal pain and flatulent
distension, pallor, lassitude and general ill-health. Alteration in bowel habit is less
frequent. Occasionally there is diarrhoea.
Transverse and descending colon
There is increasing constipation alternating with diarrhoea. Occasionally there is blood
and mucus. May also present with fistulation, e.g. gastrocolic – vomiting faeces.
Sigmoid and rectal
Rectal bleeding is the most frequent presentation. It is usually slight, with alteration in
bowel habit and spurious morning diarrhoea. The patient wakes and passes mucus in the
presence of constipation and tenesmus. Severe pain may indicate extension into surround-
ing tissues and a poor prognosis. May also present with fistulation, e.g. colovesical.
Guidelines
Specific guidelines which identify those patients considered to be at high risk of colorectal
cancer (and therefore warranting urgent referral and investigation) were published by the
National Institute for Health and Clinical Excellence (NICE) in 2005. High-risk groups
were identified as the following.
✧ Patients aged 40 and above with rectal bleeding and a change in bowel habit to looser
stools and/or increased stool frequency persisting for six weeks or more.
 COLON, RECTUM AND ANUS 211

✧ Patients aged 60 and above with rectal bleeding persisting for six weeks or more
without a change in bowel habit but in the absence of anal symptoms.
✧ Patients aged 60 and above with a change in bowel habit to looser and/or more
frequent stools persisting for six weeks or more in the absence of rectal bleeding.
✧ Patients with a right iliac fossa mass consistent with colonic involvement, irrespective
of age.
✧ Patients with a palpable intraluminal (not pelvic) rectal mass.
✧ Men of any age with unexplained iron deficiency anaemia (haemoglobin <11 g/100 ml)
irrespective of age.
✧ Non-menstruating women with unexplained iron deficiency anaemia (haemoglobin
<10 g/100 ml)
Examination
Perform a general colorectal examination. Examine for the presence of jaundice, anaemia
and weight loss. Perform an abdominal examination: examine for a palpable mass,
e.g. in RIF due to caecal lesion; or enlarged liver indicating metastases. Perform rectal
examination: 75% of all rectal tumours and approximately a third of bowel tumours can
be palpated. Determine the location, mobility and extent of spread around bowel and
into surrounding tissues.
Investigations
Do FBC, U&E, LFTs, CXR and ECG. Determine pre-operative CEA level. Perform
Proctososcopy: determine size, site, extent and distance from anal verge. Flexible sig-
moidoscopy needs bowel preparation with a phosphate enema. All patients suspected of
possible carcinoma of the colon should undergo rigid sigmoidoscopy and barium enema
or colonoscopy. Suspicious lesions detected on barium should undergo colonoscopy and
biopsy. CT scans of the chest and abdomen are used to stage the disease (looking for liver
and lung metastases) and to look for local complications such as duodenal or ureteric
involvement. Alternatives include the use of liver ultrasound and CXR, but these are
considered less sensitive.
Barium enema
Double contrast is more reliable but still has a false negative rate of more than 2%.
Features of malignancy are mucosal destruction, abrupt cut-off of barium and localised
lesion with sharp demarcation from the involved areas (‘apple-core lesions’).
Colonoscopy
This is generally considered the first-line investigation if there is a high suspicion of
cancer, or if barium enema is equivocal. Full examination of colon should be made to
demonstrate additional pathology, e.g. synchronous carcinoma (present in 2–5% of
cases), diverticula disease. If it cannot be performed pre-operatively due to a stenosing
primary lesion, arrange for full examination of the colon within three months after the
operation to remove the primary lesion.
Endoluminal ultrasound
This is useful in rectal tumours for defining the involvement of the rectal wall and extent
of extra-rectal involvement and adjacent lymph nodes.
MRI
This is increasingly used to locally stage rectal cancers, to determine their relation-
ship to the mesorectal fascia and to select patients likely to benefit from pre-operative
radiotherapy.
212 GENERAL SURGERY OUTPATIENT DECISIONS

Treatment
All patients should be discussed at the multidisciplinary team (MDT) meeting (involving
surgeons, oncologists, radiologists and pathologists, amongst others) where potential
alternative management strategies can be discussed. Pre-operative radiotherapy may be
recommended in patients with large rectal tumours where the potential circumferential
resection margin is threatened. It is also considered when local excision of a small rectal
cancer is contemplated in poor-risk patients. Ongoing trials may suggest a survival benefit
for all rectal cancer patients undergoing curative surgery.
Bowel preparation
This varies widely according to local policy, but there is a current trend away from the use
of mechanical bowel preparation, with its attendant side effects and negative impact on
post-operative recovery, unless on-table colonoscopy is likely to be needed or there is a
high likelihood of forming a defunctioning stoma, in which case many consider a column
of faeces between the stoma and anastomosis to be undesirable. Right-sided colonic
lesions do not require preparation. Bowel preparation agents include Picolax, Fleet,
Klean-Prep and polyethylene glycol. All can cause electrolyte disturbances and dehydra-
tion, and patients should be given concurrent intravenous fluids to prevent profound
drops in blood pressure on the induction of anaesthesia. Do not use in obstructing lesions
– use on-table lavage instead.
Ward prophylaxis
Peri-operative antibiotics (commonly used but with little evidence except for a potential
reduction in wound infection rates), deep vein thrombosis (DVT) prophylaxis with TED
stockings and subcutaneous heparin.
Even in the presence of liver metastases the patient’s best interests may be served by
removal of the primary tumour.
Abdominoperineal resection
Used when the tumour is very close to the anal verge or invading the anal sphincters. End
colostomy in the left iliac fossa.
Anterior resection
Used when the tumour is situated more proximally in the rectum such that adequate distal
clearance can be attained with acceptable post-operative functional results. Sometimes
a covering colostomy/ileostomy is fashioned to mitigate against the consequences of
anastomotic leakage (stomas do not prevent leaks). Patients undergoing radical rectal
surgery should be warned of the possibility of sexual and urinary dysfunction following
surgery due to inadvertent damage to the pelvic nerves.
Locally advanced tumours
En bloc resection. Radical approach can give survival rate of 50% at five years depending
on the stage.
Small cancers of the rectum
These are mobile in the rectal mucosa. They especially occur in the elderly. Perform local
excision with a 0.5–1.0cm margin of healthy tissue. Transanal endoscopic microsurgery
(TEM) allows accurate local full thickness excision but even in T1 lesions, lymph node
metastases have been reported in up to 17% of patients with tumours invading the lower
one-third of the submucosa.
Palliative transanal resection (often with a urological resectoscope – TART) can be used
to palliate those with rectal cancers who are unfit for radical surgery.
Local radiotherapy is not widely accepted.
 COLON, RECTUM AND ANUS 213

Multiple colonic tumours

Synchronous tumours: incidence is 2–5%, and they often require total colectomy.
Hepatic metastases – suitability for liver resection
The aim of liver resection (resectability) is to remove all macroscopic disease with clear
margins, leaving sufficient functioning liver. Considerations include the following.
✧ Patients with solitary, multiple and bilobar disease who have had radical treatment of
the primary colorectal cancer are candidates for liver resection.
✧ The ability to achieve clear margins (R0 resection) should be determined by the
radiologist and surgeon in the regional hepatobiliary unit.
✧ The surgeon should define the acceptable residual functioning volume, approximately
one-third of the standard liver volume, or the equivalent of a minimum of two
segments.
✧ The liver surgeon and anaesthetist should make the clinical decision regarding fitness
for surgery.
✧ If deemed medically unfit for surgery, patients should be considered for ablative
therapy.
✧ Extrahepatic disease that should be considered for liver resection includes:
∝ resectable/ablatable pulmonary metastases
∝ resectable/ablatable isolated extrahepatic sites, e.g. spleen, adrenal or resectable
local recurrence
∝ local direct extension of liver metastases to, for example, diaphragm/adrenal, that
can be resected.
Follow-up
In suspected colorectal cancer, urgent endoscopic investigation should be performed
and patients should be seen at regular appropriate intervals to give the results of biopsies
and staging investigations and to agree a treatment plan. If surgery is indicated explain
all possible procedures to the patient, including the possibility of a colostomy/covering
ileostomy. Referral to the stoma service pre-operatively is helpful. There is a good case
for colonoscopy screening for those patients with familial colonic polyposis, family his-
tory of colonic malignancy, previous colorectal cancer and adenomas and inflammatory
bowel disease.
Inoperable and recurrent tumour
Provide regular review and discuss palliative chemotherapy with an oncologist. Consider
involving the palliative care team early, as they can offer advice on the amelioration of
symptoms as well as terminal care.
Monitor CEA and CA 19-9. If the levels of these markers rise it may indicate recurrence
(assuming a high pre-treatment level fell to normal following initial surgery). However,
a large number of recurrences are associated with no rise in their levels.
Post-operative follow-up
Review with the histology to determine adequate tumour resection; for grading and
stag ing of the tumour; and to discuss subsequent oncological follow-up, although
this is increasingly arranged during the MDT meeting. Examine for complications of
laparotomy and general anaesthetic.
Complications of anterior resection include anastomotic leak, usually detected in an
in-patient, but it may present later as a pelvic abscess/collection. Investigate by water-
soluble enema to detect leak and CT scan to define collection. If anastomosis has been
protected by a covering colostomy and the leak is small and the patient well, conservative
management can be pursued and resolution expected. Defunctioned patients should
214 GENERAL SURGERY OUTPATIENT DECISIONS

have a water-soluble contrast enema arranged six weeks following surgery to exclude
‘radiological’ leaks prior to arranging reversal of the covering stoma.
Patients in whom direct evaluation of the entire colon was not possible prior to surgery
(stenosing lesions, emergency surgery) should have a completion colonoscopy within
three months to exclude a synchronous tumour not detected at operation.
Opinion is divided as to the most appropriate follow-up strategy following colorectal
cancer resection. The benefits of intensive follow-up depend to a point on the fitness of
the patient to undergo subsequent hepatic or pulmonary resections should metastases
be diagnosed. In some studies the major benefit from following patients for five
years following surgery has been psychological support, with very few asymptomatic
recurrences being detected. To resolve this question the FACS Trial (Follow up After
Colorectal Surgery) is ongoing to assess the cost-effectiveness of intensive versus minimal
follow-up following resection of potentially curable colorectal cancer.
Most patients currently followed up in hospital undergo abdominal palpation to look
for hepatomegaly, rigid sigmoidoscopy to assess for anastomotic recurrence in the case of
low anastomoses, and regular ultrasound or CT scans according to local protocols.
Adjuvant therapy for colorectal carcinoma
Chemotherapy is generally considered for those with node positive disease (Dukes’ C).
five-year survival is 82% for Dukes’ A, 69% for Dukes’ B and 54% for Dukes’ C.
Irritable bowel syndrome (IBS)
Generally, IBS describes a syndrome of recurrent symptoms of abdominal pain, bloating
and/or altered bowel habit with no underlying organic disease. However, the lack of
organic disease does not diminish the distress the symptoms can cause. Psychological
factors and stress play an important role in the symptoms, although most patients have
no obvious psychological or personality disorder. In middle-aged and older patients,
a diagnosis of IBS should be made only after carcinoma or other organic disease has
been excluded by the appropriate investigations. In younger patients, cancer is less
likely but not unknown, and a difficult balance has to be obtained between unnecessary
investigation and missing the occasional tumour. The less-experienced surgeon should
probably err on the side of caution.
History
Take a general colorectal history. Classically, the IBS patient presents before the age of 35
and gives a history of recurrent abdominal pain that can occur at various sites around
the abdomen. They may complain of abdominal bloating and describe some relief on
passing flatus or faeces. Faeces are more frequent and smaller and may be loose or like
string or sheep droppings. There may be associated passage of mucus and a feeling of
incomplete evacuation. Typically the symptoms seem out of proportion to the patient’s
apparent well-being. Take a careful dietary history and note the intake of fibre. Take a
history of smoking, alcohol consumption, ongoing stress and psychological disturbances
past and present.
Ask about other psychological symptoms – anxiety, stress, depression drugs – and
about referral to hospital to investigate similar anxiety-related symptoms affecting other
body systems, e.g. difficulty swallowing. Coeliac disease is an important differential
diagnosis and should especially be considered in the presence of mild anaemia.
Examination
Perform a general colorectal examination. Look to exclude underlying pathology.
Determine the site of pain. Palpate for masses or palpable colon in the left iliac fossa,
which may indicate thickening or spasm. Make a rectal examination to exclude rectal or
anal pathology.
 COLON, RECTUM AND ANUS 215

Investigations
Investigate with proctoscopy, sigmoidoscopy and AXR. If insufflation of air at sigmoido-
scopy reproduces pain this is highly suggestive of irritable bowel syndrome. Further
investigation e.g. colonoscopy/barium enema, ultrasound scan, is only indicated if
underlying pathology is suspected, or in the presence of alarm features including onset
after age 50, bleeding and weight loss. In patients without such features investigation
should be kept to a minimum as they may simply increase the patients’ anxiety.
Treatment
Give an explanation of symptoms, empathy and reassurance. A high-fibre diet may
improve symptoms or make them worse, but is often tried initially. Sorbitol and caffeine
may exacerbate symptoms. Peppermint oil may be tried to reduce gut spasm, as may
anticholinergic drugs such as dicycloverine and hyoscine butylbromide, but there is no
convincing trial evidence to suggest that they are better than placebo. Tricyclic antidepres-
sants in low doses have been shown to be beneficial, possibly working via gut serotonin
receptors. Some patients have a good result from cognitive behavioural therapy but often
these are difficult patients to manage and they are victims of long-term management.
Follow-up
Once organic disease is excluded, further investigation should be kept to a minimum. After
this, time should be given for dietary manipulations or other treatments to work, but if
these fail patients may benefit from referral to physicians with a special interest in IBS.
Pneumatosis coli
These are gas-filled cysts found in the subserosal and submucosal planes. They are
thought to result from lymphatic stasis, and the dilated channels then fill with gas.
History
The patient is asymptomatic or presents with colicky abdominal pain. A fulminant form
exists, which may present with abdominal pain and bloody diarrhoea associated with
pneumoperitoneum.
Examination
Examination may be normal or there may be evidence of abdominal distension.
Investigations
They are often detected as an incidental finding on AXR and barium enema.
Treatment
No active treatment is necessary. Cysts can be induced to disappear by oxygen therapy
over 3–4 days. In fulminant disease the patient should be treated symptomatically, but
if they deteriorate to the point of laparotomy the outlook is bleak and surgery generally
involves excision of the affected segments and exteriorisation of both bowel ends.
Volvulus of the large bowel
Sigmoid volvulus
Predisposed by a long, redundant loop of sigmoid colon with a narrow base of attachment
of the sigmoid mesocolon. It is classically seen in those with a long history of constipation
and possibly laxative abuse, perhaps in long-term care due to neuropsychiatric disorders.
Patients may present with an anticlockwise torsion of 180 degrees, which reverts
spontaneously, leading to intermittent symptoms of abdominal pain, distension and
constipation. If rotation of 360 degrees or more occurs, reduction is required to prevent
216 GENERAL SURGERY OUTPATIENT DECISIONS

perforation secondary to closed-loop obstruction. The chronic form may cause symptoms
over many years.
History
Take a general colorectal history. In the chronic form patients may present to the out-
patient clinic with a history of recurrent episodes of colicky central abdominal pain
associated with distension and complete constipation. Motility disorders such as
Hirschsprung’s and Chagas diseases may predispose.
Examination
Perform a general examination. Examination may be normal between episodes, or during
episodes there may be abdominal distension, tinkling bowel sounds and an empty rectum
with blood on the glove.
Investigation
AXR shows a markedly distended loop of colon originating from the left iliac fossa and
extending into the right upper quadrant (‘coffee bean’). U&Es may reveal dehydration
and other electrolyte abnormalities. FBC may reveal anaemia. Between episodes, barium
enema may reveal a large redundant sigmoid loop, which suggests the diagnosis.
Treatment
Resuscitate if acute. Colonoscopic reduction is successful in 80%, but recurrence occurs
in 90% and therefore it should be considered a temporary measure prior to definitive
surgery.
Follow-up
Review for need for surgery. Because of the high rate of recurrence and the risks of
emergency surgery, all but the very unfit should be considered for elective repair. Options
include resection with or without stoma; fixation of the redundant loop (sigmoidopexy);
or novel minimally invasive treatments such as percutaneous endoscopic colostomy
(PEC), which involves fixation of the colonic loop to the anterior abdominal wall using
PEG tubes.
Caecal volvulus
This occurs with a congenitally mobile caecum that twists up into the left upper quadrant
of the abdomen. It often occurs in younger patients than does the sigmoid volvulus and it
can be precipitated by pregnancy, recent surgery, left colonic obstructions and congenital
malrotation/bands. The majority are really ileocolic; 10% are purely caecal; 11% of people
have failure of fusion.
History
Patients may present acutely or with indolent obstructive symptoms with recurring vague
indigestion and cramp-like abdominal pain.
Examination
Examination may be normal between episodes or the patient may present with abdominal
distension arising from the right iliac fossa.
Investigations
During acute episodes, AXR reveals a large bowel loop arising from the RIF to the left
upper quadrant. Between episodes a barium enema may reveal a chronically enlarged
caecum, which suggests the diagnosis.
 COLON, RECTUM AND ANUS 217

Treatment
Acutely colonoscopic decompression is not effective and surgery is required – options
include right hemicolectomy, caecopexy and caecostomy.
Follow-up
Review with results, which may or may not suggest the diagnosis but should exclude other
causes, e.g. cancer. Decide on need for surgery.
Post-operative follow-up
Review with histology to exclude the presence of co-existing carcinoma or other
pathology. Detect any complications of laparotomy and large bowel resection.

Vascular lesions of the colon

The major vascular conditions affecting the colon can be classified as:
✧ ischaemic lesions of the large bowel
✧ angiodysplastic lesions of the colon.
Ischaemic conditions of the colon
There are three main causes of ischaemia and three main forms which present.
The main causes of ischaemic colitis include the following.
✧ Thrombosis: arterial or venous, caused by arteriosclerosis, polycythaemia rubra vera,
portal hypertension, malignant disease of the colon, hyperviscosity syndrome due to
platelet abnormalities or high molecular weight dextran infusion.
✧ Emboli: left atrium (AF), left ventricle (MI), atheromatous plaque in the aorta.
✧ Vasculitis: polyarteritis nodosa (PAN), systemic lupus erythematosus (SLE), giant cell
arteritis (Takayasu’s arteritis), Buerger’s disease, Henoch-Schönlein purpura.
✧ Surgical trauma to vessels: aortic reconstruction (with an inadequate marginal artery),
resection of adjacent intestine.
✧ Non-occlusive ischaemia: shock-hypovolaemia or septic, congestive cardiac failure (an
uncommon but frequently fatal complication of cardiopulmonary bypass).
✧ Spontaneous ischaemic colitis.

The three forms of ischaemic colitis are gangrenous, transient and stricturing.
Gangrenous
This presents with several days of abdominal pain and rectal bleeding. There is mild
to moderate abdominal tenderness. Proctoscopy shows bleeding above the level of the
proctoscope (‘red-currant jelly’). The disease occurs most commonly at the splenic flexure
(so-called ‘Griffiths’ point’: the watershed between the superior and inferior mesenteric
artery territories). On AXR, ischaemic colitis shows thumb printing, picket-fence
thickening of folds and sacculation. Thumb printing is due to submucosal oedema and
haemorrhage. Arteriography may show complete occlusion of the vessel. Colonoscopy
may reveal haemorrhagic nodules and ulceration, but should be performed with care due
to the risk of perforation.
Treatment is initially supportive with total parenteral nutrition (TPN). If it deteriorates
it needs surgery with resection of the bowel.
Transient
This occurs in patients who are middle-aged, with known peripheral vascular disease;
collaterals form.
218 GENERAL SURGERY OUTPATIENT DECISIONS

Stricturing
This may present with symptoms of chronic obstruction with a history of vascular
disease (cardiac or peripheral). Strictures form due to scarring following the chronic
ischaemia.
Vascular ectasia of the colon
This condition tends to affect the over-60 age group. They are acquired disorders, also
known as angiodysplasia or arteriovenous malformations. They produce anaemia
from chronic blood loss, generally of venous origin, or sudden haemorrhage. They are
usually small and not detectable at operation and are only diagnosed by angiography.
They mostly occur in the caecum and right colon. The cause is unknown but there is
a 20% correlation between aortic stenosis and angiodysplasia. It is also associated with
microaneurysm and collagen diseases.
History
Obscure colonic bleeding. There may be a history of intermittent episodes of fresh rectal
bleeding.
Examination
Chronic cases may present with anaemia with otherwise normal examination findings.
Acute cases may present with shock and fresh rectal bleeding.
Investigation
Give OGD and colonoscopy to rule out other causes of bleeding. Radio-labelled red-cell
scans or selective mesenteric angiography can help to identify the site of bleeding and
therapeutic angiography can be used to embolise the affected vessel.
Treatment
Treat with angiographic embolisation or segmental colectomy as guided by imaging
studies.
Follow-up
Follow up at short intervals (1–4 weeks) until the cause is identified.

Inflammatory bowel disease (IBD): ulcerative colitis and Crohn’s

IBD describes conditions associated with inflammation of the large bowel. The main
differential diagnosis is between ulcerative colitis (UC) and Crohn’s.
Other conditions that enter the differential diagnosis include tuberculous infections,
amoebic dysentery, bilharzial infestations of the colon, Salmonella enteritis and colitis,
Campylobacter infections, antibiotic-associated pseudomembranous colitis, necrotising
enterocolitis, radiation-induced colitis and enteritis, ischaemic colitis (rare under age
60), complicated diverticular disease (especially with internal fistula), pneumatoides
cystoides intestinalis (early stages) and primary cytomegalovirus colitis (can simulate or
complicate UC).
Diseases that mimic Crohn’s and exhibit similar X-ray signs include small bowel
adenocarcinoma, lymphomas and small bowel phytobezoar.
Differentiation between ulcerative colitis and Crohn’s
Crohn’s disease can affect the entire gastrointestinal tract, from mouth to anus, and is
characterised by discontinuous ‘skip’ lesions, while UC affects only the colon, except for
backwash ileitis in patients with diffuse and severe disease who have an incompetent
 COLON, RECTUM AND ANUS 219

ileocaecal valve. It tends to do so in a confluent manner from the rectum, extending

variable distances proximally (note that in some patients with UC there is relative ‘rectal
sparing’). UC and Crohn’s describe a spectrum of disease, and those patients with colitis
that cannot be differentiated into either category are labelled ‘indeterminate colitis’.
IBD is covered in full in the section describing disorders of the small bowel.
Pseudomembranous colitis
This is a specific form of infective colitis generally seen in hospitalised patients receiving
antibiotics. It is caused by Clostridium difficile. It is more common in elderly patients,
after surgical intervention, in patients with intestinal neoplasm and in patients with
atherosclerotic ischaemia.
History/examination
The mild form consists of watery mucoid diarrhoea which is offensive; the severe form
results in toxic dilatation and a risk of perforation.
Investigations
It is diagnostic by colonoscopy and biopsies, where an off-white slough of necrotic
mucosa and exudates (the ‘pseudomembrane’) is characteristic. Stool culture is used to
identify C. difficile or its toxin.
Treatment
Give oral vancomycin for 1–2 weeks, or give intravenous metronidazole.
Neutropenic colitis
This may develop in patients undergoing chemotherapy. It is caused by super-infection,
e.g. Clostridium septicum.

Rectal and anorectal disorders

Proctitis
Proctitis is an inflammation of the bowel similar to ulcerative colitis but inflammation is
confined (initially) to the rectum and anal canal. The causes of proctitis can be divided
into sexually transmitted infections, other infective causes, inflammatory bowel disease
and trauma (mechanical, radiation).
✧ Sexually transmitted infections include gonorrhoea, herpes, Chlamydia and
lymphogranuloma venereum. They are common in those engaging in unprotected
receptive anal intercourse.
✧ Non-sexually transmitted infections include group ‘A’ Streptococcus.
✧ Inflammatory bowel disease: a non-specific variation of UC accounts for many cases
of non-infective proctitis. While in most cases the course is benign, the condition may
result in late rectal strictures. Crohn’s and UC may also present initially with isolated
proctitis.
✧ Trauma: often related to the insertion of foreign bodies into the rectum for sexual
gratification or to radiation injury following radical radiotherapy for prostate cancer
(see below).
History
Take a general colorectal history. Mainly in young adults, who present with rectal bleed-
ing, diarrhoea, tenesmus and passage of mucus or mucino-sanguinous discharge. Take a
sexual history to identify possible infective or factitious causes.
220 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
Perform a general examination. Examination may be normal but examine for general fea-
tures of ulcerative colitis. In the rectal examination look for other perianal conditions.
Investigations
Sigmoidoscopy shows mucosa oedematous and hyperaemic. Perform biopsies for
histology; colonic involvement is excluded by colonoscopy.
Treatment
Give bowel sedatives and stool softeners, prednisolone suppositories and enemas,
sulphasalazine tablets or enemas. Any co-existent perianal disease (fissure, abscess, fistula,
haemorrhoids) is treated by the appropriate surgical procedure.
Neutropenic anorectal infections
There is a high incidence of anorectal bacterial infections in neutropenic patients, caused
by E. coli, S. aureus, Klebsiella. Diagnosis can be late in patients who are unable to mount
a white cell response, and the development of large abscesses or necrotising fasciitis is
possible. They are treated by intravenous antibiotics; by drainage of pus and limited
debridement of slough and necrotic areas; and by formation of colostomy in cases where
the condition progresses and conservative management fails.
Radiation proctitis
Rectal bleeding following pelvic irradiation has been reported in up to 95% of patients
in retrospective studies, with symptoms peaking at one year from treatment and tending
to resolve after 18 months. Some authors have suggested that up to 5–10% of patients
require surgery for complications of radiation proctitis. There is increased incidence in
diabetics and those with significant cardiovascular disease. Symptoms may appear within
two weeks of treatment.
History
Symptoms are frequency, diarrhoea, rectal blood and mucus and tenesmus. Occasionally
symptoms are delayed and the patient is found to have a large rectal ulcer which requires
biopsy to exclude cancer.
Other symptoms may result from rectal fistulation into the vagina or urinary tract.
There may also be damage to the small bowel and transverse colon.
Examination
Examine for lower abdominal tenderness. Rectal examination may be normal or an
indurated area may be palpable. Look for blood on the glove on withdrawal.
Investigation
Investigate with sigmoidoscopy with biopsy for diagnosis and to determine the extent
of the disease.
Treatment
Treatment is medical initially, using 5-ASA/steroid enemas if symptoms are persistent
or troublesome. With severe symptoms consider topical formalin solution (requires
anaesthetic) or laser coagulation. Formalin is effective in 80% of patients after 1–2 appli-
cations but 30% develop recurrent symptoms. Surgery is reserved for those with severe
complications (perforation, fistula, stricture). Defunctioning sigmoid loop colostomy is
provided for 6–12 months to rest the bowel. However, haemorrhage and tenesmus may
continue.
 COLON, RECTUM AND ANUS 221

Alternatively a Hartmann’s procedure can be performed (although acceptable leak

rates are reported in those with isolated segments of radiation injury undergoing primary
anastomosis).
Follow-up
Flexible sigmoidoscopy and biopsy are needed to make the diagnosis, define the extent of
affected bowel and exclude other causes such as cancer. Trial of medical treatment can be
attempted in those with debilitating symptoms, but close review is required to monitor
response. In severe cases consider admission for in-patient care.
Post-operative follow-up
Review with histology to confirm the diagnosis and detect complications of the procedure.
Determine if the surgical procedure has been successful in relieving the symptoms and
review accordingly. Decide whether to reverse any colostomies at 6–12 months. Symptoms
should have settled completely before this is performed.

Involvement of the colon by gynaecological pathology

This is involvement of the sigmoid colon by ovarian carcinoma, which can present with
symptoms suggestive of bowel cancer. Also, endometriosis can implant onto the serosa
of the sigmoid colon and rectum and cause characteristic symptoms.
Endometriosis of the bowel
Although endometriosis (defined as the presence of functioning endometrial tissue
outside of the uterus) occurs in 4–17% of women of reproductive age, only 5–10% of
these will have colorectal involvement.
History
Take a general colorectal and gynaecological history. Dysmenorrhoea, dyspareunia, cyclical
rectal bleeding (occurs in up to one-third of patients but very few have involvement of
the bowel mucosa) and painful defaecation just before menstruation are characteristic.
Pain is relieved once menstruation starts. Occasionally bowel obstruction is caused.
Differential diagnosis includes malignancy (primary or metastatic), diverticulitis, IBD,
pelvic inflammatory disease (PID) and radiation colitis.
Examination
Perform a general examination, including full abdominal and pelvic examination. Usually
examination is normal and the diagnosis is suspected on the history.
Investigations
Sigmoidoscopy; laparoscopy and biopsy for histological diagnosis; joint care with
gynaecologists.
Treatment
Treat with hormone manipulation initially (combined oral contraceptive pill,
gonadotropin-releasing hormone (GnRH) analogues). Treat with Hysterectomy, oopho-
rectomy and rectosigmoidectomy.
In younger patients, excise endometrial implants.
Follow-up
Follow up at short intervals until diagnosis is obtained.
222 GENERAL SURGERY OUTPATIENT DECISIONS

Post-operative follow-up
Review with histology to confirm diagnosis. Recurrence requires further laparoscopy.
Rectovaginal fistulas
Causes include:
✧ obstetric injury
✧ IBD (Crohn’s)
✧ radiation injury
✧ infection (cryptoglandular, Bartholin’s gland, lymphogranuloma venereum)
✧ neoplasm (anal, rectal, vaginal)
✧ trauma (foreign body, iatrogenic: vaginal or anorectal surgery)
✧ congenital.

History
Take a general colorectal and gynaecological history. History will include the occurrence
of a foul vaginal discharge resistant to normal therapy progressing to the passage of flatus
or faeces per vagina. Symptoms may be intermittent or constant. Recent prolonged labour
preceding the onset of symptoms may be a feature, as may recent perineal irradiation.
Examination
Perform a general examination including abdominal, rectal and vaginal examination.
Investigations
Rigid sigmoidoscopy may reveal the fistula. Some authors recommend the rigid sig-
moidoscope to examine the vagina as well in this circumstance and it is better than
the speculum at identifying the vaginal component of the fistula. Fistula may also be
demonstrated by barium enema or vaginal contrast study. Examination under anaesthetic
(EUA) may be required in difficult cases. Inserting a tampon into the vagina and instilling
methylene blue into the rectum can help to prove the existence of a fistula that is hard
to demonstrate.
Treatment
Treatment depends on the cause and height of the fistula. All sepsis should be adequately
drained before attempts at repair are made. Very superficial tracks can sometimes be
treated by simple fistulotomy; medical treatments such as infliximab may be useful in
Crohn’s fistulae. Defunctioning stoma should be considered for recurrent fistulae and
complex cases.
Transanal repair: rectal advancement flap, sleeve (circumferential) advancement flap
(used if defect is large).
Transperineal repair: laying open of fistula and immediate overlapping sphincter repair,
transverse transperineal repair (fistula track divided along with perineal body and vaginal
and rectal defects closed separately).
Transvaginal repair: inversion of fistula (into rectum), vaginal advancement flap.
Transabdominal repair: dissection of rectovaginal septum, interposition of omental or
gracilis muscle flap, with or without limited rectal excision.
Follow-up
Follow up at short intervals until cancer is excluded. Prompt treatment is required to
avoid complications from sepsis.
Post-operative follow-up
Review with histology to exclude cancer. Determine the success of the procedure and
decide a date for possible closure of any covering colostomy.
 COLON, RECTUM AND ANUS 223

Recto-urinary fistulas
Causes include diverticulitis, Crohn’s, carcinoma, irradiation of the bladder and
tuberculosis of the prostate. Most recto-urinary fistulas result from injury, mainly as a
result of prostatic or urethral instrumentation. Retroprostatic fistulas are rare and result
from complications of transrectal needle biopsy of the prostate.
History
Take a general colorectal and urological history. Usually there is a history of recurrent
urinary tract infections or the passage of flatus (pneumaturia) or faeces (faecaluria) in
the urine. Other features of the history may be suggestive of one of the causes above.
Examination
Perform a general examination. Examine for evidence of sepsis, anaemia and renal
impairment. Examine for features of one of the underlying causes.
Investigations
Take FBC, U&Es and urine and blood cultures. Sigmoidoscopy may identify the fistula
and help identify any underlying disorder. Contrast studies of the bowel may identify the
fistula. CT scan may give more detailed information for planning definitive surgery.
Treatment
Treatment is by insertion of a urinary catheter and definitive diagnosis and treatment of
the underlying pathology. Post-traumatic fistulas are amenable to direct repair either by
perineal, trans-anal or trans-sphincteric approach.
Follow-up
Follow up at short intervals until cause is identified. Treatment should be arranged
promptly to avoid the development of sepsis and deterioration in renal function.
Post-operative follow-up
Review with histology to confirm the diagnosis. Determine the success of the operation
and detect any complications of the procedure.

Disorders of the anorectal musculature

Rectal prolapse
A partial prolapse involves the mucosa only; a complete prolapse involves the entire
thickness of the rectal wall. In children under two, prolapse is not uncommon (it is
often associated with a diarrhoeal illness or prolonged coughing) but usually resolves
spontaneously (it is, though, associated with cystic fibrosis and so a sweat test should
be performed). The differential diagnosis in adults includes haemorrhoids and large
polypoidal tumours.
History
Take a general colorectal history. In children the prolapse is usually incomplete and has
been noticed by the parent. Adults tend to complain either of the prolapse itself and
resulting soiling of underclothes from mucus, blood and faeces, or a varying degree of
faecal incontinence. The prolapse will tend to be noticed at defaecation or on coughing
or straining.
Examination
Perform a general examination. In children the prolapse can be viewed when sitting the
224 GENERAL SURGERY OUTPATIENT DECISIONS

child on a potty. In adults the anus may be patulous with decreased tone. Active contrac-
tion of the anal sphincter onto the examining finger is weak. The patient experiences no
discomfort on rectal examination, and anal and rectal sensation are decreased. Bearing
down produces the prolapse. If complete, two complete layers of bowel wall are palpable
between the fingers. Generally a prolapse of greater than 5cm in length is complete and
less than 5cm needs careful examination to differentiate complete from incomplete.
Procidentia of the uterus may often co-exist, and a combined approach to treatment
between gynaecologist and surgeon is required.
Investigations
Proctoscopy and sigmoidoscopy are performed to exclude underlying rectal disorders.
Anorectal physiology is useful to detect any underlying pathology, investigate the
incontinence aspect of the disorder and plan appropriate treatment.
Treatment
For babies do nothing. It will spontaneously resolve. In children, if it is incomplete it is
self-limiting; give laxatives and ensure regular defaecation with or without enemas. For
older children inject sclerosants into the lower rectal mucosa.
In adults, if anal sphincter function is satisfactory and the prolapse partial (i.e. anterior
mucosal prolapse) then a careful mucosal excision (similar to a haemorrhoidectomy) can
be perfomed.
If poor sphincter tone is a contributory factor, sphincteric exercises may help.
Surgery
✧ Perineal procedures: Delorme’s (mucosal stripping and muscle placation), Altemeier’s
(perineal rectosigmoidectomy).
✧ Abdominal procedures: include laparoscopic/open suture rectopexy, Ivalon® sponge/
mesh rectopexy, resection rectopexy.
✧ Transabdominal rectopexy has a 90% success rate, but is a major abdominal procedure.
There is a risk of sexual dysfunction, which needs to be included in the consent
process. For frail or elderly patients, a Delorme’s procedure may relieve symptoms
and does not preclude a second procedure but has a high recurrence rate.
Follow-up
Intervals are short until serious underlying pathology has been excluded. Thereafter, a
decision on surgical treatment or expectant management should be made.
Post-operative follow-up
Patients are reviewed to determine the success of the procedure and to detect any com-
plications. After transabdominal rectopexy the commonest complication is constipation,
which occurs in a third of patients. If prosthetic mesh has been used there is the risk
of deep-seated infection, which, if it fails to settle, requires removal of the mesh. Some
patients may complain of sexual and urinary disturbances due to disruption of the pelvic
nerves.
Descending perineum syndrome
Excessive straining leads to a prolonged reflex inhibition of musculature with an abnormal
descent of the perineum and bulging of the anterior rectal wall towards the anal canal.
History
Take a general colorectal history. There are generally non-specific symptoms of difficulty
passing faeces, tenesmus and incontinence. Associations include a long history of
 COLON, RECTUM AND ANUS 225

constipation, vaginal deliveries, previous rectal/perineal surgery, rectocoeles and

enterocoeles.
Examination
Perform a general examination. On straining, the anus descends to 1cm below the inter-
ischial line.
Investigation
Investigate with sigmoidoscopy to exclude rectal disease and detect any complications,
e.g. solitary rectal ulcer. Anal physiology studies may be helpful in difficult cases, as may
defaecating proctography.
Treatment
Advise the patient to avoid straining, give Bisacodyl suppositories and bulk-forming
laxatives. Inject sclerosants or surgically excise any mucosal prolapse. Biofeedback may
be beneficial.
Follow-up
Non-urgent review to determine the success of the treatment in helping defaecation.
Once stabilised, discharge with advice.
Post-operative follow-up
Review to determine success of operation and detect any complications. Otherwise
follow-up is the same as non-operative.
Solitary rectal ulcer
These may be multiple and not all cases have ulceration. Symptoms result from an internal
rectal prolapse or intussusception, which causes trauma to the rectal wall. Persistent rectal
symptoms are due to rectal ulceration, which is commonly situated 7–10cm from the anal
verge on the anterior or anterolateral wall. There are well-defined indurated edges, with a
grey base with surrounding mucosa which may look normal or oedematous or nodular.
The mechanism of ulceration may be rectal prolapse, failure of relaxation of puborectalis
muscle or insertion of foreign bodies.
History
Take a general colorectal history. This condition is characterised by a long history of
prolonged and multiple visits to the toilet associated with prolonged, unproductive
straining, although rectal bleeding and passage of mucus during and between defaecation
may occur. There may be a deep-seated perineal pain and the sensation to defaecate may
be so strong that the patient becomes desperate and inserts fingers or other objects into
the rectum in an attempt to empty the already empty rectum.
Examination
General examination may be normal with some lower abdominal discomfort. Rectal
examination reveals rectal soreness and an indurated area internally.
Investigations
Investigate with sigmoidoscopy and biopsies. Sigmoidoscopy reveals haemorrhage or
oedema, or in 50% an ulcer adjacent to a valve of Houston on the anterior surface,
approximately 5–8cm from the anal verge. This may look like a rectal carcinoma but
repeated biopsy reveals only non-specific inflammatory changes or fibromuscular hyper-
plasia of the lamina propria.
A defaecating proctogram may reveal an internal intussusception.
226 GENERAL SURGERY OUTPATIENT DECISIONS

Treatment
Explain the condition to the patient. There is no medical therapy, although rectal steroids
have been used. Biofeedback has been proposed to modify the harmful toilet habit. With
severe symptoms use abdominal rectopexy to treat prolapse, or rectal excision and end-
colostomy, although fewer than two-thirds of patients derived a benefit from rectopexy
in some series.
Follow-up
Follow up at short intervals of 1–2 weeks until cancer is excluded. Thereafter see the
patient after 1–3 months to try different therapies, assess severity of symptoms and decide
on the need for surgery.
Post-operative follow-up
Review to determine the success of the procedure in relieving symptoms and to detect
complications. Complications of rectopexy are described under rectal prolapse.
Faecal incontinence
This is the involuntary passing of flatus or stool. Its incidence is underestimated but may
be up to 1–2%. Causes include old age, childbirth, chronic constipation, anal dilatation
or fistula surgery, dementia and faecal impaction, low rectal tumours and autonomic
neuropathy associated with diabetes mellitus. It can be classified as:
✧ traumatic: obstetric, surgical, accidental/war
✧ colorectal disease: haemorrhoids, rectal prolapse, IBD, tumours
✧ congenital: spina bifida, surgery for imperforate anus, Hirschprung’s
✧ neurological: cerebral, spinal, peripheral
✧ miscellaneous: behavioural, faecal impaction.

Anal continence depends on a variety of mechanisms, including stool consistency, rectal

capacity/compliance, sphincter function, anal sensation and an intact rectoanal inhibitory
reflex. The underlying mechanisms in incontinence may include either damage to the
anal sphincter or perineal descent due to excessive straining over many years leading to
a traction neuropathy of the pudendal nerve.
Severity of incontinence
Browning and Parks’ grades are shown in Table 9.2.
TABLE 9.2 Incontinence grades.
Grade A normal continence to solid, liquid and flatus
Grade B incontinence of flatus but no faecal leakage
Grade C acceptable control over solid stool, but no control over liquid or flatus
Grade D continuous faecal leakage

History
Take a general colorectal history. Enquire about the above causes and the severity of
incontinence.
Examination
Perform a general examination. Examine for perineal scars from obstetric injury or fistula
surgery. Note the degree of perineal descent at rest and on straining and any associated
prolapse. Exclude abnormality of lumbosacral plexus.
 COLON, RECTUM AND ANUS 227

In a rectal examination, look for faecal impaction or rectal tumours. Examine sphincter
integrity at rest and on contraction.
Investigations
Investigate with proctoscopy and sigmoidoscopy.
If recognised causes of faecal incontinence are not found, the patient is said to have
idiopathic faecal incontinence. Less severe cases require no further investigation and can
be treated symptomatically with loperamide.
Severe cases
✧ Anal manometry measures the presence of and relaxation after rectal distension by
balloon. Anal canal pressures at rest reflect activity of the internal sphincter (50–80cm
H2O) and voluntary contraction of the external sphincter (squeeze pressure) will
increase the pressure of the anal canal to 150cm H2O. It is used to diagnose a short
and weak sphincter.
✧ Sphincter EMG can detect silent areas of a sphincter defect and localise the ends of
the muscle pre-operatively. Also traction neuropathy of the pudendal nerve – some
muscle fibres lose their innervation.
✧ Anorectal sensation: rectal compliance balloon or thermal stimulation.
✧ Trans-anal ultrasound to image defects in the sphincter.
✧ Defaecating proctogram to detect prolapse.
Treatment
Mild cases
Give counselling, and give constipating agents if loose stool is present. Advise physio-
therapy with anal sphincter and pelvic floor exercises, or biofeedback methods. Leakage
after passing motion may indicate incomplete evacuation, which can be treated by a
glycerine suppository after each motion or by a daily phosphate enema.
Severe cases
Severe cases may require operative treatment with sphincter repair when defects are
identified. Reconstructive options include graciloplasty or the insertion of artificial neo-
sphincters. Sacral nerve stimulation has recently emerged as a potential new treatment.
Follow-up
Follow up at short intervals initially to assess severity and review with investigations. Mild
cases can be discharged to the GP when serious underlying pathology has been excluded.
Severe cases need a decision made regarding surgery when appropriate investigations
have been completed.
Post-operative follow-up
Review to assess the success of the procedure and to detect any complications of the
procedure. Recurrence not amenable to further surgery may require a stoma.
Anorectal suppuration and anorectal abscesses
These can be caused by both aerobic (Staphylococcus, Streptococcus, E. coli and Bacillus
pyocyaneus) and anaerobic (Clostridium welchii and Bacteroides) bacteria.
Particularly susceptible are leucopenic, ulcerative colitis (15%), Crohn’s (25%) and
diabetic patients.
Perianal skin infections are caused by Staphylococcus aureus and nearly all heal with
simple incision and drainage.
Perianal abscess of bowel origin starts internally in glands in the intersphincteric
space (cryptoglandular). Spread to the skin immediately adjacent to the anus is termed a
228 GENERAL SURGERY OUTPATIENT DECISIONS

perianal abscess. Spread laterally into the buttock is termed an ischiorectal abscess. These
may originate from high intersphincteric infection or from pelvirectal disease. These
abscesses can be considered as perianal fistula in which the internal openings are small,
cannot be found at operation and will heal spontaneously in the majority. In a minority
the fistulous track will persist and require formal fistula surgery.
History
Severe throbbing pain, worse on sitting and coughing. Ask about a history of predisposing
factors, e.g. malignancy, chemotherapy, UC, Crohn’s or diabetes. Often will present as
emergencies rather than to the outpatient clinic.
Examination
Red (may not be very red), tender, rounded swelling in the perianal area; there may be
some degree of induration and later some fluctuation. Ischiorectal abscesses occupy a
larger area to one side of the anus and sometimes may be bilateral.
✧ Submucous abscess presents as dull aching pain in the rectum with usually no exter-
nal evidence of infection. Rectal examination may reveal a rounded smooth area of
induration on one side of the upper anal canal and lower rectum. Pus may be seen
draining from an internal opening.
✧ Pelvirectal abscess is normally a complication of pelvic sepsis. There are signs of
infection with pyrexia, rigors, diarrhoea, weakness and lower abdominal tenderness
or even a mass. Rectal examination shows it is tender high in rectum and may have
a boggy swelling.
Investigation
Investigate with FBC to detect underlying leucopenic condition. Test blood sugar to
detect diabetes mellitus. Perform examination under anaesthetic. Pus should be sent for
microbiology. A sample of the abscess cavity wall should be sent for microbiology and
histology.
Treatment
Examination under anaesthetic; perform incision and drainage. Perform rigid sigmoido-
scopy and proctoscopy. Biopsies of inflamed mucosal lesions are taken if appropriate.
Examine for the internal opening of a perianal fistula. If the internal opening of a fistula
is seen it should be noted and left. Attempts to probe cavities for fistula tracks in the acute
setting are likely to be rewarded only by the creation of new tracks through the friable
indurated tissue, rather than by the identification of an existing track. Otherwise, incise
and drain the abscess cavity. Underlying disorders are treated appropriately.
Post-operative follow-up
Review with the results of microbiology of the pus. Infections of Staph. aureus will
all heal, and provided the wound is clean the patient can be discharged. Those with
organisms of bowel origin should be followed up until complete healing is confirmed.
Most will heal but some will not heal or will recur within a short time. These patients
should be investigated for possible perianal fistula by EUA.
Anorectal fistulas
There is usually only one internal opening, but there may be more than one external
opening. These usually start as a perianal abscess but the internal opening persists, or
perianal gland infection persists as a source of sepsis. This is particularly likely to occur
in the presence of some underlying disorder such as UC or Crohn’s or with chronic
infections such as TB, actinomycoses and lymphogranuloma venereum. Occasionally
carcinoma of the rectum can present as a fistula.
 COLON, RECTUM AND ANUS 229

Differential diagnosis
Exclude colloid rectal carcinoma, proctocolitis, Crohn’s of small intestine, TB, actinomy-
cosis and lymphogranuloma venereum.
Local conditions include pilonidal sinus, suppurative hidradenitis, chronically infected
Bartholin’s gland and vaginal and urethral fistulas.
Classification
Goodsall’s rule relates the external opening of an anal fistula to its internal opening.
Fistulas with external openings anterior to the inter-ischial line have their internal
opening on the same radius. External openings posterior to the inter-ischial line form a
horseshoe to open in the midline. Exceptions include anterior openings more than 3cm
from the anus (which may be anterior extensions of posterior horseshoe fistulas) and
anterior fistulas associated with other diseases, e.g. Crohn’s, malignancy.
Fistulas are also classified according to height and relation to the anal sphincters:
✧ subcutaneous
✧ low intersphincteric: goes underneath the subcutaneous part of the external
sphincter
✧ trans-sphincteric: track extends through the external sphincter
✧ anorectal opening between the rectum and exterior.

An alternative classification is the Park’s classification. See specialised texts.

History
Take a general colorectal history. There may be a history to suggest an underlying disorder
or previous acute perianal abscess followed by intermittent or persistent discharge or
recurrent abscess.
Examination
Perform a general examination. Rectal examination may reveal the presence of single or
multiple external openings. Granulation tissue may mark the opening or there may be
the presence of pus. The external opening may have temporarily healed and be indicated
by an area of reddish/brown induration. Induration may also be palpated inside the
rectum, indicating the site of the internal opening. Try to determine the course of the
track between the internal and external openings.
Ask the patient to squeeze the inserted finger to determine the relation of the primary
track to the puborectalis sling, which correlates to the upper extent of the external
sphincters. Then advance the finger to identify any induration above the levator
muscles.
Investigations
The main investigation is the EUA. However, in complicated disease or in cases complicated
by other diseases, fistulography may provide useful information as to the course of the
track, especially if an internal opening has not been identified. MRI scanning has an
increasing role in identifying the course of fistulas and excluding other disease, and, in
experienced hands, endoanal ultrasound (often with hydrogen peroxide contrast) can
give valuable anatomical information.
Treatment
Treat with surgery – EUA and treatment of fistula.
✧ Laying open.
✧ Seton insertion.
✧ Fibrin glue/fistula plug.
230 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Chronic: long-term metronidazole treatment.

✧ TB: treat active disease prior to treatment of fistula.

For UC/Crohn’s it is necessary to get control of the primary disease first. However,
resection of the ileocaecal region in Crohn’s, with no other apparent disease of the bowel,
often fails to heal perianal fistulas. Long-term treatment with metronidazole, salazopyrin
or azathioprine is needed, however, it may lead to amyloid deposition and death from
amyloid renal and cardiac failure. Therefore rectal excision and colostomy are acceptable
alternatives. Infliximab may be used in an attempt to heal a fistula once any associated
abscess has been drained.
Follow-up
If a fistula is suspected, the patient should go forward for EUA where it can be formally
assessed. If symptoms are atypical it may be prudent to perform a flexible sigmoidoscopy
first, or at the time of the EUA to exclude co-existing colorectal conditions.
Post-operative follow-up
If a seton has been inserted it will require attention (some patients are left long term with a
seton to control their symptoms by establishing adequate drainage). Examine for evidence
of ongoing sepsis or recurrent discharge, which may suggest unrecognised extensions of
the original disease and require either repeat surgery or an MRI to diagnose.
Hidradenitis of the perianal skin
This is not a condition of bowel origin, but it tends to be referred to colorectal clinics
because of the site. The condition consists of chronic inflammation of sweat glands leading
to recurrent infection and abscess formation. The affected area begins as induration and
may progress to sinus formation. The majority of cases occur in the axillae, but 30% are
perianal. Differential diagnosis includes pruritus ani and perianal fistula.
History
Take a general colorectal history, which will usually be normal. There is a history of
recurrent infections of the area, sometimes progressing to boils/abscess formation.
Examination
Perform a general examination. Examine the axillae to detect any disease there. The
groins and perianal area may be indurated and show evidence of scarring and chronic
inflammation. There may be multiple small boils with white heads and small amounts of
pus in the sweat area of the groins and perianal area. Rectal examination is normal.
Investigations
Few investigations are needed for a diagnosis. Bowel investigations are indicated if the
history/examination suggests a co-existing bowel condition. Microbiology of any pus
should confirm skin bacteria only. Test urine to exclude glycosuria and also test blood sugar.
Treatment
In mild cases long-term antibiotics, e.g. erythromycin, may be effective in reducing the
rate of infection, combined with conservative measures such as wearing loose airy clothing
and daily washing. More severe cases require excision of affected skin and subcutaneous
tissue to deep fascia with or without a split skin graft (plastic surgery referral).
Follow-up
Mild cases can be reviewed after 1–6 months to determine the effect of conservative
 COLON, RECTUM AND ANUS 231

measures. Failure of medical treatment or severe disease are indications to consider

surgery.
Post-operative follow-up
Review with histology to confirm diagnosis. Detect recurrence or any complications of
surgery, e.g. skin necrosis. Unless it is severe, skin necrosis can be treated conservatively with
antibiotics and dressings. Extensive skin necrosis may require a plastic surgical opinion.
Pruritis ani
This is an itchy and irritated anus. Secondary causes include anorectal and dermatological
disorders, but in many the underlying problem cannot be found. Minor degrees of faecal
soiling can lead to irritation and scratching, or to overzealous cleaning and the applica-
tion of inappropriate topical preparations. This in turn results in damage to the delicate
perianal skin and further irritation, and a vicious circle results.
Dysfunction of the internal anal sphincter allows anal leakage, and skin tags prevent
adequate cleaning of the anus, as do perianal warts. There may be mucus discharge from
haemorrhoids, benign or malignant rectal tumours, anal fissures and fistulas. All may be
made worse by the ingestion of spicy foods and caffeine.
Secondary causes can be classified as the following.
✧ Fungal infection: secondary infection due to Candida, Trichomonas or Tinea crura.
✧ Parasitic infestation: threadworms, scabies etc.
✧ Other infections: gonococcal proctitis and Condyloma acuminatum, Herpes simplex.
✧ Dermatological disorders: contact dermatitis, psoriasis, lichen planus, eczema.
✧ Neoplasia: rectal adenoma, rectal adenocarcinoma, squamous cell anal carcinoma,
malignant melanoma, Bowen’s disease, Paget’s disease.
✧ Benign anorectal: haemorrhoids, fistula, fissure, prolapse, sphincter dysfunction,
incontinence, radiation proctitis, ulcerative colitis.
History
Take a general and colorectal history to detect any of the causes outlined above. Perianal
and anal itching may be severe and worse when warm. Enquire about the length of
symptoms, change of bowel habit, diet, recent travel etc. In children, suspect Enterobius
infestation. Enquire about an itchy or irritating rash elsewhere on the body.
Examination
Perform a general examination to detect any general skin conditions. Long-standing
irritation causes excoriation and icthyosis, and the perianal skin is corrugated, making
removal of faecal particles difficult. In advanced cases skin becomes atrophic and
excoriated with oedema and thickening of the underlying dermis.
Examine the anus resting and straining. On rectal examination assess the anal tone and
squeeze pressure. Palpate for polyps, fissures, fistulas and neoplasms.
Investigations
Perform urinalysis, blood sugar and FBC. Examine the affected area under a Wood’s
light. Corynebacterium minutissimum is diagnosed by the presence of bight pink-orange
fluorescence (beware – Anusol fluoresces purple). Perform proctoscopy and sigmoidoscopy
to detect any underlying colorectal condition, e.g. neoplasm, haemorrhoids, prolapse.
Perform biopsies and arrange colonoscopy as indicated.
Biopsy affected skin if suspicious. Skin scrapings are taken for fungal elements.
For detection of threadworms in children, a piece of ‘Sellotape’ is applied to the anus
and then stuck onto a clean glass slide. This is repeated for two days, in the mornings.
Microscopy reveals the ova deposited on the perianal skin overnight.
232 GENERAL SURGERY OUTPATIENT DECISIONS

Treatment
The aims are to decrease leakage, improve hygiene and prevent injury to perianal skin.
✧ Treat underlying conditions such as haemorrhoids, fissures and warts.
✧ Treat fungal infections with nystatin or clotrimazole. Treat threadworms with
piperazine.
✧ Give advice on hygiene: gentle washing with water only, no soap, wet wiping after
defaecation is more efficient at cleaning the anus than dry wiping, avoid vigorous
rubbing, wear cotton underwear, no tights.
✧ Decrease leakage: modify diet to avoid spicy foods and fibre, reduce or abstain from
alcohol and caffeine. Prescribe loperamide or codeine.
✧ Pruritus: avoid scratching. Use hydrocortisone cream for 10 days to break the cycle,
but excessive use can cause skin atrophy and itching on withdrawal of the cream.
Follow-up
Review at regular intervals (1–3 months) once diagnosis is achieved to gauge the effect
of therapies.
Haemorrhoids
Haemorrhoids are enlargements of the venous tissue in the rectum, which can cause
symptoms by prolapsing or bleeding. Haemorrhoids are very common and are a very
common cause of perianal bleeding. However, just because haemorrhoids are present
does not mean they are the only cause of the perianal bleeding. Haemorrhoids can
co-exist with cancers or other serious pathology and should not be assumed to be the
cause of rectal bleeding, especially in those over 50. Haemorrhoids may be classified as
follows.
✧ First degree: bleeding but no prolapse.
✧ Second degree: prolapse but reduce spontaneously.
✧ Third degree: prolapse and require manual reduction.
✧ Fourth degree: irreducibly prolapsed.

History
Take a general colorectal history. Commonly patients complain of prolapse and bleeding.
The bleeding is bright red on the toilet paper or dripping into the pan. Pain is uncommon
but can be present in up to 20%. Prolapse may be associated with mucoid discharge and
perianal wetness.
Examination
Perform a general examination. External inspection of the anus may be normal or the
piles may already be visible. Alternatively there may be skin tags visible, which are an
indicator of previous episodes of prolapsed piles. Occasionally, a pea-sized blue swelling is
present on the anal margin, which represents a thrombosed perianal haematoma, which is
often confused with haemorrhoids. Ask the patient to strain down and the haemorrhoids
may appear. Digital examination may be normal.
Investigations
Investigate with sigmoidoscopy to exclude higher carcinoma. Proctoscopy is the best way
to demonstrate the haemorrhoids,which prolapse into the lumen of the scope. Often
there is a history of bleeding but minimal to see on proctoscopy.
Treatment
Conservative measures include laxatives, bulk forming agents and advice to avoid
straining at stool.
 COLON, RECTUM AND ANUS 233

✧ Injection sclerotherapy: phenol in almond oil produces fibrosis. Use 3 ml injected at

the root of each haemorrhoid. Repeat after 3–4 weeks. Useful for all primary piles
and smaller second-degree piles. Contraindicated in third-degree piles, thrombosed
piles or associated anal fissure. There is a small risk of pelvic sepsis or prostatitis if
injection is misplaced.
✧ Rubber band ligation: bands are placed at the base of the piles, which strangulates a
disc of tissue. It sloughs and leaves an ulcer, which scars and fixes the mucosa in place,
preventing the mucosa from becoming engorged and prolapsing.
✧ Haemorrhoidectomy: used if failed to respond to injection sclerotherapy or rubber
banding. Late complications include pain, fissure and fistula formation along the
tracks of cutaneous wounds. Stenosis may develop by three weeks – treat with an anal
dilator. Recent advances include the introduction of ‘stapled haemorrhoidectomy’,
in which a circular stapler is introduced via the anus and fired, removing a circle of
mucosa.

Thrombosed haemorrhoids need conservative treatment (ice, analgesia, bed rest) or

immediate operation, which can be technically difficult and bloody.
Perianal haematoma
This is a bluish, pea-sized swelling at the anal margin. It can be managed conservatively
with analgesia and ice, or incised and drained with instant relief of discomfort.
Summary of treatment options for haemorrhoids
✧ First degree: dietary modification.
✧ Second degree: rubber band ligation, sclerotherapy (haemorrhoidectomy).
✧ Third degree: rubber band ligation, sclerotherapy (haemorrhoidectomy).
✧ Fourth degree: haemorrhoidectomy.
Follow-up
Once diagnosis is made (and concurrent pathology is excluded) review at six-weekly
intervals to gauge the effect of injection or banding. Discharge patients once they are
symptom-free, with advice to avoid constipation and straining at stool, or book them for
haemorrhoidectomy if not they are responding to repeated outpatient management.
Post-operative follow-up
Review to determine success of operation and to confirm healing. Complications include
prolonged healing and anal stenosis. Anal stenosis can be treated with anal dilators. For
prolonged healing, exclude any co-existing pathology or infection and allow 1–2 months
before further EUA. Incontinence may occur due to anal stretching, loss of the anal
cushions or overuse of laxatives. Most cases settle with conservative measures, but anal
physiology studies may be required for persistent cases.
Anal fissure
Anal fissures are common. They represent up to 10% of referrals to colorectal clinics.
They are longitudinal tears in the anoderm which are typically seen at 6 o’clock (posterior
midline) but may be seen anteriorly (especially in women). They are often seen in
association with a ‘sentinel pile’, a skin tag at the distal extreme of the fissure. Patients
enter a vicious cycle in which pain causes fear of defaecation, leading to constipation and
the passage of hard stool, which exacerbates the problem. Spasm of the internal sphincter
(the white fibres of which are often visible in the base of a chronic fissure) reduces the
blood supply to the anoderm (vessels penetrate the muscle and are occluded by sphincter
spasm) further reducing the ability of the sphincter to heal.
234 GENERAL SURGERY OUTPATIENT DECISIONS

Differential diagnosis
This includes atypical ulceration of the perianal margin, TB, syphilis (if suspected
requires biopsy and culture of tissue). For gross fissures, suspect UC or Crohn’s; if
indurated suspect malignancy and send tissue for histology.
History
There is severe pain for 20–30 minutes after defaecation. Bleeding on paper and slight
mucoid discharge. There may be history of proctocolitis or Crohn’s.
Investigation
Usually no investigations are necessary but the following can be performed if atypical
features are present: FBC and C-reactive protein for inflammatory bowel disease; sero-
logical tests for syphilis; rectal biopsy; biopsy of the ulcer edge with tissue for bacterial and
viral cultures if infective cause suspected; and histology if there is any suspicion that the
fissure is atypical and may in fact be a malignancy, Crohn’s etc. Perform anal manometry
if disordered defaecation is suspected.
Examination
There may be the sentinel pile – the perianal skin tag in the posterior midline. The distal
extent of the fissure may just be visible as the perianal skin is gently distracted and the
white, transverse fibres of the exposed internal sphincter in the base of a chronic fissure
may be visible. Rectal examination is frequently not possible due to the pain.
Treatment
Most acute fissures heal spontaneously in 2 to 3 weeks with laxatives and fibre supplements.
In the interim, 5% lignocaine cream applied well within the anal canal may offer symp-
tomatic relief. Glyceryl trinitrate (GTN) ointment (0.2%) applied twice daily to the anal
region decreases sphincter tone and enables healing in approximately 67% of patients.
Topical diltiazem is an alternative, notably in those who cannot tolerate the headache
frequently associated with GTN. For those who fail to heal, botulinum A toxin (Botox)
can be injected either in the outpatients department or under sedation/GA. Initial healing
rates of 70–96% have been reported, but the effect of the blockade wears off after about
three months and recurrences do occur even after this time.
Surgery is required both to exclude more serious conditions (fissure biopsy) and to
speed recovery. Operation consists of examination under anaesthetic (rectal examination,
sigmoidoscopy and biopsy if indicated) and lateral internal anal sphincterotomy
(healing rates of up to 85–95%, but incontinence to flatus in up to 35%). Uncontrolled
manual anal dilatation (the four finger stretch) is no longer recommended due to the
unacceptably high risk of sphincter injury.
Follow-up
Review at short intervals (1–4 weeks) to determine the success of conservative measures
in relieving symptoms. Failure is an indication to consider surgery.
Post-operative follow-up
Review with histology if biopsy taken. Determine success of operation in relieving
symptoms and confirm healing (may take 4–6 weeks). Continued pain or non-healing
may require further EUA to reconsider diagnosis or further treatment, e.g. advancement
skin flaps (V-Y advancement, rhomboid advancement flaps). Mild degrees of incontinence
usually recover or respond to constipating agents.
 COLON, RECTUM AND ANUS 235

Carcinoma of the anal canal and anus

Squamous cell carcinoma of the anus is rare: 1–2% of gastrointestinal malignancies,
about 500 new cases per year in the UK. Differentials include anal fissure, simple papilla,
anal condyloma, prolapsed haemorrhoids and Crohn’s.
Adenocarcinoma of the rectum may spread down and invade the anal canal. Lesions
tend to be softer and more mucoid, but are differentiated on the basis of biopsy and
histology. Predisposing factors include human papillomavirus (HPV) infection, HIV
and immunosupression.
History
Take a general colorectal history. Patients may complain of painful defaecation, rectal
bleeding or bloody discharge and/or a lump. Occasionally they may complain of
symptoms relating to a rectovaginal fistula. Patients presenting with inguinal lympha-
denopathy should always have anal cancer excluded.
Examination
Perform a general examination. Anal carcinoma may present as a warty protuberance,
flattened plaque or penetrating ulcer. Rectal examination may be difficult due to pain.
Examine for the presence of enlarged inguinal nodes.
Investigations
All suspicious lesions need an examination under anaesthetic and biopsy. Make fine-
needle aspiration of enlarged inguinal lymph nodes. Local staging is clinical, by MRI and/
or endoanal ultrasound. The presence of distant metastases (affecting 40% of patients in
the chest or abdomen) is diagnosed by CT scans.
Treatment
The primary treatment of anal cancer is chemoradiotherapy, but small lesions at the
anal margin can be treated by local excision alone with equally good results. Inguinal
lymph node involvement is seen in 10–25% of those with anal cancer and may be treated
by radiotherapy, although some advocate radical groin dissection (histological proof
of nodal involvement should be obtained before embarking on this). Surgery may be
required in four main scenarios:
✧ residual disease
✧ complications of primary treatment
✧ incontinence or fistula after tumour resolution
✧ subsequent tumour recurrence (salvage abdominoperineal excision).

Follow-up
Follow up at short intervals (1–2 weeks) until diagnosis is achieved and treatment insti-
gated. Anal cancer is increasingly being treated in regional centres in view of its relative
rarity. Lymph nodes not thought to be involved should be examined every month for the
first six months after treatment of the primary lesion, then every two months for the next
18 months. Suspicious lesions require fine-needle aspiration or lymph node dissection.
Post-operative follow-up
Review wide local excision – 55% survival at five years. If lymph nodes were involved at
presentation it is 0% survival at five years. With delayed involvement of inguinal lymph
nodes there is 60% survival at five years.
Lymph nodes not thought to be involved should be examined every month for the
first six months after treatment of the primary lesion, then every two months for the next
18 months. Suspicious lesions require fine-needle aspiration or lymph node dissection.
236 GENERAL SURGERY OUTPATIENT DECISIONS

Rare lesions of the anal region

✧ Basal cell carcinoma is a small raised and indurated lesion, occasionally ulcerated.
It is usually only 1–2cm in diameter, and good results are obtained from wide local
excision.
✧ Bowen’s disease is a rare intraepidermal cancer of the anal region, usually diagnosed
after biopsy of an unusual anal lesion. It is treated by wide local excision with or
without skin grafting.

Other rare tumours of the anal canal include basiloid (cloacogenic) carcinoma and
malignant melanoma. Malignant melanoma may mimic a perianal haematoma due to
its colour, although amelanotic lesions can occur. Its prognosis is even worse than that at
other sites so radial surgery is generally avoided.
Perianal papillomas (condyloma accuminata)
These represent one of the commonest sexually transmitted diseases, especially among
homosexual men (of whom as many as 50–75% will harbour asymptomatic condylomas).
It is caused by the human papilloma virus and is important because of the association
with malignant change and the development of anal carcinoma. Differential diagnosis
includes condyloma latum, molluscum contagiosum and hypertrophied anal papillae.
History
Take a general colorectal and sexual history. Symptoms include bleeding, discharge
causing permanent wetness and pruritus ani.
Examination
Perform a general examination. Appearance may vary from a few pink spots to a con-
fluent mass of sheet of warts.
Investigations
Proctoscopy and sigmoidoscopy may reveal papillae within the anal canal which also
require eradication if treatment is to be successful.
Treatment
Principles of treatment include the complete eradication of all lesions and biopsy of
lesions to detect malignant change.
✧ EUA and diathermy excision of perianal and intra-anal lesions.
✧ Podophyllin: requires multiple treatments. Can cause histological changes similar to
carcinoma in situ, which reverse four weeks after treatment.
✧ Bichloroacetic acid: multiple, weekly treatments are required.

Follow-up
Review with histology to exclude carcinoma in situ and confirm healing. Recurrence
requires further treatment. Carcinoma in situ requires further follow-up and repeated
biopsies.
Pilonidal sinus disease
The name literally means ‘nest of hairs’. This disorder is commonly referred to colorectal
clinics although it is not strictly a disease involving the bowel. It is a disorder of the skin
near the anus – the natal cleft – and it occurs in men and hirsute women. It is a disease
of chronic inflammation involving the presence of hairs within sinuses in the skin. It can
be confused with perianal fistula disease and in rare cases a congenital sinus originating
from the spinal cord.
 COLON, RECTUM AND ANUS 237

History
Take a general colorectal history, which is usually normal. The onset of the disease is after
puberty and the presence in childhood should raise the possibility of a congenital spinal
sinus. The disease can present either as an acute abscess or as chronic sinus periodically
discharging pus. There may be a history of previous surgery in the area.
Examination
Perform a general examination, which is usually normal. Examination of the perianal area
reveals usually one or more midline pits within the skin of the natal cleft. Some of these
pits may have lateral extensions. Some sinuses may be inflamed and indurated. Pressing
may produce some pus from the pits, or hairs may exude from them. There may be scars
or unhealed wounds from previous surgery.
Investigations
Investigations are usually not required, apart from urinalysis to exclude glycosuria.
Imaging such as CT or MRI may be required if a congenital spinal abnormality is
suspected.
Treatment
Asymptomatic pits do not require treatment.
Acute abscess
If possible, repeated aspiration and antibiotics allow the disease to settle, enabling defini-
tive surgery at a later date. The fewer operations that are performed, the better. If incision
and drainage are required, the preferred approach is incisions away from the midline and
definitive treatment of the sinus once the acute infection has resolved.
Chronic abscess
This usually requires a surgical procedure, but mild chronic disease may settle if the area
can be maintained hairless by regular shaving or the use of depilatory creams. Brushing
of the pits and injection with sclerosant has been attempted with variable success.
Surgery
A variety of surgical options exists. The choices include the following.
✧ Excision and packing (healing by secondary intent: often prolonged time to
healing).
✧ Excision and midline closure (frequent wound breakdown).
✧ Pit excision and lateral drainage (‘Bascom’ procedure).
✧ Excision with asymmetric closure: aims to keep the wound out of the midline to allow
better healing and is often combined with an approach that flattens the natal cleft to
reduce recurrence.
✧ Complex plastic surgical reconstructions (including Z-plasties and myocutaneous
flaps).
Follow-up
Review within weeks after an acute episode and arrange definitive treatment as soon as
possible. If the disease is chronic, decide whether surgery is indicated.
Post-operative follow-up
Review with histology to confirm diagnosis and monitor healing. Healing can take a
long time after incision and drainage or after definitive surgery using midline wounds.
Aim to keep the area free of hair by regular shaving until and after healing occurs. The
238 GENERAL SURGERY OUTPATIENT DECISIONS

commonest complication is the chronic non-healing midline wound. This may be due
to recurrent disease, but generally is due to the problems of healing at this site. Further
lateral surgery may be indicated. For large wounds, plastic surgical procedures may be
required.
Intestinal stomas
A stoma is a surgically constructed opening of the bowel (or urinary system) on to the
skin of the abdomen. Stomas can be permanent or temporary. The aim with temporary
stomas is to restore bowel continuity at a later date. End stomas are usually permanent
and are one end of the bowel sutured to the skin. Loop stomas are usually temporary,
where a loop of bowel is brought through the abdominal wall and the anterior wall is
opened so that two orifices, proximal and distal, are visible, but only the proximal end
discharges. Over time the distal orifice may shrink so that it is barely visible. The double-
barrelled stoma is similar, except that two ends of bowel are brought out together, usually
after the segment of bowel between has been resected. Double-barrelled stomas are
usually temporary.
Ileostomies are constructed from the terminal ileum.
Complications of stomas
Many problems may arise with stomas and present to the outpatient clinic, but they can
frequently be addressed by the stomatherapists by the use of different appliances.
One of the first considerations is to determine whether the stoma is temporary or
permanent. If significant problems arise in a temporary stoma the correct management
may be to bring forward the operation to restore bowel continuity. Most centres have
experienced stoma care nurses – always involve them in the management decisions.
✧ Constipation and diarrhoea: management may depend to a certain extent on the
underlying disorder, but this can usually be treated with appropriate drugs.
✧ Prolapse of stoma: a common problem, which often occurs when an originally dilated
obstructed bowel returns to normal calibre. It is unsightly and uncomfortable but
rarely dangerous, although ulceration and ischaemic changes at the apex can occur.
If surgery is indicated it usually involves re-siting the stoma and excising redundant
bowel.
✧ Stenosis of stoma: a stoma should usually admit a gloved index finger easily. If not,
dilators can be used but are seldom a long-term solution. Surgical re-siting is usually
necessary.
✧ Skin rashes: usually due to irritation of the skin because of a failure of the bag to fit
snugly around the stoma. Occasionally it is caused by a contact dermatitis, and a change
of appliance is required. Involve the stoma nurse for advice regarding appliances.
✧ Parastomal hernia: weakness in the abdominal wall predisposes to hernia formation
and a bulge underneath the stoma. If asymptomatic, this can be treated conservatively.
If troublesome, surgical re-siting is required, but this can be a difficult procedure.
Local repair has a high incidence of recurrence, but hernias also tend to occur in the
new site and represent a generalised weakness of the abdominal wall. Laparoscopic
repair using a prosthetic mesh is a potential solution to prevent the need for relocation
of an otherwise acceptable stoma.
✧ Bleeding stoma: may be due to lesions on the edge of the mucocutaneous junction,
or lesions further up the gastrointestinal tract. Superficial granulations respond to
silver nitrate cauterisation. Unusual lesions may need biopsy, especially if the primary
surgery was for malignancy. More troublesome bleeding requires further investigation,
including proctoscopy/sigmoidoscopy or flexible endoscopy down the stoma.
Vascular
Umar Sadat and David Cooper

TEN
Vascular surgery
Vascular surgery covers the management of a large and varied number of disorders
affecting the arterial, venous and lymphatic systems. Most arterial disorders are caused
by the effect of atherosclerosis. However, some, such as Raynaud’s, are vasospastic in
nature, while others, such as thoracic outlet syndrome, result from extrinsic compression.
Arteries are also vulnerable to inflammation (vasculitis), connective tissue disorders and
chronic degeneration (fibrodysplasia). Venous disorders are also very common, ranging
from primary varicose veins to venous hypertension and ulceration. A cross-section of
the common disorders referred to a vascular clinic will be described.

General vascular assessment

Most disorders seen by vascular surgeons are arterial and the result of atherosclerosis
causing ischaemic symptoms of an end organ. However, atherosclerosis is very common.
Evidence of arterial disease may be present without this being the primary cause of
the patient’s symptoms. In particular, symptoms affecting the lower limb may be due
to musculoskeletal or neurological pathologies and not vascular disease, even though
some element of vascular dysfunction is present. Once a vascular cause is established the
nature, site and severity of the condition is assessed to determine the need and timing
for interventional treatment.
The underlying cause of ischaemic symptoms is insufficient delivery of oxygen to the
tissues, of which diseased arteries may be considered as just the final stage of a process. A
general assessment of the patient is necessary to detect other conditions that may affect
oxygen delivery such as anaemia, cardiovascular disease and/or respiratory disease.
Although the patient may have presented with symptoms specific to one body site,
if vascular disease is identified this indicates general atherosclerosis, which affects
every artery in the body. The most common causes of death of patients presenting
with intermittent claudication are myocardial infarction and stroke. It may be possible
to reduce the risk and improve the function of the peripheral vascular system by
modification of risk factors such as smoking, lipids, control of hypertension, haemostatic
and rheological variables and diabetic control.
Vascular history
A general history is taken initially, until a vascular cause becomes apparent. A vascular
history consists of specific questions related to the presenting complaint and general
questions related to general cardiovascular status, risk-factor analysis, family and drug
history and so on. Specific questions will be covered in the relevant sections; general
questions will be covered here.
Generalised atherosclerosis is an important cause of morbidity in patients undergoing
peripheral vascular interventions. Therefore, a careful assessment of the cardiac status
is important. Enquire regarding angina or previous myocardial infarction, cardiac valve
disease, dysrhythmias and heart failure.
Aspirin 75–150 mg per day has been shown to decrease the cardiovascular risk of
patients with peripheral vascular disease but must be avoided in patients with a history
of oesophagitis or peptic ulceration, due to the risk of gastrointestinal bleeding.

239
240 GENERAL SURGERY OUTPATIENT DECISIONS

Risk factors
Much can be done to improve the prognosis and symptoms of patients presenting with
peripheral vascular disease through identification and modification of cardiovascular
risk factors.
Hypertension
This is the most significant risk factor in strokes, heart failure and ischaemic heart disease.
The majority (95%) of cases of hypertension are primary (no identifiable cause), but this
is diagnosed by elimination of the uncommon secondary causes such as renal disease,
endocrine disease, coarctation of the aorta and so on.
Smoking
Smoking is associated with a four times higher risk of peripheral vascular disease (PVD).
The majority of patients with PVD will have a significant current or past smoking
history. The amount and duration of tobacco use should be determined – this is often
underestimated. Stopping smoking is the biggest single factor in improving the short- and
long-term prognosis of all patients with PVD.
Diabetes mellitus
Suffering from diabetes mellitus is associated with a three times higher risk of PVD in
men and a five times higher risk in women. Good diabetic monitoring in the form of
blood glucose levels and foot care and neuropathy are important factors in the prevention
of serious complications of PVD.
Obesity and diet
Obesity may have several effects on vascular disease. Losing weight reduces the load and
therefore the work the muscles need to perform. Obesity usually indicates an unhealthy
diet high in saturated fat and salt. Modification to a healthier diet and controlled weight
loss may improve the long-term prognosis of these patients as well as helping to improve
their current symptoms.
Serum lipids
A raised serum cholesterol increases the risk of developing PVD up to two times. Low-
density lipoprotein (LDL) transports cholesterol from the liver to the peripheral tissues.
High density lipoprotein (HDL) transports cholesterol from the peripheral tissues to the
liver. High LDL levels and/or low HDL levels are associated with an increased risk of PVD.
High serum triglyceride levels may also be associated with the development of PVD.
Haemostatic and rheological variables
Anaemia and polycythaemia may both make the symptoms of PVD worse and can be
corrected.
Family history
Premature atherosclerosis may be due to an inherited disorder of lipid metabolism.
Brothers of patients with abdominal aortic aneurysm (AAA) have a 50% chance of also
being affected and should undergo an abdominal ultrasound scan.
Drug history
Drug history can give important clues to underlying medical conditions not previously
mentioned by the patient. Also, some medications may exacerbate PVD, e.g. beta-
blockers; while other medications may need to be stopped before vascular procedures,
e.g. metformin prior to angiography.
 VASCULAR 241

Vascular examination
A general examination is performed. Examine for signs of anaemia or hyperlipidaemia.
All peripheral pulses are palpated and the volume and character of each pulse is recorded
– radial, brachial, axillary, subclavian, carotid, aortic, femoral, popliteal, dorsalis pedis
and posterior tibial. The dorsalis pedis or posterior tibial pulse may be absent in 10%
of normal individuals. The blood pressure is measured with the patient semi-reclined.
Examine for radio-radial delay and radio-femoral delay. Listen for carotid, subclavian,
aortic, iliac, femoral and popliteal artery bruits.
Examine the respiratory and cardiovascular systems. Examine the abdomen; in
particular, palpate for any AAA. Remember, the abdominal aorta bifurcates at about the
level of the umbilicus, therefore AAAs are palpated above this, iliac aneurysms below this.
Auscultate for an aortic bruit – this may indicate aortic, renal or iliac stenotic disease. A
machinery-type murmur associated with an aneurysm may indicate an aortocaval fistula,
especially if associated with swelling of the legs.
In the legs, examine for limb swelling, ulceration or the presence of varicose veins. Port-
wine stains or differing limb size may indicate underlying arteriovenous malformations.
Examine for signs of ischaemia: relative skin temperatures, venous guttering, delayed
(greater than 2 seconds) capillary return, red shiny skin on the toes or patches of
infarction/gangrene on the toes.
Perform Buerger’s test. Raise the legs and note the angle at which the soles of the feet
turn pale. After a minute hang the legs down and note the time for the feet to develop a
brick red colour and the veins to refill. A brick red colour is positive for ischaemia.
Investigation of vascular disorders
Laboratory investigations
Biochemistry
To screen for underlying renal disease, renovascular disease, diabetes mellitus.
Serum tests: include general biochemical screen, renal function, serum lipids (HDL,
LDL, very low-density lipoprotein (VLDL), triglycerides).
Haematology
Test for anaemia, polycythaemia. Look at clotting and coagulopathies.
Immunology
Test for coagulopathies, protein C, protein S deficiencies, lupus anticoagulant. Auto-
antibody screen for connective tissue disorders (CTD) and vasculitis.
Physiology/imaging techniques
Ultrasound
The predominant imaging technique used in vascular surgery is ultrasound, but there are
many different types and applications.
Continuous wave Doppler (CWD)
CWD is the simplest form of ultrasound and is ideal for use by the doctor in the out-
patient clinic to detect flow within blood vessels. The probe is the size of a pencil and
the set is the size of a typical personal stereo. In the head of the probe are a transmitter
and a receiver, which are continuously active. The probe is moved over the area where an
artery is thought to be. When blood flow is detected the typical whoosh-whoosh sound
becomes audible.
242 GENERAL SURGERY OUTPATIENT DECISIONS

Ankle-brachial pressure index (ABPI)

In health, the systolic blood pressure at the ankle should be the same or slightly higher
than that at the arm. Atherosclerosis usually affects the leg vessels and spares the arm
vessels. To measure the ankle-brachial pressure a blood pressure cuff is placed on the
upper arm and the radial pulse is detected at the wrist using the CWD. The cuff is then
inflated until the CWD signal disappears. The cuff is deflated slowly until the signal
returns and the pressure is noted. The procedure is then repeated for the lower limb,
with the cuff applied just above the ankle and the probe placed on either the dorsalis
pedis, posterior tibial and/or peroneal arteries. The pressure at which the signal returns
is compared for the arm and the leg and expressed as a ratio – the ABPI. An ABPI of
0.9–1.0 is normal. Less than 0.9 indicates vascular disease, less than 0.5 indicates severe
vascular disease.
ABPI is unreliable in the presence of incompressible arteries. In some patients the
arteries are so calcified they are incompressible by the cuff and the patient appears to have
a high ABPI because a CWD signal can always be detected at very high cuff pressures,
even in the presence of obvious vascular disease. This commonly occurs in diabetic
patients. In this instance an experienced vascular technologist may comment that the
arterial signal sounds damped, based on the subjective interpretation of the quality of
the audio signal. This can be investigated further by measurement of the toe pressure or
by using the pole test.
Resting ABPI may miss mild cases of arterial disease or not provide sufficient evidence
to convincingly exclude vascular disease in cases where symptoms may be caused by other
disorders. Mild disease can be detected by repeating the ABPI after a period of exercise
(see exercise testing).
Pole test
In some patients the arteries are so calcified they are incompressible by the cuff and
the patient appears to have a high ABPI. This can be tested by detecting the arterial
signal in the foot and then raising the foot until the signal disappears. The height at
which the signal disappears is recorded – in health the signal should never disappear.
The measurements on the pole have been calibrated so that the height in centimetres
corresponds to the mmHg, e.g. less than 50 mmHg indicates severe ischaemia.
Toe-pressures measurement
This is an alternative method in patients with incompressible arteries. A small cuff is
inflated around the big toe until the arterial signal in the digital arteries disappears.
Smaller arteries in the digits are usually not affected by calcification and provide a more
reliable toe-brachial pressure index (TBPI). TBPI less than 0.8 indicates ischaemia. Less
than 30–35 mmHg absolute pressure measurement indicates critical ischaemia.
Treadmill exercise testing
This is particularly useful in detecting mild disease or excluding vascular disease in
patients complaining of leg pain due to other pathology, e.g. arthritis. The commonest
method utilises a treadmill. The resting ABPI is measured, then the patient walks on the
treadmill at a pace of 3.5 km/h and a gradient of 10 degrees for 10 minutes or until the
symptoms prevent further exertion. The ABPI is measured immediately on stopping the
exercise. In the presence of vascular disease the ABPI falls after exercise. A normal ABPI
after exercise that has precipitated the symptoms excludes a vascular cause.
Not all patients are capable of walking on a moving treadmill, especially those unsteady
on their feet due to arthritis. An alternative method is to walk the patient along the
corridor until symptoms are produced or to use an ankle flexion/extension.
 VASCULAR 243

Ankle flexion/extension exercise testing

This is useful in patients unable to use the treadmill. The patient sits reclined and
repeatedly flexes and extends the ankle of the affected limb against a fixed resistance
device, thereby exercising the calf muscle. The ABPI is measured before and after exercise
and is interpreted in the same way as the treadmill exercise.
This technique is more sensitive than resting ABPI in detecting or excluding significant
vascular disease. It is useful for patients who are unable to walk on the treadmill. However,
the technique simulates rather than replicates the action of walking.
Colour Duplex ultrasonography
This is the combination of B-mode images and colour-coded pulsed Doppler informa-
tion. It has become the dominant non-invasive investigation in vascular practice. Acoustic
water-based gel is applied to the skin overlying the area of interest and the probe is
applied. The depth and power of the signal is adjusted until the artery is visualised.
Doppler waveforms are then sampled from different parts of the artery. Colour coding
allows high velocity signals and turbulence within the artery to be identified, indicating
the site of possible stenoses.
Diagnostic arterial angiography
Prior to the procedure the renal function is checked by measurement of serum urea, cre-
atinine and electrolytes. A creatinine less than 125 µmol/l is acceptable, at 125–300 µmol/l
stop all non-steroidal anti-inflammatory drugs (NSAIDs) and hydrate with intrave-
nous fluids both before and after the procedure to ensure a good diuresis. Greater
than 300 µmol/l requires a nephrology opinion prior to the procedure. Metformin is
associated with a risk of lactic acidosis and renal failure and is therefore stopped 48 hours
before angiography and restarted 48 hours after angiography if renal function has not
deteriorated. Anticoagulation with warfarin is stopped and converted to intravenous
heparin. Heparin is stopped four hours prior to the procedure and restarted two hours
after the procedure. Warfarin is restarted the following day if there are no bleeding
complications.
The most common portal of entry into the vascular system is the femoral artery
(3–5Fr), although the axillary (3Fr) and brachial arteries (3Fr) can also be used. Under
local anaesthesia the femoral artery is punctured using a hollow needle through which a
floppy ended wire is passed. The needle is then removed and a plastic sheath is passed over
the wire into the artery and an injection of contrast confirms the intraluminal position.
A pigtail catheter is advanced into the aorta and contrast is injected. Radiographs are
taken as the contrast is displaced through the distal vasculature, utilising arterial digital
subtraction imaging. Repeated injections are often necessary to image the full length
of both legs. At the end of the procedure the catheter is removed and direct pressure
is applied for 10–20 minutes (sometimes longer) until the bleeding stops. The patient
then remains supine on absolute bed-rest for two to four hours after the procedure and
remains in hospital overnight for observation of the puncture wound, pulse and blood
pressure and distal circulation.
The technique provides an accurate map of the arterial tree, identifying stenoses
and occlusions. Diagnostic angiography can be combined with therapeutic balloon
angioplasty/stenting for the treatment of stenoses and occlusions.
Complications include bleeding, trauma to the artery, haematoma, retroperitoneal
haematoma, false aneurysm formation, embolisation, arterial dissection, acute limb-
threatening ischaemia occasionally leading to limb loss, allergic reactions to the contrast
and exacerbation of renal failure. All patients should be fully informed of these major
complications before consenting to the procedure.
244 GENERAL SURGERY OUTPATIENT DECISIONS

Digital subtraction angiography

Digital subtraction angiography (DSA) is a computerised technique for improving the
image quality obtained at angiography. X-ray images are digitalised and the images of
soft tissue and bone are suppressed while the images of contrast within the blood vessels
are enhanced. The increased sensitivity has enabled the intravenous delivery of contrast
to image the arterial system (IV-DSA). The venous circulation is cannulated and the
cannula tip is placed in the right atrium. Contrast is then injected and digital images
are generated of the limb in question. Larger volumes of contrast are need for IV-DSA
compared to arterial DSA.
CT angiography
A computed tomography (CT) scan is performed with injection of intravenous contrast.
The technique can be used with standard CT but is more sensitive when combined with
spiral (helical) CT. Spiral CT consists of the patient moving through a continuous X-ray
field. The digital images obtained are processed to enhance the images and generate 3-D
reconstructions and superior imaging of vascular structures. CTA is useful for assessing
the anatomy of large vessels, e.g. AAA, but is less sensitive for the assessment of small
vessels.
Magnetic resonance imaging (MRI) angiograph
Either moving blood is used, as its own contrast, or contrast is given. For imaging of small
vessels additional small coils are placed over the area concerned. Improved images can be
obtained with the intravenous injection of gadolinium and T1 acquisition.
The technique is not applicable to patients with significant metal implants. Images are
still not accurate enough for small vessels.
Ascending venography
A vein in the foot is cannulated and low osmolar contrast is injected with a tourniquet
inflated at the ankle at sufficient pressure to prevent filling of the superficial veins and to
direct the contrast into the deep veins. This is an invasive technique and cannot reliably
identify reflux. Much of the information can be obtained by colour Duplex.
Descending venography
The common femoral vein is cannulated and contrast is injected. Reflux is induced by
generating a standardised Valsalva manoeuvre by the patient blowing into a manometer
device for 10 seconds with 60 degrees head-up tilt on the X-ray table. The technique was
once used to demonstrate the extent of deep and superficial venous incompetence, but it is
an invasive technique and most of the information can be obtained by colour Duplex.
Varicography
Contrast is injected directly into a varicose vein to demonstrate the distribution and
connections with the deep venous system and to identify the origin of recurrent varicose
veins. This invasive technique has been largely replaced by colour Duplex.
Contrast lymphangiography
A mixture of local anaesthetic and vital blue dye is injected subcutaneously into the first
webspace. The dye is taken up by the lymphatics and outlines the main channels in the
foot. One of these channels is cannulated and contrast is infused over a period of an hour.
Serial X-rays of the leg, groin, pelvis, abdomen and chest are taken over the first few hours,
at 24 hours or even several days later.
The technique provides anatomical detail of the lymphatics. It is useful for imaging the
thoracic duct, lymph leaks in the pelvis, abdomen, and chest, and distinguishing reactive
 VASCULAR 245

from malignant lymph nodes. It is an invasive technique, largely superseded by isotope

lymphangiography.
Isotope lymphangiography
Radio-labelled technetium colloid is injected into the second or third web space of the
toes. Gamma cameras track the progress of the marker.
This is a very specific method that can demonstrate such abnormalities as delayed
transit, presence of collaterals, dermal backflow and reduced uptake in one or more
groups of nodes.

Vascular disorders
Atherosclerotic disorders of the arteries
Atherosclerosis is the major cause of lower limb ischaemia, which is the condition
most frequently seen in vascular surgical outpatients. The overwhelming majority of
patients presenting with intermittent claudication or rest pain will be suffering from
atherosclerosis. However, there are other causes of lower limb ischaemia, especially in
younger patients, which may need to be considered. These include cystic adventitial
disease, popliteal entrapment, fibromuscular dysplasia and Buerger’s disease.
Intermittent claudication
Intermittent claudication occurs when stenosed arteries cannot supply sufficient blood
to the exercising muscles during exercise. The patient describes cramp-like symptoms
in the lower legs, most commonly the calf muscles, occurring at a predictable distance,
which is quickly relieved by rest. Once the pain is relieved the patient may then describe
the ability to walk further the second time before the pain returns. These symptoms need
to be differentiated from other causes of pain in the legs when walking, such as arthritis
or sciatica.
The decision to treat is based on the severity of the symptoms and the effect on the
patient’s lifestyle. Severity is not decided purely on the distance walked. A claudication
distance of 400 yards may be an occasional inconvenience to a retired patient but may be
job-threatening to a manual worker.
History
Take a general vascular history.
Calf claudication
This is commonly associated with femoral artery disease. A typical history of vascular
calf claudication is pain in one or both calves that occurs after walking a certain distance
and is relieved by rest. The distance tends to be constant but may be gradually getting
less over weeks and months as the disease progresses. The pain is quickly relieved by rest
(for one to two minutes).
Buttock claudication
This is commonly associated with aortoiliac disease. It is slightly different in character to
calf claudication. Patients describe more aching and weakness or complain of their hip
giving way. However, the pain is exacerbated by exercise and relieved by rest. Male patients
with bilateral aortoiliac disease may admit to impotence on questioning.
Foot claudication
This is very rare and occurs only in patients with Buerger’s disease and occlusive disease,
which affects the distal arteries first and spreads proximally. Patients describe pain and
246 GENERAL SURGERY OUTPATIENT DECISIONS

numbness that affects the forefoot with exercise. This is often diagnosed as an ortho-
paedic pain and may have progressed to persistent rest pain by the time a vascular opinion
is sought.
Other common causes of pain in the calf or leg
Arthritis
Arthritis of the knee or ankle may cause referred pain to the calf. Arthritis of the spine or
hip may produce symptoms similar to buttock claudication.
However, arthritic symptoms tend to vary in severity from day to day or with weather
conditions. The pain may occur at rest or start with exercise. The amount of exercise
necessary to produce symptoms varies and the pain may persist for hours after the
exercise stops.
Nocturnal cramp
Nocturnal cramp is pain in the calf that typically occurs in bed and wakes the patient, and
it is relieved by massage of the calf or getting out of bed and walking around.
Spinal stenosis
There is usually a history of arthritis, and the condition is caused by osteophytes nar-
rowing the spinal canal. The pain occurs on walking and is relieved by rest but especially
by bending forward. However, this pain can also be precipitated by prolonged standing.
There may be associated numbness and paraesthesia, especially around the perineum.
Chronic compartment syndrome
This often affects athletes with large calf muscles. The symptoms are similar to claudication
but a large amount of exercise is required to produce the symptoms. Popliteal entrapment
syndrome and cystic adventitial disease need excluding in young patients presenting with
claudication.
If the symptoms are typical of vascular claudication, determine the distance walked
before symptoms start. Determine how this affects the patient’s lifestyle. If the walking
distance is very small (less than 50 yards) ask about rest pain (pain in the toes at rest),
especially at night in bed.
Risk factors
Smoking, diabetes mellitus, family history, cardiac history, hypertension, high-fat diet.
Examination
Palpate all the pulses and auscultate for bruits. Look for general stigmata of vascular
insufficiency, e.g. loss of hair in the lower leg, atrophic skin and so on. Claudication is
usually but not always associated with absent pulses – pulses may be present at rest but
disappear with exercise. Try to determine the site of the arterial disease, e.g. an absent
femoral pulse suggests iliac artery disease. Perform Buerger’s test. Examine for evidence
of distal embolisation, e.g. focal spots of skin infarction in an otherwise well-perfused
foot (e.g. iliac artery disease).
Investigations
Perform a routine atherosclerotic screen – dipstick urinalysis, full blood count (FBC),
urea and electrolytes (U&Es), serum lipids and electrocardiogram (ECG). Check ankle-
brachial pressure index (less than 0.9 indicates underlying vascular disease). A treadmill
test may reveal ankle pressure drop after exercise. Colour Duplex arterial scan can identify
the site and length of stenoses/occlusions. Arteriogram identifies the site and nature of
arterial disease, and is usually combined with angioplasty treatment.
 VASCULAR 247

Treatment
Mild claudication
Where mild claudication is not interfering with the patient’s lifestyle, correct any under-
lying disorder such as hyperlipidaemia. Advise daily walks, losing weight and stopping
smoking. Improve cardiac and respiratory function.
Moderate claudication
Where moderate claudication is affecting the patient’s lifestyle but not severely so, treat
as for mild disease but review earlier and proceed to active treatment if conservative
measures fail. Some centres advocate a supervised exercise programme under the control
of a physiotherapist. Results may be comparable to angioplasty without the risk of com-
plications and they represent a non-interventional alternative.
Severe claudication
In cases severely affecting daily living, more active treatment is indicated. First choice is
angiogram and angioplasty. If the patient is not suitable for angioplasty or angioplasty fails,
consider for arterial bypass surgery (operations described under critical ischaemia).
Post-treatment follow-up
Mild claudication
Review in three months. If improved, discharge with advice. If stable or deteriorated,
decide whether a further trial of conservative treatment is indicated. This is usually the
case unless the symptoms have become severe.
Moderate claudication
Review in three months. Decide whether to continue conservative management or
whether symptoms have become severe enough to merit angioplasty.
Severe claudication
Review after angiogram/plasty. Decide whether further angioplasty or surgical intervention
is indicated.
Post-operative follow-up
Review after four to six weeks to determine the success of the procedure and detect any
complications. Angioplasties for critical ischaemia have a re-occlusion rate of up to
40% in the first six months, but may have remained patent long enough to allow ulcer
healing. A recurrence of severe symptoms or critical ischaemia requires urgent Duplex
reassessment and reangioplasty or bypass if necessary. Complications include groin
haematoma and false aneurysm formation. Both can be assessed by Duplex.
The post-operative follow-up of surgical procedures is described under critical
ischaemia.
Critical ischaemia, rest pain, gangrene
Ischaemic rest pain occurs when not enough blood is reaching the foot to maintain the
integrity of the foot even at rest. The pain starts at that part of the lower limb furthest
away from the heart, i.e. the tip of the big toe, and spreads proximally. If ischaemia is
not reversed then dry gangrene ensues. Gangrene also occurs when a small injury occurs
in a critically ischaemic foot. Healing tissue requires up to 10 times the blood supply
of normal tissue in order to heal. If this increase in blood supply does not occur then
the tissue dies back to the point of adequate blood supply. In this way a small wound
sustained to the tip of the big toe of a critically ischaemic foot can result in the whole leg
turning gangrenous.
248 GENERAL SURGERY OUTPATIENT DECISIONS

Ischaemic rest pain needs to be differentiated from other causes of pain in the foot
at rest, e.g. arthritis of the toes or metatarsophalangeal joints. The site of the pain is
important – it is very unusual for ischaemic rest pain to occur in the ankle without also
affecting the toes.
History
Take a general and vascular history. Rest pain may first start at night when the foot is
lifted on to the bed thereby losing the help of gravity to supply blood to the foot. Patients
may describe attaining relief from the pain by dangling the foot over the side of the bed.
Eventually, even with the leg dependent there is still not enough blood supply and the foot
is painful all the time. Pain starts at the point furthest away from the heart and spreads
proximally.
Other causes of constant lower limb pain
Embolisation
Distal embolisation (from an aortic or iliac lesion) may result in rest pain affecting the
toes, but the foot appears well perfused and foot pulses may be palpable.
Arthritis
Arthritis also causes pain in the foot or ankle at rest, but tends to be localised to the
joints or areas proximal to the toes. Metatarsalgia can occur at night and is relieved by
standing, and can be confused with vascular night pain. However, metatarsalgia tends
to run a fluctuating course, causing symptoms for several days or weeks with similar
asymptomatic periods. Confusion can occur when the two conditions co-exist.
Painful peripheral neuritis
This condition tends to occur in diabetics and is characterised by a constant burning pain
affecting both lower legs. The pain is worse at night when the legs become warm.
Reflex sympathetic dystrophy
This produces a burning pain similar to painful peripheral neuritis. The condition is
ill-defined but there may be a history of preceding trauma that may be relatively minor.
The limb becomes swollen and is initially warm and dry but later becomes cool, mottled
and cyanotic. However, the arterial tree is normal.
Causalgia
This results from incomplete nerve injury and produces a similar constant burning
pain.
Examination
Palpate all the pulses and listen for bruits. Look for signs of peripheral ischaemia – loss of
hair, thin shiny skin or atrophic musculature. The foot may be oedematous from chronic
dependency. Note that a critically ischaemic foot may actually appear erythematous
with good capillary return. This appearance may prompt doctors to think that the
foot is infected, when in fact the appearance is due to an inflammatory reaction to the
underlying ischaemia. The appearance is similar to a positive Buerger’s test.
Investigations
Peform a routine atherosclerotic screen of urinalysis and blood tests. Plain X-rays may
be indicated if joint disease is suspected. On the ankle-brachial pressure index, a ratio of
less than 0.9 indicates peripheral vascular disease; a ratio of less than 0.5 indicates severe
ischaemia. Peripheral disease may exist in the presence of apparently normal ABPI, due
 VASCULAR 249

to incompressible arteries. Colour Duplex scan of the leg arteries is a very useful non-
invasive technique that is very reliable in identifying stenoses/occlusions when performed
by an experienced operator. Diagnostic angiography may be combined with therapeutic
angioplasty if this is appropriate for the lesion and the patient.
Treatment
It is usually too late for conservative therapy and some form of active intervention is indi-
cated. Patients usually require admission for adequate pain relief, elevation of the limb
to reduce tissue oedema and intravenous antibiotics if indicated. Improve cardiac and
respiratory function. Different hospitals vary in their criteria for angioplasty or opera-
tive treatment. In unfit patients who would be high risk for a long surgical procedure,
angioplasty is preferred if the lesion is suitable.
Operative treatment
Treatment depends on the site of the disease. As a general rule the most proximal lesion
is corrected first, and ischaemic skin lesions have the best chance of healing if there is a
continuous channel of blood into the pedal arch. Many different operations are available.
Only the commonly performed procedures will be described.
Aortobifemoral bypass
Occlusive disease of the iliac arteries can be bypassed using a prosthetic bifurcated graft
from the aorta to both femoral arteries. The patient must be fit enough to withstand
clamping of the aorta. In unfit individuals an axillobifemoral graft is a less invasive
alternative. It is unusual for gangrene or rest pain to be associated with aortoiliac
occlusions alone.
Femoropopliteal bypass
Occlusive disease of the superficial femoral artery can be bypassed by using either a
prosthetic graft or the patient’s own vein. Vein has the better long-term patency but
prosthetic graft to the above knee popliteal artery is acceptable, and patency of prosthetic
grafts to the below popliteal artery is improved when a cuff of vein (Miller cuff) is
interposed between the graft and the artery.
Femorodistal bypass
Bypass operations performed to the distal run-off vessels (posterior tibial, anterior
tibial and peroneal) require autologous vein to be used to obtain reasonable long-term
patency.
Chemical lumbar sympathectomy
This procedure is reserved for trying to achieve skin healing in very unfit individuals with
extensive distal disease for whom neither angioplasty nor bypass is possible.
Follow-up
Investigations and treatment need to be performed and reviewed within days or weeks,
depending on the severity. In the case of tissue loss or gangrene, admission to hospital
for in-patient assessment is justified.
Post-operative follow-up
When angioplasty and/or arterial bypass operations have been performed for critical
ischaemia, long-term regular follow-up is indicated to detect recurrence, progression of
disease or complications developing in the graft.
250 GENERAL SURGERY OUTPATIENT DECISIONS

Vein-graft surveillance
When autologous vein has been used to bypass occlusions in the leg arteries, many
hospitals follow patients with regular Duplex ultrasound scans of the vein to detect sub-
clinical stenoses rather than requiring regular attendance at clinic. Significant vein-graft
stenoses are treated by urgent angioplasty or operative vein patch angioplasty. Patients
are advised to seek urgent medical attention if the leg turns white, cold, numb or painful
between scans, as the graft may have occluded and may be salvaged if operated on soon
enough. Surveillance is performed on all patients for the first year and extended for a
second year for grafts that are considered at risk. Thereafter patients are reviewed in
the outpatient department (OPD) with Duplex scans at 6–12 months and discharged if
symptom-free.
Complications
Complications include wound infections. Superficial infections should be treated aggres-
sively with antibiotics and weekly review. Deeper infections may require in-patient
treatment and intravenous antibiotics, especially if prosthetic grafts have been used.
If the wound near an anastomosis becomes infected or opens up, in-patient therapy is
mandatory as there is a real risk of secondary haemorrhage.
Wound haematomas and lymph collections can be managed conservatively provided
they do not become infected. Limb swelling is normal after arterial bypass surgery and
can be treated conservatively if deep-venous thrombosis (DVT) and cellulitis have been
excluded.
Cystic adventitial disease
Cystic adventitial disease (CAD) is an uncommon cause of lower limb ischaemia in
younger patients. The adventitia of the popliteal artery undergoes a degenerative process
and develops a cyst. When the pressure of the contents of the cyst exceeds arterial
pressure, the cyst may compress the artery, causing sudden-onset ischaemia.
The differential diagnosis includes popliteal aneurysm, popliteal entrapment and
simple knee joint cysts. Exclude cardiac source for emboli, vasculitis and/or CTD.
History
Patients are usually young males and complain of claudication of recent onset. Symptoms
may be severe due to the lack of collateral development. Patients may describe ischaemic
neuropathy symptoms of burning, paraesthesia and cold.
Examination
There is usually a lack of atherosclerotic signs in other body sites. All pulses in the affected
limb may be present at rest but foot pulses disappear on flexion of the knee. Palpation of
the affected artery may simulate a popliteal aneurysm. A popliteal bruit may be audible.
Later, if occlusion of the popliteal artery occurs, pulses are lost.
Investigations
Colour Duplex may demonstrate the compression of the artery and also identify the
cyst and exclude a popliteal aneurysm. CT and MRI scans may better define the lesion in
relation to other anatomical structures. Arteriography demonstrates a smooth localised
stenosis behind the knee.
Treatment
Angioplasty tends not to be successful, because the walls are compliant and cyst content
may embolise distally. Aspiration of cysts under CT scan control can be attempted but
lesions tend to recur. Surgical evacuation of the cyst is effective treatment if the artery
 VASCULAR 251

has not progressed to occlusion, when resection and interposition vein graft repair is
required.
Follow-up
Review with results of investigations to confirm diagnosis.
Post-operative follow-up
Review after four to six weeks to confirm the success of the procedure. If aspiration has
been performed, medium-term follow-up may be required to detect recurrence. Follow-
up of bypass procedures is described under critical ischaemia.
Popliteal entrapment syndrome
Popliteal entrapment is an uncommon disorder but should be excluded in all young
patients complaining of lower limb ischaemia. Its most common form is caused by
compression of the artery by the medial head of the gastrocnemius muscle. Other forms
are caused by abnormal strips of muscle or fibrous bands. Exclude cardiac emboli,
vasculitis and/or CTD.
History
Most patients are young and active and describe typical symptoms of claudication associ-
ated with physical exercise. Patients may describe atypical features such as numbness of the
foot, blanching, paraesthesia or pain on walking but not running. Enquire regarding cardiac
abnormalities and arrythmias or possible vasculitic pathologies, CTD and the like.
Examination
Exclude cardiac or other sources of embolisation. There is usually a lack of atherosclerosis
affecting other arteries. Pulses may be palpable at rest but disappear on dorsiflexion or
forced plantar flexion of the foot. Later cases may have absent pulses due to popliteal
occlusion. Alternatively, some patients may have post-stenotic aneurysmal degeneration
of the popliteal artery.
Investigations
Perform FBC, plasma viscosity/erythrocyte sedimentation rate (PV/ESR) and autoantibody
screen to investigate haematological or vasculitic causes. Consider echocardiogram to
exclude cardiac source of emboli. Duplex ultrasound may demonstrate compression of
the artery and identify aneurysmal dilatation. MRI scanning is being increasingly used
to identify the soft tissue abnormalities in this condition. Angiography is used to confirm
the diagnosis and exclude any arterial abnormality. In cases of occlusion, angiography
defines the distal run-off vessels.
Treatment
All confirmed cases are treated surgically, with release of the constricting band or muscle
and reconstruction of the artery if necessary.
Follow-up
Review with results (at one to three months), confirm diagnosis and plan treatment.
Popliteal entrapment tends to be bilateral and symptoms may develop in the other limb
with time.
Post-operative follow-up
Review to determine the success of the procedure and detect any complications. If a vein
interposition graft has been used, the regular vein graft surveillance is appropriate to
detect stenoses and prevent occlusion.
252 GENERAL SURGERY OUTPATIENT DECISIONS

Carotid artery disease

The most common carotid conditions are transient ischaemic attacks (TIA) and strokes
caused by carotid artery stenotic disease. Data from a number of randomised trials have
identified that patients with embolic neurological symptoms originating from significant
stenosis of the internal carotid artery benefit from carotid endarterectomy compared to
medical therapy alone.
Carotid disease is primarily an embolic disease and the degree of stenosis is only an
indirect marker of the severity of the atheroma. Increasingly, patients are assessed in TIA
clinics by a multidisciplinary team consisting of a vascular surgeon, neurologist or stroke
physician and a radiologist. Patients have their symptoms assessed, their arteries scanned
and treatment arranged at the one visit. The medical opinion is particularly useful for
patients with non-specific or non-hemispheric conditions, for which the differential
diagnosis includes epilepsy, brain tumours, hypoglycaemia, migraine, cardiac arrythmias
and vertebrobasilar ischaemia.
Other rare causes of stroke include systemic lupus erythematosus (SLE), polyarteritis
nodosa (PAN), giant cell arteritis, migraine, brain tumours and fibromuscular dysplasia
(FMD).
History
The classic embolic neurological event is the transient ischaemic attack (TIA). A TIA
is a mini stroke (e.g. limb weakness, speech defects, facial weakness) which recovers
completely within 24 hours. The symptoms affect the limbs on the opposite side to
the stenosed artery. Amaurosis fugax (fleeting blindness) occurs when an embolus
temporarily occludes the main stem or branch of the retinal artery causing temporary
blindness. Amaurosis fugax consists of transient monocular blindness that occurs on the
same side as the stenosed artery. All or part of the visual field may be lost, but usually
the embolus breaks up and vision returns. Occasionally, loss of vision is permanent and
complete (central retinal artery occlusion).
Patients with residual motor or visual defects may still be considered for endarterec-
tomy if they have a good quality of life and/or if a further stroke would threaten their
independence.
Non-specific or non-hemispheric symptoms such as blackouts, drop attacks, fainting,
dizziness, double vision or vertigo are more suggestive of cardiac, neurological or ear, nose
and throat (ENT) disease, and further investigation or referral to the relevant speciality
should be considered. However, some of these symptoms may indicate vertebrobasilar
ischaemia (VBI), which may have a primary vascular cause, and this should be excluded
(see VBI section).
Examination
Perform a general and vascular examination. Listen for bruits over the carotid and
subclavian arteries. Note that the absence of a carotid bruit does not exclude the presence
of a severely stenosed carotid artery. Perform a general neurological examination and
record any existing neurological deficits. Perform a cardiac examination. In particular
examine for arrythmias, valve abnormalities and heart failure.
Investigations
Colour Duplex ultrasonography can determine the degree of stenosis and is reliable
when performed by an experienced operator. Carotid angiogram is useful to confirm
total carotid artery occlusion, which may be difficult to diagnose on colour Duplex, or
to identify aortic arch, brachiocephalic or subclavian artery disease. Computed tomog-
raphy angiography/magnetic resonance angiogram (CTA/MRA) scans are less invasive
 VASCULAR 253

alternatives to carotid angiography. CT/MRI brain scans may be indicated to exclude

neurological disease.
Treatment
All patients should receive the best medical therapy – aspirin, anti-hypertensives and
lipid-lowering agents.
Symptomatic carotid stenosis
Male patients with carotid stenosis greater than 50% benefit from early surgery. Females
benefit if stenosis is greater than 70%.
Asymptomatic carotid stenosis
Fit male patients under the age of 75 with carotid stenosis greater than 50–60% benefit
from surgery. Female patients (and males over the age of 75) may benefit depending on
co-morbidities and low surgical morbidity/mortality rates.
Follow-up
Investigations need to be performed and reviewed as soon as possible. For those patients
confirmed to have a severe symptomatic carotid stenosis, carotid endarterectomy is
most effective within two days of the onset of symptoms. In those patients with mild/
moderate carotid stenoses, best medical therapy should be instituted and the patient
reviewed either in the surgical or medical clinic to monitor effectiveness. For patients in
whom carotid artery disease is excluded, consider referral for neurology, cardiac, ENT or
ophthalmological opinion as indicated by the results of the assessment performed.
Post-operative follow-up
Patients are seen four to six weeks after operation to check on local complications related
to the wound. In some centres a further Duplex scan is performed on the operated artery
to identify restenosis or asymptomatic occlusion. Restenosis is usually due to intimal
hyperplasia, which does not cause embolic symptoms. Other complications following
CEA include cranial nerve lesions, infection (superficial and deep) and false aneurysm.
Transient cranial lesions occur in up to a third of patients and usually resolve within
12 months. Superficial infection is treated aggressively with antibiotics, especially if
prosthetic patch angioplasty was performed, and most resolve. Persistent and deep
infections may require admission and intravenous antibiotics and repeated Duplex
scanning to confirm the integrity of the patch angioplasty. There is a risk of potentially
fatal secondary haemorrhage.
Vertebrobasilar ischaemia (VBI)
The symptoms of vertebrobasilar ischaemia are less common than those of carotid
ischaemia, and the criteria for surgical treatment are less well defined. Symptoms of VBI
may be embolic or haemodynamic and arise from disease of the vertebral artery itself
or from the subclavian artery proximal to the origin of the vertebral artery. The cause of
symptoms may not be primarily vascular, e.g. the vertebral arteries may be compressed
by osteophytes associated with cervical spondylosis. Other neurological pathologies,
orthostatic hypotension, cardiac arrhythmias, ENT and other non-vascular causes may
need to be excluded.
History
Determine exactly the circumstances when symptoms occur, e.g. head turning. This may
indicate the non-vascular causes outlined in the introduction.
254 GENERAL SURGERY OUTPATIENT DECISIONS

Vertebrobasilar symptoms (TIAs)

At least three of the following symptoms occurring simultaneously are required for
diagnosis of vertebrobasilar syndrome (isolated symptoms are less significant): unilateral
or bilateral simultaneous motor/sensory deficits, ataxia, diplopia, dysarthria, dysphagia,
bilateral homonymous hemianopia, vertigo, tinnitus, transient global amnesia. Drop
attacks or loss of consciousness may be the result of embolisation, or, if they coincide
with vigorous use of the arm, represent the subclavian steal syndrome. Enquire regarding
other neurological, ENT or cardiac pathologies.
Examination
Listen for supraclavicular and carotid bruits. Examine the neck for tenderness and range
of movement. Examine the arms for evidence of upper limb ischaemia. Examine for
cardiac abnormalities.
Investigations
Colour Duplex of the carotid subclavian and vertebral arteries is sensitive enough to
detect significant disease. Definitive identification of lesions requires angiography. CT
brain scan may be required to exclude brain tumours producing similar symptoms. 24-
hour ECG may be required to investigate cardiac arrythmias.
Treatment
Embolic symptoms are treated initially with correction of vascular risk factors and low-
dose aspirin. If this does not work, anticoagulation may be necessary. For haemodynamic
lesions, angioplasty of subclavian stenoses/occlusions may be undertaken.
Indications for surgery include severe (greater than 70%) stenoses of the vertebral
artery, short occlusions of both vertebral artery origins or stenosis of one remaining
or dominant artery causing symptoms. Surgical reconstruction of the vertebral artery
is a specialised technique performed mainly for recognised embolic or haemodynamic
disease and consists of carotid to vertebral artery bypass or transposition of the vertebral
artery to the carotid.
Follow-up
Review within short intervals (1–6 weeks) with results of investigations until diagnosis is
made. Decisions regarding treatment are made and patients are reviewed to confirm the
effectiveness of the various therapies. Patients are discharged once serious causes have
been excluded or symptoms have stabilised. Neurology, ENT or cardiac referrals may be
indicated.
Post-operative follow-up
Review to determine the success of the procedure and detect any complications, e.g. graft
occlusion and/or recurrence of symptoms.
Carotid artery aneurysm
Carotid artery aneurysm is rare, but more frequently affects the common carotid artery
than the internal or external carotid arteries. Causes include atherosclerosis, trauma,
mycotic and fibromuscular dysplasia (FMD). Most aneurysms are fusiform rather than
saccular.
Differential diagnosis includes tortuous carotid artery, carotid body tumour, lymph
nodes overlying the artery, branchial cyst and cystic hygroma.
History
Most patients present because they have noticed a pulsatile swelling in the neck. Most are
asymptomatic, but some present with carotid territory TIAs or stroke. High aneurysms
 VASCULAR 255

of the internal carotid artery can cause symptoms due to cranial nerve neuropraxia, e.g.
dysphagia, hoarse voice, facial pain. There may be a history of trauma or of an infective
episode suggesting possible mycotic aneurysm.
Examination
Common carotid artery (CCA) aneurysms present with a pulsatile swelling at the angle
of the jaw; internal carotid artery (ICA) aneurysms present as a swelling in the posterior
pharynx. Bruits may be audible. Perform a neurological examination and examine for
cranial nerve lesions.
Investigations
Colour Duplex scan will usually confirm or exclude the diagnosis. Alternatively,
angiography can be used. In difficult cases or where surgery is considered, a CT/MRI
scan of the neck is useful to define the relation of the aneurysm to other structures.
Treatment
Most aneurysms require surgical repair. Fusiform aneurysms require excision and
vein graft bypass. Saccular aneurysms can be treated by aneurysmectomy and patch
angioplasty. Very high aneurysms at the skull base can be treated by endovascular
embolisation after test occlusion or other investigations have confirmed adequate
collateral flow around the circle of Willis.
Follow-up
Patients should be reviewed quickly with results (within one to four weeks) to confirm
or exclude the diagnosis. The majority of pulsatile lumps turn out to be a prominent
or tortuous but otherwise normal carotid artery and the patient can be reassured and
discharged. In very tortuous arteries investigate for FMD, especially if the patient is also
hypertensive (see renal artery stenosis section). Confirmed carotid aneurysms require
prompt treatment. Other causes are managed appropriately.
Post-operative follow-up
Review to confirm the success of the operation and to detect complications. The com-
plications are the same as for carotid endarterectomy. Patients can be discharged once
healed and symptom-free.
Carotid body tumour (CBT)
The carotid body is derived from neural crest cells of the third branchial arch and is
located behind and between the internal and external carotid arteries. The correct term
for a tumour of this gland is a paraganglioma. When these occur, 5% are bilateral and
10% are malignant. Although not strictly a vascular condition, these lesions are often
referred to vascular surgeons because treatment sometimes requires reconstruction of the
carotid arteries. Some rare cases may be associated with phaeochromocytoma.
Differential diagnosis includes carotid artery aneurysm, lymph node mass, branchial
cyst and cystic hygroma.
History
Patients commonly present because they have noticed a pulsatile swelling in the neck.
Other symptoms include headache, neck pain, dizziness, hoarse voice and dysphagia
caused by local invasion or cranial nerve compression. CBTs seldom cause cerebral
ischaemia, but occasional symptoms of flushing, dizziness, arrythmias and hypertension
are caused by neuroendocrine secretion by the tumour.
256 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
A mass in the neck may be palpable. This mass may feel pulsatile because of its close
proximity to the carotid arteries but, unlike an aneurysm, is not expansile. Classically
these tumours can be moved from side to side but not up or down. Perform a
neurological examination, looking for cranial nerve lesions (IX, X, XI, XII). An indirect
laryngoscopy may be required. Occasionally there may be a Horner’s syndrome. Examine
for neuroendocrine effects.
Investigations
Growth of the tumour tends to splay the carotid bifurcation, which can be detected by
colour Duplex or angiography. The blood supply from the external carotid artery (ECA)
and the very vascular nature of these tumours may also be demonstrated. A CT/MRI scan
may be useful to define the relation of the tumour to other structures, to define its extent
and to exclude bilateral disease. The Shamblin classification grades these tumours from
I to III based on size, site and degree of difficulty. Grade III may require resection of ECA
or ICA and vein graft repair.
Treatment
Tumours require surgical excision and sometimes carotid artery reconstruction. Some
centres recommend pre-operative embolisation of the blood supply of the tumour to
reduce vascularity.
Follow-up
Patients should be reviewed quickly with results (within one to four weeks) to con-
firm or exclude the diagnosis. The majority of pulsatile lumps turn out to be a
prominent or tortuous but otherwise normal carotid artery, and the patient can be
reassured and discharged. Confirmed CBTs require prompt treatment. Other causes
are managed appropriately. Exclude phaeochromocytoma in hypertensives (urinary
catecholamines).
Post-operative follow-up
Review with histology to confirm complete excision and exclude malignancy. Malignant
lesions require oncology referral and long-term follow-up. The complications of operation
are the same as for carotid endarterectomy. Patients can be discharged if unilateral benign
disease is confirmed, wounds have healed and the patient is symptom-free.

Inflammatory (vasculitic) disorders of the arteries

Vasculitis is the term used to describe a group of conditions characterised by inflammation
of the blood vessel wall. Vasculitis tends to present to the vascular surgeon as skin
ischaemia of the lower limbs, which mimics large vessel disease or embolic phenomena.
Suspicion is raised by finding a raised ESR, PV or C-reactive protein, and screening for
autoantibodies is performed. However, arterial biopsy is required for a diagnosis in most
cases and should be considered in all suspicious cases unless tissues are too ischaemic to
support wound healing.
Buerger’s disease (thromboangiitis obliterans)
This uncommon disorder can affect all races but is more common in the Middle and
Far East. It occurs only in smokers and predominantly affects men, although women are
increasingly affected. Buerger’s is an inflammatory occlusive disease involving muscular
medium-sized arteries of the extremities, which produces a granulomatous reaction with
giant cells within the thrombus. Later the occluded artery becomes contracted, with the
 VASCULAR 257

artery and vein bound tightly together by fibrous tissue. The disease affects the very distal
arteries first and progresses proximally.
History
Smoking history is positive. Foot claudication is the characteristic symptom caused by
involvement of the foot arteries. Calf claudication can occur with infrapopliteal disease.
The majority of patients are male and most have three to four limbs affected. It is very
rare to have a single limb affected, although upper limb symptoms may predominate and
resemble Raynaud’s. Initial symptoms include coldness, paraesthesia, skin colour changes,
skin lesions, rest pain and intermittent claudication. Note – gangrene and ulceration may
precede claudication.
Examination
Perform a general and vascular examination. Affected digits are purplish red, cold and
damp. Venous filling in the foot is very slow. Gangrene and ulceration may be present.
Proximal pulses are normal. In the acute phase there may be redness and tenderness of the
skin over the affected vein/artery. There may be phlebitis migrans. There may be evidence
of an underlying CTD in women.
Investigations
Perform a general atherosclerotic screen and PV/ESR and autoantibody screen. If tobacco
is denied, measure cotinine levels in the urine (greater than 50 ng/ml indicates smoking).
ABPI ankle pressures may be normal in the presence of disease affecting foot arteries
only – compare ankle and toe pressures.
Arteriography tends to be diagnostic, showing multiple segmental occlusions of distal
extremity arteries. Occlusions may be tapered or abrupt, with extensive reticular collat-
erals around each occlusion (corkscrew collaterals). The arterial walls are smooth, not
irregular as in atherosclerosis. Biopsy of the artery provides a histological diagnosis.
Treatment
Correct positive risk factors. Advise stopping smoking and walking training for foot
claudication to develop collaterals. To heal ulcers, intra-arterial prostaglandin E1 (PGE1)
or prostacyclin (PGI2) infusions may be effective, as may sympathectomy. Hyperbaric
oxygen therapy has also been proposed. Epidural analgesia for short periods (1–2 weeks)
may be useful to allow pain-free time for healing to occur. Transcutaneous electric nerve
stimulation (TENS) is an alternative for long-term analgesia. Surgical debridement and
amputations are performed as appropriate.
Follow-up
Follow-up depends on severity and patient behaviour. If the patient stops smoking and
the condition is mild, it tends to stabilise. Review at regular intervals (1–3 months) and
discharge once stable. More severe cases need to be reviewed at shorter intervals to detect
the need for in-patient therapy.
Post-operative follow-up
Review to determine the success of procedures. This usually consists of ensuring the
healing of amputation sites.
Takayasu’s disease (non-specific aorto-arteritis)
Takayasu’s disease is an arteritis mainly affecting the aorta and its branches, causing
segmental stenosis, occlusion, dilatation and aneurysm formation. It occurs all over
the world, but is commonest in females from the Far East, usually under the age of 40.
However, it can affect people of any age. Lesions are characterised by intimal proliferation
258 GENERAL SURGERY OUTPATIENT DECISIONS

and fibrosis of the medial and adventitial layers. Active lesions have a lymphoplastic
infiltrate, Langhans and foreign body giant cells.
In the acute phase patients complain of non-specific fever, myalgia, arthralgia, weight
loss and pain over the arteries. Pulses are present, blood pressure is elevated and there
are bruits and early ischaemia.
In the late phase inflammation has settled, pulses are absent and symptoms of vascular
insufficiency predominate.
✧ Type I affects the aortic arch.
✧ Type II affects the descending and abdominal aorta.
✧ Type III combines types I and II.
✧ Type IV is type II and pulmonary artery disease.

The most commonly affected vessels are subclavian, descending aorta, renal, carotid,
mesenteric, ascending aorta and abdominal aorta.
History
General symptoms include dizziness, syncope, claudication, angina, stroke, myocardial
infarction (MI) and upper or lower limb ischaemia, depending on which arteries are
affected.
Examination
Pulses may be absent, especially the carotid and upper limbs. Hypertension may be
present secondary to renal artery stenosis or coarctation of the aorta. This may result in
congestive cardiac failure due to hypertension, aortic insufficiency or coronary ischaemia.
Erythema nodosum and pyoderma gangrenosum may be present and associated with
juvenile rheumatoid arthritis, sarcoid and inflammatory bowel disease.
Investigations
In the acute phase FBC may show anaemia and a leucocytosis, and the ESR is raised. An
autoantibody screen should be performed to exclude CTD. Angiography is diagnostic
and may show either variable lengths of narrowing of the aorta and other arteries pro-
gressing to segmental occlusion or arterial dilatation and fusiform and saccular aneurysm
formation – or a combination of the two (the majority).
Treatment
Treat with long-term steroids, cyclophosphamide or methotrexate. Angioplasty is useful
in the chronic stage, especially for renal artery stenosis.
Surgery should be avoided in the acute phase if possible. Bypass from and to arteries
free of disease on angiography. Endarterectomy is seldom possible. Therefore carotid and
vertebral disease is treated by bypass procedures taken from the ascending aorta.
Aneurysms are resected in younger patients.
Follow-up
Joint care with relevant physicians. All patients require long-term follow-up. The condition
is monitored using serial Duplex scanning, angiography or MRI angiography.
Post-operative follow-up
Routine post-arterial surgery follow-up depending on procedure performed.
Polyarteritis nodosa
PAN is a systemic necrotising vasculitis affecting small and medium-sized muscular
arteries. It is associated with hepatitis B and most frequently diagnosed in men between
 VASCULAR 259

the ages of 40 and 60, although any age can be affected. Damage to the blood vessel wall
can result in aneurysm formation.
History
Symptoms depend on the artery affected. General symptoms include malaise, abdominal
pain, weight loss, fever and myalgia. Gastrointestinal involvement is common and
manifests as abdominal pain, nausea and vomiting. This can proceed to bowel perforation
and haemorrhage.
Examination
Perform a general and vascular examination. Hypertension is a frequent finding due to
renal artery involvement. Skin manifestations include nailfold infarcts, palpable purpura,
and livedo reticularis. Aneurysm may be palpable. Mononeuritis multiplex commonly
occurs, and other important sites to examine are the testes and retina.
Investigations
Urinalysis may reveal proteinuria with renal failure developing in two-thirds of patients.
A FBC may reveal anaemia and the ESR may be elevated. Antineutrophil cytoplasmic
antibody (ANCA) may be raised. Hepatitis B surface antigen and antibody should be
determined in all patients.
Angiography shows the characteristic findings of saccular or fusiform aneurysms
and arterial narrowing. Arterial biopsy may reveal a vasculitis, which is diagnostic when
combined with the angiographic appearance.
Treatment
Treat with corticosteroids with cyclophosphamide if control is difficult. Angioplasty may
be useful once the acute disease has settled.
Post-treatment follow-up
Follow up at regular intervals by relevant physician to determine the course of the disease.
Long-term follow-up is required to detect late arterial complications.
Wegener’s granulomatosis
This is a systemic necrotising vasculitis which preferentially affects the upper respiratory
tract, lungs and kidneys. Cutaneous manifestations include cutaneous ulceration,
subcutaneous nodules and palpable purpura.
Investigations include sinus radiographs or CT scans, which show mucosal thickening
and sinus opacification of air-fluid levels, and the CXR is abnormal. Diagnosis is made
through biopsy. Elevated c-ANCA levels are associated with Wegener’s. Treatment is with
immunosuppressant therapy and follow-up by relevant physicians.
Giant cell arteritis
This is a systemic granulomatous vasculitis that affects large and medium-sized blood
vessels, commonly the cranial branches of the aorta and in particular the ophthalmic
artery, causing sudden blindness. It occurs mainly in the over-fifties and is three to five
times more common in women.
History
Fever, weight loss and fatigue may be the earliest symptoms, but these are often missed.
Classically, patients present with severe headache. Jaw claudication is described in over
half of patients, due to facial/maxillary artery involvement. Once blindness is complete
it is permanent, but amaurosis fugax is reversible with steroid treatment.
260 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
Perform a general and vascular examination. Tenderness of the scalp over the superficial
temporal artery region may be elicited. Examine for disease of the carotid, vertebral and
subclavian arteries.
Investigations
Diagnosis is usually based on the clinical findings, a raised ESR (positive in 80%) and
positive granulomatous histology from a temporal artery biopsy (negative in 50% due to
skip pattern). Therefore, a negative biopsy in the presence of a strong clinical suspicion
should still be treated with steroids. Exclude other causes of amaurosis fugax, e.g. Duplex
of carotid arteries.
Treatment
High-dose steroids initially, gradually tailing down to a maintenance dose.
Post-treatment follow-up
Usually by physicians, with patients referred to vascular surgeons to perform the temporal
artery biopsy.
Post-operative follow-up
Review with histology and confirm wound healing. Refer to relevant speciality for further
management.
Cutaneous vasculitis
This typically occurs in the post-capillary venules, although capillaries and arterioles
are also involved. Most patients have a single episode that is self-limiting and requires
no special treatment. Patients with severe or recurrent episodes are investigated by skin
biopsy and treated with steroids.
Idiopathic cutaneous vasculitis
This is the most common form. It produces symmetrical palpable purpura typically
affecting the lower leg. Lesions occur in crops, appearing as a macular erythema
progressing to purpura. The condition is distinguished from urticaria because lesions
last longer than 24 hours. Biopsy of lesions shows leucocytoclastic vasculitis with
endothelial swelling, often necrosis, haemorrhage, fibrin deposition and infiltration with
polymorphonuclear neutrophils.
Necrotising vasculitis
This form is associated with infections, drugs or CTD. Infections are often viruses affecting
the upper respiratory tract, e.g. Henoch-Schönlein purpura. The commonest drugs are
penicillin and sulphonamides. Diuretics and NSAIDs can also cause it. Histology shows
a leucocytoclastic vasculitis.
Cutaneous vasculitis as a manifestation of systemic disease
The most common disease is SLE. Other diseases are Churg-Straus and Behçet’s
disease.

Non-atherosclerotic, non-inflammatory disorders of the arteries

Arterial fibrodysplasias
Fibrodysplasia describes a group of disorders of unknown aetiology that are neither
inflammatory nor atherosclerotic, and which result in stenoses, occlusions and aneurysms.
 VASCULAR 261

Variations of the disorders include intimal fibroplasia, medial hyperplasia, medial fibro-
plasia and perimedial dysplasia. The most important of these conditions is renal artery
fibrodysplasia, which affects 0.5% of the population and is the second most common
surgically correctable cause of hypertension.
The pathogenesis is unclear, but the underlying cause may represent mural ischaemia
from inadequate vaso-vasorum blood flow.
Intimal fibrodysplasia
Primary intimal fibrodysplasia presents in children and young adults as a focal smooth
stenosis or web in otherwise normal arteries and may represent residual or persistent
neonatal intimal cushions.
Medial hyperplasia
This is hyperplasia of the media causing a stenosis but without accompanying fibrosis.
This is rare, affects mainly females, age range 40–50s, and presents as a focal stenosis in
the main renal artery.
Medial fibroplasia
This represents 85% of dysplastic renovascular disease. Two forms are recognised:
peripheral, which is confined to outer media; and diffuse, which affects the whole media.
It tends to progress from the periphery. Compact fibrous tissue replaces smooth muscle
and ground substance. Adventitial tissues are not involved but the internal elastic lamina
fragments.
Perimedial dysplasia
Perimedial dysplasia represents 10% of renal artery dysplasias and may co-exist with
medial fibrodysplasia. It produces focal or multiple stenoses of the main artery but
without aneurysmal formation. Microscopically there are collections of amorphous tissue
in the adventitia.
Renal artery fibrodysplasia
See renal artery stenosis section.
Carotid and vertebral artery fibrodysplasia
Intimal and medial fibrodysplasia affect these arteries and both are associated with
elongation, kinking and coiling of the arteries. Medial fibrodysplasia almost totally occurs
in females, at a mean age of 55. ICA and vertebral artery (VA) disease co-exist with renal
artery fibrodysplasia in 50% of cases and intracranial aneurysm in 25%.
Carotid artery
It affects the mid-carotid artery adjacent to the 2–3 cervical vertebrae, but involvement
of the ICA origin is rare (unlike atherosclerosis). It produces serial stenoses, which are
often bilateral.
Vertebral artery
The lower part of the vertebral artery is affected more than the upper segments. Multiple
stenoses and aneurysms are produced, but not the ‘string of beads’ appearance seen on
angiography in renal artery fibrodysplasia.
History
Take a general and vascular history. These lesions may be incidental asymptomatic
findings or may present with TIAs, stroke, rupture or acute dissection affecting the
262 GENERAL SURGERY OUTPATIENT DECISIONS

relevant vascular territory. Patients may complain of a pulsatile mass in the neck. A
history of hypertension raises the possibility of renal artery stenosis.
Examination
Perform a general and vascular examination. Examine the carotid, vertebral and subclavian
arteries for bruits. The finding of a pulsatile mass in the neck often raises the suspicion
of an aneurysm or carotid body tumour, but usually is due to coiling and kinking of the
artery. However, fusiform aneurysmal dilatation can occur with FMD.
Investigations
Colour Duplex helps to identify the coiled and elongated artery or aneurysm formation.
Carotid body tumour can be excluded. Angiography is indicated to define the disease
and identify intracranial aneurysms and renal artery stenosis. If hypertension is a feature,
angiographic examination of the renal arteries is particularly indicated.
Treatment
Treatment is indicated for symptomatic disease and includes resection and interposi-
tion vein bypass. Angioplasty is indicated for non-embolic, non-aneurysmal stenotic
disease.
Follow-up
Review with results of investigations and decide on a treatment plan. The finding of
intracranial aneurysms is referred for a neurosurgical opinion. Renal artery stenosis is
treated as appropriate (see renal artery stenosis section).
Post-operative follow-up
Review after 4–6 weeks to determine the success of the operation. Complications are
similar to those for carotid endarterectomy. Long-term follow-up with annual Duplex
scans to detect FMD in the contralateral side and other arteries should be considered.
Iliac, femoral, popliteal and tibial artery fibrodysplasia
FMD can affect any of these arteries, but is rare. It most commonly affects the external
iliac artery, producing serial stenoses with intervening mural aneurysms affecting the
proximal third of this vessel. It affects females in the 50–60s age range. There is associated
renal artery disease in 1–6%. Management consists of excluding renal artery disease and
treatment of the stenoses by angioplasty or bypass surgery.
Subclavian, axillary and brachial artery fibrodysplasia
Smooth focal or long tubular stenoses produce symptoms of arm ischaemia. It is difficult
to differentiate from Takayasu’s. Once again, these lesions are rare and tend to respond
to angioplasty.
Splanchnic artery fibrodysplasia
This has origins of coeliac, SMA and IMA stenoses and occasional aneurysms, e.g. splenic
artery aneurysm. Stenoses caused by FMD may be a rare cause of intestinal ischaemia,
which respond well to angioplasty. FMD is one of the causes of splenic artery aneurysms,
which occur particularly in multiparous young women and can cause fatal rupture during
pregnancy. Therefore these aneurysms should be repaired when detected.

Aneurysmal disorders of the arteries

A true aneurysm is an abnormal dilatation of an artery that affects all three layers of the
 VASCULAR 263

wall of the artery. It is considered significant if it causes symptoms if or the dilatation

exceeds twice its normal diameter. The cause of 90% of aneurysms is degenerative
secondary to atherosclerosis. Aneurysms can be associated with other disease processes
including FMD, SLE, Takayasu’s, giant cell arteritis, PAN, Behçet’s, Marfan’s, and Erhler’s
Danlos. Aneurysms can also arise as a result of systemic infection (mycotic aneurysms)
or dissection of the wall of the artery or they can be secondary to trauma including post-
stenotic.
False aneurysms occur secondary to an escape of blood from the artery, which is
contained only by the adventitia and usually occurs secondary to cannulation of the
artery followed by inadequate compression.
It is useful to consider true aneurysms as peripheral, visceral and central, based on the
site and behaviour of the aneurysms.
✧ Peripheral aneurysms affecting the limb arteries seldom rupture but commonly
embolise or thrombose, causing distal ischaemia.
✧ Visceral artery aneurysms seldom embolise but are prone to rupture.
✧ Central aneurysms such as thoraco-abdominal and abdominal aortic and iliac
aneurysms can both embolise distally, causing ischaemia, and/or rupture.
Central aneurysms
Thoraco-abdominal aneurysms (TAA)
Thoraco-abdominal aneurysms are classified as types I–IV.
✧ Type I affects the descending thoracic aorta and abdominal aorta to just above the
renal arteries.
✧ Type II affects all the descending thoracic and abdominal aorta and can include the
ascending thoracic aorta.
✧ Type III affects most of the descending thoracic aorta and all the abdominal aorta.
✧ Type IV affects all the abdominal aorta from the diaphragm.

The aetiology of thoraco-abdominal aneurysms includes medial degenerative disease,

aortic dissection, atherosclerosis, aortitis, infection and trauma.
These aneurysms can present with complications associated with compression or
erosion of neighbouring structures such as nerves or viscera in the chest or abdomen.
Surgical repair of these aneurysms is a major surgical undertaking, which only the
fittest patients are likely to survive.
History
Many patients are asymptomatic, but if symptoms are present they may include pain
in the chest or abdomen secondary to expansion or compression. Compression of the
trachea or bronchus can cause cough, wheeze or evidence of chest infection. Compression
of the oesophagus can cause dysphagia. Compression of liver or bile ducts may cause
jaundice. Vagus nerve traction may present as a hoarse voice. Thrombosis of spinal
arteries may present with paraplegia.
Assess cardiorespiratory fitness to undergo surgery, e.g. exercise tolerance, angina,
shortness of breath (SOB) and so on.
Examination
Examine for evidence of atherosclerosis and aneurysmal disease. Assess cardiorespiratory
fitness.
Investigations
A CT scan with intravenous contrast is required to determine the extent of aneurysm
and whether it is suitable for endovascular repair. Angiogram is performed if there
264 GENERAL SURGERY OUTPATIENT DECISIONS

is evidence of visceral, renal or limb stenotic disease. Lung function tests and cardiac
assessment (e.g. echocardiogram) are obtained together with an anaesthetic opinion.
Liaison with cardiothoracic surgeons for all thoraco-abdominal aneurysms other than
type IV is indicated.
Treatment
Treatment involves correction of risk factors and improvement of cardiorespiratory
function. Patients who are suitable undergo operation, consisting of either open or
endovascular repair. Hybrid procedures consist of both open and endovascular surgery.
Follow-up
Review with results to classify the extent of the aneurysm and assess the fitness of the
patient to withstand surgery. Liaise with cardiothoracic surgeons if indicated.
Post-operative follow-up
Review to determine the success of the operation. This will usually have been apparent
before the patient was discharged from hospital. Major complications include paraplegia,
limb loss and death.
Abdominal aortic aneurysm (AAA)
The commonest site of the abdominal aorta to be affected by aneurysmal disease is below
the renal arteries, and it may involve the iliac arteries. Aneurysms affecting the aorta above
the renal arteries (suprarenal, supracoeliac) require much more complex surgery to repair
and may require referral to a tertiary centre (see thoraco-abdominal aneurysm repair).
Once an AAA ruptures the operative mortality is approximately 50%, therefore the aim
of surgery is to operate before rupture occurs, when the mortality is approximately 5%.
However, not all aneurysms rupture and a number of patients will die of other causes
without the aneurysm ever causing any symptoms. Recent research has identified that
once an AAA reaches 5.5cm diameter, elective surgery should be considered. Surgery
should also be performed on smaller aneurysms that become symptomatic.
History
Take a general and vascular history. The majority of AAAs are asymptomatic and are
detected on routine clinical examination, on USS of the abdomen performed by another
speciality, e.g. urology, or on an aneurysm screening programme. Patients may present
having noticed a pulsatile swelling in the abdomen. Symptoms such as backache or
abdominal pain may indicate a rapidly enlarging aorta, which requires urgent assessment.
Assess cardiorespiratory fitness, e.g. angina and exercise tolerance. Enquire regarding
family history, especially brothers.
Examination
Perform a general and vascular examination with the aim of confirming the diagnosis,
detecting aneurysms or stenotic disease affecting other arteries and determining the
general cardiorespiratory fitness of the patient should surgery prove to be necessary.
Investigations
Perform a general atherosclerotic screen of urinalysis and blood tests. USS is usually
adequate to confirm the diagnosis of AAA and gives an accurate estimate of the diameter.
USS should also confirm the AAA arises below the renal arteries and whether it extends
to involve the iliac arteries. A CT scan with intravenous contrast is performed to
determine suitability for endovascular repair (EVAR). Angiography is performed if
the patient has evidence of stenotic/occlusive disease of leg arteries, which may require
 VASCULAR 265

bypass, or evidence of renal artery stenosis meeting the criteria for revascularisation.
Investigations performed prior to surgery include lung function tests, cardiac assessment
(e.g. echocardiogram) and an anaesthetic opinion.
Treatment
Correct risk factors and optimise cardiorespiratory function. Asymptomatic AAA greater
than 5.5cm diameter should undergo operative repair. Smaller aneurysms are considered
for surgery if they are symptomatic.
Open aneurysm repair
This is the established operation, performed via a large midline or transverse abdominal
incision. The aorta is clamped above and below the aneurysm, and the aorta is replaced
with an artificial graft. Clamping the aorta puts a major strain on the heart and lungs,
which is why a pre-operative assessment is necessary, and care in the intensive care unit
is necessary post-operatively.
Endovascular aneurysm repair (EVAR)
This involves stenting of the AAA via delivery systems inserted through the femoral
arteries. EVAR is currently being performed in designated centres and its major advantage
is that its less invasive approach is associated with a lower 30-day peri-operative mortality
rate – but at a cost of increased rate of reintervention (40%), lifelong surveillance and no
improvement in long-term survival over open repair.
Follow-up
Asymptomatic aneurysms less than 5.5cm in diameter undergo USS at regular intervals
to detect any increase in size. Initially this should be every three months, increased to six
months or even yearly if the aneurysm appears stable and not increasing in size. Smaller
aneurysms that become symptomatic should be repaired. Aneurysms approaching 5.5cm
are scanned more frequently again or undergo a CT scan with contrast as there is some
evidence that USS may underestimate the aortic diameter compared to CT. All patients
are counselled as to the nature of the disease and advised that any abdominal or back
pain should be considered secondary to a leaking AAA requiring urgent admission to
hospital.
Post-operative follow-up
Open repair
At first visit confirm wound healing and return to normal activity. Most complications
of aneurysm surgery occur immediately after surgery, e.g. distal embolisation causing
trash foot, ischaemic toes etc; renal failure; or ischaemic bowel. Long-term complications
include graft infection, indicated by non-specific general malaise and loss of appetite. An
urgent CT scan is performed and infection is suspected if fluid or even air is detected
around the graft. Graft infection may result in false aneurysm formation or even an
aorto-enteric fistula, which may present with haematemesis or rectal bleeding. All must
be investigated urgently as an in-patient. Other complications may result from adhesions
causing intermittent bowel obstruction. Impotence may result from damage to the
autonomic nerves on the anterior surface of the aorta. Anastomotic stenoses may develop
resulting in ischaemic symptoms. Incisional hernias are not uncommon.
Endovascular repair
A CT scan is performed at three months to check for complete repair on the aneurysm
and yearly thereafter. ‘Endoleak’ is the term given to incomplete sealing and it is classified
from type I to IV.
266 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Type I represents a leak from one of the ends of the stent graft and requires urgent
repair.
✧ Type II represents backbleeding from the IMA or lumbar arteries. Usually these can
be monitored, and as long as the AAA does not increase in size, no intervention is
required.
✧ Type III represents a leak from a join where two stents have been placed together and
requires urgent action.
✧ Type IV is a breach in the stent material and requires urgent repair.

Other complications include occlusion of a limb or the whole graft, which presents either
urgently with acute ischaemia or as chronic ischaemia causing claudication/rest pain.
Buttock claudication can occur because one limb of the stent graft has covered the
internal iliac artery, either intentionally or unintentionally.
Deterioration in renal function can occur due to a renal artery being covered by the
stent.
Iliac artery aneurysm
Iliac artery aneurysm tends to refer to aneurysm of the common and/or internal iliac
arteries. The external iliac artery is seldom aneurysmal. Common iliac artery aneurysms
often occur in conjunction with AAA, and the two are repaired together using a bifurcated
graft. Occasionally common iliac aneurysms occur in isolation, or are associated with a
small AAA, and merit repair because they have reached a size at risk of rupture or are
associated with distal embolisation. Internal iliac aneurysms are less common but may
also rupture or embolise. Repair of these aneurysms is important because the blood
supply to the bowel has to be considered.
History
Like AAAs, the majority of iliac aneurysms are asymptomatic and are detected on routine
clinical examination or on USS. The patient may have noticed a pulsatile swelling in
the abdomen. Symptoms such as backache or abdominal pain may indicate a rapidly
enlarging aneurysm that requires urgent assessment. Iliac artery aneurysms may give
rise to embolisation, and the patient presents with distal limb ischaemia. Internal iliac
aneurysms may compress structures in the pelvis, such as nerves, producing symptoms
of sciatica or obturator neuralgia.
Examination
Perform a general and vascular examination with the aim of confirming the diagnosis,
detecting aneurysms or stenotic disease affecting other arteries and determining the
general cardiorespiratory fitness of the patient should surgery prove to be necessary. The
aorta bifurcates at the level of the umbilicus so an iliac aneurysm is palpable below the
umbilicus.
Investigations
Perform a general atherosclerotic screen of urinalysis and blood tests. USS is usually
adequate to confirm the diagnosis and give an accurate estimate of size. CT scan with
contrast defines the extent of the aneurysm and its relationship to surrounding structures
and suitability for endovascular repair. In some cases it is possible to repair an iliac
aneurysm without clamping the aorta, but all patients should be prepared for theatre
assuming that the aorta will have to be clamped. Therefore, lung function tests, cardiac
assessment and an anaesthetic opinion are obtained.
 VASCULAR 267

Treatment
The normal diameter of the common iliac artery is 1.0–1.5cm. Any aneurysm greater than
3cm or any symptomatic aneurysm should be considered for operative repair.
Isolated common iliac aneurysm (normal diameter 1–1.5cm)
Endovascular stenting or open repair with Dacron inlay graft.
Common iliac aneurysm and co-existing AAA
Bifurcated aortic aneurysm repair.
Internal iliac aneurysm (normal diameter 0.75–1.0cm)
If the contralateral internal iliac artery is normal, ligate the aneurysmal internal iliac. If
both internal iliac arteries are aneurysmal, ligate one and use polytetrafluoroethylene
(PTFE) or vein to revascularise the other.
External iliac aneurysm (normal diameter 1–1.5cm)
Seldom aneurysmal.
Follow-up
Review with investigations and decide on need and fitness for surgery.
Post-operative follow-up
Follow-up and complications are the same as for AAA.
Peripheral artery aneurysm
A peripheral artery is aneurysmal when it is two times the normal diameter. When
the underlying cause is atherosclerosis, a number of arteries are commonly affected
together, e.g. femoral and popliteal arteries. Other causes include trauma, congenital,
FND, arteritis and infection (mycotic). When infection is the cause, the aneurysm often
arises suddenly and is related to a systemic infective episode, e.g. Salmonella infection.
The main complication of peripheral aneurysm is not rupture (although this can occur)
but thrombosis or embolisation resulting in ischaemia.
True aneurysm is a dilatation of all three layers of the vessel wall; false aneurysm results
from bleeding from the lumen underneath the adventitia, resulting in expansion of just
the adventitia. False aneurysms commonly affect the femoral artery and are caused by
cannulation of the artery, e.g. angiogram followed by inadequate compression.
History
Try to identify an underlying cause from those listed above. Determine whether the
aneurysm is asymptomatic or symptomatic. False aneurysm will usually have been
preceded by some trauma or puncture of the artery, most commonly by the performance
of an angiogram. Symptoms may consist of pain due to expansion or pressure on adjacent
structures, distal embolisation or ischaemia.
Examination
Perform a general and vascular examination. Palpate all peripheral arteries and pulses to
detect co-existing aneurysm or evidence of arterial occlusion and distal ischaemia. Palpate
for co-existing iliac or AAA. True aneurysms are pulsatile and expansile. False aneurysms
are pulsatile but not expansile.
Investigations
Duplex USS is the primary investigation, which will confirm the diagnosis, differentiate
268 GENERAL SURGERY OUTPATIENT DECISIONS

between true and false aneurysms and provide an accurate estimate of the size and extent
of the aneurysm. Also scan the aorta to exclude co-existent AAA disease. Blood cultures
are indicated if mycotic aneurysm is suspected.
Treatment
Common femoral aneurysm (normal diameter 1–1.5cm)
Open repair with Dacron or PTFE inlay graft.
Superficial femoral artery aneurysm (normal diameter 0.75–1.0cm)
Focal aneurysm affecting one segment of artery; or fusiform aneurysmal disease affecting
the whole length of the artery. For focal disease, open repair with PTFE or Dacron inlay
graft. For fusiform disease, bypass the whole length of the artery using vein or PTFE with
ligation of the superficial femoral artery (SFA) proximally and distally.
Popliteal artery aneurysm (normal diameter 0.5–1.0cm)
Saccular or fusiform extending into SFA. Saccular or fusiform bypass using vein or PTFE
with proximal and distal ligation of the aneurysm.
Carotid artery aneurysm
Open repair and vein bypass (see carotid aneurysm section).
Subclavian/axillary artery aneurysm
Open repair and PTFE graft, often associated with a cervical rib or band, which will also
need treatment.
Follow-up
Review with results of investigations and decide on those patients suitable for surgery.
Post-operative follow-up
Review to determine the success of the operation and to detect any complications.
Complications are specific to the procedure. Vein grafts are entered into the vein graft
surveillance programme with regular Duplex scans to detect developing stenoses.
Otherwise discharge when all wounds have healed and patient is symptom-free.
Visceral artery aneurysms
Visceral artery aneurysms are very rare, but are associated with a high mortality rate if they
rupture. Therefore most are repaired. Causes include infection (mycotic), fibromuscular
dysplasia or atherosclerosis. Urgent angiography is indicated for symptomatic or large
aneurysms, and prompt surgical repair in patients suitable for surgery. In patients unfit
for surgery endovascular embolisation may be successful.
Vasospastic disorders of the arteries
Raynaud’s phenomenon
Most commonly, Raynaud’s describes an abnormal arterial vasospasm in response to cold,
usually affecting the fingers. Classically the fingers turn white and numb on exposure to
cold, the static blood becomes deoxygenated producing a blue colour, then the vasospasm
is released and a reactive hyperaemia occurs and the fingers turn bright red. Two forms
are recognised.
Raynaud’s disease (primary)
This is the more common form and has no underlying disease. The symptoms are usually
mild and seldom produce tissue loss.
 VASCULAR 269

Raynaud’s syndrome (secondary)

This form has an underlying disease, although Raynaud’s symptoms may precede the
systemic illness by 20 years. The symptoms are usually more severe and associated with
ulceration and tissue loss.
There are numerous variations to the classic description. Triphasic colour change is
not necessary; for diagnosis; blanching and reactive hyperaemia are sufficient. Vasospasm
can be provoked not only by cold but also by emotion, hormones, trauma, chemicals,
vibration and tobacco exposure. Vasospasm does not just affect the fingers – toes are
also commonly affected and the vasospasm can be systemic, affecting the nose, ear-
lobes, cerebral and coronary arteries, lung vessels (producing pulmonary fibrosis) and
oesophagus (producing dysphagia).
Venous spasm produces intense venous congestion and purple colour change and has
the same primary and secondary forms as Raynaud’s. Acrocyanosis is the term for venous
vasospasm and venous infarcts are commonly known as chillblains.
Underlying disorders
Immunological
Systemic sclerosis (90%), SLE, mixed connective tissue disease, dermatomyositis/poly-
myositis, rheumatoid arthritis, cryoglobulinaemia, Sjogren’s.
Occupational
Vinyl chloride workers, ammunition workers, outside workers, frozen food packers.
Vibration white finger.
Obstructive
Thoracic outlet, Buerger’s.
Drugs
Ergotamines, betablockers, cytotoxics, cyclosporin.
Other
Malignancy, endocrine (hypothyroidism), uraemia, hepatitis B, reflex sympathetic
dystrophy, A-V fistula.
History
A history of blanching is usually adequate for diagnosis. Recent onset, especially in
childhood or middle age, is suggestive of secondary Raynaud’s. Determine the provoking
factors. Enquire about underlying disorders according to the list above. Raynaud’s is
usually bilateral. Raynaud’s affecting just one hand is suspicious of a local traumatic or
obstructive cause, e.g. cervical rib. Confusion can also be caused by Buerger’s disease,
predominantly affecting the upper limbs.
Examination
Perform a general and vascular examination. In primary Raynaud’s the fingers are usually
normal to inspection and all pulses are present and normal. In severe and secondary
Raynaud’s there may be scars on the finger pulps from previous ulcers or ulcers may be
present. Look for evidence of secondary infection. Examine for any underlying causes.
Absent pulses may suggest an atherosclerotic cause, Buerger’s disease or a mechanical
cause such as thoracic outlet compression syndrome. Use an ophthalmoscope on
high power to examine the skin proximal to the nailfold. Normally, capillary vessels
underneath the skin are not visible. If they are, this is evidence of significant ischaemia
usually associated with secondary Raynaud’s.
270 GENERAL SURGERY OUTPATIENT DECISIONS

Investigations
The diagnosis of Raynaud’s is mainly clinical. Some centres define Raynaud’s as a drop
in systolic finger pressure on cooling the hand under controlled laboratory conditions,
but the results are not totally sensitive and specific. The most important investigations
are to exclude a secondary cause.
Take FBC, TFTs (hypothyroidism), ESR/PV and urinalysis for renal disease in CTD or
diabetes. Use CXR to detect lung fibrosis or malignancy, thoracic inlet views to detect a
cervical rib. Upper limb Duplex is useful to exclude major arterial disease. Immunological
tests include autoantibody screen for RhF, antinuclear antibodies (ANA) for SLE,
anticentromere for localised systemic sclerosis (SS) and antitopoisomerase for diffuse
SS. These investigations may need to be repeated every few years if the symptoms persist
or deteriorate.
Treatment
General measures include stopping smoking, changing occupation, changing medications
and stopping the contraceptive pill if there is a clear link. Heated gloves and socks or
chemical handwarmers may be advised. Advise regarding The Raynaud’s and Scleroderma
Association, Alsager, Cheshire for practical advice and support.
Mild to moderate primary Raynaud’s will often respond to a combination of these
general measures to control the symptoms. If the symptoms are still affecting lifestyle or
employment, or secondary Raynaud’s is present, drug therapy may be necessary.
Drugs
Nifedipine retard 10 mg once a day taken at bedtime is effective and taken at this time
minimises the headache and dizziness that can occur. The dose can be gradually increased
to 20 mg bd/tds if tolerated. It is not licensed for use in pregnancy, so inform patient of
this. Amlodipine, diltiazem and isradipine are also useful second-line drugs.
Inositol nicotinate (Hexopal) 4 g/day may take three months to have any effect.
Naftidrofuryl oxylate (Praxilene) 200 mg tds may decrease frequency and severity of
attacks.
In-patient treatment
Iloprost infusion, a stable prostocyclin analogue, may be given intravenously for six
hours for 3–5 days per treatment. This may terminate a prolonged attack and reduce the
frequency of further attacks.
Sympathetomy
Lumbar sympathetomy is effective for the lower limb, not for the upper limb.
Treat any infection or ulcers aggressively with antibiotics. Note – usual signs of infec-
tion are often absent. Severe ulceration or gangrene may require surgical debridement
or amputation.
Treatment of underlying connective tissue disorder may be needed.
Follow-up
After the first consultation, patients should be reviewed at short intervals (1–4 weeks)
until secondary causes are excluded. Mild/moderate disease can be reviewed at longer
intervals (1–6 months) to give a chance for treatment to become effective; or be reviewed
only in winter when symptoms occur. Severe cases tend to have symptoms all year round
and may need to be reviewed at shorter intervals with open appointments to attend the
clinic if an attack fails to resolve quickly.
 VASCULAR 271

Post-operative follow-up
This is usually confined to reviewing the results of lower limb sympathectomy and/or
amputations of digits. For amputations, wound healing can be prolonged and the normal
signs of wound infection may not be present. Treat early with antibiotics based on culture
and sensitivities.

Disorders of the venous system

By far the commonest venous disorder presenting to the vascular clinic is primary
varicose veins. However, certain vascular malformations may present with dilated veins
in the leg, e.g. arteriovenous fistulas or venous malformations. The Klippel-Trenaunay
syndrome presents with a dilated varicose vein running down the outside of the leg, but
is associated with hypoplasia of the deep veins. Dilated superficial veins may be secondary
collateral veins in the presence of damaged, occluded or absent deep veins.
Chronic superficial and/or deep venous incompetence may present as varicose veins,
leg swelling or venous eczema/ulceration.
Primary varicose veins
Varicose veins are dilated superficial veins in the leg caused by incompetent valves
allowing high-pressure blood to reflux from the deep veins into the superficial veins. In
the long term (years) this may lead to venous stasis, ankle oedema, lipodermatosclerosis
and eventually ulceration. Most varicose veins referred to the vascular clinic consist of
primary varicose veins affecting the long or short saphenous systems. However, up to
20% of patients present with recurrent varicose veins arising from previous varicose vein
treatment. Other patients may present with dilated superficial veins that are not varicose,
or they are worried about the cosmetic appearance of thread veins with or without
associated varicose veins. Occasionally, visible veins are either normal or caused by some
congenital abnormality or underlying pathology for which varicose vein surgery would
be inappropriate.
History
Take a general vascular history. Most patients will describe the presence of these veins
for several years. In females their appearance may coincide with pregnancy. Exclude
previous deep vein thrombosis or conditions that may have led to this, e.g. long bone
fractures, prolonged bed rest, plaster of Paris use. Determine the symptoms caused by
the veins. Patients may complain of local tenderness in the region of a prominent vein
or general symptoms of discomfort, aching or throbbing. There may be a history of
acute haemorrhage from a prominent vein or episodes of superficial thrombophlebitis.
Alternatively there may be no symptoms and the main concern is cosmetic.
Examination
Examine the patient standing and determine whether the varicose veins affect the
long saphenous (medial side of thigh and calf) or short saphenous system (mainly
lateral calf and originating from the popliteal fossa – but not all). Determine the site of
incompetence using the tourniquet. Occasionally there is a communicating vein between
the two systems. Examine for signs of venous stasis: oedema or lipodermatosclerosis
spreading from the medial malleolus.
The presence of venous stasis should prompt investigations to exclude deep venous
incompetence. Examine for the presence and extent of thread veins. Thrombophlebitis
may result in firm, tender cord-like veins caused by thrombosis and fibrosis surrounded
by erythema.
272 GENERAL SURGERY OUTPATIENT DECISIONS

Investigations
For straightforward long saphenous varicose veins, no further investigation is necessary
prior to treatment. Continuous wave Doppler examination may be helpful in experienced
hands, but, where available, colour Duplex ultrasonography is preferable for confirming
the site of incompetence, identifying short saphenous reflux and excluding deep venous
reflux. Varicography is the more invasive alternative.
Treatment
Conservative treatment consists of compression hosiery (class II compression stockings),
but most patients opt for operative therapy unless they are a high operative risk.
Isolated long saphenous vein reflux
This is usually treated operatively with a Trendelenburg tie, stripping of the vein to the
knee and lower leg avulsions. In young, fit patients this can be performed as a day-case
providing the patient meets the day-case criteria. Newer local anaesthetic techniques
include endovenous laser ablation (EVLA) and VNUS® Closure. Ultrasound-guided foam
sclerotherapy is an outpatient technique and represents a non-operative alternative.
Isolated short saphenous vein reflux
This is treated by short saphenous ligation in the popliteal fossa. However, the sapheno-
popliteal junction is variable and can originate from the mid-posterior thigh. Therefore,
pre-operative Duplex marking of the junction is recommended. Combined long and short
saphenous vein reflux can be treated during the same operation but requires turning of
the patient halfway though the operation. Bilateral long saphenous incompetence can be
treated simultaneously but is usually considered inappropriate for day-case surgery.
Co-existing superficial and deep venous reflux
This condition usually precludes superficial surgery. This is because in the presence of deep
venous reflux, superficial surgery is ineffective and may impair the venous circulation of
the limb. Surgery may be indicated if ambulatory venous pressure measurements indicate
that superficial vein occlusion improves venous refilling time or the superficial veins are
causing specific symptoms, e.g. bleeding.
Co-existing venous and occlusive arterial disease
The arterial disease is treated first.
Threadveins
Most patients can be treated by sclerotherapy.
Follow-up
Most of these problems are routine and there is no urgency for investigations unless
deep-venous thrombosis is suspected.
For those patients who have undergone EVLA, VNUS® or sclerotherapy, late compli-
cations include local skin ulceration due to extravasation of sclerosant (slow to heal but
no specific treatment). Superficial thrombophlebitis is caused by a clot in the vein due to
inadequate compression. The clot can be aspirated under local anaesthetic. If there is an
allergic skin rash to the bandage put a cotton stocking under the bandage. Nerve damage
is usually transitory. Skin staining mostly fades with time.
Post-operative follow-up
Patients are usually reviewed at 4–6 weeks after operation. Common complications
are usually related to the wound. Deep vein thrombosis is no more common than after
 VASCULAR 273

other operations. Patients may be concerned about prominent residual or ‘missed’ veins.
The best course of action is reassurance and review in 6–12 months time rather than to
proceed immediately to further surgery. By that time the residual veins may not be such
a concern, or further veins may have become prominent, which would have been missed
by immediate re-operation. Repeat the Duplex scan and treat appropriately according
to findings. Residual veins not associated with reflux can be treated by avulsions under
local anaesthetic or sclerotherapy.
Complications of varicose vein surgery include bruising in the groin or along the track
of the treated long saphenous vein. A cord of thrombus may be palpable along the line of
the stripped vein. Both will usually resolve.
There may be small areas of skin paraesthesia in relation to the groin wound or
avulsion site due to damage to cutaneous nerves. Once again, this should resolve if mild.
Saphenous neuritis is caused by damage to the great saphenous nerve. This can cause
distressing pain, tingling, and paraesthesia in the distribution of the great saphenous
nerve. Referral to the pain clinic may be required in some cases.
Tattooing of the skin can occur if incisions are made through ink marks placed
pre-operatively to mark the vein. Plastic surgical referral may be necessary for severe
tattooing.
Avulsions at certain sites should be avoided to remove the risk of damage to other
structures, e.g. around the neck of the fibula to avoid the common peroneal nerve, the
posterior tibial vessels behind the medial malleolus and the sural nerve in the medial line
of the posterior calf.
Superficial thrombophlebitis
Thrombophlebitis is inflammation of a vein due to thrombosis. It can occur in normal
or varicose veins.
When thrombophlebitis occurs in normal veins it may indicate an underlying condition
such as thrombophilia or occult malignancy, and patients should be investigated to
exclude these.
When thrombophlebitis occurs in varicose veins it is usually as the result of stasis, but
all patients with thrombophlebitis are at increased risk of DVT (25% association) and
this should be excluded.
Patients who have thrombophlebitis extending to the saphenofemoral junction may
have a tongue of thrombus protruding into the femoral vein and are at risk of pulmonary
embolus.
History
Patients complain of tender inflammation over the superficial limb veins. There may be
a history of varicose veins and/or DVT. Enquire regarding symptoms of systemic disease.
Enquire about a family history of thromboses.
Examination
Perform a general and vascular examination. Examine for the presence of varicose veins
and limb swelling. The skin overlying the affected vein is red, inflamed and tender and
may appear infected (but is not). The vein may be palpable as a firm thrombosed cord
underneath the skin. Determine the extent of the thrombophlebitis.
Investigations
The diagnosis is essentially clinical. Duplex will define the extent of the thrombus and
exclude protrusion of the thrombus through the saphenofemoral junction (SFJ) and a
DVT.
FBC, PV/ESR and thrombophilia screen are performed to investigate underlying causes.
274 GENERAL SURGERY OUTPATIENT DECISIONS

Depending on the result of the history and examination, appropriate investigations are
performed to exclude underlying malignancy.
Treatment
Uncomplicated thrombophlebitis is treated with analgesia, NSAIDs and compression.
DVT is treated with anticoagulation. Varicose veins are treated appropriately once
inflammation has subsided. Extensive thrombophlebitis extending to the SFJ is treated
by immediate ligation of the SFJ and anticoagulation, e.g. low molecular weight heparin
or warfarin, is considered. Underlying causes are treated as appropriate. Females with
thrombophlebitis should stop the contraceptive pill and be counselled regarding their
increased risk of DVT.
Follow-up
If extensive thrombophlebitis or DVT is suspected, admit for further investigation and
anticoagulation as an in-patient. Otherwise, review promptly (1–4 weeks) with results
of investigations. Refer to relevant speciality if an underlying cause is found. Advise
regarding increased risk of DVT.
Post-operative follow-up
As for varicose veins.
Recurrent varicose veins
Approximately 20% of patients presenting to the vascular clinic with varicose veins have
had previous treatment and complain that the varicosities have returned.
Usually these patients can be separated into three groups.
✧ Persistent veins: varicose veins that were not adequately removed at the original
operation and have never gone away.
✧ New varicose veins: varicose veins developing in a system, e.g. short saphenous vein
(SSV) not part of the original operation.
✧ True recurrent varicose veins: varicosities have recurred in the same system that
was originally operated on. Recurrence may be due to inadequate saphenofemoral/
saphenopopliteal junction disconnection, a residual untreated mid-thigh perforator
vein or new growth of veins reconnecting the saphenofemoral/saphenopopliteal
system.
History
Determine the nature of the original surgery. Assess the symptoms caused by the
recurrent veins.
Examination
Perform a general examination of the distribution of the varicose veins, including
tourniquet tests.
Investigations
Colour Duplex scan to define the source of recurrence and plan surgery.
Treatment
As with primary varicose veins, treatment is either conservative with compression hosiery
or active with sclerotherapy or surgery. Reflux arising from a non-operated venous system
is treated by the relevant procedure.
 VASCULAR 275

Follow-up
Review with the results of investigations and decide on appropriate therapy. There is
usually no urgency unless ulceration is present.
Post-operative follow-up
Review to assess the success of surgery and detect any complications of surgery.
Chronic venous insufficiency
Chronic venous insufficiency occurs when the venous return is impaired by reflux,
obstruction and calf muscle pump failure. Sustained venous hypertension leads to oedema
and leg swelling; eczema, especially around the medial malleolus; lipdermatosclerosis and
eventually ulceration. Swelling initially consists of oedema fluid but eventually results in
subcutaneous fibrosis and induration.
History
Take a general and vascular history. Previous history of deep vein thrombosis, leg swelling,
prolonged immobilisation, plaster of Paris use or long-bone fractures may suggest deep
venous incompetence, while the presence of varicose veins, past or present, may suggest
a superficial venous cause.
Symptoms associated with chronic venous hypertension include pruritis, aching pain
and limb swelling. Occasionally the patient may complain of venous claudication, which
consists of a bursting calf pain on walking a certain distance, not relieved purely by rest
but also requiring elevation of the limb.
Examination
Perform a general and vascular examination. Examine for the presence of varicose veins,
limb swelling, lipodermatosclerosis (LDS), ulceration and co-existent arterial disease.
Investigations
Colour Duplex scanning is useful to identify both superficial and deep venous reflux
and may identify scarred, thickened or obstructed deep veins. In the absence of reliable
Duplex, ascending venography is useful to identify scarred, thickened or obstructed deep
veins, while descending venography is useful to identify deep and superficial reflux. The
resting and post-exercise venous pressure and refilling time at the ankle can be measured
directly by ambulatory venous pressure measurements. ABPI or arterial Duplex scans
are performed to exclude co-existing arterial disease, especially if compression therapy
is considered. Compression in the presence of arterial disease can result in critical
ischaemia, gangrene and limb loss.
Treatment
Treatment is conservative. Bed rest with the legs elevated reduces the venous pressure at
the ankle to 12–15 mmHg and is useful for reducing leg swelling in grossly swollen legs
prior to compression therapy.
Graduated compression bandaging (Charing Cross four-layer) generates compression
of approximately 40 mmHg at the ankle and 18 mmHg at the knee and is used to heal
venous ulcers in the absence of arterial disease.
Compression stockings are used to prevent ulceration in non-ulcerated or healed legs
with deep venous incompetence. Class I stockings generate less than 25 mmHg pressure
at the ankle; class II generate 25–35 mmHg; class III generate 35–45 mmHg and class IV
generate 45–60 mmHg. Below-knee stockings class II are adequate for most patients, but
compliance can be a problem due to difficulties putting the stockings on or discomfort
in hot weather. Non-compliance is greater for class III–IV and full-leg stockings.
276 GENERAL SURGERY OUTPATIENT DECISIONS

Surgical treatment is indicated for patients with isolated superficial venous incom-
petence. This is sufficient to heal ulcers with or without compression therapy.
Surgical options for deep venous outflow obstruction include Palma’s procedure
for iliac vein stenosis/occlusion or thigh vein bypass for thigh vein occlusion. These
procedures are rarely performed.
Follow-up
Review with results of investigations and decide on appropriate treatment. Venous ulcers
undergoing compression are reviewed (1–3 months) until healing is underway, and the
patient can be discharged with advice to progress to compression stockings once the ulcer
is completely healed and four-layer bandaging is no longer necessary. Patients prescribed
compression stockings may be reviewed once to confirm compliance and improvement
in symptoms, then discharged with advice as to lifelong use.
Post-operative follow-up
Review to determine the success of the operation and to detect complications of varicose
vein surgery (see primary varicose veins section). Patients can be discharged once they
are symptom-free and wounds have healed.
Leg ulceration
The commonest cause of leg ulceration is venous disease, and up to a quarter of these
patients will have co-existing arterial insufficiency. Approximately 10% of ulcers are due
to pure arterial insufficiency. Other causes include diabetes mellitus and rheumatoid
arthritis.
✧ Venous ulceration: the cause of venous ulceration is sustained venous hypertension,
which can be due to superficial and/or deep venous incompetence. Venous hypertension
causes the typical leathery skin of lipodermatosclerosis around the medial malleolus,
which eventually leads to venous ulceration. Venous stasis ulceration can occur in the
presence of normal veins, due to the non-function of the calf muscle pump secondary
to arthritis of the ankle, or severe arthritis in other lower limb joints limiting mobility
and contraction of the calf muscles.
✧ Arterial ulceration: arterial insufficiency can produce ulceration anywhere on the
lower limb. These ulcers usually result from some minor trauma to the skin. Healing
skin requires up to 10 times the blood supply of ordinary skin. If the diseased arterial
system cannot supply this extra blood the wound never heals and an ulcer develops.
✧ Neuropathic ulceration usually occurs on the sole of the foot or over pressure points.
The absence of sensation means the patient is not aware that something is pressing
or rubbing on the foot until an ulcer is produced. This is most commonly seen with
diabetic neuropathy.
✧ Vasculitic ulceration: a vasculitis disease produces small infarctions of the vessels
supplying the skin, resulting in areas of the skin dying and producing ulcers. Initially
these start as a number of small ulcers with surrounding vasculitic skin changes, but
eventually the ulcers may coalesce to form a larger ulcer. There is usually a known
vasculitis process, e.g. rheumatoid arthritis.
✧ Infective ulcers: primary infective ulcers are rare in the UK. More common is second-
ary infection of existing ulcers.
✧ Neoplastic ulcers: primary skin cancers forming ulcers on the leg are uncommon.
However, long-standing ulcers from other causes may turn malignant (Marjolin’s
ulcer).
✧ Mixed pathology: often ulceration may have more than one cause and all underlying
causes need to be addressed, e.g. mixed arterial and venous ulcers.
 VASCULAR 277

History
Take a general and vascular history. A history of claudication or rest pain suggests an
arterial cause. Note any risk factors for venous disease, as outlined for chronic venous
insufficiency.
Symptoms associated with chronic venous hypertension include pruritis, aching pain
and limb swelling. Occasionally the patient may complain of venous claudication, which
consists of a bursting calf pain on walking a certain distance, that is not relieved purely
by rest but also requires elevation of the limb.
Ulcers occurring over the pressure points of the foot in diabetics or patients with other
neurological conditions suggest a neuropathic cause, but there may also be co-existing
arterial or venous disease. History of a skin rash progressing to multiple small ulcers
suggests a vasculitic cause. Ulcers presenting for several years that start to deteriorate
may indicate neoplastic change.
Examination
Perform a general and vascular examination. Varicose veins and absent pulses are noted.
An ulcer occurring in an area of lipodermatosclerosis, with or without visible varicose
veins or leg swelling, suggests a venous cause. Examine the distribution of any visible
veins. A pale ulcer in a leg with no pulses suggests an ischaemic cause. Ulcers occurring on
the sole of the foot or over the pressure points suggest a neuropathic cause. An ulcer with
a raised exophytic edge suggests possible malignant change. Arthritis limiting movement
of the ankle joint may be associated with venous stasis ulcers.
Investigations
Do a general atherosclerosis screen, FBC, U&Es, immunology and plasma viscosity.
Obtain Duplex USS of the superficial and deep venous systems of the leg and ABPI of
the ankle arteries with arterial Duplex scan or arteriography if abnormal. X-rays of ulcers
occurring over bones and joints are performed to exclude underlying osteomyelitis.
Microbiological swabs are taken of ulcers thought to be infected. A bluish-green discharge
suggests possible Pseudomonas aeruginosa infection. Potentially malignant or vasculitic
ulcers undergo biopsy for histology.
Treatment
Treatment consists of treatment of the ulcer and treatment of the underlying cause.
Generally ulcers are treated with non-adherent dressings while the underlying cause is
corrected. Infected ulcers with spreading cellulitis are treated with systemic antibiotics
(flucloxacillin, cefuroxime) guided by the results of microbiological assessment. Infected
ulcers not associated with spreading cellulitis can be treated with topical antibiotics or
activated charcoal dressings, but their use may be associated with allergic skin reactions.
Pseudomonas infection responds to silver sulphadiazine cream or combined activated
charcoal and silver sulphadiazine preparations applied daily for 1–2 weeks. Ulcers are
then re-swabbed.
Chronic ulcers
Chronic ulcers covered in adherent slough or eschar should be surgically debrided back
to bleeding tissue to speed healing. Generally, topical desloughing agents are slow and
inefficient.
Venous ulcers
Varicose veins in the presence of competent deep veins are treated by standard varicose
vein surgery. If superficial venous incompetence co-exists with deep venous incompetence,
superficial vein surgery is unlikely to improve the situation. Ulcers associated with deep
278 GENERAL SURGERY OUTPATIENT DECISIONS

venous incompetence in the absence of arterial disease are treated by compression

bandaging (Charing Cross four-layer). Compression bandaging is changed at twice-weekly
to weekly intervals or when there is strike-through. Copious exudate not controlled by
this regime may require admission for bed rest and leg elevation. Valvuloplasty, or valve
transposition for deep venous incompetence, are still experimental procedures.
Patients with venous stasis ulcers with normal veins but arthritis of the ankle limiting
function of the calf muscle pump are referred to the physiotherapy department to try to
improve mobility at this joint.
Venous outflow obstruction
Surgical options include Palma’s procedure for iliac vein stenosis/occlusion or thigh vein
bypass for thigh vein occlusion – rarely performed procedures.
Arterial ulcers
These ulcers will not improve unless the blood supply to the limb is improved. This is
achieved by either angioplasty or vascular bypass surgery.
Mixed arterial-venous ulcers
Correct the arterial problem first. Once normal ankle pressures are restored, venous
surgery can be performed, or use three-layer compression bandaging under close surveil-
lance to detect an ischaemia.
Neuropathic ulcers
There is usually joint management with diabetologists, who arrange pressure-relieving
footwear and so on. Arterial insufficiency can co-exist with neuropathic ulceration and
should be corrected if this might impair ulcer healing.
Skin grafting: split skin or full-thickness pinch grafts can be used to speed up ulcer
healing, but they are most successful if venous reflux has been corrected and there is no
infection.
Follow-up
Infected ulcers are reviewed at regular intervals (1–4 weeks) until the infection is under
control. Occasionally admission for intravenous antibiotics is required.
Chronic venous ulceration is reviewed at longer intervals (1–3 months) until healing
is well established. Patients can then be discharged with an open appointment when
complete healing is anticipated. Patients are prescribed two pairs of compression
stockings to wear every day to prevent ulcer recurrence once healing is achieved. Patients
are instructed in the correct fitting of compression stockings. Usually class II stockings
are preferred, but if these are too tight or difficult for an old person to put on, class I are
acceptable.
Neuropathic ulcers are generally followed up in the diabetic foot clinic.
Post-operative follow-up
Arterial ulcers are reviewed at regular intervals (2–6 weeks) after any procedure to improve
the blood supply, until healing is established. Deterioration in the ulcer after a period of
healing may indicate the artery has re-occluded and this should be investigated.
Venous ulcers treated by surgery should heal within 1–6 months if surgery has been
effective, irrespective of whether compression bandaging is also employed. Failure to
improve after this time should prompt investigation with a Duplex ultrasound scan to
confirm adequate surgery. Further surgery is performed if indicated.
 VASCULAR 279

The swollen limb

This most commonly refers to lower limb swelling, although upper limb swelling also
occurs. The cause of swelling is generally due to tumour, overgrowth of normal tissue or
oedema. The aetiology of the swollen limb can be classified according to whether one or
both legs are swollen; and whether the onset is acute or chronic, primary or secondary.
The rarer causes develop in childhood and include congenital conditions such as
primary lymphoedema, gigantism and arteriovenous fistulae.
In adulthood the general causes of bilateral limb swelling include heart failure, liver
failure, renal failure, hypoproteinaemia, fluid overload, myxoedema and lymphoedema.
Sudden-onset single limb swelling may be due to trauma, deep vein thrombosis,
cellulitis, allergy or rheumatoid.
Chronic limb swelling in the adult may be venous: varicose veins; deep venous incom-
petence; intrinsic and extrinsic obstruction to venous return, e.g. pregnancy, pelvic
tumours; inferior vena cava (IVC) obstruction; and postphlebitic limb. Other causes
include aortocaval fistula, popliteal or femoral aneurysm, lymphoedema, vascular mal-
formations, paralysis – failure of calf muscle pump, and chronic dependency of the limb
due to immobility.
Acquired secondary causes include filiariasis, malignant involvement, surgical block
dissection, radiotherapy, trauma, cellulitis, chronic inflammatory eczema and rheumatoid
arthritis.
History
Take a general and vascular history. The onset of the swelling is important. Swelling present
from birth, even though it is now getting worse, suggests one of the congenital causes.
Sudden-onset, single limb swelling suggests one of the acute causes or lymphoedema.
Bilateral swelling may indicate a general cause or lymphoedema.
Take a venous history regarding previous venous pathology. Assess the patient’s
mobility – one of the commonest causes of limb swelling in the elderly is chronic
immobility, sitting in a chair all day with dependent legs. Enquire about periods of
infection or cellulitis, previous malignancy and radiotherapy.
Examination
Perform a general and vascular examination. Is one leg affected or both? In younger
patients look for skin staining or soft tissue or bony overgrowth, which may suggest
a vascular malformation or tumour. Examine for dilated veins and determine their
pattern. Examine for the typical lipodermatosclerosis of chronic venous insufficiency.
Lymphoedema starts with toes and makes them square – inability to pinch a fold of
skin at the base of the second toe is known as Stemmer’s sign. It then spreads up the
legs and can produce huge limbs. Chronic lymphoedematous limbs display the typical
furry lichenification. Assess the mobility of the patient. Examine for the signs of a DVT
or cellulitis.
Investigation
History and examination should indicate the affected system. Investigations are then
directed to confirming the diagnosis. Duplex ultrasound is the standard investigation
of most venous causes, although venography may be helpful. Duplex can also identify
the typical ‘honeycomb’ appearance in the subcutaneous tissues of lymphoedema.
Lymphangiography may be used to demonstrate hypoplasia or blockage of more
proximal lymphatics. Ultrasound is also useful to identify or exclude pelvic masses,
although CT/MRI is more specific.
280 GENERAL SURGERY OUTPATIENT DECISIONS

Treatment
Treatment is appropriate for the underlying cause. The management of chronic lym-
phoedema consists of specialised massage and compression bandaging techniques. Class I
or II compression hosiery can be used to keep swelling under control once arterial disease
has been excluded. Repeated episodes of cellulitis progressively destroy more lymphatic
channels, so long-term flucloxacillin is indicated to reduce infective episodes. Tissue
reduction and mesenteric bridge operations for lymphoedema are specialised operations
(see lymphoedema section).
Follow-up
Review with results of investigations and assess the effect of treatment. Acute cases may
require hospital admission for investigation. More chronic cases can be reviewed at longer
intervals (1–3 months). Once the condition has stabilised patients can be discharged or
given an open appointment to return if deterioration occurs.
Lymphoedema
The primary causes of lymphoedema may be familial or non-familial and present at
different ages. Lymphoedema congenita occurs before one year of age (Milroy’s); praecox
occurs before 35 years; tarda occurs in those older than 35.
Secondary lymphoedema occurs due to a blockage of primarily normal lymphatics
by malignant disease, surgery, radiotherapy, and infection (parasitic, pyogenic – beta
haemolytic Streptococcus, Staphylococcus aureus, TB).
Lymphoedema can also be classified according to the mechanism of lymphoedema
as follows.
✧ Obliterative: the lymphatics are progressively obliterated from distal to proximal.
Represents 80% of lymphoedema cases, predominantly affects females.
✧ Proximal obstructive: lymphatic obstruction is caused by disease in the abdominal,
pelvic or inguinal lymph nodes. Usually unilateral.
✧ Lymphatic valvular incompetence and hyperplasia: the lymphatic equivalent of
varicose veins.
History
The history is one of slow progressive swelling of the limb or limbs, starting at the toes and
spreading proximally. There may be an episode of trauma or infection that precipitates
the swelling, which persists despite healing of the original condition. Decrease in swelling
overnight suggests a reversible cause. Enquire about possible secondary causes. Enquire
about recurrent episodes of cellulitis.
Examination
Lymphoedema swelling tends to be uniform, non-inflamed and non-pigmented, and it
pits on pressure in the early stages. The toes are affected early and become square. Later
there may be hyperkeratosis of the toes and skin fissuring secondary to fungal infection.
Chylous vesicles may appear on the pretibial area, but ulceration in pure lymphoedema
is rare. Examine for evidence of secondary causes and chest, abdominal and pelvic
pathology.
Investigation
The diagnosis of lymphoedema is mainly clinical. Colour Duplex is often performed to
exclude venous disorders. The diagnosis can be confirmed and the type of lymphoedema
classified using isotope or contrast lymphangiography. CT/MRI scan can be used to
exclude pelvic and abdominal disease and can also demonstrate the typical honeycomb
appearance of the lymphatic tissue in the tissues of the affected limb.
 VASCULAR 281

Treatment
The aims of treatment are to decrease limb swelling and weight, decrease the risk of infec-
tion and improve function. Lymphoedema can be reduced by regular massage (manual
lymphatic drainage – MLD), compression bandaging, exercise and breathing exercises.
Diuretics are useful as a short-term treatment only. Improvement in leg swelling can be
maintained by compression stockings, but note that lymphoedema compression stock-
ings are different to venous compression stockings. Recurrent episodes of cellulitis are
treated by long-term prophylactic flucloxacillin to prevent further damage to lymphatic
channels. Secondary fungal infections are treated with diethylcarbamazine. The legs are
washed daily and the feet protected with well-fitting, comfortable shoes.
Indications for surgical therapy include gross lymphoedema, inability to walk or work,
lymphorrhagia and recurrent lymphangitis. Generally, debulking operations are indicated
for obliterative causes and bypass procedures for proximal obstruction. These procedures
are rarely performed these days and the mainstay of therapy is MLD.
Follow-up
Follow up at regular intervals to review the results of investigations, monitor the effect-
iveness of treatment and detect complications. Once a long-term management plan has
been instituted and is controlling symptoms the patient can be discharged with advice
to return if deterioration occurs.
Post-operative follow-up
Review to determine the success of the procedure and to detect complications.
The diabetic foot
The feet of diabetic patients are prone to the development of infection, ulceration and
gangrene due to a combination of neuropathy, peripheral arterial disease and arthropathy.
Sensory neuropathy reduces the sensation of the feet and makes then more prone to
minor injury, which leads to the development of ulcers. Autonomic neuropathy leads to
dry skin, prone to injury. Motor neuropathy leads to muscle imbalance and increased
shear stresses on the skin, which can also cause ulceration. This also leads to joint and gait
abnormalities, which increase shear stress on the skin and decrease the efficiency of the
ankle joint and the calf muscle pump, decreasing the efficiency of the venous circulation
in the leg, which also predisposes the limb to ulceration. Peripheral arterial disease
renders the tissues more prone to ulceration, and once ulceration has occurred healing is
delayed or prevented until the blood supply to the area can be improved.
Assessment of diabetic foot problems requires a multidisciplinary approach involving
a diabetologist, vascular surgeon, orthopaedic surgeon, orthoptist and chiropodist.
History
Take a general and vascular history. Assess the diabetic control. Assess the neurological
system – symptoms of central neuropathy include fainting spells, dizziness, nausea,
vomiting of retained foods and impotence. Symptoms of peripheral neuropathy include
motor weakness, dry feet, numbness or loss of sensation in the feet, hyperaesthesia
(burning feet) or pain in the legs. Vascular symptoms include claudication, although rest
pain or ulceration may be the first symptom in diabetics. Ask about previous ulcers and
healing. Ask about other vascular causes of ulceration, e.g. venous incompetence.
Examination
Perform a general examination. Assess the characteristics of the ulcer. Assess the
neurological, vascular and orthopaedic systems.
✧ The ulcer: site, size, character, neuropathic. Vascular or mixed, simple or complicated.
282 GENERAL SURGERY OUTPATIENT DECISIONS

✧ Neuropathy: usually a glove and stocking pattern. Examine the lower limb for de-
creased sensation to light touch (cotton wool), sharp and blunt, vibration (tuning fork
on the big toe or malleoli), temperature (coldness of tuning fork on the skin).
✧ Vascular: perform a general vascular examination.
✧ Orthopaedic: observe the patient walking for abnormalities of gait. Examine the foot
for evidence of muscle imbalance, e.g. pes cavus, hallux valgus. Examine the joints of
the lower limb for swelling, tenderness, range of movement, crepitus.
Investigations
Carry out more quantitative tests for neuropathy: nerve conduction studies, thesiometer,
Semmes-Weinstein fibres. Arterial ABPI are performed. If the arteries are incompressible
ABPI is unreliable, although arterial stenoses may be suspected from the detection of
abnormal waveforms. Toe-pressures and/or the toe-pole test are alternative tests. Arterial
colour Duplex scans are required and/or angiography with magnified foot views. Take
X-rays of joints and bones underlying ulcers for evidence of osteomyelitis. Make tests of
diabetic control. Venous Duplex if indicated. Microbiology swabs of ulcers. Take biopsy
if long-standing, to exclude Marjolin’s or vasculitis.
Treatment
Treat complicated ulcers with antibiotics; clean the ulcer; advise bed rest and limb eleva-
tion; and perform debridement.
For simple ulcers, if predominantly neuropathic, advise bed rest, remove callus around
ulcer, use total contact plaster, moulded insoles and surgical shoes, silicon implants.
Diabetic arthropathy is similar to Charcot’s. It needs correct footwear and surgery to
stabilise the foot.
For neuropathy, improve diabetic control. Advise bed rest, remove callus around ulcer,
use total contact plaster, moulded insoles and surgical shoes, silicon implants.
Vascular ulcers may need angioplasty or bypass, including popliteal-pedal bypass, or
amputations.
Follow-up
Multidisciplinary diabetic foot clinic to assess results of investigations and monitor the
effect of treatment.
Post-operative follow-up
Standard vascular follow-up, depending on procedure performed.

Vascular lesions of the upper limb

The same arterial, venous and lymphatic pathologies can occur in the upper limb as in
the lower limb. However, the frequency and pattern of disease tends to be different. Also,
the anatomy of how blood vessels leave the chest and how nerves leave the neck to pass
over the first rib and under the clavicle to enter the arm plays an important role in the
development of pathology in this region – the thoracic outlet syndrome.
Atherosclerosis is less common in the vessels of the arm, but when it does occur it
tends to affect the aortic arch and the brachiocephalic and subclavian arteries proximal
to the origin of the vertebral artery. Because of the origin of the vertebral artery, stenotic
or embolic disease of the brachiocephalic and subclavian arteries may present with
symptoms of vertebrobasilar ischaemia (VBI) rather than arm ischaemia.
Venous thrombosis and obstruction can occur as a result of thoracic outlet obstruction
and present with a swollen cyanotic arm, but this is uncommon. Iatrogenic causes are much
more common, such as subclavian vein cannulation. Lymphoedema and other causes of
a swollen arm can occur and the underlying pathologies are similar to the lower limb.
 VASCULAR 283

Arterial lesions of the upper limb

Atherosclerosis occurs less frequently in the arm than in the leg, but is still the commonest
cause of ischaemia, though not the commonest cause of ischaemic-like symptoms (see
thoracic outlet compression syndrome (TOCS)).
Atherosclerosis affects the aortic arch and the brachiocephalic and subclavian artery
proximal to the origin of the vertebral artery, and it may give rise to ischaemic and embolic
symptoms in the arm. The source of emboli to the upper limb may be the arterial lesions,
but is more commonly the heart, originating from atrial fibrillation or mural thrombus
associated with myocardial infarction. Emboli can present with an acutely ischaemic
arm, or chronic microembolisation may present to the outpatients with a Raynaud’s-type
picture affecting the one hand. Untreated, this may eventually lead to occlusion of the
radial and ulnar arteries. Emboli originating from the subclavian and brachiocephalic
arteries may also cause vertebrobasilar transient ischaemic attacks (TIA).
Occlusions of the proximal subclavian artery may also cause haemodynamic vertebro-
basilar symptoms – the subclavian steal syndrome.
Non-atherosclerotic disorders of the arteries of the arm include Takayasu’s and giant
cell arteritis and Buergers. Irradiation of the chest and/or axilla for malignancy, e.g. breast
cancer, may result in long strictures of the subclavian, axillary and brachial arteries.
Localised arterial lesions distal to the origin of the vertebral artery are most commonly
due to compression resulting from TOCS. This may result in occlusion of the subclavian
artery causing chronic arm ischaemia or in aneurysm formation causing neurogenic
compression and distal embolisation.
History
Take a general and vascular history. History of general atherosclerosis affecting the heart
and the lower limbs suggests atherosclerosis as the cause of the arm symptoms. A history
of cardiac arrhythmias or recent myocardial infarct may suggest a cardiac source of
emboli. Patients may present with symptoms related to the arm, but also enquire about
vertebrobasilar symptoms.
✧ Arm symptoms include forearm fatigue, cold hand, rest pain in the hand and history
of embolisation: episodes of a pale, cold, painful, weak hand. Symptoms may be
similar to Raynaud’s but are unilateral. Symptoms may be constant, with pain,
paraesthesia, weakness and coldness, or intermittent with claudication, swelling and
colour change.
✧ Vertebrobasilar symptoms (TIAs): isolated symptoms are of limited significance. At
least three or more of the following symptoms are required for a diagnosis of VBI:
unilateral or bilateral simultaneous motor/sensory deficits, ataxia, diplopia, dysarthria,
dysphagia, bilateral homonymous hemianopia, vertigo, tinnitus, transient global
amnesia. Drop attacks or loss of consciousness may be the result of embolisation,
or if they coincide with vigorous use of the arm, may represent the subclavian steal
syndrome.
Examination
Perform a general cardiovascular examination. Examine the hands for evidence of
ischaemia and embolisation, e.g. splinter haemorrhages, skin infarcts. Examine for muscle
wasting. Note the rate and rhythm of the pulse. Examine for radial-radial delay. Palpate
all the pulses and listen for bruits. Examine the supraclavicular fossae for the presence
of cervical ribs or subclavian aneurysms. Perform Roos’ test. Perform a neurological
examination of the arms. Perform a musculoskeletal examination of the neck and
shoulder. Perform Tinel’s and Phalen’s test for carpal tunnel syndrome.
284 GENERAL SURGERY OUTPATIENT DECISIONS

Investigations
Compare the blood pressure in both arms using the Doppler. Repeat the measurements
with the cuff at the upper arm, upper forearm and lower forearm to detect segmental
occlusions of the brachial and forearm arteries. A pressure drop greater than 15 mmHg
is significant, but it may require exercise to produce it. Listen with the Doppler over the
thenar and hypothenar eminences for arterial signals from the plantar arch.
Take colour Duplex of the subclavian, axillary and brachial arteries in different positions
to detect stenoses, occlusions, aneurysms or compression. If vertebrobasilar symptoms
are present this should be combined with insonation of the carotid and vertebral arteries.
Visualisation of the brachiocephalic and proximal subclavian arteries is difficult with
colour Duplex, but disease in these segments may be associated with damped waveforms
more distally. Arch aortogram and selective brachiocephalic/subclavian angiogram is
necessary to define the lesions and determine the distal run-off vessels.
CXR, cervical spine and thoracic inlet views are required if thoracic outlet syndrome
is suspected, and these will define bony lesions, e.g. cervical ribs. MRI scan may detect
fibrous bands.
If a cardiac source of emboli is suspected, ECG and cardiac enzymes can be performed.
An echocardiogram may be indicated on the advice of a cardiologist.
If an arterial and cardiac lesion is excluded, suspect neurogenic TOCS and investigate
as appropriate (see TOCS section).
Treatment
Embolisation to the arm or vertebrobasilar circulation is treated with aspirin initially and
anticoagulation if this fails to control the symptoms.
Stenoses of the brachiocephalic and subclavian arteries can be treated with angioplasty
alone or combined with stenting. This treatment is also suitable for stenoses secondary
to arteritis or irradiation.
Lesions unable to be treated endovascularly may be considered for surgical repair.
Surgery consists of thoracic and extrathoracic procedures. Extrathoracic procedures
tend to be preferred because they are less invasive, e.g. subclavian-carotid transposition,
carotid-subclavian bypass, axillo-axillary bypass.
Disease distal to the vertebral origin requires vein bypass. Severe multi-segment disease
responds poorly to bypass and may respond better to upper thoracic sympathectomy or
intermittent prostocyclin infusions.
Subclavian artery stenosis, occlusion or aneurysm associated with thoracic outlet
syndrome requires resection of the constricting rib or band and repair or bypass of the
arterial defect.
Follow-up
If embolisation is suspected, admit the patient for in-patient investigation or start
antiembolic therapy and review at short intervals (1–3 weeks) with the results of investi-
gations until the source is identified or serious causes excluded and symptoms controlled.
Similarly, severe symptoms of ischaemia should be promptly investigated until an arterial
lesion has been excluded or confirmed.
Post-operative follow-up
Review after operation or endovascular treatment to determine the success of the pro-
cedure. Detect any residual neurogenic symptoms and treat as appropriate.
Thoracic outlet compression syndrome (TOCS)
The arteries, veins and nerves of the upper limb pass through a narrow space over the first
rib, between the sternomastoid and scalene muscles and under the clavicle to supply the
 VASCULAR 285

arm. In some patients this space is very narrow and these structures can be compressed,
resulting in the symptoms and signs of the TOCS.
In most patients (95%), symptoms are caused by compression of the nerves of the
upper or lower brachial plexus. In 5% of patients the subclavian artery and/or vein is
compressed. However, lesions of the subclavian artery may be limb threatening and
should be excluded in every case.
The causes of TOCS include cervical ribs, abnormal scaleneus anterior or medius
muscles, fibromuscular bands, abnormal first rib, callus or exostoses from the clavicle or
first rib, and neoplasms near the thoracic outlet.
Conditions that may cause similar symptoms in the arm and need to be excluded
include cervical spondylosis, cervical disc herniation, cervical spinal cord and plexus
lesions, shoulder joint and capsule abnormalities, ulnar nerve compression at the elbow,
median nerve compression (carpal tunnel syndrome), multiple sclerosis, motor neurone
disease and cardiac angina.
History
Most patients describe symptoms of pain, paraesthesia, weakness, coldness, numbness,
claudication, swelling or colour change. Symptoms may have occurred spontaneously
or have been precipitated by trauma or physical overactivity, e.g. painting the ceiling.
Symptoms may be worse during physical activity of the arm, e.g. carrying the shopping,
or occur when the arms are elevated, e.g. hanging out the washing. Symptoms may
become constant in long-standing cases.
✧ Upper plexus symptoms (C5, 6, 7) are suggested by pain in the neck, shoulder-tip,
upper chest, supra-scapular area, outside of upper arm, volar surface of thumb and
index finger.
✧ Lower plexus symptoms (C8, T1) are suggested by pain in the back of the neck and
adjacent scapular area, axilla, medial side of arm, ring and little fingers.

Colour change, numbness and paraesthesia can simulate Raynaud’s but represent
chronic microembolisation from an arterial lesion. Other arterial symptoms include arm
claudication, arm fatigue and weakness with exercise.
Venous symptoms include limb swelling and cyanotic colour change, heaviness accen-
tuated by exercise and relieved by rest. Elevation of the arm may aggravate the symptoms
by increasing the compression of the subclavian vein at the thoracic outlet.
Ulnar nerve compression at the elbow produces symptoms in the ulnar nerve distri-
bution distal to this point. Median nerve compression at the wrist, which is called carpal
tunnel syndrome, affects the median nerve in the hand only.
Lateral cervical disc prolapse tends to press on one nerve root, causing burning pain
in the relevant dermatome and muscle weakness and decreased reflexes in the relevant
myotome. Simultaneous pressure on half the spinal cord may cause Brown-Séquard
syndrome.
Intraforaminal osteophytes occurring with cervical spondylosis can effect and cause
symptoms in several nerve roots without an associated Brown-Séquard syndrome.
Examination
Examine the hands for evidence of ischaemia and embolisation, e.g. splinter haemor-
rhages, skin infarcts. Note the rate and rhythm of the pulse. Examine for radial-radial
delay. Palpate all the pulses and listen for bruits. Examine the supraclavicular fossae for
the presence of cervical ribs or subclavian aneurysms. Examine for arterial lesions as
described above.
Examine for muscle wasting of the arm and hand and perform a neurological
examination. Examine for muscle tone and motor weakness, reflexes and loss of
286 GENERAL SURGERY OUTPATIENT DECISIONS

sensation to pin prick and light touch. Perform Tinel’s and Phalen’s test for carpal tunnel
syndrome.
Perform Roos’ test. The arms are raised to the level of the shoulders, 90 degrees
abducted, and externally rotated – like a soldier surrendering. The hands are then
repeatedly clenched and unclenched for 1–2 minutes. Patients with TOCS can seldom
complete more than 30–40 seconds before pain forces them to stop. The hand may also
go pale and become hyperaemic when the position is released.
Perform a musculoskeletal examination of the neck and shoulder. Palpate for tenderness
and restricted movement, which may indicate cervical spondylosis, disc prolapse or
shoulder joint lesions, e.g. rotator cuff injuries.
A cyanotic, swollen arm with prominent venous collaterals suggests venous TOCS.
Investigations
Investigate arterial lesions as described above. Usually colour Duplex scan is sufficient to
investigate both arterial and venous TOCS; however, arteriograms and venograms may
be necessary.
CXR, cervical spine and thoracic inlet views are required if thoracic outlet syndrome
is suspected, and these will define bony lesions, e.g. cervical ribs. MRI scan may detect
fibrous bands.
Nerve conduction studies, electromyography and other neurophysiological tests are
often normal in TOCS, but are useful to exclude other neurological causes, e.g. spinal
cord lesions, ulnar and median nerve lesions.
Ultimately the diagnosis of neurogenic TOCS is clinical, after exclusion of other
pathologies by the investigations described.
Treatment
In the absence of arterial and venous lesions the initial management of neurogenic TOCS
is conservative, with analgesia, NSAIDs and physiotherapy to strengthen the neck and
shoulder girdle.
Embolic symptoms are treated with aspirin or anticoagulation initially, or with treat-
ment of the embolic source.
Surgery is reserved for cases where conservative measures have failed to relieve symp-
toms, there is impaired function of the limb or there are associated arterial or venous
lesions.
✧ The transaxillary approach is used if lower brachial plexus symptoms predomi-
nate, for resection of the first rib and if there is no cervical rib or arterial or venous
compression.
✧ The supraclavicular approach is used for excision of a cervical rib. It is used if upper
brachial plexus symptoms predominate; if there are lesions of the subclavian artery
or vein which need correction; or if fibrous bands or scalene muscle requires division.
If the first rib requires resection then a second infraclavicular incision is required to
access the anterior part of the rib.
Follow-up
The presence of arterial or venous lesions requires review at short intervals (1–4 weeks)
until the lesion is defined and the symptoms are stabilised. Neurogenic TOCS can be
reviewed at longer intervals (1–6 months) with the results of investigations and to assess
the effect of physiotherapy.
Post-operative follow-up
Patients are reviewed to assess the success of the procedure and to detect complications.
Initial complications include traction injuries to the brachial plexus or phrenic and long
 VASCULAR 287

thoracic nerves, and these will resolve within six months. Injuries may also occur to the
subclavian vessels and the thoracic duct.
Twenty per cent of patients develop recurrent TOCS within 18 months of the original
procedure. If severe, re-operation is required, performing whichever procedure was not
performed at the first operation, consistent with symptoms and physical signs.
Renal artery stenosis
Renal artery stenosis (RAS) is a potentially curable cause of hypertension and deteriorating
renal function. There are two main disease processes: atherosclerosis and fibromuscular
dysplasia (FMD). Other less common causes include Takayasu’s arteritis, renal artery
aneurysm, arteriovenous malformation, neurofibromatosis and Marfan’s syndrome.
Atherosclerosis tends to be associated with an atherosclerotic aorta and effects mainly
the ostia of the renal arteries. FMD is more common in women and affects the more
distal renal artery and its branches. FMD is a particularly common cause of renovascular
hypertension in children.
History
Patients may be referred with hypertension that is difficult to control, often requiring 3–4
antihypertensive agents. There may be episodes of flash pulmonary oedema, or they are
referred because of deteriorating renal function, especially after starting an ACE inhibitor.
In renal artery stenosis, contraction of the efferent glomerular arteriole is a protective
mechanism maintaining glomerular filtration. ACE inhibitors prevent this and renal
function deteriorates.
Examination
Perform a general and vascular examination. Measure the blood pressure. Evidence of
general atherosclerosis suggests this as the cause of renal artery stenosis. There may be
absent pulses and audible abdominal and flank bruits.
Investigation
Dipstick urine and perform routine haematology, biochemistry and serum lipids testing.
Perform abdominal USS to measure the length of the kidneys – less than 8–9cm indicates
an irretrievable loss of renal parenchyma, and correction of the renal artery stenosis is
pointless. Duplex of the renal arteries may identify stenoses, but is difficult due to bowel
gas.
Captopril renography is performed before and after a dose of ACE inhibitor. The
second renogram is worse than the first in the presence of RAS. This is sensitive only for
stenoses greater than 50% and does not differentiate between FMD and atherosclerosis.
Contrast arterial angiography is the gold standard, using lateral and oblique views
to define the RAS. FMD gives the classical string of beads appearance of alternating
stenoses and microaneurysm formation. Angiography also demonstrates ostial disease
and atherosclerotic aorta. Ask for lateral views of SMA and coeliac arteries as well, in case
extra-anatomical bypass is to be considered. Angiography will also demonstrate renal
artery aneurysms.
Treatment
This includes treatment of hypertension, hyperlipidaemia and renal failure.
Angioplasty
Angioplasty is the treatment of choice for FMD. Recurrent and renal artery branch
lesions also respond well. Angioplasty is less successful for atherosclerosis, and the main
indication is to try and preserve existing renal function. For atherosclerotic RAS causing
288 GENERAL SURGERY OUTPATIENT DECISIONS

hypertension, the most suitable cases for angioplasty consist of a unilateral stenosis with
a normal contralateral kidney. If hypertension has caused nephrosclerosis in the non-
stenosed kidney there will be improvement in the hypertension.
Surgical treatment
Nephrectomy is indicated for a small, scarred kidney producing significant amounts of
renin (renal vein renin ratio >1.5) causing hypertension, with a normal kidney on the
contralateral side.
Revascularisation
Revascularisation procedures are particularly appropriate where there is co-existing
aortic disease or angioplasty has failed and for bilateral RAS caused by atherosclerosis.
Surgery is the first-choice option for the solitary failing kidney.
Branch renal artery disease
FMD, renal artery aneurysm, dissection, diffuse atheroma and arteritis usually require
removal of the kidney, bench surgery to correct the abnormality and reimplantation
(autotransplantation).
Follow-up
Review with results of investigations and decide whether and which intervention is
indicated.
Post-operative follow-up
Long-term follow-up is required to detect recurrent disease causing deterioration in renal
function or hypertension so that secondary procedures can be instituted. Follow-up may
be performed by the relevant physician and referred back when required.
Intestinal ischaemia
Intestinal ischaemia is most commonly encountered as an acute emergency caused by
mesenteric artery embolism or thrombosis or by mesenteric venous thrombosis. Both
conditions are associated with high mortality despite prompt surgical intervention. In
the outpatient clinic, patients may be referred for investigation of symptoms attributed
to chronic mesenteric ischaemia.
The blood supply of the intestinal tract is particularly rich in collaterals. Therefore,
mesenteric ischaemia only occurs if two out of the three main intestinal arteries are
occluded or severely stenosed. Isolated mesenteric artery disease is unlikely to result
in mesenteric ischaemia unless previous abdominal surgery has been performed and
the collateral pathways have been disrupted. The most important artery for intestinal
blood supply is the SMA. Therefore, isolated stenosis of the coeliac or IMA rarely causes
intestinal ischaemia.
History
Take a general, gastrointestinal and vascular history. Typically, patients describe a constant
history of severe epigastric or periumbilical pain developing 30–45 minutes after food
every time they eat. The pain is increasing in severity but the patient may have learned
to reduce the pain by eating smaller meals, inducing vomiting before the 30–45 minutes
or avoiding eating completely. There is usually a history of severe weight loss. There may
be other symptoms of atherosclerosis, e.g. claudication, angina. There may be a history
of extensive investigation for gastrointestinal or psychiatric disease.
 VASCULAR 289

Examination
Perform a general, gastrointestinal and cardiovascular examination. There may be evi-
dence of severe weight loss and generalised atherosclerosis. Abdominal bruits may be
audible.
Investigation
Carry out a routine atherosclerotic screen, haematology, biochemistry including LFTs,
and serum lipids. Exclude more common causes of abdominal pain and weight loss, e.g.
carcinoma of the tail of the pancreas – CT or MRI scan is recommended if not previously
performed.
Duplex ultrasonography may identify mesenteric stenoses but examination is difficult
and a negative result does not exclude disease.
Mesenteric angiography with lateral aortic views is the gold standard. This may reveal
ostial occlusions, stenoses and disease of the aorta, renal arteries and other branches.
MRI scans and spiral CT angiography may also demonstrate disease.
Treatment
Consider if diagnosis is confirmed. Medical management consists of correction of pain,
fluid and electrolyte disturbances and malnourishment. Consider parenteral nutrition
until lesions can be treated.
Definitive treatment consists of angioplasty or surgery. Angioplasty of ostial lesions
tends to be difficult because of co-existent aortic disease. Complications of angioplasty
carry a high mortality and some centres recommend that angioplasty is reserved for
patients unfit for surgery.
Surgery is indicated in otherwise fit patients or after failed angioplasty. Procedures
consist of transaortic endarterectomy, mesenteric artery bypass or reimplantation of the
SMA. Occasionally, a median arcuate band from the crura of the diaphragm compresses
the coeliac artery and SMA. Release of this band relieves the stenosis. However, for
revascularisation procedures always revascularise the SMA and revascularise more than
one mesenteric artery if possible. Prolonged parenteral nutrition may be required in the
post-operative period.
Follow-up
Review at short intervals (1–6 weeks) with the results of investigation until cancer is
excluded and the mesenteric ischaemia is confirmed or excluded. Institute medical
therapy prior to definitive treatment.
Post-operative follow-up
Most patients will spend a long time in hospital after any procedure so the success or
otherwise of the procedure will be determined during this period. Long-term follow-up
with regular Duplex scans is indicated to detect recurrent disease, for which angiogram
and angioplasty may be appropriate. Redo surgery may be indicated for graft occlusion.
Vascular malformations
In contrast to common terminology, ‘vascular malformations’ refers to arterial and
venous abnormalities that have normal endothelial turnover, are present from birth, but
may not cause symptoms until later in life. Haemangiomas occur in infants, develop after
birth, demonstrate endothelial hyperplasia and tend to resolve spontaneously, although
this may not be complete.
Vascular malformations may be classified as high flow lesions or low flow lesions. High
flow lesions consist of arteriovenous malformations. Low flow lesions may be capillary,
venous, lymphatic or mixed malformations, but there is no arteriovenous shunting.
290 GENERAL SURGERY OUTPATIENT DECISIONS

Acquired arterial and venous abnormalities may result from trauma or iatrogenic
procedures. Certain malignant tumours may mimic the features of a vascular
malformation and must be excluded. The tumours include angiosarcomas and renal
and thyroid metastases.
Objectives
Differentiate vascular malformation from haemangioma; exclude malignant tumour;
classify vascular malformation into high flow and low flow; treat lesions conservatively
or with intervention.
History
Patients may describe a lesion that has been present from birth but may have become
symptomatic or increased in size at puberty, pregnancy or after an episode of trauma.
Patients with high flow lesions may complain of pain, excessive sweating over the lesion
and even ulceration and bleeding. Extremities may be painful due to ischaemia caused
by arteriovenous shunting proximal to their blood supply.
Patients with low flow lesions also complain of pain. For capillary lesions, pain may
be a predominant symptom, with little skin staining or swelling evident, though local
hyperhidrosis is common. Large venous lesions may cause pain due to engorgement
and episodes of spontaneous thrombosis. Pain may be worse after exercise and last for
days. Limb soft tissue and skeletal overgrowth is common, as is overlying eczema and
ulceration.
Lymphatic lesions are associated with deformity and exudation of fluid and are prone
to cellulitis.
For acquired vascular malformations there may be a history of trauma or iatrogenic
injury.
Examination
Perform a general and vascular examination. Assess the cardiac status. Note that exami-
nation may be normal despite the presence of a significant lesion. A small cutaneous
discoloration may indicate a large underlying malformation. If a mass is present, examine
it for size, consistency, tenderness and pulsation bruits. Venous lesions tend to be soft
and easily compressible with rapid refilling, and they engorge with dependency. Calcified
phleboliths may be palpable with the lesions. Lymphatic lesions may transilluminate.
High flow lesions tend to be firm, pulsatile and poorly compressible.
Examine for limb length and soft tissue and skeletal hypertrophy, e.g. the Parkes-
Weber limb. Tissue in such a limb does not pit on pressure, tends to be warmer than the
contralateral limb and may be associated with a machinery-type murmur. Such a limb
may demonstrate Branham’s sign – inflation of a tourniquet above arterial pressure
proximal to the high flow lesions is associated with slowing of the pulse, indicating a
significant arteriovenous shunt.
Traumatic lesions may be associated with scars.
Investigation
Duplex is a useful first-line investigation for differentiating high flow from low flow
lesions. MRI scan or spiral CT is then used to define the extent of the lesion and identify
any suspicious characteristics. X-rays may be useful to define bony lesions, and biopsy
for histology may be required to exclude malignancy.
For those lesions where intervention is considered appropriate, angiography for high
flow lesions, or venography for low flow lesions, is useful to delineate the lesions and plan
appropriate treatment.
 VASCULAR 291

Treatment
Treatment is multidisciplinary, involving a vascular surgeon, vascular radiologist, cardi-
ologist, plastic surgeon, orthopaedic surgeon and sometimes a maxillofacial surgeon.
Half of all lesions can be managed satisfactorily with compression hosiery and analgesia
as required. In addition, small superficial arteriovenous malformations may be cured by
surgical excision. For larger lesions not suitable for conservative treatment because of site
or size, or for symptoms not controlled by conservative measures, further intervention
consists of embolisation or surgical treatment.
✧ High flow lesions tend to be treated by repeated bouts of arterial or direct puncture
embolisation to control symptoms over many years. Those lesions thought to be
suitable for surgical excision can be pre-treated with embolisation to decrease intra-
operative vascularity and blood loss.
✧ Low flow lesions are treated by direct puncture sclerotherapy under imaging control
and either local or general anaesthetic. This tends to control the lesion rather than
cure it and may need to be reviewed at regular intervals.
Bony and tissue overgrowth abnormalities are treated by the plastic and orthopaedic
surgeons.
Follow-up
Patients are reviewed at short intervals (1–4 weeks) with the results of investigations until
malignant tumours are excluded and the extent of the lesions is defined. Patients con-
sidered suitable for conservative therapy are reviewed at regular intervals (1–6 months)
until the symptoms and condition are stable. They are then discharged or given an open
appointment.
Post-operative follow-up
Complications of embolisation include inadvertent embolisation of other arteries,
passage of emboli into the venous circulation and the post-embolisation syndrome of
pyrexia, leucocytosis and malaise. Most of these complications occur while the patient is
an in-patient, but post-embolisation syndrome may last for weeks. Infarction of overlying
skin is not uncommon but usually resolves.
Lesions are seldom cured by therapeutic procedures, e.g. embolisation, and need to
be repeated if and when the symptoms return as the lesion enlarges again. Therefore,
long-term follow-up with repeated Duplex ultrasound to monitor the size of the lesions
is advised.

Amputation
Unfortunately, treatment of vascular disease is not always successful or in the patient’s
best interest. Amputation of a gangrenous, ulcerated or critically ischaemic limb becomes
the only way to relieve the patient’s symptoms and sometimes to save his or her life.
Although the original treatment may not have been successful, it is important to maintain
a positive outlook for the overall well-being and to approach each amputation as an
interesting challenge.
Goals of surgery
The aim of amputation is to achieve the most distal level consistent with the causal
condition and a well-healed non-sensitive stump.
The goals of surgery are: firstly, ablation and secondly, reconstruction.
Many factors have to be taken into account when considering the level of amputation
and the procedure to be performed. Is the patient likely to walk with a prosthesis? Can
the knee joint be preserved?
292 GENERAL SURGERY OUTPATIENT DECISIONS

Other considerations include the pathology, anatomy of the proposed level of ampu-
tation, surgery, prosthesis and personal factors (age, sex, occupation and so on).
Phases
Amputation can be divided into three phases: pre-operative, operative and post-
operative.
✧ The pre-operative stage involves counselling, time to accept the decision (see breaking
bad news), limb fitting service, talking to a prosthetist and a rehabilitation plan.
✧ The operative stage involves antibiotics, DVT prophylaxis, anaesthesia: local
anaesthesia (LA) – sciatic, femoral block. Regional – spinal, epidural. GA. Perform
the correct procedure with good surgical technique.
✧ The post-operative stage involves pain relief (oedema, infection, DVT, medical
problems). Physiotherapy – early mobilisation – between bars, on crutches, pneumatic
post-amputation mobility (PPAM) aid after 7–10 days. Children and young adults get
immediate post-operative fitting. Exercise for balance, control of prosthesis, strength,
donning and doffing, toilet, stairs, home. Removal of sutures at three weeks.
Complications
Complications include non-healing, pain (acute, chronic), phantom limb pain, protrusion
of the bone end and inability to mobilise.
Non-healing is the most frustrating and demoralising complication for the patient.
Factors affecting healing are:
✧ tissue blood flow – pulses, arteriogram, cellulitis
✧ poor nutritional status
✧ infection, diabetes, medical conditions
✧ suboptimal surgical technique
✧ poor post-operative stump management.

Limb amputation operations

Below knee transtibial amputation
✧ Advantages: preserves knee joint, better mobility.
✧ Disadvantages: non-healing.
✧ Transection level: 12–15cm measured from the joint line, the shortest length to
preserve the tibial tubercle.
✧ Techniques: long posterior (Burgess) flap, sagittal – equal medial and lateral, skew
flap. All myofasciocutaneous flaps.
Above knee transfemoral
✧ Advantages: healing.
✧ Disadvantages: poor mobilisation.
✧ Transection level: as long as possible.
✧ Techniques: anterior-posterior flaps, long medial-sagittal flaps.
Through knee and Gritti-Stokes amputation
✧ Advantages: long stump, less traumatic, better for bilateral amputations, suitable for
hemiparesis with risk of hip and knee contractions.
✧ Disadvantages: non-healing.
✧ Techniques: knee disarticulation – end weight-bearing but bulky stump.

For Gritti-Stokes, remove the end of the femur and articular surface of the patella. The
cut surface of the patella is then fixed to the cut surface of the end of the femur. Non-end
weight-bearing stump.
 VASCULAR 293

Non-union between the patella and the end of the femur is the main problem.
Hip disarticulation, transiliac and sacroiliac amputations are more specialised
techniques.
Syme ankle disarticulation
✧ Advantages: stump tolerates end pressure, long lever, ability to walk without prosthesis,
good for trauma and congenital deformities.
✧ Disadvantages: non-healing in vascular and diabetic patients, for women it is less
cosmetic.
✧ Technique: disarticulate calcaneum and talus and remove end of tibia. Bring up heel
skin pad over end of stump.
Partial foot amputations
✧ Distal toe.
✧ Whole toe: racquet incision.
✧ Transmetatarsal: two levels head or base of metatarsal but always through cancellous
bone.

Amputations of arm, wrist and fingers are less commonly performed.

 Lumps and bumps
Miles Banwell and Michael Irwin
ELEVEN

Skin lesions
The skin consists of epidermis, dermis and adnexal structures, which include hair follicles,
sebaceous glands and eccrine and apocrine sweat glands.
Benign and malignant lesions can arise from any of these elements.
Benign lesions of the epidermis
Skin tags (squamous papillomas)
History
Skin tags are common (found in 25% of adults), particularly in obese patients. They begin
in the second decade, increasing in frequency up to the fifth decade. The axilla, neck and
inguinal regions are most affected. The skin tags can catch on clothing or jewellery.
Examination
The squamous papilloma appears as a small non-inflamed tag of skin. It is skin-coloured,
oval and mobile, with no deep fixation or induration of the base. A short broad-to-
narrow stalk lengthens and narrows as it grows. It rarely exceeds 1cm diameter.
Investigations
None.
Treatment
Excision biopsy.
Post-operative follow-up
Review with histology and check wound healing.
Common wart
The common wart is caused by the papillomavirus. It may occur anywhere on the body
but is commonly found on the hands and feet.
History
Occurs as slow-growing lesions, usually in the second decade of life. Painful if on the soles
of the feet (verrucas), or may catch and bleed.
Examination
Appears as exophytic growth or hard, tender, black area on the sole of the foot.
Investigations
None.
Treatment
Cryotherapy, curettage, topical preparations (40% salicylic acid or 5-fluorouracil (5FU)),
laser ablation. May regress spontaneously.
Post-treatment follow-up
Rarely indicated.

294
 LUMPS AND BUMPS 295

Seborrhoeic keratosis
This is associated with old age.
History
Painless, pigmented warty plaques that are unsightly and may catch on clothing and
bleed.
Examination
Appears as a ‘stuck-on’ brown warty plaque, often with variegated pigment and truncal
predominance. The plaque may grow quite large (to 1–2cm in diameter). Has a greasy
texture.
Investigations
None.
Treatment
Treat by curettage or excision. Other modalities include cryotherapy or topical
trichloroacetic acid.
Post-treatment follow-up
Review with histology and discharge.
Keratoacanthoma (molluscum sebaceum)
Benign, rapidly growing, self-healing skin tumour. Currently regarded as well-
differentiated, low-grade squamous cell carcinoma (SCC) and managed as such.
History
Found from fifth decade onwards, more commonly in males than females (by a 3:1 ratio),
and typically on the face or dorsum of the hand. It has a rapid six-week growth phase,
then involutes over the next six months. Usually painless, but may catch and bleed.
Examination
Appears as a globular tumour, with keratin plug/horn and radial symmetry.
Investigations
Excision biopsy.
Treatment
Excision. May require reconstruction, depending on size and position.
Post-operative follow-up
Review with histology.
Pre-malignant lesions of the epidermis
Actinic and solar keratosis
These are pre-malignant lesions. They usually occur on skin chronically exposed to
sunlight (face and hands). Approximately 5% become squamous cell cancers.
History
Occur from middle age onwards. The patient presents with erythematous macules and
papules with coarse adherent whitish scales. They are slow-growing lesions, not usually
associated with pain or bleeding.
296 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
The patient has erythematous, rough or scaly macules or papules, which may be ulcerated.
Examine lymph node fields.
Investigations
An excision biopsy is often indicated; especially in immunosuppressed (e.g. renal trans-
plant) patients, as these have a higher conversion rate to SCC.
Treatment
Cryotherapy, topical 5FU, excision. Less commonly, topical immune modulator
(imiquimod) or photodynamic therapy (PDT) is required.
Post-treatment follow-up
Long-term follow-up is required to detect recurrence or new lesions in the same or other
areas.
Bowen’s disease (intraepidermal SCC in situ)
The principal aetiology is sun damage. Bowen’s disease of glans penis is termed erythro-
plasia of Queyrat. Bowen’s disease of the nipple is associated with underlying ductal
carcinoma.
History
Bowen’s disease is a slow-growing, red, scaly plaque that may irritate and occasionally
bleed.
Examination
Examination shows a well-defined red hyperkeratotic plaque. There is clear potential for
invasive transformation. Ulceration suggests invasion.
Investigations
Skin biopsy under local anaesthetic. It is critical to exclude an underlying malignancy
(e.g. in the breast).
Treatment
Cryotherapy, 5FU, PDT, excision.
Post-treatment follow-up
No long-term follow-up is required once adequately treated.
Malignant lesions of the epidermis
Basal cell carcinoma (rodent ulcer) (BCC)
This is the most common skin cancer in white races. It is locally invasive, and metastasis
is extremely rare.
History
A slow-growing skin lesion that gradually ulcerates and may bleed. It is not painful unless
advanced.
Examination
Basal cell carcinomas are usually found on skin chronically exposed to sunlight and in
areas rich in pilosebaceous follicles. Hence more than 90% are found on the face. The
lesion is characterised by a pinkish colour, pearly edges and telangiectasia. There are
 LUMPS AND BUMPS 297

many subtypes, which may be broadly grouped as: localised (e.g. nodular/nodulocystic),
superficial, or infiltrative (e.g. morphoeic). Superficial BCCs are less easy to diagnose
clinically as they may simply present as a persistent erythematous macule. Infiltrative
(morphoeic) lesions tend to ‘ghost’ under the skin.
Investigations
Incision/excision biopsy if the diagnosis is uncertain. Uncommonly, in advanced lesions,
morbidity arises from invasion into underlying structures – nares/sinuses/external
auditory meatus/orbit/brain – and therefore may require magnetic resonance imaging or
computed tomography (MRI/CT). Gorlin’s syndrome (autosomal dominant inheritance)
comprises lifelong multiple BCCs, palmar pits and jaw cysts.
Treatment
Surgical excision with a 2–3mm margin. A wider margin (5mm) is required if the border
is indistinct or for larger lesions. For superficial BCCs, consider dermatology referral for
topical 5FU, topical imiquimod or PDT. Recurrent or infiltrative BCCs in anatomically
sensitive areas may require Mohs micrographic surgery. Also consider radiotherapy,
particularly in elderly patients.
Post-operative follow-up
Review with histology and discharge if excision is complete. Incomplete excision generally
requires further excision. Long-term follow-up is required for multiple recurrences or in
lesions narrowly excised in anatomical areas at high risk of deeper invasion.
Squamous cell carcinoma (SCC)
This is the second most common skin cancer in white races, yet its incidence is still only
one-quarter that of BCC’s. Associated factors include exposure to sunlight, Bowen’s
disease, chronic ulcers and burns (Marjolin’s). SCCs are prone to local recurrence (if
well differentiated there is a 7% risk, if poorly differentiated there is a 28% risk) and
metastases (there are lymph node metastases at presentation in 2–3%). Increased
metastatic potential is determined by location (sun exposed, e.g. lip and ear), diameter
(greater than 2cm), depth of invasion (greater than 4mm thick), poor differentiation and
perineural invasion and host immunosuppression.
Differential diagnosis includes keratoacanthoma, basal cell carcinoma, Bowen’s disease,
actinic keratosis, malignant melanoma, pyogenic granuloma and traumatised seborrhoeic
keratosis. Keratoacanthoma is now regarded as well-differentiated, low-grade SCC.
History
Patients describe a quickly growing lump that ulcerates and bleeds.
Examination
The edge of the ulcer is often raised and everted. Examine for regional
lymphadenopathy.
Investigations
Diagnosis is confirmed by biopsy.
Treatment
Wide local excision (5–10mm margin). Carry out therapeutic lymph node dissection
if indicated. Treatment should be co-ordinated through the local skin cancer
multidisciplinary team (MDT). Radiotherapy may be considered by the MDT if there is
a close margin or if the condition is recurrent or inoperable.
298 GENERAL SURGERY OUTPATIENT DECISIONS

Post-operative follow-up
Discuss within the forum of the local MDT. Review with histology to confirm the
diagnosis and that there was complete excision. Incomplete excision generally requires
further surgery. Long-term follow-up by a plastic surgeon/dermatologist is indicated if
high-risk lesions are found, as determined by histological thickness, if they are poorly
differentiated or in a difficult anatomic site.
Benign lesions of the dermis
Dermatofibroma (fibrous histiocytoma)
History
This is a usually slow-growing, irritating, brownish nodular lesion. Approximately 20%
are preceded by trauma or insect bite.
Examination
Dermatofibroma presents as a well-circumscribed reddish-brown nodule, which is firm
to palpation due to abundant fibrous stroma. It usually occurs on the legs, and is typically
less than 1cm in diameter.
Treatment
Excision biopsy.
Post-operative follow-up
Review with histology.
Hypertrophic scar
This is an abnormal scar limited by the initial boundary of the incision or wound.
Proposed aetiologies include increased wound tension, infection and delayed healing.
There is higher risk with an anatomical site (sternum, shoulders, deltoid). Hypertrophic
scars often regress spontaneously as they mature.
History
The scar develops within weeks of a wound healing and shows some degree of improve-
ment with time. There is little in the way of familial history.
Examination
It presents as a raised, thickened, pinky-red, often irritating scar confined to an injury
site.
Investigations
None.
Treatment
The first treatment is time (expectant). Otherwise, topical silicone gels/silicone sheets or
pressure garments (for at least six months). Finally, re-excision should be considered only
if the aetiology is clear. There is otherwise a high risk of recurrence. Liaise with plastic
surgery.
Keloid scar
This is an abnormal scar that develops months after injury, shows no regression and may
get worse between six and twelve months. It is more common in black African races, and
it has a familial tendency. Common sites include the face and earlobes (from piercing),
 LUMPS AND BUMPS 299

as well as those anatomical sites prone to hypertrophic scarring (see above). Original
wounds are often trivial and not under tension.

History
Exuberant scar formation progressing beyond six months. Itchy, hard and often painful.
There may have been a similar reaction in previous wound scars.

Examination
It presents as a heaped-up, exuberant, overgrown scar. It is defined by firm scar tissue that
extends beyond the boundaries of the incision or wound. By contrast, a hypertrophic scar
does not extend beyond these boundaries.

Investigations
None.

Treatment
These are generally referred to plastic surgeons for management. Intralesional steroid,
pressure garments or topical silicone may be indicated. Excision surgery is a last resort
and should be performed only in conjunction with other modalities, such as steroid
injection, pressure splints or radiotherapy.

Post-treatment follow-up
The response rates for all treatments are variable and follow-up depends on the treatment
modality. There is a high chance of recurrence, whichever is chosen.

Malignant lesions of the dermis

Metastatic carcinoma
This is the most common in tumours of the breast, lung and bowel.

History
There are small, hard, painless nodules in the skin, which may or may not be related to
the site of a previous tumour or irradiation.

Examination
Small hard nodules are found in an area adjacent to a previous surgical scar or radio-
therapy field. If arising in independent areas, exclude undiagnosed underlying primary
malignancy.

Investigations
Incision/excision biopsy.

Treatment
Excision, if possible. Defects from larger lesions may require plastic surgical reconstruction.
Otherwise, consider adjuvant therapies as appropriate. Ensure adequate ongoing
management of primary cancer.

Post-operative follow-up
Confirm diagnosis with histology and arrange appropriate therapy as indicated for
primary tumour.
300 GENERAL SURGERY OUTPATIENT DECISIONS

Pigmented skin lesions

Most suspicious pigmented lesions are referred to a dermatology or plastic surgery clinic
for excision if malignancy is suspected. However, knowledge of these lesions is necessary
for the general surgeon as they may be referred as simple skin lesions for day-case excision
without the appreciation that they may be malignant, especially if not pigmented.
Melanocytes are specialised cells located at the basal layer of the epidermis. They
synthesise melanin and store it in vesicles called melanosomes. Melanosomes are
distributed to surrounding cells. Melanin production is stimulated by sunlight and a
pituitary hormone, melanocyte-stimulating hormone (MSH). All races have approxi-
mately the same number of melanocytes, but the baseline activity of these cells varies.
Naevus cells are melanocytes that have entered the dermis and have a distinct pheno-
type. They are more spherical, have fewer dendritic processes and display aggregation in
nests.
Benign pigmented lesions
Benign pigmented lesions may be subdivided into those containing melanocytes
(melanocytic naevi) and those containing naevus cells (naevocellular naevi).
Melanocytic naevi
✧ Simple lentigo is a benign melanocytic naevus of the epidermis characterised by a tan
or brown macule with slightly irregular borders.
✧ Blue naevus is a benign melanocytic naevus of the dermis. It appears as a round area
of blue-black discolouration deeper in the skin.
Naevocellular naevi
✧ Benign naevocellular naevi include congenital (giant hairy naevus or non-giant hairy
naevus), acquired (junctional, compound, intradermal) or special (spitz, dysplastic,
halo) forms.
✧ Congenital naevus is histologically similar to a compound naevus, containing
junctional and intradermal components. It may be disfiguring, causing great parental
anxiety and concern. It appears as dark brown papules of variable size, and can be very
large and often hairy (giant hairy naevus). There is 1–2% malignant transformation,
mainly within the first five years of life. Sacral lesions are associated with spina bifida
or meningocoele. Treatment is by serial excision, also dermabrasion, curettage and
laser treatment.
✧ Junctional naevus is formed by nests of naevus cells clustered at the epidermal-dermal
junction. It is a deeply pigmented macule with a well-defined border. It is often found
on the trunk. It typically appears in the first and second decades. It progresses to
compound or intradermal naevus with age.
✧ Intradermal naevus is formed by nests of naevus cells clustered within the dermis. It
appears as a flesh-coloured or light tan dome-shaped papule. It is often found on the
face or neck. It typically appears in the second and third decades.
✧ Compound naevus contains junctional and intradermal components. It appears as a
dark brown papule with well-defined regular borders. It is often found on the trunk.
It typically arises up to early adulthood.
✧ Dysplastic (atypical) naevus has an irregular outline, variegated pigmentation and a
diameter greater than 5mm. It is often multiple (dysplastic naevus syndrome). There
is a 5–10% risk of malignant change to superficial spreading melanoma.
Treatment
Excision biopsy if recent changes create suspicion of melanoma (see below).
 LUMPS AND BUMPS 301

Post-operative follow-up
Follow up with a histology review. For dysplastic naevi, re-excision with wider margins
(up to 5mm) may be indicated.

Malignant pigmented lesions

There are a number of pigmented malignant skin lesions (e.g. pigmented BCC). However,
by far the most important to exclude is malignant melanoma, due to its high metastatic
potential and unpredictability. Absence of pigment does not exclude melanoma. A
diagnosis of amelanotic malignant melanoma should always be considered.

Malignant melanoma
Malignant melanoma is a malignant tumour of epidermal melanocytes. There are four
main subtypes.
✧ Superficial spreading melanoma is the commonest type of melanoma (60%). It has a
flat, irregular border, heavy and irregular pigmentation and a raised surface. Ulceration
indicates invasion. There is equal incidence in males and females, particularly in sun-
exposed areas – backs in men, lower legs in women. Radial growth occurs prior to
vertical growth.
✧ Nodular melanoma is the second most common melanoma (20%). It has early vertical
growth and therefore a poorer prognosis. It is typically uniformly black, but may be
amelanotic.
✧ Melanoma arising in lentigo maligna accounts for 5–10% of all melanomas. The
precursor lesion is lentigo maligna (Hutchinson’s freckle), which equates to melanoma
in situ (radial growth only), 40% of which will become invasive.
✧ Acral lentiginous melanoma accounts for 2–8% of all melanomas in Caucasians, and
40–60% in dark-skinned races. It arises on palms, soles, mucocutaneous junctions
and subungually. In subungual melanoma the great toe is the most common location,
then the thumb. A biopsy is needed to distinguish it from pigmented naevus of the
nail matrix. It is treated by amputation of the affected digit.
✧ Secondary melanoma (primary not identified) has a lymph node disease as its
main presentation (primary lesion regressed). Non-lymph node metastatic sites
include skin, brain, lung, bone, spinal cord and adrenals. Abdominal obstruction or
intersusception is a possible presentation of metastasis.

Treatment objectives
These are to exclude melanoma and to stage and treat melanoma in the context of the
regional melanoma MDT meeting.

History
Most patients present because they have noticed a new mole or a change in an existing
mole. National Institute for Health and Clinical Excellence (NICE) suspected cancer
referral guidelines (2005) detail three ‘major’ suspicious features of a mole: change in
size, irregular shape and irregular colour. There are four ‘minor’ features: largest diameter
greater than 6mm, inflammation, oozing and change in sensation. Major features score
two points, minor features one point; and a total of three points should trigger referral
to the local melanoma service for excision biopsy.

Examination
Examine the lesion for suspicious features (above). Check for satellite nodules, in-transit
metastases, palpable regional nodes, lymphoedema and hepatomegaly.
302 GENERAL SURGERY OUTPATIENT DECISIONS

Investigations
All suspicious pigmented lesions, which are not obviously benign on clinical examination,
require full thickness excision biopsy for histological confirmation. At this stage ensure
a minimal (2mm) margin until the histological diagnosis is certain. A cuff of subdermal
fat should be included in the biopsy to allow accurate histological analysis of depth of
invasion. Orientate the excision biopsy ellipse on limbs in a longitudinal axis to facilitate
future wide local excision. Histological analysis of the depth of invasion provides useful
prognostic information. The Breslow thickness (BT) classification measures the depth
of invasion from the stratum granulosum of the epidermis to the deepest part of the
tumour.
Melanoma staging is based on the tumour, node and metastasis (TNM) system, with
modifications from the American Joint Committee on Cancer (2001). Invasion of less
than 1.0mm carries a good prognosis. Invasion greater than 2.0mm carries a high risk of
metastases. Other histological features associated with poor prognoses include ulceration,
mitotic activity, neurovascular invasion and microscopic satellites.

Treatment
Treatment must be in accordance with NICE cancer service guidelines. Early referral to
the local melanoma service is mandatory, with referral prior to excision biopsy if there
is a high clinical index of suspicion. There must be immediate referral to the regional
melanoma MDT following the excision biopsy diagnosis. Subsequent management will
include wide local excision down to fascia, with margins determined by BT (1cm if BT
less than 1mm, 2cm if BT greater than 1mm). Therapeutic regional lymphadenectomy
is undertaken for nodal metastases and local control. Sentinel node biopsy remains
controversial and is undertaken only in selected centres in the context of clinical trials.
Chemotherapy, radiotherapy and immunotherapy, as guided by the oncologist in the
context of clinical trials, should be considered.

Post-operative follow-up
Undertaken by plastic surgery, dermatology and oncology.

Vascular skin lesions

Campbell de Morgan spots (cherry angiomata)
These are small (1–3mm) bright red spots found on sun-exposed skin in older patients.
They are an arteriovenous (AV) fistula of a dermal capillary. They are benign and require
no treatment.

Pyogenic granuloma
This is a rapid-growing benign vascular nodule, consisting of proliferating capillaries in a
loose stroma of connective tissue. Differential diagnosis includes amelanotic melanoma,
glomus tumour and Kaposi’s sarcoma.

History
There is usually a history of trauma at the site followed by a rapidly growing lesion, which
may bleed.

Examination
It presents as a dark red nodule of exuberant granulation tissue which may have ulcerated.
Common sites are fingers, upper chest, lip and toes.
 LUMPS AND BUMPS 303

Investigations
Excision biopsy to exclude malignancy.
Treatment
The condition often recurs after cautery, as proliferating vessels extend deep into the
dermis. Hence, it generally requires excision biopsy.
Post-operative follow-up
Review with histology and discharge.
Port wine stain
Port wine stain is usually present at birth (0.3% of live births). It is classified as a capillary
vascular malformation. It appears as a deep reddish-blue discolouration of the skin;
mostly on the face (cranial nerve V distribution), rarely on the trunk and extremities.
It grows in proportion to the child and persists lifelong. Two-thirds of patients develop
hyperplastic skin changes (cobblestoning) by adulthood. The most well-known syndromic
association is Sturge-Weber syndrome (ophthalmic CNV1 distribution) characterised
by intracranial lesions causing intractable epilepsy. Others include Klippel-Trenauney
syndrome (extremity distribution) and Cobb syndrome (truncal distribution). Treatment
is by cosmetic camouflage or argon/pulsed-dye laser therapy. However, laser therapy
shows no benefit in 20%, and the condition may recur in 50% after four years.
Strawberry naevus
Strawberry naevus is a red, soft, compressible, fleshy lesion arising on the head and neck
within or just after the first two weeks of life. It is classified as a capillary haemangioma.
It is relatively common. Multiple haemangiomas may be associated with internal hae-
mangiomas of major organs. There is a cycle of proliferation (strawberry phase) and
involution. Lesions tend to grow for six to eight months and then the majority regress
with time. Typically, 50% of lesions will have regressed by age five. Therefore, treatment
generally is non-operative and observation only is required. However, urgent treatment
is required for periorbital haemangiomas if they are obstructing visual fields (there is a
risk of deprivation amblyopia). If they are symptomatic (bleeding) or in an anatomically
difficult site, then refer for plastic surgery. Excision, pulsed-dye laser or intralesional
steroid injection may all be considered. Regressed lesions may leave a redundant skin
fold requiring excision.
Spider naevus (acquired telangiectasia)
This is a small red lesion (angioma) consisting of a central feeding arteriole with radiating
capillaries. It blanches on pressure. The presence of up to five is normal. It is common
in pregnancy but disappears in puerperium. Large numbers are associated with cirrhosis
of the liver. It also occurs in hyperthyroidism, carcinoid, post-irradiation, post-topical
steroid use, systemic lupus erythematosus (SLE) scleroderma and dermatomyositis. It
may be treated with pulsed-dye laser treatment.
Glomus tumour (angioneuromyoma)
Glomus bodies are small arteriovenous anastomoses involved in thermoregulation.
Tumours are associated with nerve and muscle and classically occur in fingers and toes,
particularly in the nail bed, where they cause nail ridging. They are dark bluish-red, cold
intolerant and exquisitely tender due to association with nerves. Treatment is by surgical
excision.
304 GENERAL SURGERY OUTPATIENT DECISIONS

Kaposi’s sarcoma
This is a malignant tumour of endothelial cells and perivascular connective tissue cells.
It may occur in immunosuppressed patients and is commonly seen in AIDS patients
(50%).
History
Patient complains of a slightly tender raised nodule. There may be a history of
immunosuppression.
Examination
Examination finds a raised purplish nodule, which may be single or multiple.
Investigations
Excision biopsy.
Treatment
Excision biopsy. Local radiotherapy or cytotoxic therapy may be indicated for
multi ple lesions. Ensure aetiological factors are investigated and managed (e.g.
immunosuppression).
Post-operative follow-up
Refer to the appropriate speciality: dermatology, plastics, or infectious diseases.

Lesions of skin appendages

Epidermoid cyst (sebaceous cyst)
These arise due to blockage of the duct of a sebaceous gland. Sebaceous glands are
common on the scalp, face, neck and back.
History
An epidermoid cyst appears as a slow-growing lump, which occasionally discharges or
becomes infected and inflamed.
Examination
Examination finds a soft/firm spherical lump with a central punctum on the skin surface.
It arises within the dermis and often extends deeper, but it is tethered to the epidermis.
It may discharge through the punctum.
Investigations
None.
Treatment
Treat by surgical excision. If the cyst is acutely infected, allow to settle first with antibiotics.
An abscess may require incision and drainage. At excision, failure to remove the cyst wall
completely may result in recurrence.
Post-operative follow-up
Review with histology and confirm wound healing. Wound infection is common,
especially if the cyst ruptures during excision. It usually responds to antibiotics.
Dermoid cyst
Dermoid cysts may be congenital or acquired. Congenital cysts are usually present in
 LUMPS AND BUMPS 305

young children. They are most common at the embryological fusion lines of the head
and neck (inclusion cysts), usually at the outer angle of the eyebrow (external angular
dermoid). Acquired cysts are a complication of trauma, where a piece of epidermis is
translocated into deeper tissue (implantation cyst). They are commonly seen following
hand injuries.
History
There is a firm subcutaneous lump arising at a site of trauma or previous surgery.
Alternatively, a soft slow-growing lump, with no history of trauma and typically at the
eyebrow, is noticed in early childhood.
Examination
Examination finds a firm discrete lump under the skin, located at embryological fusion
lines (congenital) or associated with a previous scar (acquired).
Investigations
Excision biopsy. Congenital cysts are referred to paediatric surgery/plastics for work-up
(CT/MRI is indicated for deep extension).
Treatment
Excision biopsy.
Post-operative follow-up
None.
Pilonidal sinus
Pilonidal sinus is a chronic infection of the skin caused by penetration of hairs into
the skin and subcutaneous tissues. A sinus is formed that leads to a cavity filled with
hair and granulation tissue. Common sites include the natal cleft, between the fingers
(hairdressers) or occasionally the umbilicus or axilla.
Differential diagnosis includes perianal fistula, hidradenitis suppurativa and simple
boils.
History
Pilonidal sinus is seen as a chronically discharging skin infection that fails to clear despite
courses of antibiotics. There may be repeated episodes of inflammation and discharge.
Examination
Perform a general examination. Depending on the site, there will usually be evidence of
one or more sinuses, and hairs may be visible within these. There is usually evidence of
chronic inflammation or discharging sinus.
Investigations
Microbiology, blood sugar, urine dipstick.
Treatment
Treat conservatively with careful wound toilet and shaving of surrounding hair. Use
antibiotics in acute phases, incision and drainage for acute abscesses. Surgical excision
may be required for chronic disease; and it may require plastic surgical reconstruction.
Consider laser depilation to prevent recurrence.
306 GENERAL SURGERY OUTPATIENT DECISIONS

Post-operative follow-up
Review with histology and to confirm healing.
Hidradenitis suppurativa
This is a chronic indolent disease of skin and subcutaneous tissue in apocrine gland-
bearing areas, characterised by recurrent deep abscesses in axillae, groins, perineum and
perianal areas. Staphylococcus aureus is the usual organism, but occasionally coliforms
are cultured.
Differential diagnosis includes folliculitis, carbuncle, cellulitis or, in the perianal area,
pilonidal sinus or perianal fistula.
History
There is recurrent inflammation and infection that fails to respond to repeat courses of
antibiotics. It is most common in young adult females.
Examination
There is an involved area of skin that is indurated and fibrotic, with evidence of chronic
inflammation. Chronically discharging sinuses may be present.
Investigations
Microbiology.
Treatment
Non-surgical treatment should include advice on weight loss and stopping smoking
(both are strong risk factors). Encourage careful personal hygiene and antiseptic washes
(chlorhexidine). Consider dermatology referral for advice on long-term antibiotics
(clindamycin) and antiandrogens (cyproterone acetate) in females. Abscesses require
incision and drainage. In severe disease, excision of the affected hair/gland bearing skin
may be indicated. Healing is by secondary intention or primary closure for small defects.
Alternatively, larger defects are reconstructed with split skin grafts or a local flap (plastic
surgery).
Post-treatment follow-up
Review at regular intervals (1–3 months) to monitor the effect of conservative therapy
and decide if surgical intervention is indicated.

Subcutaneous lesions
Lipoma
A lipoma is a soft benign tumour of adipose tissue. Lipomas usually occur singly, but may
be multiple. They are commonly subcutaneous, but can be intramuscular. Lipomas are
normally painless. If the tumour is tender, then it is more likely to be an angiolipoma.
Rarely, liposarcomatous change can occur in a benign lipoma. There is a higher index of
suspicion for malignant change if the lesion is large, rapidly growing or painful.
History
Appears as a slow-growing lump under the skin; is usually asymptomatic.
Examination
Examination finds a lump in the subcutaneous tissue not attached to the dermis. It is
often lobulated. The absence of a punctum helps differentiate it from an epidermoid cyst.
The contraction of the underlying muscle helps to distinguish between subcutaneous and
intramuscular locations.
 LUMPS AND BUMPS 307

Investigations
There are usually none. If diagnosis is uncertain or there are unusual features, ultrasound
(USS) or CT/MRI scan is indicated. Consider FNA cytology if the lesion is suspicious.
Treatment
Most lipomas can be excised (shelled out) under local anaesthetic. Large or intramuscular
lipomas require general anaesthetic excision. Liposuction may be considered with larger
lesions to minimise scarring, but it is associated with a higher recurrence rate.
Post-treatment follow-up
None, unless reviewing with result of investigations or to assess wound healing following
large lipoma removal.
Neurofibroma
A neurofibroma is a benign tumour arising from neural tissue and supporting stromal
cells. It is a soft fleshy tumour, which is either sessile or pedunculated. Neurofibromatosis
(von Recklinghausen’s disease) patients have multiple tumours, arising throughout life. It
is a disfiguring condition that causes great distress to sufferers. It is commonly caused by
autosomal dominant inheritance following sporadic mutation. Type 1 neurofibromatosis
is associated with mainly cutaneous features, and type 2 neurofibromatosis is associated
with central nervous system (CNS) tumours (neurofibromas). Occasionally, malignant
change to neurofibrosarcoma occurs (with increase in size and pain).
History
A single lump or, more commonly, multiple soft cutaneous lumps over the body.
Otherwise asymptomatic, although it may become traumatised, leading to inflammation
or infection. There may be a positive family history.
Examination
There are usually several fleshy lesions, which may be tender to palpation. Neurofibromatosis
is associated with café-au-lait patches and axillary freckles.
Investigation
Excision biopsy to confirm the diagnosis.
Treatment
Treatment is by excision if symptomatic or if there is suspicion of neurofibrosarcomatous
change. Delayed healing is common.
Post-operative follow-up
Review with histology and confirm wound healing. Discharge with advice or refer to
clinical genetics.

Disorders of the nails

Ingrowing toenail (onychocryptosis)
Ingrowing toenail is a common condition, mainly in young people. It usually affects
the lateral edge of the great toenail. A sharp edge of the nail traumatises the nail bed
causing pain, ulceration, infection and a granulation tissue response, which exacerbates
the condition.
308 GENERAL SURGERY OUTPATIENT DECISIONS

History
There is a history of pain, recurrent inflammation and infection at the side of the nail.
Examination
The condition most commonly affects the lateral side of the great toe but can affect both
sides or other toes. The affected skin at the side of the nail is inflamed, boggy and swollen,
with onycholysis and creeping over-granulation.
Investigations
Usually none. Microbiology, including fungal scrapings, if diagnosis unclear.
Treatment
Mild cases may respond to antibiotics and chiropody.
Other cases require surgical treatment. Surgical procedures include simple nail
avulsion, wedge excision and phenolisation, and Zadek’s procedure (total excision of the
germinal matrix).
Post-treatment follow-up
Follow up at regular intervals (1–3 months) if using conservative management. Proceed
to surgery if such management fails.
Post-operative follow-up
Review to determine wound healing. Complications include infection, prolonged wound
healing and recurrence.
Onychogryphosis
This is a ‘rams horn’ deformity of the toenail, usually affecting the big toes of elderly
people.
History
Patients complain of increasing thickening and deformity of the nail, which is difficult
to cut and interferes with footwear.
Examination
The nail is thickened, yellow and hooked. Aetiology includes trauma and fungal
infections.
Investigations
Microbiology (fungal scrapings).
Treatment
Initial treatment is chiropody. Otherwise removal of the nail or Zadek’s procedure.
Post-operative follow-up
Review to confirm healing. Complications are the same as for ingrowing toenail.
Subungal exostosis
This is a bony lump arising from the distal phalanx, which grows underneath the nail. It
usually affects the great toe.
History
A young patient complains of pain and deformity of the toenail. The nail may have failed
to respond to treatment for ingrowing toenail.
 LUMPS AND BUMPS 309

Examination
The toenail appears to be pushed up by a lesion arising underneath the nail bed.
Investigations
An X-ray of the toe reveals the bony exostosis.
Treatment
Consider plastic or orthopaedic surgery referral for removal of the nail and excision of
the bony nodule, with careful nail bed preservation.
Post-operative follow-up
Review with histology before discharge.

Groin lumps
One of the most common presentations in general surgery is with a lump in the groin.
The differential diagnosis is large but in practical terms the main distinction is between
hernias and other causes. Differential diagnosis of a lump in the groin:
✧ skin and soft tissues
∝ sebaceous cyst
∝ lipoma
✧ hernias
∝ inguinal
∝ femoral
✧ vascular
∝ femoral artery aneurysm
∝ sapheno varix
✧ lymphadenopathy
∝ generalised versus localised
✧ renal/urogenital system
∝ ectopic or maldescended testis
∝ transplanted kidney.

Inguinal hernias
History
There may be a sudden onset related to abdominal straining. There is a reducible lump,
which may be increasing in size.
Examination
There is a reducible lump in the groin arising from above the inguinal ligament (usually
above and medial to the pubic tubercle). There is an expansile cough impulse. Direct
hernias appear medial to the deep ring.
Investigations
None, or USS.
Treatment
Conservative if unfit for surgery, but most are repaired surgically.
Post-treatment follow-up
None, or review with results of investigations.
310 GENERAL SURGERY OUTPATIENT DECISIONS

Post-operative follow-up
Review to confirm successful repair and wound healing at around six weeks.
Femoral hernias
History
There may be sudden onset related to abdominal straining, typically in the female. There
is a reducible lump, which may be increasing in size.
Examination
Examination finds a reducible lump in the groin arising below the medial end of the
inguinal ligament (below and lateral to the pubic tubercle).
Investigations
None, or USS.
Treatment
Surgical repair.
Post-operative follow-up
Review to confirm successful repair and wound healing at six weeks.
Lymph node mass
Enlarged lymph nodes in the groin can be a great source of diagnostic confusion.
The femoral canal normally contains a lymph node, which if enlarged can be mistaken
for a femoral hernia. Lymph nodes overlying the femoral artery may transmit the
pulsation and resemble a femoral artery aneurysm.
If enlarged lymph nodes are recognised, their management is the same as lymph nodes
elsewhere in the body.
The objective is to determine whether the enlargement is localised or whether it is part
of a generalised lymphadenopathy. If it is localised, examine the whole drainage area for
a cause, i.e. infective, neoplastic.
History
Ask about local symptoms for the drainage area of that group of lymph nodes, e.g. leg,
perineum, anus, scrotum, lower abdomen or back. Ask about other lumps elsewhere on
the body. General symptoms include weight loss and night sweats.
Examination
Examine the lump, noting size, consistency and so on. Determine whether the lump is
isolated or part of a general enlargement. Perform a general examination of all lymph
node sites including the liver and spleen. Perform a thorough examination of the drainage
area of the lymph node for a possible infective or neoplastic cause of lymph node
enlargement. Include a rectal examination for possible anal tumour.
Investigations
Excision biopsy of the enlarged lymph node is not the first investigation. Laboratory
tests include FBC and blood film, plasma viscosity/erythrocyte sedimentation rate (PV/
ESR) and Monospot/Paul Bunnel (for glandular fever). Perform fine-needle aspiration
of non-pulsatile lumps for cytology, and use microbiology, including Ziehl-Neelsen (ZN)
stain and TB culture. Use USS to exclude other causes. Perform an excision biopsy for
lymphoma.
 LUMPS AND BUMPS 311

Treatment
Treatment depends on the results of investigations.
In children and young people, once lymphoma is excluded, the cause is usually infective
and will settle. Similarly, the management of TB lymphadenopathy is the relevant
chemotherapy.
In cases related to generalised lymphadenopathy, e.g. lymphoma/leukaemia or
glandular fever, the management is of the underlying condition. Local causes may include
SCC, melanoma, genital infection/neoplasm or an infective lesion on a leg.
Follow-up
Review at short intervals until cancer is excluded. Determine whether excision biopsy is
necessary.
Post-operative follow-up
Review with histology and confirm wound healing. Treat any underlying condition
appropriately.
Possible complications include damage to surrounding structures, lymphocoele,
infected lymphocoele and non-healing. Non-healing is particularly associated with TB
or neoplastic causes and responds to treatment of the underlying condition.
Lipoma
(see above)
Sebaceous cyst
(see above)
Hydrocoele of the cord
Usually, the hydrocoeles are confined to the scrotum. Isolated hydrocoeles can occur in
the spermatic cord and present with lumps in the inguinal canal.
History
There is a slow-growing, non-reducible lump in the groin.
Examination
Examination finds a non-reducible lump in the groin that does not arise from the deep
inguinal ring. The lump is usually mobile, has no expansile cough impulse and may be
made to transilluminate. The lump moves down with traction on the ipsilateral testis.
Investigations
None, or USS and/or FNA.
Treatment
Aspiration or surgical excision.
Follow-up
None, or review with results of investigations (at four to eight weeks).
Post-operative follow-up
Review with histology and to confirm wound healing (at four to six weeks). Complications
are similar to those for inguinal hernia.
312 GENERAL SURGERY OUTPATIENT DECISIONS

Undescended/maldescended testis
Undescended testes are seldom palpable in the groin except in the thinnest of individuals,
but maldescended testes may lie in an abnormal position after emerging through the
external inguinal ring.
History
There is a tender lump in the groin, upper thigh or lower abdomen. There is an absent
testicle on one side of the scrotum. Ask whether the testicle has always been absent or has
been noticed in the scrotum at some time. Maldescended testes are usually asymptomatic.
If symptoms occur it may be that the testicle is now diseased.
Examination
Examination reveals an absent testis in the scrotum. There is a testicle-like lump in one
of the above sites.
Investigations
None, or USS to identify testicular internal architecture.
Treatment
If the patient is pre-pubertal, replace in the scrotum if the testis is normal to inspection at
operation. After puberty, orchidectomy is performed, as the testis is unlikely to function
and carries an increased risk of tumour formation.
Follow-up
Review with results of investigations (at four to eight weeks).
Post-operative follow-up
Review with histology (if orchidectomy performed) and confirm wound healing.
Complications are similar to those for inguinal hernia or hydrocoele repair.
Sapheno varix
A sapheno varix may be best described as a venous aneurysm of the long saphenous vein
just before its junction with the femoral vein in the groin.
History
There is a soft lump in the groin which disappears on lying down. Usually there is a
history of varicose veins.
Examination
Examination finds a soft reducible lump in the groin arising below the middle of the
inguinal ligament. The lump disappears on lying down. Varicose veins are usually visible
in the affected leg.
Investigations
None, or venous Duplex scan.
Treatment
Varicose vein operation.
Post-treatment follow-up
Review with results of investigations (at one to three months)
 LUMPS AND BUMPS 313

Post-operative follow-up
Review to determine the success of the operation and to confirm wound healing.
Complications are those described for varicose vein operation.
Femoral artery aneurysm
True femoral aneurysms involve all three layers of the artery wall and often occur in
conjunction with abdominal aortic or popliteal aneurysms, which may also require
treatment. False femoral aneurysms usually occur after arterial injury or cannulation of
the femoral artery. Blood escapes from the lumen of the artery but is ‘contained’ by the
adventitia of the artery to produce a swelling that transmits a pulsation.
History
True femoral aneurysms usually present with a history of a gradually increasing firm
pulsatile lump in the groin. Femoral aneurysms may embolise and block off distal
arteries, so ask about claudication, rest pain or blue toes. If there is a history of recent
injury or cannulation, e.g. cardiac angiography, then consider false femoral aneurysm as
the cause.
Examination
Look for a pulsatile lump in the groin that does not reduce or disappear when the patient
is lying down. A true aneurysm is expansile in three directions at once (medial, lateral,
anterior). A false aneurysm has only transmitted pulsation.
Examine all other arteries for aneurysmal disease. Examine for evidence of distal
embolisation and peripheral ischaemia.
Investigations
Duplex ultrasound of aorta, iliac, femoral and popliteal arteries.
Treatment
Surgical repair of both forms of aneurysm.
Follow-up
Review with investigations (at one to three months)
Post-operative follow-up
Review to confirm graft function and wound healing.

Scrotal lumps/testicular swellings

Although disorders of the testes and scrotum are increasingly being referred to urologists,
they are still a common problem in general surgery clinics.
By definition, scrotal lumps originate in the scrotum, and on examination it nearly
always is possible to get above the lump. If the lump is confirmed as scrotal, the next
question is whether the swelling involves the whole scrotum or whether it is localised to
one side or one part of the scrotum. Does the swelling arise from the skin and connective
tissue of the scrotum, the coverings of the testicle, i.e. tunica vaginalis, the appendages of
the testicle, e.g. epididymis, or the body of the testicle itself? Is the lump cystic or solid?
The most important objective in all scrotal lumps is to exclude testicular cancer.
Skin
Problems may include sebaceous cysts, warts, chancre and skin cancer, e.g. epithelioma
(most common in chimney sweeps and tar workers).
314 GENERAL SURGERY OUTPATIENT DECISIONS

Connective tissue
Idiopathic lymphoedema occurs spontaneously or in response to friction and other
triggers. Secondary lymphoedema may result from generalised oedema, e.g. CCF, renal
failure. Infections may cause lymphatic obstruction, e.g. Wuchereria bancrofti produces
the well known elephantiasis of the scrotum. Pelvic cellulitis, ascites and skin infection
are other causes.
Tunica vaginalis
This describes a double walled covering of the testis. In health this contains a small
amount of fluid which acts as a lubricant for movement of the testis. A large amount of
fluid can accumulate to produce a hydrocoele. Hydrocoeles may occur spontaneously or
be secondary to underlying disease of the testis, e.g. infection, tumour. Blood may also
accumulate in the same way and is known as a haematocoele. In cases of gross infection
pus may accumulate to produce a pyocoele.
Testicular appendages
Cysts and swellings occur in the epididymis and spermatic cord, producing lumps that
are palpable and separate from the testis, e.g. epididymal cyst, varicocoele.
Testis
Lumps arising from the body of the testis are tumours until proven otherwise.
Hydrocoele
Hydrocoeles are a collection of fluid in the tunica surrounding the testes.
Hydrocoeles may be primary or secondary. Primary hydrocoeles occur spontaneously
and there is no underlying cause. They usually occur in men aged over 40. In secondary
hydrocoeles, fluid accumulates because of underlying inflammation, infection, trauma
or tumour of the testis, and it occurs in younger men.
Primary hydrocoeles may be classified as the following.
✧ Vaginal hydrocoele, which occurs within the tunica vaginalis and surrounds the testis
and does not communicate with the peritoneal cavity.
✧ Congenital hydrocoele, which is associated with a hernial sac and communicates with
the peritoneal cavity.
✧ Infantile hydrocoele, which extends from the testis to the deep inguinal ring but does
not communicate with the peritoneal cavity.
✧ Hydrocoele of the cord, which occurs anywhere along the spermatic cord, and can
occur in women as hydrocoele of the Canal of Nuck.
Objectives
Treatment objectives are to diagnose the hydrocoele, differentiate primary from secondary,
treat the hydrocoele and treat the underlying cause.
History
Patients complain of a gradually increasing swelling of the scrotum. In primary
hydrocoeles, this is usually painless, although patients may report a dragging sensation. In
secondary hydrocoeles, there may be a history of tenderness, inflammation and systemic
illness. Ask about genito-urinary infections. In children with congenital hydrocoeles these
may fill up during the day when upright and empty at night when supine.
Examination
Examine the scrotum, inguinal region and the testes. Confirm the presence of a scrotal lump
and assess the swelling according to the criteria in the introduction to scrotal lumps.
 LUMPS AND BUMPS 315

If the testis is not palpable separate from the lump, then a hydrocoele is likely. Does the
lump transilluminate? All primary hydrocoeles transilluminate because they contain clear
watery fluid. Secondary hydrocoeles may not transilluminate to the same extent because
they may contain turbid fluid, pus or blood. A hydrocoele of the cord moves down when
traction is applied to the testis. Aspiration of a tense hydrocoele may be necessary to allow
palpation of the testis.
Investigations
For primary hydrocoeles, USS may confirm difficult cases. A sample of fluid may be
aspirated and sent for cytology and microbiology. The testis is then palpated to confirm
a normal shape, contour and smooth surface.
For secondary hydrocoeles, USS is usually performed to confirm the presence of a
hydrocoele and to examine the underlying testis. A sample of fluid may be aspirated and
sent for cytology and microbiology. If tumour is suspected, ultrasound is mandatory,
and so are determinations of serum alpha-foetoprotein (AFP) and human chorionic
gonadotropin (beta hCG). If urinary tract infection is suspected, a sample of urine is
sent for microbiology.
Treatment
For primary hydrocoeles, aspirate to dryness and review in two to four weeks. If the
hydrocoele recurs, a further attempt at aspiration is justified. In the elderly and unfit this
can be repeated every two to three months, but in most patients surgery is indicated if
the hydrocoele recurs.
In children with a congenital hydrocoele, an inguinal operation is required to deal with
the accompanying hernia sac.
For secondary hydrocoele, treatment is primarily of the underlying disorder.
Follow-up
Secondary hydrocoeles should be reviewed at short intervals (one to four weeks) until
cancer is excluded. Thereafter, review at regular intervals until evidence shows that the
underlying condition is responding to treatment. In primary hydrocoele, review every
one to three months and aspirate or arrange for surgery. Complications of aspiration
include infection and haematoma.
Post-operative follow-up
In primary hydrocoele, review after four to six weeks to determine the success of the
operation and to check wound healing.
Epididymal cyst
Epididymal cysts are similar collections of fluid to hydrocoeles but are separate from
the testis. Spermatocoeles are similar to epididymal cysts but consist of turbid fluid that
contains spermatozoa. Both may be multiple or multilocular.
Objectives
Treatment objectives are to diagnose the cyst, exclude other causes and treat the cyst.
History
Patients complain of a gradually increasing lump separate from the testes. There is seldom
any secondary history, although patients may report an aching or dragging sensation in
the testicle, groin or lumbar region.
316 GENERAL SURGERY OUTPATIENT DECISIONS

Examination
Perform a general and abdominal examination. Confirm the presence of a scrotal lump –
you can get above it. The lump is smooth, oval and separate from, above and to the lateral
side of a normal testis. Epididymal cysts usually transilluminate, and may be multiple
and bilateral.
Investigation
None, or ultrasound in difficult cases. Lumps may be aspirated to dryness. Aspiration of
clear watery fluid confirms the diagnosis (whitish turbid fluid suggests a spermatocoele).
Blood-stained fluid should be sent for cytology and microbiology.
Treatment
Aspirate to dryness in the clinic and review. Epididymal cysts tend to recur after
aspiration.
Post-treatment follow-up
Review at one- to three-monthly intervals. If the cyst recurs more than twice, surgery is
indicated. Complications of aspiration include haematoma and infection.
Post-operative follow-up
Determine the successful removal of the cyst and wound healing. Generally the scrotum
heals very well. Wound infections respond to antibiotics. Successful removal of one cyst
does not prevent others from forming in the future.
Haematocoele
Haematoceles are similar to hydrocoeles but contain blood instead of fluid.
Haematoceles may result from aspiration of a hydrocoele if the needle causes bleeding
within the scrotum. Haematoceles may also complicate surgical procedures of the groin
or scrotum, e.g. hydrocoele, scrotal hernia repair. Other causes include trauma, torsion
or tumour.
Objectives
Treatment objectives are to diagnose haematocoele, exclude cancer and treat the
haematocoele.
History
Determine the onset of the swelling and any precipitating cause, e.g. surgical procedure
or trauma. Onset related to trauma or torsion is usually rapid. Tumour causes a more
gradual onset. However, sudden onset may occur due to rupture of a small vessel involved
in the growth. Patients may ascribe this to an episode of trauma, which may be mild.
Testes involved with tumour are more prone to bleeding after trauma.
Examination
Examine the scrotum, inguinal region and testes. A haematocele is usually a tense, firm
scrotal lump, similar on examination to a hydrocoele except it does not transilluminate.
In addition, there may be ecchymosis of the scrotal skin.
Investigations
Aspiration of blood confirms the diagnosis but does not establish the underlying cause.
If tumour is suspected then USS should be performed to define testicular architecture,
and measure serum beta-hCG and AFP.
 LUMPS AND BUMPS 317

Treatment
If the condition presents acutely, admit for exploration and evacuation of haematoma
once tumour has been excluded. In elderly unfit patients, or if the haematocele is chronic,
i.e. organised haematoma, a conservative course can be followed with analgesia and a
scrotal support.
Post-treatment follow-up
If immediate exploration is not indicated, review at short intervals (one to four weeks)
until cancer is excluded. If a conservative course is being followed, review at regular
intervals (one to three months) until there is evidence of resolution. Then discharge or
give an open appointment.
Post-operative follow-up
Review to confirm the success of the operation and wound healing (at four to six weeks).
Complications are similar to those for hydrocoele repair.
Varicocoele
Varicocoele is a malformation of dilated veins surrounding the testis in the scrotum.
Varicocoeles may be primary or secondary. The vast majority are primary and are
congenital. Their importance is that they may inhibit sperm production because they
maintain the testis at a higher temperature than is optimal for spermatogenesis. Secondary
varicocoeles are rare but may be caused by obstruction to the testicular vein as it joins the
renal vein, by thrombus or tumour extending along the renal vein or by fibrosis caused by
excess adrenaline in the blood draining from an adrenal phaeochromocytoma.
Objectives
Treatment objectives are to diagnose the varicocoele, detect secondary causes, treat the
varicocoele and treat any underlying cause.
History
Usually young men (teens and early twenties) complain of a generalised swelling in
the scrotum that is worse on standing. A patient may also complain of a heaviness or
dragging sensation. Varicocoeles may occur in older age groups or in patients with
systemic symptoms suggesting kidney tumours or phaeochromocytomas. There may be
a history of infertility.
Examination
On standing the scrotum feels full – like a bag of worms. The swelling reduces considerably
and may disappear on lying down and on elevation of the scrotum. The testis is normal
to palpation.
Investigations
USS of testis and, if indicated, of kidney and adrenal gland. If secondary causes are
suspected CT/MRI of kidney and adrenal, and investigation of urinary free catecholamine
levels, FBC, urea and electrolytes.
Treatment
Mild cases do not require treatment, especially if they are unilateral. The dragging
sensation may be helped by a scrotal support. More severe cases can be treated by ligation
of all but one of the veins in the spermatic cord in the groin or laparoscopically by
clipping the veins inside the peritoneal cavity.
318 GENERAL SURGERY OUTPATIENT DECISIONS

Post-treatment follow-up
If unilateral and mild, advise and discharge or review once (at four to six weeks) after
use of scrotal support to relieve symptoms. If symptoms are persistent or severe, surgery
may be indicated.
Post-operative follow-up
Review after four to six weeks to determine the success of the operation (gauged by relief
from heavy sensation and resolution of veins) and check wound healing.
Chronic epididymo-orchitis
Epididymitis describes inflammation/infection confined to the spermatic cord and
epididymis. Orchitis describes inflammation/infection confined to the testis. Epididymo-
orchitis describes infection/inflammation affecting both. It can be acute or chronic.
Acute infections are usually investigated and treated as an in-patient procedure and will
not be described again here. Chronic infections may be referred to the outpatient clinic
due to repeated episodes of inflammation or for investigation of a testicular swelling or
hydrocoele.
In children and in men over the age of 35, acute epididymo-orchitis is usually second-
ary to bacterial infection of the urinary tract, which may have disordered anatomy
allowing infection. In younger men the urinary tract is normal and epididymo-orchitis
is usually due to sexually transmitted organisms, e.g. Neisseria gonorrhoea, Chlamydia,
Herpes simplex and Trichomonas vaginalis.
In all age groups, epididymitis can be secondary to systemic disease, e.g. TB,
Brucella, sarcoid and Cryptococcus. Other rare causes of testicular infection include the
following.
✧ Pyogenic orchitis, which may occur following an episode of generalised sepsis and
occasionally destroys the testis.
✧ Viral orchitis, which may occur secondary to influenza and coxsackie virus infection
but most commonly is secondary to mumps. It occurs exclusively in post-pubertal
patients and starts four to six days after the parotitis to give testicular swelling and a
hydrocoele.
✧ Granulomatous orchitis, which may occur following trauma, infection, chemicals or
post-vasectomy. The testis becomes enlarged and tender.
Objectives
Objectives are to diagnose epididymitis, exclude tumour or underlying systemic disease,
exclude abnormalities of the urinary tract, treat epididymitis and treat any underlying
condition.
History
Take a general history for symptoms, which may suggest a systemic cause. Usually,
symptoms are confined to the genito-urinary tract, and patients describe recurrent
episodes of pain in the epididymis and testis following episodes of dysuria or urethral
discharge. This may settle with a course of antibiotics but not completely resolve and
it may be a continuing source of symptoms over weeks or months. Ask about sexual
encounters to determine the risk of infection and symptoms affecting the patient’s sexual
partner.
If indicated, ask questions to exclude the rarer causes outlined above.
Examination
Perform a general examination. The scrotum may be erythematous, swollen and tender.
A hydrocoele may be present. Try to determine the point of maximal tenderness, i.e.
 LUMPS AND BUMPS 319

epididymis or testis or both. The epididymis may feel thickened and hard. The testis may
be enlarged, irregular and firm.
Investigations
Investigations include midstream specimen of urine (MSU) or microscopy, and culture
and sensitivity (C&S) test of urethral discharge. If cultures are not diagnostic, send blood
for immunology for IgG and IgM antibodies to Chlamydia. Check U&Es to exclude
evidence of renal impairment. In children and elderly men, further investigation of the
urinary tract may be indicated to exclude congenital abnormalities or obstruction.
If tumour cannot be excluded, a USS of the testis is indicated, as well as estimations of
serum AFP and beta-hCG. If the USS suggests disordered testicular architecture, surgical
biopsy/orchidectomy of the testis may be indicated, which may also be necessary for the
diagnosis of tuberculosis, sarcoid, malakoplakia and some other conditions.
Treatment
Symptomatic treatment includes analgesia, scrotal support and occasionally drainage of
a tense hydrocoele. Children and older men are treated for common urinary pathogens.
Chronic epididymo-orchitis in young men may require prolonged treatment with
doxycycline, erythromycin or similar drugs. Treatment of secondary conditions is of the
underlying condition. Treatment of mumps orchitis is symptomatic.
Post-treatment follow-up
Follow up at short intervals (one to four weeks) until acute infection settles and tumour
or serious causes are excluded. Thereafter, follow up at longer intervals (one to three
months) to allow time for treatment to work and inflammation to settle. Remember
to arrange further investigation of the urinary tract in children and elderly men.
Complications of epididymo-orchitis include abscess formation, testicular infarction
and obstruction of sperm. Abscess formation is suspected if infection fails to settle and
pain and swelling persist. USS may demonstrate pus. Treatment requires incision and
drainage or orchidectomy.
Post-operative follow-up
Review with histology and treat the underlying cause appropriately. Complications
include wound infection, hydrocoele and scarring.
Testicular tumours
Testicular tumours are the commonest tumours affecting young men. The management
of such tumours is specialised, and the general surgical management consists mainly
of diagnosis and referral to a urologist and oncologist. It is important to consider the
diagnosis in any patient with scrotal pathology, especially since complete cure can be
expected if diagnosis is made early enough.
Tumours may arise from all tissue components in the testis, but 90% of tumours are
either teratomas (ages 25–30) or seminomas (ages 35–40). Other tumours account for the
remaining 10% and include lymphomas (which tend to develop in elderly men), Sertoli
cell and Leydig cell tumours.
Carcinoma in situ has been identified with increasing use of testicular biopsy for
investigation of infertility. These patients have a 50% risk of developing testicular cancer
within five years.
Objectives
Objectives are to diagnose testicular cancer, stage the cancer and treat the cancer.
320 GENERAL SURGERY OUTPATIENT DECISIONS

History
Take a general history. The classical history is of painless enlargement of the testis, but the
condition can present mimicking infection, hydrocoele and trauma. The diagnosis should
be considered in all scrotal swellings. Weight loss, back pain or shortness of breath may
indicate extensive disease. Headaches may indicate brain metastases.
Examination
Perform a general examination. Examine the scrotum and determine the characteristics
of the lump or swelling. Examine for distant spread. Examine the supraclavicular fossae
for lymph nodes and the chest for bronchial lung metastases, pleural effusions and so on.
Examine the abdomen for central lymph node masses and other signs.
Investigations
USS of both testes. Serum estimation of B-hCG and AFP, which is raised in 50–90%
of non-seminomatous tumours. These levels may also be raised in seminomas with a
teratomatous element.
Definitive diagnosis is by inguinal exploration of testis and testicular biopsy, performed
by an experienced urologist. Initial staging is by CXR and by thoracic and abdominal CT
scan. Bone and brain scans may be indicated by clinical findings.
Treatment
Treatment is administered by a urologist and oncologist with a special interest. It consists
of radiotherapy and chemotherapy, depending on the stage of the tumour.
Post-treatment follow-up
Follow-up is undertaken by the urologist/oncologist.
GENERAL SURGERY
OUTPATIENT DECISIONS
second edition

Few doctors receive formal training in how to conduct an outpatient consultation or how to compose
and dictate an outpatient letter. Trainee surgeons in each new speciality spend their first few weeks in
outpatient clinics learning by experience with all the pitfalls this entails. Much work involves seeing
patients who have been brought back for review by their predecessors. Problems are caused by
inexperience, unfamiliarity, fear of making mistakes, the pressure of patient numbers and lack of training.
New doctors will find little help in the standard textbooks on how to follow-up patients. This book
provides the necessary background information to enable rational decision making in a concise and
economical style. It describes reasonable and safe lines of management suitable for most patients, ideal for
when discussion with a senior colleague is not possible.
The information in this new edition has been revised, expanded and presented in the context of today’s
specialist clinics and multidisciplinary teams. This new edition is multi-authored to take account of the
multidisciplinary approach.
As well as an overall review of general outpatient issues, every major speciality is covered, with clear notes
for each condition covering history, examination, investigations, results, treatment, follow-up and post-
operative follow-up. The book can be read before or during clinics, and enables trainees to have an action
plan in mind before they walk into a consultation.
All surgeons have to be trained to go through the process of dealing with unfamiliar clinical conditions
for the first time. Surgeons will use this book as a useful foundation on which to build their own personal
knowledge.
other radcliffe books of related interest
Handbook of General Surgical Emergencies
Sam Mehta, Andrew Hindmarsh and Leila Rees
Safe Sedation for All Practitioners
a practical guide
James Watts
Treating Common Diseases
Hugh McGavock and Dennis Johnston

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