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Obstetric Anesthesia and
Uncommon Disorders
2nd edition
Edited by

David R. Gambling
M. Joanne Douglas
Robert S. F. McKay
CAMBRIDGE UNIVERSITY PRESS
Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo

Cambridge University Press

The Edinburgh Building, Cambridge CB2 8RU, UK
Published in the United States of America by Cambridge University Press, New York
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© Cambridge University Press 2008

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 CONTENTS

List of plates page vi 12 Chronic pain in pregnancy

List of contributors vii Hector J. Lacassie and Holly A. Muir 229
Preface ix
Section 4 Metabolic disorders 239
Section 1 Cardiovascular and respiratory disorders 1
13 Disorders of intermediary metabolism
1 Structural heart disease in pregnant women Stephen Halpern and Bhadresh Shah 239
Brendan Carvalho and Ethan Jackson 1
14 Liver and renal disease
2 Disorders of cardiac conduction M. J. Paech and K. Scott 249
Jean E. Swenerton, Ravishankar Agaram, and Victor F. Huckell 29
15 Malignant hyperthermia
3 Vascular diseases M. Joanne Douglas 269
David R. Gambling 57
16 Rare endocrine disorders
4 Respiratory disorders in pregnancy J. M. Mhyre and L. S. Polley 275
John Philip and Shiv K. Sharma 75
Section 5 Other disorders 293
Section 2 Musculoskeletal disorders 101
17 Blood disorders
5 Myopathies M. Joanne Douglas and Penny Ballem 293
Chantal Crochetiere 101
18 Infectious diseases in pregnancy
6 Parturients of short stature Gabriela Rocha Lauretti and Robert S. F. McKay 321
Andrea J. Fuller, Sheila E. Cohen, and Emily F. Ratner 115
19 Dermatoses
7 Disorders of the vertebral column Robert S. F. McKay and John E. Schlicher 343
Edward T. Crosby 129
20 Psychiatric disorders in pregnancy
8 Miscellaneous skeletal and connective tissue disorders Timothy J. G. Pavy 363
in pregnancy
Caroline Grange 145 21 Malignancy and pregnancy
Holly A. Muir, Michael Smith, and David R. Gambling 371
Section 3 Nervous system disorders 167
22 Pregnancy and transplantation
9 Disorders of the central nervous system in pregnancy
Kerri M. Robertson 381
J. Martinez-Tica and R. B. Vadhera 167

23 Autoimmune diseases
10 Spinal cord disorders
Caroline Grange 405
Roanne Preston 191

Index 423
11 Peripheral neuropathy
Felicity Reynolds 215

v
 PLATES

Plate section between pages 278 and 279

Figure 14.1 page 262

Figure 17.1 296

Figure 17.3 305

Figure 17.4 307

Figure 19.1 346

Figure 19.2 349

vi
 CONTRIBUTORS

Ravishankar Agaram, MBBS, MD (Anes), FRCA David R. Gambling, MB, BS, FRCPC
Specialist Registrar Clinical Associate Professor
Department of Anaesthetics Department Anesthesiology, University of California, San Diego
Glasgow Royal Infirmary San Diego, CA, USA
Glasgow, UK Staff Anesthesiologist, Sharp Mary Birch Hospital for Women

Penny Ballem, BSc, MSc, MD, FRCPC Caroline Grange, MBBS

Clinical Professor Consultant Anaesthetist
Department of Medicine Nuffield Department of Anaesthetics
School of Hematology The John Radcliffe Hospital
Faculty of Medicine Oxford, UK
University of British Columbia
Vancouver, BC, Canada Stephen Halpern, MD, MSc, FRCPC
Professor, Department of Anesthesia
Brendan Carvalho, MB, BCh, FRCA University of Toronto
Department of Anesthesia Director of Obstetrical Anesthesia
Stanford University School of Medicine Sunnybrook and Women’s College Health Sciences Centre
Stanford, CA, USA Toronto, Ontario, Canada

Sheila E. Cohen, MB, ChB, FRCA Victor F. Huckell, MD

Professor of Anesthesia and of Obstetrics and Gynecology Clinical Professor of Medicine
Department of Anesthesia University of British Columbia
Stanford University School of Medicine Vancouver, BC, Canada
Stanford, CA, USA
Ethan Jackson, MD
Chantal Crochetiere, MD, FRCPC Clinical Assistant Professor of Cardiothoracic Anesthesia
Assistant Professor Director of Intraoperative Transesophageal Echocardiography,
University of Montréal and Division Chief of Adult Congenital Cardiothoracic Anesthesia
Department of Anesthesiology Stanford University Medical Center and
Sainte-Justine Hospital Lucille Packard Children’s Hospital at Stanford University.
Chemin Côte-Ste-Catherine Stanford, CA, USA
Montréal QC, Canada
Hector J. Lacassie, MD
Edward T. Crosby, MD, FRCPC Associate Professor
Department of Anesthesiology Anesthesiology Department
Ottawa Hospital – General Campus Pontificia Universidad Católica de Chile and
Ottawa, Ontario, Canada Visiting Associate, Duke University Medical Center
Durham, NC, USA
M. Joanne Douglas, MD, FRCPC
Department of Anesthesia Gabriela Rocha Lauretti, MD, PhD
BC Women’s Hospital Professora Associada (Anestesiologista)
Vancouver, Canada Universidade de São Paulo
Faculdade de Medicina de Ribeirão Preto
Andrea J. Fuller, MD Av. Bandeirantes
Northern Colorado Anesthesia Professional Consultants Ribeirão Preto-SP, Brasil
Staff Physician
Fort Collins, CO, USA J. Martinez-Tica, MD
Associate Professor
Department of Anesthesiology
University of Texas Medical Branch
Galveston, TX, USA

vii
List of contributors

Robert S. F. McKay, MD Felicity Reynolds, MB BS, MD, FRCA, FRCOG ad eundem

Clinical Professor and Chair Emeritus Professor of Obstetric Anaesthesia
Department of Anesthesiology St Thomas’s Hospital
University of Kansas School of Medicine – Wichita London, UK
Wichita, KS, USA
Kerri M. Robertson, MD
J. M. Mhyre, MD Associate Clinical Professor
Robert Wood Johnson Clinical Scholar Chief, GVTCCM Division
Lecturer, Department of Anesthesiology Chief, Liver Transplantation
Division of Obstetrical Anesthesiology Department of Anesthesiology
Duke University Medical Center
Holly A. Muir, MD Durham, NC, USA
Vice Chair Clinical Operations Department of Anesthesiology
Chief, Division of Women’s Anesthesia John E. Schlicher, MD, FAAD
Duke University Medical Center Private Practice Dermatologist
Durham, North Carolina, USA Beatrice Keller Clinic
Sun City West, AZ, USA
M. J. Paech, MB
School of Medicine and Pharmacology K. Scott, BM, FRCA
The University of Western Australia Specialist Registrar in Anaesthesia
Department of Anaesthesia and Pain Medicine Oxford Radcliffe Hospitals NHS Trust
King Edward Memorial Hospital for Women Oxford, UK
Subiaco, Western Australia
Bhadresh Shah, MB, BS, MD
Timothy J. G. Pavy, MBBS, FANZCA, FRCA, FFPMANZCA, DA, DIP, Fellow in Obstetrical Anesthesia
MID, COG Sunnybrook and Women’s College Health Sciences Centre
Staff Specialist Anaesthetist and Head of Department Toronto, Ontario, Canada
Department of Anaesthesia and Pain Medicine
King Edward Memorial Hospital Shiv K. Sharma, MD, FRCA, Professor
Subiaco, Western Australia Department of Anesthesiology and Pain Management
Obstetric Division
John Philip, MD, Associate Professor University of Texas Southwestern Medical Center
Department of Anesthesiology and Pain Management Dallas, TX, USA
University of Texas Southwestern Medical Center
Dallas, TX, USA Michael Smith, MD
Chief Resident in Anesthesiology
L. S. Polley, MD Department of Anesthesiology
Associate Professor of Anesthesiology University of Kansas School of Medicine – Wichita
Director, Obstetric Anesthesiology Wichita, KS, USA
University of Michigan Health System
F3900 Mott Children’s Hospital Jean E. Swenerton, MD, FRCPC
Ann Arbor, MI, USA Clinical Associate Professor
Division of Obstetric Anesthesia
Roanne Preston, MD, FRCPC Faculty of Medicine
Department of Anesthesia The University of British Columbia
BC Women’s Hospital Canada
Vancouver, BC, Canada
R. B. Vadhera, MD, FRCA, FFARCSI
Emily F. Ratner, MD, DABMA Director, OB Anesthesia
Associate Professor Department of Anesthesiology
Co-Director, Division of Medical Acupuncture University of Texas Medical Branch
Department of Anesthesia Galveston, TX, USA
Stanford University School of Medicine
Stanford, CA, USA

viii
 P R E F A C E TO TH E S E C O N D E D I T I O N

It has been almost ten years since the first edition of Obstetric This book is dedicated to my wife Kimberley and children
Anesthesia and Uncommon Disorders was published. Over the Carwyn, Jake, and Samantha. David R. Gambling
past few years colleagues have asked the editors when they
This book is dedicated to my family: my mother, Bill, Matthew,
could expect to see a new edition. We had some hesitation, not
Sheila, Erin, and Mark, who fill my life with joy.
least of which was because we felt that many practioners could
M. Joanne Douglas
find most of this information for themselves using the internet or
subspecialty journals. Upon reflection, we recognized that there We dedicate this book to the many anesthesiologists who work
is no substitute for a textbook that contains information gathered long hours to provide safe care to mothers and babies, and to their
and carefully reviewed by a number of devoted specialists. Hence, families who make the sacrifices that allow their loved one to
spurred on by those requests for a second edition it was decided provide this care. Thank you Susan, Lindsey, and Katie.
to create a revision that provides more recent references and Robert S. F. McKay
reflects some of the changes in obstetric anesthesia practice
To the memory of Dr Clive Meintjies a wonderful friend, mentor
that have occurred over the past ten years. With the assistance
and doctor.
of a third editor, Robert S. F. McKay, we recruited some outstand-
ing new contributors from around the world and created a second
edition that we trust the reader will find useful. We have contin-
ued to use chapters based on body systems and diseases. We have
consolidated some chapters, split others, and added two new
chapters, namely ‘Chronic pain in pregnancy’ and ‘Malignancy
and pregnancy’. There are now 23 chapters each illustrated with
figures, tables, and photographs, and each chapter is accompa-
nied by a comprehensive list of updated references.
We thank our new publishers, Cambridge University Press, for
giving us the opportunity to produce this revision, and we would
like to thank each and every contributor for their hard work and
commitment to this project.
Finally, we want to thank our families for their patience while
we spent hours, too numerous to count, fine tuning each chapter.

ix
 SECTION 1: CARDIOVASCULAR AND RESPIRATORY DISORDERS

1 STRUCTURAL HEART DISEASE IN PREGNANT WOMEN

Brendan Carvalho and Ethan Jackson

Introduction Pregnancy exerts a progressive cardiovascular stress that peaks

at approximately 28–32 weeks of gestation.9 Cardiac output (CO)
This chapter will outline the physiological changes, hemodynamic
starts to increase by the tenth week of gestation and continues to
goals, management, and anesthetic options with regards to patients
rise to a peak of 30–50% above baseline by 32 weeks’ gestation.
with acquired or congenital structural heart disease during preg-
The increase in CO is due to increased stroke volume (SV) – up to
nancy, labor, and delivery. There is no consensus as to the optimal
30% above baseline – in the first half of pregnancy. This is in
anesthetic technique for the conditions being discussed. General
contrast to the latter half of pregnancy when CO is maintained
and regional anesthesia can have significant cardiovascular effects
by an increase in heart rate (HR) – up to 15% above baseline – in
on a parturient with cardiac disease. In addition, many pharmaco-
addition to the increased SV. Plasma volume increases by 40–50%
logical agents commonly used in anesthetic and obstetric practice
from prepregnant levels. This raised plasma volume exceeds the
can have adverse hemodynamic effects (Table 1.1).
increase in red blood cells resulting in a relative anemia that may
Due to the nature and the rarity of the cardiac diseases discussed,
compromise oxygen delivery. Blood pressure (BP) usually falls
there is a lack of randomized controlled studies to guide our
during pregnancy due to progesterone-induced vasodilatation
practice. As a result, case reports and expert opinion will form the
and the low resistance placental bed. Pulse pressure widens due
basis of discussing the anesthetic techniques. However, management
to a greater reduction in diastolic BP compared to systolic BP.
options and anesthetic techniques must be individualized and
Hyperventilation associated with pregnancy results from the
based on the prevailing hemodynamic condition and obstetric needs.
respiratory stimulating effects of progesterone and leads to hypo-
carbia (PaCO2 27–34 mmHg) and a mild respiratory alkalosis (pH
Scope of the problem of 7.40–7.45).
Labor pain, periodic changes in venous return due to uterine
An estimated 0.2–3.0% of pregnant patients have cardiac disease,1 contractions, and maternal expulsive efforts increase CO approxi-
an increasing cause of maternal mortality.2,3 The 2000– 2 Confidential mately 45% above prelabor levels. These physiological stresses
Enquiries into Maternal Deaths in the United Kingdom reported that can be minimized by good analgesia and anesthesia, careful fluid
cardiac disease was the second most common nonobstetric cause and hemodynamic management, as well as careful positioning to
of maternal death after psychiatric disease.4 Cardiac disease is avoid aortocaval compression.10
also more common than the leading direct causes of maternal Further increases in preload occur after delivery due to auto-
death.4,5 The maternal mortality rate ranges from 0.4% in New transfusion from the contracting uterus and relief of aortocaval
York Heart Association (NYHA) class I–II women to 6.8% in class compression.11 These fluid shifts cause further stress on an
III–IV (Tables 1.2 and 1.3). Despite a dramatic decline over the last already potentially compromised cardiac lesion. Postpartum nor-
few decades in the incidence of rheumatic heart disease among malization of systemic vascular resistance (SVR) and loss of the
women of childbearing age in the developed world, more women low resistance placental bed increases afterload. Careful fluid and
with partially or fully corrected congenital heart disease (CHD) hemodynamic monitoring for days to weeks postpartum are
are surviving to reproductive age because of improved surgical essential to minimize potential problems in this crucial period.
techniques and advances in medical management.6,7
The principal danger for a pregnant woman with a heart lesion
is cardiac decompensation because of the inability to meet the Symptoms and signs of normal pregnancy
additional demands imposed by the physiological changes of preg- and heart disease
nancy and parturition. In addition, infection, hemorrhage, and Easy fatigability, dyspnea, and orthopnea of normal pregnancy
thromboembolism can compound the risk. Maternal and neonatal may simulate heart disease. Orthopnea is more common in obese
outcomes can both be improved by meticulous peripartum care. women and may be due to limitation of diaphragmatic motion.
However, some women with serious cardiac disease may still suffer Chest pain during pregnancy is most often due to hiatal hernia,
significant morbidity and mortality despite optimal medical care.4,8 esophageal reflux, or distension of the ribcage. Tachycardia is
normal in pregnancy, as are premature atrial and ventricular
depolarizations. Orthostatic syncope may occur with sudden
Physiology of pregnancy
assumption of the upright position. Syncope occurring in later
A comparison between normal cardiopulmonary parameters in pregnancy is usually due to supine hypotension secondary to
the pregnant and nonpregnant states is shown in Table 1.4. inferior vena caval compression.

Obstetric Anesthesia and Uncommon Disorders, eds. David R. Gambling, M. Joanne Douglas and Robert S. F. McKay. Published by Cambridge University Press.
# Cambridge University Press 2008.
1 Cardiovascular and respiratory disorders

Table 1.1 Cardiovascular effects of commonly used anesthetic and obstetric drugs

Cardiac Myocardial
Heart rate Blood pressure SVR output contractility Venodilation

Etomidate « « or # « or # « « «
Ketamine "" " " or « " "a «
Thiopental " ## « to " b # # "
Propofol " or « # ## « to # # "
Succinylcholine « to # with « to " « to " « « « to #
repeat doses
Atracurium « or " « to # « « « « to "
Pancuronium " " « to " " " «
Rocuronium « or " « « « « «
Vecuronium « « « « « «
Fentanyl # « to # « « « «
Meperidine « or " # # # # "
Morphine « or # # # # # "
Halothane « or " # # « or # ## #
Isoflurane "" # ## « or " # #
Sevoflurane " # # « or # ? # «
Nitrous oxide « or " « or " « or " # or " « « or #
Lidocaine « « « " " " if used for regional
anesthesia
Lidocaine toxicity # # " # # "
Midazolam « or " # « or # « « or # «
Ergometrine " "" " " " #
Oxytocin « or " « to " « to # « « « to "
(<10 U)
# (>10 U
bolus dose)
Magnesium sulfate « or # # # « « "
Nitroglycerin « ## « to # # « ""
Terbutaline " « to # « to # " « to " "

The response is represented by a five-point scale from a marked increase ("") to marked decrease (##), « is no effect, " is a slight increase, # is a slight
decrease.
a
Secondary effect from endogenous catecholamine release
b
May decrease due to histamine release
There are various caveats in the interpretation of these data. Some values are derived from animal studies, some from human volunteers, and some
from patients. Values may vary depending on whether a patient is mechanically ventilated or breathing spontaneously. In addition, the hemodynamic
effects of these agents may change in the presence of other anesthetic agents. Finally, the hemodynamic response may be different in patients who are
hypovolemic, have sympathetic overactivity, or a sympathectomy. The values and ranges indicated in this table are the authors’ opinion of the most
likely clinical response for most patients and have been taken in part from the following texts:
Bowdle, T. A., Horita, A. & Kharasch, E. D. (eds). The Pharmacologic Basis of Anesthesiology: Basic Science and Practical Applications. New York:
Churchill Livingstone, 1994 and Norris, M. C. (ed). Obstetric Anesthesia. Philadelphia: J. B. Lippincott, 1993.

Some cardiovascular findings on physical examination may pressure is not elevated and the hepatojugular reflex is not posi-
be confusing. Peripheral edema occurs in 60–80% of pregnant tive. Pseudo-cardiomegaly is related to displacement of the apex
individuals, and is attributed to hemodilution, a fall in plasma by the gravid uterus. There is often a third heart sound due to
oncotic pressure, and an increase in capillary pressure secondary volume loading and right ventricular outflow tract murmurs
to raised venous pressure in the legs. However, this is not asso- are common.
ciated with hepatomegaly. Rales are likely the result of upward Certain symptoms and signs suggest the presence of heart
displacement of the diaphragm. Prominent peripheral and neck disease. A careful history and physical examination will allow
veins are related to the hypervolemia of pregnancy and the these to be differentiated beyond the symptoms and signs of
vasodilatory effects of progesterone. However, mean right atrial normal pregnancy. Symptoms suggestive of heart disease

2
 Chapter 1

Table 1.2 New York Heart Association (NYHA) functional capacity and objective assessment a

Functional capacity Objective assessment

Class I. Patients with cardiac disease but without limitation of physical activity. No objective evidence of cardiovascular disease.
Ordinary physical activity does not cause fatigue, palpitations, dyspnea, or angina.
Class II. Patients with cardiac disease resulting in slight limitation of physical Objective evidence of minimal cardiovascular disease.
activity. They are comfortable at rest. Ordinary physical activity results in fatigue,
palpitation, dyspnea, or angina.
Class III. Patients with cardiac disease resulting in marked limitation of physical Objective evidence of moderately severe cardiovascular
activity. They are comfortable at rest. Less than ordinary activity causes fatigue, disease.
palpitation, dyspnea, or angina.
Class IV. Patients with cardiac disease resulting in inability to carry on any physical Objective evidence of severe cardiovascular disease.
activity without discomfort. Symptoms of heart failure or angina may be present
even at rest. If any physical activity is undertaken, discomfort is increased.

a
AHA medical/scientific statement: 1994 revisions to classifications of functional capacity and objective assessment of patients with diseases of the
heart. Circulation 1994; 90: 644.

Table 1.3 Maternal mortality associated with heart disease in Table 1.4 Normal hemodynamic and ventilatory parameters
pregnancy in the nonpregnant and pregnant patient

Group 1: Mortality <1% Percentage

Atrial septal defect Nonpregnant Pregnant change
Ventricular septal defect
Cardiac output (l/min) 4.3  0.9 6.2  1.0 þ 45%
Patent ductus arteriosus
Heart rate (beats/min) 71  10 83  10 þ 17%
Pulmonary/tricuspid disease
Systemic vascular 1530  520 1210  226  21%
Tetralogy of Fallot, corrected
resistance
Bioprosthetic valve
(dyne.sec.cm5)
Mitral stenosis, NYHA class I and II
Pulmonary vascular 119  47 78  22  34%
Group 2: Mortality 5–15% resistance
2A Mitral stenosis NYHA class III–IV (dyne.sec.cm5)
Aortic stenosis Mean arterial pressure 86  8 90  6 NSC
Coarctation of aorta, without valvular involvement (mmHg)
Uncorrected Tetralogy of Fallot Pulmonary capillary 6.3  2.1 7.5  1.8 NSC
Previous myocardial infarction wedge pressure
Marfan syndrome with normal aorta (mmHg)
2B Mitral stenosis with atrial fibrillation Central venous 3.7  2.6 3.6  2.5 NSC
Artificial valve pressure (mmHg)
Group 3: Mortality 25–50%
NSC ¼ no significant change.
Primary pulmonary hypertension or Eisenmenger syndrome
Adapted from: Clark, S. L., Cotton, D. B., Lee, W. et al. Central
Coarctation of aorta, with valvular involvement
hemodynamic assessment of normal term pregnancy. Am. J. Obstet.
Marfan syndrome with aortic involvement
Gynecol. 1989; 161: 1439–4.
Adapted from: Foley, M. R.: Cardiac disease. In Dildy, G. A., Belfort,
M. A., Saade, G. R., Phelan, J. P., Hankins, G. D. & Clark, S. L. (eds.),
Critical Care Obstetrics, 4th edn. Malden: Blackwell Science, 2004, General management principles of pregnant
pp. 252–74. women with heart disease
1. Take a detailed history and follow up patients regularly during
include severe or progressive dyspnea, progressive orthopnea, pregnancy
paroxysmal nocturnal dyspnea, hemoptysis, syncope with Patients with significant heart disease are usually diagnosed
exertion, and chest pain related to effort or emotion. Physical prior to pregnancy and may develop worsening of symptoms
findings strongly suggesting the presence of heart disease during their pregnancy. However, some cardiac lesions asso-
include cyanosis, clubbing, persistent neck-vein distension, ciated with few symptoms in the nonpregnant state may
palpable murmurs, diastolic murmurs, dysrhythmias, and true become symptomatic for the first time in mid to late pregnancy.
cardiomegaly. The hemodynamic changes that occur in pregnancy represent a

3
1 Cardiovascular and respiratory disorders

significant stress test. Most women with cardiac disease who

remain asymptomatic throughout pregnancy usually tolerate Table 1.5 Endocarditis prophylaxis risk stratification
labor and delivery. Conversely, women who are breathless at High-risk category (endocarditis prophylaxis recommended)
rest (NYHA IV) and groups 2 and 3 listed in Table 1.3, usually Prosthetic cardiac valves, including bioprosthetic and homograft valves
tolerate pregnancy poorly. Functional class NYHA III–IV patients Previous bacterial endocarditis
with surgically correctable lesions should be assessed for correct- Complex cyanotic congenital heart disease (e.g. single ventricle states,
ive surgery before pregnancy. transposition of the great arteries, Tetralogy of Fallot)
2. Understand the physiological changes of pregnancy Surgically constructed systemic pulmonary shunts or conduits
It is essential to understand the impact of physiological
Moderate-risk category (endocarditis prophylaxis recommended)
changes of pregnancy on the specific heart lesion in order to
Most other congenital cardiac malformations (other than those above
properly manage these patients.12
and below)
3. Multidisciplinary team approach
Acquired valve dysfunction (e.g. rheumatic heart disease)
Pregnant women with significant or complex heart disease
Hypertrophic cardiomyopathy
should be managed by a team in a specialist center.13 This
Mitral valve prolapse with mitral regurgitation  thickened leaflets
team should include representatives from obstetrics and peri-
Negligible-risk category (no greater risk than the general population
natology, anesthesiology, neonatology, cardiology, intensive
and endocarditis prophylaxis not recommended)
care, nursing, and social work. Patients should be seen regu-
Isolated secundum atrial septal defect
larly throughout their pregnancy and a management plan
Surgical repair of atrial septal defect, ventricular septal defect, or
should be formulated early in pregnancy before the onset of
patent ductus arteriosus (without residua beyond 6 months)
labor. High-risk women should be managed by senior anesthe-
Previous coronary artery bypass graft surgery
siologists experienced in treating pregnant patients with cardiac
Mitral valve prolapse without mitral regurgitation
lesions. Pediatric involvement is important, as there is a 5–15%
Physiologic, functional, or innocent heart murmurs
chance that the fetus will be affected by the same cardiac
Previous Kawasaki disease without valve dysfunction
defect.14 In addition, the fetus may be compromised by the
Previous rheumatic fever without valve dysfunction
mother’s cardiopulmonary insufficiency.15 In-utero echocar-
Cardiac pacemakers (intravascular and epicardial) and implanted
diography at 18 weeks’ gestation can detect most fetal cardiac
defibrillators
defects.16,17 Avoidance of pregnancy, or consideration of an
early therapeutic termination, in women with very high-risk From: Dajani, A. S., Taubert, K. A., Wilson, W. et al. Prevention of
cardiac disease (e.g., pulmonary hypertension) is prudent. bacterial endocarditis. Recommendations by the American Heart
4. Infective endocarditis antibiotic prophylaxis Association. Circulation 1997; 96: 358–66.
Although the risk of bacteremia following normal delivery
is low (0–5%),13 appropriate antibiotic coverage should be
provided for high-risk patients (especially those with prosthe- placenta and appears safe in women who breast-feed. Heparin
tic valves or a history of endocarditis) prior to labor, delivery, or is used to prevent and treat thromboembolism. For UFH, the
other surgical procedures (Tables 1.5 and 1.6).18 activated partial thromboplastin time (aPTT) should be mon-
5. Anticoagulation during pregnancy and peripartum itored because heparin requirements increase as pregnancy
Pregnancy is a hypercoagulable state, which increases the risk of progresses. Platelet count should be measured before neuraxial
thromboembolic events, especially in the cardiac patient with a blocks in patients on UFH for more than 4 days because of the
prosthetic heart valve, valvular heart disease, or heart failure.1 risk of heparin-induced thrombocytopenia.24 For LMWH,
Anticoagulant therapy should be considered in these high-risk monitoring of aPTT or anti-Xa level is not predictive of the
patients to prevent thromboembolism or thrombus formation. risk of bleeding and is therefore not always necessary or recom-
mended.24 Low molecular weight heparin offers potential
Warfarin: The use of oral anticoagulants during pregnancy is advantages over UFH including lack of need for laboratory
relatively contraindicated. Warfarin therapy in the first trimester monitoring, greater bioavailability, once-a-day dosing because
is associated with an increased incidence of fetal death and birth of its long half-life, and less thrombocytopenia and osteoporo-
defects (‘‘warfarin embryopathy’’). Warfarin use later in preg- sis. Its efficacy in preventing and treating thromboembolism
nancy is associated with prematurity and low birthweight, as (as well as the above mentioned advantages) are leading to the
well as neonatal cerebral hemorrhage.19,20 Despite these risks, widespread use of LMWH in obstetrics.
warfarin is sometimes administered in combination with low Thrombolytics: Streptokinase and urokinase are relatively con-
dose aspirin (80–100 mg/day) to patients with mechanical valves traindicated in pregnancy because of reports of placental abrup-
because of concerns about the efficacy of heparin in preventing tion and postpartum hemorrhage.25 Streptokinase has been used
systemic embolism.21,22 Warfarin can be used in the postpartum successfully to treat prosthetic mitral valve thrombosis during
period and appears safe in women who breast-feed.23 pregnancy.26 The thrombosis was confirmed by echocardio-
Heparin: Heparin, unfractionated (standard, UFH) or low graphy and fluoroscopy at 28 weeks’ gestation in a woman with
molecular weight (LMWH), is the drug of choice during preg- a history of progressive exertional dyspnea. Valve function
nancy because it is a large molecule that does not cross the returned to normal within 18 hours of commencing treatment.

4
 Chapter 1

Table 1.6 Adult antibiotic prophylaxis for genitourinary/gastrointestinal procedures

Situation a Agents Regimen b

High-risk patients Ampicillin plus Ampicillin 2.0 g i.m. or i.v. plus gentamicin 1.5 mg/kg (not to exceed 120 mg) within
gentamicin 30 min of starting procedure; 6 h later, ampicillin 1 g i.m./i.v. or amoxicillin 1 g orally
High-risk patients allergic Vancomycin plus Vancomycin 1.0 g i.v. over 1–2 h plus gentamicin 1.5 mg/kg i.v./i.m. (not to exceed
to ampicillin/amoxicillin gentamicin 120 mg); complete injection/infusion within 30 min of starting procedure
Moderate-risk patients Amoxicillin or ampicillin Amoxicillin 2.0 g orally 1 h before procedure, or ampicillin 2.0 g i.m./i.v. within 30 min
of starting procedure
Moderate-risk patients Vancomycin Vancomycin 1.0 g i.v. over 1–2 h; complete infusion within 30 min of starting
allergic to ampicillin/ procedure
amoxicillin

i.m. ¼ intramuscular; i.v. ¼ intravenous

a
Endocarditis prophylaxis not recommended for routine C/S and prophylaxis is optional for high-risk patients undergoing vaginal delivery.
b
No second dose of vancomycin or gentamicin is recommended.
From: Dajani, A. S., Taubert, K. A., Wilson, W. et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association.
Circulation 1997; 96: 358–66.

Table 1.7 ASRA guidelines for regional anesthesia in the anticoagulated patient a

Anticoagulant/thrombolytic Neuraxial placement considerations After placement / epidural catheter removal

2
Low dose LMWH (e.g. enoxaparin 10–12 hours after the last LMWH dose. After placement: first dose 6–8 hours; second dose no
0.5 mg/kg/day, dalteparin 120 U/kg sooner than 24 hours after the first dose.
q 12 h) After removal: minimum of 2 hours.
High dose LMWH b, c (e.g. enoxaparin No sooner than 24 hours. After placement: no sooner than 24 hours. Indwelling
1 mg/kg q 12 h) catheters should be removed prior to starting
LMWH.
After removal: minimum of 2 hours.
Heparin IV d, f 1 hour before any subsequent heparin 1 hour.
administration or 2–4 hours after the last
heparin dose.
Prophylactic heparin SC d, e, f None. None.
Warfarin Discontinue 4–5 days prior; INR <1.5 before Neuraxial catheters should be removed when INR
considering regional anesthesia. <1.5.
Aspirin and NSAIDs No special dosing or timing considerations. No special dosing or timing considerations.
Platelet inhibitors (e.g. ticlopidine, 14 days for ticlopidine. 14 days for ticlopidine.
clopidogrel, GP IIb/IIIa) 7 days for clopidogrel. Platelet GP IIb/IIIa 7 days for clopidogrel. Platelet GP IIb/IIIa inhibitors:
inhibitors: eptifibatide and tirofiban (8 h) eptifibatide and tirofiban (8 h) to abciximab (48 h).
to abciximab (48 h).
Thrombolytics (e.g. streptokinase) Avoid except in highly unusual circumstances. Avoid except in highly unusual circumstances.

a
Adapted from the ASRA 2002 published guidelines: Horlocker, T. T., Wedel, D. J., Benzon, H. et al. Regional anesthesia in the anticoagulated patient:
defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg. Anesth. Pain Med. 2003; 28: 172–97.
b
LMWH therapy should be delayed for 24 hours if the presence of blood during needle and catheter placement occurs.
c
Higher doses may require more caution.
d
It may be prudent to confirm that partial thromboplastin time (PTT) is within normal range prior to removal.
e
The risk of neuraxial bleeding may be reduced by delaying the heparin injection until after the block, and may be increased in debilitated patients or
after prolonged therapy.
f
Due to heparin-induced thrombocytopenia, patients receiving heparin >4 days should have a platelet count prior to neuraxial block.

Anesthetic considerations: Many women with cardiac disease The American Society of Regional Anesthesiology (ASRA) guide-
will be treated with anticoagulants to avoid thromboembolism. lines should be considered when performing any regional
The decision to perform neuraxial anesthesia in a patient receiv- anesthetic on a patient taking anticoagulants (Table 1.7).24 The
ing thromboprophylaxis should be made on an individual basis. patient’s coagulation status should be optimized and level of

5
1 Cardiovascular and respiratory disorders

anticoagulation carefully monitored before spinal or epidural

placement and at epidural catheter removal. In patients who Table 1.8 Hemodynamic advantages and disadvantages of
have received neuraxial blocks, postprocedure neurological vaginal birth and elective cesarean section
monitoring needs to be carried out at regular intervals (<2 hours Vaginal birth Cesarean section
between neurologic checks). The epidural infusion should be
Advantages Minimize blood loss Predictable and planned
limited to dilute local anesthetics that minimize sensory and
Minimize surgical stress Timed delivery
motor block to aid neurological assessment.24
Quicker recovery All personnel
Hemodynamic stability immediately available
6. Uterotonic agents
Disadvantages Unpredictable timing Increased surgical stress
Care should be exercised when administering oxytocin to
Potentially prolonged Higher blood loss
patients with cardiac disease since a large bolus can cause
Painful and stressful Longer recovery
hypotension and tachycardia and has been shown to cause
Potentially ‘‘after-hours’’ Higher potential
increases in cardiac stress.27 A slow infusion of a dilute oxyto-
postoperative
cin solution is usually well tolerated. Other uterotonic agents
complications
such as ergometrine can induce systemic hypertension and
coronary vasoconstriction. Prostaglandin F2-alpha has the
potential to cause severe pulmonary hypertension if large phase and Valsalva maneuvers. Although induction of labor in
doses are injected directly into the circulation.28 pregnant patients with cardiac disease is safe,33 there are
7. Peripartum monitoring higher maternal and neonatal complications compared to
The level of monitoring, beyond standard American Society of healthy controls.
Anesthesiology guidelines, should be appropriate for the sever- 10. The critical postpartum period
ity of the cardiac lesion and the planned obstetric or anesthetic The immediate postpartum period is critical, especially if pul-
intervention. Invasive monitoring is advised in symptomatic monary hypertension is present. Most fatalities occur in the
patients with known cardiac defects. Monitoring of radial artery first week after delivery, but others occur as late as three to
pressure  central venous pressure (CVP)  pulmonary artery four weeks postpartum. For this reason invasive monitoring
catheter  transesophageal echocardiography (TEE) allows pre- should not be discontinued immediately after delivery, and full
cise, continuous measurement of hemodynamic variables and therapeutic and monitoring support in a critical care setting
guides appropriate use of fluid and drug therapy. When the should be provided. Postoperative pain management (e.g.,
pathophysiology of critically ill obstetric patients cannot be epidural analgesia) is useful in reducing the cardiovascular
explained by noninvasive hemodynamic monitoring and the stress response following C/S. In addition, a neuraxial-induced
patient fails to respond to conservative medical management, sympathectomy may improve microvascular flow and reduce
invasive hemodynamic monitoring may be helpful in guiding the risk of perioperative deep vein thrombosis.
further management.29 The benefits of additional hemody-
namic data provided by invasive monitoring should be weighed
against the risks associated with invasive line insertion.30,31
Valvular lesions
8. Basic hemodynamic goals Women with stenotic lesions do not tolerate the changes in HR or
Although care must be individualized to the cardiac lesion and increases in CO that occur during pregnancy. Any woman with a
patient condition, basic maintenance of hemodynamic goals symptomatic stenotic lesion warrants very close attention and
are applicable to most cases. possible correction before or during pregnancy.
 Avoid sudden alterations in HR and maintain normal sinus
rhythm.
Mitral stenosis
 Maintain preload and minimize sudden increases or decreases
in central blood volume. Pregnant patients with cardiac disease Mitral stenosis (MS) accounts for 90% of rheumatic heart disease
are at increased risk of developing pulmonary edema. in pregnancy, with 25% of patients developing symptoms for the
 Avoid sudden decreases in afterload and SVR. Decreases in first time during late pregnancy. Mitral stenosis is the most com-
SVR are compensated for by increasing HR, which can lead mon cardiac pathology associated with acute pulmonary edema
to worsening cardiac function. in pregnancy, followed by aortic valve disease and primary myo-
9. Vaginal versus cesarean delivery cardial disease. Symptoms depend on the severity and include
There are advantages and disadvantages of both vaginal and fatigue and dyspnea on exertion initially, but may progress to
cesarean section (C/S) with no convincing evidence that either paroxysmal nocturnal dyspnea, orthopnea, and shortness of
option is clearly superior (Table 1.8).32 The delivery plan breath at rest. Mitral stenosis is considered severe when the
should be individualized according to the woman’s condition. valve area is 1 cm2 or less. Overall mortality is around 1% in
Vaginal delivery may be preferable if obstetrically indicated, mild disease or 5–15% in severe mitral valve disease.
however, limits to the duration should be discussed and pre- Predictors of adverse events include:7,34,35
parations for a potential C/S considered. Assisted delivery is  mitral valve area <1.5 cm2
recommended to avoid prolonged pushing, a rapid expulsive  NYHA functional class >II