4 5771463918631256090

CO RE TO PICS IN O BSTETRIC ANAESTHESIA
C OR E TOP I C S I N OB ST E T R I C
A N A E ST HE SI A
Edited by
Kirsty MacLennan
Consultant Obstetric Anaesthetist, St Marys Hospital, Central Manchester University Hospitals NHS
Trust, Manchester, UK
Kate OBrien
W. Ross Macnab
University Printing House, Cambridge CB2 8BS, United Kingdom
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Library of Congress Cataloguing in Publication data
Core topics in obstetric anaesthesia / edited by Kirsty MacLennan, Consultant
Obstetric Anaesthetist, St Marys Hospital, Central Manchester, University
Hospitals NHS Trust, Manchester, UK, Katherine OBrien, Consultant Obstetric
Anaesthetist, St Marys Hospital, Central Manchester, University Hospitals NHS
Trust, Manchester, UK, William MacNab, Consultant Obstetric Anaesthetist,
St Marys Hospital, Central Manchester, University Hospitals NHS Trust,
Manchester, UK.
pages cm
ISBN 978-1-107-02849-4 (hardback)
1. Anesthesia in obstetrics. I. MacLennan, Kirsty. II. OBrien, Katherine,
1962 III. MacNab, William, 1969
RG732.C68 2015
617.9682dc23
2015021141
ISBN 978-1-107-02849-4 Hardback
Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party internet
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Every effort has been made in preparing this book to provide accurate and up-to-date information which is in accord with accepted
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Contents
List of contributors
Preface
Section 1
Basic science, epidemiology and service organization
1 Physiology of pregnancy
N. J. Nirmalan and M. Nirmalan
2 Placental physiology
Carolynn Wai and W. Ross Macnab
3 Pharmacology relevant to pregnancy

Christopher Kelly and Malachy Columb
4 Maternal morbidity and mortality

Kate OBrien
Section 2
Obstetric aspects
5 Maternal critical care
Sarah Wheatly and Kate OBrien
6 Obstetrics for the anaesthetist

Emma Ingram, Alex Heazell and Edward D. Johnstone
7 Antenatal assessment
Allison C. L. Howells
Section 3
Provision of anaesthesia
8 Incidental anaesthesia during pregnancy
Desiree M. A. Choi and Kim G. Soulsby
9 Non-regional analgesia techniques for labour

Gordon Yuill
10 Regional analgesia techniques for labour

Lawrence C. Tsen
11 Regional anaesthesia for operative delivery

Cathy Armstrong and Khaled Girgirah
12 General anaesthesia for caesarean section and transverse abdominal plane block
Suraj Jayasundera and Karen Butler
13 Anaesthesia for other obstetric indications: cervical suture, external cephalic version,
controlled ARM, manual removal of placenta and perineal repair
John R. Dick
Section 4
Medical conditions in pregnancy
14 Hypertension in pregnancy, pre-eclampsia and eclampsia
Suna Monaghan, Jenny Myers and Lorna A. Howie
15 Sepsis and influenza in pregnancy

Tim Holzmann and Dougal Atkinson
16 Cardiac disease in pregnancy

W. Ross Macnab, Anita Macnab and Akbar Vohra
17 Respiratory disease in pregnancy

Christopher Kelly, Simon Maguire and Craig Carroll
18 Obesity and ultrasonography for central neuraxial blocks
Sophie Bishop and Preye Zuokumor
19 Endocrine disease in pregnancy including diabetes mellitus, thyroid and adrenal

disease
Jenny Myers and Dan Mallaber
20 Renal disease
Jessica Longbottom and W. Ross Macnab
21 Haematologic disease in pregnancy

Pavan Kochhar, Andrew Heck and Clare Tower
22 Neurosurgical and neurological disease in pregnancy

Kirsty MacLennan and Craig Carroll
23 Immunology, including testing and management of allergy during pregnancy

Gareth Kitchen, Tomaz Garcez and Nigel J. N. Harper
24 HIV and infectious disease in pregnancy, including herpes, syphilis and hepatitis
Jacqueline E. A. K. Bamfo, Matthew D. Phillips, M. Kingston, K. Chan and Ian Clegg
Section 5
Postpartum complications and obstetric emergencies
25 Maternal collapse, including massive obstetric haemorrhage, amniotic fluid embolism
and cardiac arrest
Kate Grady and Tracey Johnston
26 Postpartum complications, follow-up and maternal satisfaction

Richard Wadsworth and Kailash Bhatia
Section 6
Service organization
27 Multidisciplinary teaching and training on the delivery unit
Catherine Robinson and Cathy Armstrong
28 Clinical governance and patient safety

Kate OBrien
29 Ethics, consent and the law

Andrew Heck and Ross Clark
Index
Contributors
Cathy Armstrong
Consultant Anaesthetist, Manchester Royal Infirmary, Manchester, UK
Dougal Atkinson
Consultant in Anaesthesia and Critical Care, Central Manchester University Hospitals,
Manchester, UK
Jacqueline E. A. K. Bamfo
Subspeciality Trainee in Maternal Fetal Medicine, Fetal Medicine Unit, St Marys Hospital,
Manchester, UK
Kailash Bhatia
Consultant Anaesthetist, Department of Anaesthesia, Central Manchester University Hospitals
NHS Foundation Trust, Manchester, UK
Sophie Bishop
Consultant Anaesthetist, University Hospital of South Manchester, Wythenshawe, UK
Karen Butler
Consultant Anaesthetist, Anaesthetic Department, Blackburn Hospital, Blackburn, UK
Craig Carroll
Consultant Neuroanaesthetist, Salford Royal Hospital NHS Foundation Trust, Salford, UK
K. Chan
Consultant Obstetrician, Department of Obstetrics and Fetal Medicine Unit, St Marys Hospital,
Manchester, UK
Desiree M. A. Choi
Consultant Obstetric Anaesthetist, Nuffield Department of Anaesthetics, John Radcliffe Hospital,
Oxford, UK
Ross Clark
Consultant Obstetric Anaesthetist, Central Manchester University Hospitals NHS Foundation
Ian Clegg
Consultant Anaesthetist, East Lancashire Hospitals NHS Trust, UK
Malachy Columb
Consultant in Anaesthesia and Intensive Care Medicine, University Hospital of South
Manchester, Wythenshawe, UK
John R. Dick
Consultant Anaesthetist, University College London Hospital, London, UK
Tomaz Garcez
Consultant Clinical Immunologist, Central Manchester University Hospitals NHS Foundation
Khaled Girgirah
Specialty Trainee in Anaesthesia, North West Deanery, Central Manchester Childrens Hospital,
Manchester, UK
Kate Grady
Consultant Anaesthetist, University Hospital of South Manchester, Manchester, UK
Nigel J. N. Harper
Alex Heazell
Senior Clinical Lecturer and Honorary Consultant in Obstetrics, St Marys Hospital,
Manchester, UK
Andrew Heck
Specialty Trainee in Anaesthesia, North West Deanery, Department of Anaesthesia, St Marys
Hospital, Manchester, UK
Tim Holzmann
North Western Deanery, Manchester, UK
Consultant Anaesthetist, Central Manchester University Hospitals NHS Foundation Trust,
Manchester, UK
Lorna A. Howie
Specialist Trainee in Anaesthesia, North West Deanery, St Marys Hospital, Manchester, UK
Emma Ingram
Academic Health Science Centre, Manchester, UK
Suraj Jayasundera
Specialty Trainee in Anaesthesia, North West Deanery, Royal Manchester Childrens Hospital,
Manchester, UK
Tracey Johnston
Consultant Obstetrician, Birmingham Womens NHS Foundation Trust, Birmingham, UK
Edward D. Johnstone
Senior Clinical Lecturer, St Marys Hospital and Central Manchester University Hospitals NHS
Foundation Trust, Manchester, UK
Christopher Kelly
Specialty Trainee, in Anaesthesia, North West Deanery, University Hospital of South
Manchester, Wythenshawe, UK
M. Kingston
Consultant Physician in Genitourinang Medicine, Manchester Royal Infirmary, Manchester, UK
Gareth Kitchen
Specialty Trainee in Anaesthesis, North Western Deanery, Manchester, UK
Pavan Kochhar
Consultant Obstetric Anaesthetist, St Marys Hospital, Manchester, UK
Jessica Longbottom
Specialty Trainee in Anaesthesia, North West Deanery, Manchester, UK
Kirsty MacLennan
Anita Macnab
Consultant Cardiologist, University Hospital of South Manchester, Manchester, UK
W. Ross Macnab
Simon Maguire
Consultant Anaesthetist, South Manchester University Hospital Trust, Manchester, UK
Dan Mallaber
Manchester, UK
Suna Monaghan
Manchester, UK
Jenny Myers
Senior Clinical Lecturer, Maternal and Fetal Health Research Centre, St Marys Hospital,
Manchester, UK
M. Nirmalan
Professor of Medical Education and Honorary Consultant in Anaesthesia, Manchester Royal
Infirmary, Manchester, UK
N. J. Nirmalan
Senior Lecturer, Programme Leader, Biomedical Sciences, University of Salford, Manchester,
UK
Kate OBrien
Matthew D. Phillips
Manchester Royal Infirmary, Manchester, UK
Catherine Robinson
Consultant Anaesthetist, Manchester Royal Infirmary, Manchester, UK
Kim G. Soulsby
Specialist Registrar in Anaesthesia, Oxford University Hospitals, Oxford, UK
Clare Tower
Consultant in Obstetrics and Maternal and Fetal Medicine, Central Manchester University
Hospitals NHS Foundation Trust, Manchester, UK
Lawrence C. Tsen
Associate Professor, Harvard Medical School, Department of Anesthesiology, Perioperative
and Pain Medicine, Brigham and Womens Hospital, Boston, MA
Akbar Vohra
Consultant Anaesthetist Central Manchester University Hospitals NHS Foundation Trust,
Manchester, UK
Richard Wadsworth
Carolynn Wai
Specialty Trainee in Anaesthesia, North West Deanery, Manchester, UK
Sarah Wheatly
Consultant Anaesthetist, University Hospital of South Manchester, Manchester, UK
Gordon Yuill
Consultant Anaesthetist, Department of Anaesthesia, Stepping Hill Hospital, Stockport, UK
Preye Zuokumor
Manchester, UK
Preface
Navigating through the minefields of obstetric anaesthesia is becoming more and more challenging.
Obstetric anaesthetists are encountering a much broader range of pathologies owing to the ever
increasing morbidity affecting women of childbearing age. This book aims to provide healthcare
professionals caring for parturients with a wealth of up-to-date information on a broad range of
aspects affecting obstetric care.
The book is divided into six sections. Section 1 addresses the basic sciences, including expected
physiological and pharmacological alterations associated with pregnancy, and epidemiology. Section
2, entitled obstetric aspects, includes maternal critical care, antenatal assessment and a chapter
authored by an obstetrician, dedicated to obstetrics for the anaesthetist.
Section 3 covers all aspects of provision of anaesthesia, including incidental anaesthesia (for
those parturients requiring non-obstetric surgery whilst pregnant), regional and non-regional
analgesia for labour, regional and general anaesthesia for operative delivery and anaesthesia for
specific obstetric indications. Section 4 is divided into easily navigable chapters that cover the
common conditions encountered during pregnancy, ranging from obesity and pre-eclampsia to allergy,
sepsis and HIV. Dedicated chapters for individual systems detail commonly encountered conditions,
how these conditions can be affected by pregnancy and suggested peripartum management plans.
Section 5 focuses on postpartum complications and maternal collapse. Section 6 changes the
direction away from clinical practice and addresses ethics and consent, clinical governance and
multidisciplinary training for members of the delivery suite.
By combining obstetric and anaesthetic authorship on many chapters, we aspire to give the
reader a well-founded knowledge base with which to approach situations on the delivery suite. This
book is a must have for current, easily accessible opinion, making it valuable for anaesthetic trainees
sitting examinations, occasional dabblers in obstetric anaesthesia and full-time obstetric anaesthetic
consultants alike. Most up-to-date literature and initiatives, including National Audit Project 5,
Cochrane reviews, guidelines and enhanced recovery after surgery are discussed.
We hope that this addition to the core topic range will assist healthcare professionals in the
rapidly changing complex field of obstetric anaesthesia.
Kirsty MacLennan, Kate OBrien and W. Ross Macnab
Section 1

Basic science, epidemiology and service

organization
Chapter 1
Physiology of pregnancy

N. J. Nirmalan and M. Nirmalan
Introduction
Maternal physiology undergoes complex changes during pregnancy in order to enable the female
reproductive system to nurture and adapt to the fetus and placenta. The changes are predominantly
either secondary to hormonal responses to female sex hormones or physical adaptations to increasing
fetal size. The definition and detailed understanding of the normal physiological changes occurring in
the antepartum, intrapartum and postpartum periods of pregnancy are crucial to recognize
pathophysiological deviations as a result of disease and anaesthesia. Even though the changes are in
fact quite widespread, this chapter will focus on some of the key physiological systems that are of
direct relevance to the anaesthetists management of a pregnant woman during the peripartum period.
Haematological system
Antepartum period
Pregnancy and the neonatal period result in significant changes in the haematological system with an
associated increased risk for the development of complications, such as anaemia, thromboembolism
and consumptive coagulopathies. Most haematological parameters are progressively altered during
pregnancy and are reflected in laboratory investigations. Blood and plasma volumes increase,
resulting in an adaptive hypervolaemia. An increase of 3045% in the blood volume occurs, with
changes starting at 68 weeks and peaking at 2834 weeks, approximately 1.5 L higher than the
prepregnant state. The increased blood volume is accompanied by increases in red cell mass
secondary to increased erythropoiesis stimulated by high circulating levels of renal erythropoietin
(Epo). The changes in erythropoiesis begin by week 10 and progressively accelerate through the
second and third trimesters and are accompanied by erythroid hyperplasia of the bone marrow and an
increase in the reticulocyte counts. While the early increases in erythropoietin may be due to the
decreased oxygen-carrying capacity, in the last two trimesters, the increase is thought to be induced
by progesterone, prolactin and human placental lactogen. Pregnancy-induced physiological changes
are also responsible for a rise in red blood cell 2,3 diphosphoglycerate (2,3-DPG) levels leading to a
gradual rightward shift of the maternal oxygenhaemoglobin dissociation curve, with improved
oxygen transfer from mother to fetus. Red cell parameters like the mean corpuscular volume (MCV)
and mean corpuscular haemoglobin concentration (MCHC) remain relatively stable in the absence of
iron deficiency anaemia.
Circulating oestrogen and progesterone act directly on the kidney, inducing the release of renin
with activation of the aldosteronereninangiotensin mechanism resulting in Na+ retention and an
associated increase in total body water. The resultant increase in plasma volume (~45%) is relatively
greater than accompanying increases in red cell mass (~33%). The consequent haemodilution causes
decreases in haematocrit (3339% at term) and haemoglobin concentrations (~150 g/L prepregnancy
to ~120 g/L in the third trimester) leading to physiological anaemia of pregnancy. White cell counts
can increase by ~8% from the second month of pregnancy, predominantly due to an oestrogen-induced
neutrophilia. While T- and B-lymphocyte counts do not change, their function is suppressed leading to
increased susceptibility to infections. Platelet levels generally remain within the normal range during
pregnancy. There is some evidence of increased production and increased consumption. Gestational
thrombocytopenia is a physiological condition that occurs in a small number of parturients.
Hypervolaemia and the ensuing haemodilution can cause significant changes in other plasma
components as well (plasma proteins, electrolytes, lipids, enzymes, serum iron etc.). Total plasma
protein is reduced by 1014%, particularly during the first trimester. Despite an absolute increase in
serum albumin concentrations, the relative decrease due to haemodilution results in decreased oncotic
pressure, contributing to oedema, which is further aggravated by increased venous hydrostatic
pressure in the third trimester. The albumin-to-globulin ratio decreases due to absolute and relative
increases in globulin concentrations. Increases in fibrinogen levels of 5080% are reported in
pregnancy, which, together with elevations in serum globulins, cause progressive elevations in the
erythrocyte sedimentation rate (ESR) in pregnancy. A combination of hypervolaemia and effects of
alterations in the respiratory system (low CO2 levels) result in a decrease of serum electrolyte levels
with reduced plasma osmolarity. Increases in serum lipids (4060% at term), particularly cholesterol
and phospholipids, occur due to increased fetal and placental demands. With poor iron
supplementation, serum iron and ferritin levels decrease. Reduction of serum ferritin a more precise
indicator of reticuloendothelial iron stores peaks in the second trimester in parallel with the rapid
expansion in maternal red blood cell mass. An increase in serum alkaline phosphatase is a common
finding and is usually attributed to increased placental production.
Pregnancy induces a hypercoagulable state with an increased risk of thrombosis and
coagulopathies due to an intrinsic activation of the coagulation system in the uteroplacental
circulation. The majority of the coagulation factors are elevated, particularly Factors I, VII, VIII, X,
XII, prekallikrein and the von Willebrand factor (vWF). Activated partial thromboplastin time
(APTT) and prothrombin time (PT) decrease after mid pregnancy, while the bleeding time remains
normal. The overall effect on the coagulation system during pregnancy is an increase in thrombin
generation due to increased activity of procoagulant proteins and suppression of the fibrinolytic
system. The resultant hypercoagulable state facilitates and stabilizes clot formation. Haematological
changes occurring in pregnancy are summarized in Table 1.1 below.
Table 1.1 The most significant haematological changes in pregnancy
Physiological anaemia
Neutrophilia
Mild thrombocytopenia
Increased procoagulant factors
Diminished fibrinolysis
The physiological changes in the haematological and haemostatic system during pregnancy are
essential to meet the demands of the fetus and protect against intrapartum blood loss. An
understanding of the normal physiological process is vital, given the influence of these changing
parameters on the interpretation of laboratory investigations and the increased susceptibility to
thromboembolism and coagulopathies. The haematological changes revert to prepregnancy status at 2
weeks post partum.
Intrapartum and postpartum phases
Maternal adaptions in the haematological system during the intrapartum phase of the pregnancy are
primarily aligned to coping with and minimizing the impact of significant blood loss associated with
the delivery of the fetus. The efficacy of this adaptation is reflected in the ability to withstand losses
of up to 1000 mL of blood (~500 mL in a normal vaginal delivery; up to ~ 1000 mL for a caesarian
section or normal twin delivery) with minimal resultant effects on the blood and pulse pressures
estimated to be around half the extra blood volume acquired antepartum.
A stress-induced increase in erythropoiesis coupled with muscular exertion and dehydration
result in haemoconcentration and mild increases in haemoglobin levels in the peripartum period. The
stress response also contributes to neutrophilia and increased WBC counts that could confound or
mask the diagnosis of infection. Some authors have documented a physiological increase in white cell
counts of up to 30 000 mm3 in the postpartum period.
An enhancement of the hypercoagulable state of pregnancy and activation of the clotting
cascades and platelets ensures a more stringent control on the blood losses in the peripartum phase. In
order to minimize blood losses from the endometrial placental separation site, fibrinolytic activity
decreases during partus, promoting clot formation. Placental and decidual tissue factor, a membrane
bound protein that initiates coagulation, increases during labour, as does Factor VIII complex and
Factor V. Prothrombin time decreases, particularly in the final stages of labour.
The reduction of fibrinolytic inhibitor levels following placental detachment results in normal
fibrinolytic activity 48 h after the delivery. By week 6 post partum, the haemostatic system returns to
the prepregnant state. These changes in the pro- and anticoagulation systems account for the marked
increase in the risks of venous thrombosis in women during this period.
The cardiovascular system

Physiological changes in pregnancy
The increased metabolic demands of the mother and fetus during pregnancy result in a range of
physiologically significant, but reversible adaptive changes in the maternal cardiovascular system. In
most instances, the increased demands on the maternal cardiovascular system are met adequately by
the ensuing physiological adaptations. If, however, there is underlying maternal cardiovascular
compromise due to disease, or the normal physiological haemodynamic changes fail to occur, the
adverse effects on the uteroplacental circulation could result in fetal and maternal disease.
Most cardiovascular and haemodynamic changes are initiated in the early stages of pregnancy
due to high circulatory levels of the vasoactive reproductive hormones oestrogen, progesterone and
prostaglandins (PGE1 and PGE2). The resulting vasodilation and reduction in systemic and
pulmonary vascular resistance (~20%) cause a fall in systolic and diastolic blood pressures
triggering reflex increases in the stroke volume (~2530%) and heart rate (~1020), and increases in
cardiac output by approximately 3050% of the prepregnancy states. Changes in heart rate and stroke
volume are detected as early as 5 weeks and 8 weeks, respectively. Stroke volume peaks around 16
24 weeks and decreases in the last trimester to reach prepregnancy values by term. The increased
cardiac outputs are facilitated by physiological hypertrophy and dilatation of the left ventricles and,
together with increases in total blood volume, plasma volume and red cell mass, aid in increasing the
capacity of the maternal cardiovascular system to effectively respond to the increased demands
imposed by the fetal and uteroplacental circulations. A further increase in cardiac output may occur
during labour in response to the sympathetic and catecholamine drives.
Maternal blood volume increase starts as early as 6 weeks gestation and progressively rises
through pregnancy peaking at 30% at 2832 weeks of gestation. Increases in the total volume are
consequent to increases in plasma volumes and red blood cell volumes. While changes in the blood
volume during pregnancy are mediated primarily by hormonal effects, vasoactive mediators like
nitric oxide are largely responsible for the vasodilatation that is commonly seen within the maternal
circulation. This combination of increased circulating volume and vasodilatation will result in an
increase in stroke volume and cardiac output. While much of the increased cardiac output is
redistributed in the uteroplacental circuit, organs like the mammary glands, skin, uterus and kidneys
also have increased perfusion. Uterine blood flow increases from ~50 mL/min at 10 weeks gestation
to 500600 mL/min at term. The elasticity of the uterine spiral arteries is severely compromised,
resulting in permanent dilatation and unresponsiveness to circulating vasopressor agents and the
autonomic nervous system. The resulting pooling of uterine blood aids in the maintenance of the
uteroplacental blood circulation.
Arterial and venous blood pressures during pregnancy do not show increases, despite the
significant perturbations in blood volume and cardiac output. Inferior vena caval compression,
particularly post 20 weeks of gestation, may result in decreases in cardiac output and placental
perfusion and cause maternal hypotension. Positional changes in blood pressure are more evident in
diastolic pressures, with average decreases of 1015 mmHg, while systolic blood pressures remain
constant. Consequent to these changes the pulse pressure increases in the third trimester.
Some of the physiological changes in pregnancy may also be reflected in an electrocardiogram
(ECG) and need to be defined in order to be differentiated from pathological changes. Diaphragmatic
elevation due to increased uterine size causes a deviation of the position of the heart to the left. A 15
left axis deviation may be seen with Q waves in leads III and AVF. Unspecific ST changes and
inverted T waves in lead III may also occur.
Figure 1.1 The relationship between the gravid uterus and the IVC in the supine and lateral
positions.
Table 1.2 Summary of key cardiovascular changes in pregnancy
Parameter Change
Stroke volume +30%
Heart rate +1520%
SVR 5% (approximately)
SBP 10 mmHg
DBP 1520 mmHg
MAP 1520 mmHg

Oxygen consumption +20%
Cardiac output +5070% (increase is more dramatic in late

pregnancy)
Intrapartum period
The stress-induced release of catecholamines and an increased sympathetic drive during labour and
delivery of the fetus result in significant haemodynamic and cardiovascular perturbations. A
significant increase occurs in cardiac output as a result of the additional circulatory load secondary to
each uterine contraction (approximately 300500 mL). Cardiac output rises progressively throughout
labour, peaking immediately after delivery. Rises in systolic and diastolic blood pressure occur
during the contractions. Heart rate changes in the intrapartum period are variable, although SVR
remains constant. Arrhythmias may occur in subjects with pre-existing cardiac diseases and
occasionally in subjects with no previous cardiac disease in response to these changes. These
arrhythmias include sinus tachycardia/bradycardia, supraventricular tachycardia and premature
ventricular/atrial and nodal contractions.
Postpartum period
While blood loss during delivery can be significant (up to 10% (500 mL) with vaginal deliveries and
1530% with caesarean sections), the compensatory increase in stroke volume and therefore cardiac
output seen in early pregnancy could last for up to 2 hours after delivery of the fetus. The cardiac
output continues to decline by a further 30% over 2 weeks, reaching prepregnant values by 612
weeks in most cases.
The respiratory system

Antepartum period
The increased demands of pregnancy require an associated expansion in the efficacy of tissue
oxygenation, and maternal alterations during pregnancy are designed to accommodate this. A 3050%
increase in the minute ventilation is achieved through a series of hormonal and biochemical changes,
ensuring enhanced oxygen availability and more efficient carbon dioxide removal. In addition to
hormonal effects, several mechanical factors influence respiratory function.
The progressive enlargement of the gravid uterus causes progressive cranial displacement and
alterations in the movement of the diaphragm. The increased intra-abdominal pressures lead to a
flaring of the lower thorax and an increase in the thoracic circumference by ~ 6 cm. The hormonal and
biochemical effects on respiration may occur through either central effects on the respiratory centre or
via direct local effects in the respiratory smooth muscles. Increasing levels of serum progesterone, a
known respiratory stimulant, are primarily responsible for these changes, aided by high circulating
levels of oestradiol and prostaglandins. The mechanism of action is postulated to be a progesterone-
induced enhanced sensitivity to CO2 (up to 60% by 20 weeks), a lowering of the carbon dioxide
thresholds in the respiratory centre and a consequent increase in minute ventilation. The consequent
reduction in maternal PaCO2 facilitates a greater carbon dioxide pressure gradient (PaCO2) between
the maternal and fetal circulations resulting in a more efficient transfer via the placental circulation.
In addition, progesterone-induced relaxation of the bronchial and tracheal smooth musculature results
in decreased airway resistance and increased respiratory air volumes in pregnancy, often causing
symptoms attributed to asthma to lessen in pregnancy. The increased respiratory rate and increased
minute ventilation result in a fall in PaCO2 (to ~ 4.1 kPa, 31 mmHg) by the end of the first trimester.
A small increase in PaO2 (to ~ 14 kPa, 105 mmHg) is also observed during the third trimester.
Nearer to term however, the inability of increases in cardiac output to fully compensate for the
increased oxygen demand results in a small reduction in PaO2 to less than 13.5 kPa (101 mmHg). The
changes in PaO2 alluded to above, however, are too small to have any important consequences on
maternal or fetal physiology. O2 consumption and CO2 production increase by 60% of prepregnant
values at term.
Changes in respiratory volume become apparent at around 20 weeks gestation and progress
throughout the pregnancy. A 3040% increase in tidal volume (Vt) is accompanied by an increased
inspiratory reserve volume (IRV) and decreases in expiratory reserve volume (ERV, 2030%),
residual volume (RV, ~20%) and functional residual capacity (FRC, 20%). The decrease in FRC as a
result of decreases in ERV and RV could make parturients more prone to respiratory collapse in the
supine position. The vital capacity (VC), forced expiratory volume in 1 second (FEV1) and the
FEV1/VC ratios remain unchanged during pregnancy. An increase in the physiological dead space up
to a volume of ~60 mL may occur. The reduction in FRC by approximately 20% and an increase in
minute ventilation by 3050% have major implications for changes to alveolar gas compositions
(anaesthetic agents as well as PaO2) in response to changes in alveolar ventilation. This includes a
faster rise in the concentration of anaesthetic agents during induction of anaesthesia and a faster fall in
PaO2 in response to upper airway obstruction or central respiratory depression.
Airflow is mainly determined by bronchial smooth muscle tone and the degree of congestion in
the bronchial capillaries, particularly in the smaller airways. The net effect on airway resistance is
probably determined by the balance between factors enhancing bronchoconstriction (e.g. PFG2a,
decreased RV and decreased PaCO 2) and those enhancing bronchodilatation (PGE2 and
progesterone). In the small airways (< 1 mm), airway closure in pregnancy occurs above the FRC
nearer term with a higher tendency for closure in the supine position. This may result in an alteration
in PaO2 due to ventilationperfusion (V/Q) mismatch in the lung bases.
Table 1.3 Changes in lung function tests during the late stages (third trimester) of pregnancy
Respiratory rate Unchanged
FEV1 Unchanged
PEFR Unchanged
Minute volume/ventilation Increased by 3050%
Tidal volume Increased by 3050%
FVC Unchanged
FEVI/FVC Unchanged
Maximum mid-expiratory flow rate (forced expiratory Unchanged

flow rate 2575)
Functional residual volume Decreased by 18%
Diffusing capacity, a measure of the ease with which gas transfers across the pulmonary
membrane, may show an increase in early pregnancy, although the changes are not deemed to be
clinically significant.
Changes in the intrapartum and postpartum periods

The specific changes during these phases will largely be dependent on the effect of pain, anxiety,
airway congestion and posture on alveolar ventilation, airflow resistance and arterial PaCO2 levels
along the lines described above. As the size of the gravid uterus gets smaller, the FRC and minute
ventilation are returned to prepregnant values over the first few weeks after delivery.
Acidbase regulation in pregnancy

Pregnancy induces a state of respiratory alkalosis and a left shift of the oxyhaemoglobin dissociation
curve. The respiratory alkalosis drives CO2 transfer from the fetus to the mother by increasing the
arterial CO2 pressure gradient between the maternal and fetal circulations. Increased renal excretion
of bicarbonate metabolically compensates for the respiratory alkalosis, with maternal pH levels at the
higher end of normal values (pH 7.47.45). Changes are stable throughout pregnancy until the onset of
labour. Maternal hyperventilation associated with labour results in an acute left shift of the
oxyhaemoglobin dissociation curve. The resultant increase in the affinity of maternal haemoglobin for
oxygen compromises oxygen delivery to the fetus. In addition, prolonged, painful labour results in
increases in the basic metabolic rates and oxygen demand, which cannot be compensated by further
increases in cardiac output. Effective administration of regional anaesthesia could prevent further
exacerbations in BMR and hyperventilation and serve to minimize potentially detrimental effects on
the fetus.
Oxygenhaemoglobin dissociation curve in pregnancy

The oxygen dissociation curve demonstrates the equilibrium between the partial pressure of oxygen in
the blood (PaO2) and the saturation of haemoglobin with oxygen. The sigmoid nature of the curve
dictates that once the plateau stage has been reached, large changes in oxygen partial pressures are
required to make relatively small differences in percentage haemoglobin saturation (SaO2). The
left/right shift in the position of the curve is determined by the affinity of haemoglobin for oxygen,
with a shift to the right implying lowered affinity, and vice versa. The affinity is expressed by the P 50
values, i.e. the oxygen tension at 50% haemoglobin saturation. The normal adult P50 (at pH 7.4,
37 C) is 26 mmHg (3.4 kPa). Throughout pregnancy there is a gradual rightward shift of the curve
due to a progressive increase in P50. At term, the P 50 is approximately 30 mmHg, resulting in
decreased haemoglobin affinity and therefore increased oxygen transfer to the fetus. These changes
are mediated by increases in 2,3-DPG levels seen throughout pregnancy. The median concentration of
red cell 2,3-DPG in the first trimester of pregnancy is approximately 16.1 mol/gHb and this may
increase to a level of approximately 17.0 mol/gHb by the end of the third trimester. Red cell 2,3-
DPG levels decrease rapidly during the postpartum period. These changes in 2,3-DPG levels and the
consequent reduction in oxygen affinity may partially compensate for the physiological anaemia seen
during pregnancy.
The gastrointestinal system

Anatomical and physiological alterations in the maternal gastrointestinal and hepatic systems during
pregnancy are essential to support the increased nutritional demands of the fetus. The changes are
primarily due to either mechanical changes imposed by the growing fetus and/or hormonal effects of
progesterone and oestrogen. Appetite and food consumption are increased during pregnancy, although
variations can occur in the food types desired, with avoidance of certain items and cravings for
others. Although the basis for these changes is unclear, a combination of hormonal changes
(oestrogens and progesterone), insulin/glucagon levels and alterations in taste etc. are postulated to
have a role to play.
A combination of increased abdominal pressure due to the growing fetus and a progesterone-
induced decrease in the lower oesophageal sphincter tone result in gastro-oesophageal reflux in as
many as 80% of term parturients. Most of the clinical changes occur in the third trimester at about 36
weeks. The flattening of the hemidiaphragm could result in the reduction of the normally acute gastro-
oesophageal angle, thereby contributing to the reflux. The alterations in lower oesophageal sphincter
tone are also primarily responsible for heartburn in pregnancy. Although a progesterone-induced
decreased gastric tone can result in delayed gastric emptying and increased gastric volumes during
pregnancy, the effects are more significant during labour. The effects may be exaggerated due to the
administration of opiate analgesics and general anaesthetics, thereby increasing the risk of vomiting
and aspiration pneumonia on induction of general anaesthesia. Preventive measures include
administration of H2 blockers, neutralization of gastric contents and rapid sequence induction with
cricoid pressure.
Similarly, a progesterone-induced decrease in smooth muscle tone and motility can also occur in
pregnancy, prolonging intestinal transit times, particularly during late pregnancy. Histological
changes in the intestinal villi show villus hypertrophy and increased absorptive capacity to cope with
corresponding increases in demand. Together with the increased absorptive surface, decreased
motility allows for increased absorption of fluids and nutrients, including amino acids, glucose,
sodium chloride and water. Iron absorption in the duodenum increases twofold by the third trimester.
Calcium absorption is enhanced primarily due to increased levels of 1,25-dihydroxy-vitamin D. All
pregnancy-associated changes to the gastrointestinal system are thought to revert to normal by 48
hours post partum.
The hepatic system

Pregnancy-associated changes in the hepatic system are primarily related to the effects of oestrogens
on liver metabolism. The enlarging uterus displaces the liver superiorly, posteriorly and anteriorly.
Small but significant increases in the plasma concentrations of all liver enzymes, including gamma-
GT, ALT, AST and LDH are demonstrable in pregnancy. In most patients, however, these changes do
not imply liver dysfunction and are clinically insignificant. These small increases in liver enzymes
and the presence of some of the clinical signs usually attributed to liver disease, such as spider
naevi and palmar erythema, in otherwise normal pregnancies may render the diagnosis of liver
disease more challenging in pregnant women. The placenta is a rich source of alkaline phosphatase
and consequently plasma concentrations of alkaline phosphatase may be increased almost threefold in
the late stages of pregnancy. Pregnant women also have a slightly greater tendency to develop gall
stones due to a progesterone-induced reduction in cholecystokinin release and a reduced contractile
response of the gall bladder, resulting in biliary stasis. Plasma cholinesterase levels may be almost
25% lower in the third trimester due to reduced hepatic synthesis and, theoretically, this reduction
may prolong the duration of action of succinylcholine. Even though these differences are not clinically
important in the majority of women who receive suxamethonium, a small group of women with
increased succinylcholine sensitivity (who are heterozygote for an abnormal cholinesterase gene) may
show prolonged neuromuscular block following the administration of suxamethonium during
pregnancy.
Renal system
As a result of an increase in blood volume, stroke volume and cardiac renal blood flow, and renal
plasma flow and glomerular filtration rate are increased in pregnancy. In fact, renal plasma flow and
GFR may be 4065% greater in a pregnant woman at term when compared to her prepregnant values.
This is reflected by an increased clearance of urea, creatinine, urate and excretion of bicarbonate,
resulting in a corresponding reduction in the plasma levels of these solutes. Through increased
activity of the reninangiotensinaldosterone axis and the effects of circulating progesterone,
increased free water retention is seen and this leads to a reduction in plasma osmolality. It has been
shown that plasma osmolality starts to decline soon after conception and reaches a value almost
10 mosmol/kg lower than preconception values by the 10th week of pregnancy, changing very little
after this. Glycosuria can be observed in 40% of parturients secondary to increased filtration (due to
raised GFR) and the filtered load of glucose exceeding the tubular maximum for glucose.
Urinary tract infections are also more common in pregnant patients due to urinary stasis from
progesterone-mediated ureteric smooth muscle relaxation and the direct effects of the gravid uterus on
the bladder. Finally the changes in the ECF volume and GFR may alter the volume of distribution and
clearance of some drugs that are of considerable importance to anaesthetists. For example, although
some studies show conflicting results, it is generally seen that the plasma concentrations of
anticonvulsant drugs may be decreased considerably in the third trimester of pregnancy. A
combination of factors including changes to protein binding, increased GFR and expansion of plasma
volume may account for these observed changes in the pharmacokinetics of some of the common
drugs used in clinical practice
Figure 1.2 Relationship between filtered/reabsorbed glucose levels and the inability of the renal
tubules to indefinitely reabsorb all the filtered glucose due to saturation of the relevant transport
systems. When the filtered load exceeds the tubular transport systems, glucose will appear in the
urine renal glycosuria.
Endocrine system
Endocrine system
Pregnancy is frequently associated with increased insulin production and increased insulin resistance.
These changes are brought about largely through the effects of human placental lactogen (HPL), which
is also known as the human chorionic somatomammotropin (HCS). HCS is a polypeptide placental
hormone that is secreted by the syncytiotrophoblast of the developing embryo. Structurally and
functionally HCS mimics the effects of human growth hormone and modifies the metabolic state of the
mother during pregnancy. The changes brought about by the actions of HCS facilitate the constant and
uninterrupted supply of glucose and other energy substrates to the growing fetus. HPL has anti-insulin
properties and consequently relative hyperglycaemia and impaired glucose tolerance is common in
pregnancy. Approximately 6% of pregnancies are complicated by maternal diabetes mellitus (80% of
which are gestational). Maternal hyperglycaemia can result in fetal hyperglycaemia, which is usually
accompanied by fetal hyperinsulinism. This results in large fetal sizes (macrosomia), which may have
considerable implications for delivery and hypoglycaemia during the immediate peripartum periods.
In addition to the above, pregnancy is also associated with an increase in the production of prolactin,
parathyroid hormone and the adrenal cortical hormones, such as cortisol and aldosterone.
Table 1.4 Changes in GFR in pregnancy
Normal adult female 106 to 132 mL/min
Trimester one 131 to 166 mL/min
Trimester two 135 to 170 mL/min
Trimester three 117 to 182 mL/min
Key points
1. The complex changes in maternal physiology are predominantly secondary to hormonal
responses to female sex hormones or physical adaptations to increasing fetal size.
2. Significant changes in the haematological system increase the risk for development of
anaemia, thromboembolism and consumptive coagulopathies.
3. Cardiovascular adaptations occur early, with an increase in stroke volume and heart rate and
a reduction in SVR, PVR and blood pressure.
4. The respiratory system undergoes significant changes to improve efficacy of tissue
oxygenation.
5. Acidbase regulation changes alter normal non-pregnant parameters.
6. Gastrointestinal, hepatic, endocrine and renal physiology undergoes significant alterations to

support the development of the fetus.
Further reading
Bassell, G. M. and Marx, G. F. (1981). Physiological changes of normal pregnancy and parturition: In
E. V. Cosmi (ed.), Obstetrical Anaesthesia and Perinatology. New York: Appleton Century-Crofts.
Blackburn, S. T. (2007). Maternal and Fetal Neonatal Physiology: A Clinical Perspective, 3rd edn.
Philadelphia, PA: Elsevier Saunders.
Cunningham, F. G., Leveno, K., Bloom, S. et al. (2005). Williams Obstetrics, 22nd edn. New York:
McGraw-Hill.
Duffy, T. P. (2004). Haematological aspects of pregnancy. In Burrows, G. N., Duffy, T. P. and Copel,
J. A. (eds.), Medical Complications During Pregnancy, 6th edn. Philadelphia, PA: Saunders.
Hellgren, M. (2003). Haemostasis during normal pregnancy and puerperium. Semin. Thromb.
Hemost., 29, 125.
McAuliffe, F., Kametas, N., Costello, J. et al. (2004). Respiratory function in singleton and twin
pregnancy. BJOG, 108, 980.
Monga, M. (2004). Maternal cardiovascular and renal adaptations to pregnancy. In Creasy, R. K.,
Resnik, R. and Iams, J. D. (eds.), Maternal-Fetal Medicine: Principles and Practice, 5th edn.
Philadelphia, PA: Saunders.
Pritchard, J. A. (1965). Changes in blood volume during pregnancy and delivery. Anaetheioslogy, 26,
393.
Van Thiel, D.H. and Shade, R. R. (1996). Pregnancy: Its physiologic course, nutrient cost and effects
on gastrointestinal function. In Rustgi, V. K. and Cooper, J. N. (eds.), Gastrointestinal and Hepatic
Complications in Pregnancy. New York: John Wiley & Sons, Inc.
Wise, R. A., Polito, A. J. and Krishnan, V. (2006). Respiratory physiologic changes. Immun. Allergy
Clin. North Am. 26, 1.
Chapter 2
Placental physiology

Carolynn Wai and W. Ross Macnab
Introduction
The placenta is an organ that connects a developing fetus to the uterine wall for exchange of oxygen,
nutrients, antibodies and hormones between the mother and fetus. It is required for the removal of
waste products. The development of the placenta is essential for normal fetal growth, development,
and the maintenance of a healthy pregnancy.
Embryological development
The placenta begins to develop upon implantation of a blastocyst into the maternal endometrium,
leading to rapid proliferation and differentiation of trophoblasts. This leads to the formation of two
layers: the cytotrophoblast and syncytiotrophoblast. As the blastocyst implants in the uterine lining,
vacuoles and lacunae form within the syncytiotrophoblast. This network of lacunae eventually
become the intervillous spaces. The cytotrophoblast erodes deeper into the endometrial tissues
leading to formation of chorionic villi, which will cover the entire surface of the chorionic sac.
Transformation of the narrow spiral arteries into wide uteroplacental arteries also takes place, due to
invasion of cytotrophoblasts into the vascular smooth muscle and endothelial cells. The maternal
endometrium undergoes various changes, known collectively as the decidual reaction, forming the
decidua, which is shed at delivery.
Anatomical structure
The placenta is discoid in shape with a diameter of 15 to 25 cm. A full-term placenta is
approximately 23 cm thick and weighs about 500600 g. The growth of the placenta roughly
parallels that of the expanding uterus and covers approximately 15 to 30% of the internal surface of
the uterus. It consists of two components: a fetal and a maternal portion.
The fetal component of the placenta is formed by the wall of the chorion (chorionic plate). The
villi that arise from it project into the intervillous spaces which contain maternal blood. The maternal
component of the placenta, on the other hand, is formed by the decidua basalis, which is the
endometrium, deep into the fetal component of the placenta. The two components are held together by
the cytotrophoblastic shell. Wedge-shaped areas of decidual tissues, known as placental septa, form
as the villi invade the decidua, leading to grooves when viewed from the maternal side of the
placenta. Cotyledons are easily recognizable bulging areas that are covered by a thin layer of decidua
basalis. These areas of irregular convexities within the fetal part of the placenta result from the
formation of the placental septa. These septa contain two or more stem villi and their branches.
Anastomoses are formed between the dilated spiral arteries from the decidua and endometrial veins.
These anastomoses result in the formation of sinusoids which drain into the lacunar network,
establishing the uteroplacental circulation (see Figures 2.1 and 2.2).
Figure 2.1 Anatomical structure of the placenta.
Figure 2.2 Structure of the placenta.
Placental circulation
The placenta receives the highest blood flow of any fetal organ (40% of fetal cardiac output). The
maternal and fetal circulations are separated by a placental membrane consisting of fetal tissue.
Maternal placental circulation

Maternal blood fills the intervillous space through 80 to 100 spiral arteries in the decidua.
Remodelling of these arteries causes them to be wider and less convoluted, and this in turn increases
maternal blood flow to the placenta. This pulsatile flow of blood bathes the fetal villi with
oxygenated blood. The pressure from the arteries forces the blood deep into the intervillous spaces to
allow gas and metabolic exchange. As the pressure decreases, the deoxygenated maternal blood re-
enters the circulation through the endometrial veins. There is a total of approximately 150 mL of
blood within the intervillous spaces of a mature placenta. It is replenished about three to four times a
minute and is affected by uterine contractions.
Placental membrane
This membrane separates the maternal and fetal blood. In the first four months of pregnancy, it
consists of four layers: the endothelial lining of the fetal vessels, the connective tissue of the villus,
the cytotrophoblast layer and the syncytiotrophoblast layer. This gradually thins out to permit closer
contact between the fetal endothelium and the syncytial membrane, allowing greater exchange of
compounds between mother and fetus. Although also called a barrier, this is a misnomer, as many
substances pass through freely.
Fetal placental circulation

Deoxygenated fetal blood leaves the fetus through umbilical arteries to the placenta. The umbilical
arteries then branch radially, forming the chorionic arteries at the junction of the umbilical cord and
the placenta; these arteries further branch into cotyledon arteries. Within the villi, the vessels form an
extensive arteriocapillaryvenous system, bringing the fetal blood extremely close to the maternal
blood. There is no intermingling of fetal and maternal blood; however, small gaps exist within the
placental membrane, leading to small amounts of fetal blood entering the maternal circulation.
Oxygenated fetal blood passes into thin-walled veins that map the placental arteries back to the
site of attachment of the umbilical cord. Here, they merge to form the umbilical vein, which supplies
oxygenated blood to the fetus.
Placental transfer
The efficient exchange of compounds between maternal and fetal circulation occurs at the
syncytiotrophoblast layer and utilises several mechanisms:
1. Passive transport:
a. Simple diffusion
b. Osmosis
c. Facilitated diffusion
2. Active transport:
a. Carrier-mediated active transport
b. Ion channels
3. Vesicular transport:
a. Endocytosis
b. Exocytosis
Functions
The placenta has three main functions: metabolism, exchange of metabolic and gaseous products
between maternal and fetal circulations, and the production of hormones.
Metabolism
The placenta has the ability to synthesize glycogen, protein, cholesterol and fatty acids, which serve
as a source of nutrients and energy for the developing fetus. Glycogen is synthesized and stored as an
energy reserve for the fetus.
The high demand for cholesterol by the fetus is initially supplied by maternal cholesterol, but as
gestation progresses, the placenta synthesizes cholesterol from fatty acid stores. Placental cholesterol
is an important precursor for placental production of steroid hormones, such as progesterone and
oestrogen.
Lactate is produced as a waste product of metabolism by the placenta and has to be removed via
the maternal circulation.
Exchange of metabolic and gaseous products
Gaseous transfer
The placental membrane is highly permeable to oxygen and carbon dioxide, which cross the placenta
rapidly by simple diffusion. Therefore, the rate-limiting step for exchange is the blood flow. Fetal
haemoglobin has a higher affinity for oxygen and a lower affinity for carbon dioxide in comparison to
maternal haemoglobin. This therefore favours oxygen uptake by the fetus and carbon dioxide
excretion to the mother.
Glucose and carbohydrates

The fetus relies on glucose as the primary substrate for its oxidative metabolism. The placenta is
unable to produce sufficient amounts of glucose until later in gestation and therefore relies on transfer
of glucose from the maternal circulation. This is achieved via protein-mediated facilitated diffusion.
A few glucose transporters (GLUTs) have been identified in the human placenta, with GLUT1 being
the most abundant subtype.
Proteins and amino acids

Amino acids are essential for protein synthesis by the fetus. The maternal transfer of amino acids
occurs via the microvillous and basal membranes of the syncytiotrophoblast, utilizing an active
transport mechanism.
Lipids and fatty acids

Fatty acids are essential components for fetal development. Many lipids are bound to plasma
proteins, which can be released by lipoprotein lipase found on the maternal surface of the placenta.
Free fatty acids and glycerol cross the placental membrane via simple diffusion, as well as facilitated
diffusion via fatty-acid binding proteins. They are re-esterified when they reach the cytoplasm of the
placental trophoblast.
Immunoglobulins and antibodies

The fetus is unable to produce antibodies until well after birth, and placental transfer of maternal
antibodies confers passive immunity to the fetus. Immunoglobulin G is the predominant means of fetal
immunity and is transported via pinocytosis.
Water and electrolytes

These compounds are freely exchanged between maternal and fetal circulations. The basal membrane
of the placenta contains a Na+-K+ pump but net movement of Na+ and Cl is by simple diffusion. This
maintains similar concentrations of these ions between maternal and fetal circulations. Water passes
freely by osmosis, whilst Ca2+ utilizes an active transport mechanism, which is still poorly
understood. Fetal ionized Ca2+ levels are higher compared to maternal levels and are regulated by
parathyroid hormone-related peptides (PTHrP).
Drugs
Most drugs and metabolites cross the placental membrane by simple diffusion, but a few may utilize
any of the transport mechanisms described above. This is dependent on the drugs molecular weight,
degree of ionization, lipid solubility, protein binding and the blood flow.
Hormone production
The placenta has no innervation and therefore relies on secretion of humoral agents to communicate
between maternal and fetal circulations. These substances can act locally within the placenta or the
uterus (autocrine and paracrine regulations). The two main groups of hormones produced by the
placenta are peptide and steroid hormones.
1. Peptide hormones are mainly produced by the trophoblast cells of the chorionic villi. The
main ones are:
a. Human chorionic gonadotrophin (hCG)
b. Human placental lactogen (hPL)
c. Insulin-like growth factors (IGFs)
d. Corticotropin-releasing hormone (CRH)
2. Steroid hormones are derived from a common precursor, cholesterol. They are lipophilic
molecules which readily cross the cell membranes:
a. Progesterone
b. Oestrogen
c. Glucocorticoids
3. Others
a. Growth factors, including vascular endothelial growth factors and placental growth factors
b. Cytokines, chemokines, eicosanoids.
Key points
1. Placental development begins at the point of blastocyst implantation into maternal
endometrium.
2. Two layers are formed, the cytotrophoblast and the syncytiotrophoblast, that develop into the
chorionic villi and intervillous spaces, respectively.
3. Placental function includes exchange of metabolic and gaseous products, metabolism and
hormone production.
Further reading
Baker, P. and Kenny, L. (eds.) (2011). Obstetrics by Ten Teachers, 19th edn. Boca Raton, FL: CRC
press.
Moore, K., Persaud, T. and Torchia, M. (eds.) (2012). The Developing Human, 9th edn. Philadelphia,
PA: Saunders.
Roberts, V. and Myatt, L. (2014). Placental development and physiology, UpToDate

http://www.uptodate.com/contents/placental-development-and-physiology (accessed April 2015).
Langman, J. and Sadler, T. (2012). Langmans Medical Embryology, 12th edn. Philadelphia, PA:
Lippincott Williams & Wilkins.
Gude, N. M., Roberts, C. T., Kalionis, B. and King, R. G. (2004). Growth and function of the normal
human placenta. Thromb. Res., 114, 397407.
Chapter 3
Pharmacology relevant to pregnancy

Christopher Kelly and Malachy Columb
There are specific issues with regard to therapeutics and pharmacology in the expectant mother and
during the postpartum period. There are general changes in the pharmacokinetics and
pharmacodynamics, considerations relating to the placenta, potential effects on the fetus and impacts
on breastfeeding.
Pharmacokinetics
Bioavailability
The absorption of a drug is the method by which it moves into the body and into the circulating blood,
and is characterized as the bioavailability. This can be via a wide range of routes, those used most
commonly by the anaesthetist are intravenous (IV), inhalational, epidural, intrathecal, oral,
intramuscular (IM), sublingual, intranasal, rectal and transdermal. Despite the enhanced cardiac
output in pregnancy, the absorption of drugs is minimally affected, but pregnancy-induced emesis may
reduce the bioavailability of orally administered drugs. The increased minute ventilation associated
with pregnancy can speed the onset and offset of inhalational agents.
Volume of distribution (VD)
The distribution of a drug throughout the body is dependent on various factors: physicochemical
characteristics of the drug (molecular size, lipid solubility, ionization and protein binding), regional
blood flow and any cellular transport mechanisms. The volume of distribution (VD) can be greatly
affected by pregnancy. Increases in circulating blood volume and total body water provide a larger
VD for most drugs. Pregnancy alters the plasma protein profile, potentially changing binding
characteristics and the fraction of free drug available for action. Increased cardiac output will speed
the distribution of drugs.
Placental transfer
The fetus is also, in effect, an additional compartment into which drugs may distribute. The factors
affecting the extent to which drugs cross the placenta into fetal circulation are similar to those for any
phospholipid membrane bilayer. Placental transfer will be facilitated for more lipid-soluble drugs,
compared to hydrophilic polar or ionized molecules. Likewise, the greater the proportion that is free
drug or in the unbound state, the faster it will equilibrate. The extents to which the drug is ionized and
protein bound may be different in mother and fetus because of the reduced pH in the fetus, and this
may impact on the effective concentration gradients. This situation may change or be exacerbated by
labour, during which maternal and fetal acidoses may develop.
Metabolism
Metabolism of drugs is largely unaffected by normal pregnancy. It is possible that the pathological
state of HELLP (Haemolysis, Elevated Liver enzymes, Low Platelets) syndrome may impair liver
function and thus the metabolism of drugs. A special situation is the relative reduction in the levels of
circulating plasma cholinesterases as a result of the increased plasma volume in pregnancy. This can
lead to prolonged duration of action of drugs metabolized by these enzymes e.g. suxamethonium.
Elimination of most drugs is increased during pregnancy. Glomerular filtration rate is increased by
50%, peaking at the end of the first trimester, leading to greater plasma clearance. Pre-eclampsia is a
potential exception to this, with associated reduction in renal function.
Pharmacodynamics
In general, pharmacodynamics are relatively unaffected by pregnancy. An important exception is the
reduction in minimum alveolar concentration (MAC) of inhaled anaesthetic agents that is required for
anaesthesia in pregnancy with a resulting increase in the relative potencies of these agents. Likewise
the potencies of local anaesthetics are increased in pregnancy and the altered coagulation of the
pregnant state may affect the efficacies of anticoagulants.
Local anaesthetics
A local anaesthetic is an agent that produces temporary blockade of neuronal transmission when
applied to a nerve axon. The amide local anaesthetics bupivacaine and ropivacaine are commonly
used for analgesia in obstetric patients in the UK.
At rest, the interior of a nerve is negatively charged due to the greater concentration of sodium
ions in the extracellular space relative to the intracellular. The propagation of an action potential is
dependent on opening of sodium channels in the cell membrane, allowing net influx and
depolarization of the cell. Local anaesthetics prevent this sequence of events by first diffusing into the
cell in an unionized state, then, having been ionized in the more acidic cytoplasm, binding the
cytosolic aspect of the sodium channel. This prevents sodium influx and depolarization and hence
propagation of the action potential.
The physiochemical properties of local anaesthetics affect their behaviour clinically. As with all
anaesthetic agents, potency is related to lipid solubility. The more lipid soluble drugs are more
potent. Unlike general anaesthetics, there appears to be a ceiling effect; above an oil:water partition
coefficient of four there is no further increase in potency. Bupivacaine is more lipid soluble than
lidocaine and concentrations of 0.25%wt/vol compared to 1%wt/vol will produce anaesthesia.
Greater protein binding of the drug will lead to a longer duration of action. The longer the
aliphatic chain on the compound the greater the protein binding will be. Both bupivacaine and
ropivacaine are extensively (95% and 94%, respectively) bound to both albumin and 1-acid
glycoprotein hence the relatively long duration of action. Lidocaine is only 64% bound and
consequently has a shorter duration of action.
The pKa of the agent impacts the time to onset of action of the drug because it determines the
ratio of the ionized to the unionized lipid-soluble fraction at any given pH. A large fraction of lipid-
soluble unionized drug will facilitate diffusion of the anaesthetic into the axon where it will take
effect. In practice, the lower the pKa of these basic compounds, the greater the unionized fraction at
physiological pH and the faster the onset of action. Lidocaine, for example, has a pKa of 7.9 so is
33% unionized at pH 7.4, whereas bupivacaine, with a pKa of 8.1, is only 15% unionized at the same
pH.
Local anaesthetic agents become toxic once they reach sufficient plasma concentrations.
Although guidance is given for maximum safe doses, there are a variety of factors in determining
toxicity. The vascularity and presence of fat, which fixes local anaesthetic, at the injection site will
influence eventual plasma concentration. There is also evidence to suggest that the rate of change of
the plasma concentration will impact toxicity as well as peak concentration. So, as well as mass of
the drug, its concentration and speed of administration will be relevant.
As blood concentrations increase, central nervous system (CNS) symptoms will develop.
Initially there is a period of excitation (due to inhibition of inhibitory fibres) followed by generalized
depression and eventually respiratory arrest. Cardiovascular effects will follow the onset of CNS
features, but vary from agent to agent. Bupivacaine is said to be maximally cardiotoxic causing re-
entrant tachyarrhythmias and eventually ventricular fibrillation and cardiac arrest. The situation is
then worsened as the patient becomes more acidotic, reducing protein binding and increasing free
drug. Resuscitation attempts can be prolonged and intralipid is recommended to reduce free drug
concentrations. The ratio of concentrations required for CNS to cardiovascular toxicities is
considered to be a safety margin. This is lower for bupivacaine than all the other agents in use.
Because of these safety concerns, the pure S-enantiomer of bupivacaine, levobupivacaine, has
been developed with a more favourable side effect profile. Likewise, ropivacaine is a pure S-
enantiomer, which is also less cardiotoxic and less potent than bupivacaine.
Systemic analgesia
A variety of systemic analgesics are in common use today. Generally they are cheap, easy to
administer and have few contraindications. They can be of great value when epidural analgesia is
refused or contraindicated. Parenteral opioids have a long history of use and are still popular today.
Pethidine
Since 1950 in the UK it has been legal for midwives to administer pethidine to labouring women and
so it is the most commonly administered analgesic. It is a synthetic opioid and phenylpiperidine
derivative, and is usually given at a dose of 1 mg/kg IM by midwives. There is some evidence to
suggest that the reduction in pain scores is greater when administered by the IV route with no
associated increases in negative outcomes. The efficacy of pethidine has been questioned by a
National Childbirth Trust (NCT) survey showing that women more often find it unhelpful than helpful.
This is likely due to side effects of the drug on the mother. CNS effects include sedation, confusion
and dysphoria. Pethidine is metabolized by the liver to inactive pethidinic acid and norpethidine
which has half the activity of pethidine. Norpethidine (N-desmethyl pethidine) may accumulate in
renal failure and has been linked to grand mal epilepsy. For this reason it is relatively contraindicated
in patients with raised blood pressure or other potential for seizures, such as eclampsia.
Pethidine reduces gastric motility and will lead to increased aspiration risk should general
anaesthesia be required. It is common practice to co-administer ranitidine and metoclopramide in an
attempt to offset this effect. Like other opioids there is the potential to cause nausea and vomiting,
although phenothiazine antiemetics should be avoided specifically with pethidine because of the
increased sedation and antagonism of the analgesia that may ensue. There is a dose-dependent
respiratory depression with all opiates. The dosage should be titrated to effect and respiratory rate.
This can be particularly problematic if the patient is also using Entonox. Pethidine has not been
shown to have any effect on uterine contractility.
The fetus and neonate can also be affected by the administration of opiates. Pethidine is nearly
30 times more lipid soluble than morphine and as a result will equilibrate across the placenta within
minutes. Here the half life is around 20 hours, as compared to 3 hours in the mother. Fortunately this
does not appear to be detrimental to the neonate, although some authors argue that the maternal
respiratory alkalosis associated with pain will facilitate ion trapping of pethidine base within the
relatively acidic fetal circulation. Cardiorespiratory effects have been noted. Heart rate variability
may be reduced and some studies have shown reduced SpO2 values in mother and baby while
sleeping, but none of these findings have been associated with adverse long-term outcomes.
Morphine
Morphine is a naturally occurring phenanthrene derivative. It is typically given as a bolus of 25 mg
IV or 510 mg IM. It shares many of the systemic effects of pethidine, but is cleared more quickly,
with duration of action of 34 hours. There is deemed to be less potential for accumulation of active
metabolites than with pethidine and a reduced concern for convulsions. This drug can only be
prescribed by doctors, so does not allow midwives the autonomy afforded with pethidine.
Diamorphine
Diamorphine is a diacetylated morphine derivative; it is a prodrug with 1.5 to 2.0 times the potency
of morphine. The NCT survey found that mothers and midwives rated it more useful than pethidine. It
is more lipid soluble than morphine and as a result would be expected to have a faster onset of action.
This drug is not available for clinical use in the US. It is associated with the same sedation,
respiratory depression and nausea that come with all opiates.
Patient-controlled analgesia (PCA)

There has been great enthusiasm for PCA in labour. Many different agents have been administered in
this way because of the potential benefits to patients, fetus and staff:
Increased patient satisfaction
Lower total dose of drug delivered
Less respiratory depression
Less nausea and vomiting
Increased patient autonomy and less intensive for carers
Few contraindications.
Remifentanil is an ultra short-acting pure -opioid agonist that is rapidly metabolized by non-specific
plasma esterases. With a half life of only 37 minutes, independent of hepatic or renal function, it
would appear to be ideal for rapidly fluctuating pain in labour. Recently this has been used to good
effect in patients refusing epidural analgesia or where it is contraindicated. Mothers must be taught to
coordinate the timing of the bolus dose to cover their contraction. Monitoring of SpO2 and one to one
nursing care is advised, although any respiratory depression is likely to be short lived and naloxone
is rarely required. The initial bolus is often set at 0.25 g/kg of lean body weight, with a three minute
lockout. This can then be titrated to effect.
Ketamine
Ketamine is a phencyclidine derivative presented as a mixture of two enantiomers and at low doses
can have potent analgesic effects. It has a reasonably short duration of action of around 10 minutes but
may accumulate with repeated doses. It may be helpful during the second stage of labour, but use is
limited by the potential for psychomotor effects and at higher doses increased uterine tone. Interest
has been renewed in this agent with the advent of the pure S-enantiomer, which may have fewer side
effects.
Inhalational analgesia
A wide range of inhalational anaesthetic agents have been used over more than 150 years. During this
time they have been shown to be effective and safe. Some of the oldest anaesthetics such as ether and
chloroform gave way to trichloroethylene and methoxyflurane, subsequently the more recent agents
such as isoflurane, sevoflurane and desflurane have also been used. Despite this, the most commonly
used agent by far is a 50:50 nitrous oxide in oxygen mix known as Entonox.
Nitrous oxide has a low blood:gas partition coefficient of 0.47, leading to rapid onset and offset
of action. Although quick, the peak effect does not come on immediately and mothers must be taught
the timing to begin inspiring the mixture 2030 seconds before the peak pain sets in. Incorrect timing
can lead to the unfortunate situation of poor analgesia then disproportionate sedation following the
contraction. It is thought to act at the -opioid receptor and can transiently give analgesia of similar
potency to morphine.
The Medical Research Council, in conducting studies with different ratios of nitrous oxide to
oxygen, concluded that the 50:50 mix was safest. Although higher proportions of nitrous oxide would
be more efficacious, there is increased risk that patients would become unduly sedated. Less than
0.5% of mothers will become excessively drowsy with Entonox alone, but this figure would rise if
other respiratory depressants are co-administered. Whether or not any significant desaturation occurs
with the use of Entonox, it is estimated that 25 million administrations occur in the USA annually
without obvious problems.
Drugs affecting the uterus

Drugs reducing uterine tone
Tocolysis is indicated to prevent preterm labour and to aid intrauterine resuscitation of the fetus. Due
to the pressure in the uterus there is no blood flow to the fetus during contractions. Because of this,
once a decision has been made to proceed to operative delivery, attempts are often made to improve
blood flow. A variety of agents are in use to reduce uterine tone, none of these have been studied
extensively and a degree of controversy exists over their use.
-adrenoceptor agonists such as salbutamol and terbutaline (ritrodrine is no longer available as
it has been discontinued) will bind 2 receptors in the myometrium. There is subsequent activation of
adenylyl cyclase with increasing concentrations of the secondary messenger 3-5-cyclic adenosine
monophosphate (cAMP). The increased concentrations reduce free ionized calcium, which is
required for the interaction of myofilaments, hence the smooth muscle of the uterus relaxes. These
agents can be given orally or by infusion and can cause tremor, restlessness and tachycardia. Rarely
pulmonary oedema is seen, but this is thought to be an indirect mechanism partially due to fluid
overload.
The calcium channel dihydropyridine blocker nifedipine blocks voltage-gated calcium channels,
which then limits the release of calcium into the sarcoplasmic reticulum and prevents muscle
contraction. None of the other calcium channel blockers are used for this purpose.
Atosiban is the only oxytocin antagonist available. It has similar effect to the outmoded
ritrodrine, but has a more favourable side effect profile. The usual rise in intracellular calcium that is
prompted by secondary messenger systems is blocked by atosiban. An advantage of this agent is that
it can be used in conjunction with other tocolytics with potentially synergistic effect.
Glyceryl trinitrate (GTN) acts as a nitrate donor and increases concentrations of nitric oxide in
the smooth muscle of the uterus. Nitric oxide is normally responsible for regulating blood flow within
the uterus. The lipophilic molecule easily crosses cell membranes, where it activates guanylyl
cyclase. This enzyme increases intracellular concentrations of cyclic guanosine monophosphate
(cGMP) and thus activates protein kinases, protein phosphorylation and causes smooth muscle
relaxation. The drug can be given sublingually or intravenously and can lead to the familiar side
effects of headache, hypotension and reflex tachycardia. Pulmonary oedema has been reported with
its use, potentially due to changes in vascular permeability.
Magnesium sulfate has a wide range of clinical applications, several of which are relevant to the
obstetric anaesthetist. Magnesium is the fourth most common cation in the body and is involved in a
variety of body systems. Its effects as a tocolytic arise from the physiological antagonism of calcium.
This is mediated via two separate mechanisms: high intracellular concentrations of magnesium
prevent influx of calcium in a non-competitive way and there appears to be competitive inhibition of
calcium binding at the sarcoplasmic reticulum.
The volatile anaesthetic agents all cause dose-dependent reductions in uterine tone.
Drugs that stimulate the uterus

Oxytocin is the first-line drug for prophylaxis and treatment of uterine atony. Endogenous oxytocin is
produced in the supraoptic nucleus of the hypothalamus and stored in the neurohypophysis or
posterior pituitary gland. It is normally responsible for controlling lactation and acts at receptors in
the uterine myometrium. In early pregnancy there are few of these receptors and so the response to
oxytocin is greatly reduced when compared to that at term. The exogenous drug was historically
derived from animal extracts and had significant quantities of antidiuretic hormone (ADH) in the
mixture. This is far less of a problem with newer synthetic agents such as syntocinon, but there is still
potential for the problem because the nine amino-acid polypeptide oxytocin differs from ADH by
only two amino acids. It is therefore possible that small quantities of ADH are present. This is part of
the rationale for the administration of syntocinon in normal saline to prevent excessive doses.
Syntocinon will increase the frequency and force of contractions via its action on the oxytocin
receptors in the myometrium. It also causes clinically significant reductions in systemic vascular
resistance at therapeutic doses, resulting in hypotension and tachycardia. These side effects can be
reduced by ensuring that large doses (>5 units) are not given and that the drug is not given quickly.
Many authors suggest giving the dose as an infusion over several minutes to reduce haemodynamic
instability and to allow compensatory responses. It follows that patients with a fixed cardiac output
state, such as those with aortic stenosis or pulmonary hypertension would be particularly susceptible
to the deleterious effects of reduced afterload. The effects of the drug, however, are only short lived
and have a half life of approximately 10 minutes, potentially adding further weight to the argument for
infusion rather than bolus injection of the drug.
The ergot alkaloids are second-line agents used in the treatment of uterine atony, a class of
chemicals produced by a common fungus. Ergometrine is the most commonly used agent today and has
activity at -adrenergic, dopaminergic and serotoninergic (5-HT3) receptors. In addition to causing
uterine tetany, it causes generalized vasoconstriction, hypertension, bronchospasm and nausea. The
drug should therefore be used only with caution in patients with pre-existing hypertension, pre-
eclampsia, pulmonary hypertension or asthma. It is generally not given IV because the IM route is
preferred as onsets of action are comparable and there is some potential to reduce some of the side
effects. Interestingly the combination of syntocinon (5 units) and ergometrine (500 g) known as
syntometrine seems to reduce the side effect profile further and is said to be safer in patients with
asthma when given IM.
Should first- and second-line treatments fail in treating uterine atony, prostaglandins (PG) E and
F may be useful. Endogenous PG concentrations increase during labour and are responsible for
uterine contraction after placental separation; however, this system may be deficient in some women.
The effects of PG are twofold; they directly increase the concentration of free intracellular calcium
and potentiate the effect of the oxytotics. 15-Methyl PG F2 (carboprost, Hemabate) is now the agent
of choice, given at a dose of 250 g IM and has been given directly to the myometrium. Doses can be
repeated not more than every 15 minutes to a maximum dose of 2 mg. Common side effects are fever,
flushing, diarrhoea, nausea and vomiting. Carboprost may also cause bronchospasm, ventilation
perfusion inequality and shunt leading to hypoxaemia. For this reason it is relatively contraindicated
in asthmatics. PG E2 is an alternative option for those with asthma as it causes bronchodilatation and
in some studies has caused increases in PaO2.
Anaesthetic agents and pregnancy

Anaesthesia may be necessary during the course of the pregnancy and there are special considerations
to consider. As for any patient a safe anaesthetic must be provided for the mother but minimizing the
potential for teratogenesis and maximizing fetal viability are additional challenges. This can be aided
in part by timing of surgery, but choice of agents is paramount.
Induction agents
Thiopentone is the sulfur analogue of pentobarbitone. It is used for induction of anaesthesia and
treatment of status epilepticus. Animal studies in rats and mice have not demonstrated any adverse
effects at anaesthetic doses and indeed this agent has a long history of use in pregnant women without
any evidence of teratogenicity. There is a theoretical risk with barbiturates at very high doses when
used to control seizure activity in that it has been suggested that dysmorphism in children of mothers
with epilepsy may not be entirely due to complications of convulsions.
There is evidence from animal models that thiopentone causes a significant (20%35%)
reduction in uterine blood flow. This is transient and of unknown significance to viability of the
pregnancy, but it has been postulated that this could be associated with reduced birthweight and
increased risk of miscarriage.
Propofol has animal data to support its use in that it is not known to be teratogenic and has not
been shown to affect oocyte maturation. It has been used in many pregnant women both for
anaesthesia and sedation in intensive care without obvious problems. The manufacturer data sheets,
however, do not recommend use during pregnancy. Similar studies to those performed with
thiopentone have been performed in sheep and despite maternal hypotension on induction, uterine
blood flow remained stable. This provides a theoretical advantage to the use of propofol.
Ketamine is perhaps less well studied than some other agents and less experience has been
amassed. There is no evidence to suggest that it is teratogenic in doses used clinically for anaesthesia.
Again knowledge of response to this drug comes from studies in sheep. During the third trimester
ketamine causes hypertension and increases uterine blood flow, but earlier in pregnancy it causes
profound uterine hypertonus. This almost certainly has negative implications for fetal blood flow.
Etomidate is not recommended for use in expectant mothers. Although no evidence exists for
teratogenicity it is accepted that cortisol levels are suppressed with its use. This may have
consequences for glucose homeostasis in the unborn child.
Benzodiazepines (BDZ) do have some evidence to suggest teratogenicity. Retrospective studies
showed an association between BDZ use in the first trimester and cleft lip or palate, although this
finding is not universal. Indeed, prospective investigations have not repeated the finding and many
experts do not consider these to be teratogenic. Most authors agree that the risk posed by single-dose
short-acting agents is of negligible risk. Large doses of BDZ immediately prior to delivery can have
lasting impact on the neonate. Hypotonus, respiratory depression and hypoxia have all been reported,
so it is advised to avoid these agents if possible. When required, personnel trained in neonatal
resuscitation should be present at delivery.
Opioids have been investigated thoroughly in animal models. Early concerns that these agents
may cause growth and developmental problems have been put down to study design and the
consequent effects of opiates such as respiratory depression and reduced nutritional intake. These
issues have been circumvented by improved study design and even large sustained doses of opiate
such as 500 g/kg/day fentanyl and 8 mg/kg/day alfentanil through pregnancy have shown no
teratogenic effects whatsoever. Observational studies in mothers on methadone programmes have not
found congenital anomalies, but systematic study is lacking in this area. It is highly unlikely that
standard dosing of opioid analgesia for surgery is of any risk to the fetus.
Muscle relaxants
There are obvious difficulties when testing for the teratogenicity of muscle relaxants. The agents are
not usually given in clinically relevant doses alone and there is always potential for hypoxia and
hypercarbia, both of which are known to have deleterious effects on the fetus. Observational studies
have not demonstrated any problems with the use of non-depolarizing agents. Cultured rat embryo
studies have shown dose-dependent growth retardation and morphological changes, but only at
concentrations 30 times clinical levels. These bulky polar molecules do not readily cross the placenta
where typically concentrations are one-tenth the levels found in maternal blood. It is widely accepted
they are safe to use, particularly if they facilitate ventilation and oxygenation where the balance of
risk certainly favours them.
Volatile anaesthetics
As with agents discussed so far, much of the evidence we have on volatile agents comes from animal
models and observational studies in human populations. Similar problems arise from experiments
with inhaled anaesthetics as with muscle relaxants, namely distinguishing between genuine
teratogenicity and consequences of hypoxia, hypercarbia, hypothermia and nutritional issues.
Attempts have been made to see if either prolonged low-dose or intermittent, but frequent, high-dose
exposures have deleterious effects.
Chronic exposure to sub-anaesthetic concentrations of halothane in pregnant rats caused growth
restriction, but no other abnormalities. Although repeated and prolonged exposures of mice to
clinically relevant concentrations of halothane (4 MAC hours per day) caused skeletal abnormalities,
it is not clear if this link is causal. Indeed in other studies in rats where temperature, feeding and
sleep patterns were preserved halothane, isoflurane and enflurane showed no teratogenicity. Most
authors agree that isoflurane is safe to use in pregnancy as no studies have shown conclusive effects.
Since halothane has a theoretical impact on pregnancy it is suggested that it is not given to expectant
mothers.
There is a paucity of information on agents more commonly used in anaesthetic practice today.
Sevoflurane and desflurane have been animal tested by manufacturers in unpublished work. Their
suggestion is that pregnancies were only negatively impacted by concentrations associated with
maternal mortality. It is widely accepted that these agents are safe to use in pregnancy.
Nitrous oxide has been shown to have teratogenic effects in animal models when administered in
concentrations greater than 50% for prolonged periods. It was initially hypothesized that the
inhibition of the methionine synthase-tetrahydrofolate reductase system was causing impaired DNA
synthesis and hence abnormalities. This was shown to be incorrect because the effect could not be
blocked by folinic acid supplementation, which should correct this effect. Perhaps surprisingly the
effect is corrected by the co-administration of volatile anaesthetics. The precise mechanism by which
this happens has not been confirmed. Observational studies in humans during the 1960s and 1970s
suggested that members of the healthcare professions in theatre environments were more prone to
spontaneous abortion and congenital malformations. This was, at the time, attributed to chronic
exposure to sub-anaesthetic doses of the volatile agents. The study design was criticized and felt to be
impacted by reporting bias. Subsequent studies have failed to find such a link and prospective trials
have reported female anaesthetists to have similar rates of reproductive success as other female
physicians.
Antiemetics
Nausea and vomiting unfortunately affect many mothers and hyperemesis gravidarum is a potential
cause of serious morbidity for mother and fetus. As a consequence, the arsenal of drugs usually
employed perioperatively to combat nausea and vomiting has been used extensively in pregnant
women.
Prochlorperazine has been assessed in a large prospective clinical study and not found to have
negative sequelae. Despite this, manufacturers advise caution following case reports of jaundice in
late-term mothers taking large doses of this antiemetic. It can be considered safe.
Metoclopramide is a popular agent when treating pregnancy-related nausea. As well as many
years of experience of the drug in this population, animal studies have not demonstrated teratogenic
effects. There is, however, controversy in the literature as to how effective an antiemetic it is.
Cyclizine has no evidence to suggest that it causes problems during pregnancy. Manufacturers do
advise caution because a related piperazine-derived antihistamine has caused teratogenicity in high
doses in rats.
The serotonin (5-HT3) antagonists, such as ondansetron, have not been found to be teratogenic in
animal studies. Since these agents have been in general use for less time than other agents, there are
fewer data from human studies. For this reason caution is advised, particularly in the first trimester.
NSAIDs
The non-steroidal anti-inflammatory drugs (NSAIDs) have a long history of use perioperatively in
pregnancy in spite of some evidence from animal models that they may be harmful at very high
concentrations. The Collaborative Low-dose Aspirin Study in Pregnancy (CLASP) study followed
the children of mothers through early childhood and found no increased congenital or behavioural
abnormalities from the background rate.
A possible exception in this class is ketorolac, where the product literature provided by the
manufacturer described studies in which rats given the drug had offspring with high rates of vascular
malformations. Aside from this specific case NSAIDs are thought to be safe in early pregnancy. In
later pregnancy (after 32 weeks gestation) these agents may have a range of unfavourable impacts on
the unborn child. By inhibiting cyclo-oxygenase enzymes the NSAIDs alter the synthesis of
prostaglandins, impacting the circulatory system. Indeed these drugs can cause premature closure of
the fetal ductus arteriosus, with resulting pulmonary hypertension and if severe enough, tricuspid
incompetence. Paradoxically they may also cause delayed closure of the ductus arteriosus after birth,
which can be refractory to standard medical treatments. The manufacturers also express caution with
regard to the consequences of platelet dysfunction with intracranial and gastrointestinal haemorrhage
and perforation. There are possible links with renal failure and necrotizing enterocolitis.
Acetaminophen
There is no known teratogenic effect with acetaminophen (paracetamol) and it has been used
extensively in pregnancy without cause for concern. Pregnancy does not seem to alter the kinetics or
dynamics of this useful drug. It does not appear to cause any lasting changes to the expression of
prostaglandins.
Catecholamines and the vasoactive drugs

Should surgery be required, it is desirable to keep maternal haemodynamics as stable as possible.
There are additional considerations when manipulating the blood pressure of the pregnant patient,
paramount in this is the maintenance of blood flow to the uterus and placenta. Blood flow is
dependent on the arterial to venous pressure gradient and vascular resistance of the uterus. Pregnancy
reduces the sensitivity to vasopressors, but this reduction in sensitivity is not consistent, nor is it the
same for all vascular beds to all agents. It was argued in the past that ephedrine was the agent of
choice in treating maternal hypotension relating to regional or general anaesthesia. The justification
for this was that the -adrenergic effects of the drug would increase cardiac output. This increased
output would offset the increase in uterine vascular resistance and maintain or correct reductions in
uterine blood flow. This was supported by some early work demonstrating favourable umbilical cord
pH values with the use of ephedrine. Equally, it was noted that stressed women, due to pain or
anxiety, with elevated blood pressure in response to endogenous norepinephrine had reduced uterine
blood flow.
More recently some carefully designed studies have demonstrated value in using the -
adrenoceptor agonist phenylephrine by infusion to maintain normotension. Previous fears that this
would cause disproportionate constriction of the uterine vessels compared to systemic vasculature
have not materialized. Research has not confirmed that umbilical cord pH and fetal outcomes are
improved with phenlyephrine delivered this way and it has become standard practice in many centres
to combat hypotension associated with intrathecal block. Both of these agents have an established
history of use in the pregnant woman without any observed teratogenic effect. Equally they have been
studied extensively in animal models of uteroplacental blood flow without any risk of congenital
malformation. As is often the case, the risk of hypoperfusion of the placenta with ensuing hypoxaemia
and acidosis is a far greater risk to the fetus than the theoretical potential these drugs may have for
teratogenicity.
Antihypertensive agents
It may become necessary to pharmacologically reduce blood pressure in the pregnant patient mother,
particularly in the event of craniofacial surgery in response to conditions raising intracranial
pressure.
Labetalol has combined - and -adrenoceptor blocking effects, -blockade is specific to 1
receptors but -blockade is non-specific. The ratios of the relative activities at these two receptors
vary, depending on the route of administration from 1:7 for intravenous to 1:3 for oral. IV
administration has been shown to lower blood pressure in hypertensive, pregnant rats. This reduction
in blood pressure is not accompanied by reduction in uterine blood flow, presumably because of -
mediated vasodilatation. It is for this reason it has become so popular for use in hypertensive
pregnant women and those with pre-eclampsia.
Esmolol is a cardioselective ultra-short-acting 1-blocker that undergoes rapid ester hydrolysis
in the plasma. It is a highly lipophilic agent that crosses the placenta readily and is responsible for a
degree of -blockade in the fetal heart with resultant bradycardia. This, coupled with the tendency to
significantly reduce uterine blood flow, can cause fetal metabolic disturbance. For these reasons this
otherwise useful agent should be avoided in pregnancy.
Hydralazine is a direct-acting vasodilator. The precise mechanism of action is not clear, but is
thought to involve activation of guanylyl cyclase increasing concentrations of cGMP and resultant
reduction in intracellular calcium. This relaxes smooth muscle and causes vasodilatation. It is
effective in lowering blood pressure and seems to have favourable characteristics for uterine blood
flow in animal models. Some argue it should be used with caution in situations of raised intracranial
pressure or cerebral irritation as it markedly increases cerebral blood flow. It is a useful agent for
women with pre-eclampsia, particularly where -blockers are contraindicated, such as in asthma.
GTN reduces smooth-muscle tone and reduces blood pressure by mechanisms discussed
previously. Animal models of uterine blood flow do not demonstrate significant reductions, even
when maternal blood pressure has fallen. Furthermore, prolonged infusion has not been shown to
cause metabolic disturbance in the sheep fetus.
Sodium nitroprusside is becoming increasingly rare as a choice for treatment of hypertension.
The production of cyanide as a by-product of metabolism has been of concern in all patient groups,
but this may be even more so when the fetus will also be exposed. There are case reports of it being
used successfully in pregnancy during neurosurgery, but it appears to have negative effects on uterine
blood flow. Its use cannot be routinely recommended.
Dihydropyridine calcium-channel blockers such as nifedipine and nimodipine have been used to
treat hypertension in pregnancy. They are often used in neurosurgical conditions because their
benefits go beyond those of blood pressure control. They are particularly useful in the treatment of
cerebral artery vasospasm. There have, however, been animal studies in sheep that have
demonstrated fetal hypoxaemia and acidosis in response to infusions of these drugs. These unwanted
effects can persist even after the drug is discontinued. For this reason most authors now agree that
calcium-channel blockers should not be used routinely unless the secondary benefits on brain
vasculature are required.
Magnesium sulfate has a wide range of interesting uses for the anaesthetist including an
antiadrenergic effect by inhibiting the release of catecholamines. It slows cardiac conduction and
reduces force of contraction while reducing afterload. In normotensive and hypertensive animals it
can increase uterine blood flow by 10%. Although it poorly crosses the bloodbrain barrier it
interferes with the release of all neurotransmitters and accordingly has antiseizure activity. This
combination of features explains why it has been shown to be so useful in the management of pre-
eclampsia. Infants born to mothers given magnesium sulfate show reduced rates of cystic
periventricular leucomalacia and cerebral palsy. Magnesium is presumed to have neuroprotective
effects by blocking N-methyl, D-aspartate (NMDA) receptors and acting as a calcium antagonist and
reducing calcium influx into cells. Other proposed mechanisms include protection against free
radicals, vasodilatation, increased vascular stability, reduced hypoxic damage, attenuated cytokine
and catecholamine-induced cell damage and antiapoptotic actions. Oligodendrocytes in the
periventricular white matter seem to benefit most from this protection and these have previously been
shown to be the main site of injury in cerebral palsy. Three meta-analyses and a Cochrane review
concluded that magnesium sulfate given to women at risk of preterm birth substantially reduces the
risk of cerebral palsy in their offspring with a relative risk of 0.68 (95% CI 0.540.87). There is
currently no consensus on dose or timing, but 4 g IV loading dose over 2030 minutes followed by a
1 g/h infusion for 24 hours or until delivery has been adopted by many units. Magnesium sulfate IV
can cause hypotension, flushing, nausea and vomiting, sweating and pain at the injection site.
Breastfeeding and anaesthesia

Mothers are often highly motivated to breastfeed their infant. Should they require anaesthesia during
this period it is reasonable to assess the safety of continuing with breastfeeding. We can assess the
dose of any given drug likely to be passed to the infant by knowledge of the concentration in the
maternal plasma, the ratio of that concentration to the concentration in breast milk and the volume of
milk taken by the infant.
Although most of the agents used in anaesthesia are highly lipid soluble there is a higher fat
content in the human brain than there is in breast milk. So the conscious level of the mother can be
used as an accurate guide to the concentrations of drugs such as induction agents, volatile anaesthetic
agents, opioids, BZDs and local anaesthetics. Assuming that the mother is alert and conscious, there
is unlikely to be unsafe levels in the plasma. Additional safety margins are provided by the usually
low milk-to-plasma ratio and the fact that the infant will be taking any quantity of drug by the enteral
route further reducing the likely blood concentration in the infant. Most authorities suggest that
breastfeeding can continue as normal, assuming that the standard anaesthetic medications have been
used and the mother feels well enough to continue.
Non-anaesthetic drugs
Anticoagulation
The normal enhancement of coagulation that accompanies pregnancy may have the unfortunate side
effect of increased rates of deep vein thrombosis and thromboembolism. These conditions should be
treated in a similar fashion in the pregnant population as the non-pregnant. Equally, some women will
be anticoagulated prior to conception and require maintenance of therapy.
Warfarin is often the treatment of choice for long-term anticoagulation in non-pregnant patients.
It is, unfortunately, not suitable during gestation. It is a well-documented teratogen; the characteristic
features of chondrodysplasia punctata are similar to ConradiHunerman syndrome and are very likely
a result of multiple microhaemorrhages during the course of development.
Heparins are large water-soluble polar molecules that do not cross the placenta to any great
extent. This makes them the treatment of choice for anticoagulation. There is no evidence to suggest
they are teratogenic and their effect can be reversed rapidly if so required.
Antibiotics
Coincident infections during pregnancy may require treatment. On the whole, antibiotics tend to be
large water-soluble molecules that do not cross the placenta in great quantities. The penicillins are
widely accepted to be safe and are used with reasonable frequency. Equally the cephalosporins and
erythromycin can be used confidently.
Tetracyclines have not been shown to have teratogenic effects per se, but they are known to bind
to tooth enamel and cause discolouration if given up to the sixth month of pregnancy. For this reason
another agent should be sought where possible.
Aminoglycosides have been associated with ototoxicity in the newborn. This appears to be a
dose-related phenomenon. Advice is against the use of these antimicrobials, but if no other choices
exist then close monitoring of levels is advised and reduction of the therapeutic course to the
minimum possible time.
Metronidazole has been used safely in pregnancy and no evidence exists that it is harmful. Only
when animals were given toxic concentrations of the antimicrobial did any fetal effects arise.
Anticonvulsants
All anticonvulsants cross the placenta and teratogenicity is well recognized with a twofold increase
in congenital malformations. Major malformations include orofacial cleft and congenital heart
defects. Sodium valproate and carbamazepine have a higher incidence of neural tube defect (13.8%
and 1% respectively). Fetal anticonvulsant syndrome may also present in a variety of ways, such as
dysmorphic features, hypoplastic nails or developmental delay. Newer second-line agents may be
preferable. Management should aim to control seizures at the minimum dose of anticonvulsants
possible.
Caffeine
Caffeine has been examined in large population studies and has not been shown to cause any harm to
the unborn child. Early concerns that it may be associated with increased rates of spontaneous
abortion and low birth weight have been allayed as it seems this was an effect confused with that of
tobacco smoking.
Key points
1. Drugs and therapeutics for the mother can be challenging. It is important for maternal and fetal
health that appropriate treatments are continued or modified. Attention must be paid to minimize
the potential for teratogenesis and maximize fetal wellbeing.
2. Factors that affect the extent and speed of placental transfer of drugs are lipid solubility,
ionization, protein binding and amount of free unbound drug.
3. Metabolism of drugs is largely unaffected by normal pregnancy.
4. With drugs and breastfeeding, it should be noted there is usually a low milk-to-plasma ratio.
There is a further reduction in infant blood concentration due to the enteral route of ingestion.
Further reading
Chestnut, D. H., Polley, L. S., Tsen, L. C. and Wong, C.A. (eds.) (2014). Chestnuts Obstetric
Anaesthesia: Principles and Practice, 5th edn. Philadelphia, PA: Saunders.
Collis, R., Plaat, F. and Urquhart, J. (2011). Texbook of Obstetric Anaesthesia. Greenwich:
Greenwich Medical Media.
Evers, A. S., Maze, M., and Kharasch, E. D. (eds.) (2013). Anesthetic Pharmacology, 2nd edn.
Cambridge: Cambridge University Press. https://www.rcog.org.uk/en/guidelines-research-
services/guidelines/
Peck, T. and Hill, S. (2014). Pharmacology for Anaesthesia and Intensive Care, 4th edn. Cambridge:
Cambridge University Press.
Smith, S., Scarth, E. and Sasada, M. (2011). Drugs in Anaesthesia and Intensive Care, 4th edn.
Oxford: Oxford University Press.
Suresh, M. S., Segal, B. S., Preston, R. L., Fernando, R. and Mason, C. L. (2012). Shnider and
Levisons Anaesthesia for Obstetrics. Philadelphia, PA: Lippincott Williams & Wilkins
Yentis, S., May A. and Malhotra, S. (2007). Analgesia, Anaesthesia and Pregnancy: A Practical
Guide, 2nd edn. Cambridge: Cambridge University Press.
Chapter 4
Maternal morbidity and mortality

Kate OBrien
Introduction
Until the mid-1930s maternal mortality was high in the Western world with the maternal mortality
rate (MMR) about 450 per 100,000 births (UK); the current MMR is 8 per 100,000 births.
The vast majority of maternal mortality occurs in the developing world. The Millennium
Development Goals is an initiative to improve maternal health in developing countries. The aim is to
reduce the maternal mortality ratio by three quarters from 1990 to 2015.
National maternal mortality statistics have been recorded in the UK for over 150 years. The
Maternal Death enquiries have been published every three years since 1952; this is the longest
running continuous medical audit in the world. The enquiries review and assess maternal deaths and
recommend service changes to make childbirth safer.
History of maternal mortality

The maternal mortality rate in England and Wales was fairly static from 1880 to the mid-1930s and
the risk of dying in childbirth was the same as in the Victorian era. Mortality from infectious diseases
and infant mortality started to fall in the late 1890s. This was due to an increased standard of living:
better housing, hygiene and nutrition; however, this was not translated into lower rates of maternal
mortality until the mid-1930s. After this there was a steep decline in maternal mortality rates, which
continued for the next 50 years. This pattern was consistent throughout the developed world.
The exception was in northwestern European countries: Sweden, Norway, the Netherlands and
Denmark. In these countries there were well-trained midwives who used aseptic techniques from
their inception (18901900) and there was a tradition of minimal surgical intervention whether at
home or in hospital. This led to low rates of maternal mortality.
Another success story was the midwives in the Kentucky Frontier Nursing Service. The
midwives travelled on horseback to help with childbirth. Despite the fact that these women lived in
poor rural communities the maternal mortality rates were ten times less than those in the city of
Lexington.
Medical interference
The UK maternal mortality figures showed a significant trend upwards in the 1890s; the maximum
excess of deaths was, at its worst, 250 per 100,000 births. This was in the main due to the use of
chloroform and unnecessary forceps deliveries.
Medical interference causes iatrogenic mortality. In Kentucky the maternal mortality rate was
highest when physicians were involved in the delivery (19251937):
Kentucky Frontier Nursing Service MMR 6070 per 100,000 births
White women of Kentucky MMR 440530 per 100,000

births
White women delivered by physicians in hospital in MMR 800900 per 100,000

Lexington births
Factors for the decline in the UK maternal mortality rates

1930s onwards
1. Sulfonamides for the treatment of puerperal sepsis
2. Introduction of ergometrine
3. Blood transfusions
4. Introduction of penicillin
5. Improved training
6. Improved anaesthetic techniques
7. Less interference in normal labours
8. Improvements in maternal care.
Confidential Enquiries into Maternal Deaths (UK)

This is the longest running continuous medical audit in the world. The enquiries look at all maternal
deaths whether they are directly or indirectly related to pregnancy. The enquiries initially only
applied to women in England and Wales, but were extended to Scotland and Northern Ireland in
1985.
In the 19521954 enquiry:
There were 1,403 direct maternal deaths (2,052,000 confinements)
The risk of dying directly from a pregnancy-related condition was 1:1,500.
In the 20002002 enquiry:
There were 106 direct maternal deaths (2,016,136 births)
The risk of dying from a pregnancy-related condition was 1:19,020.
The aim of the enquiry is to improve the quality of maternal care by providing guidance and
recommendations based on the assessment of each case.
The overall death rate has decreased over the years, but the number of deaths associated with
substandard care has stayed static at about 60%. The recommendations from the reports advise ways
in which maternity services can improve the quality of care to prevent maternal morbidity and
mortality.
Recent advice includes conditions where poor care has been identified:
1. Sepsis: is often poorly recognized and managed. Before the previous report was published, an
alert was published warning about the increased number of deaths due to community acquired -
haemolytic streptococcus A. The deaths had increased from 3 in 20002 to 13 in 20068.
2. Failure to recognize serious acute illness:
a. Delay in contacting anaesthetists or critical care specialists
b. Postpartum haemorrhage
3. Pre-eclampsia/eclampsia: treat systolic hypertension, consider early invasive arterial
pressure monitoring
4. Increasing numbers of women with chronic illness and co-morbidity:
a. These women need multidisciplinary planning prior to delivery
b. Obesity
5. Specialist clinical care: women with serious medical conditions require prompt
multidisciplinary care.
In 2012 the body Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries
across the UK (MBRRACE-UK) is to continue the Maternal Death Enquiries. The collaboration is
under the umbrella of the Maternal, Newborn and Infant Clinical Outcome Review Programme (MNI-
CORP), and has been appointed by the Healthcare Quality Improvement Partnership (HQIP).
The process
1. Identification of the cases:
a. A maternal death for the enquiry is defined as all deaths of pregnant women and women up
to one year following the end of their pregnancy
b. This is regardless of the place or circumstances of death
2. Information collection:
a. All health professionals who cared for the woman write an unnamed summary of their
involvement
b. They are also asked to provide a reflection on the care given and any lessons learnt
3. A national panel of experts assesses the data. The case is assessed for the real cause of death
and any remediable factors associated with the death
4. Findings and lessons learnt are collated to provide a triennial report; this contains
recommendations and guidelines, using up-to-date evidence, to improve future practice.
The deaths are divided into categories:
1. Direct deaths:
a. Maternal mortality rate for mothers who died from medical conditions that could only be a
result of pregnancy
b. For example, obstetric haemorrhage or pre-eclampsia
2. Indirect deaths:
a. The mortality rate for mothers deaths from indirect causes
b. From pre-existing or new medical or mental health conditions aggravated by pregnancy e.g.
heart disease, suicide
3. Coincidental deaths:
a. Accidents, lightning strikes
4. Late deaths:
a. Deaths that occur from 42 days after the end of pregnancy to one year later.
The recommendations of the Maternal Death Enquiries (MDE) have been a major influence in
improving maternal care at a professional and governmental level. Since the MDEs first report there
has been a significant decrease in the number of anaesthetic-related deaths; it was the third most
common cause of death in the 1960s and is now an uncommon event. This is due to a number of
factors, increased supervision of trainees, improved monitoring equipment, a huge shift to regional
rather than general anaesthesia for operative intervention and the introduction of antacid prophylaxis.
In the last MDE (20062008) there were six direct deaths attributable to anaesthesia; two of
these were airway-related deaths. One of the specific recommendations in the report was:
Management of failed intubation/ventilation is a core anaesthetic skill that should be rehearsed and
assessed regularly.
National Audit Project 4, Major Complications of Airway Management in the UK (2001), also
highlighted deficiencies in airway management and failure to alter airway management according to
the situation. This data is very similar to an audit of failed intubation in one UK region where in half
the women there was a failure to follow a failed intubation protocol.
The last MDE report shows, for the first time in many years, a decline in overall maternal
mortality. The rate for direct deaths has fallen from 6.24 to 4.67 per 100,00 maternities (P = 0.02);
however, the indirect deaths have not changed significantly.
The commonest indirect cause of death is cardiac disease:
Cardiomyopathy
Ischaemic heart disease/myocardial infarction
Aortic dissection.
The MDE reports do not just show in-hospital mortality, but show inequalities in healthcare
provision, particularly in vulnerable women. There are also top ten recommendations to emphasize
to Trusts and other professional bodies that these require action as a top priority.
The first reports targeted better management of haemorrhage, sepsis and anaesthesia. More
recently thromboembolism was highlighted and the deaths have significantly fallen from 41 deaths
(20032005) to 18 deaths (20062008).
The report covering 20002002 showed startling statistics:
Socially excluded pregnant women faced up to a higher than 20-fold greater risk of dying than
the more privileged
Black African women, particularly asylum seekers, were also at higher risk
This resulted in redefining how maternity services are now provided, making sure that
antenatal care is more accessible to these women (20062008)
The result is a downward trend in maternal mortality in Black African women and also from
women from White ethnic backgrounds
Maternal mortality has been significantly reduced in relation to the area of the mothers
residence (deprivation score and postcode).
Maternal mortality in the developing world

There is a huge inequality in maternal mortality in the developed and developing world. Every day
800 women die of preventable causes; 99% of all maternal deaths occur in developing countries. In
2013, it is estimated that 289,000 women died during pregnancy or following childbirth. The majority
of these deaths were in poorly resourced settings.
The greatest risk of maternal mortality is in adolescent girls aged 15 or younger. In this group
pregnancy-related complications are the leading cause of death.
Data collected by the World Health Organization (WHO), in 2013, clearly shows these
inequalities:
Country Maternal mortality rate per 100,00 live births
Spain 4
United Kingdom 8
India 190
Cameroon 590
Sierra Leone 1100
The Millennium Development Goals (MDGs)

There are eight international development goals that were agreed upon at the Millennium Summit of
the United Nations in 2000. All the UN member states committed to achieve these goals by 2015.
The MDG5 goal was to improve maternal health:
1. 5A: reduce the maternal mortality ratio (MMR) by three quarters between 1990 and 2015:
a. Maternal mortality ratio
b. Proportion of births attended by a skilled birth assistant
2. 5B: universal access to reproductive health by 2015:
a. Contraceptive prevalence rate
b. Adolescent birth rate
c. Antenatal care coverage
d. Unmet need for family planning.
At the time that MDG5 was instituted the maternal death rate per year was 529,000. The lifetime risk
of dying with complications of pregnancy and childbirth was 1:4,000 women in a developing country
and 1:16 in sub-Saharan Africa.
Between 19902013 maternal deaths have fallen by 45%. The MMR has fallen 2.6% per year;
to achieve the MDG5 goal it should be 5.5% per year.
Other regions have had significant reductions in maternal mortality, particularly in North Africa
and Asia.
Causes of death
In the developing world, 75% maternal mortality is related to pregnancy or childbirth. The
commonest reasons are:
Haemorrhage mostly after childbirth 27%
Infection puerperal sepsis 11%
Hypertensive complications related to 14%

pregnancy
Complications from delivery 12%
Obstructed labour
Thrombotic complications
Unsafe abortion 8%
Pre-existing disease 28%
Malaria
HIV and AIDS, this is prevalent in sub-

Saharan Africa
AIDS-related indirect maternal deaths
Botswana: MMR 170 per 100,00 live births 23.5%
South Africa MMR 150 per 100,00 live 41.4%

births
Access to healthcare in pregnancy

There are factors that prevent women from accessing adequate healthcare in pregnancy and in the
peripartum period. This is seen in both sub-Saharan Africa and South Asia.
The factors are:
Distance from healthcare facilities
Inadequate healthcare facilities
Poverty
A lack of information
Cultural beliefs
Lack of trained skilled health workers midwives, trained nurses and doctors.
UK Obstetric Surveillance System (UKOSS)

UKOSS is a national system to study rare disorders of pregnancy.
The objective of the project is to develop a UK-wide Obstetric Surveillance System to
describe the epidemiology of a variety of uncommon disorders of pregnancy.
Maternal mortality is the tip of the iceberg compared to severe maternal morbidity. There are
pregnancy-related conditions and indirect conditions that lead to this morbidity and mortality. Each
individual maternity unit will have only limited exposure to these uncommon conditions. Aggregating
clinical information using this reporting system should result in a greater understanding of the disease
process with the aim to improve outcomes for these women.
UKOSS methodology is a monthly prospective case collection from each maternity unit; this is in
the form of a reporting card, which includes a nothing to report box.
The data is collected centrally from a data collection form, which is different for each study.
The criteria for a condition to be studied by UKOSS are:
An important cause of maternal morbidity or mortality
Uncommon < 1:2,000 births
Methodology is suitable
Other data sources exist to enhance case ascertainment.
UKOSS was launched in 2005 as a joint venture between the Royal College of Obstetricians and
Gynaecologists and the National Perinatal Epidemiology Unit.
The first interim reports were published in 2007 and have been subsequently published yearly.
The studies encompass all types of morbidity from Failed tracheal intubation in obstetric
anaesthesia to H1N1v influenza in pregnancy.
Scottish Confidential Audit of Severe Maternal Morbidity (SCASMM)
For the last 10 years, data (20032012) has been collected on severe maternal morbidity in all
consultant-led maternity units in Scotland. There are 14 definitions of maternal morbidity that are
used in the audit.
Practice is assessed according to published guidelines and this is used to identify variance in
practice and good practice. Two types of morbidity were analysed in more detail:
1. Massive obstetric haemorrhage
2. Eclampsia.
All other domains of morbidity were calculated and a National Rate per 1,000 births was
calculated.
The main findings in the last 10 years are:
1. An increase in the rate of massive obstetric haemorrhage
2. Overall rates of eclampsia have fallen, this may be attributable to the routine use of
magnesium sulfate in severe pre-eclampsia
3. All other morbidities have remained stable.
Sadly the 10th Annual Report will be the last.

The reports have provided valuable data on the frequency of maternal morbidity. The results of
the reports should be used to benchmark every maternity units practice. Analysis of severe morbidity
can improve outcomes and is a valuable tool for teaching and training.
Key points
1. There are unacceptable differences in maternal mortality between the developed and
developing world.
2. Midwives or other suitably trained birth attendants are the key to lowering maternal mortality
rates.
3. The maternal death enquiries have an important role in maternal safety and aid in changing
policy in maternal care.
4. The mortality rate in most of the developed world is small. Looking at maternal severe
morbidity in detail can lead to further improvements in the quality and safety of maternal care,
resulting in better maternal and perinatal outcomes.
Further reading
Loudon, I. (1986). Deaths in childbed from the eighteenth century to 1935. Med. Hist. 30: 141.
The Confidential Enquiries into Maternal Deaths. https://www.npeu.ox.ac.uk/mbrrace-uk (accessed

April 2015).
Millennium Development Goals (2013). New York: United Nations.
UKOSS: https://www.npeu.ox.ac.uk/ukoss
Scottish Confidential Audit of Severe Maternal Morbidity: 10th Annual Report: Healthcare
Improvement Scotland.
http://www.healthcareimprovementscotland.org/our_work/reproductive,_maternal_child/programme_r
Section 2

Obstetric aspects
Chapter 5
Maternal critical care

Sarah Wheatly and Kate OBrien
Introduction
Maternal critical care is an evolving sub-speciality, encompassing the multidisciplinary care of the
pregnant or recently pregnant woman needing organ support and/or intensive monitoring. Whilst some
unwell women will need to be admitted to a general critical care facility, it has been recognized that
critical care can and should be provided within the maternity unit, and that this may be advantageous
to both mother and baby.
It is estimated that approximately 5% of obstetric patients will require critical care either on the
delivery unit or a general critical care facility.
The maternal population has changed significantly over the last 20 years:
Increase in obesity and in particular morbid obesity
Increase in numbers of type 2 and gestational diabetes
Increase in number of women having children in their 30s40s
Increase in maternal co-morbidity e.g. congenital heart disease, ischaemic heart disease.
Level 2 care can generally be provided on the delivery unit; however, level 3 care usually requires
transfer to a general intensive care unit. The standard of care provided must be the same whether the
woman is managed on a delivery unit or general critical care unit.
The Critical Care Minimal Data Set (CCMDS) is the tool that defines the level of care required
for the patient (see Table 5.1).
Table 5.1 Levels of Care
LEVEL 0 Needing hospital admission
LEVEL 1 Recently discharged from a higher level of care

In need of additional monitoring
Requiring critical outreach service support
LEVEL 2 Needing preoperative optimization

Needing extended postoperative care
Stepping down from level 3 care
Needing single organ support:
Basic respiratory
Basic or advanced cardiovascular (count as single organ

support)
Renal
Neurological
Hepatic
Dermatological
LEVEL 3 Advanced respiratory support alone

Support of 2 or more organs
There are a number of conditions requiring critical care on a delivery unit, see Table 5.2, for
example:
1. Complications related to pregnancy:
a. Massive obstetric haemorrhage
b. Hypertensive disorders (pre-eclampsia, eclampsia)
c. Genital tract sepsis
2. Medical complications:
a. Respiratory disease, e.g. pneumonia, asthma
b. Cardiac disease, e.g. ischaemic heart disease, cardiomyopathy, congenital heart disease
c. Sickle cell disease
d. Renal disease.
The Intensive Care National Audit and Research Centre (ICNARC) [2005] reported on a subset of
women aged 1650, who were pregnant or recently pregnant, admitted to general critical care. The
purpose of the study was to evaluate the APACHE II scoring system in obstetric admissions.
Table 5.2 Most likely criteria for organ support on a labour ward
Respiratory
Basic
>50% O2 via facemask
Deteriorating respiratory function requiring close observation
Recent extubation (within 24 hours) after >24 hours of mechanical ventilation
Cardiovascular
Basic
CVP line for monitoring and/or access for delivery of titrated fluid boluses in hypovolaemia
Arterial line for monitoring and/or sampling
Single IV vasoactive drug to support or control BP, output or perfusion

includes labetalol OR hydralazine, but not uterotonics e.g. syntocinon
Advanced
Multiple IV vasoactive or rhythm-controlling drugs

includes labetalol and hydrallazine used simultaneously
Continuous cardiac output monitoring
Neurological
Continuous IV medication to control seizures and/or continuous cerebral monitoring

at present includes use of magnesium to treat eclampsia, but not for prevention
Intracranial pressure monitoring
The results were:
1. Direct obstetric admissions were 0.7% of the ICU population
The mortality was 1.7%
2. Indirect or coincidental admissions
The mortality was 4.2%
3. Non-obstetric female admissions
The mortality was 14.7%.
This data seems to show that pregnancy or recent pregnancy confers an increase in survival following
critical illness. The reasons are not immediately clear; however, it may be due to the physiological
changes of pregnancy combined with delivery of the fetus.
Background
Maternal critical care has developed with the increasing need to care for mothers who develop
complications of pregnancy, new disease, or exacerbations of underlying disorders during or
immediately after pregnancy. A number of national reports have been key in its establishment. These
reports, and the resulting developments include the following.
UK Maternal Death Reports

These triennial reports are the longest running clinical audit study in the world. The enquiry looks
into the causes and factors associated with all reported maternal deaths. Recommendations are made
to improve care and patient safety to reduce deaths.
Causes of deaths are divided into direct, indirect, late and coincidental. Whist the number of
deaths has fallen significantly over the years, there is concern that the percentage of deaths associated
with substandard care (meaning that the deaths may have been avoidable) has remained static at
about 60%.
This has resulted in a recommendation since the mid-1990s that high-dependency care should
be available on the delivery unit; in addition there was a further recommendation that invasive
monitoring should be used more widely (2001).
Despite all these recommendations, there was no guidance from any professional body on how
to implement this in clinical practice.
Comprehensive Critical Care

This review of adult critical care services in the UK was published in 2000 in response to the need to
improve the provision of care for the critically ill. The recommendations were:
1. Integration of critical care services within each hospital:
a. Critical care without walls
b. Care provided in the most suitable location for the patient
2. Network development both within and between hospital Trusts:
a. Standardization of care
b. Regional guidelines
c. Care bundles
3. Workforce development to balance staff skill mix with level of care needed:
a. The standard of care should be the same wherever the patient is cared for
b. Competency-based assessment for staff looking after these patients
4. Data collection:
a. Evidence base to support clinical governance
b. Workforce and service planning.
Safer Childbirth
Published in 2007, from the Royal Colleges of Obstetricians and Gynaecologists, Midwives,
Anaesthetists and Paediatrics and Child Health, this was a comprehensive report on recommendations
for standards of care in labour.
Included within this were the recommendations that:
1. High-dependency care should be available on or near the labour ward
2. There should be a core of midwives with experience and expertise in the management of the
critically ill woman
3. The Critical Care Minimum Data Set (CCMDS), the national format for data collection on
critical care patients, should be used on labour wards.
However, this report did not define what was meant by high-dependency care, nor did it specify how
midwives should be trained in the management of the critically ill woman.
Levels of Care
Published in 2009, this report from the Department of Health refined and updated the levels of care
first described in Comprehensive Critical Care. It followed the approach of allocating levels of
care according to clinical need and not location or nurse-to-patient ratio (Table 5.1).
Basic and advanced organ support was defined with descriptive examples. The definitions
reflect data needed for the CCMDS, which in turn supports funding for critical care. Critical care is
now thought of as level 2 and level 3 care only.
Awareness of the definitions and recommendations in the above reports and concerns about the
exclusion of obstetric patients led to a Department of Health meeting of the Critical Care Information
and Advisory Group (CCIAG) with representatives from obstetrics, midwifery and anaesthesia in
2007. It was agreed that the definitions of levels of care could be used for obstetric patients.
Following this, updated versions of the CCMDS have included obstetric patients and it became
officially recognized that critical care could be provided on a delivery unit. Most importantly the
term critical care could be used for maternity patients. The term maternal critical care was used to
reflect the fact that this care is provided by a skilled multidisciplinary team centred on the mother.
Providing Equity of Critical and Maternal Care for the Critically Ill Pregnant or Recently
Pregnant Woman
This 2011 document was produced by a multidisciplinary working group commissioned by the Joint
Standing Committee of the Royal College of Obstetricians and Gynaecologists, and the Royal College
of Anaesthetists in response to concerns about the lack of national guidance on the care of the
critically ill mother.
The remit of the Working Group was to summarize existing standards and recommendations
relevant to the care of the critically ill parturient, and to provide guidance for the first time on the
management of parturients who become critically ill.
The document included:
1. A definition of maternal critical care
2. An estimation of numbers of women needing maternal critical care
3. A description of different settings for provision of maternal critical care
4. An outline of relevant competencies required to provide maternal critical care
5. A list of appropriate equipment needed.
Importantly, the document emphasized the need for critically ill parturients to be cared for with their
babies where possible, and to have the same standard of care, from professionals with the same level
of competencies, whether in a general critical care area or a maternity unit.
Steps in starting a critical care facility in the delivery unit:
1. Champions:
a. Need a group of like-minded people that want to set up the critical care facility
b. Assess the burden of critical care on the delivery unit (DU). The data capture can be
difficult and will almost always understate the numbers
c. Once the baseline numbers are collected, then you produce a statement of need
d. This is circulated to the directorate responsible for maternity to assess the application,
consider funding and decide which model of care is required. This may well be different in
high-volume units with tertiary referrals compared to smaller units.
2. Multidisciplinary team (minimum):
a. Lead consultant obstetrician
b. Lead consultant anaesthetist
c. Midwifery lead
d. Critical care consultant

e. Critical care nurse:
i. Lead nurse for critical care
ii. Lead nurse responsible for critical care on the delivery unit
f. Midwife education practitioners
g. Representation from obstetric and anaesthetic directorates
i. The directorates have to apply to the local critical care network to recognize the
designated area in DU as a critical care facility
3. Identify triggers for admission and discharge to and from:
a. Maternal critical care
b. General critical care (see Figure 5.1)
c. Other specialties e.g. cardiology and renal services
4. Identify a designated critical care area on the DU:
a. This may be in single rooms or a 24-bedded unit
b. These areas must have fixed monitoring to be designated as critical care rooms; they need
to have:
i. Enough space
ii. Adequate lighting
iii. Electricity supply
iv. Piped oxygen and air
v. Suction
vi. Storage
vii. Data points
c. The following should also be immediately available:
i. Syringe pumps
ii. Fluid infusion pumps

iii. Intravenous fluid warmers
iv. Forced air warmers e.g. Bair hugger
v. Rapid infusor and warmer e.g. Belmont, Level 1
vi. Airway trolley
vii. Emergency haemorrhage trolley
viii. Blood fridge
ix. Eclampsia box
x. Blood gas analyzer
xi. Near patient coagulation testing e.g. TEG, ROTEM
xii. Transfer monitor and ventilator
5. CCMDS collection:
a. This is an essential part of defining how many level 2/3 women are receiving maternal
critical care
b. This needs to be part of general critical care data collection
c. The tariff for this is set by the CCMDS
d. Level 1 patients also are reported on; these are women that do not require level 2 care, but
are at risk for deterioration and need to be intensively monitored. This hidden burden on the
DU can be fed into the commissioning process to ensure that the tariffs are commensurate with
the medical and midwifery time caring for these women.
e. Accurate coding of each maternal critical care episode
6. Benchmarking:
a. Assessment of severe maternal morbidity
b. Data incorporated into the critical care network data set.

Figure 5.1 Maternal critical care flowchart.
Staffing
Nursing
It is essential for parturients requiring level 2 or 3 care to have their nursing needs met by staff who
are trained and competent in critical care; midwives normally provide nursing care on the DU.
Current midwifery training in the UK concentrates on normal pregnancy and labour, and does not
require a general nursing background. Further training is therefore needed if midwives are to attain
the knowledge, skills and competencies required to care for critically ill parturients. Several different
courses with varying levels of practical experience are currently available, many now being
university based. A useful framework for the skills and competencies required can be adapted from
the DOH document Competencies for Recognising and Responding to Acutely Ill Patients in
Hospital and the National Competency Framework for Adult Critical Care Nurses.
Recognition of critical illness is often poor, as highlighted in a number of Confidential
Enquiries. Midwives benefit from undertaking acute illness management training to pick up patient
deterioration before overt maternal collapse; there are a number of these courses throughout the UK.
This involves lectures and scenarios and then a competency assessment.
A combination of critical care nurses and midwives with enhanced competencies to care for
level 2 women has been shown to work well in some units with both the critical care nurses and the
midwives find that the combination of the two plays to their strengths.
All the critical care nurses have an induction programme; this includes lectures, sessions in
clinics and simulation. The course is open to midwives who are gaining enhanced competencies to
look after level 2 women and covers all aspects of maternal physiology, pathophysiology and
common emergency scenarios (see Chapter 26).
Medical
Obstetricians in units providing level 2 critical care will need additional training in care of the
critically ill as this is not currently included in speciality training. A number of general courses are
available, though none specific to obstetricians or maternal critical care. This may be an area for
development, using adaptations of existing intensive care courses, and core competencies in intensive
care medicine as a framework.
Dedicated 24-hour anaesthetic cover from anaesthetists with a minimum of Step 1 intensive care
competencies should be available for units providing critical care.
UK anaesthetic training includes a significant amount of intensive care at present, though most
consultant obstetric anaesthetists do not have regular sessions in critical care. As maternal critical
care evolves there is scope for consultants to have a dual role in both general critical care and
maternity and this may also be an area for development.
The multidisciplinary team (MDT)

The MDT is an essential part of maternal critical care. There needs to be effective leadership,
communication, including comprehensive handover, and appropriate referral to other specialties as
required.
The MDT consists of midwives, obstetricians, anaesthetists and in some units critical care
nurses. The ward rounds must be regular (46 hourly) to ensure that there is no deterioration of the
patients condition.
Transfer
There are many situations in which a critically ill parturient may need to be transferred: either within
one hospital, or from one facility to another. This is most commonly either for:
1. Transfer to general or cardiac intensive care
2. Investigations e.g. CT scan.
Guidelines should be available for transfer of critically ill women. The triggers for transfer will be
different for each unit, but these triggers must be clear for transfer to ICU and for discharge back to
the DU (see Figure 5.1). The decision to transfer should be multidisciplinary, involving obstetricians,
midwives, anaesthetists, intensivists and any other relevant speciality.
Key points
1. Women who have a need for maternal critical care generally have a good outcome.
2. The burden of maternal critical care will continue to rise from co-morbidity and the
increasing caesarean section rate.
3. Midwifery and obstetric training should encompass illness recognition and management
training. This needs to be urgently addressed by the RCOG and the RCM.
4. Transfer triggers, specific to the hospital, to general critical care need to be stated clearly.
5. The delivery unit often is the best place for many women with critical illness.
Further reading
Department of Health. (2000). Comprehensive Critical Care: A Review of Adult Critical Care
Services. London: Department of Health.
Royal College of Obstetricians and Gynaecologists. (2007). Safer Childbirth: Minimum Standards for
the Organization and Delivery of Care in Labour. London: RCOG.
Royal College of Obstetricians and Gynaecologists. (2011). Providing Equity of Critical and
Maternity Care for the Critically Ill Pregnant or Recently Pregnant Woman. London: RCOG.
Department of Health. (2008). Competencies for Recognising and Responding to Acutely Ill Patients
in Hospital. London: Department of Health.
Department of Health. (2012). National Competency Framework for Adult Critical Care Nurses.
(2012). London: Department of Health.
Chapter 6
Obstetrics for the anaesthetist

Emma Ingram, Alex Heazell and Edward D. Johnstone
Intrapartum care at or near term gestation

Intrapartum care is a challenging and rapidly changing environment for all health professionals. As an
obstetrician the key question is often Do I need to intervene? And if so, how much time do I have to
do this? Fetal monitoring, recommendation of mode and timing of delivery is aimed at reducing poor
neonatal outcomes.
Within the scope of this chapter it is not possible to cover all potential intrapartum events that
may require anaesthetic assessment and input. The aim of this chapter is to provide enough
information on fetal monitoring to enable the anaesthetist to understand the urgency of a delivery and
how this is determined in high-risk cases such as twins and vaginal breech delivery.
Intrapartum fetal monitoring

Intrapartum fetal monitoring techniques have enabled obstetricians to intervene and prevent the
development of a severe hypoxia. However, these techniques are far from perfect. The mainstay of
fetal intrapartum monitoring remains the cardiotocograph (CTG), which records the fetal heart rate
(FHR) and the presence of uterine contraction activity using the tocograph. This is recommended by
NICE for all high-risk labours. Although not exhaustive, indications for continuous intrapartum CTG
monitoring are listed below:
Meconium-stained liquor
Abnormal FHR detected by intermittent auscultation

Maternal pyrexia of 38 C on one occasion or 37.5C on two occasions, 2 hours apart
Fresh bleeding developing in labour
Oxytocin use for augmentation
Multiple pregnancy
Vaginal breech delivery
Maternal request
Fetal growth restriction
Preterm labour
Maternal disease (pre-eclampsia, obstetric cholestasis).
The evidence for these recommendations is derived from observational studies rather than
randomized controlled trials. The poor quality of these studies, which were performed more than 20
years ago, has resulted in a lack of evidence for CTG use in low-risk women. Therefore although it
might seem counterintuitive to the anaesthetist to reduce the amount of monitoring information
available to doctors and midwives caring for women in labour, current NICE guidance does not
support the use of CTG in this group. A Cochrane review on continuous CTG during labour
demonstrated a reduction in neonatal seizures, but no significant differences in cerebral palsy or
infant mortality rates. This was offset by increases in caesarean section and instrumental vaginal birth
rates.
Interpretation of CTG
The interpretation of a fetal heart rate (FHR) trace should take into consideration the presence or
stage of labour, its progress, maternal observations and other risk factors present. CTG interpretation
is subject to high intra- and interobserver variation related to experience, training and time of day.
Computerized CTG interpretation software has been developed to support decision-making in the
management of labour. Its use in labour is currently being evaluated in the multicentre randomized
controlled INFANT study.
A documented interpretation of a CTG should be performed every hour, or with any clinical
concern. Interpretation is based on four features rate, variability, accelerations and decelerations.
Based on these features the CTG can be classified as normal, suspicious or pathological (Table 6.1).
Figure 6.1a Normal and abnormal CTGs.
A normal cardiotocograph trace. The baseline is 135 beats/min variability 25 beats/min
accelerations present and no decelerations.
Figure 6.1b A pathological cardiotocograph trace demonstrating late decelerations. The radar of
the deceleration and the peak of contraction are marked with arows.
Table 6.1 CTG parameters and interpretation
Feature Baseline (bpm) Variability (bpm) Decelerations Accelerations
Reassuring 110160 5 None Present
Non-reassuring 100109 <5 for Typical variable The absence of

161180 4090 minutes decelerations accelerations with
with over 50% of otherwise normal
contractions, trace is of
uncertain
occurring for over
significance
90 minutes
Single
prolonged
deceleration for
up to 3 minutes
Abnormal <100>180 <5 for >90 Either atypical

Sinusoidal minutes variable
pattern 10 decelerations
minutes with over 50% of
contractions or
late decelerations,
both for over 30
minutes
Single
prolonged
deceleration for
more than 3
minutes
Category Definition
Normal An FHR trace in which all four features are classified as reassuring
Suspicious An FHR trace with one feature classified as non-reassuring and the
remaining features classified as reassuring
Pathological An FHR trace with two or more features classified as non-reassuring

or one or more classified as abnormal
Baseline rate
The normal fetal heart rate is 110160 bpm, with the mean tending to fall as gestation progresses. A
low baseline (100110 bpm) or a tachycardia (160180 bpm), where accelerations are present and
no other adverse features appear is not regarded as suspicious. This may represent a baseline
reduction following opiate administration, or a tachycardia with an active fetus, both of which may
eventually settle. FHR is affected by maternal pyrexia and/or tachycardia and usually rises by 10
15 bpm. A slow rise in baseline over the duration of a labour may indicate increasing fetal acidosis
and should be regarded as suspicious. A baseline rate of <100 or >180 is always abnormal.
Variability
Variability is defined as the beat-to-beat variation, and should be greater than 5 bpm; it represents the
fetal autonomic nervous system function. A reduction in variability for up to 40 minutes may be
normal with the fetal sleep cycle. A reduction in variability has low sensitivity but high specificity
for fetal acidosis.
Accelerations
The presence of accelerations in the FHR of greater than 15 bpm for 15 seconds is a reassuring
feature suggesting fetal activity. The presence of accelerations has a high specificity for excluding
fetal acidosis, although the absence of accelerations does not denote a suspicious or pathological
CTG trace.
Decelerations
The presence of decelerations is a non-reassuring or abnormal feature on a CTG, and is classified
according to the type (early, late and variable), duration and frequency. Early decelerations are
uniform in size, shape and duration and are likely to represent head compression in the late first or
second stages of labour rather than hypoxia. Critically, early decelerations start with uterine
contractions and the FHR has normally returned to baseline as the contraction finishes.
Late decelerations are so called because the deceleration in FHR starts to occur after the uterine
contraction peaks, and persists after the contraction finishes. Late decelerations are more indicative
of fetal hypoxia.
Variable decelerations are more common, accounting for more than 80% of decelerations seen.
They are defined as a reduction from the baseline more than 15 bpm for 15 seconds with varying
length, amplitude and uniformity. Commonly as a result of cord compression, variable decelerations
are sub-classified into typical (which may be found near the end of the second stage of labour) or
atypical. Atypical variable decelerations are more concerning and may show a loss of shouldering
(accelerations before and after the deceleration), a smooth decline, with a slow recovery to baseline
which may overshoot, or be biphasic in shape.
When a CTG is normal the baby is very likely to be well, but the majority of abnormal CTGs
occur in babies who are not distressed. A suspicious CTG requires review by an obstetrician for a
management plan, which will depend on the overall clinical picture and the duration of concern. For
example, the presence of variable decelerations in early labour is of more concern than near delivery.
Suspicious features may respond to simple measures that can be performed to optimize placental
perfusion.
These techniques may include:
Changing of maternal position
Adequate hydration with intravenous crystalloid fluid
Avoiding uterine hyperstimulation by judicious use of oxytocin
Reduction of maternal pyrexia by paracetamol and/or antibiotics.
If suspicious features persist, then consideration of further assessment with fetal blood sampling
should be made. Unlike a CTG classified as suspicious, a pathological CTG requires action. This
may mean expediting birth by instrumental delivery if imminent or by further assessment of fetal
wellbeing by fetal blood sampling. If labour is not advanced enough to permit this (<3 cm dilated), or
is contraindicated, then delivery by emergency caesarean section is required if pathological features
persist.
Fetal blood sampling (FBS)

As an abnormal CTG has a relatively low positive predictive value (PPV) for acidosis, FBS is
performed in most UK units in an attempt to reduce false positive diagnosis of fetal compromise and
corresponding unnecessary intervention. Fetal blood sampling provides current fetal pH and base
excess.
Serious adverse sequelae in the newborn period are rare after birth with umbilical cord pH
greater than 7.0 or base excess less than 12 mmol/L.
FBS should be performed with the consent of the mother with full understanding that the
subsequent result may influence the mode and urgency of delivery or that the FBS may need repeating
should the CTG continue to be pathological. FBS is ideally performed in the left lateral position to
optimize placental perfusion. Contraindications to FBS include gestation earlier than 34 weeks,
maternal blood-borne infection (HIV, active hepatitis B and C) and potential inherited fetal bleeding
disorders. Should there be a pathological trace where FBS is contraindicated, technically impossible
due to dilatation, a failure of collection or the mother refuses the FBS, delivery should be expedited
on the presumption of fetal acidosis.
FBS results should be interpreted in the context of the progress of labour (Table 6.2). FBS
should not be performed with obvious fetal compromise as indicated by prolonged (>4 minutes)
bradycardia or when vaginal delivery can be easily achieved using ventouse or forceps. In these
cases immediate delivery should be expedited.
Table 6.2 FBS results and recommendations
FBS result (pH) Interpretation Appropriate action
7.25 Normal Appropriate sampling should be repeated no

more than 60 minutes later if the FHR trace
remains pathological, or sooner if there are
further abnormalities
7.217.24 Borderline Sampling should be repeated no more than 30

minutes later if the FHR trace remains
pathological, or sooner if there are further
abnormalities
7.20 Abnormal Consultant obstetric advice should be sought,

with a view to an urgent birth
An abnormal FBS result requires urgent delivery. The delivery should be performed by the
fastest and safest mode relevant to the operators skill and experience.
Classification of urgency of delivery

The Sentinel Caesarean Section Audit suggested that in cases such as cord prolapse, a decision-to-
delivery interval (DDI) of 15 minutes was feasible. However, in many Category 1 decisions, delivery
within 30 minutes was not achieved. Once a decision to deliver has been made, delivery should be
carried out with the urgency appropriate to the risk for that baby and the safety of its mother (Tables
6.3 and 6.4). Evidence suggests that delay is often associated with transfer to theatre.
Table 6.3 Classification of urgency for caesarean section
Category
1 Immediate threat to the life of the woman or fetus
2 Maternal or fetal compromise that is not immediately life-threatening
3 No maternal or fetal compromise but needs early delivery
4 Delivery timed to suit woman or staff
Table 6.4 Suggested DDI target times
Category Time from decision to delivery
1 30 minutes
2 75 minutes
3 24 hours
4 Timed to suit patient and staff
In cases of suspected or confirmed acute fetal compromise, such as that of a pathological CTG
or abnormal FBS result, delivery should be accomplished as soon as possible. Thirty minutes has
become the accepted standard for Category 1 deliveries, and is often used as an audit tool to monitor
performance.
Many units have implemented DDI timings to aim towards; this can aid in focusing the team on
the urgency of the delivery, allow planning of the labour ward workload and allow auditing of key
indicators. Although far from universal, commonly implemented target times are shown below.
Despite a DDI interval of 30 minutes being suggested, studies have demonstrated this was only
achievable in two-thirds of emergency caesareans for fetal distress. A DDI interval of up to 75 mins
had no significant increase in neonatal or maternal morbidity. However, during acute hypoxia, such as
a fetal bradycardia, pH reduces by 0.1 units/min; the degree of acidosis will depend on the starting
pH of a potentially already compromised fetus.
Fetal ECG (ST analysis)
Whilst the majority of units use CTG and FBS as their main methods of fetal monitoring, some units
employ fetal ECG as an adjunct. Whilst, as with a CTG, an anaesthetist would not be expected to
interpret a fetal ECG, it is important to understand the additional information it can provide and how
this may alter clinical decisions. NICE suggests that fetal ECG may reduce intervention, but doesnt
significantly alter neonatal outcome. The additional costs and complexities of staff training have
meant its not a common finding on delivery units at present.
The fetal ECG, like an adult ECG, displays P, QRS and T waves. Hypoxia during labour can
alter the waveform of the fetal ECG. Repolarization of myocardial cells is sensitive to metabolic
dysfunction caused by hypoxia. Hypoxia in the fetus changes the ST segment. Fetal ECGs are
performed with ruptured membranes through a fetal scalp electrode (rather than an abdominal
transducer, which is most often used for CTG) with computer analysis of the waveform. Progressive
changes in the T/QRS ratio can be determined if applied before evidence of fetal stress, usually
commenced at the beginning of labour to determine changes from the baseline (i.e. the fetal ECG
cannot be applied once CTG abnormalities have commenced). Unlike CTG, fetal ECG does not
require FBS to confirm hypoxia so delivery is indicated on the basis of fetal ECG analysis
recommendation. Unfortunately, once a fetal ECG becomes abnormal then the safe delivery window
is 20 minutes or less. This tight delivery window is another reason why many departments have not
adopted the technology.
Instrumental delivery
Instrumental delivery is more common in primiparous women and those with epidural analgesia. The
obstetrician will normally allow an hour of active pushing before considering intervening both to aid
the mother and prevent prolonged second stage complications such as postpartum haemorrhage. Prior
to performing an instrumental delivery the obstetrician will assess the cervical dilatation, fetal
presentation (head = cephalic, bottom = breech), station of presenting part (relative to ischial spines),
position, moulding (overlapping of fetal skull bones), presence of caput (fetal scalp oedema) and
pelvic outlet capacity. In the UK, obstetricians will only perform instrumental deliveries at full
cervical dilatation with the fetal head at or below the ischial spines. Having determined the
suitability for instrumental delivery the obstetrician must determine the fetal head position using
anatomical features felt on the fetal head. The occipito-anterior (OA) position presents the smallest
relative fetal head diameter and is the easiest to deliver vaginally. Malposition occurs when the fetal
head is not OA and is in an alternative position (See Figure 6.2). Occipito-posterior (OP) and
occipito-transverse (OT) and variations on this (right occipito-posterior ROP= the occiput is 1020
to the right, etc.) present a larger relative fetal head diameter and will often require rotation to OA by
the obstetrician to achieve delivery.
Figure 6.2 Diagrammatic representation of fetal presentation.
The majority of instrumental deliveries are performed within the delivery room with the fetal
head in the occipito-anterior (OA) position. However, if delivery is anticipated to be more
complicated, instrumental delivery in theatre is recommended, the so-called trial of instrumental
delivery. Transfer to theatre allows adequate analgesia with either spinal or epidural, which
improves associated pain and maternal concordance and allows a rapid conversion to Caesarean
section if required. In general, deliveries that are anticipated to be more difficult or likely to fail,
such as those with a high presenting part, malposition, macrosomic infant or a high maternal BMI,
will be performed in theatre. Sometimes transfer to theatre is necessary for maternal analgesia alone.
In cases of fetal distress when a difficult trial of instrumental delivery for malposition is considered it
may be prudent to perform an FBS prior to transfer to provide an accurate assessment of fetal
acidosis.
The choice of instrument depends on fetal head position, operator preference and experience.
Whilst ventouse has a reduced incidence of perineal trauma, fetal traction is more limited than with
forceps, meaning it is more likely to fail. Therefore, in situations with extensive caput, a large baby
or poor maternal effort, forceps are usually the preferred choice even if the fetus is in OA position. If
fetal head rotation is required to correct malposition then this can be achieved manually, with
posterior cup ventouse or Keillands forceps. The success of attempts to rotate the fetal head and
deliver the baby in theatre are very dependent on obstetrician experience and the anaesthetist should
be prepared for sudden changes in the mode of delivery in such circumstances, particularly in dealing
with less experienced staff. Further awareness of difficulty should also be raised if multiple
instruments (i.e. ventouse and forceps) are used. Instrumental deliveries are also associated with
perineal trauma including 3rd and 4th degree tears and postpartum haemorrhage. In theatre the
anaesthetist can provide essential input with regards to the physiological signs of blood loss and take
a lead role in co-ordinating its management.
Conversion to caesarean section after an unsuccessful attempted instrumental delivery presents
the obstetrician with a high-risk surgical case where bleeding and uterine trauma frequently occur. As
an obstetrician, a full dilation section after instrumentation creates a low impacted head, and a very
friable vascular lower segment. It may be necessary to aid the delivery of the head by adjustment of
the theatre table to a lower level or in reverse Trendelenburg position. Tocolytics or conversion to
general anaesthetic may also be required. In these situations time is critical and anticipation or
suggestion of these techniques by the anaesthetist can be helpful. Should the head remain impacted it
may be necessary to push the head from below, which requires the cooperation of theatre staff in
maternal positioning. Such deliveries may be stressful for the delivering obstetrician, particularly in
the case of concurrent potential fetal compromise. Support from the anaesthetist including prompts
about blood loss and any potential requirements for cross-matching can be helpful.
Intrapartum management of twins

Twins are regarded as high-risk pregnancies with a perinatal mortality rate five times higher than that
of singletons. The increased perinatal mortality is largely related to prematurity, fetal growth
restriction and complications of monochorionicity, such as twin-to-twin transfusion. However,
intrapartum complications are also more common, especially with delivery of the second twin.
Vaginally delivered second twins have a fourfold increased risk of intrapartum death, compared to
planned caesarean section. An understanding of the types of twins, their subsequent management
options and the potential intrapartum complications is essential.
For the purpose of mode of delivery, twins can be divided into those which share an amniotic
sac and those which are separate. Dichorionic diamniotic twins, which have separate placentas and
are within separate sacs, and monochorionic diamniotic twins who have a shared placenta but
separate sacs, are potentially suitable for vaginal delivery. Monochorionic monoamniotic (MCMA)
twins share both an amniotic sac and a placenta; therefore the bodies can become interlocked,
preventing vaginal birth. Caesarean section is recommended for all monoamniotic twins and higher
multiples.
Timing of twin deliveries is important due to increasing morbidity and mortality with advancing
gestation. In this situation its the shared placenta that becomes most significant. In dichorionic twin
pregnancies delivery should be planned after 3738 completed weeks and in uncomplicated
monochorionic twins at 3637 completed weeks. MCMA twins have the highest risk of stillbirth and
cord entanglement and so should be delivered by 3234 completed weeks. Due to the nature of twin
pregnancy, one-third will go into spontaneous preterm labour before 37 weeks.
Mode of delivery remains a contentious issue. Some suggest that the risk of mortality and
morbidity for the second twin advocates caesarean section in all cases. A Cochrane review suggests
that caesarean section does not change neonatal outcome, whilst increasing maternal morbidity. A
large randomized trial, the Twin Birth Study, aimed to answer the question of planned mode of
delivery. Recent publication of the study demonstrated that planned caesarean delivery did not
significantly decrease or increase the risk of neonatal death or serious morbidity, when compared
with planned vaginal delivery.
Thus, the mode of delivery in uncomplicated twins is dependent on the presentation of the
leading twin. With breech presentation of the first twin, which occurs in 20% of cases, the woman
should be offered an elective caesarean section. Cephalic presentation of the leading twin would
permit a trial of vaginal delivery.
To deliver twins, adequate experienced midwifery and obstetric staff is essential, and a theatre
and anaesthetist should be readily available. Twins should have their fetal heart rate monitored
throughout labour. As it is critical to differentiate between the two fetal heart rates this may be
achieved by a fetal scalp electrode on twin one and an external CTG transducer on twin two. If CTG
concerns arise in the leading twin an FBS can be performed as normal. CTG concerns with the
second twin require a decision regarding operative delivery, as there are no measures to confirm
whether twin two is acidotic. After delivery of the first twin, the second is stabilized to control lie
and an ultrasound performed to confirm presentation, which can change in 20% of cases. Oxytocin
should be ready for augmentation should contractions stop and the second twin should be allowed to
descend into the pelvis before the membranes are ruptured. The second twin can deliver either
cephalic or by breech extraction. During this technique internal podalic version is performed initially.
The operator grasps the fetal foot within the uterus and gently and continuously pulls until in the
pelvis. The breech delivery is then continued as described, but with continuous traction. Following
delivery of the second twin, postpartum haemorrhage should be anticipated due to atony of the over-
distended uterine myometrium.
Anaesthetic involvement in twin deliveries may involve placement of epidural anaesthesia,
which can facilitate manoeuvres to deliver a breech second twin or provide anaesthesia for an urgent
recourse to delivery. The anaesthetist should be readily available for emergency caesarean section
and for management of postpartum blood loss.
Vaginal breech delivery

Breech presentation occurs in 34% of pregnancies at term. The Term Breech Trial recommended
caesarean section as the safest mode of delivery for breech presentation at term in nulliparous
women. This recommendation was based on a relative risk of neonatal mortality or serious neonatal
morbidity of 0.33 for planned caesarean section compared to planned vaginal birth, although the
absolute risks were small at 1.6% for planned caesarean section to 5% for planned vaginal birth.
Recommendations were rapidly implemented and experience with vaginal breech deliveries has
diminished amongst obstetricians and midwives since, with major implications on training. Options
for a woman with a diagnosed breech at term are external cephalic version or caesarean section.
Woman are counselled that vaginal breech delivery increases the risk of perinatal morbidity and
mortality. Some women opt for a planned vaginal breech delivery, whilst some will present with an
undiagnosed breech in labour. Vaginal breech deliveries can proceed as long as the woman is
counselled appropriately and offered a caesarean section. There should be no other contraindications
to vaginal delivery and essential conditions should be met throughout the delivery in order to
optimize safety. The women should be:
Labouring spontaneously
On a consultant-led labour ward with suitable experienced staff onsite willing to perform or
supervise the delivery
Appropriately counselled with an understanding that early recourse to CS may be required

(approx. 50% of breech labours in nulliparous women will end in CS)
Have an appropriate sized fetus (weight not <2000 g or > 3800 g)

Continuous CTG monitoring with no signs of fetal distress
Progressing adequately in labour without the use of oxytocin augmentation.
A vaginal breech delivery requires one-to-one care. As the anaesthetist, regional analgesia may be
helpful with possible delivery interventions. There needs to be a readiness to transfer to theatre for an
emergency caesarean section should there be fetal distress, poor progress in labour or cord prolapse.
Once full dilatation is confirmed, the woman should be placed in the lithotomy position and the
bladder emptied. The breech should be allowed to descend without traction or manipulation to the
introitus, the fetus should be in the sacro-anterior position throughout. With distension of the introitus,
an episiotomy should be considered and maternal effort should allow steady advancement to the
umbilicus. It may be necessary to manipulate the legs free with gentle pressure behind each popliteal
fossa. As the body continues to descend with contractions, the scapula will become visible and the
arms should deliver spontaneously if flexed. Lovsets manoeuvre may be required to deliver nuchal
arms by rotation through 90 in either direction. The baby should be allowed to descend further until
the nape of the neck is visible. Delivery of the head is now possible with flexion by pressure on the
occiput (MauriceauSmellieViet manoeuvre) or by lifting the feet upwards in an arc (Burns
Marshall technique) (Figure 6.3). If neither of these manoeuvres is successful, forceps can be applied
to deliver the head with the feet raised above. Breech delivery is more traumatic for the baby, and its
more likely to become cold. A paediatrician should be available after delivery for possible
resuscitation and review.
Figure 6.3 Breech delivery.
Complications of breech delivery include cord prolapse, fetal distress or inadequate progress of
labour, all of which require recourse to caesarean section. A more distressing and unusual situation is
head entrapment, which more commonly occurs with preterm infants. This is an obstetric emergency,
which requires senior multidisciplinary assistance. In this situation the head may be trapped by a
bony abnormality or an incompletely dilated cervix. The initial aim is to increase the dimensions of
the pelvic outlet by the McRoberts position and trying suprapubic pressure. Should this fail,
tocolytics may be required or incisions to the cervix. In order to perform cervical incisions, adequate
analgesia is required and haemorrhage may ensue. Drastic measures may require caesarean section
with the baby being supported and pushed from below.
Key points
1. Interpretation of the CTG is based on rate, variability, acceleration and deceleration. It can be
classified as normal, suspicious or pathological.
2. Normal fetal heart rate is between 110 and 160 beats per minute, a baseline rate of less than
100 and greater than 180 is always abnormal.
3. Suspicious CTGs require review and a management plan. This plan will depend on overall
clinical picture, duration of concern and the consideration and results of further assessments.
4. Decision-to-delivery times can be used as a tool to monitor team performance and help
towards improvements in the delivery of care.
5. Caesarean section after a failed instrumental delivery can be a challenging surgical

procedure.
Further reading
Alfirevic, Z., Devane, D. and Gyte, G. M. L. (2013). Continuous cardiotocography (CTG) as a form
of electronic fetal monitoring (EFM) for fetal assessment during labour (Review). Cochrane
Database Syst. Rev., 2013(5), Art. No. CD006066.
Armstrong, L. and Stenson, B. J. (2007). Use of umbilical cord blood gas analysis in the assessment
of the newborn. Arch. Dis. Child Fetal Neonatal Ed., 92(6), F430F434.
Barrett, J., Hannah, M., Hutton, E. et al. (2013). A randomized trial of planned caesarean or vaginal
delivery for twin pregnancy. New Engl. J. Med. 369 (14), 12951305.
Hannah, M. E., Hannah, W. J., Hewson, S. A. et al. (2000). Planned caesarean section versus vaginal
birth at term: a randomised multicentre trial. Lancet 356, 13751383.
National Institute of Health and Clinical Excellence (2011). Caesarean Section. CG132. 3235.
National Institute of Health and Clinical Excellence (2007). Intrapartum care. CG55. 4448.
Royal College of Obstetricians and Gynaecologists (2006). The Management of Breech Presentation.
Green-top guideline No. 20b. London: RCOG Press.
Royal College of Obstetricians and Gynaecologists (2011). Operative Vaginal Delivery. Green-top
Guideline 26. London: RCOG Press.
Shah, D. (2013) Clinical Progress in Obstetrics and Gynaecology. New Delhi: Jaypee Brothers.
Smith, G. C., Pell, J. P. and Dobbie, R. (2002). Birth order, gestational age and risk of delivery
related perinatal death in twins: retrospective cohort study. BMJ 325, 10041008.
Thomas, J., Paranjothy, S. and James, D. (2004). National cross sectional survey to determine
whether the decision to delivery interval is critical in emergency caesarean section. BMJ 328, 665.
Tuffnell, D. J., Wilkinson, K. and Beresford, N. (2001). Interval between decision and delivery by
caesarean section: are current standards achievable? Observational case series. BMJ 322, 1330.
Chapter 7
Antenatal assessment

In 2007 the Department of Health published Maternity Matters: Choice, Access and Continuity of
Care in a Safe Service. The over-riding aim of any maternity service is to provide safe, high-quality
care to women and their partners, thus enabling a safe pregnancy and birth for both mother and baby
and to provide a confident start to family life.
For the majority of women, midwives and obstetricians will deliver care, but there are an
increasing number of women whose pregnancy, labour or delivery require anaesthetic input.
Over the past decade the Centre for Maternal and Child Enquiries (CMACE), the Royal College
of Obstetricians and Gynaecologists (RCOG), the Obstetric Anaesthetists Association (OAA) and
the Association of Anaesthetists of Great Britain and Ireland (AAGBI) have all produced guidance
emphasizing the need for good communication between all the speciality groups providing antenatal
care. Antenatal anaesthetic assessment is pivotal in planning peripartum care, particularly for those
with co-existing disease, to ensure the best outcome for these women. The most recent guidance from
the OAA/AAGBI states there should be an agreed system whereby the anaesthetist is given sufficient
notice of all potentially high-risk patients. In the majority of obstetric units this would be done as a
referral to an antenatal anaesthetic assessment clinic.
Antenatal anaesthetic clinic

There are increasing numbers of parturients presenting with co-existing, complex medical conditions.
This may, in part, result from the advances in medicine that have rendered such conditions more
stable and have seen these women surviving to childbearing age. Many women are now choosing to
have children later in life, resulting in an increase in acquired co-morbidity. The prevalence of
morbid obesity has significantly increased in the UK (1.4% in 1993, 2.9% in 2005). This was echoed
by data published by the World Health Organization, demonstrating that the prevalence of obesity has
nearly doubled between 1998 and 2008.
The anaesthetic service not only provides intrapartum analgesia and anaesthesia, but also assists
in the delivery of peripartum care to women with complications related to their pregnancy or co-
existing medical disease.
The aim of the antenatal clinic is to carry out a review of the womans history, assess the impact
of any co-morbidities and provide information. The outcome of the visit should be an individualized
anaesthetic management plan for labour and delivery. Women with complex medical problems need
to be discussed at a multidisciplinary forum, so that obstetricians, anaesthetists, midwives and other
medical specialities are aware of the issues that might arise in the peripartum period.
In 1993 Rosaeg et al. published a review of patients seen in their anaesthetic clinic over a 6-
year period. The review showed that the clinic provided a valuable service, not only to the pregnant
woman, but also to the anaesthetist and other healthcare professionals involved in the womans care.
Another highlighted benefit was the provision of consistent advice and information regarding
anaesthetic management that may impact on obstetric care to the obstetricians.
When setting up an anaesthetic assessment service it is essential that there is suitable
infrastructure to support the clinic:
Consultant time made available in job plans to run the clinics
Consultation room dedicated to the clinic
Setting appropriate referral criteria (see Table 7.1)
Consultant review of referrals prior to booking
Secretarial support
Booking women into the clinic
Appointment and clinic letters
Point of contact for the women
Retrieval of notes from other hospitals
Interpreting services
Dissemination of the findings from the clinic visit to all relevant personnel
A system that ensures there is easy access to the clinic letters if a woman is admitted to the
delivery unit out of hours
Database of all the referrals
Audit of the clinic service.
Table 7.1 Example of referral criteria taken from referral guidelines at St Marys Hospital,
Manchester
Anaesthetic Previous difficulties with general or regional

anaesthesia
Severe reaction to drugs including anaesthetic
agents or local anaesthetics
Cardiac Congenital heart disease

Coronary heart disease
Previous cardiac surgery
Arrhythmias/pacemaker or ICD in situ
Respiratory Severe asthma

Cystic fibrosis
Restrictive lung disease
Musculoskeletal Scoliosis
Achondroplasia
Previous spinal surgery/injury
Muscular dystrophies
Neurological History of brain injury/surgery

Myopathy
Multiple sclerosis
Spina bifida
Any spinal cord abnormality
Stroke
Haematological Haemaglobinopathy
Coagulopathy
Endocrine Thyroid disease/phaeochromocytoma/other endocrine

disorder
Obstetric Risk of major obstetric haemorrhage
Others Severe obesity BMI > 40 kg/m2

Difficult venous access or needle phobia
Refusal of blood products
Learning difficulties or significant problems with
consent
Other severe disease
Who should be seen?

In an ideal world, all parturients would be reviewed in the antenatal period; however, personnel and
financial constraints make this unworkable.
Locally agreed referral criteria enable patients at higher risk and women who have had
problems with previous pregnancies to be referred to the anaesthetic antenatal clinic.
The recent OAA/AAGBI guidance on provision of obstetric services recommends that referral
criteria for antenatal anaesthetic clinics should include:
Women that might present difficulties should analgesia or anaesthesia be required (this could
include women with poor venous access, e.g. due to intravenous drug use or severe burns, or
those with learning difficulties or mental health problems)
Women at high risk of obstetric complications
BMI > 40 kg/m2 at booking (as recommended by Joint CMACE/RCOG guideline on the
management of women with obesity in pregnancy)
Previous difficulty with or complications of regional or general anaesthesia
Women with significant medical conditions.

This list is not exhaustive and should be tailored to the needs of each individual obstetric unit.
It is important to have formal referral criteria, regardless of whether the parturient is seen in an
anaesthetic clinic or on an ad hoc basis, as it will increase the number of appropriate referrals and
highlight the presence of the service. When introducing or amending referral guidelines it is vital to
ensure that they are communicated to the healthcare professionals making the referrals and to provide
a point of contact should there be any uncertainty over which patients to refer.
Once guidelines have been agreed and circulated, referrals can be made through an electronic
booking system, written referral or standardized proforma, whichever is suitable for each obstetric
unit. Referrals can be made either at the time of the booking visit or later in pregnancy, it is essential
that there is clear guidance where the referral is sent to be reviewed by an anaesthetic consultant.
Where should they be seen?

A survey of UK obstetric units in 2005 showed that 70% of the units did not have formal anaesthetic
clinics. This figure will have undoubtedly changed over the past 10 years, as with increasing pressure
on the anaesthetic antenatal service, more obstetric units have changed from providing reviews on an
ad hoc basis to a formal clinic environment.
Whether patients are seen on an ad hoc basis or in a clinic there should be a dedicated room
available to allow the consultation to be conducted without interruption.
When should they be seen?

Once the referral has been made by the obstetrician or midwife and been reviewed by the
anaesthetist, a decision needs to be made as to the timing of the antenatal anaesthetic assessment. The
RCOG Good Practice Guideline 13 for Cardiac Disease and Pregnancy suggests that women with
pre-existing cardiac disease should be seen by a multidisciplinary team at 3234 weeks to discuss
her delivery plan. While this recommendation is for women with pre-existing cardiac disease, it can
be used to guide timing of an antenatal anaesthetic review for the majority of women. The timing of a
womans clinic visit will ultimately depend on the condition she is referred with; some women may
well need to be assessed in the second trimester if their medical condition means they have a
significant chance of preterm delivery.
If possible it is best to match the anaesthetic assessment with a planned antenatal clinic
appointment, this prevents multiple visits to the hospital and improves non-attendance rates. Most
women are referred in a timely manner; however, it is important to have some leeway in the clinic
bookings for women who book late or who were not identified as high-risk earlier in their pregnancy.
Who should see the patient?

Recommendations and guidance from various bodies, including The Confidential Enquiries into
Maternal and Child Health, RCOG, OAA and AAGBI, all suggest that a senior anaesthetist carries
out the antenatal anaesthetic review. The clinics should be consultant led; if for any reason the
consultant is not available, each case should be discussed with a consultant at the earliest
opportunity, to ensure appropriate advice has been given to the woman.
The clinic appointment

This appointment allows the anaesthetist to make a thorough assessment of the parturient and to plan
for delivery, whilst giving the patient an opportunity to discuss any concerns they may have and make
an informed choice about the options available to them during labour and delivery.
A full history of medical and obstetric conditions, and drug history, including any drug allergies,
should be taken together with a full anaesthetic history. It would be a shame to miss the chance to
elicit a history of suxamethonium apnoea in a woman referred with back pain due to a mild scoliosis.
History-taking will always need to be focused on specific areas of concern, but should also take into
account the physiological changes in pregnancy, which may significantly worsen any pre-existing
condition.
Examination will be guided by the patients condition, but should always include airway
assessment, examination of the back, paying particular attention to the lumbar spine, and an
assessment of venous access. Examination of the back should include visual inspection for scars,
palpation of the vertebrae and where appropriate, ultrasound-guided estimation of the depth of
epidural space. This can provide an invaluable source of information during labour or delivery when
regional anaesthesia is required.
Discussion with the woman should be tailored to their reason for referral and how that may
affect labour and delivery. Information should be provided and recommendations made regarding
their choices for analgesia and anaesthesia and the need for any further investigations. Any specific
concerns regarding their condition, analgesic options, mode and place of delivery can also be
addressed. Patient information leaflets can be given for the patient to read at home and they need to
have contact information should they require any further advice. [(www.oaaformothers.info)
translations of these leaflets are available in many languages on this website]
Once the consultation has finished, a detailed record of the history, examination, investigations,
discussion and any outstanding issues should be made. Ideally this should be documented in the
womans notes, either in the form of a written entry or a dictated letter. A shortened version of the
consultation should also be written in the womans handheld notes in case of presentation at another
hospital. It is also useful to keep a second copy of the consultation record on the delivery suite so that
the information is readily available to consultant anaesthetists and anaesthetic trainees, in cases
where there is a delay obtaining a patients notes.
Depending on the co-morbidity, additional information or investigations can be requested; the
appointment can also ensure that there is time to arrange other speciality involvement.
This includes:
Further information from the GP
Further information and discussion with other specialities
Multidisciplinary review to decide timing and mode of delivery; this may need to be
reviewed in light of any change in the womans condition
Arranging further investigations, e.g. echocardiography, spinal imaging
Booking cell salvage for caesarean section e.g. placenta praevia, women refusing blood
products
Booking critical care and specialist theatre space, e.g. women with significant heart disease,
women who may require respiratory support in the peripartum period.
Another important aspect of an anaesthetic assessment clinic is education. As previously mentioned,

the antenatal anaesthetic clinic should be a consultant-delivered service. This environment provides
the perfect educational opportunity for midwives, anaesthetists and obstetricians in training.
Observers to the clinic will gain insight into the necessity for forward planning to ensure delivery of
a safe and high standard of maternal care.
Key points
1. Anaesthetic antenatal assessment is critical in the planning of peripartum care in the presence
of significant maternal co-existing disease.
2. An appropriate locally agreed referral criteria system is recommended.
3. A senior anaesthetist should carry out the review.
4. The timing of the visit will depend on the reason for referral, but most can be seen early in the
third trimester.
Further reading
Centre for Maternal and Child Enquiries (CMACE). (2010). Maternal Obesity in the UK: Findings
from a National Project. London: CMACE.
Centre for Maternal and Child Enquiries (CMACE). (2011). Saving mothers lives: reviewing
maternal deaths to make motherhood safer: 200608. The Eighth Report on Confidential Enquiries
into Maternal Deaths in the United Kingdom. Br. J. Obstet. Gynaecol., 118 ( 1), 1203.
Cormack, C., Francis, S. and Yentis, S. (2007). Antenatal anaesthetic assessment of the pregnant
woman. Anaesth. Intensive Care Med. 8, (7), 269272.
Department of Health. (2007). Maternity Matters: Choice, Access and Continuity of Care in a Safe
Service. London: Department of Health.
Obstetric Anaesthetists Association/Association of Anaesthetists of Great Britain and Ireland.

(2013). Guidelines for obstetric anaesthetic services. London: AAGBI and OAA.
Rai, M. R., Lua, S. H., Popat, M. and Russell, R. (2005). Antenatal anaesthetic assessment of high-
risk pregnancy: a survey of UK practice. Int. J. Obstet. Anaesth., 14, 219222.
Rosaeg, O. P., Yarnell, R. W. and Lindsay, M. P. (1993). The obstetrical anaesthesia assessment
clinic: a review of six years experience. Can. J. Anaesth., 40(4), 346356.
Royal College of Obstetricians and Gynaecologists. (2008). Standards for Maternity Care: Report of
a Working Party. London: RCOG.
Royal College of Obstetricians and Gynaecologists. (2011). Cardiac Disease and Pregnancy. Good
Practice no.13. London: RCOG.
The Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European
Society of Cardiology (ESC). (2011). ESC Guidelines on the management of cardiovascular diseases
during pregnancy. Eur. Heart J., 32, 31473197.
Section 3

Provision of anaesthesia
Chapter 8
Incidental anaesthesia during pregnancy

Desiree M. A. Choi and Kim G. Soulsby
Introduction
Parturients may require anaesthesia during their pregnancy in order to facilitate obstetric or non-
obstetric surgical procedures. Common obstetric procedures required in pregnancy include cervical
cerclage, ovarian cyst interventions and fetal surgery. The incidence of incidental or non-obstetric
anaesthesia in pregnancy has been reported as ranging from 1:50150 pregnancies, with
appendectomy, cholecystectomy and pelvic laparoscopy being the most commonly encountered
procedures.
Incidental anaesthesia must minimize the risk of interrupting the pregnancy and affecting fetal
development. Alterations in maternal physiology accentuate anaesthetic risks and the approach to
anaesthesia must be modified accordingly.
Fetal considerations
Anaesthesia may impact on the fetus in two ways: it may interrupt the pregnancy, resulting in either
pregnancy loss or premature delivery, or it may impact on fetal development, either by teratogenic
pharmacological effects or because of derangements in the physiological milieu.
The effects of a teratogenic insult depend on the gestation of the fetus at the time of exposure.
Teratogens cause an all or nothing effect in the early pluripotential developmental phase, such that
the embryo will either die or be unaffected and develop normally. However, days 31 to 71 of human
gestation correspond to the organogenesis phase, where exposure to teratogens may impair the
structural development of organ systems. First trimester anaesthesia has been linked with increased
neonatal central nervous system and eye malformation, particularly hydrocephalus and cataracts. In
the phase following organogenesis, teratogen exposure is more likely to affect the fetal central
nervous system, which undergoes development and maturation throughout pregnancy. These effects
are likely to result in functional behavioural effects rather than structural malformations.
Drug teratogenicity
Organogenesis phase
There is theoretical reason to suspect that drugs used in anaesthesia may be teratogenic: the cellular
mechanisms for differentiation and organogenesis include mechanisms known to be targeted by drugs
used in anaesthesia. Neurotransmitter and receptor mechanisms, as well as signalling and second
messenger systems are all known to be affected by drugs used in anaesthesia. This theoretical risk of
teratogenicity has been difficult to quantify in a practical clinical context, because of difficulties
extrapolating animal research data to human development (teratogenicity is species specific) and the
obvious ethical and logistical problems of research on human fetal exposure to teratogens.
Later pregnancy
Drugs used in later pregnancy may have direct effects other than structural organogenesis impairment.
Benzodiazepines in late pregnancy may result in fetal benzodiazepine dependence and
withdrawal (although unlikely in the short-term context of a single anaesthetic). Used peripartum, they
are associated with fetal hypotonia, respiratory depression and hypothermia, and are probably best
avoided in a viable gestation pregnancy.
Opioids have similar potential for fetal dependence and withdrawal, but again this is unlikely to
result from short-term anaesthetic use. Peripartum opioid use results in reversible respiratory
depression.
Non-steroidal anti-inflammatory drugs in the third trimester have been linked to premature
closure of the ductus arteriosus, tricuspid incompetence and pulmonary hypertension. They have been
associated with a range of fetal and neonatal effects consistent with their side-effect profile
(including platelet dysfunction and intracranial haemorrhage, renal impairment and gastrointestinal
bleeding), and their use should be avoided after 32 weeks gestation.
Neuromuscular blocking agents are polar molecules that do not readily cross the maternal
placental barrier and are safe to use in late pregnancy.
The antiemetic prochlorperazine has been associated with neonatal jaundice and extrapyramidal
side effects when used in high dose late in pregnancy.
Fetal effects of deranged maternal physiology
Organogenesis phase
There is some evidence that chronic hypercarbia and hyperthermia may be teratogenic, but it seems
unlikely that anaesthesia would result in such exposure.
Later pregnancy
Derangements in maternal physiology that are precipitated or exacerbated by anaesthesia are likely to
impact on the fetus by their effects on uteroplacental perfusion and oxygen delivery. Regardless of the
cause of reduced uteroplacental perfusion, the fetal effects are similar: acidosis and fetal hypoxaemia
will result. The insult may result in fetal injury, ranging from transient mild acidosis or hypoxaemia to
brain injury, and ultimately to fetal death if the injury is unrecognized or untreated.
Uteroplacental blood flow

Reduced uteroplacental blood flow results most commonly from aortocaval compression, and is
preventable with careful positioning during anaesthesia. Unrecognized and untreated reduction in
circulating volume (whether absolute, as in haemorrhage, or relative as in sepsis) will reduce
placental perfusion, and may do so without overt maternal hypotension because of the additional
mobilized cardiac reserve in pregnancy.
Oxygen homeostasis
Fetal compensation to moderate, transient maternal hypoxaemia occurs by increased oxygen
extraction, and may be well tolerated by the healthy fetus. This compensation is facilitated by fetal
haemoglobin HbF, which has a high affinity for oxygen and which avidly binds maternal oxygen.
However, an acidotic fetus will demonstrate a rightward shift in the oxygen dissociation curve, with
reduced affinity for maternal oxygen. An acidotic fetus does not tolerate maternal hypoxia well.
In severe maternal hypoxia the maternal compensatory response is to divert flow to vital
maternal organs, and away from the placenta. Uterine vasoconstriction results, reducing oxygen
delivery to the fetus.
Carbon dioxide homeostasis

Carbon dioxide and its effects on acidbase balance may affect the fetus directly, by diffusing into the
fetal circulation, and indirectly by the affecting uterine blood flow. Maternal hypercarbia results
directly in fetal hypercarbia and respiratory acidosis. This results in a rightward shift in the fetal
oxygen dissociation curve, with a consequent reduction in fetal oxygen extraction, leaving the fetus
vulnerable to the effects of co-existent hypoxia. Fetal hypercarbia and acidosis also impair fetal
myocardial contractility.
Maternal hypercarbia results in uterine vasodilation and increased uteroplacental flow, although
severe hypercarbia may reduce uteroplacental flow by causing vasoconstriction. Maternal hypocarbia
is poorly tolerated by the fetus, because hypocarbia and alkalaemia result in uterine vasoconstriction,
reducing uteroplacental blood flow.
Miscarriage and premature delivery

The evidence for an increased risk of miscarriage following anaesthesia and surgery in pregnancy
comes mainly from large retrospective studies of pregnancy outcomes following incidental surgery
and anaesthesia. Further evidence is extrapolated from epidemiological studies linking occupational
exposure to nitrous oxide and volatile anaesthetic agents with increased miscarriage rates.
Brodsky et al. showed an increase in the spontaneous abortion rate from the baseline of 5.1% to
8% in the first trimester pregnancies following anaesthesia and surgery. This seemed to be unrelated
to the site of surgery, and abdominal and pelvic surgery was not more likely than remote surgery to
induce miscarriage.
The increase in spontaneous abortion in the second trimester from 1.4% baseline to 5.9% was
shown in pregnancies exposed to incidental surgery and anaesthesia, again irrespective of the
anatomical site of surgery.
Once a pregnancy is of viable gestation, incidental surgery and anaesthesia may increase the risk
of premature labour and delivery. This appears to be higher for gynaecological and abdominal
surgery, which involves manipulation of the uterus. A systematic review found the rate of premature
delivery following non-obstetric surgery to be 3.5%, with appendectomy carrying the highest risk of
premature delivery. The trend towards the use of laparoscopic techniques in parturients has raised
concerns regarding the risk of direct injury from laparoscopic instruments, and from indirect effects
of hypercarbia and pneumoperitoneum. However, a number of subsequent studies have suggested that
laparoscopy is not associated with increased risk of pregnancy loss or poor fetal outcome.
Maternal considerations and the conduct of anaesthesia

during pregnancy
A detailed review of the physiology of pregnancy has been covered in Chapter 1. This chapter
considers the changes relevant to anaesthesia and the conduct of anaesthesia in pregnancy. An
appreciation of the normal physiology of pregnancy in each trimester is important, because
maintenance of normal physiological parameters during anaesthesia is important for both the
parturient and the developing fetus. Equally, the altered physiology of pregnancy impacts on the way
the parturient responds to anaesthesia, and on the potential risks of anaesthesia and anaesthetic
procedures including tracheal intubation.
Planning and preoperative preparation

Elective operations should not be undertaken during pregnancy, and should be postponed until after
delivery where possible. If surgery is necessary, ideally it should be delayed until the second
trimester in order to avoid the organogenesis phase. Surgery in the third trimester is associated with a
risk of premature labour. Deferring surgery until six weeks post partum allows a return to the non-
pregnant state, thus reducing the incidence of perioperative thromboembolism.
When consent is sought from a pregnant woman for incidental surgery, the risks of anaesthesia
both to her, the pregnancy and the fetus should be discussed.
Consideration should be given to where the surgery is performed. If the pregnancy is viable,
surgery should be conducted where facilities for obstetric and neonatal care are available. Planning
should involve a multidisciplinary approach, and should include obstetric, midwifery and
neonatology teams where appropriate. The pregnancy will require monitoring postoperatively, and
might affect where postoperative care is delivered.
Preoperative assessment should include a thorough airway assessment. Prokinetics and antacid
premedication should be administered.
Mode of anaesthesia
There is no evidence that regional anaesthesia is less likely than general anaesthesia to result in
miscarriage or premature delivery. There are other reasons, however, to consider a regional or local
anaesthetic technique where possible. Fetal exposure to drugs is less with a regional technique.
Regional techniques avoid instrumentation of the airway and the risks of difficult and failed
intubation, gastric contents regurgitation and aspiration, and the derangements in maternal oxygen and
acidbase homeostasis that result from mechanical ventilation.
General anaesthesia
Respiratory and airway

The incidence of difficult or failed tracheal intubation is higher in the obstetric population than in the
general population, with an estimated frequency of 1:224. For similar reasons, mask ventilation may
be more difficult as pregnancy progresses. Nasal intubation is not recommended as nasal mucosal
congestion increases the risk of bleeding.
Perioperative hypoxia can be attributed to increased maternal oxygen consumption, compounded
by a reduced functional residual capacity that is further compromised in a supine position. Thorough
preoxygenation and denitrogenation is therefore important.
The tendency to acid reflux from early in the second trimester results in an increased risk of
aspiration of gastric contents during general anaesthesia. Protection of the airway by performance of
rapid sequence induction with cricoid pressure and endotracheal intubation is advised from the
second trimester in order to minimize the risk.
Cardiovascular
Compression of the inferior vena cava by the gravid uterus in the supine position must be avoided by
anaesthetizing parturients in a left lateral tilt position, or by manual lateral displacement of the uterus.
As pregnancy progresses, cardiac output increases as a result of an increased stroke volume,
heart rate and circulating blood volume. This increased cardiovascular reserve allows the healthy
parturient to compensate efficiently for reduction in blood volume from haemorrhage. It is important
to appreciate that a reduction in blood pressure may be a late sign of hypovolaemia.
Pregnancy is a prothrombotic state and measures to reduce the risks of perioperative deep
venous thrombosis should be taken.
General anaesthetic drugs

A reduction in blood flow to the uteroplacental unit can occur with intravenous induction agents that
precipitate maternal hypotension. A comparison of the effects of propofol and thiopental can be found
i n Chapter 11. Studies have shown that propofol obtunds the maternal hypertensive response to
laryngoscopy and intubation to a greater extent than thiopental. A study has shown that maximal
noradrenaline concentrations are higher in parturients induced with thiopental compared with
propofol (although adrenaline concentrations are similar). This could lead to uterine vasoconstriction
and reduced uterine blood flow; however, in the study neonatal outcomes were the same. Ketamine
may increase uterine flow in the third trimester, by increasing cardiac output and blood pressure, but
there are concerns about its tendency to increase uterine tone, and its potential for causing persisting
behavioural changes even after a single-dose fetal exposure. Etomidate has been used for caesarean
section, but unproven concerns exist over its potential to suppress fetal cortisol production and render
the fetus vulnerable to hypoglycaemia.
Volatile anaesthetic agents during pregnancy can reduce uterine perfusion by reducing maternal
blood pressure; however, these effects are partially compensated by uterine vasodilation and
relaxation, which tend to increase uterine blood flow. All volatile agents appear to be safe for use in
pregnancy, although nitrous oxide is teratogenic in animals under certain conditions. Pregnancy
increases sensitivity to volatile agents, reducing the minimum alveolar concentration value.
Neuromuscular blocking agents are safe to use in pregnancy, and cross the placenta only
minimally. It should be borne in mind that their effects may be prolonged slightly by altered hepatic
metabolism (rocuronium and vecuronium) or reduced plasma cholinesterase levels (suxamethonium)
in pregnancy.
Uterine blood flow should be maintained by avoiding maternal hypotension. Phenylephrine has
been shown at caesarean section to maintain uterine flow, while preserving fetal acidbase status,
and is the suggested drug for treating maternal hypotension.
Intraoperative hypertension results in uterine vasoconstriction and reduced uterine flow, and
should also be avoided. Labetalol, hydralazine, glyceryl trinitrate and magnesium sulfate are all safe
alternatives for lowering blood pressure in pregnancy.
Postoperative analgesia should be optimized to avoid maternal catecholamine surges that can
lead to a reduction in uterine blood flow. Regional anaesthetic techniques, opioids and simple
analgesia are all safe. Non-steroidal anti-inflammatories should be avoided.
Regional anaesthesia
Regional anaesthesia is the preferred technique, where possible, for surgery during pregnancy. It may
be precluded, however, by the nature of the proposed surgery, maternal refusal, sepsis or coagulation
concerns (including pregnancy-induced thrombocytopenia which occurs in 1% of pregnancies).
Amide anaesthetics bupivacaine, lidocaine and ropivacaine have been shown to be safe in pregnancy,
and central neuraxial block techniques are widely used in obstetric anaesthetic practice. A smaller
dose is required per dermatomal block in pregnancy. Fetal compromise may occur when maternal
hypotension is untreated, and care must be taken to treat hypotension and maintain adequate
circulating volume.
Fetal monitoring
Previability (2325 weeks) it is good practice for fetal heart auscultation using hand-held doppler to
be performed before and after elective surgery to reduce maternal anxiety and prevent any potential
litigation.
After viability, fetal assessment with ultrasound or CTG may be appropriate. This depends on
the nature of the surgery and whether it is elective or emergency. Intraoperative monitoring of the fetal
heart is not necessary as if concerns regarding fetal wellbeing are present then obstetric involvement
is needed, as delivery of the fetus may be necessary.
Key points
1. Surgery during pregnancy should be avoided and deferred where possible.
2. The risk of miscarriage is lowest in the second trimester, and the risk of premature labour and
delivery is highest in the third trimester.
3. Most anaesthetic drugs appear to be clinically safe in pregnancy, and have been used with no
apparent maternal or fetal harm.
4. Some drugs should be avoided in later pregnancy.
5. Careful maintenance of the normal physiology of pregnancy is important, both for maternal
wellbeing and for fetal outcome.
6. Considered planning for incidental surgery in pregnancy should involve a multidisciplinary

team approach, with thought for timing, location, personnel involved and the need for
perioperative fetal monitoring.
Further reading
Boivin, J-F. (1997). Risk of spontaneous abortion in women occupationally exposed to anaesthetic
gases: a meta-analysis. J. Occup. Env. Med., 54(8), 541548.
Brodsky, J. B., Cohen, E. N., Brown, B. W. Jr, Wu, M. L., Witcher, C. (1980). Surgery during
pregnancy and fetal outcome. Am. J. Obstet. Gynecol., 138, 165167.
Cohen-Kerem, R., Railton, C., Oren, D., Lishner, M., Koren, G. (2005). Pregnancy outcome
following non-obstetric surgical intervention. Am. J. Surg., 190(3), 467473.
Hudspith, M. (2002). Anaesthesia during pregnancy. In Collis, R., Plaat, F., Urquhart, J. (eds.),
Textbook of Obstetric Anaesthesia. London: Greenwich Medical Media Ltd.
Iwamoto, H. S. (1993). Cardiovascular effects of acute fetal hypoxia and asphyxia. In Hanson, M.,
Spencer, J. A. D., Rodeck, C. H. (eds.), Fetus and Neonate: Physiology and Clinical Applications.
Cambridge: Cambridge University Press.
Mazze, R. I. and Kallem, B. (1989). Reproductive outcome after anesthesia and operation during
pregnancy: a registry study of 5405 cases. Am. J. Obstet. Gynecol., 161, 11781185.
Mickley, G. A., Kenmuir, C. L., McMullen, C. A. et al. (2004). Long-term age-dependent behavioral
changes following a single episode of fetal N-methyl-D-aspartate (NMDA) receptor blockade. BMC
Pharmacol., 4(1), 28.
Reitman, E. and Flood, P. (2011). Anaesthetic considerations for non-obstetric surgery during
pregnancy. Br. J. Anaesth., 107(1), 7278.
Sadot, E., Telem, D. A., Arora, M. et al. (2010). Laparoscopy: a safe approach to appendicitis during
pregnancy. Surg. Endosc., 24(2), 383389.
Sylvester, G. C., Khoury, M. J., Lu, X. and Erickson, J. D. (1994). First-trimester anesthesia exposure
and the risk of central nervous system defects: a population-based case-control study. Am. J. Public
Health, 84(11), 17571760.
Chapter 9
Non-regional analgesia techniques for labour

Gordon Yuill
On 19 January 1847, James Young Simpson used diethyl ether to anaesthetize a woman with a
deformed pelvis for delivery, to widespread opposition and consternation from his contemporaries,
questioning its safety and his wisdom.
The controversy about the delivery of Queen Victorias eighth child, Prince Leopald, in 1853
was such that her Court physicians publically denied that John Snow had anaesthetized her with ether
to ease the pain. Four years later the issue was less controversial and it was widely acknowledged
that Queen Victoria had received an anaesthetic to help her with the birth of Princess Beatrice, her
ninth child. Anaesthesia for childbirth had become part of medical practice by 1860, in large part in
response to the demands of women.
Our armamentarium for the management of labour has thankfully grown somewhat since the
nineteenth century. This chapter will discuss the non-regional techniques (non-pharmacological and
pharmacological) that are available in the UK.
The Cochrane Collaboration

In 2012 The Cochrane Collaboration summarized the evidence from Cochrane and non-Cochrane
systematic reviews on the efficacy and safety of non-pharmacological and pharmacological
interventions to manage pain in labour. This represented over 300 trials within 18 systematic reviews
and they were able to categorize the interventions into: What works (epidural, combined spinal and
epidural, inhaled analgesia), What may work (immersion in water, relaxation, acupuncture,
massage, local anaesthetic nerve blocks, non-opioid drugs) and Insufficient evidence to make a
judgement (hypnosis, biofeedback, sterile water injections, aromatherapy, transcutaneous electrical
nerve stimulation (TENS), parenteral opioids).
Non-pharmacological methods
Many non-pharmacological methods have been tried for the relief of labour pain, with varying
success and much interindividual variability. Women may consider these options as an integral and
important part of their labour experience, despite the benefits often being intangible and not easily
documented by scientific method. It is important that the anaesthetic provider is aware of some of
these techniques, their benefits and limitations, in order to be able to have a full and informed
discussion with their patient. The 2012 Cochrane overview found some evidence to suggest that
immersion in water, relaxation, acupuncture and massage may work, whilst there was insufficient
evidence for hypnosis, biofeedback, sterile water injections, aromatherapy or TENS. Table 9.1
provides a useful summary.
Table 9.1 Complimentary methods of pain relief.
Mechanism of action Advantages Disadvantages Evidence
TENS Based on gate theory Non- Useful only in Systematic review of

invasive, early labour, eight RCTs failed to
easy to use, cost demonstrate analgesic
good for implications effect
back pain
Immersion Sensation of warm water Popular, Cannot use Cochrane review of

inhibits pain backed by with other three trials. No
transmission and Government methods, difference in pain
supports gravid uterus Health limited relief between
Committee accessibility, immersion groups.
temporary Systematic review of
seven RCTs: mixed
results
Massage Inhibits pain Perceived as Labour One RCT with 28

transmission, provides highly intensive women showed
support and distraction effective by physical and
those using it emotional benefits
Acupuncture Stimulates specific Drug free Invasive, need One RCT with 100
(acupressure, points on body with fine trained women in Sweden
needles (or pressure or therapist, can comparing
laser
laser); may inhibit pain take 30 min for acupuncture suggested
acupuncture) transmission or produce effect former group needed
natural endorphins less analgesia,
including epidurals
Waterblocks Injection of 0.1 ml sterile Easy to Temporary Two double-blind

water in four spots over perform, relief only RCTs showed
sacrum. Action similar to (4590 min), reduction in labour
good for
TENS initial burning pain, but other work
back pain sensation showed they were not
rated by women as
effective as other
methods
Continous Presence of trained Popular, None Cochrane review of

support support person can useful in any 15 RCTs involving
improve the stage 12,791 women. Those
physiological and with continuous
psychological aspects of support, as opposed
labour to conventional care,
were less likely to
have intrapartum
analgesia, operative
birth or be
dissatisfied with their
experiences
Hypnosis Entering a hypnotic state Non- Not all women Cochrane review of
to have better control invasive susceptible three RCTs: one
over the pain (1020% are reported less
not), time anaesthesia and
consuming, can another less narcotic
be harmful use, but overall meta-
analysis showed no
difference in the need
for pain relief
Aromatherapy Use of essential oils of Non- Individual One small (n=22)
plants and flowers for invasive sensation of RCT compared ginger
therapeutic effect smell, so oils with lemongrass no
need to be difference in pain
tested scores or
pharmacological pain
relief
Homeopathy A minute amount of a Needs to be No RCTS

substance can be used to individualized
alleviate symptoms (like
cures like)
RCT = randomized controlled trial, TENS = Transcutaneous electrical nerve stimulation
(Reproduced from Fortescue C, Wee MYK (2005). Analgesia in labour: non-regional
techniques. Continuing Education in Anaesthesia, Critical Care & Pain; 5: 913 with permission
from Oxford University Press.)
Pharmacological methods
Although a whole array of drugs has been used for the pain of labour, parenteral opioids and
inhalational analgesia have formed the mainstay of non-regional methods. Despite being less
efficacious than regional analgesia, they are more widely available, cheaper, more simple to
administer, less labour intensive and often more culturally acceptable. Thus, opioids and inhalational
techniques are more widely used around the world, especially in areas where epidural availability is
poor.
Parenteral opioids
Opioids have a long history as labour analgesics. They can be given via numerous routes (sub-
cutaneous, intramuscular or intravenous), by either an intermittent bolus or patient-controlled
technique. As -agonists that readily cross the placenta, they are all capable of maternal sedation,
respiratory depression, loss of protective airway reflexes, and the risk of neonatal depression.
The Cochrane overview in 2012 concluded that there was insufficient evidence that parenteral
opioids were more effective than placebo or other interventions for pain management in labour.
Intermittent bolus
Pethidine (meperidine)
Pethidine was introduced into obstetric practice in the 1940s. It has remained the most widely used
intermittent bolused opiate worldwide. It was first made legally available in 1950 in the UK for
midwives to use independently. A survey of UK practice in 2008 found that 84% of UK units still
used pethidine for labour analgesia despite significant doubts to its efficacy. This is probably due to
familiarity, ease of administration, low cost and lack of evidence of a superior alternative. Some
women find they are more able to cope with their labour pains due to its ability to provide sedation,
dysphoria and amnesia.
It is a synthetic, phenylpiperidine derivative that is an agonist at - and -opioid receptors. It is
used in a dose of 50150 mg IM, which may be repeated 4 hours later. Onset of pain relief occurs
within 45 minutes and lasts 2 to 3 hours.
The Cochrane overview in 2012 found that compared to other opioids more women receiving
pethidine experienced adverse effects, including impaired capacity to engage in decision-making
about care, sedation, hypoventilation, hypotension, prolonged labour, urine retention, nausea,
vomiting and a slowing of gastric emptying.
It rapidly crosses the placenta, equilibrating within 6 minutes, and it has been shown to cause
decreased fetal heart rate variability within 25 to 40 minutes that can last for an hour. It has a
maternal half-life of 2.5 to 3 hours, but a more prolonged neonatal half-life of up to 18 to 23 hours.
Pethidine is metabolized in the liver to its active metabolite norpethidine, which is a potent
respiratory depressant with convulsant properties, which can accumulate with repeated doses, and
has a half-life in the neonate of 60 hours. It should be used with caution in women with severe pre-
eclampsia and other causes of renal impairment. The babies of women who have received pethidine
in labour have been shown to be sleepier, less attentive, at risk of neonatal respiratory depression
and hypothermia, and less able to establish breastfeeding, despite normal Apgar scores at birth.
However, about 10% of neonates will have a 1 minute Apgar score of <6 if pethidine is given 23
hours before delivery, as this coincides with peak fetal concentrations. The incidence is reduced if
given before or after this.
Diamorphine
Diamorphine is a synthetic derivative of morphine and is widely used as a labour analgesic in the
UK. In the 2008 UK survey of practice it was found that diamorphine was used in 34% of units, and
more frequently than pethidine in some areas. In other surveys it is rated better than pethidine and
Entonox by both midwives and parturients. It is essentially a pro-drug that is rapidly metobolized to
6-mono-acetylmorphine, an active metabolite that is more lipid soluble than morphine, before further
breakdown to morphine. This increased lipid solubility accounts for its rapid onset, but also for its
speed across the placenta, suggesting that infants born shortly after maternal diamorphine
administration are at greater risk of respiratory depression. It is usually given in a dose of 57.5 mg
IM. Most studies comparing pethidine and diamorphine find that neither drug works well, with almost
50% of women reporting poor pain relief and up to 40% of women requesting second-line analgesia.
However, patients who receive pethidine are more likely to report no pain relief and the incidence of
vomiting is lower in the diamorphine group. Pethidine was also associated with lower Apgar scores
at 1 minute.
Morphine
Morphine is possibly the first opiate used as an analgesic in labour. Morphine is rarely prescribed in
labour in the UK. Its dose is 2 to 5 mg IV or 5 to 10 mg IM. It rapidly crosses the placenta, but rapid
maternal elimination decreases fetal exposure. Its side effects are dose-related and similar to those of
pethidine, without having a pro-convulsant metabolite. Some studies have shown that neither
pethidine nor morphine reduce pain scores, but they do both increase sedation. It was popular in the
1920s and 1930s, and used with hyoscine to induce twilight sleep for labour and delivery. Women
frequently had little memory of labour or of being in pain.
Fentanyl
Fentanyl is a tertiary amine, which is a synthetic phenylpiperidine derivative. It is a highly selective
-agonist, is highly lipid soluble and has an analgesic potency 100 times that of morphine and 800
times that of pethidine. Its high lipid solubility gives it a rapid onset, which combined with a short
duration of action and a lack of metabolites makes its use in labour attractive. However, it may
accumulate after large or multiple doses and studies have shown it to have a similarly poor analgesic
effect as pethidine.
Other opioids
Other opioids, including those with partial agonist and agonist/antagonist properties have been used
in labour.
The systemic opioids that are used for labour analgesia are summarized in Table 9.2.
Table 9.2 Systemic opioids for labour analgesia.
Drug Usual Dose Onset Duration Comments
Meperidine 2550 mg IV 510 min IV 23 h Has an active metabolite

50100 mg IM 4045 min IM with a long half-life
Maximal neonatal
depression 14 h after dose
Morphine 25 mg IV 35 min IV 34 h More neonatal respiratory

510 mg IM 2040 min IM depression than meperidine
Has an active metabolite
Diamorphine 57.5 mg IV/IM 510 min IM 90 min Morphine pro-drug

More euphoria, less
nausea than with morphine
Fentanyl 2550 g IV 23 min IV 30 Usually administered as an

100 g IM 10 min IM 60 min infusion or by PCA
Accumulates during an
infusion
Less neonatal depression
than with meperidine
Nalbuphine 1020 mg IV/IM 23 min IV 36 h Opioid against/antagonist

15 min IM/SQ Ceiling effect on
respiratory depression
Lower neonatal
neurobehavioural scores
than with meperidine
Butorphanol 12 mg IV/IM 510 min IV 34 h Opioid against/antagonist

1030 IM Ceiling effect on
respiratory depression
Meptazinol 100 mg IM 15 min IM 23 h Partial opioid agonist

Less sedation and
respiratory depression than
with other opioids
Pentazocine 2040 mg IV/IM 23 min IV 23 h Opioid against/antagonist

520 min Psychomimetic effects
IM/SQ possible
Tramadol 50100 mg IV/IM 10 min IM 23 h Less efficacy than with

meperidine
More side effects than
meperidine
IM, intramuscular; IV, intravenous; PCA, patient-controlled analgesia; SQ, sub-cutaneous

(Reproduced from Chestnut DH, Polley LS, Tsen LC, Wong CA (2009). Chestnuts Obstetric
Anesthesia: Principles and Practice, 4th Edition. Philadelphia, PA: Elsevier. ISBN: 978-0-323-
05541-3 with permission from Elsevier.)
Patient-controlled analgesia
Patient-controlled analgesia (PCA) for labour has been used clinically since the 1970s, offering an
attractive alternative when neuraxial anaesthesia is unavailable, contraindicated or unsuccessful. By
giving the parturient a degree of control it offers high levels of satisfaction, despite only average
reductions in pain scores. Concerns about the potential to cause harm should not be taken lightly
though. Respiratory depression is a real possibility when the use of potent opioids and the reliance on
safe administration, dosing and equipment are combined. Opioids such as pethidine, morphine,
diamorphine, fentanyl, alfentanil and nalbuphine have all been used in this way, but the most
appropriate drug, dose and dosing schedule has not been defined.
The introduction of remifentanil in the 1990s has led to an explosion in interest in using
remifentanil patient-controlled analgesia for labour.
Remifentanil patient-controlled analgesia

Remifentanil is a 4-anilido-piperidine derivative of fentanyl, which is an ultra-short acting -1
opioid receptor agonist. It has a low volume of distribution, low lipid solubility, a terminal half-life
of <10 minutes, and its context-sensitive half-life of 3.5 minutes is independent of the duration of the
infusion. Bloodbrain equilibrium occurs in 1.2 to 1.4 minutes and it is rapidly metabolized by
plasma and tissue esterases to an inactive metabolite. In theory, the rapid onset of analgesia offers
advantages for labour analgesia. The timing of delivery of each bolus is crucial: if it occurs at the
beginning of a 70-second contraction it is likely to be effective for the following one. It crosses the
placenta rapidly; however, the mean umbilical artery-to-umbilical vein concentration ratio is 0.29,
demonstrating that the drug is rapidly metabolized and redistributed in the fetus. This pharmacokinetic
profile gives remifentanil an advantage over other opioids used for labour analgesia. It has been
shown to be superior to inhalational analgesia, pethidine IM and PCA, and fentanyl PCA in labour,
with greater reduction in pain scores, lower rates of conversion to epidural analgesia and better
overall satisfaction. It seems that remifentanil produces clinically effective, but not complete,
analgesia, with about a 10% conversion rate to neuraxial analgesia.
Whilst no ideal regimen has been identified, the timing of dose administration, the rate of bolus
delivery and the lockout interval are important to analgesia outcome. In the UK it is available in over
one-third of units, with almost half of all other units expressing an intention to introduce it. One-third
of those using remifentanil offer it as a routine method of pain relief, the remainder limit its use to
those who cannot have regional analgesia. The most popular regimen in the UK is a 40 g bolus with
a 2-minute lockout. There is some debate about whether a 3-minute lockout would be more
appropriate, as shorter lockouts allow additional doses to be received before maximal side effects
(and peak analgesic effects) have occurred. There is a wide interindividual variability and tolerance
has been shown to occur.
Maternal side effects are transient, and include sedation, hypoventilation, oxygen desaturation,
nausea and vomiting. However, there is no room for complacency, as case reports of respiratory
and/or cardiac arrest demonstrate. Thus, a strict protocol is mandatory. The most important criterion
is continuous one-to-one care with a competency-assessed midwife. The other essential requirements
include: a dedicated intravenous cannula, an antireflux valve on the administration line, monitoring of
sedation level and respiratory rate and continuous oxygen saturation monitoring (see Table 9.3).
Table 9.3 Suggested guidelines for remifentanil PCA in labour.
Eligibility
Informed consent
No opioid use in the previous 4 h

Dedicated IV cannula for remifentanil administration
PCIA protocol
PCIA bolus: 40 g
Lockout interval: 2 min
Continuous observations
SaO2 (pulse oximetry)
Nursing supervision: one-to-one
30-min observations
Respiratory rate
Sedation score
Pain score
Indications for contacting the anaesthesia provider
Excessive sedation score (not arousable to voice)
Respiratory rate <8 breaths/min
SaO2 <90% while breathing room air
Sample guidelines adapted from those used by the Ulster Community and Hospitals Trust, Ulster,
United Kingdom. Labour nurses must establish competency in the use of remifentanil PCIA before
providing care.
PCIA patient-controlled IV analgesia.
(Reproduced from Hinova A, Fernando R (2009). Systemic Remifentanil for Labor Analgesia.
Anesthesia and Analgesia 109: 19251929 with permission from Wolters Kluwer Health.)
Despite concerns about neonatal depression, fetal heart rate abnormalities and accumulation in
the neonate, no study has identified an increased incidence of non-reassuring fetal heart rate
recordings, and Apgar scores, neurobehavioural scores and umbilical cord gases have all been at
least as good as those using pethidine or epidural analgesia.
Inhalational methods
As we have already seen, inhalational analgesia for childbirth has been used since the nineteenth
century. The most commonly used agent is nitrous oxide, with some interest in halogenated agents.
Entonox
Entonox is the trade name given to a 50/50 mixture of oxygen and nitrous oxide. It was invented by Dr
Mike Tunstall in 1961, approved for unsupervised use by midwives in 1965, and available in 99% of
obstetric units in the UK in 1990, being used by 60% of parturients. It is uncommon in the USA, but is
used in up to 86% of units in Canada. Its low blood-gas solubility (0.47) means that it equilibrates
rapidly with blood, and as it washes out of the lungs rapidly there is minimal accumulation. At normal
temperatures both components are present in pressurized cylinders in the gaseous phase (due to the
Poynting effect); liquefaction of nitrous oxide and separation of the two components may occur at
temperatures of 7 C.
Evidence for the efficacy of Entonox is conflicting, although distraction, relaxation and sense of
control all increase its subjective benefit. Technique of use and maternal cooperation are required.
Parturients should be trained to time maximum effect with peak contraction pain, by inhaling from the
very beginning of the contraction through to its end.
Adverse effects include drowsiness, disorientation and nausea. The risk of maternal
hypoventilation, diffusion hypoxia and desaturation are increased with concomitant use of opioids.
There is a theoretical risk of bone marrow suppression with prolonged use, and there may be an
occupational risk to midwives if not scavenged or used in poorly ventilated rooms.
Halogenated agents
Up to the 1970s, chloroform, trichloroethylene, and methoxyflurane had all been used by midwives
for labour analgesia. This is no longer allowed and an anaesthetist must now be present. This, and the
need for specialized equipment, concerns for their tocolytic effects, environmental pollution, and the
potential for maternal amnesia, altered consciousness and loss of protective airway reflexes,
currently limits the routine use of inhaled halogenated agents.
Isoflurane
Isoflurane was first reported for labour analgesia in 1975, and at a level of 0.75% in air it produces
better analgesia than Entonox, but with an increase in maternal sedation. Lower levels (0.25% in air)
also produced better analgesia than Entonox, but maternal satisfaction was no better.
Desflurane
Desflurane has a lower blood-gas partition coefficient (0.42) than nitrous oxide, thus also allowing
rapid onset and offset of action. When 1% to 4% desflurane in oxygen was compared to 30% to 60%
nitrous oxide analgesia, scores were found to be similar, but at the expense of a high amnesia rate
(23%).
Sevoflurane
Sevoflurane has been studied and found to have an optimal concentration of 0.8% for labour
analgesia. At this level it is more effective than Entonox without desaturation, apnoea, or change in
end-tidal CO2. Apgar scores were unaffected. Its odour does have to be tolerated and subjective
sleepiness seems to be increased compared with Entonox.
Key points
1. A wide variety of non-pharmacological pain-relief methods have been used with varying
success. It is important to empower and support the parturient who wishes to utilize these
methods.
2. Parenteral opioids have a long history as labour analgesics. They are easy to utilize, have
well recognized side-effect profiles and so are commonly used worldwide.
3. PCA offers parturients a level of control that is reflected in its high satisfaction scores.
4. Remifentanil has many desirable characteristics as a labour analgesic, but the rigorous use of
protocols is mandatory.
Further reading
Fairlie, F. M., Marshall, L., Walker, J. J. and Elbourne, D. (1999). Intramuscular opioids for
maternal pain relief in labour: a randomised controlled trial comparing pethidine with diamorphine.
Br. J. Obstet. Gynaecol., 106, 11811187.
Fortescue, C. and Wee, M. Y. (2005). Analgesia in labour: non-regional techniques. CEACCP, 5,

913.
Fernando, R. and Jones, T. (2009). Systemic analgesia: parenteral and inhalational agents. In
Chestnut, D. H., Polley, L. S., Tsen, L. C. and Wong, C. A. (eds.) Chestnuts Obstetric Anesthesia:
Principles and Practice, 4th edn. Philadelphia, PA: Elsevier.
Harries, S. and Turner, M. (2008). Non-regional labour analgesia. In Clyburn, P., Collis, R., Harries,
S. and Davies, S. (eds.) OSH Obstet. Anaesth. Oxford: Oxford University Press.
Smith, S., Scarth, E. and Sasada, M. (2011). Drugs in Anaesthesia and Intensive care, 4th edn.
Oxford: Oxford University Press.
Hinova, A. and Fernando, R. (2009). Systemic remifentanil for labor analgesia. Anesth. Analg. 109,
19251929.
Hughes, D. and Foley, P. (2013). The case for remifentanil PCA as labour analgesia. RCA Bull., 78,
68.
Jones, L., Othman, M., Dowswell, T. et al. (2012). Pain management for women in labour: an
overview of systemic reviews. Cochrane Database Syst. Rev. 2012(3), Art. No.: CD009234.
Muchatuta, N. A. and Kinsella, S. M. (2013). Remifentanil for labour analgesia: time to draw breath?
Anaesthiology, 68, 231235.
Oloffson, C., Ekblom, A., Ekman-Ordeberg, G. et al. (1996). Lack of analgesic effect of systemically
administered morphine or pethidine on labour pain. Br. J. Obstet. Gynaecol., 103, 968972.
Tuckey, J. P., Prout, R. E. and Wee, M. Y. (2008). Prescribing intramuscular opioids for labour
analgesia in consultant-led maternity units: a survey of UK practice. Int. J. Obstet. Anesth., 17, 38.
Chapter 10
Regional analgesia techniques for labour

Lawrence C. Tsen
Introduction
Regional analgesia, which is pain relief delivered to a discrete region of the body, encompasses a
variety of methods (Table 10.1), of which central neuraxial [e.g. epidural, spinal, combined spinal
epidural (CSE) and dural puncture epidural (DPE)] techniques provide the most effective analgesia
for all stages of labour and delivery (Box 10.1).
Table 10.1 Regional analgesia techniques
Regional technique Method Obstetric stages of Comments

labour
Paracervical block Nerve ganglion block 1st stage May cause fetal
by uterine cervix bradycardia from fetal
absorption
Lumbar sympathetic In lumbar region 1st stage Multiple, technically

block challenging injections
Pudendal block Terminal pudendal 2nd stage Not effective for

nerve blockade uterine cavity, cervix
or upper vaginal repair
Perineal infiltration Terminal sensory 2nd stage Effective for blocking

nerves in perineum perineal sensation only
Neuraxial techniques 1st, 2nd and 3rd stages Spinal opioids alone
will provide analgesia
limited to early 1st
stage
Box 10.1 Stages of labour and delivery
Stage Parameters Source of Pain Spinal Cord Level
First Onset of labour until Peripheral nociceptors in Visceral afferent neurons,

complete cervical the lower uterine segment enter 10th to 12th thoracic
dilation and cervix and 1st lumbar spinal
segments
Second Pushing and delivery of Distention of vagina and Somatic afferent fibres in
the fetus perineum pudendal nerve, enter 2nd
to 4th sacral spinal
segments
Third Delivery of the placenta Distention of vagina and Somatic afferent fibres in
perineum pudendal nerve enter 2nd
to 4th sacral spinal
segments
Patient benefits and concerns

The benefits of neuraxial techniques during labour include improved pain scores when compared to
other forms of analgesia, minimal fetal exposure to analgesic medications, and improved maternal
satisfaction with the overall birth experience. Biochemically, neuraxial techniques reduce maternal
plasma concentrations of stress catecholamines, which may improve uteroplacental perfusion and the
effectiveness of uterine contractions; hyperventilation is also reduced, which diminishes the leftward
shift in the maternal oxyhaemoglobin dissociation curve and improves fetal oxygen delivery.
Neuraxial techniques improve the success of external cephalic versions, the delivery of multiple
gestation infants and the removal of products of conception. Finally, the presence of catheter-based
neuraxial techniques for labour analgesia can provide for the rapid conversion to anaesthesia should
an emergent operative procedure occur; avoidance of the maternal airway, which can undergo
significant engorgement during pregnancy and labour is a favourable action plan, given the untoward
implications of a difficult intubation or extubation on maternal and fetal wellbeing.
Among the most frequent concerns vocalized by parturients is whether neuraxial analgesia
affects the progress and outcome of labour. In parturients of mixed parity, a prolongation of the first
and second stages of labour by 42 minutes and 14 minutes, respectively, has been observed with the
use of epidural analgesia compared to parenteral opioids. Moreover, maintenance of epidural
analgesia with intermittent boluses of 0.25% bupivacaine (which is more concentrated than that
typically used in contemporary practice) has been associated with a higher proportion of instrumental
deliveries, when compared to CSE techniques or parenteral opioids. However, the rate of caesarean
delivery is not increased with the use of neuraxial techniques. Of interest, CSE techniques may have
salutary effects on labour progress. In nulliparous parturients at less than 3 cm cervical dilation, the
use of a CSE labour analgesia technique results in faster cervical dilation and delivery by an average
of 30 minutes when compared to an epidural technique with 0.125% bupivacaine. Moreover, a
significantly shorter median time from initiation of analgesia to complete dilatation has been
observed with the CSE technique versus systemic analgesia (295 min vs. 385 min, P < 0.001); time to
vaginal delivery was shorter as well (398 min vs. 479 min, P < 0.001).
An additional concern expressed by parturients is whether the fetus is affected by neuraxially
administered medications. Indirectly, neuraxial techniques may affect uteroplacental blood flow
through alterations in maternal blood pressure and uterine tone. Correction of blood pressure
alterations can be remedied quickly, with minimal to no known adverse fetal effects. FHR changes,
which are more commonly observed following spinal or CSE analgesia, can be minimized with the
avoidance of higher opioid doses (i.e. fentanyl >50 g, and sufentanil > 7.5 g). Although most
analgesic medications, including local anaesthetics and opioids, readily cross the placenta, the doses,
when administered neuraxially, are very small, particularly in comparison to the amount of systemic
medications required to provide similar analgesia; minimal, if any, direct effect of these agents on
FHR activity or fetal wellbeing has been observed.
Indications and contraindications

Neuraxial techniques are particularly useful in patients with a difficult airway (e.g. high body mass
index), worsening co-morbidities (e.g. pre-eclampsia), or the likelihood of an urgent operative
delivery (e.g. placenta praevia, trial of labour after caesarean [TOLAC], high-order multiple
gestation or breech presentation). Such patients may be suitable for an early (prophylactic)
placement of a catheter-based neuraxial technique; aside from a small test dose (3 to 5 mL of 1.5% to
2% lidocaine) to indicate a bilateral sensory block, the catheter need not be dosed until an analgesic
or anaesthetic is requested or required.
The major contraindications to neuraxial techniques are patient refusal and the presence of an
underlying infection (e.g. meningitis, abscess), cardiac issue (e.g. hypotension), coagulation issue
(e.g. haematoma) or neurologic process (e.g. cranial herniation, puncture of tethered spinal cord)
(Box 10.2). Severe obstetric haemorrhage in the antepartum period, including uterine rupture and
acute, severe fetal distress, may also contraindicate neuraxial anaesthesia procedures because of the
time necessary to establish a surgical anaesthetic. The most controversial conditions are those
involving a decreasing platelet count, an evolving infectious process, or a fluctuating neurologic
examination.
Box 10.2 Contraindications to neuraxial techniques
Absolute contraindications
Patient refusal or inability to cooperate
Localized infection at the insertion site
Sepsis
Severe coagulopathy
Uncorrected hypovolaemia
Relative contraindications
Mild coagulopathy
Severe maternal cardiac disease (including congenital and acquired disorders)
Neurologic disease (including intracranial and spinal cord disorders)
Severe fetal depression.

Ultimately, the risks and benefits of neuraxial analgesia should be individualized, with the
patient engaged in an informed consent discussion. Included in these decisions should be the
experience of each individual anaesthetist and the environment in which care is being provided.
Types of neuraxial techniques

Epidural analgesia
Placement of a catheter into the epidural space provides an effective, reliable and titratable form of
labour analgesia (Table 10.2) that can be converted to surgical anaesthesia for an instrumental or
operative delivery, laceration repair or postpartum tubal ligation.
Table 10.2 Selection considerations for neuraxial analgesic techniques for labour.
Technique Advantages Disadvantages Comments
Continuous epidural Ability to titrate Technically more

duration, density and difficult, with possible
level of block
inadvertent epidural
needle dural puncture
Slow onset
Large drug doses
Patchy, one-sided
blocks can occur
Continuous spinal Ability to titrate Large dural puncture Complete analgesia for
st
duration, density, and with risk of headache if early 1 stage labour
with opioid alone
level of block epidural needle used
Rapid onset Possible adverse
Low drug doses events if mistaken, and
Ability to use dosed, as epidural
puncture created catheter
inadvertently with
epidural attempt
Combined spinal- Ability to titrate Delayed verification of Spinal needle can
epidural (CSE) duration, density and epidural catheter function as a finder
functionality
level of block needle to minimize
Rapid onset inadvertent dural
Low drug doses puncture with epidural
Rapid sacral spread needle
Bilateral coverage Complete analgesia
for early 1st stage
labour with opioid
alone
Dural puncture Ability to titrate Large drug doses Spinal needle can
epidural (DPE) duration, density and function as a finder
level of block needle to minimize
Ability to verify inadvertent epidural
functionality of needle dural puncture
epidural catheter Technically similar
Intermediate onset to CSE, but spinal
Intermediate sacral drugs are not given
spread through spinal needle
Improved bilateral
coverage
Single-shot spinal Technically simple Density and level

Rapid onset cannot be augmented
Low drug doses Pruritus
Rapid sacral spread
Bilateral coverage
The selection of agents for epidural administration depends on the degree and duration of pain
relief desired, with an overall goal of providing lumbar and sacral sensory analgesia with minimal
motor blockade. Epidural opioids alone can provide analgesia during the early first stage of labour;
however, a combination of opioids with local anaesthetic agents is necessary thereafter. Use of this
combination minimizes the doses, and side effects, of each component, including pruritus (e.g. an
opioid effect) and motor blockade (e.g. a local anaesthetic effect). An epidural bolus of fentanyl
100 g, with or without local anaesthetic, can be of assistance during the second stage of labour when
patchy analgesia or perineal sparing cannot be remedied with local anaesthetics alone.
Once the initial sensory blockade has been established, epidural analgesia can be maintained
with dilute solutions of local anaesthetic agents with opioids, administered by intermittent bolus
injections, continuous infusion, or both techniques simultaneously. The development of programmable
infusion pumps has enabled patient-controlled intermittent bolus top-up injections, which reduces the
total amount of medication used, decreases the amount of motor blockade, and increases patient
satisfaction when compared to a continuous infusion or intermittent bolus methodologies alone.
Spinal analgesia
The finite duration of action of a single injection (i.e. single-shot) and the increased risk of post
dural-puncture headaches with multiple injections, limit the utility of the spinal technique for labour
analgesia. However, single injection spinal techniques can be used immediately prior to vaginal
breech delivery, outlet forceps or vacuum extraction, or postpartum repairs of extensive tears or
lacerations. Various doses and types of local anaesthetics may be used; however, the selection should
consider the likelihood for caesarean delivery. Clear communication between the obstetrician and
anaesthetist is essential for the appropriate technique and agents to be chosen.
The placement of a catheter into the spinal space (i.e. spinal catheter or continuous spinal
technique) is particularly useful in patients where incremental dosing is desired (e.g. a cardiac
disorder requiring adequate filling pressures) or the expected complexity or duration of the case is
unknown (e.g. multiple gestation, morbid obesity, placenta accreta). A spinal catheter technique is
also an attractive option when an inadvertent dural puncture occurs during a planned epidural
technique.
A spinal catheter presents a significantly greater risk of a post dural puncture headache (PDPH),
particularly when a 17 or 18 gauge epidural needle and a macro- (e.g. 19 or 20 gauge) epidural
catheter is used. Smaller microcatheters (e.g. 27 to 32 gauge) allow the use of a smaller needle, but
are associated with greater technical difficulties, failures, and complications (e.g. cauda equina
syndrome, from repeated, generous dosing in an attempt to augment the level or density). Whether the
spinal catheter should remain in situ for 24 hours following delivery in an attempt to reduce the
incidence of a PDPH is controversial; the retained catheter should be knotted with the hub removed
or taped to the skin under a transparent dressing to prevent inadvertent use.
Combined spinal-epidural technique

The CSE technique consists of the insertion of an epidural needle, placement of a longer spinal
needle through the shaft of the epidural needle into the subarachnoid space (e.g. the needle-through-
needle approach), administration of spinal medications, removal of the spinal needle and placement
of an epidural catheter. In comparison to the epidural technique, the CSE technique has a number of
advantages, including a more rapid sacral sensory blockade (by approximately 6 minutes), smaller
initial drug dose and lower incidence of epidural catheter failure (Table 10.2).
A lipid-soluble opioid (fentanyl or sufentanil) is an appropriate initial spinal drug during early
labour; spinal opioid analgesia can preserve haemodynamic stability in preload-dependent cardiac
patients. Limitations with the CSE technique include spinal opioid-associated pruritus and fetal
bradycardia, which can be reduced with fentanyl doses < 50 g or sufetanil doses < 7.5 g. The CSE
technique also cannot determine if the epidural catheter is properly sited, until it is used to provide
analgesia. Moreover, with any dural puncture, the risk for PDPH and infection is present, albeit
uncommon with small-gauge (2527 gauge) pencil-point needles and good aseptic technique,
respectively.
The likelihood of a dural puncture with a 1920 gauge epidural catheter passing through a 2527
gauge spinal needle is low. However, drugs placed in the epidural space can pass through the 2526
gauge spinal dural hole and improve sacral analgesia with very low risk for high spinal blockade
(see DPE below).
Dural puncture epidural technique

The dural puncture epidural (DPE) technique consists of the insertion of an epidural needle,
placement of a longer spinal needle through the shaft of the epidural needle into the subarachnoid
space (e.g. the needle-through-needle approach), removal of the spinal needle and placement of an
epidural catheter. No medications are directly administered through the spinal needle; instead,
epidurally administered medications enter the subarachnoid space through the conduit made by the
spinal needle.
Figure 10.1 Mechanism of dural puncture epidural effect. The dural puncture epidural (DPE)
technique. Following the introduction of a 17 to 18 gauge epidural needle through the ligamentum
flavum, a longer 25 to 26 gauge spinal needle is introduced through the epidural needle and
punctures the dura (dural ligament or sac). The spinal needle is removed, and an epidural catheter
is placed. Medication is dosed through the epidural catheter, which translocates though the spinal-
needle-created passageway, into the subarachnoid space.
In comparison to the epidural technique, the DPE technique has a number of advantages,
including a faster sacral blockade, greater bilateral coverage and a lower epidural catheter failure
rate (Table 10.2). In addition, the epidural catheter is immediately tested with medications for correct
placement; this is the principal advantage over the CSE technique, particularly for parturients with a
difficult airway or a high probability of an instrumental or operative delivery.
As with any dural puncture technique, the risk for a PDPH and infection is present, but
uncommon.
Preparing for a neuraxial technique

History, physical, testing and informed consent
Prior to proceeding with any neuraxial technique, a focused review of the obstetric, anaesthetic,
medical and surgical history should be performed, accompanied by a brief physical examination with
vital signs. Routine platelet count and blood typing with screening or cross-matching are not
necessary; however, lab and additional testing (i.e. electrocardiogram or imaging) should be dictated
by the current condition of the patient and anticipated likely outcomes. Communication with the
multidisciplinary team is encouraged.
A discussion of the potential risks and consent for the procedure should be undertaken
antenatally if possible, or at the earliest possible convenience when in labour. The presence of labour
pain does not preclude an informed consent; however, care should be taken to query and document the
comprehension of the information discussed.
Medications, equipment and monitors

As expected and unexpected physiologic sequelae may occur following neuraxial techniques,
intravenous access should be established, with medications and equipment available to respond to
common (e.g. hypotension) and less frequent side effects and complications (e.g. high spinal, local
anaesthetic toxicity; see below). Medications to have readily available include ephedrine and
phenylephrine, but also atropine, epinephrine, naloxone, calcium chloride and lipid emulsion.
Emergency equipment, including a self-inflating bag and mask, an oxygen source, a cardiac
resuscitation trolley and a difficult airway trolley should be immediately available in a known,
accessible location.
The maternal blood pressure should be measured between contractions at baseline, and every 1
to 3 minutes after neuraxial technique placement for approximately 20 minutes, or until
haemodynamic stability has been demonstrated. Subsequently, throughout labour, maternal blood
pressure should be measured every 15 to 30 minutes, or in accordance with local guidelines.
Continuous pulse oximetry is useful to monitor maternal heart rate and saturation, and should be
considered throughout labour in selected patients (e.g. sleep apnoea, cardiac disease, etc.).
Assessment of the sensory level and motor ability should occur regularly (Box 10.3).
Box 10.3 Sensory and motor assessment
Sensory evaluation
Cold, pinprick or touch sensation from caudad to cephalad orientation in the midaxillary line
Motor evaluation
Bromage scale (modified)-degree of blockade
None: Full flexion of knees and feet
Partial: Partial ability to flex knees, able to move feet
Almost Complete: Inability to flex knees, able to move feet
Complete: Unable to move knees or feet
Fetal heart rate (FHR) monitoring should occur before and after the administration of neuraxial
analgesia; opioid administration within the subarachnoid versus epidural space is associated with a
higher incidence of non-reassuring FHR patterns. Continuous external FHR monitoring is often used
for the remainder of the labour; however, it may not be necessary or possible in every clinical setting.
In some cases, particularly when external monitoring proves difficult (e.g. high BMI), a fetal scalp
electrode may be indicated.
Hydration and position

Insertion of an intravenous catheter (>18 gauge) is an absolute requirement prior to the placement of a
neuraxial technique, to allow for correction of hypovolaemia and treatment of the sympathectomy-
induced hypotension with fluids or vasopressors (e.g. phenylephrine 40 g, or ephedrine 10 mg). A
fixed volume of fluid prior to the administration of a neuraxial technique is not necessary, and recent
investigations with spinal anaesthesia-induced hypotension during caesarean delivery indicate that
fluid administration at the time of neuraxial technique administration (co-loading), versus in advance
(preloading), is more effective. A balanced crystalloid solution (e.g. lactated Ringers or Hartmanns
solution) without dextrose is the most commonly used fluid in labouring women; however, colloid
solutions, which have a longer intravascular dwell time and consequently a more prolonged effect on
preload and cardiac output, may be valuable, particularly when hypovolaemia is initially present or
when the presence of even modest hypotension would be detrimental (e.g. aortic stenosis).
Although the sitting position is the most common position used for the initiation of neuraxial
techniques, the lateral decubitus position may offer greater maternal comfort, less orthostatic
hypotension, and improved ability to monitor FHR and maintain optimal maternal and fetal
positioning. Moreover, the lateral position offers the option of providing a neuraxial technique in the
setting of a presenting fetal part or cord prolapse. The sitting position may facilitate identification of
the midline in high body mass index patients and improved respiratory mechanics in patients with
respiratory issues. FHR monitoring during positioning may provide information on optimal
positioning for fetal perfusion; aortocaval compression must be avoided at all times.
Insertion of a neuraxial technique

The timing of neuraxial technique insertion should be based on a conversation between the patient, the
obstetric care team and the anaesthetist. The initiation of neuraxial analgesia early vs. late in labour
does not affect the caesarean delivery rate. The choice of neuraxial technique, agents and dosages is
based on a number of factors, including patient and provider preferences.
Prior to commencing the technique, the patient should be asked to confirm her identity and
understanding of the anticipated technique, and the anaesthetist should verbally review aloud the
relevant medical, obstetric and anaesthetic issues; these steps serve to improve patient safety.
The epidural space should be identified with a loss of resistance to intermittent or continuous
pressure with either air, saline or their combination. Midline and paramedian approaches have been
used. A specific epidural approach, method or medium used for loss of resistance has not been
uniformly found to be better in ensuring successful placement, improving analgesia or minimizing
risks.
If the epidural loss of resistance is equivocal, or the intent is to perform a CSE or DPE
technique, a longer spinal needle (10 to 15 mm longer than the epidural needle when completely
inserted) can be advanced as a finder needle through the shaft of the epidural needle (needle-
through-needle method) into the dural sac with cerebrospinal fluid (CSF) confirmed. If CSF is not
obtained, the epidural needle may be of insufficient depth (thereby not allowing the spinal needle to
reach the dural sac) or off the midline (allowing the spinal needle to miss the dural sac). If CSF is not
confirmed, but the epidural catheter is threaded and dosed, a higher failure rate of the resulting
analgesia or anaesthesia has been observed.
If during the epidural needle placement an inadvertent dural puncture (i.e. wet tap) occurs, an
epidural catheter can be inserted into the subarachnoid space and used as a continuous spinal catheter
technique. The patient, as well as the catheter itself and patients chart, should be marked to clearly
indicate the presence of a spinal catheter. Safety with the continuous spinal technique is reliant on all
practitioners having familiarity and comfort in managing such a catheter; if accidentally dosed as an
epidural catheter, a high spinal is likely.
Epidural catheters should be inserted 5 cm into the epidural space; catheter insertion less or
greater than this amount may result in a greater incidence of failed block (due to movement out of the
epidural space) or a one-sided block (due to the catheter residing towards one side), respectively.
The spinal catheter insertion depth has not been well studied; however, most clinicians insert the
catheter 3 to 5 cm into the subarachnoid space.
Test dose
Neuraxial techniques may be complicated by the inadvertent placement of the needle or catheter into
intravenous, subdural or subarachnoid spaces. This typically occurs during the insertion process,
although catheter migration may occur, perhaps through a defect created during the placement. To
date, there is not an ideal test that can reliably distinguish the location of the needle or catheter.
A commonly used test dose is composed of 3 mL of 1.5% lidocaine with epinephrine (1:200,000
solution = 15 g/3 mL). When given intravascularly, the lidocaine component may provide limited
symptoms (e.g. tinnitus, palpitations, light-headedness, dizziness), but the epinephrine should increase
heart rate. However, the heart rate may increase by only 10 beats per minute (bpm) within 45
seconds, instead of 20 bpm in non-pregnant individuals; a transient decrease in FHR from uterine
artery constriction may be observed as well. A test dose should be avoided during uterine
contractions, when pain may also increase the heart rate. When a test dose enters the subarachnoid
space, the lidocaine dose will provide a quick onset (within 3 minutes) sensory and motor blockade
and an anaesthetic block within 10 minutes; this contrasts with a slower onset of less dense analgesia
if the test dose is within the epidural space. Subarachnoid epinephrine will have minimal effects.
The best test for an incorrectly placed needle or catheter is an astute clinician, who can
critically assess haemodynamic and neuraxial blockade responses, as well as the often subtle
symptoms parturients may experience. Good practice dictates that every clinician-administered bolus
through any neuraxial catheter begins with aspiration, inspection of any aspirate, fractionation of the
desired dose into smaller increments (0.5 mL spinal, 3 mL epidural), and evaluation of the effects.
Labour analgesia agent selection

Agents used to create labour analgesia include lipid-soluble opioids and long-acting local anaesthetic
agents (Table 10.3). Opioids alone can provide sufficient analgesia for early first stage of labour in
the intrathecal space only. A combination of opioids with local anaesthetics is necessary during this
stage in the epidural space, as well as for later stages of labour in both the subarachnoid and epidural
spaces. The combination of agents allows for smaller doses of both agents to be used, thereby
minimizing undesirable side effects (e.g. opioid-induced pruritus, local anaesthetic-induced motor
blockade), and provides faster onset.
Table 10.3 Drugs for initiation and maintenance of labour analgesia
Drug Epidural analgesia Spinal analgesia
Local Anaestheticsa
Initiation/Maintenance
Bupivacaine 0.0625%0.125% 1.252.5 mg
L-Bupivacaine 0.0625%0.125% 1.252.5 mg
Ropivacaine 0.08%0.2% 2.54.5 mg
Breakthrough/Delivery
Bupivacaine 0.125%0.25% NA
L-Bupivacaine 0.125%0.25% NA
Ropivacaine 0.2%0.4% NA
Lidocaineb 0.75%1.0% NA
Opioids
Initiation/Maintenance/Breakthrough
Fentanyl 50100 g 1525 g
Sufentanil 510 g 1.55 g
Morphine NA 0.1250.25 mg
NA = not applicable.
a The volume used to initiate an epidural labour analgesic is 1020 mL of local anaesthetic
solution.
b Lidocaine and bupivacaine 0.25%, L-bupivacaine 0.25% and ropivacaine 0.4%
The dermatomal spread of analgesia is dependent on the total dose of local anaesthetic agents in
the subarachnoid space, and the volume of local anaesthetic administered is a more relevant factor in
the epidural space. Opioids and local anaesthetic solutions have a lower specific gravity relative to
CSF (i.e. hypobaric), which allow for cephalad extension of the sensory blockade. A T-10, sensory
dermatome level is necessary for labour analgesia. Initiation of epidural analgesia with 15 to 20 mL
of < 0.125% bupivacaine or ropivacaine with sufentanil (0.20.3 g/mL) or fentanyl (0.2 g/mL)
results in effective labour analgesia for vaginal delivery.
Maintenance of neuraxial labour analgesia

A variety of methods can be used to maintain analgesia, including intermittent bolus, continuous
infusion or their combination. Intermittent bolus methods can be administered by the anaesthetist, the
patient (e.g. patient-controlled epidural analgesia; PCEA) or a pump (e.g. timed bolus). Clinician-
administered boluses are typically the most variable, given alterations in timing and therapy
administered; by contrast, the PCEA method yields more control to the patient, resulting in more
immediate delivery of the analgesia when desired and greater maternal satisfaction.
Typical epidural bolus doses of a dilute local anaesthetic with opioid combination (e.g. 0.125%
bupivacaine with fentanyl 0.2 g/mL) range from 5 to 8 mL or 8 to 12 mL in the presence or absence
of a background infusion of 48 mL/h, respectively. Lockout intervals are generally 10 to 15 min. The
use of a background infusion, typically with one-third to one-half of the total hourly dose volume,
provides better analgesia than a pure bolus-only approach, with fewer unscheduled interventions.
Additional epidural top-up doses for breakthrough pain use higher volumes and/or concentrations of
local anaesthetics; 0.25% bupivacaine or 0.375% ropivacaine 6 to 8 mL is commonly used. The
requirement for concentrations of local anaesthetic agents sufficient for operative anaesthesia is
typically unnecessary for labour analgesia (Figure 10.2) and may indicate a need for a replacement
technique.
Figure 10.2 The continuum of epidural analgesia to anaesthesia effects due to anaesthetic
concentration.
PCEA pumps should be locked to prevent tampering with the contents or settings and patients
should be instructed to be the exclusive operator of the demand button. The labour and delivery suite
should have clear policies on which personnel may adjust the content, rate or volume of pump settings
or bolus doses. Records of the technique and all agents administered should be kept at the bedside.
Patient monitoring
The use of neuraxial analgesia, regardless of whether PCEA is used, mandates periodic (every 90
120 minutes) patient assessment to evaluate the quality and spread of analgesia, maternal symptoms
and signs (blood pressure), and FHR responses. An inappropriately high level may suggest a subdural
or subarachnoid migration of medication, whereas a low level may signal migration of the catheter
intravenously or out of the intended space, or the administration of an inadequate dose. Assessments
should be recorded on an analgesic record by the patients bedside.
Neuraxial labour analgesia for peripartum interventions
The larger somatic nerve fibres that enter the spinal cord at sacral segments 2 to 4 frequently require
the administration of a higher concentration or greater volume of local anaesthetic solution than that
previously used for the visceral fibres during the first stage of labour. Because drug volume
administered into the lumbar epidural space spreads mostly in a cephalad orientation, patients should
be monitored for high sensory levels and associated haemodynamic and respiratory alterations.
Dense analgesia, and sometimes even anaesthesia, is required for delivery, particularly in the
setting of an episiotomy, intended external or internal version, or forceps or vacuum-extraction
delivery (Table 10.3; Figure 10.2) . Postpartum, extensive vaginal and cervical repairs most often
require anaesthesia, and may benefit from movement to an operating room for better obstetric
visualization, surgical repair and response to postoperative issues. During this immediate peripartum
period, open and clear communication between care providers is essential, so that relevant and
timely expectations, plans and responses can be made.
Side effects
Hypotension
Neuraxial-induced sympathetic blockade results in peripheral vasodilation, increased venous
capacitance and reduced venous return to the heart. Hypotension, defined as systolic blood pressure
less than 100 mmHg or a 20% to 30% decrease from baseline, can be observed in approximately
10% of pregnant women following initiation of neuraxial analgesia. During pregnancy, hypotension
may be compounded by aortocaval compression by the gravid uterus. Persistent hypotension may
result in decreased uteroplacental perfusion, fetal hypoxia and acidosis, and thus the FHR should be
monitored.
Preventive measures include maternal intravascular volume expansion (preloading with IV fluid,
usually 500 to 1000 mL of crystalloid such as Hartmanns solution) and the avoidance of aortocaval
compression by uterine displacement. Treatment includes assessment of the sensory and motor
blockade (to rule out high blockade or inadvertent subarachnoid or subdural blockade), the titration
of IV doses of vasopressors such as ephedrine (510 mg) and phenylephrine (40100 g) and the use
of volume expansion. Vasopressor use can significantly reduce the nausea and vomiting following a
spinal technique, which may be associated with reductions in sympathetic tone, blood pressure and
cerebral blood flow.
Pruritus
The incidence and severity of pruritus is dose dependent and greater with the spinal vs. epidural
administration of opioids. The aetiology is most likely related to sensory modulation, central opioid
receptor activation and central inhibitory neurotransmitters (e.g. -aminobutyric acid [GABA] and
glycine) antagonization. The co-administration of spinal bupivacaine appears to lower the incidence
of pruritus.
Opioid-induced pruritus is typically self-limiting, although an effective treatment is the
administration of a centrally acting agonist (which acts as a competitive antagonist; e.g. naloxone,
naltrexone) or partial agonistantagonist (e.g. nalbuphine). The use of these agents should be limited
to prevent complete reversal of the desired analgesia. Because the release of histamine is not
believed to be involved in the mechanism of opioid-induced pruritus, the observed benefit from the
provision of antihistamines (e.g. diphenhydramine) is most likely due to the resulting sedation.
Nausea and vomiting

The anatomic and hormonal changes in gastric emptying associated with pregnancy can frequently
result in nausea and vomiting; these symptoms may also be in response to neuraxial opioids or
hypotension.
Treatment should be guided towards correcting hypotension if it exists. Antagonists to the 5-HT 3
(e.g. ondansetron), dopamine (e.g. prochlorperazine, metoclopramide), H1 (e.g. diphenhydramine)
receptors, as well as anticholinergics (e.g. hyoscine), benzodiazepines (e.g. midazolam) and steroids
(e.g. dexamethasone) have been observed to be helpful in treating nausea and vomiting. Many of these
agents should be administered slowly (over several minutes) to minimize extrapyramidal side effects
or hypotension.
Fever and shivering

In some women with neuraxial labour analgesia, there is a small (< 1C) increase in core
temperature, particularly if labouring in a warm ambient environment. Shivering may also occur in
this setting, independent of temperature increases. A non-infectious, inflammatory process appears to
be the aetiology for the temperature increase, with a higher thermoregulatory sweating threshold and a
reduction in pain-induced hyperventilation being partially involved. The clinical diagnosis of fever is
a temperature greater than 38C. Women with longer, more uncomfortable, dysfunctional labours (e.g.
nulliparous, larger babies, non-vertex presentation) and infections (e.g. chorioamnionitis) are more
likely to request neuraxial techniques and exhibit fever.
Maternal fever may result in both maternal and fetal infection/sepsis evaluations and result in
exposure to antibiotics. Peripartum maternal fever should always prompt consideration and
monitoring for an infectious aetiology. Acetaminophen (paracetamol) 650 to 1000 mg PO can be
given to manage maternal fever, which provides some analgesia as well. Meperidine 12.5 mg IV can
be administered for the treatment of shivering, acknowledging that increased sedation may occur; its
use is most often relegated to the postpartum period, given the accumulation of normeperidine, which
has been related to neonatal seizure activity with repeated in utero exposure.
Complications
Failed analgesia
The definition of analgesia failure can include an absence of analgesia, incomplete or patchy
analgesia or the need for a replacement technique. Neuraxial techniques that include a spinal
component (i.e. spinal, spinal catheter, CSE, DPE) have a lower incidence of failed analgesia than
the epidural technique. Obstetric factors (e.g. progress of labour, occiput posterior fetal
presentation), maternal anatomic factors (e.g. distended bladder) and analgesic factors should be
evaluated when significant changes in the quality of analgesia are reported. A sensory and motor
evaluation should be conducted in the traditional caudad to cephalad direction, with adequate caudad
evaluation to determine the presence of sacral blockade.
Treatment should be guided by the patients symptoms and sensory evaluation. If an epidural,
CSE, or DPE blockade spread is inadequate, one sided or patchy, administer 6 to 10 mL,
remembering that the epidural space is volume sensitive, of a dilute local anaesthetic solution (e.g.
0.125% bupivacaine). If the sensory (and perhaps motor) blockade has been extended, and an interval
analgesic improvement is observed, but remains inadequate, administer 6 to 10 mL of a more
concentrated local anaesthetic solution (e.g. 0.25% bupivacaine). If interval analgesic improvement
is again observed, but still inadequate, consider using a more concentrated local anaesthetic solution
(e.g. 1% lidocaine), the addition of an opioid (e.g. fentanyl 100 g) or replacement of the catheter.
The requirement for even higher anaesthetic doses adequate for surgical interventions should prompt
consideration of technique replacement (Figure 10.2). With a spinal catheter, CSF may not be able to
be aspirated each time; however, the administration of 1 to 2 mL of 0.25% bupivacaine (or
equivalent) should provide additional comfort; if analgesia remains insufficient, consider 1 to 2 mL
of hyperbaric lidocaine 1.5%, and then, if insufficient, consider replacing the catheter.
All analgesic interventions should be considered in the context of the patient and obstetric needs;
if the discomfort is intense or delivery imminent, the higher dose regimens may be employed earlier.
However, administration of anaesthetic agents through neuraxial catheters should never sacrifice
safety and should always employ the use of catheter aspiration before and between each dose;
incremental, fractionated dosing; and appropriate pauses to evaluate intended and unintended (e.g.
intrathecal or intravascular migration) effects.
High neuraxial blockade

A high total spinal neuraxial blockade may be produced from local anaesthetic agents administered
in the epidural, subdural and subarachnoid spaces. Subarachnoid and subdural injection occurs with
an incidence of 1:2,900 and 1:4,200, respectively, with a high/total spinal occurring in 1:1,400 cases.
Within the epidural space, large volumes (>30 mL) of local anaesthetic would be required to achieve
a high spinal. By contrast, an inadvertent and unrecognized subarachnoid or subdural puncture may
allow a relatively small volume of local anaesthetic to spread quickly.
Total spinal blockade manifests with rapidly ascending sensory and motor changes, bradycardia
and hypotension, dyspnoea, with difficulty swallowing and limited ability to phonate, and loss of grip
strength. Unconsciousness and respiratory depression may soon follow, most commonly as a result of
hypoperfusion of the brain and brainstem. Medications within the subdural space may result in
Horners syndrome (i.e. anhydrosis, enophthalmos, ptosis and miosis) and a patchy sensory and motor
blockade. A total spinal blockade with analgesic concentrations of local anaesthetic agents causes a
more rapid and dense sensory and motor blockade than a subdural or epidural blockade (see Table
10.4).
Table 10.4 Comparison of epidural, sub-dural and sub-arachnoid blockade during intended epidural
technique
Epidural Sub-dural Sub-arachnoid
Incidence 0.025 (0.0170.033) 0.035 (0.020.04)

Onset Slow Intermediate Rapid
Spread Higher than expected, Higher than expected,
but with patchy sensory but with present
blockade sensory blockade
Motor blockade Minimal Minimal Dense
Hypotension Less than spinal and Less than spinal, Dependent on height of
subdural; dependent on greater than epidural; sensory blockade
height of sensory dependent on height of
blockade sensory blockade
Treatment includes assessment of the patients symptoms and evaluation of the neuraxial
catheter. Aortocaval compression should be avoided, 100% oxygen administered and the provision of
positive pressure ventilation via an endotracheal tube if necessary. Maternal vital signs, EKG and
FHR should be evaluated, with maternal circulation supported with vasopressor agents and fluids.
Inadvertent dural puncture

The incidence of an inadvertent dural puncture with an epidural needle or catheter is approximately
1% to 3%. When detected during the insertion of the epidural technique, the procedure may be
reattempted at another interspace, or the epidural catheter may be placed into the subarachnoid space
for the provision of a continuous spinal analgesic technique for labour and delivery. This continuous
spinal technique minimizes the risk of a repeat dural puncture at another site, particularly in the
setting of anatomic or pathologic issues of the back (e.g. obesity, scoliosis), or passage of a sufficient
amount of local anaesthetic agent or opioid through the dural puncture into the subarachnoid space,
resulting in a high neuraxial blockade. A spinal catheter can be efficiently titrated for both analgesia
and anaesthesia (see above).
The patient should be followed up for a post dural puncture headache, with pain relief provided
by bed rest, hydration and the oral intake of caffeinated and analgesic products (including Fioricet or
Fiorinal) for 24 to 48 hours. If correctly diagnosed as a PDPH, the administration of an epidural
blood patch, whereby 10 to 20 mL of autologous blood is placed in the epidural space, is associated
with a high (80%) success rate. Neurologic complications (e.g. peripheral neuropathy, subarachnoid
bleed) as a result of spinal anaesthesia in the obstetric population are extremely rare; however,
should these events occur, a consultation with a neurologist may assist in the diagnosis and
management.
Intravascular injection of local anaesthetic

The incidence of intravascular injection during attempted epidural labour analgesia is 1:5000.
Physiologic responses to intravascular injection are dependent on the amount and type of agents used.
Initially, CNS symptoms (e.g. tinnitus, dizziness, restlessness, difficulty speaking, seizures and loss of
consciousness) occur, which may be followed closely by cardiovascular signs (e.g. initial increases
in blood pressure from sympathetic stimulation, followed by bradycardia, ventricular dysfunction,
tachycardia and fibrillation) and collapse.
Prevention begins with meticulous attention to the technique and observation of the patient while
delivering fractionated doses. Treatment includes suspension of further injection, calling for
assistance, providing 100% oxygen with positive-pressure ventilation if necessary, avoiding
aortocaval compression, monitoring and supporting maternal vital signs, monitoring FHR and
preparing for emergency caesarean delivery within 4 minutes. The administration of 20% lipid
emulsion (i.e. IV bolus 1.5 mL/kg followed by a continuous infusion of 0.25 to 5 mL/kg/min for 10
minutes or longer) should be considered; barbiturates or benzodiazepines may also be given to arrest
seizure activity.
Key points
1. Neuraxial techniques, including spinal, epidural, combined spinal-epidural (CSE) and dural-
puncture epidural (DPE) techniques, are commonly used in modern obstetric care for the
provision of labour analgesia and anaesthesia for instrumental and operative deliveries.
2. The basic properties of spinal, epidural, CSE and DPE techniques may be advantageous for
specific situations.
3. A catheter-based neuraxial technique can allow flexibility in titrating the onset and duration of
the blockade; however, the spinal catheter technique is less commonly used due to the size of the
dural puncture and the resulting high incidence of headache.
4. A number of analgesic and anaesthetic options exist for labour and delivery, including non-
pharmacologic modalities, systemic agents and peripheral nerve blocks.
5. Whether neuraxial analgesia affects the progress and outcome of labour remains
controversial, in part due to the complexity in study design. However, the majority of studies
appear to indicate little overall effect of epidural analgesia on progress and outcome of labour.
Anaesthetic and obstetric practice styles may influence who ultimately receives an instrumental
or operative delivery.
6. Although the aetiology remains unclear, epidural labour analgesia appears to increase
maternal temperature; however, a delay of 4 to 5 hours is observed prior to a mean increase of
approximately 0.1C/h following epidural initiation. The impact of these changes remains
controversial, and deserves further investigation.
7. Awareness and communication of the indications and implications of neuraxial techniques

among the entire obstetric care team, including obstetric, anaesthetic, neonatal and nursing care
providers, remain of paramount importance to the continued welfare of the expectant mother and
fetus.
Further reading
American Society of Anaesthetists Task Force on Obstetric Anaesthesia. (2007). Practice guidelines
for obstetric anaesthesia: an updated report by the American Society of Anaesthetists Task Force on
Obstetric Anaesthesia. Anesthesiology, 106, 843863.
Bucklin, B. A., Hawkins, J. L., Anderson, J. R. and Ullrich, F. A. (2005). Obstetric anaesthesia
workforce survey: twenty-year update. Anesthesiology, 103, 645653.
Cappiello, E., ORourke, N., Segal, S. and Tsen, L. C. (2008). A randomized trial of dural puncture
epidural technique compared with the standard epidural technique for labour analgesia. Anesth.
Analg., 107(5), 16461651.
Leo, S., Ocampo, C. E., Lim, Y. and Sia, A. T. (2010). A randomized comparison of automated
intermittent mandatory boluses with a basal infusion in combination with patient-controlled epidural
analgesia for labour and delivery. Int. J. Obstet. Anesth., 19, 357364.
Loubert, C., Hinova, A. and Fernando, R. (2011). Update on modern neuraxial analgesia in labour: a
review of the literature of the last 5 years. Anaesthesia, 66, 192212.
Mercier, F. J. (2011). Fluid loading for caesarean delivery under spinal anaesthesia: have we studied
all the options? Anesth. Analg., 113(4), 677680.
Ngan Kee, W. D. (2010). Prevention of maternal hypotension after regional anaesthesia for caesarean
section. Curr. Opin. Anaesthesiol., 23, 304309.
Simmons, S. W., Taghizadeh, N., Dennis, A. T. and Cyna, A. M. (2012). Combined spinal-epidural
versus epidural analgesia in labour. Cochrane Database Syst. Rev., 10, Art. No.: CD003401.
Halpern, S. H. and Abdallah, F. W. (2010). Effect of labor analgesia on labor outcome. Curr. Opin.
Anaesthesiol., 23, 317322.
Wong, C. A., Scavone, B. M., Peaceman, A. M. et al. (2005). The risk of caesarean delivery with
neuraxial analgesia given early versus late in labour. N. Engl. J. Med., 52, 655665.
Chapter 11
Regional anaesthesia for operative delivery

Cathy Armstrong and Khaled Girgirah
Introduction
The rate of general anaesthesia (GA) for caesarean section (CS) has fallen from 55% (19891990) to
9.4% (20112012). Over the same time period there has been an increase in CS rates from 11.3% to
25%. Despite the rise in CS rate there are approximately 70% fewer obstetric GAs performed per
year nationally.
The reasons for this include:
Increasing awareness of the risks of general anaesthesia in the parturient. The UKOSS study
demonstrated a 1:224 risk of failed intubation
The introduction of pencil point spinal needles, which have reduced the risk of post dural-
puncture headache to an acceptable level (0.25%)
Changes in maternal demographics: increasing numbers of women with morbid obesity and
other co-morbidities
Alteration in maternal expectations. Better information antenatally regarding the risks and
benefits of regional anaesthesia vs. general anaesthesia allows women to make informed
choices.
Benefits of regional anaesthesia (RA) for the woman include:
The partner can be present throughout the delivery

Maternal/neonatal skin-to-skin contact at the time of delivery can facilitate bonding
The drugs used to provide RA do not affect uterine tone and there is minimal, if any, direct
effect of these agents on fetal heart rate activity or fetal wellbeing
The addition of neuraxial opioids provides excellent postoperative analgesia
A reduction in the need for general anaesthesia reduces risks e.g. failed intubation.
Audit standards from the Association of Anaesthetists are that the proportion of CS under regional
anaesthesia should be:
Category 1 CS >50%
Category 23 CS >85%
Category 4 CS >95%.
Types of central anaesthetic neuraxial blockade

The CNB technique for delivery is dictated by:
The experience of the anaesthetist
The urgency of the decision-to-delivery interval (DDI):
Category 1: immediate threat to the life of the mother or fetus (< 30 minutes)
Category 2: no immediate threat to the life of woman or fetus (< 75 minutes)
Category 3: requires early delivery (> 75 minutes)
Category 4: at a time to suit the woman and the maternity service
Co-morbidities, e.g.:
Obesity
Pre-eclampsia
Cardiac disease
Respiratory disease
Whether the in-situ epidural is satisfactory enough to top-up.
The contraindications to CNB are detailed in Chapter 10.

The absolute contraindications are:
Patient refusal
Sepsis local to the insertion site and systemic
Coagulopathy:
Pathological
Iatrogenic.
There are a number of situations where there is a judgement that the risks of CNB are less than the
risks associated with GA, e.g. a woman that has a stable platelet count of 70 109/L, with a normal
coagulation screen. She may be considered unsuitable for a labour epidural, but an acceptable risk for
siting a spinal for operative delivery.
The multidisciplinary team should be made aware of any woman with morbidities that could
complicate the performance of CNB as this may result in a delay in decision-to-delivery time.
Complex cases should be supervised by a senior anaesthetist.
Preparation for central neuraxial blockade is as follows:
1. Patient:
a. A full medical history, to assess the womans suitability for CNB
b. Early identification of women who have an increased risk of operative delivery e.g. twin
pregnancy, morbid obesity, medical co-morbidities, induction of labour
c. Appropriate examination and review of relevant investigations in light of the history
d. A full explanation of the procedure, including the benefits and risks of CNB (See Table
11.1)
e. Prompt access to translation services
f. Antacid prophylaxis
2. Equipment required prior to commencing CNB:
a. Full standard monitoring

b. A large bore cannula (16G or higher)
c. Emergency drugs, including vasopressors, must be immediately available in the location

(delivery unit room or theatre)
d. A selection of different length Tuohy and spinal needles.
Table 11.1 Risks of central neuraxial blockade
Risks Epidural Spinal
Hypotension 1:50 1:5
Failure of CNB, resulting in GA conversion 1:20 1:125
Post dural puncture headache 1:100 1:400
Neurological damage 1:1,000 (temporary)
1:13,000 (permanent)
Epidural abscess 1:50,000
Meningitis 1:100,000
Epidural haematoma 1:170,000
Accidental unconsciousness 1:5,000
Severe injury, including being paralyzed 1:250,000
Spinal anaesthesia
Operative delivery encompasses caesarean section, forceps and ventouse deliveries. Spinal
anaesthesia is the commonest way of providing anaesthesia for operative delivery and is the most
reliable of CNB techniques. The woman can be positioned in the sitting or lateral position, this may
be dictated by the patient, fetal monitoring requirements or uncommon events such as cord prolapse.
Skin preparation
Controversy remains over the most appropriate antiseptic solution with which to clean the skin prior
to insertion of CNB. The Royal College of Anaesthetists, The American Society of Anesthesiologists
and The American Society of Regional Anesthesia all recommend the use of chlorhexidine in alcohol
as the skin disinfectant of choice for CNB. A UK working party review in 2014 (see Further Reading)
recommend the use of 0.5% chlorhexidine in alcohol for CNB, this being the agent that gives the best
balance for risk of neurotoxicity vs. the risk of infection.
Chlorhexidine gluconate has the following characteristics:
Potent and broad spectrum
Effective against bacteria and yeast
Fast onset and long duration of action (when compared with povidone iodine)
Efficacious even in the presence of blood
Lower incidence of skin reactions (when compared with povidone iodine)
Chlorhexidine in alcoholic solution has improved bacteriostatic profile when compared with
chlorhexidine in aqueous solution
There is an established risk of neurotoxicity in vitro and in animal studies; the risk of
developing chronic adhesive arachnoiditis is extremely rare
There is limited in vivo evidence regarding the alterations in efficacy between 0.5% and 2%
chlorhexidine
Meticulous attention should be given to reducing the risk of contamination of CNB equipment
with chlorhexidine. Some advocate the use of pre-soaked sponge applicators or sprays; time
must be allowed for the solution to dry
Hypersensitivity reactions have been described; most anaphylactic reactions have resulted
from topical application to mucous membranes and the use of chlorhexidine-impregnated
devices, although they can occur following contact with intact skin (see Chapter 23).
Other precautions (as per National Audit Project 3 recommendations) that should be employed at the
time of CNB include:
Thorough hand washing with appropriate preparation
Hat, mask, sterile gown, gloves and drape

The recommended level for siting a spinal needle (2527 gauge) is L3/4. Use of higher intervertebral
spaces may result in damage to the cauda equina, particularly in view of the lack of reliability in
confirming lumbar levels when using bony landmarks. See Chapter 18 for ultrasound of spine.
Spinal anaesthesia relies on distribution of local anaesthetic and/or opioids in the cerebrospinal
fluid (CSF). Glucose levels in CSF are approximately two-thirds of that in venous blood. Use of a
glucometer can help to confirm CSF if there is doubt. Whilst performing CNB, good communication
with the woman is essential; it is important for the woman to report any issues with pain or
paraesthesia on injection. If this occurs, then changing the direction of the needle can remedy the
situation, if not then resiting the block is the safest option.
A reduced spinal dose of local anaesthetic (2.23.0 mL of 0.5% heavy bupivacaine) is required
in the parturient as there is a smaller CSF volume in the lumbar region and greater sensitivity of nerve
fibres to local anaesthetic. The cephalad displacement of CSF from the lumbar region is a result of
caval compression and increased fat in the epidural space. Opioid analgesics are generally added to
the local anaesthetic mixture to enhance the efficacy of the spinal block. The main contraindications to
spinal opioid analgesia are opioid allergy and an active herpetic eruption.
Assessment of the block

The sensory block height should be assessed and documented prior to skin incision. Sensory
examination should move caudad to cephalad bilaterally in the midaxillary or midclavicular lines.
The adequacy of regional anaesthesia for caesarean section has been assessed using a range of
sensory modalities, including light touch, pinprick and cold. Absence of light touch sensation up to T5
dermatome is widely accepted to indicate an adequate level of block for caesarean section. Sacral
anaesthesia is also essential as the S2S4 dermatomes innervate the peritoneum overlying the lower
uterine segment. Instrumental deliveries do not require the same height of block and can be
commenced when certain of sacral anaesthesia and a block to T8. However, should the instrumental
delivery be unsuccessful, the anaesthetist must assess the block height to ensure that it has reached an
appropriate level to proceed to caesarean section under regional anaesthesia.
A survey of UK obstetric anaesthetists in 2010 showed that 74% still checked the block height
with cold sensation to ethyl chloride alone. Concerns regarding the reliability of use of cold sensation
to evaluate block height relate to the multimodal transmission of sensation. Cold, transmitted by A
fibres, may not be distinguished from cold discomfort, transmitted by C fibres. A fibres may also be
activated, transmitting light touch and possibly pressure sensation.
When sharp pinprick is used to assess block height, it is important to document the exact end
point:
Total loss of all sensation to the pinprick
The pinprick is recognized as a touch
The pinprick is recognized as being sharp, but is less sharp than normal
The pinprick feels normal.
If the block is inadequate prior to skin incision then there are three options, which need to be
discussed with the obstetricians:
Repeat the spinal anaesthetic, the second dose is dependent on the block height from the
previous spinal (1.02.2 mL 0.5% heavy bupivacaine)
Postponement of the case in the elective setting
Conversion to GA.
Pain during CS under regional anaesthesia is one of the most common causes of obstetric anaesthetic
litigation. It is essential to document thoroughly the womans concerns and offer alternative solutions,
e.g. low-dose intravenous opioid analgesia, local anaesthetic infiltration by the surgeon or conversion
to GA. Each step must be acted on promptly and the outcome of the intervention recorded.
Combined spinal epidural (CSE)

Indications for a combined spinal epidural approach for operative delivery include:
Anticipated prolonged surgery with the potential to exceed the anaesthetic duration of a single
shot spinal (e.g. multiple previous CS, obesity, combined CS and tubal ligation):
a standard intrathecal dose is administered; the epidural catheter is in place for

intraoperative supplementation if the spinal block regresses over time
Parturients with cardiac co-morbidities where sudden cardiovascular changes are

undesirable:
a reduced intrathecal volume (1.02.0 mL) is injected to lessen the hypotension from
sympathetic blockade; the block height can then be extended using the epidural catheter,
thus minimizing cardiovascular instability.
There are two recognized techniques for CSE insertion:
1. Needle-through-needle technique: This is the commonest approach. The epidural space is

located with a Tuohy needle, a spinal needle is passed through the Tuohy needle to puncture the
dura and deposit medication in the CSF. The spinal needle is withdrawn and a catheter is then
threaded into the epidural space. The risks of this technique include:
a. Threading the epidural catheter through the dural puncture created by the spinal needle
b. Failure to enter the intrathecal space with the spinal needle despite the Tuohy needle being
located in the epidural space
c. Potential problems threading the epidural catheter after spinal injection (i.e. blood in
catheter, persistent pain on insertion), leading to abandonment of the epidural
d. Reduced block height from the spinal anaesthetic due to increased time in sitting position
while epidural catheter is placed.
2. Separate insertion of an epidural catheter and a spinal at different lumbar levels. The epidural
is sited prior to spinal insertion. Risks include:
a. The risk of damaging the epidural catheter on insertion of the spinal needle; however, this
is minimized by insertion of the spinal at a level below the epidural site.
Both techniques rely on an epidural that is effectively untested and may fail when attempting to
extend the block.
Epidural top-up for operative delivery

The maternity Hospital Episode Statistics (HES) shows that the risk of conversion to GA with
epidural anaesthesia is 2.2%, whereas the risk of conversion with spinal anaesthesia is 0.8%.
Epidural analgesia is commonplace on consultant-led delivery units and the majority work well
in labour. Epidural top-up for Category 1 and 2 CS in low- and high-risk women is an invaluable
technique to ensure a prompt and effective anaesthetic block, e.g. difficult airway, morbid obesity and
twin pregnancies. If the epidural block is inadequate there should be discussion with the woman
about resiting the epidural.
It is vital that women with epidural analgesia are reviewed regularly. There are only two
statistically significant factors that predict a failed anaesthetic top-up:
1. More than one anaesthetist top-up in the room
2. Increased maternal height.
An effective top-up requires:
A good labour analgesic effect
Testing to ensure there is a good sacral block
Enough time to top-up safely.
This ensures that only epidurals that are working well are topped-up for operative delivery.
If there is doubt about the efficacy of the epidural, the catheter should be removed and a spinal
anaesthetic sited in theatre. Cases must be assessed on an individual basis.
Top-ups for epidural anaesthesia can be performed in theatre or in a delivery room. If the top-up
occurs in a delivery room it is mandatory that the anaesthetist remains in attendance. Full monitoring
and access to emergency drugs is essential (see preparation for CNB).
Intrathecal catheters
Indwelling intrathecal catheters used in labour and theatre have the potential to deliver the ideal
labour analgesia/anaesthesia with a reliable analgesic block in labour that could be topped up to
provide a dense and fast anaesthetic.
Table 11.2 Examples of epidural top-up regimens
Lignocaine, adrenaline, bicarbonate (+/ fentanyl) mixture (LEB)

18 mL 2% lignocaine, 100 g adrenaline (0.1 mL 1:1000) 50100 g fentanyl
Pros: this is the fastest-acting mixture, almost halving the times of other mixtures, the addition of
fentanyl further shortens the time to surgical anaesthesia
Cons: has to be mixed by the anaesthetist, this may result in drug errors, particularly with those
unfamiliar in the technique. Increased analgesic supplementation during the CS
0.75% Ropivacaine
1020 mL 50100 g fentanyl
Pros: same time to surgical anaesthesia as levobupivacaine, but less supplementation during CS
Cons: slower onset to surgical anaesthesia
O.5% Levobupivacaine
1020 mL 50100 g fentanyl
Pros: widely used and familiar to most anaesthetists, no cardiotoxicity compared to racemic
bupivacaine
Cons: slower onset of surgical anaesthesia
Intrathecal catheters left in situ following inadvertent dural puncture at epidural insertion can be
topped up for theatre using small volumes of local anaesthetic. However, intentional insertion and use
of intrathecal catheters is currently not common practice in the UK.
Use of indwelling intrathecal catheters for labour & delivery was developed in the 1980s,
however their safety was questioned following cases of cauda equina syndrome and nerve damage.
There was also a high incidence of post dural puncture headache. However, recent development of
microcatheters (26G32G) has led to renewed interest and may change practice in the future. Further
research into long-term complication rates needs to be completed before widespread use can resume.
Risks of CNB
The 3rd National Audit Project (NAP3) of the Royal College of Anaesthetists on major complications
of central neuraxial block in the United Kingdom reported that CNB performed for obstetric analgesia
or anaesthesia appears to be acceptably safe. Obstetric CNB was associated with fewer major
complications than in other areas, likely as a result of a generally healthy patient population with
short durations of epidural catheterizations. Although neurological complications in obstetric practice
may be a result of the CNB, obstetric causes must also be considered. Risk factors for neuraxial
infection following CNB include multiple attempts at insertion accompanied by massive obstetric
haemorrhage. Post CNB headache should be investigated appropriately (see Chapter 26). Wrong
route drug errors were more common in the obstetric group. Meticulous attention to epidural infusion
connection and drug checking may help.
Less than 6% of all CNB reported in NAP3 were combined spinal epidurals. This group,
however, accounted for over 13% of the reports of harm.
Hypotension
All types of CNB can cause maternal hypotension. Epidural and small-volume CSE blocks tend to
take longer to provide surgical anaesthesia so the incidence is less frequent than for spinal
anaesthesia. Approximately 80% of women will become hypotensive unless they are given a
vasopressor; phenylephrine or ephedrine are commonly used.
The hypotension, due to preganglionic sympathetic blockade, causes a dramatic fall in systemic
vascular resistance. In normal pregnancy the uterine arteries are maximally dilated, resulting in
pressure-dependent blood flow. Studies have shown no adverse effects on oxygen supply to the fetus
when phenylephrine infusion is used to maintain baseline blood pressure (BP).
Which vasopressor?
1. Phenylephrine:
Most effective drug to prevent hypotension associated with spinal anaesthesia
Most effective drug for prevention of nausea
Does not induce fetal acidosis
Decreases heart rate and cardiac output (clinically insignificant in low-risk pregnancies)
A suggested regime would be to commence a phenylephrine infusion (concentration 100 g/mL)

at a rate of 30 mL/h, titrated to blood pressure.
2. Ephedrine:
Freely crosses the placenta
Higher rate of nausea and vomiting, despite similar BP
Can induce fetal acidosis; this is likely to be a direct -adrenergic effect resulting in an
increase in fetal metabolic rate.
Table 11.3 Adjuvants table
Agent Doses used and Site of action Information

studied
Ketamine 0.5 mg/kg Non-competitive Limited data for post

NMDA antagonist caesarean section
analgesia
Not recommended
Would require
further research
Clonidine Intrathecal 75400 g 2 receptor: Can cause significant

Epidural 100 peripheral, hypotension and
800 g spinal, brainstem sedation
Analgesic benefit
when used in
combination with
opiates
Neostigmine Intrathecal 12.525 g Spinal nicotinic and Limited use due to side
muscarinic receptors effects
Not enough data to
use epidurally
Requires more
research
Magnesium Intrathecal 50 mg Non-competitive Requires more

Epidural 500 mg NMDA antagonist research
Used in combination
with local and opiates
Midazolam Intrathecal 2 mg GABA receptors More research

required
Potential beneficial
side effect profile
Epinephrine Intrathecal receptors, local Prolongs duration of

200 g vasoconstriction action
Epidural
2.530 g
General advice: Adjuvants should always be reviewed in the context of risks and benefits. Agents can
be used as sole agents, but are usually used in combination with opioids. All adjuvants have some
benefits as an analgesic agent or on the duration of action of drugs. They will also alter the side-effect
profile. More data is available for use as adjuvants in non-obstetric patients and all agents require
further research to be able to give definitive advice.
NMDA N-methyl-D-aspartate, GABA
Pre-eclampsia
The high systemic vascular resistance seen in severe pre-eclampsia (PET) often negates the need for
vasopressor support following spinal anaesthesia.
Vasopressors must be immediately available, but should be given with caution owing to their
exaggerated response in this condition.
Post dural puncture headache/neurological damage

The management of these complications can be found in Chapters 26 and 22, respectively.
High central neuraxial block

The risk factors for a high block are:
Epidural top-up:
The catheter can be intrathecal or subdural (see Chapter 10)
High concentration solutions of local anaesthetic
Too much volume of high concentration local anaesthetic
Spinal anaesthesia: the following situations may lead to a quicker, more extensive spread of
local anaesthetic. This is thought to result from lumbar thecal compression resulting in rapid
rostral spread.
Following a recent epidural top-up, if the catheter has been removed for either speed or
anticipated failure of top-up
Women with raised BMI
Multiple pregnancies.
Management
This is dependent on the height of the block and the womans symptoms.
The block should be assessed as soon as possible after the patient has been positioned supine
following regional anaesthesia.
The features of high block include:
Bradycardia
Hypotension
Respiratory compromise
Loss of consciousness.
Tilting the table early into reverse Trendelenburg may prevent any further extension of the block.
Respiratory compromise or loss of consciousness necessitate prompt action, including securing the
airway. Ventilation and sedation should be maintained until adequate spontaneous respiration is
resumed.
Hypotension and bradycardia are treated with:
Intravenous fluids
Vagolytics: atropine
Sympathomimetics: ephedrine, adrenaline
Vasopressors: phenylephrine, metaraminol.
Postoperatively, following a high block, it is important to debrief the woman. She should receive a
full explanation of events and should have time to ask any questions that she might have.
Intraoperative side effects

Local anaesthetic (LA) toxicity
This can occur secondary to inadvertent intravascular administration of LA or epidural absorption of
high volumes of high concentration LA agents. Management is supportive with administration of
intralipid (Table 11.4).
Table 11.4 AAGBI safety guideline: Management of severe local anaesthetic toxicity
1 Signs of severe toxicity:

Recognition Sudden alteration in mental status, severe agitation or loss of
consciousness, with or without tonicclonic convulsions
Cardiovascular collapse: sinus bradycardia, conduction blocks,

asystole and ventricular tachyarrhythmias may all occur
Local anaesthetic (LA) toxicity may occur some time after an initial
injection
2 Stop injecting the LA

Immediate Call for help
management
Maintain the airway and, if necessary, secure it with a tracheal tube
Give 100% oxygen and ensure adequate lung ventilation

(hyperventilation may help by increasing plasma pH in the presence of
metabolic acidosis)
Confirm or establish intravenous access
Control seizures: give benzodiazepine, thiopental or propofol in small

incremental doses
Assess cardiovascular status throughout
Consider drawing blood for analysis, but do not delay definitive

treatment to do this
3 In circulatory arrest Without circulatory arrest

Treatment Use conventional
Start cardiopulmonary resuscitation therapies to treat:
(CPR) using standard protocols
Hypotension
Manage arrhythmias using the same Bradycardia
protocols, recognizing that arrhythmias
Tachyarrhythmia
may be very refractory to treatment
Consider the use of cardiopulmonary

bypass if available
Give intravenous lipid emulsion (following the Consider intravenous lipid
regimen overleaf) emulsion (following the
regimen overleaf)
Continue CPR throughout treatment with
lipid emulsion Propofol is not a
Recovery from LA-induced cardiac suitable substitute
arrest may take >1 h for lipid emulsion
Propofol is not a suitable substitute for Lidocaine should not
lipid emulsion be used as an

antiarrhythmic
Lidocaine should not be used as an
therapy
antiarrhythmic therapy
4 Arrange safe transfer to a clinical area with appropriate equipment and

Follow-up suitable staff until sustained recovery is achieved
Exclude pancreatitis by regular clinical review, including daily

amylase or lipase assays for two days
Report cases as follows:
in the United Kingdom to the National Patient Safety Agency (via

www.npsa.nhs.uk)
in the Republic of Ireland to the Irish Medicines Board (via

www.imb.ie)
If Lipid has been given, please also report its use to the international
registry at www.lipidregistry.org. Details may also be posted at
www.lipidrescue.org
Your nearest bag of lipid emulsion is kept:

This guideline is not a standard of medical care. The ultimate judgement with regard to a particular
clinical procedure or treatment plan must be made by the clinician in the light of the clinical data
presented and the diagnostic and treatment options available.
The Association of Anaesthetists of Great Britain & Ireland 2010
Nausea and vomiting

This common side effect is most often seen in association with spinal anaesthesia. The most frequent
cause of nausea and vomiting is hypotension: in studies looking at maintenance of BP using
phenylephrine, if the BP is kept at 100% of baseline the incidence was 4%, compared to 16% when
the BP is maintained at 90% of baseline.
Other factors include parenteral opioids, increased vagal activity, surgical stimuli and uterotonic
agents.
The current evidence does not seem to favour either routine or rescue administration of
antiemetics, so it would seem prudent to use them only if there is a specific indication.
Shivering
A significant number of women will experience shivering following CNB; some reports show this to
be as high as 60%. The mechanism is unclear and is likely to be multifactorial, e.g. altered
thermoregulation, intrathecal drugs and autonomic blockade. Shivering increases the metabolic rate
and is often distressing for the parturient.
A study of shivering in parturients following institution of epidural anaesthesia for CS
randomized parturients to receive either 50 mg pethidine or 0.9% saline intravenously post delivery.
The results showed a decrease in shivering from 87% to 35% (p < 0.01) and a decrease in severe
shivering from 57% to 0% (p < 0.01) in the pethidine group with no statistical change in those who
received 0.9% saline. The effect of administering pethidine was apparent after 2 minutes.
Doses of 25 mg IV pethidine usually suffice. Tramadol has a similar effect, but causes more
nausea and drowsiness.
Postoperative considerations
Analgesia
The management of postoperative pain should be multimodal. When time allows, addition of an
opioid to the CNB will improve the quality of the anaesthetic block, postoperative analgesia and
patient satisfaction.
In time-pressured caesarean sections, it may be safer to forego the addition of opioid to the
CNB. An opioid PCA and transverse abdominal plane blocks should be considered (see Chapter 12).
Paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) are routinely prescribed
regularly. A number of situations preclude the use of NSAIDs, e.g. renal dysfunction, lupus nephritis
and pre-eclampsia; it is essential to perform an assessment of the womans suitability for these drugs.
Oral opioid drugs should also be prescribed.
Thromboprophylaxis
Thromboembolism is a particular risk for the parturient following caesarean section.
Thromboprophylaxis is recommended for a minimum of 7 days or longer in those groups at high risk.
In order to reduce the risk of spinal haematomas, thromboprophylaxis is prescribed 4 hours following
instrumentation of the back, i.e. following insertion of a spinal needle or removal of an epidural
catheter.
If there is concern about the coagulation status, then the multidisciplinary team will make an
assessment regarding when to commence low-molecular-weight heparin. Pneumatic boots and
compression socks can be used in the interim.
Follow-up
All patients who have had a CNB should be followed up by the anaesthetic team within 24 hours.
Follow-up data records patient satisfaction and any untoward side effects of regional anaesthesia (see
Chapter 26).
Enhanced recovery after caesarean section

Recent years have seen an increase in activity in the area of enhanced recovery after caesarean
section. NICE guidance would support safe discharge of parturients 24 hours following elective
caesarean section if they are recovering well, are apyrexial and do not have complications following
CS. Many units are working towards this by embracing the principles of enhanced recovery:
Focus on patient education antenatally
Reduction in starvation times
Preference for regional anaesthesia
Reduction in the duration of urinary catheterization
Active management of postoperative pain with regular oral pain-relieving medication
Active management of postoperative nausea and vomiting
Early reestablishment of oral intake and removal of intravenous cannula
Encouragement of early mobilization.
Programmes such as these can only be instituted with good patient information, adequate community
support and easy contact with the hospital should the need arise.
Key points
1. Regional anaesthesia for operative delivery is increasing.
2. A reduced spinal dose of local anaesthetic is required in the parturient owing to smaller CSF
volume and greater sensitivity of nerve fibres to local anaesthetic.
3. Assessment and documentation of block height should be performed prior to commencement

of surgery.
4. Combined spinal epidurals may offer prolongation of surgical anaesthesia and reduced
cardiovascular instability.
5. Prior to top-up of a labour epidural for operative delivery ensure that the epidural is
functioning well and that sufficient time is allowed.
6. Complications of CNB are rare; however, the anaesthetist must remain vigilant
postoperatively.
Further reading
Further reading
Allam, J., Malhotra, S., Hemingway, C. and Yentis, S. M. (2008). Epidural lidocaine-bicarbonate-
adrenaline vs levobupivacaine for emergency caesarean section: a randomised controlled trial.
Anaesthesia, 63, 243249.
Campbell, J. P., Plaat, F., Checketts, M. R. et al. (2014). Safety Guidelines: skin antisepsis for
central neuraxial blockade. Anaesthesia, 69, 12791286.
Goring Morris, J. and Russell, I. F. (2006). A randomised comparison of 0.5% bupivacaine with a
lidocaine/epinephrine/fentanyl mixture for epidural top-up for emergency caesarean section after
low dose epidural for labour. Int. J. Obstet. Anaesth., 15, 109114.
NHS Information Centre. (20112012). HES online NHS maternity statistics. Health and social
care information centre (HSCIC). http://www.hscic.gov.uk/catalogue/PUB09202.
Royal College of Anaesthetists. (2012). Raising the Standard: A Compendium of Audit Recipes, 3rd
edn. London: Royal College of Anaesthetists, 220221.
Royal College of Obstetricians and Gynaecologists. (2015). Reducing the Risk of Venous
Thromboembolism during Pregnancy and the Puerperium. Green Top Guideline No. 37a. London:
Royal College of Obstetricians and Gynaecologists.
https://www.rcog.org.uk/globalassets/documents/guidelines/gtg-37a.pdf
Royal College of Obstetricians and Gynaecologists. (2010). Classification of Urgency of Caesarean

Section: A Continuum of Risk. Good Practice No. 11. London: Royal College of Obstetricians and
Gynaecologists.
https://www.rcog.org.uk/globalassets/documents/guidelines/goodpractice11classificationofurgency.pd
Russell, I. F. (1995). Levels of anaesthesia and intraoperative pain at caesarean section under
regional block. Int. J. Obstet. Anaesth., 4, 7177.
Russell, I. F. (2004). A comparison of cold, pinprick and touch for assessing a level of spinal block
at caesarean section. Int. J. Obstet. Anaesth., 13, 146152.
Sanders, R. D., Mallory, S., Lucas, D. N. et al. (2004). Extending low-dose epidural analgesia for
emergency caesarean section using ropivicaine 0.75%. Anaesthesia, 59, 988992.
Yentis, S. M. (2006). Height of confusion: assessing regional blocks before caesarean section. Int. J.
Obstet. Anaesth., 15, 26.
Chapter 12
General anaesthesia for caesarean section and
transverse abdominal plane block

Suraj Jayasundera and Karen Butler
Introduction
Over the last 40 years, the caesarean section delivery rate in developed countries has increased
substantially; 9% of deliveries were by caesarean section in England in 1980 compared with 24.6%
in 20082009. The reason for the increase is likely multifactorial including:
Advancing maternal age at first pregnancy
Improved safety of the procedure (both surgically and anaesthetically with the increase in
regional anaesthesia)
Changes in womens preferences
Increasing numbers of parturients who have had a previous caesarean section.
The variation in overall caesarean section rates in hospitals in England can mainly be attributed
to the variation in rates of emergency caesarean section. The use of electronic fetal monitoring and
fetal scalp blood sampling, partograms, active management of labour and consultant involvement in
decision-making have all been shown to affect caesarean section rates.
General anaesthesia and caesarean section

The early Confidential Enquiries report anaesthesia as the third most common cause of direct
maternal death, after hypertensive disease and thromboembolism; this was mainly attributed to
general anaesthesia. General anaesthesia is now more than 30 times safer than it was in the 1960s.
Neuraxial anaesthesia, with its superior safety profile and improved patient experience, has
largely replaced general anaesthesia as the technique of choice for caesarean section. The Royal
College of Anaesthetists, in the Compendium of Audit Recipes, 3rd edition 2012, recommends that
less than 15% of Category 13 caesarean sections and less than 5% of elective caesareans, be
performed under general anaesthesia. General anaesthesia was used for 8% of all caesarean sections
in England and Wales in 2013 (Hospital Episode Statistics HES data).
General anaesthesia will always have a role in obstetric theatres and it commands special
precautions, compared to general anaesthesia in the non-pregnant population.
Indications
One of the principal indications for general anaesthesia is speed. In the circumstance of a Category 1
caesarean section (immediate threat to life of woman or fetus), general anaesthesia is still the
quickest and most reliable method of ensuring surgical anaesthesia.
Other indications include maternal preference, contraindication to neuraxial block, failure of
neuraxial block and certain emergencies, including severe haemorrhage.
The advantages of general anaesthesia include speed of onset, definitive control of the airway
and ventilation and reduced hypotension when compared with spinal anaesthesia.
Risks
General anaesthesia in the parturient poses its own particular risks. These are further exacerbated in
the labouring woman.
Airway complications
The Confidential Enquiry into Maternal and Child Health 19761978 reported 16 deaths from failed
intubation, oxygenation, and aspiration and airway problems compared with 2 deaths in 20062008.
Failed intubation remains a major cause for concern amongst obstetric anaesthetists. A recent
surveillance conducted by United Kingdom Obstetric Surveillance System (UKOSS), over a 2-year
period, reported an estimated rate of failed intubation at 1 in 500 (up to four times that of the non-
obstetric population). In 2013, Quinn et al. reported the incidence to be 1 in 224.
Although airway complications in obstetric practice are rare, a number of factors further add to
the complexity, including:
Alterations in physiology whilst pregnant with a reduction in respiratory reserve and

increased oxygen consumption
Altered anatomy with short neck, airway oedema and large breasts
Increasing prevalence of obesity
Isolated location
Active labour.
Failure to oxygenate the patient not failure to intubate causes death. This was highlighted in the 8th
CMACE report and further alluded to in the obstetric review in NAP4, both recommending that
obstetric anaesthetists must maintain their airway skills such that they are able to effectively manage
failed intubation. NAP4 further recommends the need for familiarization with a broad range of
supraglottic airway devices that may reduce the risk of aspiration and facilitate the insertion of a
definitive airway. Fibreoptic equipment and skill should be available when required.
Each trust will have a policy for managing failed intubation, including a failed intubation
algorithm. The algorithm for managing an obstetric failed intubation should follow the DAS
guidelines for unanticipated difficult intubation during RSI in the non-obstetric adult patient, with
the emphasis on oxygenation and when to wake the mother up.
The decision to wake a mother, following a failed intubation, with ongoing fetal distress is
difficult; abandoning GA may lead to fetal death, but arguably maternal wellbeing is paramount and
waking the patient in order to proceed with a regional technique would be appropriate. NAP4
suggests that waking a mother should not be an automatic reaction should an airway difficulty be
encountered, particularly if a supraglottic airway device is successfully being used that can also aid
intubation. Ultimately, this will depend on the quality of the airway and the specific obstetric
circumstances.
Aspiration
Mendelsons syndrome (described in 1941 by Mendelson, a New York obstetrician) refers to the
chemical pneumonitis caused by aspiration during anaesthesia, particularly in pregnancy.
Historically, aspiration pneumonitis is said to occur if greater than 25 mL of gastric content of pH
< 2.5 enters the lungs, although there is little evidence supporting this. In pregnancy, the lower
oesophageal sphincter tone is reduced and labour pains and opiates decrease gastric emptying,
leading to increased gastric volumes. These factors, combined with the reduction of oesophageal
sphincter tone during general anaesthesia, place the labouring parturient at significant risk of
aspiration.
Rapid sequence induction

Performance of a rapid sequence induction with preoxygenation, cricoid pressure, rapid
administration of induction agent and quick, short-acting muscle relaxant and tracheal intubation
became standard practice by the 1960s. This initially led to a surge in deaths from failed intubation,
failed oxygenation and other airway problems until the mid-1980s. This has now become rare, due to
a combination of better training and assistance, and use of failed intubation drills along with
capnography.
Critics allege that cricoid pressure provides no benefit in reduction of aspiration and can be
detrimental to laryngoscopic view. Although it is difficult to demonstrate benefit, as many
interventions were introduced at the same time (antacid prophylaxis, starvation in labour, tracheal
intubation, capnography, improvement in training), it would also be difficult to demonstrate no benefit
as trials would be unethical. Studies have shown that cricoid force, particularly in the optimum range
of 2030 N, does not distort the view at laryngoscopy. If, however, it is distorting the view, it is
entirely acceptable to release, decrease or increase force.
Other risks of general anaesthesia include:
Awareness
Respiratory complications
Dental damage
Corneal abrasion
Anaphylaxis
Sore throat
Uterine atony secondary to anaesthetic agents
Post operative nausea and vomiting

Neonatal depression.
Preoperative assessment
In the emergency situation, time is limited and preoperative assessment must be comprehensive and
focused in order to reduce the risks from anaesthesia. See Table 12.1.
Figure 12.1 Obstetric failed intubation algorithm.
Table 12.1 Proposed template for obstetric preoperative assessment
Problems with previous anaesthetics
Family history of anaesthetic reactions
Co-morbidities:
Most parturients are ASA 1. However, maternal age, co-morbidity and obesity are
increasing and pre-existing cardiac or respiratory disease is not uncommon
Obstetric history:
Pre-eclampsia being of particular relevance
Placental site
Allergies
Medications
Airway assessment
Starvation times
Recent blood results including group and save or cross-match if appropriate
Premedication
Premedication aims to reduce the risk of aspiration and should be given to all parturients planned for,
or at risk of, operative delivery.
Ranitidine (H2 receptor antagonist) blocks the action of histamine on gastric parietal cells,
decreasing gastric acid production. The oral preparation reaches peak plasma concentrations within
13 hours. There is a relationship between plasma concentrations of ranitidine and suppression of
gastric acid production, but wide interindividual variability exists. Aim for oral administration 6090
minutes prior to anaesthesia (or 30 minutes for IV administration). Its effects are sustained for up to 8
hours. It is recommended to be administered 6 hourly when in high risk labour.
Metoclopramide (dopamine antagonist) inhibits gastric smooth muscle relaxation. It accelerates
intestinal transit, increases the lower oesophageal sphincter resting pressure, increases amplitude of
oesophageal peristaltic contractions and raises the threshold of activity in the chemoreceptor trigger
zone. Given orally it can take between 30 and 75 minutes to act, but 13 minutes when given IV. Its
effects are sustained for 12 hours. Use of prokinetic agents in labour is not as widespread as it once
was.
Sodium citrate 0.3 M 30 mL has the benefit of instantaneous efficacy as an acid-neutralizing
agent; however, its effects are short lived. It is best used within 20 minutes of induction.
Anaesthesia
Induction
Successful performance of a Category 1 caesarean section under general anaesthetic requires the
anaesthetist to maintain clear communication, with good leadership and team working skills.
Of UK obstetric units, 70% perform anaesthesia for caesarean section in the operating theatre
rather than an anaesthetic room; this reduces the time from induction to delivery.
To minimize delay, intravenous induction is performed once the patient is catheterized, the
abdomen draped and surgeons scrubbed. The patient is positioned with left lateral tilt to avoid
aortocaval compression. Some practitioners also advocate a 30 head-up tilt, arguing improvement in
maternal wellbeing through an increased functional residual capacity (FRC), reduced breast
interference with intubation and reduced gastro-oesophageal reflux.
The ramped position, with the parturient sat up approximately 15, with the tragus of the ear
lying in the same horizontal plane as the sternal notch and the head extended, is particularly useful for
the obese parturient; reducing the risk of acid reflux, pulmonary shunting and improving the view at
laryngoscopy. Preoxygenation in this position is improved as FRC is increased compared to the
supine position, prolonging the safe apnoeic time after induction.
Aside from the importance of a tight-fitting oxygen mask, there is little consensus regarding the
conduct of preoxygenation. Described techniques include tidal volume breathing for 3 min or
performing 4, 5, or 8 vital capacity breaths. Regarding adequacy of preoxygenation, there is debate
that use of a set time period for preoxygenation should be abandoned in favour of a target FE02 (>0.8).
Induction agent
Properties of an ideal induction agent for obstetric anaesthesia include:
Fast onset
Clear end point
Reliable dose range
Cardiovascular stability
Minimal adverse maternal and neonatal effects
Ample user experience
Appropriate licensing
Low cost
No premixing.
In a survey of UK consultant OAA members 2011, 93% of obstetric anaesthetists favoured

thiopentone as the induction agent of choice for an obstetric RSI with only 7% of respondents using
propofol. Of those surveyed in 2013, 55% hardly or never used thiopentone outside of obstetric
practice.
See Table 12.2.
Table 12.2 Summary of comparison of thiopentone compared with propofol for obstetric anaesthesia
Thiopentone Propofol
Availability Sole UK manufacturer No manufacturing or availability issues

Long-term
production of drug not
guaranteed
Association with Long history of Introduced into clinical practice in 1980s

obstetric anaesthesia association Comparatively short history of association.
Most commonly used induction agent for general
anaesthesia in obstetrics outside of UK (2013)
Awareness No difference Lack of evidence of increased awareness

(although studies small To minimize maternal awareness dose
with poor
suggested 2.5 mg/kg
standardization and
power). To minimize
maternal awareness
dose suggested not less
than 5 mg/kg
Neonatal outcome Small number of No evidence that propofol advantageous
studies showing better Some studies show no difference in Apgar
Apgar scores scores
Longer-term studies
of neurodevelopment
post maternal GA
lacking
Maternal Higher maximal Less hypertension at laryngoscopy and intubation

haemodynamics maternal noradrenaline More hypotension
concentrations In combination with suxamethonium can cause
Less hypotension severe maternal bradycardia
User experience Still extensively used Extensively used for elective anaesthesia
for obstetric emergency Good experience profile for all grades of
anaesthesia. Largely
anaesthetist
replaced by other
induction agents for
non-obstetric
emergencies owing to
lack of familiarity
Drug error Highlighted by the UK Minimal risk

patient safety report as Nil reconstitution
a risk in obstetric Distinctive appearance
practice
Reconstitution error
Syringe-swap with
antibiotics
Summary of product Reconstituted drug Should not be used for obstetric anaesthesia
characteristics
should be used within unless clearly necessary
7 hours However, used worldwide by countries
Pre-filled syringes where thiopentone not available e.g. USA
90 day shelf life
Can be used
without adverse effects
in pregnancy (in doses
not exceeding 250 mg)
Opiates
Only 15% of UK consultant OAA members surveyed in 2011 routinely administer opiates at
induction. To avoid neonatal depression, opiate administration is traditionally withheld until after
umbilical cord clamping. Parturients with pre-eclampsia and cardiac disease require an
individualized approach regarding predelivery administration of opiates in order to obtund the
potentially hazardous hypertensive effects of laryngoscopy and to maintain maternal cardiovascular
stability. Short-acting opioids (alfentanil, remifentanil) are used and clear communication with the
neonatal team ensures anticipation of potential neonatal respiratory depression.
Total intravenous anaesthesia (TIVA)

One published case series, using TIVA with remifentanil infusions in the semi-elective setting,
reported that 6 out of the 10 neonates required mask ventilation briefly. Time required for TIVA
preparation may limit its use in elective general anaesthesia.
Muscle relaxants
Succinylcholine has a long association with obstetric general anaesthesia, producing excellent
intubation conditions within less than a minute, with the additional benefit of rapid offset. However,
under-dosing of suxamethonium may worsen intubating conditions; even a dose of 1.5 mg/kg may be
inadequate due to the increased volume of distribution in pregnancy.
Its undesirable side effects include anaphylaxis, trigger for malignant hyperpyrexia and
prolonged action in plasma cholinesterase deficiency. A reduction of up to 35% in
pseudocholinesterase concentration can lengthen the effects of suxamethonium. Return of spontaneous
breathing should be observed prior to administering a non-depolarizing muscle relaxant.
Suxamethonium-induced fasciculations increase oxygen consumption and may hasten onset of
hypoxia.
Rocuronium has less undesirable side effects. At doses of 1 mg/kg it produces equivalent
intubating conditions at 1 minute. Sugammadex (ORG 25969) rapidly reverses rocuronium-induced
neuromuscular blockade. With increasing familiarity this may become a more popular combination.
Maintenance
Anaesthesia is typically maintained with a volatile anaesthetic and nitrous oxide. There is limited
evidence regarding volatile agent use for caesarean section. Sevoflurane, with its rapid offset, is
commonly used. The sympathetic stimulation produced by desflurane should be considered prior to
use in hypertensive or pre-eclamptic parturients. Concomitant use of nitrous oxide allows a lower
concentration of volatile, thus reducing the potential for uterine atony. Of surveyed anaesthetists in
2010, 85% used nitrous oxide in obstetric cases. Minimum alveolar concentration is decreased by up
to 40% for pregnant patients; however, sufficient end tidal volatile is necessary to avoid awareness.
Following umbilical cord clamping, 5 IU oxytocin is slowly administered intravenously as a
uterotonic (as per NICE guidance).
Antibiotic prophylaxis should be administered within 60 minutes prior to surgical incision to
reduce maternal infectious morbidity (specifically endometritis). In an emergency this should not
delay surgery and should be administered when possible.
Postoperative analgesia
Opioids (morphine), paracetamol and NSAIDs can be administered if there are no contraindications
following umbilical cord clamping. Antiemetics are administered as required.
TAP blocks
In an attempt to anaesthetize the abdominal wall, various techniques have been employed, including
local anaesthetic wound infiltration, bilateral ilioinguinal blocks and more recently transversus
abdominis plane (TAP) blocks.
TAP blocks were first described by Rafi in 2001. Abdominal field blocks have long been used
in clinical practice. TAP blocks, however, are unique in requiring a single injection site. Incisions
below T10 derive most benefit from TAP blocks, thus it is ideal for the commonly used Pfannenstiel
incision. For classical incisions, its utility may be questionable as local anaesthetic spread is
variable above the T10 dermatome. Supplementation with sub-costal blocks may solve this problem.
TAP blocks do not negate the need for opiates altogether as they do not block visceral pain.
Studies of analgesia outcomes in ultrasound-guided TAP blocks, for caesarean sections, have been
mixed:
Improved analgesia has been demonstrated in two clinical trials. Both of these showed that
TAP blocks had significant benefits if primary analgesia was established with intravenous
opioids.
One trial, comparing TAP blocks to intrathecal morphine, demonstrated inferior analgesia. In
another recent trial, combining TAP block with intrathecal morphine failed to demonstrate any
improvement in analgesia.
Anatomy
The innervation of the anterolateral abdominal wall arises from the anterior spinal nerves T7L1.
Having arisen from the intercostal space, these nerves travel between transversus abdominis (TA)
muscles and internal oblique (IO) muscles. There is a lateral branch at the mid-axillary line and
anterior branches that pass through the rectus muscle to supply the overlying muscles and skin. Hence,
the nerves may be conveniently blocked posteriorly in the plane that exists between the IO and TA
muscles: the transverse abdominis plane (TAP). The ilioinguinal and iliohypogastric nerves (L1 with
some contribution from T12) have a slightly different course in that they generally remain deep to the
TA muscle and are not found in the TAP until a more anterior position (once medial to the anterior
superior iliac spine).
Block technique
Rafi originally described a landmark double pop needle technique through the triangle of Petit. This
area can be identified caudally by the iliac crest, anteriorly by the external oblique muscle and
posteriorly by the latissimus dorsi muscle. To improve reliability and arguably safety, the block
should ideally be performed under ultrasound guidance. The TAP block is typically described by
placing a high frequency (510 MHz) ultrasound probe in the transverse plane between the lower
costal margin and the iliac crest in the mid-axillary line. The structures readily identifiable are: sub-
cutaneous fat, external oblique, internal oblique, transversus abdominis, peritoneum and bowel.
Figure 12.2 Local anaesthetic infiltrated into TAP layer. External oblique (EO), internal oblique
(IO), transverse abdominis (TA) and peritoneum (P).
Using sterile precautions, a 50 mm needle is usually sufficient; however, a longer needle may be
required in the obese parturient. The needle is inserted in plane, from the medial aspect, making sure
that the needle tip is visible at all times. On entering the plane between IO and TA, a pop is usually
felt. When local anaesthetic is injected in this plane, the shape of a convex lens is created. There
should be minimal resistance to injection. The block needs to be placed bilaterally for a caesarean
section, hence a low concentration, high volume mixture (1520 mL each side) of long-acting local
anaesthetic is ideal.
For lower abdominal incisions (Pfannenstiel), injecting local anaesthetic at this mid-axillary site
may miss blocking the L1 nerves and could account for the reported failure rate. These nerves do not
enter the TAP until the anterior one-third of the iliac crest. To reliably block these nerves, it is
important to perform the block near the iliac crest and not go too posterior, as described in the
traditional approach.
Complications
Complications of TAP blocks are rare, particularly when guided by ultrasound; however, there has
been a case report of liver injury using ultrasound guidance. Reported complications of the blind
technique include liver laceration, bowel perforation and intraperitoneal placement of a TAP
catheter.
Figure 12.3 Diagrammatic representation of ideal probe and needle position.
Extubation
Prior to emergence, consideration should be given to reduce gastric volume and pressure, with gentle
in and out insertion of a wide-bore orogastric tube, if a full stomach if suspected (Lessons Learnt
from 8th Confidential Enquiry). Ensure adequate reversal of neuromuscular blockade. Extubate once
the parturient is awake, with full return of airway reflexes and in the left lateral position. In cases of
morbid obesity or poor respiratory reserve it may be more suitable to extubate in the sitting position.
Postoperative care
The mother should be recovered in an appropriately staffed postoperative care unit. Further
analgesia, if required, can be given in the form of titrated intravenous opioid. Opioid patient-
controlled analgesia (PCA) systems are commonly used. Midwifery input is essential to support
breastfeeding, bonding and care of the newborn.
Key points
1. Caesarean section delivery rates are increasing.
2. General anaesthesia is considered to be the quickest and most reliable method of ensuring
surgical anaesthesia for caesarean section for immediate life-threatening cases.
3. Obstetric anaesthetists must maintain their airway skills to ensure safe management of failed
intubation.
4. Antacid premedication is recommended for all labouring women at risk of operative

intervention.
5. Thiopentone remains the most commonly used IV induction agent in the UK.
6. TAP blocks can be used as opiate-sparing adjuncts to analgesia.

Figure 12.4 Ultrasound image demonstrating needle orientation when performing TAP block.
Illustrations reproduced with permission from Ultrasound Guided Procedures in Anaesthesia,
Barrington and Royse, www.heartweb.com.au
Further reading
Centre for Maternal and Child Enquiries (CMACE) (2011). Saving mothers lives: reviewing
maternal deaths to make motherhood safer: 20062008. The eighth report on confidential enquiries
into maternal deaths in the United Kingdom. BJOG, 118 (1), 1203.
Hebbard, P., Barrington, M. and Royse, C. E. (2008). Ultrasound Guided Procedures in Anaesthesia.
www.heartweb.com.au (accessed May 2015).
Knight, M., Spark, P., Fitzpatrick, K., Misztela D., Acosta, C. and Kurinczuk, J. J. on behalf of
UKOSS (2011). United Kingdom Obstetric Surveillance System (UKOSS) Annual Report 2011.
Oxford: National Perinatal Epidemiology Unit.
Levy, D. and Meek, T. 2006. Traditional rapid sequence induction is an outmoded technique for
caesarean section and should be modified. IJOA, 15(3), 227232.
McDonnell, N. J. and Paech M. J. (2012). Editorial. The transversus abdominis plane block and post-
caesarean analgesia: are we any closer to defining its role? IJOA, 21(2), 109111.
Murdoch, H., Scrutton, M. and Laxton, C. H. (2013). Choice of anaesthetic agent for Caesarean
section: a UK survey of current practice. IJOA, 22(1), 3135.
Rafi, A. N. (2001). Abdominal field block: a new approach via the lumbar triangle. Anaesthesia,
56(10), 10241026.
Royal College of Obstetricians and Gynaecologists (2004). Why Mothers Die 20002002. Report on
Confidential Enquiries into Maternal Deaths in the United Kingdom. London: RCOG.
Van de Velde, M., Teunkens, A., Kuypers, M. et al. (2004). General anaesthesia with target
controlled infusion of propofol for planned caesarean section: maternal and neonatal effects of a
remifentanil-based technique. IJOA, 13(3), 153158.
Chapter 13
Anaesthesia for other obstetric indications:
cervical suture, external cephalic version,
controlled ARM, manual removal of placenta
and perineal repair

John R. Dick
Cervical cerclage
Introduction
Preterm birth is defined as delivery before the 37th week of pregnancy and accounts for 7.6% of all
live births. Prematurity is the leading cause for perinatal death and disability. With improvements in
neonatal care, infants that reach 26 weeks gestation have a survival rate of approximately 80%;
however, up to 50% will have some form of disability, e.g. neurodevelopmental deficits,
gastrointestinal and lung disease. The incidence of prematurity is increasing, in the UK from 7%
(1995) to 8.6% (2010) and in the USA 9.5% (1981) to 12.8% (2006); this is mainly from an increase
in medically indicated preterm delivery e.g. pre-eclampsia and fetal growth restriction. The
economic burden as a result of prematurity is immense, in the UK it was 939 million/year (2009)
and in the USA $2.9 billion/year (2007).
The causes of spontaneous preterm birth are multifactorial; however, one of the strongest
predictors of spontaneous preterm labour is short cervical length.
Cervical insufficiency is characterized by recurrent painless cervical dilation and spontaneous
mid-trimester birth; the diagnosis relies on previous clinical history. The Cochrane Collaboration
reviewed the evidence for cerclage for preventing preterm birth in a singleton pregnancy in 2012. The
nine randomized trials included showed that compared to expectant management the placement of
cervical cerclage in women at risk of preterm birth significantly reduces the risk of pre-term births.
However there is a lack of neonatal outcome and follow-up data.
Types of cervical cerclage

1. History indicated: should be offered to women with three or more previous preterm births
and/or second trimester losses. Usually performed at 1218 weeks gestation.
2. Ultrasound indicated: women with a history of one or more mid-trimester losses or preterm
births who are undergoing ultrasound surveillance should be offered ultrasound-indicated
cerclage if the cervix is 25 mm or less and before 24 weeks gestation.
3. Transabdominal cerclage: this can be used following failed vaginal cerclage or extensive
cervical surgery. This requires laparotomy or laparoscopy.
4. Rescue cerclage: the decision to perform rescue cerclage needs to be made by a senior
obstetrician; the evidence of improved neonatal outcome in this situation is very limited.
Contraindications to cervical cerclage insertion:
1. Active preterm labour
2. Clinical evidence of chorioamnionitis
3. Continual vaginal bleeding
4. Preterm prelabour rupture of membranes
5. Evidence of fetal compromise
6. Lethal fetal defect
7. Fetal death.
Immediate complications for all types of cerclage include rupture of membranes, preterm labour and
bleeding.
Transvaginal cerclage
Technique involves a transvaginal approach to the cervix and the placement of a sub-mucosal stitch at
the level of the internal os of the cervix. The Shirodkar suture is harder to remove and is associated
with a higher rate of caesarean delivery than the McDonald suture. The latter technique, which uses a
purse-string of tape, has the advantage that it can be removed without anaesthetic either antepartum or
intrapartum to allow for vaginal delivery (see Figure 13.1).
Figure 13.1 Insertion of McDonald suture.

(Source Gabbe et al., 2013, with permission of Elsevier.)
Abdominal cerclage
This is reserved for patients with an extremely short cervix or in patients with a history of failed
transvaginal cerclage. This procedure is usually done by laparotomy or laparoscopy at around 12
weeks gestation and requires a general anaesthetic. The suture is often left in situ and baby delivered
by caesarean section.
Anaesthetic technique for transvaginal cerclage

For history-indicated cerclage there is a choice of spinal, epidural or general anaesthetic. There is
one randomized trial comparing spinal and general anaesthesia for planned second-trimester
cerclage. Yoon et al. measured oxytocin levels (as a surrogate of uterine stimulation) before, 1 hour
after and 24 hours after the procedure and found no significant change in either group. A regional
block will need to extend from T10 to S4 to cover both components of cervical innervations. The
majority of practitioners use hyperbaric bupivacaine 0.5% (1012.5 mg) with fentanyl (1520 g). In
terms of intrathecal dose of bupivacaine, although a lower block height is required compared to
caesarean section at term, spinal dose requirements are greater up to 20 weeks.
If the cervix is dilated and the membranes are prolapsing through the cervix, this may necessitate
emergency cerclage. The choice of anaesthesia should be discussed with the obstetrician. General
anaesthesia may confer some advantage if uterine relaxation is required; however, the risk of
coughing and vomiting is increased compared to the use of spinal anaesthesia. In a rescue cerclage,
especially with prolapsing membranes, the lateral position can be helpful in reducing intra-abdominal
pressure and minimizing the risk of ruptured membranes during the procedure. If a regional technique
is used then uterine relaxation can be achieved for 12 minutes with the use of nitroglycerin (GTN).
For general anaesthesia the patients trachea should be intubated if there is an aspiration risk, but
for fasted subjects before 18 to 20 weeks gestation, a laryngeal mask airway (preferably a second-
generation LMA with a gastric drainage tube) may be acceptable and may help to reduce coughing
and straining on emergence. The choice of induction agent is between thiopentone and propofol, with
propofol being best for laryngeal mask use and smoother recovery. There is no evidence to support
the routine use of antibiotics for elective or emergency cerclage, although it is usual to provide cover
for carriers of Group B streptococcus. For viable fetuses, usually defined as beyond 24 weeks, it may
be wise to monitor the fetal heart rate periprocedure.
External cephalic version (ECV)

The incidence of breech presentation at term is about 34%. This has resulted in increases in
caesarean section rate, due to concerns about and risks encountered with vaginal breech delivery (see
Chapter 6). Breech presentation can be converted to a vertex presentation with ECV. Two recent
meta-analyses published in 2011 concluded the success rate of ECV can be significantly improved if
neuraxial block is utilized and there was no significant increase in fetal or maternal compromise.
Controlled artificial rupture of membranes (ARM)

This procedure is performed in theatre because of either polyhydramnios or unstable lie. This carries
a risk of cord prolapse or malpresentation, which may lead to an emergency caesarean section. For
safety, this procedure may be performed in theatre with fetal heart rate monitoring.
It is important to thoroughly discuss the options with the woman prior to the procedure:
1. No anaesthetic for ARM, then if there is a cord prolapse or malpresentation, the choice is
either general anaesthesia or spinal anaesthesia if there is no fetal compromise.
2. Spinal anaesthesia, this may be appropriate if there are airway difficulties or other maternal
morbidity, e.g. morbid obesity.
3. Combined spinal epidural technique, with a low-dose spinal for the ARM and an epidural
catheter placed for labour. The CSE technique may allow the option to quickly extend the block
for emergency caesarean in the event of cord prolapse.
In the event of a cord prolapse, available techniques to prevent the presenting part compressing the
cord include manual displacement, filling the bladder and lateral position. These techniques can buy
time to extend the epidural block for surgery, but the anaesthetist should be at all times prepared to
induce general anaesthesia if requested.
Manual removal of placenta (MROP)

With active management of the third stage (i.e. uterotonic plus controlled cord traction), 95% of
placentas will deliver within 15 minutes. A retained placenta is defined as failure to deliver within
30 minutes of birth. This increases to 60 minutes for passively managed third stage of delivery. Most
commonly, the cause is placenta adherens, which is caused by a failure of contraction of the
retroplacental myometrium. This type comes away easily with MROP. A trapped placenta occurs
where the placenta is already separated, but is trapped by the cervix. There may also be placenta
accreta (invasion of myometrium) that may require piecemeal removal. Ultrasound is useful for
differentiating between the three types of retained placenta. It is recommended that a vaginal
examination be performed just prior to transfer to theatre to assess for spontaneous delivery of the
placenta if there is a delay between diagnosis and going to theatre.
Patients with retained placentas will continue to bleed from a failure of contraction of the
placental bed, and can be significantly hypovolaemic. Whilst any delay in going to theatre increases
blood loss, some patients will spontaneously complete the third stage at the expense of acceptable
blood loss (a wait of 90 minutes prior to surgery resulted in a 55% placental delivery rate with
estimated 400 mL blood loss), thus avoiding an intervention. Fortunately deaths associated with this
condition are rare in the UK (two since 1967 from triennial reports) compared with less well-
resourced countries (e.g. 13 deaths associated with retained placenta in 1999 alone), which is
probably due to prompt diagnosis and management.
Anaesthetic management involves prompt assessment of patient for estimation of blood loss and
volaemic status. Hypovolaemia should be corrected prior to theatre with timely planning for blood
and blood products where indicated. If there is an epidural catheter in situ and the patient is
haemodynamically stable then epidural anaesthesia can be used. A block from T10 extending to S4 is
required. Similarly a spinal anaesthetic may be used to produce a similar block, but again this should
only be used with extreme caution and after adequate resuscitation. In cases involving ongoing or
major maternal haemorrhage a general anaesthetic is always preferred.
An oxytocin infusion is often started when the diagnosis of retained placenta is made; however,
this can make MROP more difficult by causing the cervix to contract. GTN may be used to help relax
the cervix and uterus (50100 g IV bolus or 1 mg sublingually) if a regional anaesthetic is being
used. The use of direct umbilical vein injections of oxytocin has been the subject of a study, but
showed no benefit. The role of intravenous prostaglandins may be beneficial in reducing the need for
MROP in patients with retained placenta, although this trial used sulprostone, which is not available
in the UK. There is an increased risk of infection from MROP and prophylactic broad-spectrum
antibiotics should be used. An infusion of oxytocin is used to maintain uterine tone and hence
minimize bleeding after the procedure.
Perineal repair
Perineal trauma occurs in most vaginal deliveries and will require a repair. The degree of tear needs
to be identified post delivery.
Classification of perineal trauma:

1. First-degree lacerations: injury to the perineal skin and vaginal epithelium
2. Second-degree lacerations: extend into fascia and musculature of the perineal body, anal
muscles are intact
3. Third-degree lacerations: extend into the fascia and musculature of the perineal body,
involving some or all of the fibres of the external anal sphincter (EAS) and/or the internal anal
sphincter (IAS). These are further subdivided according to which fibres are torn
4. Fourth-degree lacerations: involves all the perineal structures, EAS, IAS and the rectal
mucosa.
Assessment before theatre

Perineal tears can cause massive haemorrhage; complex second-degree tears can often bleed
profusely and may extend into the pouch of Douglas and the peritoneal cavity.
Local anaesthesia usually suffices for first- and straightforward second-degree tears, these
normally being repaired in the delivery room.
Complex second-, third- and fourth-degree tears require repair in theatre. It is vital that the
woman is adequately resuscitated prior to anaesthesia; women who are significantly hypovolaemic
may require general anaesthesia. If the woman is euvolaemic, then spinal or epidural anaesthesia is
preferable.
If an epidural catheter is in situ, then this can easily be topped up for perineal repair. Spinal
anaesthesia has to be sufficient to cover uterine innervation, particularly when the woman has a
complex vaginal tear.
All women who have a perineal repair in theatre should be given broad-spectrum antibiotics.
Third- and fourth-degree tears involve the anal sphincter and have significant associated
morbidity, including faecal incontinence, rectovaginal fistula, infection and pain. These women
should be referred to urogynaecology services 36 months after their perineal injury, for further
assessment with regards to continence, sexual dysfunction and chronic pain of the lower genital tract.
Key points
1. If there is risk of preterm birth cervical cerclage will reduce the risk.
2. Neuraxial block can significantly improve the success rate of ECV.
3. Definition of retained placenta is failure to deliver the placenta after 30 minutes or 60 minutes
if the third stage is managed passively.
4. Retained placenta is a leading cause of postpartum haemorrhage. The patient requires prompt
assessment of volume status, estimation of blood loss and appropriate correction of any
hypovolaemia.
Further reading
Arulkumaran, S., Regan, L., Papageorghiou, A. T. et al. (eds.) (2011). Preterm labour. In Oxford
Desk Reference: Obstetrics and Gynaecology. Oxford: Oxford University Press, 350351.
Berghella, V., Odibo, A. O., To, M. S., Rust, O. A. and Althuisius, S. M. (2005). Cerclage for short
cervix on ultrasonography: meta-analysis using individual patient-level data. Obstet. Gynecol., 106,
181189.
Gabbe, S. G., Niebyl, J. R., Galan, H. L. et al. (2013). Cervical insufficiency. In Obstetrics: Normal
and Problem Pregnancies. Philadelphia, PA: Saunders, Chapter 27.
Hong, J.-Y. (2006). Adnexal mass surgery and anesthesia during pregnancy: a 10-year retrospective
review. Int. J. Obstet. Anesth., 15, 212216.
Jones, G. (2011). Late miscarriage and early birth. In Baker, P. and Kenny, L. (eds.), Obstetrics by
Ten Teachers. Boca Raton, FL: CRC Press, 134135.
National Committee for Confidential Enquiries into Maternal Deaths (NCCEMD). (1999). Second
Interim Report on Confidential Enquiries into Maternal Deaths in South Africa.
http://www.gov.za/sites/www.gov.za/files/interimrep_0.pdf (accessed May 2015).
Sultan, P. and Carvalho, B. (2011). Neuraxial blockade for external cephalic version: a systematic
review. Int. J. Obstet. Anesth., 20, 299306.
van Shalkwyk, J., van Eyk, N. and The Society of Obstetricians and Gynaecologists of Canada
Infectious Diseases Committee. (2010). Antibiotic prophylaxis in obstetric procedures. J. Obstet.
Gynaecol. Can., 32(9), 878892.
Weeks, A. D., Alia, G., Vernon, G. et al. (2010). Umbilical vein oxytocin for the treatment of retained
placenta (RELEASE study); a double blind randomized controlled study. Lancet, 375, 141147.
Yoon, H. Y., Hong, J. Y. and Kim, S. M. (2008). The effect of anesthetic method for prophylactic
cervical cerclage on plasma oxytocin: a randomized trial. Int. J. Obstet. Anesth., 17, 2630.
Section 4

Medical conditions in pregnancy

Chapter 14
Hypertension in pregnancy, pre-eclampsia and
eclampsia

Suna Monaghan, Jenny Myers and Lorna A. Howie
Introduction
Hypertensive disorders of pregnancy are one of the most common antenatal complications, affecting
34% of all pregnancies:
They are a leading cause of direct maternal death in the UK and USA, with a rate of 0.83 and
0.99 per 100,000 maternities respectively
The necessity for urgent treatment of systolic hypertension (>160 mmHg) was one of the top
ten recommendations in the last Maternal Mortality Report (CMACE 20062008):
There were seven deaths associated with inadequate control of systolic hypertension
resulting in cerebral haemorrhage
Women with severe pre-eclampsia need to be managed by an effective multidisciplinary

team
There is fetal morbidity and mortality associated with pre-eclampsia:
Iatrogenic preterm delivery
Fetal death in utero and stillbirth
Fetal growth restriction

There is also growing evidence of increased long term health risks in:
Women who have had pre-eclamptic pregnancies, including cardiovascular disease, type
2 diabetes mellitus and metabolic syndrome
Children of pre-eclamptic mothers also have an increased risk of hypertension and

metabolic syndrome in later life.
Classification of hypertension in pregnancy

Hypertension in pregnancy is categorized according to gestation and cause (see Table 14.1). Before
20 weeks, it is likely to be due to chronic, pre-existing hypertension. Hypertension is often identified
for the first time in early pregnancy and it is important to rule out any secondary causes. The
commonest secondary cause is renal disease, but it is important to exclude vascular, endocrine and
immunological causes. Approximately 20% of women with chronic hypertension will go on to
develop superimposed pre-eclampsia.
Table 14.1 Hypertension in pregnancy
Condition Diagnosis
Chronic hypertension Hypertension (BP >140/90):
Present at booking
Present before 20/40
Being treated at the time of referral to

maternity services
Gestational hypertension New hypertension (BP >140/90):
Presenting after 20/40
Without significant proteinuria
Also known as pregnancy-induced

hypertension (PIH)
Affects 1 in 10 pregnancies
Pre-eclampsia New hypertension (BP >140/90):
After 20/40
With significant proteinuria
Affects 23% of pregnancies
2% can go on to develop eclampsia

(worldwide)
Severe pre-eclampsia New severe hypertension (BP >160/110):
After 20/40
With significant proteinuria
+/ symptoms (see below)
+/ biochemical impairment
+/ haematological impairment
HELLP severe expression of PET,

associated with haemolysis, elevated
LFTs and low platelets
Eclampsia Convulsive condition associated with pre-

eclampsia
Gestational hypertension complicates 10% of pregnancies and is defined as new-onset

hypertension (>140/90 mmHg) after 20 weeks, without significant proteinuria or other features
suggestive of multisystem disease.
Pre-eclampsia affects 34% of pregnancies, and is defined as new-onset hypertension with
significant proteinuria: greater than 300 mg of urinary protein in 24 hours or a urinary
protein:creatinine ratio (uPCR) > 30 mg/mmol.
Pre-eclampsia can occur at any time after 20 weeks gestation, even into the postpartum period.
Early-onset pre-eclampsia (<34/40) represents around 30% of cases and is often associated with
more severe fetal compromise. Severe maternal disease can develop at any gestation. The only cure
for the condition is delivery of the placenta.
Pre-eclampsia may take several days to resolve post delivery. Blood pressure and proteinuria
should resolve within 12 weeks of delivery. Women with early onset pre-eclampsia have a 25%
chance of ongoing hypertension and proteinuria; this suggests an underlying cause, usually related to a
renal condition, which requires further investigation.
Definitions
Hypertension
This can be deemed mild, moderate or severe (NICE) (see Table 14.2). Blood pressure readings
should be made with manual sphygmomanometers instead of an automated machine, as these tend to
underestimate systolic blood pressure.
Table 14.2 Definition of hypertension
Hypertension BP reading
Mild 140149/9099
Moderate 150159/100109
Severe >160/110
Proteinuria
Significant proteinuria:
Protein >300 mg/24 hours or
Urinary protein:creatinine ratio (uPCR) >30 mg/mmol on a spot sample.
NB. A degree of proteinuria is a normal physiological change in pregnancy.
Pathogenesis
The cause of pre-eclampsia is not well understood; however, the placenta is the organ that drives
pre-eclampsia.
The concept of a two-step model of trophoblast invasion has become widely accepted:
1. Invasion of the decidual segments of the spiral arteries (1012 weeks)
2. Invasion of the myometrial segments (1516 weeks).
In pre-eclampsia the second stage of the process is impaired and results in impairment of remodelling
the spiral arteries. The outcome is a poorly perfused and poorly developed placenta. Placental
ischaemia is thought to be the reason for release of placental factors and the resultant imbalance of
angiogenic factors. The altered placental function is associated with changes in the production and
secretion of a number of placental-derived factors, which cause widespread maternal vascular
endothelial dysfunction.
Widespread changes in the maternal vascular endothelium are characterized by vasoconstriction,
capillary leak and an activation of the maternal inflammatory and clotting cascades.
A number of placental factors have been investigated in relation to pathogenesis of pre-
eclampsia and it is likely that there is more than one aetiological mechanism that leads to placental
dysfunction and pre-eclampsia. Research has been focused on a number of angiogenic markers.
Angiogenesis is essential for normal placentation and two factors contribute to this:
Vascular endothelial growth factor (VGEF)
Placental growth factor (PlGF).
There are two antiangiogenic markers that have been studied:
Soluble FMS-like tyrokinase (sFlt-1): this peptide binds to and neutralizes the actions of
VGEF and PlGF
Soluble endoglin (sEng): the levels of this peptide normally fall between the first and second
trimesters; however, this is attenuated in women who go on to develop pre-eclampsia.
The result is an imbalance between proangiogenic and antiangiogenic peptides. These

biomarkers may provide a way of detecting pre-eclampsia before the systemic signs of the disease
appear. An elevation in sFlt and sEng with a reduction in VEGF and placental growth factor PlGF are
currently being investigated as potential predictive, prognostic and diagnostic markers.
Risk factors
Many of the risk factors associated with pre-eclampsia identify a group of women with increased risk
of vascular disease and these are the women at highest risk of developing the condition. It is likely
that they are sensitized to the stressors of pregnancy and have an exaggerated response to placental
dysfunction. The NICE guidelines recommend that women with risk factors for the development of
pre-eclampsia should be prescribed 75 mg aspirin daily from 12 weeks until delivery. Aspirin is
associated with a modest (around 15%) reduction in the rate of pre-eclampsia in high-risk groups.
See Table 14.3 for risk factors related to development of pre-eclampsia.
Table 14.3 Risk factors associated with pre-eclampsia
Moderate risk High risk
1st pregnancy Hypertensive disease during a previous
Age > 40 pregnancy
Pregnancy interval of > 10 years Chronic renal disease
Family history of pre-eclampsia Autoimmune diseases (SLE,

antiphospholipid syndrome etc.)
Multiple pregnancy
Diabetes
BMI 35
Chronic hypertension
Signs, symptoms and complications

Table 14.4 summarizes the diagnostic criteria for severe pre-eclampsia.
Table 14.4 Diagnostic criteria for severe pre-eclampsia
Severe pre-eclampsia: hypertension and proteinuria in addition to any one of the following
features:
CVS
Severe hypertension (SBP >160 or DBP >110)

Chest pain
Sudden swelling of face/hands/feet
Renal
Oliguria (decrease in GFR)
Creatinine >100 mmol/L
Cortical/tubular necrosis
CNS
Severe frontal headache
Visual disturbance including blurring and flashing in front of the eyes
Cortical blindness
Retinal oedema
Clonus
Eclampsia
Cerebral haemorrhage/oedema
Respiratory
Dyspnoea
Pharyngeal/laryngeal oedema
GIT
Nausea and vomiting
Right upper quadrant pain (as a result of liver capsule tension)
Epigastric pain
ALT > 50 IU/L
HELLP
Haematological
Thrombocytopenia (platelets <100 109)

Falling fibrinogen
Disseminated intravascular coagulation (DIC)
Prolonged clotting times
Microangiopathic haemolysis
Feto-placental
IUGR
Oligohydramnios
Abruption
Abnormal umbilical Doppler
Preterm delivery (50% in severe pre-eclampsia)
Still birth
Investigations
Pre-eclampsia represents a clinical syndrome and has a very variable presentation and progression.
Although the most typical presentation is hypertension associated with proteinuria, many other
clinical presentations exist.
In any woman with gestational hypertension or gestational proteinuria, a diagnosis of pre-
eclampsia should be considered and multisystem disease should be investigated, e.g. altered renal
function, altered liver function, activation of the clotting cascade and fetal growth restriction. The
majority of women with pre-eclampsia and eclampsia will have normal blood tests.
1. Proteinuria: the diagnosis of gestational proteinuria is qualitative and once significant

proteinuria has been established, there is no merit in repeatedly testing the urine, as protein
excretion in pre-eclampsia is highly variable day to day and does not predict the development of
maternal complications of severe pre-eclampsia. Women who are heavily proteinuric may also
have hypoalbuminaemia, which is associated with an increase in thromboembolic risk.
2. Bloods: check daily in severe PET, more frequently if abnormal:

a. U+E an increase in serum creatinine is suggestive of worsening maternal disease
b. FBC a rapid fall in platelet count is suggestive of severe pre-eclampsia
c. LFT significant increases in the transaminases are suggestive of severe disease.
d. Clotting is rarely abnormal unless another condition is present, e.g. placental abruption.
In severe pre-eclampsia, if the platelet count is rapidly falling, it can be useful to exclude
DIC.
e. Urate this test has little value in the management of pre-eclampsia as it is not predictive
of severe disease. It is occasionally grossly elevated as the first sign of renal involvement
(prior to proteinuria) in association with hypertension and can therefore sometimes be useful
as a diagnostic test. Gestational age-adjusted thresholds should be used.
Management
Women at high risk of developing the condition should be monitored more frequently with the aim of
identifying signs of the condition early.
The management of pre-eclampsia involves:
1. Maintenance of hypertension at a safe level i.e. SBP < 150 mmHg (the absolute value will be
dependent on any underlying chronic hypertension)
2. Using oral antihypertensives, e.g. labetalol, nifedipine and methyldopa
3. Regular monitoring of the mother and fetus for the development of adverse features.
Women with an established diagnosis of pre-eclampsia should be managed in the hospital setting to
ensure regular monitoring of BP, blood tests and assessment of fetal wellbeing. Ultimately delivery of
the baby and the placenta is the only curative treatment.
Women who develop severe pre-eclampsia (see Table 14.4) require level 2 care on a
consultant-led labour ward and should be managed by an experienced multidisciplinary team
comprising senior obstetricians, anaesthetists, critical care specialists, neonatalogists and physicians,
if required.
The main principles for the management of severe disease are:
1. Maintenance of safe blood pressure (< 150/80100 mmHg)

2. Fluid management
3. Cerebral protection
4. Thromboprophylaxis
5. Timely delivery.
Blood pressure
The most frequent cause of maternal death in association with pre-eclampsia is cerebral haemorrhage
secondary to severe systolic hypertension. Prompt and effective treatment of severe hypertension has
been highlighted by recent maternal mortality reports as a common area of sub-standard care.
Blood pressure should be measured manually at rest using Korotkoff V as the diastolic value,
with an appropriately sized BP cuff. Manual sphygmomanometers are the most accurate way of
measuring BP, as automatic devices tend to underestimate the systolic pressure. In severe disease,
when intravenous antihypertensives are indicated and/or multiple blood samples are required,
invasive arterial pressure monitoring may be beneficial.
Severe hypertension can be treated with oral or intravenous antihypertensives. Oral labetalol
(200 mg doses) or nifedipine (10 mg doses) can be used in the first instance. If BP control is
inadequate (SBP < 150, within 1 hour of antihypertensive medication), then intravenous labetalol
and/or hydralazine should be given. Hydralazine is often more effective in certain ethnic groups, e.g.
afrocarribean. There is no place for the administration of sublingual nifedipine; this can cause a
precipitous drop in the BP (see Table 14.6).
Table 14.5 Eclampsia management
Eclampsia management
Call for HELP
Airway
Breathing
Circulation
Magnesium sulfate
Loading dose 4 g IV over 5 mins
Maintenance dose 1 g/hr
For recurrent fits

Further 2 g magnesium over 10 mins (4 g if > 70 kg)
Second line diazepam 10 mg IV or thiopentone 50 mg IV
Consider other causes of seizures
May need CT scan once stabilized
Intubation if failure to regain consciousness.
Table 14.6 Antihypertensive agents
Drug Labetolol Nifedipine Hydralazine Magnesium Methyldopa

sulfate
Oral dose up to 10 mg (starting N/A N/A 250 mg up to

2.4g/day in dose) 1 g tds
34 divided
Available in
doses
three different
preparations:
capsules, MR od
and MR bd
(check drug
information
carefully)
Time to 30 min 60 min

effect
IV bolus 50 mg over N/A 2. 5 mg over 4 g over 5 N/A

dose 5 min 5 min 10 min
repeated repeated
every 10 min every 20 min
to a max of to a max of
200 mg 20 mg
Time to 10 min Within Within

effect minutes minutes
IV infusion 4 mL/h N/A 15 mg/h 1 g/h N/A

doubled
every 30 min
to a max of
32 mL/h
Class of Beta blocker Calcium-channel Directly Centrally acting

drug with alpha blocker acting antihypertensive
blocking vasodilator
properties
Side effects Caution in Profound Tachycardia Depression

asthmatics hypotension when Palpitations LFT
and people administered
abnormalities
with cardiac with MgSO4
disease Sedation
Haemolytic
anaemia
Antidote 10 mL 10%
calcium
gluconate IV
Fluid management
Pulmonary oedema was a frequent cause of death in women with pre-eclampsia, but the widespread
adoption of fluid restriction protocols has significantly reduced the frequency of this condition.
Women with severe pre-eclampsia have significant intravascular volume depletion; this can be as
much as 3040% less than in normal pregnancy. The decrease in oncotic pressure coupled with
widespread endothelial dysfunction and left ventricular diastolic dysfunction increases the risk of
pulmonary oedema.
An intravenous fluid regimen of approximately 80 mL/h is advised for the management of
women with severe pre-eclampsia. This should include all drugs and fluids (IV and oral).
If a syntocinon infusion is required, the diluent should be reduced to minimize fluid
administration:
1. For augmentation of labour: 30 IU syntocinon in 500 mL 0.9% saline
2. Post delivery: 40 IU syntocinon in 50 mL 0.9% saline over 4 hours.
Urine output should be measured hourly, usually via a urinary catheter and urometer to ensure an
accurate fluid balance. Diuretics should not be used to maintain urine output and their administration
should be restricted to instances of pulmonary oedema. A urine output of 0.25 mL/kg/h can be
tolerated for several hours and is rarely associated with acute renal failure unless another event
occurs, e.g. haemorrhage.
Continuous saturation monitoring and regular chest auscultation should be performed to identify
signs of pulmonary oedema. The postpartum diuresis will occur usually within 2448 hours of
delivery. Prior to this, in the presence of oliguria, regular monitoring of urea and electrolytes is
mandatory and the use of NSAIDs must be avoided.
Haemofiltration may be necessary if there is persistent acidaemia, hyperkalaemia, uraemia or
fluid overload. Central venous pressure monitoring can be misleading in pre-eclampsia as the
constricted vasculature alters venous pressures and therefore does not give an accurate representation
of intravascular fluid status.
Cerebral protection
Eclampsia occurs in 1:2000 deliveries in the UK with 38% antepartum, 18% intrapartum and 44%
postpartum. One in three fits occur before there is a measured rise in blood pressure or proteinuria;
1.8% are fatal and one in three will have ongoing neurological sequelae.
Neurological deterioration in eclampsia is secondary to cerebral vasospasm. The vasorelaxant
effects of magnesium sulfate make it the drug of choice for the prophylaxis and management of
eclampsia (Table 14.5).
In both instances a loading dose of 4 g IV over 5 min is followed by an infusion of 1 g/h
(Collaborative Eclampsia Trial). Magnesium should be continued for 24 hours from the time of
delivery or the last seizure, depending on which is later. If recurrent seizures occur, an additional 2 g
IV magnesium should be administered. It should be appreciated that magnesium sulfate does not have
significant antihypertensive effects nor does it treat the underlying disease process.
The potential of serum magnesium toxicity should be monitored using clinical signs (respiratory
depression, reduced oxygen saturations, absence of deep tendon reflexes or ECG change). A
diagnosis of magnesium toxicity can be confirmed by a serum level > 3.5 mmol/L and is a particular
risk in the presence of oliguria as magnesium is renally excreted. The antidote is 10 mL 10% calcium
gluconate IV, over 10 min.
Thromboprophylaxis
Women with pre-eclampsia are at increased risk of thromboembolic events secondary to a depletion
of the intravascular compartment coupled with the hypercoagulable state of pregnancy.
Thromboprophylaxis by pharmacological (low-molecular-weight heparin; LMWH) and physical
(compression stockings) methods should be considered for all women with pre-eclampsia. The timing
of therapeutic LMWH may need to be adjusted in relation to surgery and neuraxial
analgesia/anaesthesia.
Timely delivery
Planned delivery should be done on the best day in the best way. The timing and mode of delivery is
determined by a number of maternal and fetal factors. Maternal condition should always be optimized
prior to delivery.
In cases of pre-term delivery it is necessary, if there is time, to give steroids to the woman to
reduce the severity of respiratory distress of the newborn and enhance fetal lung maturity. The regime
for gestation <34 weeks is dexamethasone 24 mg over 2448 hours.
The timing of delivery in non-severe cases of pre-eclampsia is usually determined by gestation
of the pregnancy. Before 34 weeks, conservative management with inpatient surveillance is
recommended. It is good practice to have a care plan that outlines the circumstances that require
prompt delivery; these include evidence of progression of maternal disease or significant fetal
compromise. Delivery should take place in a unit that has adequate neonatal facilities. Between 34
and 37 weeks, the indications for delivery are less clear. If the maternal disease is stable and there is
no fetal compromise, timing of delivery should be agreed between the obstetric and anaesthetic
teams, following discussion with the mother.
After 37 weeks, there is little benefit associated with continuing the pregnancy from a fetal
perspective and therefore delivery is recommended within 48 hours of diagnosis.
Mode of delivery
The mode of delivery will be determined by several factors, including maternal condition (e.g. rapid
progression of disease), obstetric history (e.g. previous caesarean section) and fetal condition (e.g.
prematurity, growth restriction, abnormal Doppler).
Irrespective of the mode of delivery, syntometrine is absolutely contraindicated and the use of
carboprost should only be used after discussion with the obstetric team.
Labour
Epidural analgesia is often beneficial as it is associated with a reduction in the pain-mediated
hypertensive response and may aid vasodilatation of the uteroplacental bed. It also has the advantage
of allowing top-up for surgical intervention if required. Preloading with fluids is not recommended.
A maternal platelet count should have been performed within the preceding 4 hours, or more recently
if there has been a downward trend. Prophylactic LMWH should not have been administered in the
preceding 12 hours (24 hours for treatment dose). It is not possible to be certain of the lowest
acceptable platelet count using current evidence; however, in the absence of other coagulation
abnormalities, a platelet count of >80 109/L is considered to be acceptable for epidural analgesia.
In the presence of thrombocytopenia, platelet transfusions may be considered to cover potential
surgery or haemorrhage. The use of thromboelastography (TEG) is valuable if available, giving a
real-time assessment of coagulation function. In cases of severe coagulopathy, regional anaesthesia is
contraindicated and PCA opioids should be considered as an alternative.
Caesarean section
Maternal safety should not be compromised to allow emergency delivery. It is vital that maternal
condition is stabilized prior to surgery. It is particularly important that severe hypertension is treated
and maintained within safe limits (<150/80100 mm Hg).
In the absence of other contraindications, regional anaesthesia is preferable as it avoids the
potential fluctuations in BP often encountered during intubation and extubation. Spinal anaesthesia has
been shown to be safe in pre-eclampsia with less hypotension than that experienced by women
without pre-eclampsia. With increasing use of TEG some anaesthetists may accept lower platelet
counts (50 109/L) for spinal anaesthesia if the TEG is reassuring, particularly if there are other
maternal co-morbidities. In severe pre-eclampsia there is often an enhanced response to conventional
doses of vasopressors and less hypotension during regional anaesthesia. It is prudent to use titrated
doses of ephedrine (3 mg boluses) or phenylephrine (50100 g boluses) rather than an infusion of
phenylephrine.
General anaesthesia may be necessary in certain circumstances, e.g. thrombocytopenia
coagulopathy, pulmonary oedema, haemorrhage, acute fetal compromise, failed regional anaesthesia
and eclampsia. Eclampsia often resolves after one episode treated with magnesium sulfate; however,
if there is a decreased conscious level after one eclamptic fit, recurrent fits or concern about signs of
cerebral oedema, there is a need to intubate to stabilize the woman and then decide on further
management.
Obtunding the hypertensive response to intubation and extubation in pre-eclampsia or eclampsia
is essential to avoid the risk of cerebrovascular compromise, cardiac ischaemia or arrhythmias.
This may be achieved with the use of one or a combination of drugs:
Alfentanil 1020 g/kg
Remifentanil 1 g/kg
Labetolol 1020 mg
Magnesium sulfate 3040 mg/kg
Lignocaine 100 mg IV
Esmolol 1 mg/kg (only use after delivery, high risk of fetal bradycardia).
The choice of drug(s) will depend on familiarity and availability. If opioids are used, neonatologists
should be made aware of the possibility of neonatal effects. Magnesium sulfate can prolong the effect
of non-depolarizing neuromuscular blockers, contribute to uterine atony and potentiate the effect of
calcium-channel blockers, e.g. nifedipine.
Pre-eclampsia accentuates the pharyngeal and laryngeal oedema that occurs in the latter stages of
pregnancy, it is essential to anticipate the potential for a difficult airway.
Postnatal care
It is important that women are appropriately monitored in the immediate postnatal period and that
hypertension is treated where necessary. Close attention to fluid management and cerebral protection
should also be continued. Thromboprophylaxis and analgesic regimes may need modification in
instances of coagulopathy, haemorrhage, renal or hepatic dysfunction.
Women frequently require antihypertensive treatment for several weeks post delivery and this
should be gradually reduced in response to blood pressure measurements. Women who have had
severe disease or early onset disease should be offered a secondary care postnatal review to ensure
that the hypertension and proteinuria has resolved by 12 weeks. In women with persistent
hypertension and/or proteinuria, underlying disease should be investigated.
All women who develop pre-eclampsia should have the opportunity to be counselled about the
risk of recurrence in a future pregnancy (1050%, dependent on severity and gestation at onset).
Women should also be informed that they are at increased risk of developing hypertension and
cardiovascular disease in later life.
Key points
1. Pre-eclampsia is a leading cause of maternal death worldwide.
2. Management is supportive until the definitive treatment of delivery. Timing of delivery should
depend on severity of the condition and gestational age.
3. Blood pressure should be accurately recorded and managed. Systolic blood pressure
>160 mmHg requires urgent treatment.
4. Dysfunction of maternal vascular endothelium results in the systemic disease process of pre-
eclampsia.
5. Magnesium sulfate is the drug of choice for the prophylaxis and management of eclampsia.
6. Regional anaesthesia is preferable for caesarean section, in the absence of any

contraindications.
7. If general anaesthesia is required, care must be taken to manage the hypertensive response and
the potential for a difficult airway with oedema recognized.
Further reading
Cantwell, R., Clutton-Brock, T., Cooper, G. et al. (2011). Saving mothers lives: reviewing maternal
deaths to make motherhood safer: 20062008. Eighth report of the confidential enquiries into
maternal deaths in the United Kingdom. BJOG, 118(1), 1205.
Dennis, A. T. (2012). Management of pre-eclampsia: issues for anaesthetists. Anaesthesia, 67,

10091020.
Duley, L., Meher, S. and Abalos, E. (2006). Management of pre-eclampsia. BMJ, 332(7539),
463468.
Li Wan Po, J. and Bhatia, K. (2013). Pre-eclampsia and the anaesthetist. Anaesth. Intens. Care Med.,
14(7), 283286.
National Institute for Health and Care Excellence (2010). Hypertension in pregnancy: the management
of hypertensive disorders during pregnancy. NICE guidelines CG107.
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Rana, S., Karumanchi, A. and Lindheimer, M. D. (2014). Angiogenic factors in diagnosis,

management, and research in preeclampsia. Hypertension, 63, 198202.
Chapter 15
Sepsis and influenza in pregnancy

Tim Holzmann and Dougal Atkinson
Sepsis
Introduction
Sepsis is defined as SIRS (systemic inflammatory response syndrome) caused by suspected or proven
infection. SIRS is the bodys response to an insult. The physiological hallmarks of SIRS are
generalized vasodilatation and increased microvascular permeability. These changes can be triggered
by both non-infective insults (e.g. burns) and infection. The development and progression of SIRS and
sepsis are thought to be due to uncontrolled release of pro-inflammatory mediators and dysregulation
of the inflammatory response, leading to widespread tissue injury. Sepsis is a dynamic process and
can progress to severe sepsis and septic shock. Despite mortality rates improving over the last 10
years, mortality from septic shock remains high at approximately 24%.
Sepsis in obstetrics
In 2005, the World Health Organization (WHO) reported that infection and sepsis were responsible
for 15% of global maternal deaths. In the latest UK Confidential Enquiry into Maternal Deaths sepsis
was the leading cause of direct maternal death. Maternal mortality from sepsis has increased almost
threefold in the last 25 years.
Sepsis can occur at any time during pregnancy and the puerperium. Sources of infection include
both obstetric and non-obstetric causes (Table 15.1). The physiological changes of pregnancy can
mask signs of sepsis and provide diagnostic difficulty. In addition, maternal deterioration can rapidly
result in fetal compromise. Prompt diagnosis and management are essential. Close liaison between
with obstetricians, anaesthetists, microbiologists, physicians and critical care is important to ensure a
good outcome for mother and baby.
Table 15.1 Causes of sepsis in obstetrics
Obstetric:
Chorioamnionitis
Endometritis
Wound infection
Septic abortion
Non-obstetric:
Upper and lower urinary tract
Pneumonia
Meningitis
The general principles of sepsis management discussed below apply to the obstetric patient, but
must also take into account the physiological changes of pregnancy and associated conditions (e.g.
pre-eclampsia).
Definitions
The following definitions have been developed to improve the ability to diagnose, monitor and treat
sepsis:
Infection: the invasion of normally sterile tissue by organisms.
Bacteraemia: the presence of viable bacteria in the blood.
Systemic inflammatory response syndrome (SIRS): the presence of two or more of the
following:
Temperature >38.3 C or <36 C
Heart rate >90 beats/min
Respiratory rate >20 breaths/min or PaCO2 <4.3 kPa

WBC >12,000 cells/mm3 or <4000 cells/mm3.
Sepsis: SIRS due to a suspected or proven infection.
Severe sepsis: the combination of sepsis and at least one organ dysfunction (Table 15.2).
Septic shock: severe sepsis plus hypotension (MAP < 60 mmHg or < 80 mmHg if pre-existing
hypertension) despite adequate fluid resuscitation (defined as a minimum of 30 mL/kg of
crystalloids).
Table 15.2 Examples of organ dysfunction
Capillary refill time > 3 seconds
Urine output < 0.5 mL/kg for at least one hour, or renal replacement therapy
Lactate > 2 mmol/L
Confusion (new onset)
Platelet count < 100,000 platelets/mL
Disseminated intravascular coagulation
Acute lung injury or acute respiratory distress syndrome (ARDS)
Cardiac dysfunction defined by echocardiography or direct measurement of the cardiac index
Pathophysiology of sepsis
The normal host response to infection is a complex process aimed at containing and controlling
bacterial invasion, as well as initiating tissue repair. The physiological processes to combat infection
are initiated when immune cells, particularly macrophages, recognize and bind to microbial
components. This process involves specific cell-surface receptors, including TLR, NOD, MDL-1 and
TREM-1. Binding of microbial components to these receptors activates intracellular cascades
leading to the release of pro-inflammatory cytokines (e.g. TNFa, IL-1, ICAM-1 and NO). At the same
time, interactions between polymorphonuclear leucocytes (PMN) and the vascular endothelium
enable migration of PMNs to the site of injury. The release of mediators by these cells results in local
vasodilatation, increased microvascular permeability and a protein-rich oedema.
This process is regulated by the complex interactions of pro- and anti-inflammatory mediators
resulting in tissue repair and healing when the opposing elements are balanced. In SIRS and sepsis,
the above processes become generalized, with normal tissues also becoming involved. The exact
cause of this is unknown, but is likely multifactorial, including genetic susceptibility, excessive
release of pro-inflammatory mediators and specific properties of individual micro-organisms.
Mechanisms underlying the resulting organ dysfunction include tissue ischaemia from a combination
of imbalances between coagulation, anticoagulation and endothelial abnormalities, direct cell injury
by pro-inflammatory mediators and widespread apoptosis (programmed cell death) of various cells,
including lymphocytes leading to immunosuppression.
Management of sepsis: the essentials
Initial resuscitation
This focuses on the timely delivery of goal-directed therapy. The Surviving Sepsis Campaign has
developed guidelines to reduce mortality from sepsis and recommends the use of specific care
bundles and physiological targets for the initial phase of resuscitation (Table 15.3).
Table 15.3 Physiological targets for the first 6 hours of resuscitation
CVP 812 mmHg
MAP > 65 mmHg
Urine output > 0.5 mL/kg/h
Haematocrit > 30%
Superior vena cava oxygenation saturation (ScvO2) 70% or mixed venous oxygen saturation (SvO2)
65%
Within the first or golden hour of resuscitation, application of the Sepsis six care bundle
introduces the cornerstones of diagnosis (blood cultures), treatment (high-flow oxygen, IV antibiotics,
fluids) and monitoring (haemoglobin and lactate, hourly urine output). Early delivery of antibiotics is
a priority with mortality from severe sepsis and septic shock increasing with every hour
administration of antibiotics is delayed. The key principle of resuscitation is to improve oxygen
delivery to hypoperfused tissues, targeting factors of the oxygen delivery equation:
DO2 = [1.39 Hb SaO2 + (0.003 PaO2)] CO
DO2 = oxygen delivery, Hb = haemoglobin, SaO2 = oxygen saturation, CO = cardiac output.

Both serum lactate and superior vena cava oxygenation saturation (ScvO2) are surrogate markers
of tissue perfusion and can be used as resuscitation targets. Poor lactate clearance in sepsis is
associated with increased mortality.
Diagnosis
Appropriate cultures should be taken before antimicrobial therapy is initiated. However, the early
administration of antimicrobials is paramount and attempts to achieve cultures should not cause delay
in administering antibiotics (> 45 minutes). Current recommendations are to obtain at least two sets of
blood cultures (aerobic and anaerobic bottles) before antimicrobial therapy. In the presence of
vascular access devices (e.g. Hickman line) it is recommended to draw at least one set of blood
cultures percutaneously and another through each vascular access device in situ. Cultures from other
potential sources of infection (e.g. urine, placenta) should also be obtained where possible.
Antimicrobial therapy
Early administration of intravenous antibiotics reduces mortality and should be completed within the
first hour of sepsis management. Broad-spectrum antibiotics should be commenced to cover the most
likely source of infection. Early discussion with microbiology is recommended in critically ill
patients. De-escalation of antibiotics can take place following identification of a causative
microorganism.
Source control
When a source of infection is potentially amenable to intervention (e.g. retained products) urgent
investigation is indicated, either using radiology or by surgical exploration. Any intervention to
achieve source control should take place as soon as possible (and < 12 hours) following diagnosis.
This may require both resuscitation and treatment to take place in parallel. Initial intervention may not
necessarily aim for definitive management, but instead aim to minimize the physiological impact on
the patient (e.g. percutaneous vs. open surgical drainage).
Fluid therapy
The quantity of fluid required for resuscitation is less when colloids rather than crystalloids are used.
However, the use of certain colloids, especially the hydroxyethyl starches, is associated with
increased morbidity (renal impairment) and mortality.
In view of this, crystalloids are the recommended resuscitation fluid for severe sepsis and septic
shock. An initial fluid challenge of 30 mL/kg should be given to patients with sepsis-induced tissue
hypoperfusion who are suspected to be hypovolaemic.
There is no evidence to support the superiority of either Ringers lactate or 0.9% saline. The
high chloride content of 0.9% saline can, however, result in a significant hyperchloraemic metabolic
acidosis. The use of albumin in fluid resuscitation is safe, equally effective as 0.9% saline, but is
more expensive. Current recommendations are to use albumin only when patients require substantial
amounts of crystalloids.
Vasopressors
Current guidelines recommend a target mean arterial pressure (MAP) of > 65 mmHg. In life-
threatening hypotension vasopressors may be required to maintain organ perfusion.
Noradrenaline is the recommended first-choice vasopressor. Dopamine now has only a limited
role in septic shock, e.g. patients also presenting with bradycardia. When hypotension is severe it
may be necessary to add an additional agent to achieve target MAP. Adrenaline is the recommended
agent and can either be added to noradrenaline or used as a substitute.
Vasopressin is also effective in raising MAP when used in conjunction with noradrenaline and
can reduce noradrenaline requirements.
Phenylephrine is not recommended in the treatment of septic shock; the exceptions are when
noradrenaline use is associated with serious arrhythmias, blood pressure is persistently low when
cardiac output is known to be high and as salvage therapy when combined inotrope/vasopressor drugs
and low-dose vasopressin have failed to achieve the MAP target.
Although there are concerns regarding uteroplacental flow and the use of vasopressors, the
importance of restoring maternal blood pressure and hence organ perfusion is paramount to fetal
wellbeing and survival.
Inotropes
Dobutamine can be added to a vasopressor and is recommended in the context of myocardial
dysfunction and ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and
adequate MAP.
Dobutamine can be used to normalize cardiac index and improve oxygen delivery. The targeting
of supra-normal values is no longer recommended.
The early use of non-invasive cardiac output monitoring (e.g. LIDCO, oesophageal Doppler) and
imaging of the heart with echocardiography is recommended in septic shock to guide fluid
resuscitation and inotrope/vasopressor use.
Corticosteroids
Although the use of corticosteroids in septic shock results in haemodynamic improvement, a
beneficial effect on patient mortality is limited to patients at high risk of death.
The exact mechanism of corticosteroid action in sepsis is unknown. One possible mechanism is
to increase noradrenaline receptor sensitivity. In addition some patients with septic shock are thought
to have relative adrenal insufficiency. The ACTH stimulation test does not predict response to
treatment and should not be used to guide which patients receive hydrocortisone.
Intravenous hydrocortisone in the treatment of adult septic shock patients should only be given
when adequate fluid resuscitation and vasopressor therapy have failed to achieve the haemodynamic
targets. Intravenous hydrocortisone 200 mg per day should be given as a continuous infusion rather
than in traditional bolus doses.
Etomidate suppresses the adrenocortical axis and has been associated with increased mortality
in septic shock patients when used to facilitate endotracheal intubation. It should not be used in adult
patients with septic shock.
Blood product administration

The optimal haemoglobin concentration for patients with septic shock is unclear. The haemoglobin
level recommended for critically ill patients (70 to 90 g/L) can be safely applied to septic shock
patients once tissue hypoperfusion has resolved, unless the patient has severe hypoxaemia, acute
haemorrhage or myocardial ischaemia.
Abnormal clotting studies (e.g. elevated prothrombin time) are common in sepsis, but should not
be corrected unless the patient is bleeding or invasive procedures planned. Newer technologies like
the thromboelastogram (TEG) provide a more functional analysis of coagulation and can be helpful in
selecting the required components.
Thrombocytopenia is a common finding in sepsis due to a combination of decreased production
and increased consumption. Current thresholds for prophylactic platelet transfusions are counts
< 10,000/ mm3 in the absence of bleeding, and < 20,000/mm3 when the patient has a significant risk of
bleeding. In active bleeding or where invasive procedures are planned, platelet counts should be
> 50,000/mm3.
Activated protein C is involved in both inflammatory processes and coagulation and was thought
to be beneficial in patients with severe sepsis and septic shock with a high risk of death. It has not
been possible to reproduce the initial positive study results and in view of significant side effects
(bleeding) and high cost, the product has been withdrawn from clinical use.
Mechanical ventilation
Patients with severe sepsis and septic shock may require mechanical ventilation and their illness may
be complicated by development of the acute respiratory distress syndrome (ARDS).
A lung-protective ventilation strategy can not only prevent the development of ARDS, but also
reduce mortality in patients with established ARDS. Strategies utilizing tidal volumes of 6 mL/kg,
predicted ideal body weight and limiting plateau pressure to < 30 cmH2O are associated with better
outcomes, independent of the mode of ventilation (volume or pressure) used. Permissive hypercapnia
is an acceptable result of this ventilatory approach.
Positive end-expiratory pressure (PEEP) should be applied to minimize alveolar collapse and
atelectotrauma. Current guidelines recommend strategies based on higher rather than lower levels of
PEEP. Two different approaches to PEEP are described: titration to lung compliance or matching to
oxygenation deficit guided by FiO2.
In septic patients with severe refractory hypoxaemia due to ARDS (PaO2/FiO2 < 100 mmHg),
recruitment manoeuvres, including prone ventilation, may improve oxygenation and patient outcome.
In extreme situations, extracorporeal membrane oxygenation (ECMO) may be considered. High-
frequency oscillatory ventilation (HFOV) has not demonstrated benefit in sepsis patients with ARDS.
Patients with established sepsis-induced ARDS who do not have evidence of tissue
hypoperfusion benefit from limiting extravascular lung water. This can be achieved with a
conservative fluid strategy and/or diuretic use. 2-Agonists have not been shown to improve
outcomes in ARDS.
Sedation, analgesia and neuromuscular blockade in sepsis

Minimizing sedation levels and daily interruption of sedation improves patient outcomes in sepsis.
Neuromuscular blockers are associated with the development of critical-care neuromyopathy and
should be avoided where possible in patients without ARDS. If required, they can be given by
intermittent bolus or continuous infusion guided by neuromuscular junction monitoring. Depth of
anaesthesia monitoring should also be considered when using neuromuscular blocking agents.
A 48-hour infusion of cisatracurium in patients with early, moderate to severe ARDS
(PaO2/FiO2 < 150 mmHg) has been shown to reduce mortality without causing an increase in
neuropathy.
Glucose control
Blood glucose levels in septic patients should be maintained < 180 mg/dL (10 mmol/L), using
intravenous insulin where necessary. Strategies using tighter glucose control are associated with an
increase in adverse incidents (hypoglycaemia) and do not improve outcomes.
Renal replacement therapy

Both continuous and intermittent renal replacement therapies can be used in the management of
sepsis-induced renal failure, depending on local practice. Continuous therapies are recommended in
haemodynamically unstable septic patients.
Deep vein thrombosis prophylaxis

All septic patients should receive both appropriate pharmacoprophylaxis and intermittent pneumatic
compression devices, unless contraindicated.
Stress ulcer prophylaxis

All septic patients with bleeding risk factors should receive stress ulcer prophylaxis with proton
pump inhibitors. These should be stopped once risk factors are no longer present to reduce the risk of
ventilator-associated pneumonia and infection with Clostridium difficile.
Nutrition
Enteral nutrition should be started as early as possible in order to maintain integrity of gut mucosa
and prevention of bacterial translocation. The use of immunomodulating nutritional supplements is not
recommended.
Influenza
Influenza is a common viral infection that can pose a significant threat to pregnant women and their
babies.
Virology and structure (Figure 15.1)
Figure 15.1 Structure of influenza virus (http://www.cdc.gov/flu/images/influenza-virus-

fulltext.jpg accessed 25/2/2013).
Influenza viruses are single stranded RNA viruses that make up three genera (Influenza A, B and
C) of the family orthomyxoviridae.
Structurally the influenza virus consists of the following key components:
1 Central core of RNA (eight segments for A) genome and other viral proteins
2 Viral envelope containing two major types of glycoproteins:
Haemagglutinin (HA) enables virus binding to the target cell surface receptor sialic acid,
enabling entry of the viral genome into target cells by membrane fusion. Sialic acid-presenting
carbohydrates are present on several cell types in the respiratory tract, gastrointestinal tract,
heart and brain.
Neuraminidase (NA) acts as an enzyme, cleaving sialic acid from the HA molecule and
therefore facilitating release of viral progeny from infected host cells.
Both cell-surface proteins initiate host antibody responses and allow serotyping of virus. NA is
also a target for antiviral treatment.
Influenza A
This genus has one species (influenza A virus). Natural hosts include wild aquatic birds, poultry, pigs
and humans. Transmission of the virus to other species can result in devastating outbreaks (e.g.
poultry and human pandemics). Influenza A is the most virulent human pathogen, causing both
epidemics and pandemics. The virus is divided into multiple serotypes based on the antibody
response to the surface glycoproteins HA and NA. Human infection is restricted to H13, N12
serotypes.
Influenza B
This genus has one species (influenza B virus) with one serotype. It affects predominantly humans, but
is less common than influenza A and results in milder illness. Its limited host range and limited
antigenic diversity means influenza B can cause epidemics, but not pandemics.
Influenza C
This genus has one species (influenza C virus) and results in only occasional human infection.
Transmission
Infection is normally transmitted in three ways:
1 Airborne aerosols produced by coughing or sneezing
2 Direct transmission of infected mucus with infected nasal secretions
3 Contaminated surfaces and bird droppings hand-to-eye, hand-to-mouth and hand-to-nose.
Virus shedding when a host individual is infective starts the day prior to symptom onset and continues
for approximately 57 days.
Antigenic drift and epidemics

During viral replication, no RNA proofreading takes place with point mutations occurring
approximately once every newly replicated RNA. This leads to subtle changes in viral surface
antigen, helping to evade previously acquired host immunity. This results in seasonal variation in
virus. Seasonal flu is normally caused by influenza A and B and peaks in DecemberMarch each year
in the UK. A new vaccine is required each year.
Antigenic shift and pandemics

Influenza virus RNA is made up of 78 segments. If different influenza A viruses infect one cell it can
lead to a re-assortment of RNA segments and a whole new sub-type of surface antigen can result.
This provides pandemic potential. Pandemics are infrequent, but recurrent worldwide outbreaks of
influenza. They are caused by antigenic shift or direct transmission of an avian virus to humans.
There were three twentieth-century influenza pandemics resulting in millions of deaths, e.g.
Spanish influenza (191820, H1N1 sub-type, 40+ million deaths), Asian influenza (195758, H2N2
sub-type, 1+ million deaths), Hong Kong influenza (19689, H3N2 sub-type, 1 million deaths).
Influenza A H1N1 2009

This influenza A virus emerged in Mexico in February 2009 and was the result of multiple re-
assortment events between swine viruses leading to a novel gene mix not previously reported in
swine or human influenza viruses. Pandemic status was declared by the WHO in June 2009 and lasted
until August 2011.
The pandemic was considered mild with the majority of infected individuals experiencing a
self-limiting illness (50% symptom resolution within 7 days). However > 16,000 individuals died.
Pneumonia was present in up to 40% of cases admitted to hospital in the USA with viral pneumonitis
or ARDS evident in nearly half of patients admitted to ICU in Australia and New Zealand and
secondary bacterial pneumonia present in 20%.
H1N1 remains one of the seasonal influenza viruses in circulation globally.
Influenza in pregnancy
The increased risk of influenza during pregnancy is well recognized. In the 1918 pandemic and in a
series of 1350 pregnant women, over 50% developed pneumonia and over half of these died with an
overall case fatality of 27%. Half of those women of childbearing age who died were pregnant in the
1957 pandemic.
Pregnant women do not have a higher incidence of seasonal influenza but hospitalization rates
are 18-fold that of healthy non-pregnant women of childbearing age.
In the 2009 H1N1 pandemic there was a fivefold higher rate of hospital admission in pregnant
women vs. the general population, with the risk of mortality for pregnant women sevenfold that of
non-pregnant women of the same age. The WHO reported pregnant women accounted for 710% of
all hospital admissions with influenza. There were 12 maternal deaths in the UK between April 2009
and January 2010.
Infection is more common in the second and especially third trimesters and risk is further
increased in the presence of other risk factors (see later). Pregnant women are more likely to deliver
preterm and their babies are more likely to be stillborn or die in the first week of life if admitted to
hospital with influenza.
Clinical features
Uncomplicated influenza
Influenza presenting with fever, coryza, generalized symptoms (headache, malaise, myalgia,
arthralgia) and sometimes gastrointestinal symptoms, but without any features of complicated
influenza.
Complicated influenza
Influenza requiring hospital admission and/or signs of lower respiratory tract infection (hypoxaemia,
dyspnoea, lung infiltrate), central nervous system involvement and/or significant exacerbation of an
underlying medical condition.
Risk factors for complicated influenza
1. Pregnancy
2. > 65 years old
3. Chronic cardiac, pulmonary, renal, hepatic or neurological disease
4. Morbid obesity (BMI 40)
5. Immunosuppression
severe primary immunodeficiency
current or recent (< 6 months) chemotherapy or radiotherapy for malignancy
solid organ transplant recipients
bone marrow recipients
high dose systemic corticosteroids ( 40 mg prednisolone per day for 1 week and within
3 months of stopping)
currently or recently (< 6 months) receiving other immunosuppressive therapy
HIV infection.
Diagnosis
In uncomplicated cases this is often on clinical grounds. Diagnostic tests include viral culture,
serology, rapid antigen testing, PCR and immunofluorescence assays dependent on local protocol.
Samples include nasopharyngeal (NP) swab, nasal swab and nasal wash or aspirate. For rapid
detection techniques e.g. PCR, NP specimens are generally more effective.
Management
General principles
1. Low threshold for hospital assessment of pregnant women with suspected influenza and risk
factors for, or clinical symptoms of complicated influenza.
2. Standard infection control measures should be instituted as per local guidelines (patient
isolation, use of personal protective equipment) in suspected cases.
3. Follow local guidelines for diagnostic testing for influenza virus.
4. Start treatment in suspected cases before confirmation if clinically indicated and if signs of
complicated influenza present.
5. Exclude other pathologies (e.g. pneumonia), which may present with a similar clinical
picture.
6. Manage exacerbations of pre-existing co-morbid disease (e.g. asthma)
7 Early involvement of relevant medical specialties in complicated cases including obstetric,

anaesthetic, general medical, microbiology/virology. This will ensure an appropriate
management plan is established for antiviral treatment, the location of ongoing treatment, timing
of steroid administration and delivery of the baby where necessary.
8. Early involvement of the critical care team in complicated influenza. This should be based on
clinical assessment, local EWS policy and clinical triggers (Table 15.4).
Table 15.4 Clinical triggers for critical care review
Severe dyspnoea
Patients with influenza-related pneumonia or who have bilateral primary viral pneumonia
PaO2 < 8 KPa despite maximal oxygen administration
Progressive hypercapnia
Refractory hypotension (excessive fluid administration may further exacerbate respiratory

compromise)
Septic shock
Severe acidosis (pH < 7.26)
GCS < 10 or deteriorating conscious level
Antiviral therapy for treatment of influenza in suspected or confirmed influenza in

pregnancy
Current recommendations for treatment of influenza (both A and B) in the UK are for oseltamivir and
zanamivir. Both are selective inhibitors of neuraminidase (NA) preventing new virion release from
infected cells.
1. Uncomplicated influenza
Previously healthy oseltamivir PO 75 mg within 48 hours of symptoms, where possible for

5 days
Immunosuppressed zanamivir INH (Diskhaler) 10 mg bd or if unable to take inhaled

preparation oseltamivir PO 75 mg bd
2. Complicated influenza
Previously healthy oseltamivir PO/NG 75 mg bd with zanamivir INH, NEB or IV as

second-line treatment
Immunosuppressed zanamivir INH, NEB or IV.
Early administration of oseltamivir within 48 hours appeared to confer a mortality benefit in the
recent H1N1 pandemic. Critically ill patients may have the dose of oseltamivir increased to 150 mg
bd or if enteral absorption is compromised, IV zanamivir administered. This is an off-licence
indication available on compassionate grounds. Treatment courses may also be extended beyond 5
days. Discuss treatment with your local microbiologist or virologist. Both oseltamivir and zanamivir
can be administered to breastfeeding patients where clinically indicated.
Complications of influenza
These include the following:
Septic shock and multiple organ failure
Myocarditis
Encephalitis and cognitive impairment
Venous thromboembolism
Bacterial superinfectiom
Physical and psychological complications of prolonged critical illness.

Vaccination
The Health Protection Agency (HPA) recommends seasonal flu vaccination for all pregnant women in
the UK. Vaccination also protects the baby before and after delivery and can result in a significant
reduction in hospitalization rates for neonates in the first 6 months of life.
Key points
1. The incidence of sepsis and maternal mortality related to sepsis appears to be increasing.
2. The physiological changes of pregnancy can mask signs of sepsis and present challenges in
diagnosis.
3. In sepsis management appropriate cultures should be taken prior to early administration of

suitable antimicrobial agents.
4. There should be a low threshold for hospital assessment of pregnant women with suspected
influenza.
Further reading
Department of Health and the Royal College of Obstetricians and Gynaecologists (2009). Pandemic
H1N1 2009 Influenza: Clinical Management Guidelines for Pregnancy. Guidelines for Pregnancy
prepared by the Department of Health and the Royal College of Obstetricians and Gynaecologists
(http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/DH_
Levy, M. M., Fink, M. P., Marshall, J. C. et al. (2003). 2001 SCCM/ESICM/ACCP/ATS/SIS

International Sepsis Definitions Conference. Crit. Care Med., 31(4), 12501256.
Dellinger, R. P., Levy, M. M., Rhodes, A. et al. (2013). Surviving Sepsis Campaign: International
Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Crit. Care Med., 41(2),
580637
Lucas D. N., Robinson P. N. and Nel M. R. (2012). Sepsis in obstetrics and the role of the
anaesthetist. Int. J. of Obstet. Anesth., 21(1), 5667.
Chapter 16
Cardiac disease in pregnancy

W. Ross Macnab, Anita Macnab and Akbar Vohra
Cardiac disease is a significant cause of maternal mortality worldwide. In the last UK maternal
mortality report, cardiac disease was the leading cause of maternal death (2.3 deaths per 100000
maternities). Some mothers are waiting to have a family later in life and present with a variety of
acquired heart conditions. There is a 1% incidence of heart disease in pregnant patients in the UK,
which has reduced from an estimated 3% incidence due in part to a reduction in rheumatic heart
disease. However, it is expected to increase as the number of patients with corrected congenital heart
disease surviving to childbearing age increases and may also increase further as immigration patterns
change. The incidence of cardiac disease is in the order of 0.24% in the Western industrialized
countries and is about 4% in the United States. Congenital heart disease accounts for 7580% of
cardiac disease in pregnancy in the western world. Outside Western Europe and North America
congenital heart disease accounts for only 919% of the cardiac disease in pregnancy. In non-Western
countries rheumatic valvular disease causes 5589% of cardiovascular disease in pregnancy.
Of patients with congenital heart disease, 96% will live for at least 15 years if they survive
infancy. It is therefore essential to have a good knowledge of these cardiac conditions and a good
understanding of the stresses on the cardiovascular physiology caused by pregnancy. These patients
can turn up on any delivery suite in any hospital at any time.
Physiology
Important physiological changes in the cardiovascular system need to occur during pregnancy in order
to facilitate the increased demand for oxygen and nutrients by the uteroplacental unit, and that of the
growing fetus. Blood flow to the uterus increases from 50 mL/min at 10 weeks gestation to
850 mL/min at term. This is accomplished by a 50% rise in cardiac output (CO) and blood volume.
There is an increase in heart rate from 6 weeks. There is a reduction in systemic and pulmonary
vascular resistance due to vasoactive prostaglandins and nitric oxide production, thus preventing a
rise in pulmonary artery pressure from the increased circulating volume. The systolic and diastolic
pressures decrease, reaching their lowest values during the second trimester, before increasing as
term approaches, although never reaching prepregnancy values. Therefore, there is a risk of cardiac
decompensation as pregnancy progresses. If the cardiac output does not increase adequately,
placental insufficiency will occur, which will lead to fetal growth retardation. Changes in vascular
resistance can lead to changes in flows through shunts. In patients with Marfans, repaired coarctation
or bicuspid aortic valve with ascending aortopathy, the increase in cardiac output can lead to aortic
dilatation leading to dissection and rupture.
There is also a 15% reduction in colloid osmotic pressure during pregnancy, which can increase
the risk of pulmonary oedema in patients with cardiac disease.
During labour CO increases by a further 2550% with up to 500 mL autotransfusion of blood
from an increased return from the intervillous spaces during contractions. There is a further increase
in blood volume after delivery due to uterine contraction in the third stage. This can result in a
clinical deterioration in patients with cardiac disease due to the associated rise in ventricular filling
pressure and end-diastolic volume.
General approach to cardiac disease in pregnancy

Ideally, preparation should occur before pregnancy occurs. The responsible cardiologist and
obstetrician should undertake preconceptual counselling. Risks involved to the patient should be
discussed openly so informed decisions can be made. Cardiac function can be quantified with
cardiopulmonary exercise testing. Cardiac function should be optimized, which may include surgical
interventions such as valve replacement. Known teratogenic medications should ideally be
discontinued. Women should be seen early in established pregnancy in joint cardiology and obstetric
clinics. A multidisciplinary care plan can be made, including consideration of the services required
at the intended delivery unit such as cardiology, cardiothoracic surgery and cardiac or general
intensive care. An anaesthetist should review the woman at an early stage to develop a plan for
delivery and postpartum care.
In general, predictors of a primary cardiac event during the pregnancy include:
Prior cardiac event or stroke
Prior arrhythmia
New York Heart Association (NYHA) functional class >2
Left-sided heart obstruction (mitral valve area <2 cm2, aortic valve area <1.5 cm2 or outflow
tract gradient >30 mmHg
Left ventricular ejection fraction <40%.
Congenital heart disease

At almost 1% (7/1000), congenital heart disease is the most common inborn defect, with 60%
diagnosed before 1 year of age, 30% as children and 10% after 16 years of age. Of those surviving
infancy, 96% will live for at least 15 years, with the majority of deaths occurring after 20 years age.
There are approximately 150,000 patients with CHD in the UK and this number is increasing as
surgical and medical management improves. At least 17% are recognized as having a genetic basis.
The common defects are illustrated in Table 16.1.
Table 16.1 Incidence of congenital heart disease.
Defect Incidence of CHD
VSD 30%
ASD 10%
Patent ductus arteriosus (PDA) 10%
Pulmonary stenosis 7%
Coarctation 7%
Aortic stenosis 6%
Tetralogy of Fallot 6%
Transposition 4%
Other 20%
In most cases of congenital heart disease the diagnosis, functional status and any therapeutic
strategies will be well established prepregnancy. Depending on the condition, pregnancy could be
well tolerated or be classified as risk class 4 in the modified WHO classification of maternal
cardiovascular risk (Table 16.2). Risk Class IV is where pregnancy is relatively contraindicated and
termination should be discussed, if the patient presents as pregnant. If pregnancy is to continue, treat
the same as Risk Class III, with expert input for the duration of the peripartum period. High-risk
groups are illustrated in Tables 16.3 and 16.4. Pregnancy is associated with a thrombotic tendency,
which is exacerbated by the polycythaemia that occurs in patients with cyanotic heart disease.
Congenital heart disease patients also have a higher incidence of pre-eclampsia, which is associated
with high mortality in patients with Eisenmengers. In addition, they also have a tendency to develop
new arrhythmias.
Table 16.2 WHO classification of maternal cardiovascular risk
Risk Class Risk of pregnancy
I Increasing risk of mortality and morbidity

requiring increased specialist input
II
III
IV
Table 16.3 High-risk obstetric patients
Obstetric patients have an overall risk of >1%
Any cyanotic CHD
Pulmonary hypertension
Poor systemic ventricular function
Severe left heart obstruction mitral and aortic stenosis
Marfans with dilated root

Dacron patch repair of coarctation
Previous peripartum cardiomyopathy
Poor cardiac function
Table 16.4 Comparison of complications with different conditions
Obstetric risk comparison Percentage risk of complications
Healthy woman 0.005%
Average population 0.01%
Corrected Fallots 0.1%
Severe stenosis 1.0%
Uncorrected Fallots 10%
Pulmonary hypertension 33%
Eisenmengers 50%
In 50% of patients there will be intrauterine growth retardation (IUGR) with fetal indication of
early delivery. The babies have an increased risk of heart defect, which is often similar to that of the
parents (35%) (Table 16.5).
Table 16.5 Incidence of congenital heart defect in babies
Abnormality in parent Incidence in child
Marfans 50%
VSD 15%
ASD 10%
Aortic stenosis 10%
Tetralogy of Fallot 3%
Assessment
The most import part of the assessment is to identify patients that have complete repair, palliative
surgery or no repair. Those with complete correction should behave in a similar manner to normal
patients. Palliative correction or no correction is likely to be associated with primary and secondary
cardiac, pulmonary or systemic dysfunction.
These patients should be seen in clinic at fortnightly intervals in the first 24 weeks and then on a
weekly basis, looking for specific signs of deterioration (Table 16.6).
Table 16.6 Main areas of focus during outpatient assessments
Clinical assessment of deterioration
Ventricular decompensation
Incipient pulmonary oedema
Pulmonary hypertension and exacerbation
Systemic desaturation
Onset of new arrhythmias
SABE (subacute bacterial endocarditis)
History of shortness of breath and palpitations should be specifically sought and examination
should focus on signs of failure. Periodic transthoracic ECHO may also be helpful in identifying
deterioration and the need for early hospitalization and delivery. Pulse oximetry particularly before
and after exertion can be helpful in identifying patients that are deteriorating.
Fetal scans at 20 weeks will pick up 80% of major cardiac defects and should be repeated at 24
weeks. Nuchal scans help indicate fetal cardiac disease (>4 mm = Downs and cardiac disease
likely; <4 mm = 1:1000 risk of CHD).
In addition, many patients with CHD have other syndromes, which will have specific anaesthetic
implications. Noonans, Turners and trisomy can be associated with problems with airway
management as well as communication and consent. Di George syndrome, which is also called
CATCH 22 (Cardiac defect, Abnormal facies, Thymic hypoplasia, Cleft palate, Hypocalcaemia due
to chromosome 22), is associated with potential airway problems, electrolyte problems and immune
deficiency requiring the use of irradiated blood products for transfusion.
Ventriculoseptal defects (VSD)

These are graded according to the flow through the defect and its site. Therefore, unrestricted defects,
which are associated with high flow, will be associated with more problems. Small to moderate
VSDs are usually well tolerated in pregnancy and generally behave as well as repaired defects. The
main aim is to identify pulmonary hypertension or even Eisenmengers, which will be associated with
increased risk of complications.
Atrioseptal defects (ASD)

If previously undiagnosed, these patients present with an enlarged heart and murmurs in pregnancy,
usually secundum ASDs. Primum ASDs are associated with other endocardial cushion defects with
involvement of atrioventricular valves and earlier presentation. These patients may develop
arrhythmias. Pregnancy is usually tolerated well in unoperated patients unless they have developed
pulmonary hypertension.
Atrioventriculoseptal defects (AVSD)

Of complete AVSD, 75% occur in patients with Downs syndrome whilst 90% of partial AVSD
occur in non-Downs patients. Patients with partial AVSD present in a manner similar to secundum
VSD. Complete AVSD act essentially as univentricular hearts and are associated with heart failure.
These patients have a high risk during pregnancy due to the problems of cardiac failure risk, but
particularly due to a tendency to pulmonary hypertension and Eisenmengers.
Tetralogy of Fallot (TOF)

These patients are usually identified in infancy. Patients with complete repair will often behave in a
similar manner to normal patients. In patients that have not been repaired completely, pulmonary
hypertension and Eismengers is a major complication. Patients with saturations <85% have a high
incidence of IUGR and intrauterine death, in addition to a high incidence of maternal complications.
They can have right ventricular outflow tract obstruction (RVOTO), pulmonary regurgitation,
tricuspid regurgitation, right ventricular failure and arrhythmias.
Ebsteins anomaly
These patients have apical displacement of the tricuspid valve. This is associated with an enlarged
right atrium, tricuspid regurgitation and often right ventricular outflow obstruction and 50% will have
a patent foramen ovale (PFO) or a secundum ASD. Accessory conduction pathways occur in 25% and
are associated with atrial tachyarrhythmias.
Extreme forms are associated with in-utero death with hydrops fetalis. Severe forms present
with failure to thrive. Patients with moderate and less severe defects present in adolescence or
adulthood with dyspnoea, tachyarrhythmias, paradoxical emboli or cyanosis.
Pregnancy is usually well tolerated unless complicated by right heart failure, tachyarrhythmias
and cyanosis.
Fontans
These patients have had palliative surgery to improve pulmonary circulation and rely on passive flow
from the venous system to the pulmonary artery and lungs. Examples of such patients include
pulmonary and tricuspid atresia. Therefore, they normally have signs of elevated systemic venous
pressure and venous congestion with hepatic congestion and even cirrhosis. They are often on
multiple medications such as amiodarone, angiotensin converting enzyme (ACE) inhibitors and
warfarin, which can affect the fetus.
These patients often have heart failure, atrioventricular (AV) valve dysfunction and arrhythmias.
There is also tendency to bleeding as well as hypercoagulability.
Outcome of pregnancy can be good if they have good exercise tolerance and do not have signs of
heart failure, tachyarrhythmias and embolism. Hypovolaemia is poorly tolerated in these patients.
High intrathoracic pressure associated with assisted ventilation during general anaesthesia can reduce
pulmonary venous flow and increases the risk of dysfunction and hypoxia.
In historical series, there is a high (up to 50%) maternal mortality rate reported with pulmonary
hypertension, but more recent data suggests lower mortality figures of 1530%. Nevertheless the
risks are still very high. Death generally occurs in the third trimester or during the first months after
delivery due to worsening of the pulmonary hypertension, pulmonary thrombosis or right heart failure.
Causes of pulmonary hypertension are shown in Table 16.7.
Table 16.7 Commonest causes of pulmonary hypertension
Primary pulmonary hypertension
Collagen vascular disease
Congenital heart defects
Portal hypertension
HIV infection
Drugs/toxins/appetite suppressants
Most of the patients with shunts will develop cyanosis. Oxygen therapy (45 L/min) may
improve oxygenation, reduce the risk of pulmonary hypertensive crisis and improve fetal growth. All
these patients should be given anticoagulant prophylaxis. Ideally patients with significant pulmonary
hypertension should be managed in pulmonary hypertension centres where all therapeutic options
such as sildenafil, bosentan, prostacyclin and nitric oxide therapy are available.
Eisenmengers
This is invariably due to pulmonary hypertension with flow reversal and cyanosis as a consequence
of another defect of flow. Atrio-ventricular septal defects (AVSD), and patent ductus arteriosus
(PDA) and atrial septal defect (ASD) (often due to embolic phenomena) account for 7080% of these
patients. Other causes include truncus arteriosus, surgical aortopulmonary connections, complex
pulmonary atresia and univentricular heart.
Of Eisenmengers patients, 42% will survive to 25 years of age, with poor prognosis if they
develop syncope, elevated right atrial pressures or severe resting hypoxaemia (<85%). They have
many associated medical problems, as illustrated in Table 16.8.
Table 16.8 Co-morbidities in patients with Eisenmengers syndrome
Hepatic and renal dysfunction
Clotting dysfunction leading to bleeding tendency
DVT risk
Polycythaemia
Haemochromatosis
Arrhythmias
Gout
Haemoptysis
Risk of SABE
Pregnancy is associated with 3045% mortality and it should be discouraged (Table 16.9).
Table 16.9 Complications in patients with Eisenmengers syndrome
IUGR 30%
Premature delivery 50%
Stillbirth incidence 2040%
Thromboembolism 44%
Hypovolaemia 25%
Preeclampsia 18%
Worsening heart failure and progressive hypoxaemia are common. Therefore these patients need
close monitoring and hospitalization by 2530 weeks. They should be hospitalized for a further 13
weeks after delivery.
Anticoagulation should be considered after 20 weeks for these patients. Good hydration is vital
throughout pregnancy and particularly during labour. Vaginal delivery is the best option for these
patients.
Acquired heart disease
Acute coronary syndromes

As the average maternal age increases, the number of women at risk of an ischaemic event will also
increase. Acute coronary syndromes (ACS) are estimated to occur at 36 per 100,000 deliveries and
are related to the characteristic risk factors of smoking, hypertension, hyperlipidaemia, diabetes and a
positive family history. Spontaneous coronary artery dissection is more common in pregnancy,
usually occurring in the peripartum period. Maternal mortality after an ACS is estimated at 510%,
which has improved with the increased availability of primary percutaneous coronary intervention
(PCI).
The diagnostic criteria of an ACS are similar to those of non-pregnant patients. There must be a
low threshold for further investigation of parturients and postpartum women that present with chest
pain. A history of chest pain, ECG changes and troponin rise are the hallmarks, although inverted T
waves may occur in pregnancy without underlying ischaemia. PCI is the preferred therapy of choice
and stenting has been performed successfully during pregnancy. Tissue plasminogen activator does
not cross the placenta, however, it may cause catastrophic bleeding around the placenta and should
only be used in life-threatening ACS where PCI is not available. Low-dose aspirin and -blockers
are safe to use in pregnancy. If clopidogrel is indicated, it should be used for the shortest duration
possible and stopped prior to delivery.
Valvular heart disease

Stenotic valvular disease carries a higher risk than regurgitant lesions during pregnancy. In mitral
stenosis (MS), heart failure occurs frequently in those with valve areas less than 1.5 cm2, even when
previously asymptomatic. Pulmonary oedema may occur, particularly if atrial fibrillation occurs. The
third stage of labour may also precipitate pulmonary oedema in these patients, which should be
managed in the same way as for non-pregnant patients.
Those with moderate or severe MS should be advised to delay pregnancy until balloon
dilatation or valve replacement is performed. In those already pregnant, -blockers are used to
control the heart rate and allow a longer diastolic phase, and diuretics can be used to manage fluid
retention. In those who remain symptomatic, percutaneous balloon dilatation can be performed. Open
surgery to the valve should be avoided if at all possible. Vaginal delivery is appropriate for most
patients, however, those with NYHA class 3 or 4, or in those where balloon dilatation has failed,
should be considered for caesarean section.
Aortic stenosis (AS) is primarily caused by a congenital bicuspid valve at this age and causes
left ventricular outflow tract obstruction (LVOTO). LVOTO can also be sub-valvular or supra-
valvular in origin. Supra-valvular obstruction is often associated with anomalies of other major
vascular branches, such as the coronary arteries and pulmonary arteries.
This is often well tolerated if obstruction is mild or moderate. Patients with symptomatic AS and
impaired LV function are at the greatest risk of heart failure and arrhythmias from the increase in
cardiac output associated with pregnancy. These patients also have a greater risk of aortic dissection
and rupture.
A general anaesthetic for caesarean section is often utilized for patients with severe AS in order
to avoid the drop in systemic vascular resistance associated with a regional technique. However,
combined spinal and epidural anaesthesia or intrathecal spinal catheters have been used successfully.
Mechanical heart valves and anticoagulation

Mechanical heart valves are generally avoided in young women, but in patients with an existing
prosthesis, lifelong anticoagulation is required and there is additional concern of valve thrombosis
during pregnancy. There is an increased maternal risk of bleeding, osteoporosis and
thrombocytopenia. Maternal mortality risk is 2.9%, major bleeding is 2.9% and thrombus/embolus is
3.9%. The safest strategy for the mother is to continue warfarin, as this is associated with the lowest
rate of valve thrombosis. However, warfarin is associated with a risk of embryopathy (up to 80%)
and 70% incidence of poor fetal outcome, including middle trimester miscarriage, stillbirth, and fetal
internal and intracerebral haemorrhage. Unfractionated heparin (UFH) and low-molecular-weight
heparin (LMWH) are alternative methods of anticoagulation, but carry a higher risk of valve
thrombosis. LMWH may be used throughout pregnancy or in the 612-week period to avoid
embryopathy associated with warfarin. Close monitoring of the anti-Xa levels, keeping peak levels at
0.81.2 U/mL, is essential, as increased volume of distribution and renal clearance often lead to an
increase in the dose requirement. Choice of anticoagulation regimen depends on valve type, previous
thrombosis, dose of warfarin, and maternal preference. It should be explained to the woman that the
risk of embryopathy is low when the daily dose of warfarin is <5 mg. There is a 6.4% risk of fetal
teratogenicity. However, she should also be given the option to replace it with LMWH during weeks
612. The use of LMWH throughout the entire pregnancy is not recommended, although warfarin
should be switched to LMWH prior to delivery.
Endocarditis prophylaxis
The 2008 National Institute for Health and Care Excellence guideline on antibiotic prophylaxis for
infective endocarditis has advised against routine antibiotic prophylaxis for women during childbirth.
The American Heart Association suggests that those patients with conditions posing high risk for
infective endocarditis, namely prosthetic valve, congenital heart disease, previous infective
endocarditis and cardiac transplant, should receive a prophylactic antibiotic active against
enterococci (such as ampicillin, vancomycin or piperacillin) during operative procedures or prior to
urinary tract manipulation.
Aortic disease
Various conditions may predispose to aortic disease ( Table 16.10) Recommendations include
counselling about risk to the mother antenatally, imaging the aorta and close monitoring of aortic size
during the pregnancy, particularly looking for rapid increase in size. Aorta diameter of <4.0 cm is
relatively safe, whilst those with an aorta >4.5 cm are at high risk of rupture. History of a rapid
increase in size is also associated with a high risk of rupture. Aortic dissection is a potential risk and
there were seven deaths in the last UK maternal mortality report. Measures to minimize
cardiovascular stress at the time of delivery are important in patients with a dilated aorta. These
include good blood pressure control with blockade and regional anaesthesia. Caesarean should be
considered in these patients.
Table 16.10 Causation of aortic disease
Marfans syndrome
Ehlers-Danlos syndrome
Turners syndrome
Bicuspid aortic valve
Familial aortopathy
Associated with congenital heart disease coarctation; sinus of valsalva aneurysm
Patients with sinus of valsalva aneurysms should have surgical repair prior to pregnancy.
Acute pulmonary oedema

Acute pulmonary oedema is a significant cause of morbidity and mortality. It typically presents with
sudden onset breathlessness +/ agitation, and has several associated conditions/risk factors (Table
16.11) with an incidence of up to 1 in 200 pregnancies. Acute pulmonary oedema during pregnancy
can be divided into that occurring with hypertension and without hypertension. This distinction
allows appropriate management and pharmacological therapy.
Table 16.11 Causes of pulmonary oedema
Pre-existing conditions Cardiac conditions

Obesity
Endocrine disorders
Increased maternal age
Diseases in pregnancy Pre-eclampsia

Sepsis
AFE
Preterm labour
PE
Drugs -agonists
Steroids
Magnesium
Cocaine
Iatrogenic IV fluid
Fetal conditions Multiple gestation
Pulmonary oedema associated with hypertension may be due to pregnancy-induced hypertension,

essential hypertension or a combination of the two. Development of pulmonary oedema in these
patients is often associated with excessive fluid administration and increasing disease severity. Pre-
eclampsia predisposes to pulmonary oedema due to several factors, including elevated systemic
vascular resistance, increased left ventricular end diastolic pressure, a reduction in colloid osmotic
pressure and increased endothelial permeability. The precipitating event is an increased fluid load,
which may be due to sudden vasoconstriction through sympathetic nervous system activation or
excessive fluid administration. The immediate management includes activation of an emergency
medical team, support of the womans ventilation through non-invasive/invasive means, introduction
of pharmacological therapy and transfer to a high-dependency area when appropriate. Glyceryl
trinitrate (GTN) is recommended as the drug of choice and can be given intravenously or sub-
lingually. Furosemide can also be added to produce vasodilation and diuresis. If hypertension
persists despite this therapy, nifedipine can be added. Early echocardiography to assess left
ventricular function may be helpful in these patients and considered early.
Pulmonary oedema without hypertension has several causes (Table 16.11). Early identification
of at risk patients and careful fluid management in the perinatal period are essential to prevent
development of pulmonary oedema. The acute management is similar to that of non-pregnant patients
and includes furosemide, vasodilators, inotropes and ventilation when required.
Cardiomyopathy
Hypertrophic cardiomyopathy
Patients with hypertrophic cardiomyopathy are often asymptomatic and may present during pregnancy.
It is often well tolerated and symptoms, such as breathlessness, may be treated with -blockers. A
recognized complication is diastolic dysfunction, which may predispose to pulmonary oedema, so
strict fluid balance is essential.
Peripartum cardiomyopathy
Peripartum cardiomyopathy (PPCM) is a form of dilated cardiomyopathy carrying a worldwide
mortality of 30% in the past with more recent published mortality rates of 10%. It is a pregnancy-
specific disease condition causing systolic dysfunction and a decrease in left ventricular ejection
fraction. It can occur late in pregnancy in the last month or in the first 5 months postpartum. There is
no identifiable cause or any pre-existing heart disease before the last month of pregnancy. Diagnosis
should be suspected in a patient presenting with breathlessness, tachycardia and signs of heart failure,
including pulmonary oedema. A dilated ventricle and sluggish circulation predisposes to mural
thrombus formation, which may cause systemic emboli, making thromboprophylaxis essential in these
patients.
Management includes treatment of heart failure (oxygen, diuretics, vasodilators, -blockers and
inotropic support), elective delivery if antenatal and (ACE) inhibitors if postnatal. Severe cases may
require ventilation, balloon pumps, other cardiac assist devices and transplantation. Approximately
50% of women make a full recovery, however there is a risk of recurrence of PPCM in future
pregnancies. Failure of the heart size to return to normal at six months is a poor prognostic indicator.
Arrhythmias
Palpitations are a common complaint during pregnancy, with atrial and ventricular ectopics the most
common cause. The most frequently occurring arrhythmia during pregnancy is a supraventricular
tachycardia, which can be terminated in the same fashion as non-pregnant patients by use of vagal
manoeuvres and drugs (adenosine, verapamil or -blockers). Drugs to be avoided if possible during
pregnancy include amiodarone and atenolol in the first trimester. An underlying cause of an
arrhythmia should be sought, such as sepsis, pulmonary embolism or underlying structural heart
disease. Pacemakers, implantable defibrillators and DC cardioversion have been used successfully
and are thought to be safe during pregnancy.
Anaesthetic management of labour and caesarean section

In patients with cardiac disease, vaginal delivery has half the risk of caesarean section. In particular,
elective section is associated with a twofold increase in the risk of haemorrhage, threefold for DVT
and tenfold for infection.
Mode and timing of delivery

Spontaneous labour is suitable for women with normal cardiac function, otherwise induction of
labour is preferable in women with cardiac disease. The timing of this is based on maternal cardiac
status and maternal or fetal reasons. There is no consensus agreement on absolute contraindication to
vaginal delivery, so indication for caesarean section is again down to maternal reasons, cardiac
status and obstetric reasons. Caesarean section is indicated in situations, for example, when control
of the timing of delivery is important (mechanical heart valve and anticoagulation), cardiac
dysfunction (overt heart failure), minimizing CVS stress (dilated aortopathies), significant cardiac
disease (severe aortic stenosis or severe pulmonary hypertension).
The first and second stages of labour are usually well tolerated, particularly with good
analgesia. Therefore epidurals are potentially beneficial. Bearing down can be associated with
significant cardiovascular changes. Therefore, it is important to monitor this stage in order to avoid
significant prolongation. A shortened time-limited active second stage and early assisted delivery
should be considered.
During the third stage, placental delivery is associated with autotransfusion and the extra blood
in the circulation can lead to circulatory overload. Conversely, failure to contract the uterus may lead
to haemorrhage and circulatory instability due to blood loss. These two effects have to be balanced.
Ergometrine is associated with a tendency to raise blood pressure due to peripheral vasoconstriction
and can cause coronary spasm. Syntocinon can reduce blood pressure due to vasodilation and is
followed with an associated increase in cardiac output due to the autotransfusion and a reflex
tachycardia. In addition, oxytocin can have a direct effect on the heart, causing a reduction in
contractility and heart rate. If used it should be given by very slow injection or by infusion.
Additional infusion of syntocinon at 10 IU/h can be considered. Carboprost can cause bronchospasm,
pulmonary oedema and tachycardia. Its use in active cardiac conditions is not recommended.
Misoprostol does not appear to modify the cardiovascular system.
Monitoring during labour

Standard fetal monitoring is paramount. However, interpretation may be difficult when the mother is
being treated with drugs controlling heart rate, particularly -blockers. ECG, pulse oximetry and
invasive monitoring with arterial and occasionally central line may be necessary. Patients may need
ongoing higher levels of care in the obstetric HDU, critical care unit or cardiac unit after delivery.
Multidisciplinary team input after delivery and regular review is essential.
Management of caesarean section

Generally vaginal delivery should be encouraged and caesarean section should be scheduled so that
support services such as cardiac anaesthetist, cardiology and cardiac intensive care are available.
Many of these patients will require postoperative monitoring and management in a higher-care area.
Regional anaesthesia with combined spinal epidural or spinal catheters is well tolerated, even
in patients with restrictive cardiac and stenotic valve disease. It is particularly helpful in patients
with pulmonary hypertension or Eisenmengers. However, general anaesthesia is also well tolerated
with a careful approach. The use of appropriate monitoring is essential, including the use of
transoesophageal echocardiography if available. Patients occasionally may require inotropic support
perioperatively.
Antibiotic prophylaxis is indicated for the prevention of surgical site infection. The current
guidance regarding endocarditis prophylaxis should also be referred to if required.
Drugs including breastfeeding

Thromboprophylaxis should be continued after delivery, as should other cardiac medication. There
must be an assessment and a balance of risk, benefit and urgency. There are different resources that
can be used, including the US FDA resource that classifies drugs from A (safest) through B, C, D and
X (do not use, known danger).
Warfarin, flecanide and digoxin are safe, but -blockers are excreted into breast milk and can
cause neonatal bradycardia.
Key points
1. Cardiac disease is a significant cause of maternal mortality and morbidity, with an incidence
of heart disease in pregnancy of up to 4% in the western world.
2. Early assessment and risk stratification of parturients using a multidisciplinary team approach
is paramount.
3. It is essential to have a low threshold for further investigations of cardiac symptoms during
pregnancy and in the postpartum period.
4. Stenotic lesions carry more risk during pregnancy.
5. Mode and timing of delivery need careful planning. Vaginal delivery reduces maternal risk;
however, caesarean section may be preferable for reasons of timing, cardiac dysfunction and
disease, or to minimize CVS stress.
Further reading
Cardiac Disease in Pregnancy (CARPREG) Investigators (2001). Prospective multicenter study of

pregnancy outcomes in women with heart disease. Circulation, 104, 515521.
Chan, W. S., Anand, S. and Ginsberg, J. S. (2000). Anticoagulation of pregnant women with
mechanical heart valves: a systematic review of the literature. Arch. Intern. Med., 160, 191196.
Dennis, A. T. and Solnordal, C. B. (2012). Acute pulmonary oedema in pregnant women.

Anaesthesia, 67, 646659
Ginsberg, J. S., Greer, I. and Hirsh, J. (2001). Use of antithrombotic agents during pregnancy. Chest,
126, 344s370s
Hossenbaccus, E., Robinson, C., Wadsworth, R. and Vohra, A. (2007). Is there a role for enoximone
in the management of pregnant women with dilated cardiomyopathy? Int. J. Obstet. Anaesth., 16, S34,
P14.
Hossenbaccus, E., Robinson, C., Wadsworth, R. and Vohra, A. (2007). Severe mixed aortic valve
disease and cardiomyopathy. Int. J. Obstet. Anaesth., 16, S34, P41.
Lewis, G. (2007). The confidential enquiry into maternal and child health (CEMACH). Saving
mothers lives: reviewing maternal deaths to make motherhood safer 20032005. The Seventh report
on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH.
Steer, P., Gatzoulis, M. and Baker, P. (2006). Heart Disease and Pregnancy. London: RCOG.
Thaman, R. (2003). Pregnancy related complications in women with hypertrophic cardiomyopathy.

Heart, 89(7), 752756.
The Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European
Society of Cardiology (ESC) (2011). ESC guidelines on the management of cardiovascular diseases
during pregnancy. Eur. Heart J., 32(24), 31473197.
Yentis, S., May, A. and Malhotra, S. (2007). Analgesia, Anaesthesia and Pregnancy. Cambridge:
Cambridge University Press.
Chapter 17
Respiratory disease in pregnancy

Christopher Kelly, Simon Maguire and Craig Carroll
Introduction
A number of significant physiological changes occur within the maternal respiratory system
throughout pregnancy, either as a result of hormonal or neonatal effects. Chapter 1 details these
changes.
Asthma
Asthma is a common condition characterized by intermittent reversible airways obstruction, chronic
inflammation of the airways and bronchospasm. It affects approximately 5% of the population in the
UK and is more common in women than men.
Asthma may be affected by pregnancy. Meta-analysis has shown approximately one-third of
women will have improved symptoms, one-third will worsen and one-third will see no changes. Any
worsening of symptoms will typically peak at six months gestation. There is often an improvement of
symptoms during labour, perhaps due to endogenous corticosteroid production, with acute asthma
being very rare at this stage.
Well-controlled asthma is unlikely to have any impact on the pregnancy. Uncontrolled asthma is
associated with a variety of complications, including hyperemesis, hypertension, pre-eclampsia,
vaginal haemorrhage, complicated labour, fetal growth restriction, preterm birth, increased perinatal
mortality and neonatal hypoxia. Large cohort studies have shown an increased caesarean section rate
in those with moderate and severe asthma.
Treatment should be optimized during pregnancy. A large case-controlled study showed no
increased risk of congenital malformations in mothers being treated for asthma. There is good
evidence that the older therapies have no teratogenic effects and no evidence to show the newer
agents cause any harm. The risk of uncontrolled asthma is far greater than the theoretical risk of
therapy.
Acute asthma should be managed in the standard way. Poor management is associated with poor
outcomes for mother and fetus; there is no known risk to the fetus with standard treatment.
Asthma is not a contraindication to any form of labour analgesia. Should caesarean section be
required, regional anaesthesia is suitable, as those with asthma are less likely to tolerate mechanical
ventilation well.
Postpartum haemorrhage can safely be managed with syntometrine and prostaglandin E2.
Prostaglandin F2 may cause bronchospasm.
Breastfeeding is not a contraindication to any of the treatments given for asthma, none of which
are found in dangerous levels in the milk. Oral steroids may also be given safely to the breastfeeding
mother.
Pulmonary artery hypertension (PAH) is defined as mean pulmonary artery pressures >25 mmHg at
rest or >30 mmHg with exercise. This can arise from a wide variety of disease states leading to a
common end pathway of plexogenic pulmonary arteriopathy. It can be sub-classified into:
Idiopathic pulmonary arterial hypertension
Associated with left heart disease/congenital heart disease (e.g. Eisenmengers)
Associated with lung disease/hypoxaemia
Associated with chronic thrombotic/embolic disease
Miscellaneous (e.g. histiocytosis, lymphangioleiomyomatosis, sarcoidosis).
Idiopathic pulmonary hypertension is a rare disease with prevalence in the region of 10 per million. It
is three times more common in women than men. Much more commonly, PAH is associated with
cardiac or respiratory disorders giving an overall prevalence of around 100 per million.
The pathophysiology is worsened by physiological changes of pregnancy. Cardiac output fails to
rise in response to the normal reduction in systemic vascular resistance. The pulmonary vasculature
also fails in its response to an increased circulating volume. Hypercoagulability can lead to
thromboembolism and further rises in PA pressures. The situation worsens in labour with further
stress and tachycardia. This can lead to fatal pulmonary hypertensive crisis.
Women are often counselled against pregnancy as maternal mortality is between 30% and 50%,
depending on the aetiology of PAH. In the event of pregnancy a multidisciplinary team with
knowledge of the condition should be consulted.
Parturients are often started on low-molecular-weight heparin during pregnancy. Oxygen and
diuretics may reduce the burden on the pulmonary vasculature. Many pulmonary vasoactive
compounds are teratogenic, although sildenafil may be safe. There is no consensus on optimum mode
of delivery, but this should be with full invasive monitoring and the facility to administer nitric oxide
in order to reduce PVR and therefore pulmonary arterial pressure.
Mothers should be monitored closely for at least two weeks, as many deaths are in the
postpartum period.
Pulmonary embolism
Pulmonary embolism (PE) is an obstruction to the lung vasculature by a substance that has travelled
from elsewhere in the circulation. This is most commonly thrombus, but can be fat, air or amniotic
fluid.
The haemostatic changes during pregnancy include increased concentrations of factors I, II, V,
VII, VIII, X and XII, as well as reduced effectiveness of activated protein C and reduced levels of
protein S. This leads to a hypercoagulable state and increased risk of thromboembolism. Large
studies have demonstrated PE in 12 of 7000 pregnancies, most of these occurring postpartum. In the
20062008 CEMACE report there were 0.79 deaths per 100,000 maternities; this was the lowest
level since 1985. Obesity is an independent risk factor with 14 of the 16 women dying from PE
having a BMI >25 kg/m2. Other predictors of risk are pre-eclampsia, caesarean section and multiple
births.
A high index of suspicion should be employed and the clinician alert for dyspnoea or tachypnoea
with or without pleuritic chest pain and/or haemoptysis.
Investigations should be as for the non-pregnant population. Those with suspected PE should
have CT pulmonary angiography performed. The potential benefits of accurate diagnosis and
subsequent treatment should be weighed against an increased lifetime risk of maternal breast cancer
and theoretical harm to the fetus.
Current practice is an extrapolation of treatment used in non-pregnant patients and observational
studies. Low-molecular-weight heparins are the treatment of choice; warfarin is teratogenic and
should be avoided, although can be taken while breastfeeding. Unfractionated heparin is often
substituted close to delivery because of the potential for reversal in the event of haemorrhage.
Treatment should continue for the longest duration, either three months after the initial diagnosis or
six weeks post delivery.
Sarcoidosis
Sarcoidosis is a multisystem disorder, of unknown aetiology, characterized by granulomas, which can
be found in most tissues of the body, but are most commonly found in the lungs.
The condition typically presents between the ages of 20 years and 40 years and will affect an
estimated 1 in 2000 pregnancies. Although the condition usually has a benign course, fatalities are
reported.
Knowledge of sarcoidosis and pregnancy comes primarily from observational studies and case
reports. There is often a relapsing remitting course of sarcoidosis; those in remission or with stable
disease typically see no changes to their condition during pregnancy. Expectant mothers with active
sarcoidosis will often find their symptoms improve as they approach term; radiological
improvements are also recorded. Unfortunately there is often rebound exacerbation, potentially with
new manifestations, three to six months post delivery.
There does not seem to be a correlation between sarcoidosis and poor outcome from pregnancy.
There have been individual reports of preterm labour and low birth weights, but this seems to be in
keeping with the background rates.
The condition should be optimized prior to and during pregnancy. Pulmonary function tests may
be of use when planning labour strategies. Corticosteroids are the first-line treatment and have not
been shown to have major teratogenic effects in large studies of patients with asthma. If right heart
hypertrophy and/or dilatation are present due to pulmonary hypertension women should be advised
against pregnancy. The second-line agents methotrexate and cyclophosphamide are teratogenic and
should be avoided, although some agents may be safe.
Women should be actively followed up post partum in anticipation of potential worsening of
their condition.
Cystic fibrosis
Cystic fibrosis (CF) is an autosomal recessive condition affecting chloride channels found throughout
the body. It is a multisystem disorder, but morbidity and mortality arise principally from the
respiratory system. The resulting thickening of secretions causes blockages, chronic inflammation,
recurrent infections and architectural damage to the lungs.
CF occurs in approximately 1 in 25003200 live births. The prevalence is ever increasing as
median life expectancy is rising with improved care. There are more adults than children with CF in
some European countries.
Although all pregnancies in CF patients should be considered high risk, a baseline FEV1 >60%
predicted is associated with favourable outcomes. The normal physiological changes of pregnancy
can present a significant challenge to these patients. Increasing minute ventilation with little functional
reserve and raising cardiac output with existing right heart strain can be problematic. Indeed, as
previously mentioned, pulmonary hypertension can present grave risk.
Predictors of increased risk are weight gain <4.5 kg, BMI <20 kg/m2, colonization with B.
cepacia, frequent infections, diabetes mellitus, pancreatic insufficiency and recurrent infections.
These patients have increased frequency of preterm labour.
Treatment should be optimized during pregnancy and multidisciplinary input sought. Mildly
impaired mothers may labour normally with epidural analgesia. Should caesarean section be deemed
necessary, each patient must be assessed individually, as no robust evidence exists to guide treatment.
Regional anaesthesia is often preferable to reduce impact on the respiratory system and avoid
mechanical ventilation. High block should be avoided because of dependence on the accessory
muscles. A CSE technique seems a reasonable approach to allow epidural analgesia post section and
aid compliance with physiotherapy. These patients require meticulous attention to detail in the
perioperative period, with senior input from the CF team, physiotherapy and microbiology, as well as
obstetrics/midwifery/anaesthesia.
Musculoskeletal disease
Myopathies
The myopathies are a heterogenous group of diseases that affect skeletal muscle cell function. They
can be divided into different groups:
1. The hereditary dystrophies (muscular dystrophies)

These can have a dominant, recessive or sex-linked inheritance. They usually affect proximal
muscles and have no sensory involvement.
2. The hereditary myotonic disorders

Myotonic dystrophy (autosomal dominant) is the most common inherited myopathy with a
prevalence of 5:100,000.
3. Metabolic myopathies
These include the mitochondrial myopathies, as well as disorders of glycogen storage and
lipid metabolism.
4. Myasthenic syndromes
Predominantly myasthenia gravis (see below) but also EatonLambert syndrome.
5. Others, e.g. inflammatory myopathies

These are proximal myopathies associated with muscle pain, tenderness and markedly raised
muscle enzymes and include dermatomyositis and polymyositis. Associated restrictive lung
defects, conduction abnormalities and bulbar symptoms are a cause for anaesthetic concern.
These myopathies are often steroid-responsive.
These all have in common a tendency to progression and deterioration over time with a reduction in
muscle strength. The level of input from the multidisciplinary maternity team will therefore be
dictated by the symptoms at presentation and progression over the course of the confinement.
Myotonic dystrophy
Myotonic dystrophy has two clinically and molecularly distinct forms, DM1 and DM2.
DM1 is the most common form and presents earlier with more progressive symptoms, including
restrictive lung defects with carbon dioxide retention and a reduced response to hypoxia. Pulmonary
function tests and arterial blood gas analysis should be considered. Bulbar involvement and
oesophageal dysmotility increase the risk of aspiration. An ECG is essential to rule out any
conduction defect and there is also an association with cardiomyopathy. These parturients should be
screened for diabetes as they can have insulin resistance. DM2 is typically milder, with myotonia in
90%, muscle dysfunction in 82%, but less commonly cardiac conduction defects, cataract and
diabetes.
Parturients with myotonic dystrophy suffer a higher incidence of obstetric complications,
including premature labour. Providing there are no contraindications, regional anaesthesia is the
preferred choice for labour analgesia or operative intervention. Points for consideration in myotonic
dystrophy:
Spinal anaesthesia may be contraindicated in those patients with severe respiratory

involvement.
Prevent myotonic crisis by keeping the patient warm, avoiding suxamethonium and gentle
surgical technique. (Although case series have reported the use of suxamethonium without
complications in this patient group.)
Regional anaesthesia does not prevent a myotonic crisis.
Myotonic crisis can be treated with intravenous dantrolene, phenytoin or procainamide.
Use rocuronium and sugammadex to eliminate the possibility of postoperative residual

neuromuscular blockade.
Myasthenia gravis
Myasthenia gravis is a chronic, autoimmune disorder resulting from autoantibodies to the postsynaptic
acetylcholine receptors. It is more common in women and is characterized by muscle weakness and
fatigability with repetitive use of the involved muscle. Over 80% of patients have detectable
antibodies and those who do not tend to have a milder form of the illness. Treatment includes
anticholinesterase medication, thymectomy, steroids, azathioprine and plasma exchange.
Exacerbations may be provoked by stimuli, including pain, temperature fluxes, infection, stress and
many drugs. The illness tends to progress from the head down, typically with early involvement of the
eye and facial muscles, bulbar symptoms and progression to involvement of respiratory muscles and
proximal muscles of the upper limbs. It has a variable peripartum course, but symptoms are reported
to be exacerbated more frequently during the first trimester and post partum. One-third of patients
will remain clinically unchanged, one-third will improve while one-third will have an exacerbation
of their symptoms.
Anaesthetic considerations include:
Antenatal assessment to discern the degree of bulbar and respiratory involvement/impairment.
Baseline pulmonary function tests. FVC <2.6 L has been shown to be predictive of the need
for postoperative ventilation.
Anticholinesterase dosage may require alteration during pregnancy, especially if associated

with emesis.
Consider the possibility of both myasthenic and cholinergic crises if a patient presents with
worsening weakness. Intravenous edrophonium will improve a myasthenic, but not a
cholinergic, crisis.
Use magnesium sulfate with caution as it will temporarily interfere with neuromuscular
function and power.
The preferred method of analgesia or anaesthesia is a regional technique, thus avoiding the
respiratory depressive effects of opioids and the need for muscle relaxants.
Progressive bulbar involvement or deteriorating respiratory function may result in the need
for general anaesthesia and securing of the airway. Care must be taken in the use of muscle
relaxants and monitoring of neuromuscular function. These parturients may require an
increased dose of depolarizing muscle relaxant, but a significant reduction in the dose of non-
depolarizing relaxants, with atracurium the drug of choice. Prolonged postoperative
ventilation should be anticipated.
Scoliosis
Scoliosis is a major source of referral to obstetric anaesthetic assessment clinics. Mostly, these will
be minor to moderate, surgically uncorrected scoliosis. Scoliosis is more common in women and
most cases (90%) are idiopathic. There are, however, a large number of conditions associated with
scoliosis, including spina bifida, neurological disorders (e.g. cerebral palsy), myopathies (e.g.
muscular dystrophy), connective tissue disorders (e.g. Marfans) and metabolic disorders (e.g.
mucopolysaccharidosis).
Factors affecting morbidity include age of onset, cardiorespiratory involvement and other
associated pathologies.
With patients in whom scoliosis has developed relatively late in childhood and puberty,
cardiorespiratory function is usually well maintained.
Deformity from early childhood is associated with greater impact upon lung development and
may adversely affect cardiac function. The resulting restrictive lung defect can potentially progress to
chronic hypoxia and pulmonary hypertension. Investigations to detect cardiorespiratory defects
should be considered as part of anaesthetic assessment.
Factors affecting choice of anaesthesia and analgesia are discussed below.
Uncorrected scoliosis
The level of the vertebral deformity needs to be identified.
More than one curve can exist (i.e. thoracic + lumbar curve). The curve may not be evident
towards the lower region of the lumbar spine.
The defect is three-dimensional, with vertebral rotation in conjunction with curvature.
The spinal cord may not terminate at the usual level (i.e. T12L1).
The morphology of the epidural space may be altered, resulting in unpredictable passage of
epidural catheters, with an increased risk of failed block and possibly inadvertent dural
puncture.
Corrected scoliosis
Scoliosis corrective surgery consists of a number of steps that can compromise the ability to perform
regional blockade safely and effectively.
Posterior scoliosis correction surgery results in tissues superficial to the ligamentum flavum
being disrupted, posterior spinous processes are usually removed and laminae disrupted.
Decortication of bone and addition of inert bone graft will obliterate the midline and paramedian
access to the epidural space. The epidural space itself may be disrupted.
Attempts to perform epidural analgesia in the corrected scoliosis patient are therefore linked
with an increase in both complications of insertion and sub-optimal/inconsistent analgesic outcome.
The literature suggests that continuous spinal analgesia is used with increased frequency in this
patient group (either as a planned procedure or possibly as a result of inadvertent dural puncture).
Practical suggestions when contemplating regional anaesthesia in the scoliosis patient include:
Consider avoiding epidural analgesia, using spinal catheters instead.
Consent for an increased risk of failure and complications of neuraxial technique (failed
access, prolonged procedure, neuropraxia, inadvertent dural puncture, failure to thread
epidural catheter, blood in catheter, inconsistent block, unpredictable height of block, spinal
cord trauma.
Perform the technique low in the lumbar spine (L45, L5S1), where the pelvis tends to limit
the rotational element of deformity.
Avoid attempting regional analgesia through areas of surgical scarring.
Restrict the number of needling attempts; be prepared for failure.
Consider the risk of infecting metalwork with needling of the instrumented surgical area.
Lumbar spine disease

Mechanical lumbar back pain and nerve root pain are common causes for antenatal anaesthetic
consultation.
It is important to distinguish the pathology causing the symptoms so that the patient can be
appropriately consented for risks of regional anaesthesia.
Assessment and documentation of neurological function prior to performing a regional procedure
is important for both clinical and medicolegal reasons.
Nerve compression in the lumbar region can be caused by disc disease, alignment abnormalities,
tumour or osteophytes.
Alignment abnormalities
Either by anatomical or progressive traumatic/degenerative. Spondylisthesis of the lumbar vertebrae
(usually L5 on S1) results in a slip and malalignment of the vertebrae with resulting narrowing of the
exit foramen and spinal nerve compression. The listhesis itself is thought to contribute to mechanical
back pain.
True disc disease

The intervertebral disc consists of an outer annulus fibrosus and inner soft nucleus pulposus.
Pathologies include:
The annulus remains intact, but bulges, compressing the cauda and spinal nerve root.
The annulus ruptures and pulposus tissue exudes into the spinal canal causing compression
and chemically mediated irritation.
Disc prolapse can be posterolaterally or from the true posterior position (central disc prolapse).
Compression of the entire thecal sac in the latter scenario can result in cauda equina syndrome, which
consists of back or leg pain, saddle anaesthesia with loss of bladder and bowel continence these
are red flag signs and represent a neurosurgical urgency.
Lumbar spine decompression surgery

In order to understand the risks of regional anaesthesia, it is important to understand which operation
has been performed and at what level.
Laminectomy: the lamina and possibly posterior spinous process will have been removed.
The ligamentum may have been obliterated and removed at this level. The epidural space may
not exist. An epidural cannot be performed at this level. Epidural anaesthesia performed at
another level may be ineffective, as the spread of local anaesthetic past the operative level
may be impeded. Spread of spinal anaesthesia is unaffected.
Lateral approach with fenestration: The midline structures are left intact and a fenestration
made in the ligamentum at an interlaminar level (similar to the site of a paramedian approach
to the epidural space). Spread of epidural anaesthesia may be affected.
When considering regional anaesthesia do not attempt needling though the scar. (NB: surgery
may have been performed beyond the limit of the scar.)
A recent study demonstrated similar LA use for labour analgesia in women with previous
lumbar discectomy compared to controls. The only difference between the groups was the number of
interspaces attempted.
Patients with untreated thecal or spinal nerve compression may have a flattened or deviated
thecal sac. This may result in a decreased thecal target, with possible deviation from the midline and
obliteration of epidural fat, reducing the size of the epidural space.
There have been historical links between labour epidurals and long-term back pain, but all
recent studies have failed to demonstrate any link. A Cochrane Database Systematic Review in 2011
comparing epidural vs. non-epidural or no analgesia in labour found no link between labour epidural
analgesia and long-term backache.
Anaesthetic considerations:
Document existing neurology

Obtain information relating to previous diagnosis, level of disease and surgery
Counsel the patient and obtain consent before attempting neuraxial blockade
Avoid needling at the level of or close to any surgical scar
Be aware of red flag signs of back pain and features of cauda equina syndrome.
Neural tube defects

Spina bifida encompasses a range of neural tube defects from spinal bifida occulta (SBO), which
occurs incidentally in up to 25% of the population, to spina bifida cystica, a more severe form, which
occurs in 1 in 2000 live births.
SBO is often an incidental finding on X-ray and occurs when two halves of a vertebral arch
(usually at level L5S1) fail to fuse. The overlying skin is intact, but can have cutaneous angiomata,
pigmented areas, lipoma, a tuft of hair or simple dimple. It is not associated with neurological
symptoms.
Spinal bifida cystica is defined as failed closure of the neural arch with herniation of the
meninges (meningocoele) or the meninges and neural elements (meningomyelocoele). Tethering of the
spinal cord is a well-recognized association and neurological defects can occur below the level of
lesion.
Occult spinal dysraphism, sometimes confused with SBO, is a condition where bony defects of
the spine are associated with spinal cord anomalies, including tethering (in 3587% cases),
intraspinous lipomas, dermoid cysts, fibrous bands and split cord.
Issues complicating regional anaesthesia (RA) include:
Increased risk of neural/dural injury, especially at the level of defect
Abnormal spread of local anaesthetic, either excessive cranial or inadequate caudal
Performance of RA in presence of pre-existing neurology.
Recommendations:
In patients with SBO always consider occult spinal dysraphism. Patients with neurological
abnormalities, cutaneous manifestations or involvement of more than one lamina should have
MRI imaging to determine the extent of spinal involvement
Careful documentation of pre-existing neurology

Consent patient for risks of failure and complications
Perform neuraxial procedure above the level of defect.
Malignant hyperthermia
This inherited disorder (mainly autosomal dominant) results in an error in skeletal muscle calcium
control. There is a loss of control of calcium flux and an increase in the calcium concentration in the
cytosol of skeletal muscle. The proposed site of action is the Ryanodine receptor, which spans the
calcium-releasing channels on the sarcoplasmic reticulum and T-tubule.
The increase in intracellular free calcium results in the clinical picture of:
Increased skeletal muscle contraction
Increased skeletal muscle metabolism
Glycolysis
Rhabdomyolysis
Uncoupling of oxidative phosphorylation.
The triggers for this condition are volatile anaesthetic agents and suxamethonium. The majority of UK
cases are in patients with a known family history and therefore preparations can be made during
pregnancy. The two main presentations are therefore acute presentation in patients previously
undiagnosed and known cases presenting in the antenatal clinic.
Known cases should be seen antenatally in order to discuss the benefits of an early labour
epidural, which can safely provide intrapartum and intraoperative analgesia and anaesthesia.
Delivery suite and theatres should be prepared, ensuring the availability of a vapour-free
anaesthetic machine, TIVA equipment, dantrolene, rocuronium and sugammadex.
Algorithms for recognition and treatment of malignant hyperthermia should be readily available.
Key points
1 Respiratory disease can improve, remain stable or deteriorate during the antenatal and
postpartum period.
2 Evaluation of respiratory function outside of pregnancy can guide preconceptual counselling.

3 MDT management, with regular antenatal review and appropriate peripartum and postpartum
plans are essential.
4 Knowledge of pre-existing musculoskeletal disease is essential to guide intrapartum analgesic

and anaesthetic options.
Further reading
Anim-Somuah, M., Smyth, R. M. and Jones, L. (2011). Epidural versus non-epidural or no analgesia
in labour. Cochrane Database Syst Rev., 12, CD000331.
Bauchat, J. R., McCarthy, R. J., Koski, T. R. et al. (2012). Prior lumbar discectomy surgery does not
alter the efficacy of neuraxial labor analgesia. Anesth. Anal., 115(2), 348353.
British Thoracic Society. (2014). British guideline on the management of asthma. London: The British
Thoracic Society.
British Thoracic Society Standards of Care Committee Pulmonary Embolism Guideline Development
Group. (2003). British Thoracic Society guidelines for the management of suspected acute pulmonary
embolism. Thorax, 58, 470484.
Crochetiere, C. (2008). Myopathies: Musculoskeletal Disorders: Obstetric Anesthesia and

Uncommon Disorders. Cambridge. Cambridge University Press.
Huffmyer, J., Littlewood, K. and Nemergut, E. (2009). Perioperative management of the adult with
cystic fbrosis. Anaesth. Analg., 6, 19491961.
Imison, A. R. (2001). Anaesthesia and myotonia: an Australian experience. Anaesth. Intens. Care, 29,
3437.
Madden B. P. (2009). Pulmonary hypertension and pregnancy. Int. J. Obstet. Anaesth., 2, 156164.
Vahid, B., Mushlin, N. and Weibel, S. (2007) Sarcoidosis in pregnancy and postpartum period. Curr.
Respir. Med. Rev., 3, 7983.
Chapter 18
Obesity and ultrasonography for central
neuraxial blocks

Sophie Bishop and Preye Zuokumor
Obesity is a global health pandemic with increasing prevalence, and is arguably one of the biggest
challenges facing maternity services today.
Obesity is defined as a condition of abnormal or excessive fat accumulation in adipose tissue to
the extent that health may be impaired. Obesity is often expressed with reference to body mass index
(BMI). This is calculated by the persons weight in kilograms (kg) /divided by the square of their
height in meters (m2). The World Health Organization (WHO) defines obesity as a BMI of at least
30 kg/m2, which is further divided into five classes (Table 18.1).
Table 18.1 WHO classification of obesity
WHO Classification Popular description BMI (kg/m2) Risk of co-morbidity
Underweight Thin < 18.5 Low
Normal Normal 18.524.9 Average
Overweight Overweight 2529.9 Mildly increased
Obese Class 1 Obese 3034.9 Moderately increased
Obese Class 2 Obese 3539.9 Severely increased
Obese Class 3 Morbidly obese > 40 Very severely

increased
Super Obese > 50 Very severely
increased
Super Super Obese > 60 Very severely

increased
In 2011, an estimated 26% of women in the UK aged 16 years or over were obese (cf. 16% in
1993). The UK prevalence of women with a known BMI 35 kg/m2 at any point in pregnancy is ~5%
(approximately 38,478 maternities/year). The prevalence of women with a BMI 40 kg/m2 in the UK
is 2%, whilst a BMI 50 kg/m2 affects 0.19% of all parturients.
Maternal obesity is associated with a substantial increase in both obstetric and fetal morbidity,
as well as being a significant risk factor for maternal mortality (see Table 18.2).
Table 18.2 Risks related to obesity in pregnancy
Maternal Spontaneous first trimester and recurrent

miscarriage
Maternal death
Left ventricular hypertrophy/
dysfunction/failure, cardiomyopathy, ischaemic
heart disease
Obstructive sleep apnoea, asthma
Gestational diabetes (GDM)
Hypertension, pre-eclampsia
Thromboembolism
Dysfunctional labour
Lower success rate of vaginal birth after
caesarean section
Shoulder dystocia
Operative vaginal delivery (increases with
increasing BMI)
Higher caesarean section rate
Postcaesarean wound infection
Postpartum haemorrhage
Low breastfeeding rates
Fetal Stillbirth and perinatal mortality

Congenital anomalies, birth injuries
Macrosomia (birth weights >4000 g)
Neonatal intensive care admission
Possible long-term obesity problems for child
Pregnant women with obesity are at higher risk of anaesthesia-related complications. Obesity
has been identified as a significant risk factor for anaesthesia-related maternal mortality.
Prepregnancy BMI >40 kg/m2 and a delivery BMI >45 kg/m2 have been found to be predictive of a
higher incidence of anaesthetic complications, including: failure to establish neuraxial anaesthesia,
inadequate neuraxial anaesthesia requiring conversion to general anaesthesia and other anaesthesia-
related morbidity and mortality.
The Confidential Enquiry into Maternal and Child Health (CEMACH) report on maternal deaths
in the 20032005 triennium showed that 28% of mothers that died were obese, whereas the
prevalence of obesity in the general maternity population within the same time period was 1619%.
Six maternal deaths were directly related to anaesthesia, of which four patients were obese and two
were morbidly obese. As a result in 2008 the Centre for Maternal and Child Health Enquires
(CMACE) conducted a 3-year UK-wide Obesity in Pregnancy project and with the Royal College of
Obstetricians and Gynaecologists (RCOG) have published clinical guidelines on the management of
women with obesity in pregnancy (see Further reading). The CMACE report (20062008) noted
obesity was still a major contributor to maternal mortality, with 27% of mothers who died being
obese.
Physiological changes in obesity

Pregnancy induces a number of physiological changes to support the uteroplacental unit, as discussed
i n Chapter 1. Obesity also results in a number of significant physiological changes (additive with
increasing BMI). The further physiological impact of obesity on pregnancy leads to significant
functional impairment and decreased physiological reserve. The most important physiological
changes are listed in Table 18.3. These effects need to be taken into consideration when planning
regional and general anaesthesia for these patients.
Table 18.3 Physiological changes in obesity
Respiratory system
Reduced functional residual capacity (FRC) with risk of hypoxia
FRC below closing capacity resulting in shunting
Increased work of breathing due to reduced chest wall compliance (sometimes up to 30%)
secondary to increased chest wall weight and impaired diaphragm function. Increased
oxygen consumption and C02 production
Restrictive respiratory defect resulting in a rapid, shallow breathing pattern
Obstructive sleep apnoea with risk of pulmonary hypertension and cor pulmonale
Obese hypoventilation syndrome 510% of morbidly obese
Cardiovascular system
Increase in blood volume
Increase in cardiac output proportional to degree of obesity
(3050 mL/min for every 100 g of adipose tissue)
Presence of endothelial dysfunction with increased peripheral resistance
Hypertension
Left ventricular hypertrophy with subsequent systolic and diastolic dysfunction, leading to
heart failure
Increased risk of fatal gestational and peripartum arrhythmias
Peripartum cardiomyopathy (difficult to diagnose as symptoms masked and technical

difficulties in performing echocardiography)
Obese supine hypotensive syndrome due to aortocaval compression
Gastrointestinal
Raised intragastric pressure, relaxed lower oesphageal sphincter
Increased gastric acidity and volume
Increased incidence of gastro-oesphageal reflux and hiatus hernia. The volume and acidity
of gastric contents may be 5 greater
Endocrine
Type II diabetes mellitus (DM) (+/ complications of DM)
Nutritional status may be malnourished
Musculoskeletal
Difficulty in positioning patient, including left lateral tilt
Risk of rhabdomyolysis with prolonged surgery e.g. buttock ischaemia
Coagulation
Increased risk of thromboembolic disease
Airway
Obesity and pregnancy each increase the risk of difficult intubation and pulmonary aspiration during
anaesthesia. Careful assessment, planning and management of the airway are important. Poor head
positioning, a short neck, an increased fat pad at the back of neck, airway oedema and increased
breast tissue make laryngoscopy and tracheal intubation technically challenging. The incidence of
difficult intubation may be as high as 15%. The combination of Mallampati score and thyromental
distance are useful to predict difficult laryngoscopy. Mallampati class IIIIV has been found to be an
independent risk factor for difficult intubation in obese patients.
Positioning before induction of general anaesthesia remains critical for the morbidly obese
parturient, and time should be taken to do this even in an emergency situation. The optimal position is
the ramped position, where the head and neck are elevated until the external auditory meatus is in a
horizontal plane with the sternal notch, when assessing the patient from the side view. This can be
accomplished by using either a stack of blankets or a commercially available pillow such as the
Oxford Head Elevating Laryngoscopy Pillow (HELP) (Alma Medical, Oxford, UK).
Patients with a known difficult airway may require an awake oral fibre optic intubation (FOI).
(Nasal FOI is not recommended on account of mucosal congestion and risk of bleeding).
Thromboprophylaxis
Venous thromboembolic (VTE) disease is a major cause of maternal mortality in developed countries
and both caesarean delivery and obesity are major risk factors. Obese parturients are at significantly
higher risk of thromboembolic events throughout pregnancy and puerperium. Low-molecular-weight
heparin (LMWH) is recommended for antenatal and postnatal thromboprophylaxis (see Table 18.4).
This highlights the importance of documentation of the patients recent weight for appropriate dosing.
In addition mechanical methods such as graduated compression stockings and sequential calf
compression devices should be used and mobilization encouraged. Clear guidelines should be
provided regarding safe timing of neuraxial anaesthesia and analgesia following thromboprophylaxis
administration.
Table 18.4 RCOG guidelines for thromboprophylactic doses of LMWH
Weight Enoxaparin Dalteparin Tinzaparin
< 50 kg 20 mg daily 2500 units daily 3500 units daily
5090 kg 40 mg daily 5000 units daily 4500 units daily*
91130 kg 60 mg daily* 7500 units daily* 7000 units daily*
131170 kg 80 mg daily* 10000 units daily* 9000 units daily*
> 170 kg 0.6 mg/kg/day* 75 units/kg/day* 75 units/kg/day*
Reproduced from: Royal College of Obstetricians and Gynaecologists. Thrombosis and

Embolism during Pregnancy and the Puerperium. Green-top Guideline No. 37A. London: RCOG;
2009, with the permission of the Royal College of Obstetricians and Gynaecologists.
Equipment
Maternal weight should be re-measured in the third trimester to allow appropriate plans to be made
for specialist equipment and personnel required during labour and delivery (Table 18.5). Familiarity
with specialist beds for the morbidly obese is necessary in case a woman needs to be laid flat for
resuscitation.
Table 18.5 Equipment list
Maximum weight that operating table can support must be known (minimum of 160 kg)
Lateral extensions for operating table and arm boards
Weighing scales
Wide wheelchairs
Bariatric hover mattress
Slide sheets
HELP pillow or pillows to allow for ramping
Electric beds
Large gowns
Large compression stockings/mechanical calf compressors
Large blood pressure cuff
Ultrasound for IV cannulae/epidural insertion
Anaesthetic antenatal assessment

It is recommended that all women with a BMI 40 kg/m2 have an antenatal consultation with an
obstetric anaesthetist, so that potential difficulties can be identified and an anaesthetic management
plan for labour and delivery can be documented. Obstetric units may decide to use a lower BMI
threshold, taking into consideration the local prevalence of maternal obesity. Women with a BMI
<40 kg/m2 with anticipated problems related to co-morbidities, airway management, vascular access
and regional anaesthetic techniques will also require an antenatal anaesthetic consultation. All other
obese parturients should be assessed as soon as possible after arrival on delivery suite.
The CAVE assessment ( Table 18.6) is a useful mnemonic for assessment of these patients,
which includes a physical and ultrasound examination of the patients back. Tactful discussion with
the patient should include both the increased risk of difficult labour analgesia initiation and potential
failure and the goals for comfort and safety. Surveys suggest that this type of discussion rarely occurs,
possibly because of concerns of offending the patient. Lack of discussion may contribute to unrealistic
patient expectations or incomplete informed consent. The Obstetric Anaesthetists Association
(OAA) have published a leaflet Information for pregnant women with a high body mass index,
which is helpful to give to women, and also for those women not referred to the anaesthetic antenatal
clinic.
Table 18.6 CAVE assessment
C Co-morbidities
A Airway assessment
V Venous access
E Epidural (including U/S back)/Equipment

required
Anaesthetic management for labour

Delivery of the morbidly obese parturient should take place on a consultant-led delivery suite with
the senior obstetrician and anaesthetist aware. On admission, the antenatal anaesthetic plan should be
reviewed, or a CAVE assessment performed. Oral intake should be limited to clear fluids, and an H 2
antagonist commenced and continued 6 hourly whilst in labour. A large-bore intravenous cannula
should be inserted early in labour (ultrasound guidance may be needed), by those with expertise, as
multiple failed attempts may make it more difficult.
The provision of regional analgesia for labour reduces the need for entonox or systemic opioid
analgesia, which have been proven to lead to maternal drowsiness, airway obstruction and
hypoxaemia. Intramuscular diamorphine in obese patients is unreliable due to variable absorption and
effect. Increasingly, remifentanil patient-controlled analgesia (PCA) is used as a labour analgesic.
Extreme care should be taken to ensure obese women using PCA are well monitored and have
continuous one-to-one midwifery care until delivery.
As the obese parturient is more likely to require operative delivery and general anaesthesia is
associated with greater morbidity, central neuraxial block is the most effective form of analgesia in
labour. Due to the technical challenges of siting an epidural in these patients, placement of an
epidural early in labour is recommended as patient position can be optimized more easily. As
landmarks are more difficult to palpate and back flexion is limited (both factors predictive of difficult
neuraxial placement) the epidural failure rate is high and multiple attempts are not uncommon.
The sitting position is best as the midline may be identified more easily than in the lateral
position, and it reduces the distance from the skin to the epidural space. Interestingly, despite an
increased depth of epidural space with increasing weight and BMI, very few patients actually have an
epidural space that is deeper than 8 cm. However, it may be necessary to use a longer epidural
needle. Techniques to facilitate epidural insertion include the use of the patients light touch
discrimination to determine the midline, tilting of the table towards the operator to open the lumbar
interspaces and the use of a seeker needle to identify a spinous process. Ultrasound visualization is
discussed below.
In obese patients, successfully placed epidural catheters can easily be dislodged by the drag of
the back fat pad, so it is advisable to leave extra catheter length in the space i.e. 56 cm; also
tunnelling the epidural catheter may help. The catheter site should be protected whilst repositioning in
bed. Catheter position and sensory levels should be checked regularly during labour to ensure
adequate position and function. Epidural re-sites have been reported to increase with increasing BMI
and the epidural catheter should be replaced early if the block is ineffective.
There is evidence that after accidental dural puncture, the incidence of post dural puncture
headache is less in obese parturients compared with non-obese parturients. This may be due to
increased pressure in the epidural space. This effect may also result in higher than expected sensory
and motor block levels. Careful titration of local anaesthetic should be used to avoid a high block.
Anaesthesia for caesarean section

Anaesthetic challenges may lead to increased decision-to-delivery time if emergency operative
delivery is required and may increase anaesthetic morbidity. Advanced warning of such challenges
may influence the planned mode of delivery and allow appropriate staff to be made available.
General considerations for delivery in theatre
Appropriate equipment available
Surgery is technically more difficult with reduced surgical access and bleeding
Retraction of the panniculus may worsen aortocaval compression
Adequate left lateral tilt is required
Operating times are often longer
Increased risk of PPH.
Monitoring
Reliable monitoring of obese obstetric patients is essential. Measure the mid-arm circumference to
assess the appropriate size of non-invasive blood pressure (NIBP) cuff. If >33 cm (13 inches) use
large or adult thigh cuff size. Note that normal-size cuffs can be applied to the forearm to monitor BP
if larger cuffs are unavailable.
Invasive arterial pressure monitoring may be required. Central venous access may also be
necessary.
Regional anaesthesia
Extending labour epidural analgesia avoids general anaesthesia and allows a titratable level of
anaesthesia and dose, with the ability to extend the block for prolonged surgery and slower and more
controllable haemodynamic changes. For elective caesarean section, single-shot spinal is probably
the most practiced technique. However combined spinal-epidural techniques is an attractive
alternative technique, combining the advantages of rapid onset and dense block with the ability to
prolong regional anaesthesia if required. In addition, reducing the intrathecal dose may help to control
the haemodynamic effects of the block, which are compounded by aortocaval compression in this
group.
General anaesthesia
General anaesthesia can be slightly quicker than regional anaesthesia and is indicated when there is
an immediate threat to life of mother or fetus, and where central neuraxial block is contraindicated or
has failed i.e. only done when absolutely necessary. General anaesthesia for caesarean section is
associated with a much higher risk of maternal mortality than regional anaesthesia, with failed
intubation and aspiration as contributing factors. A senior anaesthetist should be present, to assist
with airway management. Standard aspiration prophylaxis must be given. Optimal patient positioning,
in the ramped position as previously discussed are and good preoxygenation vital, as rapid
desaturation is common. Careful attention to left lateral tilt even during general anaesthesia is
mandatory. A relatively high inspired-oxygen concentration may be necessary compared to non-obese
parturients and the use of pressure-controlled ventilation and positive end-expiratory pressure to
maintain adequate oxygenation. Awake extubation with adequate reversal of neuromuscular blockade,
with a 45 head-up tilt is a more favourable position than supine in the obese population.
Postpartum care
Postoperatively women with a BMI >40 kg/m2 should be assessed individually to determine if they
need an extended recovery period on the delivery suite or the high-dependency unit (likely if BMI
50 kg/m2) for the first 24 hours. If there is respiratory or cardiovascular compromise, early referral
to ITU should be considered. Common postoperative complications include hypoxia, pulmonary
atelectasis and pneumonia, so humidified oxygen supplementation should be maintained. Early
postnatal and postoperative mobilization is vital, with adequate pain control, VTE prophylaxis and
chest physiotherapy.
Ultrasonography for central neuraxial blocks in obstetrics

Ultrasonography for obstetric regional anaesthesia is a novel way of identifying the structures within
and around the lumbar vertebrae. Conventionally, siting epidurals and spinals relies on the
anaesthetists skills and ability to correctly identify the bony landmarks of the spine and pelvis, and to
introduce the needle blindly into the epidural or intrathecal space. Not surprisingly, the landmark-
based technique is associated with difficulties and failures, particularly amongst inexperienced
anaesthetists, obese patients and patients with scoliosis or previous back surgery. With the
introduction of high-resolution portable ultrasound machines, the lumbar spine can be imaged with
some degree of accuracy. When appropriately utilized, ultrasonography increases the success rate of
central neuraxial blocks, while minimizing the risks to the patient. The use of ultrasound imaging has
been shown to improve the efficacy of epidural analgesia and reduce technical difficulties.
In 2008, guidance from NICE reported that although evidence of U/S guided catheterization of
the epidural space was limited, it is safe and may be helpful in achieving correct placement.
Spinal ultrasound can be challenging, as the structures imaged are protected by an articulated
encasement of bones, limiting the acoustic windows for the ultrasound beam. The structures of
interest are located deeper than expected. Accordingly, spinal ultrasonography requires a probe that
is curved and of low frequency (25 Hz), with the ability for deep penetration. However, with deeper
penetration of the ultrasound beam there is some loss of image resolution.
There are two ways of facilitating epidural catheterization under ultrasound guidance. The first
is the most common and is referred to as prepuncture ultrasound. It is used as a guide to the
conventional technique of central neuraxial block and involves an initial ultrasound scan of the
vertebral spines to determine the midline, vertebral interspaces and depth of the space. The
interspaces can be marked on the skin to facilitate actual needle placement. The second, which is still
at its infancy in terms of development, is real-time ultrasound imaging, and this approach allows
observation of the epidural needle as it passes towards the epidural space. Subsequent discussions
will be limited to the first approach.
Sonoanatomy of the lumbar spine

The aim of ultrasound imaging of the lumbar spine is to encourage pattern recognition, which is
essential to the interpretation of images:
Patient should be placed in the position the block is to be performed, which is sitting in most
obstetric patients.
A curved array, low frequency (25 MHz) probe gives the best image quality.
The initial depth is set to 710 cm (the depth may be fixed with some devices)
For the sake of simplicity, there are two main orientations of the probe: paramedian sagittal
(PS) and transverse views. Information from each scanning plane compliments the other.
With the probe in a PS orientation 34 cm from the midline (PS transverse process view), the
Trident sign is the main feature and it represents finger-like shadows of the transverse
process. If the probe is tilted towards the midline, the sawtooth appearance of the laminae is
seen. Also, the posterior complex (ligamentum flavum, epidural space and posterior dura) and
anterior complex (anterior dura, posterior longitudinal ligament and vertebral body) will be
discernable (Figure 18.1).
With the probe still in the PS orientation, slide the probe caudally until the L5S1 interspace
is at the centre of the screen. The horizontal hyperechoic line of the sacrum is used to identify
the L5S1 interspace, and its location can be used to mark intervertebral levels (Figure 18.2).
Rotate the probe transversely to obtain a transverse interlaminar view of the desired
interspace. Optimal views may be obtained by tilting the probe cephalad or caudad. The depth
from skin surface to the posterior complex may be measured using the inbuilt electronic
calipers (Figures 18.3 and 18.4).
Indications for ultrasound imaging of the spine:
As part of preoperative assessment of obstetric patients at the antenatal anaesthetic

assessment clinic, in delivery suite or theatre
Facilitates insertion of central neuraxial block, especially in patients with difficult surface
anatomy, e.g. morbidly obese, scoliosis or previous back surgery
Previous problematic central neuraxial blocks
Previous post dural puncture headaches.
The perceived advantages of imaging of the spine include:
Prediction of depth of epidural and intrathecal spaces
Aids identification of intervertebral levels
Assists in locating important landmarks such as the midline and interlaminar spaces
Fewer puncture attempts
Higher first time success rate
Less time required to catheterize epidural space
Higher patient satisfaction
Improves teaching of regional techniques to anaesthetic trainees.

Limitations of the ultrasound spinal imaging technique:
Poor image quality in certain patient populations. In obese patients images are less distinct
because of attenuation of ultrasound waves. Patients with metal implants may distort the image
quality.
Inaccuracies of skin marking due to patient movement
Operator inexperience
May lead to delays (if an urgent caesarean section is needed).
Figure 18.1 Parasagittal (oblique) view. The laminae (L) form a saw-tooth pattern.
Figure 18.2 Parasagittal (oblique) view of L5S1 junction.
Figure 18.3 Transverse (interlaminar) view of the lumbar spine.
Figure 18.4 Transverse view showing the depth to the posterior complex.
Key points
1. Maternal obesity significantly increases both obstetric and fetal morbidity and is an
independent risk factor for maternal mortality.
2. Prepregnancy BMI >40 kg/m2 and a delivery BMI >45 kg/m2 are predictive of a higher
incidence of anaesthetic complications.
3. Antenatal anaesthetic assessment is recommended for parturients with BMI >40 kg/m2 at
booking.
4. Early epidural placement is recommended during labour. Timing in relation to administration

of LMWH may be required.
5. Spinal ultrasound may be helpful in achieving correct placement of central neuroaxial blocks.
6. Prepare for difficult laryngoscopy in the obese parturient with optimal patient positioning and
an appropriate airway plan.
7. Meticulous care is required to reduce significant postoperative risks, including respiratory

complications, thromboembolism and infections.
Further reading
Association of Anaesthetists of Great Britain and Ireland (2007). Peri-Operative Management of the
Morbidly Obese Patient. London: AAGBI.
Centre for Maternal and Child Enquires (CMACE) (2010). Maternal Obesity in the UK: Findings
from a national project. London: CMACE.
Centre for Maternal and Child Enquires (CMACE) (2011). Saving Mothers Lives: reviewing
maternal deaths to make motherhood safer: 20062008. The Eighth Report on Confidential Enquires
into Maternal Deaths in the United Kingdom. BJOG, 118(1), 1203.
Chin, K. J., Karmakar, M. K. and Peng, P. (2011). Ultrasonography of the adult thoracic and lumbar
spine for central neuraxial blockade. Anesthesiology, 114(6), 14591485.
Grau, T., Bartusseck, E., Conradi, R., Martin, E. and Motsch, J. (2003). Ultrasound imaging improves
learning curves in obstetric epidural: a preliminary study. Can. J. Anaesth., 50, 10471050.
Grau, T., Leopold, R. W., Fatehi, S., Martin, E. and Motsch, J. (2004). Real time ultrasonic
observation of combined spinal-epidural anaesthesia. Eur. J. Anaesthesiol., 21, 2531.
Knight, M., Kurinczuk, J. J., Spark, P. and Brocklehurst, P. (2010). Extreme obesity in pregnancy in
the United Kingdom. Obstet. Gynaecol., 115, 989997.
Labor, E. E. (2012). Analgesia for the obese parturient. Anaesth. Analg., 115, 889903.
National Institute for Health and Clinical Excellence (2008). Ultrasound Guided Catheterization of
the Epidural Space. London: NICE.
Obstetric Anaesthetists Association. (2013). Information for pregnant women with a high body mass
index (BMI). Available on www.oaa-anaes.ac.uk (accessed May 2015).
Chapter 19
Endocrine disease in pregnancy, including
diabetes mellitus, thyroid and adrenal disease

Jenny Myers and Dan Mallaber
Diabetes
Introduction
Diabetes mellitus (DM) is a common and growing problem, affecting approximately 650,000
pregnancies in England and Wales each year (representing 25% of the obstetric population). Women
with diabetes have an increased risk of both fetal and maternal complications, and of requiring
anaesthetic intervention. Close monitoring and treatment during pregnancy, and careful anaesthetic
management during labour and delivery, can reduce these risks and improve outcomes for both mother
and baby.
Classification
DM is a multisystem disorder of carbohydrate metabolism, which can result from a number of distinct
pathophysiological processes. Around 7.5% of pregnancies complicated by diabetes are due to type 1
and 5% due to type 2 diabetes. Gestational diabetes (GDM) accounts for the remaining 87.5%.
Type 1
Type 1 DM is attributable to an absolute lack of insulin production and secretion by the pancreatic
cells of the Islets of Langerhans. It is primarily an autoimmune disorder, although genetic and
environmental factors also play a role. It accounts for around 10% of all DM. There is an association
with other autoimmune conditions, including hypothyroidism.
Type 2
Type 2 DM is caused by a combination of both relative lack of insulin secretion and insulin
resistance in target tissues. It accounts for 90% of all DM cases and is primarily associated with
obesity. As such, its prevalence in both obstetric and non-obstetric populations is increasing and this
is particularly so amongst several ethnic groups (including people of African, black Caribbean, South
Asian, Middle Eastern and Chinese family origin).
Gestational diabetes mellitus

Gestational diabetes (GDM) is defined as glucose intolerance, which is first identified during
pregnancy. Insulin resistance is known to increase progressively during the second and third
trimesters of pregnancy due to an increase in counter-regulatory hormones (including placental
lactogen, placental growth hormone, cortisol and progesterone). GDM may therefore be thought of as
a preclinical state of glucose intolerance unmasked by the physiological changes in pregnancy. For
most mothers glucose levels return to normal, but there is an increased risk of subsequent type 2
diabetes in women diagnosed with GDM.
Diagnosis and screening

The diagnosis of type 1 DM is usually made in adolescence or early adulthood. It is confirmed by a
fasting glucose greater than 7 mmol/L, random glucose greater than 11.1 mmol/L or greater than
11.1 mmol/L 2 hours following a 75 g oral glucose tolerance test, and accompanying classical
symptoms such as thirst, weight loss, fatigue and polyuria.
Patients with type 2 DM are rarely symptomatic and the diagnosis is usually made during routine
screening. The threshold values are the same as for type 1 DM. A glycated haemoglobin (HbA1c)
level of greater than 48 mmol/mol is also considered strongly suggestive of DM.
Diagnosis of GDM can be more challenging because of the changes in carbohydrate metabolism
that occur normally during pregnancy, and the lack of international consensus on the diagnostic
criteria. Universal screening is not currently recommended and screening is currently targeted at
women who have risk factors for GDM (see Table 19.1). It is worth noting, however, that one or
more of these risk factors is found in 3050% of the pregnant population in the UK. Screening of
high-risk patients currently takes place at between 16 and 18 weeks gestation for those with previous
GDM, and 2428 weeks for those with other risk factors.
Table 19.1 Risk factors for GDM
Previous GDM
BMI > 30 kg/m2
Previous large baby (>4.5 kg or >95th centile on customized chart)
Parent, brother or sister with diabetes
Family origin (South Asian, Black Caribbean, Middle Eastern)
Screening criteria taken from NICE guidelines 2008
Management
The treatment of women with diabetes begins before pregnancy and includes optimization of
glycaemic control and cessation of medications contraindicated in pregnancy (e.g. angiotensin
converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), statins) with conversion
to alternative antihypertensive medication if required (calcium-channel blockers, -blockers). High-
dose folate (5 mg daily) is recommended preconceptually to reduce the risk of congenital
abnormalities, particularly neural tube defects. Early pregnancy assessment of women with pre-
existing diabetes should include an assessment of renal function (creatinine and urine
protein:creatinine ratio) and referral for retinopathy screening, which should be conducted each
trimester. Recent NICE guidelines also recommend low-dose aspirin (75 mg daily) from 12 weeks
gestation to reduce the risk of pre-eclampsia, which is more common in women with diabetes. Low-
molecular-weight heparin should be considered in women at increased risk of thrombosis (BMI
>40 kg/m2 and diabetic nephropathy with >3 g proteinuria).
For women with DM, rigorous glycaemic control and close monitoring during pregnancy is
associated with improved outcomes for both the woman and her baby. Preconception care and advice
should be offered to all women with pre-existing DM. Women with HbA1C >85 mmol/mol should be
advised to avoid pregnancy until glycaemic control is improved.
Women with type I diabetes are ideally managed in a joint antenatal diabetes clinic, combining
obstetric, diabetic and specialist midwifery care. If safely achievable, then fasting blood glucose
levels should be kept between 3.5 and 5.9 mmol/L and 1-hour postprandial blood glucose levels
below 7.8 mmol/L during pregnancy. Women should be warned of the significant risk of
hypoglycaemia, which may be complicated by reduced hypoglycaemia symptom awareness. Glucagon
kits should be made available and insulin therapy adjusted if hypoglycaemia is occurring frequently.
Increasingly women with type 1 diabetes are being offered continuous sub-cutaneous insulin infusion
(CSII) therapy. To date there is little evidence that use of pumps improves pregnancy outcomes, but it
may reduce the frequency of hypoglycaemic episodes. Insulin requirements increase in pregnancy, but
may decline in the last few weeks of pregnancy and during labour. Insulin doses should be reduced by
approximately 50% following delivery or adjusted to the prepregnancy regime.
Women with type 2 diabetes who have previously been treated with oral hypoglycaemic agents
(e.g. metformin, glibenclamide) are usually advised to continue these during their pregnancy, although
many women require additional insulin treatment to achieve the rigorous glycaemic control required
in pregnancy.
Women with GDM are often able to achieve adequate glycaemic control with dietary
adjustments, but 2030% will require treatment with either metformin or insulin.
Complications
Maternal complications
Acute
Diabetic ketoacidosis (DKA) occurs mainly in patients with Type I DM and is due to either failure to
administer sufficient insulin or to the development of a new source of insulin resistance (e.g.
infection, trauma, stress). Emesis, steroid and -blocker use are also important triggers during
pregnancy. The lack of insulin favours lipolysis, the -oxidation of free fatty acids and the formation
of acetoacetate. These biochemical events result in metabolic acidosis, hyperglycaemia and an
osmotic diuresis. Signs and symptoms of DKA include tachycardia, tachypnoea, hypotension, nausea
and vomiting.
The incidence of DKA in pregnancy is between 1% and 2% and occurs most commonly in the
second and third trimesters. As with the non-obstetric population, the management of DKA in
pregnant patients involves rehydration, control of glucose with an intravenous sliding scale insulin
regime and removal/treatment of any precipitating factors. All pregnant patients with DKA should be
cared for in a level 2 critical-care facility with input from both medical and obstetric teams.
The hyperosmolar hyperglycaemic state (HHS) occurs predominantly in patients with type 2 DM
and is characterized by very high blood glucose levels (frequently >40 mmol/L) without
accompanying ketosis. It is rare in pregnancy.
Hypoglycaemia poses a significant risk for pregnant women, occurring in up to two-thirds of
patients with pre-existing type 1 DM a rate up to 15 times higher than in the non-pregnant
population. It is most common before 20 weeks gestation. The intensification of treatment to achieve
tight glycaemic control and impairment of the counter-regulatory hormonal responses that accompany
insulin therapy are the main causes. Symptoms of hypoglycaemia are non-specific and include
abdominal pain, vomiting, weakness, dizziness and drowsiness. These may be absent or reduced in
pregnant women who are at an increased risk of hypoglycaemic unawareness. Hypoglycaemia is
much less common in women with type 2 DM or GDM.
Chronic
The prevalence of chronic complications generally correlates to the duration of DM and the adequacy
of glycaemic control. Atherosclerotic macrovascular complications include disease of the coronary,
cerebral and peripheral vasculature. Although rare, myocardial infarction is a potential risk and
suspected cardiovascular disease should be thoroughly investigated.
Microvascular complications include diabetic retinopathy and nephropathy. Pregnancy may
accelerate the rate of progression of both retinopathy and nephropathy.
Diabetic neuropathy can lead to autonomic cardiovascular dysfunction and gastroparesis. This
may be difficult to assess, but in the non-pregnant diabetic patient, prolongation of the QT interval on
the ECG correlates with the severity of autonomic dysfunction.
The diabetic stiff joint syndrome (also known as diabetic scleroderma) occurs in patients with
long-standing type I DM and is associated with short stature, joint contractures and tight skin.
Obstetric
Rates of gestational hypertension, pre-eclampsia, fetal macrosomia, preterm delivery, induction of
labour and caesarean section are all higher in diabetic obstetric patients. Recent studies have
suggested that the risk of pre-eclampsia and gestational hypertension can be reduced by optimal
glycaemic control during pregnancy.
Pre-existing DM, but not GDM, is associated with a 36% risk of preterm labour and delivery
approximately two to three times the non-diabetic rate. The incidence of early fetal loss, miscarriage
and still birth is also higher.
Fetal macrosomia (birth weight >4 kg) complicates up to 50% pregnancies in women with pre-
existing diabetes. There is a corresponding increase in the risk of birth trauma and shoulder dystocia.
The high rates of macrosomia, along with other obstetric complications such as pre-eclampsia, mean
that up to two-thirds of women with diabetes will be delivered by caesarean section. Shoulder
dystocia is also more common in women with both pre-existing and gestational diabetes. Warning
signs such as slow progress in labour, particularly in the second stage, should be heeded with early
recourse to operative delivery where significant fetal macrosomia is suspected.
Neonatal hypoglycaemia is more common, occurring in 5% and 12% of cases of pre-existing
DM and GDM, respectively. An increase in fetal insulin production in response to sustained
intrauterine fetal hyperglycaemia is thought to be the cause.
Anaesthetic management
Meticulous glycaemic control is the cornerstone of management of women with diabetes. Local
multidisciplinary protocols should be developed to cover the treatment of both pre-existing DM and
GDM in the intra- and postpartum periods. Ideally, an individualized management plan should be
drawn up in advance of delivery.
In labour or prior to caesarean delivery, an intravenous sliding scale insulin regime will be
necessary for the majority of women with pre-existing diabetes and for some women with gestational
diabetes. Tight glycaemic control in labour can reduce risk and severity of neonatal hypoglycaemia.
Insulin requirements may fall dramatically during labour and should be reduced by at least 50% after
delivery. Frequent blood glucose measurements (every 3060 minutes) should be performed to avoid
severe maternal hypoglycaemia or hyperglycaemia. Women who require fluid restriction because of
severe pre-eclampsia will require a modified regime to reduce infusion volumes.
The anaesthetist should be alert to the possibility of complications related to diabetes, and
history and examination should be directed accordingly. For women with long-standing diabetes with
known complications, antenatal anaesthetic review is desirable.
Autonomic cardiovascular dysfunction increases the possibility of hypotension during neuraxial
blockade. More frequent blood pressure measurement, judicious use of vasopressors and vigorous IV
hydration may be required. In severe cases, use of continuous intra-arterial blood pressure
measurement should be considered. Gastroparesis increases the risk of regurgitation and aspiration.
Antacid prophylaxis should be prescribed regularly during labour.
Women with type 1 diabetes and the diabetic stiff joint syndrome may suffer from limited
movement of the atlanto-occipital joint. Direct laryngoscopy and tracheal intubation may be more
difficult. This is in addition to the increased incidence of difficult intubation present in the non-
pregnant type 1 diabetic population. The prayer sign (an inability to approximate the palmar
surfaces of the phalangeal joints when the hands are bought together as if praying and despite
maximum effort) has been suggested as a screening test for difficult intubation. The stiff joint
syndrome is also associated with a reduction in compliance of the epidural space. Smaller volumes
of local anaesthetic may be required to avoid an unexpectedly high block.
With the above in mind, epidural or combined spinal-epidural (CSE) anaesthesia may be
preferred over single-shot spinal technique because of the slower onset of sympathetic blockade and
the greater degree of control that it affords.
Finally, diabetic patients are at an increased risk of infection. Strict aseptic technique must be
used during all procedures and surgical antibiotic prophylaxis as dictated by local guidelines given in
theatre.
Thyroid disease
Thyroid disease is common in women of childbearing age and hypo- and hyperthyroidism complicate
up to 4% of pregnancies. Its presence has implications for the mother and the developing fetus. An
understanding of the diagnosis, treatment, and the metabolic and anatomical changes that may
accompany thyroid disease are important to allow safe management in the puerperium.
Thyroid gland and pregnancy

During pregnancy there is an oestrogen-mediated increase in the plasma binding protein thyroxine-
binding globulin (TBG). This occurs up to around 20 weeks gestation, after which levels plateau.
TBG binds most circulating tri-iodothyronine (T3) and thyroxine (T4), and total levels of these show
a corresponding increase during pregnancy. It is the unbound (free) T4, however, that generally
determines thyroid activity in target tissues, and this remains unchanged, or falls slightly, during
pregnancy. Normal pregnancy is, therefore, a clinically euthyroid state.
T3 and T4 are synthesized in the follicular cells of the thyroid gland from dietary iodine. The
amount of iodine available falls in pregnancy due to a combination of fetal iodine uptake and
enhanced maternal renal clearance. Iodine deficiency may ensue in areas where intake is low and
lead to a reactive hyperplasia of the thyroid gland (goitre).
Hyperthyroidism
Hyperthyroidism is diagnosed by finding a raised serum concentration of free T4. Causes are shown
in Table 19.2. Measurement of thyroid stimulating hormone (TSH), TSH receptor antibodies (TSH-
RAb), ultrasound examination and fine needle aspiration may be needed to help differentiate the exact
pathophysiology.
Table 19.2 Causes of hyperthyroidism
Overstimulation:
Graves disease
TSH secreting pituitary tumour
Gestational trophoblastic neoplasia
Intrinsic thyroid over-activity:
Toxic adenoma
Toxic multinodular goitre
Inflammation:
Sub-acute thyroiditis
Other:
Ectopic thyroid tissue
Thyroxine ingestion
Symptoms are related to the increase in basal metabolic rate and include a hyperdynamic
circulation, tachyarrhythmias, nervousness, sweating, tremor, weakness, diarrhoea and changes in
appetite.
In pregnancy, direct stimulation of the thyroid gland by human chorionic gonadotrophin (hCG)
can result in transient gestational thyrotoxicosis. In the absence of symptoms, mild biochemical
hyperthyroidism should be monitored with repeat thyroid function tests (TFTs) and referral to an
endocrinologist made only if the derangement persists beyond 46 weeks.
Graves disease accounts for 70% to 90% of cases of overt hyperthyroidism in pregnancy,
followed by toxic multinodular goitre and toxic adenoma. Graves disease is an autoimmune disorder
with a multifactorial aetiology. Autoantibodies are directed against the TSH receptor and usually
augment (although may inhibit) its action. Some patients may also develop Graves eye disease with
exopthalmus, proptosis and irritation. Graves disease has an association with other autoimmune
conditions.
Thyroid nodules are common amongst the general population and may increase in size and
number during pregnancy.
Treatment of hyperthyroidism may be medical, surgical or a combination, and aims to keep free
T4 normal or in the upper range of normal throughout pregnancy. The drug of choice for most women
in pregnancy is propythiouracil, although carbimazole can also be used. Propythiouracil interferes
with synthesis of T3 and T4 in the thyroid gland and inhibits peripheral conversion of T3 to the more
active T4. Both can cross the placenta and potentially impair fetal thyroid function and cause fetal
goitre, so the lowest effective dose should be used. The dose may be reduced after the first trimester
and often discontinued in the third trimester.
Surgery, in the form of total or sub-total thyroidectomy, is usually reserved for patients who
have failed medical therapy. It is generally considered safe from the second trimester onwards.
Radioiodine therapy is contraindicated in pregnancy.
Uncontrolled hyperthyroidism is associated with a number of maternal and fetal complications.
Pre-eclampsia, preterm labour, miscarriage and placental abruption are all more common. TSH-
RAbs are able to cross the placenta and may lead to fetal tachycardia, growth retardation, low birth
and congenital malformations. Very high titres of TSH-RAbs are associated with an increased risk of
fetal intrauterine or neonatal thyrotoxicosis.
Severe cases of untreated or under-treated hyperthyroidism may result in a thyroid storm. This is
a life-threatening exacerbation of hyperthyroidism, which can lead to hyperpyrexia, cardiac failure,
coma and death.
The management of patients with hyperthyroidism involves giving careful consideration to both the
metabolic effects of the disease and the possibility of partial airway obstruction secondary to an
enlarged thyroid gland.
Surgery in the presence of uncontrolled hyperthyroidism carries a risk of precipitating a thyroid
storm and a high mortality. If time allows, the goal should be to render the patient euthyroid. In the
emergency situation, treatment involves supportive measures (cooling, oxygen, fluid and electrolyte
replacement), reduction of synthesis and peripheral conversion of thyroid hormones (propothiouracil,
glucocorticoids, sodium iodide) and amelioration of the metabolic effects (-blockers). Drugs
associated with tachycardia should be avoided.
Both general and neuraxial anaesthesia have been used safely. The decision must be made on an
individual patient basis, taking into account such factors as the presence and severity of any airway
compromise, cardiac involvement and electrolyte disturbance.
Patients with hyperthyroidism have a relative deficiency of glucocorticoids and should be given
supplementation. Care should be taken to protect the eyes and prevent corneal abrasions during
general anaesthesia in those with Graves eye disease and exophthalmus.
Hypothyroidism
Hypothyroidism is diagnosed by finding a low level of free T4. The causes can be split into primary
and secondary and are shown in Table 19.3. Hashimotos disease (autoimmune thyroiditis) is the
most common cause in women of childbearing age.
Table 19.3 Causes of hypothyroidism
Primary
Autoimmune:
Hashimotos thyroiditis
Atrophic thyroiditis
Iatrogenic:
Thyroid surgery
Radio-iodine therapy
Drug-induced:
Antithyroid drugs (propothiouracil, methimazole)
Amiodarone
Lithium
Congenital:
Dyshormonogenesis
Thyroid dysgenesis or agenesis
Other:
Iodine deficiency
Secondary
Pituitary dysfunction:
Radiotherapy
Surgery
Neoplasm
Sheehans syndrome
Hypothalamic dysfunction:
Radiotherapy
Neoplasm
Granulomatous disease
Symptoms can be vague and include fatigue, weight gain, muscle cramps, constipation and
memory problems. Women with hypothyroidism also have lower fertility rates. Sub-clinical
hypothyroidism is relatively common in the pregnant population and may be picked up by antenatal
screening programmes.
During pregnancy, untreated hypothyroidism is associated with an increased risk of anaemia,
pre-eclampsia, abruption, miscarriage, low birth weight and postpartum haemorrhage. The growing
fetus is dependent on maternal thyroxine, particularly during the first half of the pregnancy, and
hypothyroidism at this stage can adversely affect neuropsychological development. Outcomes for both
mother and fetus are improved with treatment.
Medical management is with oral thyroxine replacement until the patient is clinically and
biochemically euthyroid. Requirements may change during pregnancy and regular TSH measurements
are needed to allow appropriate dose titration.
As with hyperthyroidism, the patient should ideally be clinically and biochemically euthyroid before
any anaesthetic intervention. History, examination and investigations should focus on identifying the
potentially more serious consequences of prolonged or untreated hypothyroidism. These can include
myocardial dysfunction, coronary artery disease and obstructive sleep apnoea. In the emergency
situation, glucocorticoid supplementation should be given to the untreated patient as, like those with
hyperthyroidism, there is a decrease in glucocorticoid reserves and hyponatraemia. Intravenous
thyroxine is rarely indicated and its use carries a risk of precipitating myocardial ischaemia.
Hypothyroidism is a rare cause of acquired von Willebrands disease and untreated
hypothyroidism can result in abnormal platelet function, despite normal platelet levels. Laboratory
and/or near-patient testing of coagulation should therefore be performed before administering
neuraxial anaesthesia. Patients may show a blunted response to phenylephrine.
Any patient with a goitre requires careful assessment of the airway and neck to check for
retrosternal spread or evidence of tracheal deviation. A chest radiograph may be helpful. The history
should include the duration of swelling (long-standing goitre is associated with tracheomalacia) and
symptoms such as stridor or breathlessness, which may indicate dynamic tracheal compression.
Patients who have had previous thyroid surgery, or who have malignant disease may suffer from
vocal cord palsy.
Adrenal disease
Adrenal disorders (including congenital adrenal hyperplasia, Addisons disaease,
pheochromocytoma and Cushings disease) frequently have a negative impact on fertility and so are
relatively uncommon in pregnancy. Undiagnosed and untreated disease can have serious
consequences for maternal and fetal health with maternal mortality rates historically approaching
50% for untreated Addisons disease or pheochromocytoma.
Proper diagnosis and treatment of adrenal dysfunction with steroid therapy or surgery can
dramatically improve outcomes and lead to successful pregnancy and delivery. As always, patients
are best managed in joint obstetric endocrine clinics by those with experience in their management.
Addisons disease
Addisons disease, or primary adrenal insufficiency, is most commonly caused by autoimmune
adrenalitis, but can also be the result of infection, haemorrhage, metastases or genetic causes. New
onset disease in pregnancy is rare. Symptoms are vague and include weight loss, weakness, fatigue,
nausea, diarrhoea and postural hypotension. These can easily be mistaken for symptoms of pregnancy
itself or associated conditions such as hyperemesis gravidum.
Patients with known disease are initially maintained on their preconception doses of gluco- and
mineralocorticoids with regular electrolyte monitoring throughout the antenatal period. In normal
pregnancy, cortisol levels rise due to increased levels of corticosteroid-binding globulin and
decreased clearance. Doses of glucocorticoids may therefore need to be increased in the third
trimester for some patients. Intravenous steroids and hydration should be considered in any patient
suffering from nausea and vomiting. Mineralocorticoids should be stopped if the patient develops
pre-eclampsia.
Severe adrenal insufficiency is known as an Addisonian crisis and is a potentially life-
threatening medical emergency. It may be the result of previously undiagnosed Addisons or due to an
intercurrent stress (e.g. infection, trauma, labour) in someone with known disease. Signs include
hypotension, hyponatraemia, hypoglycaemia, hyperkalaemia, hypercalaemia, psychosis and
convulsions. Treatment is with IV steroids, IV hydration with saline and dextrose and correction of
the underlying cause (if any). Hyperkalaemia should be treated with dextrose and insulin.
Patients with well-controlled Addisons should receive an increased dose of parenteral steroids
for labour or caesarean delivery (e.g. 100 mg hydrocortisone IV QDS) and IV saline. After delivery,
doses can be tapered back to maintenance over 3 days.
Congenital adrenal hyperplasia
Congenital adrenal hyperplasia (CAH) refers to a heterogenous group of autosomal recessive
disorders that affect the enzymes controlling the synthesis of cortisol from cholesterol. The majority
(90%) of cases are due to 21-hydroxlase deficiency with 11--hydroxylase deficiency accounting for
a further 58%. Clinical features can include precocious puberty, virulization and ambiguous
genitalia in some females.
The treatment of choice for pregnant women with CAH is steroid replacement with
glucocorticoids, which can be inactivated by the placenta (hydrocortisone, prednisone,
methylprednisolone) to minimize the risk of fetal adrenal suppression. If the fetus is at risk from
CAH, then dexamethasone, which easily crosses the placenta, may be used to prevent masculinization
of the genitalia of female infants. Mineralocorticoids (fludrocortisone) can be added in those patients
with the salt-wasting form of the disease.
High-dose glucocorticoid therapy (e.g. hydrocortisone 50100 mg IV QDS) should be initiated
at the start of active labour, continued until after delivery and then tapered back down to the patients
normal maintenance dose. Elective caesarean delivery should be considered for patients who have
undergone previous reconstructive genital surgery. Electrolytes should be measured prior to
anaesthesia and disturbances corrected. Good hydration should be maintained, if necessary with 0.9%
saline IV.
Pheochromocytoma
Pheochromocytomas are rare catecholamine-secreting neuroendocrine tumours of chromaffin cells;
90% occur within the adrenal medulla, the other 10% arising from extra-adrenal chromaffin tissue. It
is thought to complicate only around 1 in 50,000 pregnancies.
The classical presentation is with paroxysms of headache, sweating, palpitations and anxiety
associated with severe hypertension. Patients may have postural hypotension and dizziness on
standing due to a contracted intravascular volume. Hypertension is common in pregnancy and so it is
possible for the diagnosis to be overlooked.
Raised levels of catecholamines in a 24-hour urine sample confirm the condition with a high
level of sensitivity and specificity. Catecholamine levels do not change in pregnancy and so the
biochemical diagnosis is no different from a women who is not pregnant. Once confirmed, the tumour
is localized using MRI or ultrasound examination if pregnant, to avoid ionizing radiation.
Surgical removal is the definitive treatment for pheochromocytoma and should ideally take place
prior to 24 weeks gestation. After this time the gravid uterus may make surgical exploration of the
abdomen and tumour removal difficult. The choice may then be to defer surgery until the fetus is
mature and consider adrenalectomy immediately after caesarean delivery.
Whatever the timing of surgery, preoperative management aims to control blood pressure,
correct volume depletion and prevent intraoperative hypertensive crises. This is usually achieved
using -adrenergic blockade (e.g. with phenoxybenzamine or doxazocin, both of which are safe in
pregnancy) for 1014 days prior to surgery to allow time for volume expansion. -Blockade should
not be used without adequate -blockade to avoid the risk of unopposed -adrenergic activity leading
to a hypertensive crisis. Expert help should be sought in the obstetric, surgical and anaesthetic
management of the pregnant patient diagnosed with pheochromocytoma.
The condition still carries a significant risk to mother and fetus. Maternal mortality is around 2%
if the condition is diagnosed antenatally, but rises to between 4% and 17% if diagnosed during
pregnancy, with a fetal mortality of up to 26%. Unrecognized pheochromocytoma carries a
significantly higher mortality and the diagnosis may not be made until post mortem.
Cushings syndrome
Cushings syndrome occurs very rarely in pregnancy because of the impact on fertility caused by
hypercortisolism. The spectrum of disease changes, with adrenal adenomas more commonly the cause
rather than the pituitary-dependent disease that predominates in the general population. Diagnosis is
made difficult because of the previously mentioned changes in cortisol levels during pregnancy. The
low dose dexamethasone suppression test is also inaccurate in the presence of high levels of
oestrogens.
GDM occurs in up to a third of patients with Cushings disease and rates of pregnancy-induced
hypertension are increased. Severe hypertension and congestive cardiac failure may occur in up to
10% of patients. Premature delivery occurs in two-thirds of cases, with a neonatal mortality rate of
around 15%.
Both adrenalectomy (usually early in the second trimester) and trans-sphenoidal
hypophysectomy have been successfully reported in pregnant patients. Steroid replacement should be
started immediately after surgery and the mother and neonate monitored for signs of cortisol
withdrawal.
Anaesthetic management may be complicated by obesity, poor venous access, an increased risk
of difficult intubation and of impaired respiratory muscle function in the postoperative period due to
proximal myopathy.
Vaginal delivery is preferable to caesarean delivery because of the increased incidence of poor
wound healing and wound breakdown in patients with Cushings.
Key points
1. Diabetes is associated with higher rates of gestational hypertension, pre-eclampsia,
polyhydramnios, shoulder dystocia, caesarean section and increased risk of fetal anomalies.
2. Insulin resistance increases progressively through the second and third trimester, largely due
to an increase in hormones like human placental lactogen, cortisol and progesterone.
3. Gestational diabetes is defined by glucose intolerance, which is first identified during

pregnancy.
4. In pregnancy, direct stimulation of the thyroid gland by human chorionic gonadotrophin can
result in transient thyrotoxicosis.
5 Thyroid surgery during pregnancy is usually reserved for patients who have had failed medical
therapy.
6. Undiagnosed and untreated adrenal disease can have serious consequences for maternal and
fetal health. Correct and early diagnosis, appropriate treatment of adrenal dysfunction, steroid
therapy or surgery can significantly improve outcomes.
Further reading
Wissner, R. N. (2014). Endocrine disorders. In D. H. Chestnut (ed.), Obstetric Anaesthesia,

Principles and Practice, 5th edn. Elsevier, 10031032.
National Institute for Health and Clinical Excellence (2008). Diabetes in Pregnancy: Management of
Diabetes and its Complications from Pre-conception to the Postnatal Period. CG63. London: NICE.
Centre for Maternal and Child Enquires (2010). The CEMACH/OAA Diabetes Project: A national
audit of anaesthetic records and care for women with type 1 or type 2 diabetes undergoing caesarean
section. London: CMACE.
Royal College of Obstetricians and Gynaecologists (2011). Diagnosis and Treatment of Gestational
Diabetes. Scientific Impact Paper No. 23. London: RCOG.
Chapter 20
Renal disease

Jessica Longbottom and W. Ross Macnab
Introduction
Chronic renal insufficiency occurs in 0.030.2% of all pregnancies. Although rare, these parturients
have a significantly increased maternal and fetal morbidity and mortality and can present a significant
challenge to the anaesthetist. The management of this high-risk group of patients is often complicated
and is supported by little evidence. It requires an understanding of the physiological changes of
pregnancy, the optimization of existing management, close monitoring of both mother and fetus, and
early involvement of obstetricians, nephrologists, neonatologists and anaesthetists, with early
intervention as required.
Renal insufficiency in pregnancy may be classified into three categories. These include known
pre-existing renal disease diagnosed prior to the pregnancy, sub-clinical chronic renal disease
unveiled by the pregnancy or new-onset disease that develops during the pregnancy. Although general
principles can be applied to the management of these patients, the causes, associated co-morbidities
and prognosis of these patients may differ greatly.
It is important to consider both the impact of renal insufficiency upon maternal and fetal
outcome, and the impact of a pregnancy upon the short- and long-term course of chronic kidney
disease. These patients have an increased risk of pregnancy-induced hypertension, pre-eclampsia,
preterm delivery, intrauterine growth restriction and perinatal mortality. The demands of pregnancy
may result in a transient, and sometimes a permanent decline in renal function.
The assessment of renal function in pregnancy
Pregnancy itself results in anatomical and physiological changes in the renal system (See Chapter 1).
Changes in water metabolism, extracellular fluid volume regulation, acidbase regulation and the
renal handling of electrolytes, protein and glucose result in altered normal ranges of typical
laboratory values. These values continue to change from the first to the second and third trimesters.
This complicates the diagnosis, assessment and surveillance of renal insufficiency. The gold standard
for measuring and therefore monitoring renal function remains inulin clearance, but it is difficult to
perform. Creatinine clearance measured with a 24-hour urine collection is the most well-validated
method for approximating glomerular filtration rate (GFR). Formulaic estimations of GFR lack
validity in pregnancy.
GFR and creatinine clearance typically increase by 4065% and serum creatinine concentrations
fall. It has been suggested that the upper limit of serum creatinine concentration should approximate
85, 80 and 90 mol/L in the first, second and third trimesters, respectively. A blood urea nitrogen
concentration of >13 mg/dL may also indicate renal insufficiency in pregnancy.
The associated increase in urinary protein excretion also results in an altered definition of
proteinuria during pregnancy of greater than 300 mg/day (correlating to 1+ on urine dipstick)
compared to a non-pregnant value of 150 mg/day.
For these reasons the usual prepregnancy NICE classification of the stages of chronic kidney
disease (Table 20.1) is difficult to apply during pregnancy, yet it remains a useful tool when
considering a patients prepregnancy values. Traditionally parturients have been stratified into mild
impairment serum creatinine <125 mol/L, moderate 125250 mol/L and severe >250 mol/L.
Table 20.1 Stages of chronic kidney disease
Stage a GFR (mL/min/1.73 m2) Description
1 <i</i>>90</i</i>> Normal or increased GFR with

other evidence of kidney damage
2 6089 Slight decrease in GFR with other

evidence of kidney damage
3a 4559 Moderate decrease in GFR with

3b 3044 or without other evidence of
kidney damage
4 1529 Severe decrease in GFR with or
without other evidence of kidney
damage
5 <15 Established renal failure
a Use suffix (p) to denote presence of proteinuria (protein creatinine ratio 50 mg/mmol)
Chronic kidney disease in pregnancy

There are many causes of CKD in women of childbearing age, all of which will be seen in pregnancy.
The most common include diabetic nephropathy, hypertensive nephropathy, chronic
glomerulonephritis, systemic lupus nephritis, polycystic kidney disease and chronic pyelonephritis
among many rarer causes. The underlying pathology and its associated systemic co-morbidities, as
well as the systemic manifestations of chronic renal impairment itself provide significant challenges
to the anaesthetist. The risk of adverse outcome to either mother or fetus does not appear to be related
to the specific underlying disorder, but to the degree of renal impairment and the presence or absence
of hypertension.
The effect of pregnancy on kidney disease

Pregnancy can exacerbate pre-existing renal disease and, in some cases, can cause irreversible
deterioration in renal function. Adverse outcomes tend to relate to the degree of maternal renal
function and blood pressure control. The pathogenesis is not clearly evident, but altered immune
function, increased inflammation, endothelial dysfunction and platelet aggregation resulting in
microvascular thrombi have all been implicated.
Proteinuria and associated peripheral oedema worsens in approximately 50% of cases and
hypertension may develop or worsen in 25% of cases. These features frequently resolve post partum.
Evidence suggests that patients with a normal or only mildly reduced GFR and a serum
creatinine concentration less than 132 mol/L have a less than 10% risk of a permanent decline in
renal function as a consequence of pregnancy. The presence of hypertension in this group of patients
gives a poorer prognosis. Patients with moderate renal insufficiency, a serum creatinine concentration
between 132 and 255 mol/L, are likely to experience an initial fall in serum creatinine concentration
as GFR increases, but this will continue to rise up to and beyond the baseline by the third trimester.
These patients have approximately a 50% risk of a permanent reduction in GFR and a 10% risk of
developing end-stage renal disease within 12 months of delivery. This figure may increase to 50% if
there is associated uncontrolled hypertension. In severe renal failure the likelihood of conception and
carrying a fetus to term is very low. Up to 40% of these patients will require dialysis. It is important
to note that pregnancy may result in immune sensitization and potential difficulties for future donor
matching should renal transplant be indicated. CKD also increases the risk of urinary tract infection,
which in turn may cause a rapid deterioration in renal function. Co-existing pre-eclampsia is also
associated with subsequent progression to end-stage renal disease.
The prevention of deterioration of renal function in these patients relies upon close surveillance
by a multidisciplinary team, monthly serial monitoring of maternal renal function, early detection and
treatment of asymptomatic bacteruria and aggressive treatment of maternal hypertension. Although the
management of hypertension is important, many antihypertensives are contraindicated in pregnancy.
Labetalol, -methyldopa and nifedipine are considered safe. Preterm delivery may be necessary to
preserve long-term kidney function.
The effect of kidney disease on pregnancy outcomes

A large systematic review demonstrated a fivefold higher incidence of maternal morbidity and
twofold higher incidence of fetal morbidity in the presence of maternal CKD.
Patients with CKD are more likely to develop gestational hypertension, pre-eclampsia and
eclampsia. Preterm deliveries are around twice as common and there is a recognized association with
intrauterine growth restriction and still birth. Again the risks of maternal and fetal complications seem
to be directly proportional to the degree of renal impairment and are further increased by the presence
of uncontrolled hypertension. Patients with mildly reduced GFR and well-controlled blood pressure
have very favourable outcomes. However, there may be as high as a 2030% and 40% increased risk
of pre-eclampsia in patients with moderate and severe renal insufficiency, respectively. In this
situation, the diagnosis of pre-eclampsia is often difficult. The presence of hypertension at the time of
conception increases the risk of fetal loss by up to tenfold. Significant proteinuria is also associated
with an increased risk of preterm delivery.
These patients may require weekly antenatal reviews, with close monitoring of blood pressure
to allow the early diagnosis and treatment of co-existing pre-eclampsia, in addition to aggressive
management of pre-existing hypertension. Fetal growth and wellbeing should be monitored.
The systemic manifestations of chronic kidney disease
Chronic kidney disease is a multisystem disorder with far-reaching systemic manifestations. These
may occur irrespective of the underlying pathology and have implications in the antenatal, intrapartum
and perioperative anaesthetic management of these patients (Table 20.2).
Table 20.2 The systemic manifestations of CKD
Cardiovascular system Hypertension, ischaemic heart disease,

peripheral vascular disease, aortic calcification,
calcific valvular heart lesions, uraemic
pericarditis, cardiomyopathy
Respiratory system Potential difficult airway, pulmonary oedema,

atelectasis and infection
Haematological system Normochromic normocytic anaemia, platelet

dysfunction
Low/normal platelet count
Immune system Immunosuppression, risk of hepatitis B and C
Gastrointestinal system Delayed gastric emptying, reduced gastric pH,

malnutrition
Neurological system Myoclonus, encephalopathy, convulsions,

autonomic neuropathy, peripheral neuropathies
Endocrine system Impaired glucose tolerance, tendency towards

hypothermia, reduced fertility
Fluid and electrolytes Hyperkalaemia, hyponatraemia, hypocalcaemia,

renal osteodystrophy, hypermagnesaemia
Acidbase regulation Chronic metabolic acidosis, poor buffering

capability
Pharmacokinetic changes Reduced protein binding

Accumulation of renally excreted drugs
Common underlying chronic renal disorders
Diabetic nephropathy
Diabetes, gestational or otherwise, is one of the most common diseases occurring in pregnancy.
Diabetic nephropathy most frequently occurs in those in whom type 1 diabetes has been present for
over 10 years and is characterized by proteinuria, hypertension and a reduced GFR. Patients with
good glycaemic control, microalbuminuria, well-preserved renal function and well-controlled blood
pressure are likely to have a successful outcome. However, patients with overt nephropathy
preconception are at increased risk of pre-eclampsia, fetal growth restriction, preterm delivery and
irreversible deterioration in renal function.
The principles of management include preconception assessment of nephropathy, patient
counselling and optimization of glycaemic control. Hypertension should be controlled with labetalol,
-methyldopa or calcium-channel blockers such as nifedipine. Close monitoring should continue
throughout pregnancy. Good intrapartum glycaemic control and fluid balance are important.
Systemic lupus nephritis

Systemic lupus erythematosus (SLE) is a common autoimmune disorder in women of childbearing
age. The associated nephritis presents unique challenges in pregnancy.
Lupus nephritis may have spontaneous exacerbations during pregnancy, which are associated
with a 75% chance of fetal loss. The presence of active disease at the time or within six months of
conception and the duration of disease significantly increase the risk of an exacerbation during
pregnancy. It remains unclear whether pregnancy itself is a risk factor for lupus flares.
A lupus flare is characterized by deteriorating renal function, hypertension, worsening
proteinuria and thrombocytopenia, making it difficult to distinguish from pre-eclampsia, a condition
which may also co-exist. Presentation prior to 20 weeks gestation or the presence of
hypocomplementaemia, urinary red blood cell casts, a typical rash, arthritis or serositis make lupus
nephritis more likely. The mainstay of the management is general supportive care and
immunosuppression with steroids and azathioprine, which may exacerbate pre-eclampsia. When
stabilization is not achieved, delivery may be indicated.
SLE is associated with the presence of antiphospholipid antibodies, which increase the risk of
both lupus flares and thrombotic events such as deep vein thrombosis, pulmonary embolism,
myocardial infarction and stroke. Patients should undergo preconception antibody screening. When
antibodies are present patients should receive aspirin prophylaxis with additional heparin if there is a
history of thrombotic events.
Chronic glomerulonephritis
None of the histological sub-types of glomerulonephritis appear to be associated with a particularly
good or poor prognosis. The severity of renal impairment and presence of hypertension are useful
prognostic factors.
Polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is often asymptomatic, with renal function
preserved until well after childbearing age. However, there is an increased risk of urinary tract
infection, hypertension, oedema and pre-eclampsia. Associated liver cysts may enlarge during
pregnancy, but liver function is usually preserved. Due to the association of ADPKD with cerebral
aneurysms antenatal screening should be considered.
Chronic pyelonephritis
Chronic pyelonephritis often worsens during pregnancy. Urinary tract abnormalities such as
vesicoureteric reflux are a common feature. Prophylactic antibiotics, high fluid intake and regular
screening for bacteruria minimize deterioration.
New diagnosis of chronic kidney disease in pregnancy

The increased monitoring of the pregnant patient combined with the anatomical and physiological
changes that occur in pregnancy may lead sub-clinical renal impairment to become clinically
detectable for the first time. Superimposed obstetric disorders such as pre-eclampsia may unveil
underlying renal disease.
Renal diseases most commonly diagnosed in this way include immunoglobulin A nephropathy,
focal and segmental glomerulosclerosis, polycystic kidney disease and reflux nephropathy.
Investigations that may aid diagnosis include ultrasonography and renal biopsy. Renal biopsy is often
deferred to the postnatal period due to the increased risk of complications secondary to increased
renal blood flow and difficult patient positioning. However, a sudden unexplained deterioration in
function or marked nephrotic syndrome prior to 32 weeks gestation may warrant a biopsy. Once the
diagnosis has been made, close monitoring by the multidisciplinary team, including regular
assessment of blood indices, proteinuria and protein:creatinine ratio is essential.
Acute kidney injury in pregnancy

Acute kidney injury requiring dialysis occurs in 1 in 20,000 pregnancies in Europe and North
America. In the developing world, 20% of AKI cases are pregnancy related and there is an incidence
of AKI of up to 1 in 50 pregnancies. AKI is a significant cause of maternal mortality, with little
overall change of the mortality figures in the developed world quoted between 0 and 30% and a
figure of up to 50% in the developing world. It is suggested by an acute deterioration in renal
function, reduced GFR, rise in serum creatinine, symptoms of uraemia, hyperkalaemia, hyponatraemia
and metabolic acidosis often, but not always, associated with oliguria. In the general population the
RIFLE criteria have been used to define three stages of severity of acute renal dysfunction and two
potential outcomes (Table 20.3).
Table 20.3 RIFLE criteria for AKI
Grade GFR criteria Urine output
Risk Creatinine 1.5; GFR reduced UO <0.5 mL/kg/h for 6 h

>25%
Injury Creatinine 2; GFR reduced UO <0.5 mL/kg/h for 12 h

>50%
Failure Creatinine 3; GFR reduced UO <0.3 mL/kg/h for 24 h or

>75% anuria for 12 h
Loss Loss of function >4 weeks
End stage Loss of function >3 months
Any cause of AKI that occurs in the non-pregnant population may also cause AKI in the pregnant
population. There are, however, specific pregnancy-related conditions, occurring in both early and
late pregnancy, which may result in AKI. AKI in early pregnancy is most commonly due to
hyperemesis gravidarum or septic abortion. Most cases of AKI occur after 35 weeks gestation and
may be caused by severe pre-eclampsia or HELLP syndrome, major obstetric haemorrhage, acute
fatty liver of pregnancy, urinary tract obstruction, acute pyelonephritis or exposure to nephrotoxins.
The principles of management are to identify and correct any reversible cause, careful fluid
management and the early use of renal replacement therapy although this may necessitate delivery.
Outcome of AKI will depend on cause and supportive treatments provided. When causes are
reversible function often recovers in 34 weeks. However, if bilateral cortical necrosis has occurred,
recovery will be limited. Full renal recovery is reported in up to 6090% of obstetric cases.
Thrombotic microangiopathy
Although rare, thrombotic microangiopathies (TMA), such as thombotic thrombocytopaenic purpura
(TTP) and haemolytic uraemic syndrome (HUS), are associated with significant morbidity and are
difficult to distinguish from severe pre-eclampsia, HELLP syndrome and acute fatty liver of
pregnancy. TMA is defined by the occurrence of thrombi of fibrin and/or platelets in the
microvasculature of various organs, mainly the kidney and brain. Other pathological features can
affect endothelial cells and basement membranes. In more recent times there has been a better
understanding of different mechanisms of causation and the chance for improved management
strategies.
TTP and HUS are characterized by unexplained thrombocytopaenia, microangiopathic anaemia
and renal failure. Associated hypertension, proteinuria, elevated liver enzymes or disseminated
intravascular coagulation (DIC) indicate a probable alternative diagnosis. The dominance of either
neurological features or renal failure suggests a diagnosis of TTP and HUS, respectively. The timing
of onset is also an important distinguishing factor, with TTP occurring in the second and third
trimester, HUS usually occurring post partum and severe pre-eclampsia and HELLP occurring after
20 weeks gestation. Renal failure associated with severe pre-eclampsia will most likely resolve
spontaneously, unlike in TTP-HUS where renal replacement therapy and resultant end-stage renal
disease are common. The mainstay of treatment is plasma exchange.
Acute tubular necrosis

Can occur due to hypotension, prolonged volume depletion and vasoconstriction and can be
secondary to other pathologies: PET, HELLP syndrome, sepsis. Exposure to nephrotoxins or
ischaemic injury secondary to prerenal failure may result in acute tubular necrosis. In severe obstetric
haemorrhage, acute cortical necrosis with DIC may occur, which can require renal replacement
therapy.
Acute fatty liver of pregnancy

This rare cause of acute kidney injury occurs in late pregnancy and is associated with rapidly
progressive liver failure, elevated liver enzymes, elevated bilirubin, hypofibrinogenaemia, anaemia,
thrombocytopaenia and deranged coagulation, and up to 40% of patients can develop AKI. Delivery
is often indicated and renal function usually recovers.
Urinary tract obstruction

It is important to exclude any potential postrenal cause of AKI. Relaxation of smooth muscle and
ureteric obstruction by the gravid uterus frequently results in a functional hydronephrosis, particularly
affecting the right side, but rarely results in renal failure. The presence of large uterine fibroids or
renal calculi may result in obstructive renal impairment. Most calculi will pass spontaneously, but
cystoscopy and stent insertion may be required.
The dialysis patient

Dialysis patients have a reduced fertility. Over 85% of women deliver before 36 weeks gestation
and the frequency of live births is reduced to only 3060%. Associated pre-eclampsia is the greatest
risk factor for an adverse perinatal outcome. Other poor prognostic factors include maternal age >35
years and more than 5 years on dialysis.
The management of these patients requires a multidisciplinary approach with close maternal and
fetal surveillance. The intensification of peritoneal dialysis (PD) and haemodialysis (HD) must be
significantly increased during pregnancy to maintain a predialysis serum urea concentration below
20 mmol/L and avoid metabolic acidosis. Both PD and HD have comparable perinatal outcomes;
however, there are complications associated with both (Table 20.4).
Table 20.4 Dialysis in pregnancy
Method of delivery Potential complications
Haemodialysis 57 sessions per week, total Risk of cardiovascular

20 h per week instability and reduced
Slow ultrafiltration rate to uteroplacental perfusion
avoid hypotension Continuous fetal heart rate
Minimal heparinization monitoring required
Difficult to establish target
weight
Peritoneal dialysis Increased frequency with Abdominal fullness and

reduced exchange volumes discomfort
Catheter problems
Polyhydramnios and placental
abruption
Careful attention must be paid to nutrition, particularly increasing daily protein intake (1.2 g per
kg body weight), calcium and vitamin D supplementation. Concurrent anaemia requires iron and folic
acid supplementation and erythropoietin. Hypertension should be aggressively managed.
Antihypertensives contraindicated in pregnancy must be stopped (e.g. ACE inhibitors, angiotensin
receptor blockers) and replaced with labetalol, metoprolol, nifedipine or methyldopa.
Specific anaesthetic considerations when caring for the dialysis parturient are similar to that in
the general population. Arteriovenous fistulas must be protected with appropriate positioning and
padding, and avoidance of intravenous access and blood pressure monitoring on that arm. Peripartum
blood loss on a background of anaemia should be anticipated and cross-matched blood products and
cell salvage be available as necessary. The increased frequency of dialysis in pregnancy usually
means the patient has undergone dialysis within the previous 2448 hours. Patients on haemodialysis
may have residual heparin that prohibits a neuraxial technique. Thromboelastography in combination
with routine tests of coagulation may be reassuring and support a neuraxial technique. It is important
to assess the intravascular volume of these patients prior to any anaesthetic intervention as this may
significantly fluctuate between dialysis. Patient weight compared to dry weight, heart rate, the
presence of postural hypotension and urine output (if not usually anuric) are useful indicators of
hypovolaemia. Hypovolaemia in the presence of autonomic neuropathy may result in profound
hypotension and poor uteroplacental perfusion, with the onset of sympathetic blockade. Euvolaemia
and a slow induction of CSE anaesthesia will minimize hypotension. Vasopressors should be used to
manage hypotension in the euvolaemic individual to avoid fluid overload. The altered
pharmacokinetics of the dialysis patient dictates the prudent use of highly protein bound or renally
excreted drugs. Patients on magnesium must have their loading dose and infusion rate modified and
levels monitored.
The renal transplant recipient

Compared to the dialysis patient, renal transplant recipients have a greater frequency of a successful
perinatal outcome, with live births occurring in up to 80% of occasions. However, hypertension
occurs in 50% and pre-eclampsia in 30% of these patients. Intrauterine growth restriction and low
birth weight is common and 50% of deliveries occur prior to 36 weeks gestation.
The effect of pregnancy on the renal allograft varies. If renal function is stable, pregnancy does
not have long-term adverse effects on allograft function. Severe proteinuria or a serum creatinine
concentration greater than 130 mol/L significantly increases the risk of graft loss. The incidence of
rejection is not increased, although it is advised to avoid pregnancy for 12 years post
transplantation. The diagnosis of rejection may require renal biopsy.
Care should be provided by a multidisciplinary team of nephrologists and obstetricians familiar
with these patients. Careful and regular monitoring of mother and fetus is necessary. Vaginal delivery
should be possible in most patients with a renal allograft. However, the precise location should be
assessed by ultrasound. It is particularly important to know the allografts exact location and involve
the transplant surgery team should the patient require caesarean section.
Immunosuppressants and corticosteroids have potential maternal and fetal side effects and may
interact with anaesthetic drugs and techniques. The adverse effects of chronic steroid use should be
evaluated particularly with respect to cardiovascular disease and altered glucose metabolism.
Although immunosuppressants are never entirely risk-free in pregnancy, azathioprine is considered
safe. However, potential adverse effects include life-threatening bone marrow suppression and
associated coagulopathy. Tacrolimus and cyclosporin are also used; however, they require an altered
dosing regime and close monitoring. Mycophenalate mofentil is generally contraindicated in
pregnancy. An increased risk of infection is associated with all immunosuppressant therapy,
necessitating the appropriate use of prophylactic antibiotics covering all surgical procedures and use
of a meticulous aseptic technique at all times.
The anaesthetic management of the parturient with chronic

kidney disease
Assessment and optimization
Preoperative evaluation must include the assessment of the degree of renal impairment, the systemic
manifestations of chronic renal disease and the co-morbidities and pathologies associated with the
underlying cause of renal failure. These patients will have been closely monitored in the antenatal
period and care plans may already be in place for intrapartum management.
Full blood count, urea and electrolytes and a coagulation screen are essential investigations on
admission to the delivery unit. Anaemia may require correction with iron, folic acid, erythropoietin
and a red cell transfusion. Patients with CKD often display a bleeding tendency. Conversely, the
increase in coagulation factors may also increase the risk of thrombosis. Thrombocytopenia and
platelet dysfunction in the presence of a normal platelet count are common. These patients may give a
history of easy bruising, bleeding from oral mucosa, melaena or excessive haemorrhage following
invasive procedures. Thromboelastography may be useful in evaluating global coagulation status.
There is no obvious correlation between excessive bleeding and severity of renal dysfunction.
Heparin-free haemodialysis, peritoneal dialysis, arginine vasopressin (DDAVP) and cryoprecipitate
have all been used to improve coagulation. Intravenous arginine vasopressin (usually 300 g)
increases von Willebrand factor (vWF) release for up to 8 hours. Repeated doses are less effective.
During the peripartum period, it is important to ensure the patient is euvolaemic, has electrolytes
that are stable and any metabolic acidosis is minimized. This requires careful fluid balance, close
monitoring of electrolytes, knowledge of daily diuretic doses, daily urine output and potentially
dialysis.
Left ventricular dysfunction and pulmonary oedema due to chronic fluid overload, ischaemic
heart disease or uraemic cardiomyopathy may all result in poor cardiorespiratory reserve. Patients
with severe disease of long duration or anaemia are particularly at risk. ECHO cardiography may be
useful in evaluating function. Hypertension in renal patients is very common. These patients require
screening for pre-eclampsia and aggressive management aiming for a diastolic pressure of less than
8090 mmHg.
Delayed gastric emptying and reduced gastric pH increases the risk of aspiration pneumonitis.
Premedication with ranitidine, metoclopramide and sodium citrate is advised.
Peripartum monitoring
In mild or moderate disease, standard non-invasive monitoring will usually suffice. In patients at risk
of ischaemic heart disease S-T segment monitoring may be useful. Temperature must be monitored, as
these patients possess a tendency towards hypothermia. Neuromuscular function following muscle
relaxants is unpredictable, especially after magnesium infusion, and monitoring is essential. Invasive
monitoring is indicated in the presence of uncontrolled hypertension, severe cardiorespiratory
disease or a rapidly fluctuating volume status.
Neuraxial analgesia and anaesthesia

The presence of thrombocytopenia may contraindicate neuraxial techniques for analgesia or
anaesthesia. More frequently, altered arachidonic acid metabolism, increased nitric oxide production
and defective endothelial release of vWF results in platelet dysfunction in the presence of a normal
platelet count. Normal values derived by thromboelastography in the presence of a normal
coagulation screen can support the use of a neuraxial technique. Residual heparin following dialysis
and the prolonged effect of low-molecular-weight heparin may also prohibit neuraxial techniques.
The use of low-dose epidural solutions and close monitoring of sensory and motor function will aid
early diagnosis of epidural haematomas.
Hypovolaemia, especially in the presence of autonomic dysfunction, may result in severe
hypotension with sympathetic blockade following epidural or spinal anaesthetic. It is important to
ensure euvolaemia, particularly prior to a spinal anaesthetic, and slowly load epidurals to prevent
precipitous drops in blood pressure. Excessive intravenous fluids may cause pulmonary oedema,
therefore once euvolaemic, vasopressors should be used to maintain normotension.
The pharmacokinetics of bupivacaine and ropivacaine are relatively unaffected and similar
doses produce the expected clinical response. Remifentanil patient-controlled analgesia (PCA) is
useful for labour analgesia where neuraxial analgesic techniques are contraindicated.
General anaesthesia
Patients with stable mild to moderate renal impairment may require little adaptation of general
anaesthetic technique. Severe disease, particularly in the presence of uncontrolled hypertension or
cardiorespiratory complications, may present a significant challenge to the anaesthetist.
Knowledge of preoperative fluid and electrolyte status and the patients ability to handle fluids
is extremely important for intraoperative fluid management. Invasive monitoring may be indicated.
Postoperatively, insensible loss in addition to the previous hours urine output is a common regimen.
Induction of anaesthesia is complicated by the increased risk of a difficult airway and aspiration.
Decreased protein binding, greater bloodbrain barrier penetration, uraemia and prolonged
elimination half-lives potentiate anaesthetic agents. The pharmacokinetics of propofol are unchanged.
Thiopentone, etomidate and benzodiazepine all require a reduction in dose. Suxamethonium is best
avoided if the serum potassium is unknown or greater than 5.5 mEq/L. Rocuronium will produce
acceptable intubating conditions within 90 s but duration of action will be significantly longer.
Suggamadex is safe to use in the presence of renal insufficiency. Atracurium and cisatracurium
produce predictable results, due to Hofmann degradation. Isoflurane and desflurane preserve renal
blood flow better than sevoflurane. Enflurane should be avoided. Patients on magnesium may require
a reduced infusion rate and monitoring of magnesium levels.
The active metabolite of morphine, morphine-6-glucuronide, accumulates in renal failure and
careful titration is advised. Alfentanil, fentanyl or remifentanil can provide useful, reliable analgesia
without accumulation although prolonged infusions of fentanyl may still accumulate. Regional
anaesthesia such as transverse abdominal plane block or a rectus sheath block may be a useful
analgesic adjunct. Paracetamol is safe in renal failure, however non-steroidal anti-inflammatories
should be avoided.
Many intraoperative renal protective strategies, including dopamine, furosemide, mannitol,
calcium-channel blockers or excessive intravenous fluids, have been explored, yet there is very little
evidence supporting any of them. It is important to avoid nephrotoxic drugs and hypovolaemia.
The anaesthetic management of the parturient with acute

kidney injury
The anaesthetic management of the patient with AKI is similar to that with chronic disease. The
systemic manifestations of chronic kidney disease will be absent and the underlying pathology is
different and sometimes unknown. Particular attention should be paid to assessment of fluid and
electrolyte status, blood pressure, severity and symptoms of uraemia, metabolic acidosis and urine
output as these patients may have unstable physiology. Renal replacement therapy and invasive
monitoring may be indicated. General and neuraxial anaesthetic techniques require similar
considerations to those with chronic impairment.
Key points
1. Renal disease significantly increases maternal and fetal morbidity and mortality.
2. Parturients with CKD are more likely to develop gestational hypertension, pre-eclampsia and
eclampsia.
3. Kidney disease during pregnancy may become apparent for the first time. This can be due to
the physiological and anatomical changes of pregnancy, increased levels of monitoring or
diseases associated with pregnancy e.g. pre-eclampsia.
4. Dialysis patients require a multidisciplinary approach, modification of their renal

replacement regimes and close surveillance of the mother and fetus.
5. Although in renal transplant patients a successful obstetric outcome is common, a

multidisciplinary approach is essential. Particular attention should be paid to close and regular
monitoring of mother and fetus, immunosuppression regimes and knowledge of the precise
location of the allograft. Ideally, transplant surgeons should be available if caesarean section is
required.
Further reading
August, P. and George, J. N. (2013). Acute kidney injury (acute renal failure) in pregnancy.
UpToDate (online). Available at http://www.uptodate.com (Accessed May 2015).
August, P. and Vella, J. (2013). Pregnancy in women with underlying renal disease. UpToDate
(online). Available at http://www.uptodate.com (Accessed May 2015).
Chinnappa, V., Ankichetty, S., Angle, P. and Halpern, S. H. (2013). Chronic kidney disease in
pregnancy. Int. J. Obstet. Anesth., 22(3), 223230.
Podymow, T., August, P. and Akbari, A. (2010). Management of renal disease in pregnancy. Obstet.
Gynecol. Clin. North Am., 37(2), 195210.
Chapter 21
Haematologic disease in pregnancy

Pavan Kochhar, Andrew Heck and Clare Tower
Introduction
The haematological system undergoes significant changes during pregnancy. A knowledge of these
changes is essential to enable clinicians to determine what is within normal parameters and what is
pathological. The recognized haematological changes during pregnancy are detailed in Chapter 1.
Anaemia of pregnancy
A measure of haemoglobin (Hb) levels should be made at booking and at 28 weeks gestation.
Anaemia during pregnancy may result from dilutional physiological changes, iron deficiency,
folate deficiency, new-onset pernicious anaemia, or pre-existing diseases, including
haemoglobinopathies or hereditary spherocytosis. Establishing the cause is paramount and early
treatment will minimize the harmful effects.
The 2011 UK guidelines for the management of iron deficiency in pregnancy defined anaemia as:
<110 g/L in the first trimester
<105 g/L in the second and third trimesters
<100 g/L postpartum.
Anaemia impairs oxygen delivery and results in an increase in cardiac output and oxygen demand,
with a loss of functional reserve and an increased risk of maternal and fetal ischaemia. Remember,
blood loss is expected at an uncomplicated normal delivery (500 mL) and at caesarean section
(1000 mL).
Iron deficiency is the leading cause of anaemia; this may be due to pre-existing low iron levels
secondary to menorrhagia, inadequate diet, pregnancy within the last year or due to increased iron
demands (such as multiple pregnancy). It is associated with low birth weight, preterm delivery and
increased blood loss at delivery.
Iron deficiency can be diagnosed using serum ferritin and total iron binding capacity saturation
more reliably than mean corpuscular volume or mean corpuscular haemoglobin concentration.
Without the presence of inflammatory disease, serum ferritin is the best indicator of iron stores in
pregnancy. The 2011 UK guidelines for the management of iron deficiency in pregnancy advise iron
replacement therapy for women with serum ferritin levels less than 30 g/L, as this represents early
iron depletion that will deteriorate with increasing gestation. A serum ferritin <15 g/L is diagnostic
of iron deficiency. Treatment is with 100200 mg elemental iron per day. Inhibitors to iron uptake in
the intestine, such as phytic acid and tannins, should be avoided. Parenteral iron may be indicated
when oral therapy is not tolerated, absorbed or compliance is in doubt. The World Health
Organization (WHO) recommends iron supplementation for all women. However, analysis of studies
in the Cochrane database have not provided sufficient evidence to support this.
Folate deficiency most often results from dietary deficiency, but can occur secondary to
haemoglobinopathies, anticonvulsants or specific folate antagonists.
Recombinant human erythropoietin is not recommended for use, other than in patients with end-
stage renal failure.
In women found to be markedly anaemic at the onset of labour, a careful assessment should be
made. Transfusion may be necessary for symptomatic women or those with Hb < 70 g/L. Active
management of the third stage is necessary to minimize blood loss.
Haemoglobinopathies
Sickle cell disease (SCD)
SCD describes a group of inherited single-gene autosomal recessive disorders caused by a sickle
gene. This includes HbSS (the most common homozygous form) and heterozygotes of haemoglobin S
and another abnormal haemoglobin such as haemoglobin C, D, E or -thalassaemia. About 300
newborns are diagnosed with SCD each year in the UK. Patients rarely live to their sixth decade.
Haemoglobin S results from a mutation on chromosome 11, causing a valine for glutamic acid
substitution on the -globin sub-unit. This formation is biochemically unstable and prone to
precipitating out of solution, markedly so when PO2 <6 kPa. The agglutinated masses cause vaso-
occlusive problems and the sickled red cells have a shorter life of 12 days compared to the normal
120 days.
Untreated, the consequences of sickle cell disease occur due to anaemia or occlusive end-organ
damage:
Cardiomegaly secondary to an anaemia-induced high-output state, pulmonary artery

hypertension and pulmonary infarction.
Pulmonary infarctions can lead to an acute chest syndrome with haemoptysis, dyspnoea and
pleuritic pain, which can ultimately lead to pulmonary failure.
Marrow hyperplasia causes frontal bossing and maxilla enlargement.
Lymphoid tissue enlargement may cause obstructive sleep apnoea.
Renal impairment begins in childhood.
Sequestration of red blood cells (RBCs) within the spleen can lead to severe life-threatening
anaemia.
Hyposplenism results from autoinfarction, rendering the patient immunocompromised.
Repeated microvascular occlusion causes retinopathy and aseptic necrosis of susceptible

tissues, including the femoral head.
Transient ischaemic attacks and strokes are more prevalent.
In parturients, SCD is associated with increased perinatal mortality (up to 20%), maternal death
(<1%), preterm labour, fetal growth restriction and acute painful crises. An increased risk of
infection, spontaneous miscarriage, thrombotic events and antepartum haemorrhage may also occur.
The RCOG Guidelines for the Management of SCD in Pregnancy (2011) make the following
recommendations:
1. Management should involve a multidisciplinary team comprising a haematologist and an

obstetrician with an interest in this area.
2. Preconception counselling is recommended to allow optimization of disease control and

medication adjustments. Medications contraindicated during pregnancy include ACE-inhibitors,
angiotensin receptor blockers and hydroxycarbamide (used to reduce the incidence of sickle
crisis). Folic acid supplementation (5 mg per day) is recommended to commence preconception
and vitamin D status should be optimized.
3. Evidence of end-organ damage should be sought, including echocardiography to assess

pulmonary hypertension.
4. The partners carrier status should be ascertained enabling counselling and antenatal
screening to occur if the couple wish.
5. Blood pressure and urine should be screened regularly. Multiple transfusions can result in
alloimmunization and iron overload. Serum iron should be measured.
6. All vaccinations should be up to date. Low-dose aspirin (75 mg) should be taken to reduce the
risk of pre-eclampsia.
7. The risk of venous thromboembolism should be assessed in order to guide the need for
thromboprophylaxis.
8. Ultrasound scanning to assess fetal growth is required throughout the third trimester.
9. Prophylactic top-up transfusions are contentious due to the risks of iron overload, delayed
transfusion reaction and the possible risk of precipitating a crisis. These should be administered
only on the advice of a specialist haematologist. Women with recurrent crisis managed with
regular exchange transfusions outside pregnancy should usually continue this programme
throughout pregnancy with the involvement of the specialist haematologist.
Anaesthetic management may be in the provision of aggressive treatment of a sickle crisis or

facilitating early analgesia as part of planned labour to minimize the risk of a crisis. On the labour
ward the patient should be monitored in a high-risk room, receive continuous saturation monitoring
and aim to keep saturations greater than 95%. Invasive monitoring may be required. Regional
anaesthesia should be provided when safe to do so (note timing of anticoagulants). These patients are
often opioid tolerant and pethidine should be avoided. Blood products should be at the discretion of
the joint haematology and obstetric team. In the event of a general anaesthetic, meticulous attention to
oxygenation, analgesia, temperature control, minimizing stasis and maintaining hydration is essential.
Postpartum care should be in an obstetric high-dependency unit and a high index of suspicion for
subsequent sickle crisis.
Thalassaemias
These are divided into two main groups: the -thalassaemias, where one to four of the -genes are
deleted, and the -thalassaemias, where one or two of the -genes are absent.
-Thalassaemia major is incompatible with life, with the fetus becoming severely hydropic; -
and -thalassaemia traits are usually asymptomatic, but individuals are prone to anaemia and should
be managed accordingly.
-Thalassaemia major sufferers have a defective -globin gene from each parent. Untreated, this
condition is fatal, with markedly ineffective erythropoiesis and severe haemolysis. Outcome has
improved to beyond the fourth decade now with repeated, regular transfusions. The clinical features
of this condition are the consequence of iron overload following repeated transfusion. This includes
hepatic, endocrine and cardiac dysfunction. Death occurs secondary to myocardial
haemochromatosis. Where transfusions have not been regular, the effects of marrow hyperplasia are
evident with bone deformities. Women with this disorder are usually sub-fertile without the use of
reproductive technologies. Care for these women should be in specialist joint clinics with careful
screening for the sequelae of iron overload. Preconception counselling is paramount, with
optimization of medication prior to fertility treatment and pregnancy. Chelating agents are
contraindicated during pregnancy. Closely supervised transfusion regimes may reduce the risk of
prematurity and intrauterine growth restriction. Women should be screened for Hep B+C, diabetes,
thyroid disease and cardiac insufficiency. Exclude spinal abnormalities, including osteoporosis and
scoliosis.
Thrombocytopenia
A platelet count of <150 10 9/L may occur during pregnancy due to gestational thrombocytopenia,
laboratory error (EDTA can cause Ca 2+ and platelet agglutination, artificially reducing platelet
count), platelet autoantibodies (immune thrombocytopenia, ITP) or widespread activation (e.g.
TTP/haemolytic uraemic syndrome and pre-eclampsia/HELLP). Other causes of impaired platelet
production include bone marrow suppression, folate deficiency, platelet destruction (such as
disseminated intravascular coagulation) and drugs (unfractionated heparin, thiazides, hydralazine,
digoxin, H2 blockers). Diagnosis and correction of thrombocytopenia is vital to reduce the risk of
haemorrhage at the time of delivery.
The timing and placement of neuraxial blocks in the presence of thrombocytopenia can be
challenging. The nature of the thrombocytopenia and trend of platelet count is important, and the
decision must be made on an individual basis. Discussion with senior doctors is important and
consideration must be made for the most experienced operator to perform the block.
Gestational thrombocytopenia
This accounts for 70% of all cases and is probably caused by accelerated platelet destruction.
Platelet count rarely falls below 75 109/L and most authors regard them as needing no particularly
special management other than platelet count monitoring. Regional anaesthesia is generally
considered safe when the platelet count is stable around 80 109/L, but this should be decided on an
individual basis, taking into account the absolute platelet count and the trend. An urgent full blood
count should be sent on admission in labour. Diagnostic difficulty can occur when thrombocytopenia
is identified for the first time during pregnancy, as confirmation of the cause can only be determined
with a platelet count postnatally.
Autoimmune thrombocytopenic purpura (ITP/ATP)

This condition stems from IgG destruction of platelets and was previously known as immune
thrombocytopenic purpura or idiopathic thrombocytopenic purpura. The incidence is around 0.1%
and diagnosis is essentially one of exclusion, with platelets < 100 109/L usually occurring early in
the antenatal period with normal coagulation profiles. High-dose oral corticosteroid therapy is
initiated when the count is found to be falling in the third trimester, with the aim of achieving a
platelet count of more than 50 109/L for delivery. If corticosteroids are ineffective, oral cyclosporin
can be used. Those failing to achieve a satisfactory platelet count using oral therapy can be treated
with intravenous IgG to transiently increase platelet count. Platelet transfusions are occasionally
required to cover the delivery.
Maternal IgG can cross the placenta and in around 5% of cases can cause neonatal
thrombocytopenia, theoretically increasing the risk of neonatal haemorrhage. As yet no study has
conclusively demonstrated a link between fetal platelet count and intrapartum risk. The occurrence of
neonatal intraventricular haemorrhage is rare and does not seem to correlate with the method of
delivery. A care plan should be put in place to reduce the theoretical risk to the fetus, including
potential avoidance of ventouse delivery.
The same principles regarding the appropriateness of regional anaesthesia should be applied as
for gestational thrombocytopenia.
Thrombotic thrombocytopenic purpura (TTP) and haemolytic uraemic syndrome (HUS)
TTP is a rare condition usually presenting in the second trimester. Intravascular clot formation leads
to platelet consumption and vascular occlusion. A classical pentad exists of:
1. Fever
2. Thrombocytopenia
3. Microangiopathic haemolytic anaemia
4. Focal neurology
5. Renal failure.
HUS presentation is similar, but with more pronounced renal failure and absence of neurological
sequelae. Microscopic differences in the number and cluster of von Willebrand factor deposits help
differentiate between the two conditions. Effective treatments include plasma exchange and
plasmapheresis, intravenous IgG, prednisolone and prostacyclin. Renal replacement therapy may be
required. Due to the coagulopathy present, neuraxial anaesthesia is not recommended.
Pre-eclampsia/HELLP
Pre-eclampsia is accompanied by a low platelet count in approximately 20% of cases, often with a
coagulopathy on a continuum with the more severe HELLP variant (Haemolysis, Elevated Liver
enzymes, Low Platelets). More extensive information is provided in Chapter 14. These patients
require regular monitoring of their platelet and coagulation status, with any fall indicating a
worsening of their condition. Any consideration of regional anaesthesia will be guided by this and
point-of-care testing of coagulopathy.
Congenital coagulopathies
von Willebrands disease (vWD)
vWD is a heterogenous group of mainly autosomal dominant disorders (types 1,2,3) in which there is
reduced or abnormal circulating von Willebrand factor (vWF). vWF has two functions:
1. It combines with factor VIII to produce a procoagulant complex (VIIIc) that protects factor
VIII from premature destruction.
2. It mediates platelet adhesion by binding to platelets (a reaction enhanced by ristocetin) and
collagen.
The incidence of von Willebrands disease is 1:100 to 1:2500 for the mild form and 1:200,000 to
1:2,000,000 for the severe homozygous form. Patients may present with a history of epistaxis,
menorrhagia and bleeding after dental extractions. The bleeding risk associated with delivery and the
immediate puerperal period can be significant. Women should be managed in close liaison with an
obstetric haematology team. Consideration for the fact that the fetus may also be affected is necessary.
Type 1 disease results from a partial quantitative vWF deficit. Increase in vWF and factor VIII
levels in pregnancy result in correction of this deficit by the third trimester in 8090% of cases. When
haematological abnormalities are corrected, management of labour and delivery should be as normal,
and regional anaesthesia is acceptable. Following delivery, levels typically fall rapidly to those
recorded prepregnancy. These women are at risk of primary and secondary postpartum haemorrhage.
In a minority of women, the disease does not correct, but some women will be responsive to
desmopressin (DDAVP) to increase vWF levels.
Type 2 disease (915% of cases) is a qualitative defect; the vWF is abnormal and may not
respond to DDAVP.
In Type 3 disease (<1% of cases) vWF is undetectable and factor VIII very low. Some women
will require factor replacement (fresh frozen plasma (FFP), cryoprecipitate or vWF/factor VIII
concentrates) to cover delivery of the fetus, and a detailed haematological care plan should be in
place.
Types 2 and 3 patients are more complex and should be managed on an individual basis with the
involvement of specialist haematologists. Regional anaesthesia is generally contraindicated, but has
been described after clotting correction.
Treatment is usually started when factor VIII levels reach less than 25% of normal. Levels
should be 50% for labour, and treatment should be instituted to raise this to 80% for caesarean
delivery. Factor VIII levels should be checked daily post partum and treatment instituted if levels fall
below 25% or significant bleeding occurs. There may be a role for oral tranexamic acid to reduce
blood loss in the puerperal period.
Haemophilia
Haemophilia A (factor VIII deficiency) and haemophilia B (factor IX deficiency) are X-linked traits
that classically do not affect women. Some female carriers (up to 10%) can be symptomatic and have
clinically significant clotting deficiency.
Factor VIII or IX levels of 30% or more are considered satisfactory for vaginal delivery. For
planned operative delivery, levels are increased to normal. Specialist haematology teams will guide
administration of FFP, cryoprecipitate, DDAVP, tranexamic acid or purified clotting factors.
Regional anaesthesia is generally contraindicated, but may be considered after specialist advice
following factor correction and a riskbenefit assessment of individual cases.
Half of all male children of heterozygous carriers for haemophilia A or B will have
haemophilia. These infants have an increased risk of bleeding and certain procedures should be used
only where careful balance of risks and benefits has been assessed: fetal scalp electrode; fetal scalp
pH sampling; vacuum extraction and difficult forceps delivery.
Acquired coagulopathies
DIC results from abnormal activation of the coagulation system. Procoagulant substances, including
thromboplastin, phospholipid and those resulting from endothelial injury are released into the
circulation. Stimulation of coagulation activity results in excess thrombin, consumption of clotting
factors and platelets, with concomitant activation of the fibrinolytic pathway.
Common obstetric causes of DIC include:
Placental abruption
Sepsis
Intrauterine death
Pre-eclampsia
HELLP syndrome
Acute fatty liver of pregnancy
Amniotic fluid embolus (AFE).
Diagnosis of DIC depends on the clinical presentation and laboratory tests. Patients may present with
cardiovascular, respiratory or renal failure. There may be bleeding from venepuncture sites, gums,
gastrointestinal and urogenital tracts, and also from the uteroplacental bed.
Laboratory tests can show a variable prolongation of the prothrombin time (PT) and activated
partial thromboplastin time (aPTT), decreased platelet count, decreased fibrinogen and an increase in
fibrin degradation products (FDPs) and D-dimers. The use of thromboelastography may allow rapid
assessment of the coagulation disruption and monitoring of correction.
Acute fulminant DIC should be treated aggressively, with the emphasis on maternal
resuscitation. Onset of DIC may be more insidious, e.g. pre-eclampsia and fetal demise. Removal of
the underlying triggering is paramount, which usually requires delivery of the fetus and placenta.
Management of massive obstetric haemorrhage should be by a senior team, according to local
protocols (see Chapter 25).
The management of DIC requires blood and blood products:
Packed red cells to replace ongoing losses
Fresh frozen plasma (FFP) to replace coagulation products
Platelet concentrates
Cryoprecipitate (contains more fibrinogen than FFP and should be considered if there is
haemorrhage and the fibrinogen level is <1 g/L).
The other considerations for patients in DIC are:
Regional anaesthesia is contraindicated
Removal of previously sited epidural catheter should be delayed until correction of

coagulopathy
Arterial line for monitoring and blood sampling
Central line for inotrope/vasopressor administration and for further monitoring
Remain vigilant for complications of massive transfusion, including transfusion-related acute

lung injury (TRALI)
Utilization of cell salvage is advised in massive haemorrhage
Surgical haemostasis may be difficult and may necessitate hysterectomy
Internal iliac artery balloon catheterization can be considered if some degree of coagulation
correction has been achieved and further surgical intervention is needed
Use of recombinant factor VII and prothrombin complex concentrates (PCC) has been
described
Metabolic acidosis may take a few hours to correct
Postoperative management in a high-dependency or critical care unit.
Thrombophilia/hypercoagulable states
Thrombophilia is a familial or acquired abnormality of haemostasis likely to predispose to
thrombosis. A congenital deficiency in anticoagulant activity occurs in approximately 3050% of
patients with a history of venous thromboembolism (VTE). Pregnancy is a hypercoagulable state, and
pre-existing thrombophilia increases the risk of thrombosis further, especially in the postpartum
period. Some thrombophilias have been associated with recurrent miscarriage and an increased risk
of pregnancy complications such as abruption, fetal growth restriction and pre-eclampsia. Antenatal
management should be personalized and involve assessment of VTE risk and the risk of pregnancy
complications. Management typically comprises low-dose aspirin and prophylactic subcutaneous
low-molecular-weight heparin (LMWH). This has implications for the anaesthetist with regard to
timing for regional techniques.
Congenital thrombophilias
Hereditary thombophilia is found in 2050% of women with pregnancy-related VTE. These factor
deficiencies can be quantitative and/or qualitative, hence specialist haematology input is required.
Protein C deficiency
Protein C inhibits activated factors V and VIII. The incidence of protein C deficiency is 1 in 15,000.
Protein C levels typically rise by 30% in pregnancy, but this rise does not occur in patients with
deficiency. These patients are greatly predisposed to VTE. In the absence of anticoagulation, VTE
rates of up to 25% have been reported, mostly in the postpartum period.
Protein S deficiency
Protein S is a co-factor for protein C. Protein S levels typically fall during pregnancy, thus
assessment of protein S levels must occur outside pregnancy. There may be an association with
arterial thrombosis. Treatment is as for Protein C deficiency.
Antithrombin III (AT) deficiency

AT inactivates thrombin and coagulation factors IXa, Xa, XIa and XIIa.
AT deficiency occurs in around 1 in 5,000 pregnancies, accounting for 15% of thromboembolic
events. Left untreated, the rate of VTE can be 5570%. Deficiencies can be quantitative (type 1) or
qualitative (type 2). Heparins may not be as effective in AT deficiency, as their mode of action is
antithrombin-dependent, thus effectiveness of heparin prophylaxis should be monitored using anti-Xa
levels. Different sub-types of AT deficiency are associated with different levels of VTE risk and
therefore expert advice should be sought. Treatment should start in early pregnancy and continue for 6
weeks postpartum. The use of antithrombin III concentrate has been described in women at particular
risk.
Factor V Leiden mutation

Factor V is a co-factor that allows factor Xa to activate thrombin, which cleaves fibrin from
fibrinogen.
This common hereditary thrombophilic tendency results from a mutation in a single amino acid
in the factor V gene. The mutant factor V Leiden persists for longer in the circulation. It is degraded
more slowly by activated protein C, hence leading to a hypercoagulable state. Heterozygous factor V
Leiden has an incidence of 35% and has a fivefold increase in VTE risk. Homozygous factor V
Leiden status is associated with higher VTE risk. LMWH timing will guide safety for regional
anaesthesia.
Acquired thrombophilias
Antiphospholipid syndrome is the most common cause of acquired thrombophilia. Recognized
antibodies include lupus anticoagulant and anticardiolipin antibodies. A preceding history of arterial
or venous thrombosis or adverse pregnancy outcome (defined as three or more unexplained
miscarriages before 10 weeks of gestation, a fetal death after 10 weeks of gestation or a premature
birth (before 35 weeks) due to pre-eclampsia or intrauterine growth restriction) is common.
Antiphospholipid syndrome is associated with a 5% incidence of VTE or cerebrovascular accident in
pregnancy.
Women with previous thromboses and antiphospholipid syndrome should be offered both
antenatal and 6 weeks of postpartum thromboprophylaxis. Women with persistent antiphospholipid
antibodies with no previous VTE and no other risk factors or fetal indications for LMWH may be
managed with close surveillance antenatally, but should be considered for LMWH for 742 days post
partum.
Assessment of coagulation
Assessment of coagulation begins with clinical examination of the patient and an index of suspicion
over causes of coagulopathies. Excessive bleeding or bleeding from unusual sites, e.g. gums or
venepuncture sites, can alert to the presence of a coagulopathy. Laboratory tests aid clinical
evaluation, but unfortunately there is no single blood test that will give an overall study of
haemostasis and blood coagulation.
Platelet count, PT and aPTT are measured. In normal pregnancy, an increase in coagulation
factors results in a reduction in PT and aPTT. Fibrinogen assays are also useful in massive
haemorrhage or sepsis. Gestational thrombocytopenia may lead to lower platelet counts at the end of
pregnancy. A limitation of the platelet assay is that it measures platelet numbers, but not function. A
summary of tests in clinical use is given in Table 21.1.
Table 21.1 Laboratory tests used in the assessment of coagulation
Study Measures Normal values
Bleeding time Platelets and vascular integrity 15 min
Platelet count Number of platelets 140440 109/L
aPTT Extrinsic pathway (factors II, 2436 s

V, VIII, IX, X, XI)
PT Intrinsic pathway (factors II, V, 1112 s

VII, X)
Thrombin time Factors I, II, circulating split 1620 s

products, heparin
During a rapidly changing scenario such as haemorrhage, receipt of laboratory coagulation
results often lags behind the current haematological picture. Coagulation products are often instituted
empirically. Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) evaluate
real-time measurement of whole blood coagulation. They evaluate the viscoelastic properties of the
sample, as well as coagulation factor and platelet activity. They can help with haemostatic decision-
making and blood product use during surgery and severe haemorrhage.
The TEG analyzer has a sample cup into which 360 L of whole blood sample is pipetted. This
cup constantly oscillates at a set speed through an arc of 445. A stationary pin attached to a torsion
wire is immersed in the blood. Each oscillation lasts 10 s. When fibrin first forms, it begins to bind
the cup and pin, causing the pin to oscillate in phase with the cup. The torque of the rotating cup is
transmitted to the immersed pin only after fibrin or fibrin-platelet bonding has linked the cup and pin
together. The degree of pin movement is converted into a graph (Figure 21.1) that represents the
kinetics of clot development.
Figure 21.1 TEG graph and annotation.
The reaction time (R-time) depicts the time for fibrin strands to form. It is decreased in
hypercoagulable states such as pregnancy. A prolonged R-time may reflect decreased or
dysfunctional coagulation factors leading to a delay in the formation of thrombin or fibrin.
Consideration should be given to administer FFP for correction. A prolonged R-time may also reflect
heparin activity, and this may be further evaluated using a heparinase cup that will remove the heparin
effect on the sample.
The maximum amplitude (MA) represents clot strength with the amplitude of pin oscillation
increasing with clot strength (Figure 21.1). The major contributors to clot strength are platelets (80
90%) and fibrinogen (1020%), which binds the platelets together. Therefore, MA gives an
indication as to the function of platelets present in the sample. A low MA value is indicative of
insufficient plateletfibrin clot formation due to poor platelet function, low platelet count, or low
fibrinogen levels or function. The most common treatment of a low MA in a bleeding patient is
transfusion of platelets. The amount of platelets required to reverse bleeding depends on the
magnitude of the abnormality and on the patients overall status.
Accepted non-pregnant reference ranges for R-time are 48 minutes and for MA, 5573 mm.
Studies on pregnant women reflect the hypercoagulable state of pregnancy; R-time values are shorter
and MA values are higher, but further work is needed to define pregnancy values.
A platelet function analyzer (PFA-100) can also measure platelet function. This tests platelet
activation and aggregation. Experience in obstetrics is limited and expert advice in the use and
interpretation of samples is essential.
Clinical example of the use of TEG

A 24-year-old primigravida presented to labour ward with PV bleeding at 24 weeks gestation. Her
blood pressure was 150/110 and scans revealed fetal demise. Bleeding from venepuncture sites
raised the clinical suspicion of DIC. TEG (Figure 21.2) was used as a rapid laboratory assessment
and confirmed the presence of DIC. A prolonged R-time indicated a decrease in coagulation factors.
A markedly reduced MA indicated reduced platelet activity. The concurrent blood tests revealed a
PT of 24, aPTT of 42.7 and fibrinogen < 0.6 g/L. Renal function was impaired, with creatinine
182 mol/L.
Figure 21.2 TEG at presentation.
Four units of red cell concentrate, four units of FFP, three units of cryoprecipitate and two adult
doses of platelets were infused. A repeat TEG ( Figure 21.3) showed a marked improvement in the
haemostatic profile. Blood tests confirmed the improvement with a PT of 14, aPTT of 35 and
fibrinogen of 35 g/L.
Figure 21.3 TEG after correction with blood products.
The patient proceeded to caesarean section under general anaesthesia.

Key points
1. Pregnancy is a hypercoagulable state that develops in order to reduce blood loss at delivery.
2. Clear guidelines exist for the diagnosis and management of anaemia during pregnancy,
including UK Guidelines on the Management of Iron Deficiency in Pregnancy by the British
Committee for Standards in Haematology.
3. Women with sickle cell disease should be managed by an MDT, including specialist
haematologists and obstetricians. RCOG guidelines should be consulted.
4. Thrombocytopenia can occur during pregnancy for a variety of reasons. Identification of

cause, trend in platelet count and knowledge of platelet function all guide timing and
appropriateness of regional anaesthesia.
5. Hypercoagulable states are typically managed antenatally with low-dose aspirin and low-
molecular-weight heparin. Care must be taken when timing regional anaesthesia.
6. Point-of-care assessment of coagulation is becoming more widespread and is of particular

benefit in rapidly changing scenarios such as haemorrhage.
Further reading
Association of Anaesthetists of Great Britain and Ireland, Obstetric Anaesthetists Association and
Regional Anaesthesia UK (2013). Regional Anaesthesia and Patients with Abnormalities of
Coagulation. http://www.aagbi.org/sites/default/files/rapac_2013_web.pdf (accessed May 2015).
British Committee for Standards in Haematology (2011). UK guidelines on the management of iron
deficiency in pregnancy.
http://www.bcshguidelines.com/documents/UK_Guidelines_iron_deficiency_in_pregnancy.pdf
(accessed May 2015).
Chestnut, D.H., Polley, L.S., Tsen, L.C. and Wong, C.A. (2008). Chestnuts Obstetric Anesthesia:
Principles and Practice, 4th edn. Philadelphia: Mosby/Elsevier.
Nelson-Piercy, C. (2010). Handbook of Obstetric Medicine, 4th edn. New York: Informa Healthcare.
Royal College of Obstetrics and Gynaecology (2007). Green-top Guideline No. 47: Blood
Transfusions in Obstetrics. http://www.rcog.org.uk/womens-health/clinical-guidance/blood-
transfusions-obstetrics-green-top-47 (accessed May 2015).
Royal College of Obstetrics and Gynaecology (2011). Green-top Guideline No. 61: Management of
Sickle Cell Disease in Pregnancy. http://www.rcog.org.uk/womens-health/clinical-guidance/sickle-
cell-disease-pregnancy-management-green-top-61 (accessed May 2015).
Stoltzfus, R. J. and Dreyfuss, M. L. (1998). Guidelines for the Use of Iron Supplements to Prevent and
Treat Iron Deficiency Anemia. Washington, DC: International Nutritional Anemia Consultative
Group, International Life Sciences Institute.
Yentis, S., May, A. and Malhotra, S. (2007). Analgesia, Anaesthesia and Pregnancy: A Practical
Guide, 2nd edn. Cambridge: Cambridge University Press.
Chapter 22
Neurosurgical and neurological disease in
pregnancy

Kirsty MacLennan and Craig Carroll
Neurological disease in parturient prompts the anaesthetic and obstetric team to consider many
aspects of care delivery. Pre-existing conditions may progress to cause significant compromise and
the onset of new neurological symptoms may mimic more commonly encountered conditions, such as
PET.
Even the presence of stable neurological conditions, of the spinal cord, neuro-axial skeleton or
intracranium, may require careful consideration with respect to analgesia, anaesthesia and mode of
delivery.
Quantification of anaesthetic risk is essential. A major anaesthetic concern relates to the safety
of performing neuraxial blockade. The following questions arise:
Is there risk of coning? If a CSF leak results in a discrepancy in pressure within the cranium
and infra foramen magnum (cranial: spinal CSF pressure gradient CSFCr:CSFSp), cerebellar
tonsillar herniation can occur caudally with brain stem compression (coning).
Is there risk of local trauma and neurological injury? Abnormal anatomy can result in spinal
cord, cauda equina or spinal nerve trauma following needling of the perispinal region.
Is there risk of spinal haemorrhage? Neuraxial vascular abnormalities can increase the risk of
bleeding as a result of needling the spinal canal.
Will the block work? Anatomical abnormalities can impede local anaesthetic spread.
General anaesthesia in parturients with neurosurgical pathologies is not without risks.

Cardiovascular fluctuations during induction of anaesthesia can precipitate brain swelling or
intracranial haemorrhage. Optimization of intracranial pressure (ICP), cerebral perfusion pressure
(CPP) and cerebral blood flow (CBF) is essential. It is important, when evaluating known or
perceived risk of complications of neuraxial blockade, to consider the risks of not performing the
block or proceeding to general anaesthesia (see Chapter 11).
Neurosurgical issues relevant to pregnancy

See Chapter 17 for spinal abnormalities.
Intracranial mass lesions

Mass lesions can be caused by infection, tumour, vascular abnormalities, inflammation (e.g. MS),
cystic lesions or haemorrhage. Presentation depends upon lesion size, rate of enlargement, aetiology
and location, and includes:
Asymptomatic; identified during investigation of other pathology
Focal neurological deficit
Ataxia
Global reduction in cerebral function
Headache classically worse when supine
Nausea and vomiting
Seizures.
Mass effect can cause disruption of neurological function by compression or destruction of brain
tissue, causing oedema within the brain, causing hydrocephalus by obstructing CSF flow and by
reducing cerebral compliance, thus increasing ICP and reducing CBF.
Posterior fossa lesions typically cause:
Headache (usually with nausea and vomiting)
Obstructed hydrocephalus (see later)
Ataxia and co-ordination issues

Lower cranial nerve dysfunction.
Meningiomata and vestibular schwannomata (benign tumours of the VIII cranial nerve arising in the
cerebropontine angle in the posterior fossa) are prone to marked expansion during pregnancy; this
may reflect the alterations in hormonal secretion during pregnancy. They require close monitoring.
Table 22.1 Neurosurgical issues relevant to pregnancy
Category Sub-category Relevance
Mass lesions of the cranial Intrinsic brain tumour ICP issue

vault Metastasis Altered neurology
Infective lesions Seizure
Influence on analgesia, mode
of delivery, peripartum
observation
Pituitary lesions Functional/non-functional Mass effect

lesions CSF drainage
Endocrine concerns
Acute visual events
Apoplexy
Posterior fossa abnormalities Tumours CSF drainage

Arnold Chiari malformations Brainstem compression
CSF gradient
Issues of CSF drainage Hydrocephalus CSF gradient

Benign intracranial Impact of indwelling shunts
hypertension (BIH) Acute pregnancy deterioration
Shunting and diversion of in vision
CSF flow Sub-dural haematoma
Consequences of low CSF
pressure
CSF pressure differential
Vascular lesions of the central Aneurysmal, non-aneurysmal Intracranial haemorrhage with
nervous system SAH altered cerebral blood flow
stroke Raised ICP
Cerebral venous thrombosis Mass effects
AVM Venous hypertension
Vascular tumours Cerebral infarction
The vertebral column and Disc abnormalities Neurological trauma

related surgery Previous lumbar surgery Failed regional analgesia
Scoliosis
Head injury in pregnancy Traumatic head injury Immediate resuscitation

Transfer
Prioritization of therapeutic
intervention
Anaesthesia for delivery
Investigation
If an intracranial mass lesion is suspected, discussion with neurosurgeons should ensue to decide
upon the optimal imaging procedure (CT or MRI).
Treatment
Initial therapy may be medical (e.g. dexamethasone) to reduce brain swelling or reduce tumour
volume. Surgical intervention may be initial control of CSF volume (with externalized ventricular
drain). Craniotomy or craniectomy may be required for excision, debulking and tissue diagnosis. The
timing of surgery will require a multidisciplinary approach, and will be influenced by the stage of
pregnancy or puerperium. Immediate management of mass-related intracranial hypertension may
require neurocritical care involvement.
The pituitary
The pituitary gland consists of the anterior pituitary gland (adenohypophysis) and posterior pituitary
gland (neurohypophysis). Connection to the hypothalamus is by the pituitary stalk. It receives its
blood supply from the internal carotid artery, in addition to portal circulation linked to the
hypothalamus.
The function of the anterior gland is endocrine and the posterior gland is a neurosecretory
extension of the hypothalamus (see Figure 22.1).
Figure 22.1 The pituitary.
Lesions of the pituitary

Mass lesions are usually primary adenomas of the anterior pituitary and stalk that may be secretory or
non-secretory, and are either large enough to cause a mass effect, or small and only significant on
account of their secretory activity. Patients with pituitary tumours may therefore have: hyposecretion
of one of more hormones, disease resulting from isolated pituitary hormone over-secretion,
hypersecretion of one hormone with deficient secretion of others, mass effect (compression of the
optic chiasm), headache, possibly accompanied by hydrocephalus (rare), with or without hormonal
pathology.
All anterior pituitary hormones except prolactin are under positive feedback control from the
hypothalamus. Compression of the pituitary stalk may reduce dopamine transit to the anterior pituitary
gland and results in mild hyperprolactinaemia (<2000 mIU/L).
Disruption of the posterior pituitary may result in diabetes insipidus, due to the lack of ADH and
reduced water resorption in the distal tubule and collecting ducts, characterized by hypernatraemia,
with inappropriately dilute urine.
Apoplexy (haemorrhagic infarction) is a rare event resulting from bleeding into the pituitary
fossa, in the presence of a pre-existing adenoma, causing sudden onset of mass effect and hormonal
dysfunction.
Classical presentation is with acute severe retro-orbital headache. Pituitary swelling can cause
compression of adjacent structures, resulting in visual field lesions, opthalmoplegia and cerebral
hypoperfusion. It is a serious condition and if left untreated may be fatal.
Risk factors include anticoagulation, coagulopathy, treatment with dopamine agonists (e.g.
bromocriptine) and pregnancy. Differential diagnoses include: sub-arachnoid haemorrhage, acute
ischaemic stroke (AIS), Sheehans syndrome or reversible cerebral vasoconstriction syndrome
(RCVS), a rare condition presenting with recurrent severe headaches that can progress to intracranial
haemorrhage or ischaemic stroke. It is more common post partum.
Investigation: CT Head is more easily organized in the emergency setting and requires the use of
iodine-based contrast. MRI is more detailed than CT and requires the use of gadolinium contrast.
Treatment: Any patient with suspected apoplexy requires emergency neurosurgical referral and
specialist endocrinology advice. Co-located obstetrics/neurosurgery care will be essential. Urgent
hormonal replacement will be necessary (initially hydrocortisone).
Sheehans syndrome results from haemorrhage into the pituitary gland in the peripartum period.
It may present with headache, but classically presents with insidious onset of panhypopituitarism
some weeks following delivery. Mass effect is uncommon. It is more common in parturients with
delivery blood loss >2000 mL. Incidence is reported as 12% following large postpartum
haemorrhage.
Investigation and management: Brain imaging by CT/MR is necessary. Involvement of an
endocrinologist is necessary when the diagnosis is suspected.
Lymphocytic hypophysitis is a benign self-limiting autoimmune inflammatory disease, usually
related to pregnancy. Treatment (under the guidance of endocrinology) is usually with steroids alone.
Cerebrospinal fluid
Hydrocephalus
Hydrocephalus is due to an increase in CSF volume within the cranial ventricular system, resulting in
ventriculomegaly and (usually) raised intracranial pressure (ICP). See Figure 22.2.
Figure 22.2 Cerebrospinal fluid production and flow.
Presentation is dependent upon the rate of CSF build up. Chronic impairment of flow results in
headache, visual disturbance, confusion and ataxia with progression to decreased level of
consciousness. Nausea and vomiting may exist. Acute cessation of CSF drainage results in rapid
deterioration in conscious level. Those dependent upon non-anatomical drainage (shunts) are at risk
of shunt blockage and acute hydrocephalus.
Non-communicating hydrocephalus occurs if CSF produced within the lateral ventricles fails to
reach the sub-arachnoid space via drainage from the fourth ventricle. There is a CSFbrain:CSFspinal
pressure gradient; lumbar drainage of CSF must be avoided as this can precipitate coning. Regional
neuraxial anaesthesia is contraindicated. Causes include space-occupying lesions, haemorrhage
(SAH, ICH) or CSF infection.
Communicating hydrocephalus occurs if CSF production exceeds reabsorption in the presence of
normal anatomy. Causes include infection (meningitis, ventriculitis), haemorrhage, venous sinus
thrombosis, following head injury or increased CSF protein content due to CNS tumour.
Anatomically, neuraxial anaesthesia is not contraindicated.
Investigations
CT head confirms the diagnosis and may give indication as to the cause. See Figure 22.3. MRI will
demonstrate increased ventricular size. T2-weighted images demonstrate periventricular oedema.
Figure 22.3 The two CT scan images demonstrate (a) dilated lateral venticles with a teardrop-
shaped third ventricle and periventricular oedema. (b) An image of treated hydrocephalus with a
ventricular drain in situ (this may be an EVD or ventriculo- shunt).
The presence of intracranial ventriculomegaly does not necessarily signify raised ICP; however,
in symptomatic patients with headache and/or decreased level of consciousness, CSF flow
obstruction must be assumed. Neurosurgical input is obligatory.
Treatment
Communicating hydrocephalus can be treated by CSF removal at lumbar puncture. For prolonged
CSF pressure control, shunting of CSF is required (ventriculoperitoneal (VP)/atrial or
lumboperitoneal (LP) shunt).
The standard emergency treatment of non-communicating hydrocephalus is with an externalized
ventricular drain (EVD). Endoscopic third ventriculostomy (ETV) may be appropriate in some cases,
with the aim to circumvent the aqueduct and VI ventricle by generating a fistula in the base of the III
ventricle. See Figure 22.4. CSF flows directly to the basal cisterns. When successful, no additional
CSF drainage procedure is necessary.
Figure 22.4 Endoscopic third ventriculostomy via a frontal burr hole through the base of the third
ventricle.
Ventriculoperitoneal/atrial shunt creates a conduit from the ventricular system to either

peritoneum or right atrium. The system contains a valve, both preventing back flow and also dictating
the CSF drainage pressure. This provides a permanent artificial route for CSF drainage.
Key points regarding CSF shunts in pregnancy:
Parturients have a higher incidence of complicated pregnancy and worse fetal outcomes.
Shunt malfunction can occur during pregnancy, though is more likely in the peridelivery
period.
Shunt blockage in a shunt-dependent parturient is a neurosurgical emergency.
CSF infection risk is increased. If suspected, neurosurgical guidance is necessary and

investigation is classically diagnostic LP after CT head to confirm shunt function.
LP shunts are a relative contraindication for lumbar neuraxial blockade.
Parturients with functioning ETVs and no hydrocephalus can be treated as normal.
Benign intracranial hypertension (BIH)

BIH occurs mainly in women of childbearing age and is associated with raised BMI. It is thought to
result from an abnormality in central venous sinus pressure. CSF pressure is raised, with normal-
sized ventricles. It causes chronic headache and is associated with papilloedema. Acute deterioration
may occur, threatening ocular function. Pregnancy and labour may precipitate deterioration. Signs and
symptoms can mimic cerebral venous thrombosis (CVT). Exclusion of this diagnosis must be made in
BIH patients with worsening headache or neurological signs.
Investigation
CT brain and orbit will demonstrate small ventricles. MR venogram is needed to exclude CVT.
Visual fields need charting. CSF pressure monitoring is required (LP or parenchymal pressure
monitor).
Treatment
Neurology/neurosurgery input is essential.
Therapeutic lumbar puncture can treat acute crises.
BIH is occasionally treated with lumboperitoneal shunt.
Labour and delivery have been successfully performed with epidural analgesia, lumbar
puncture/sub-arachnoid anaesthesia. Specialist neurosurgical advice should be sought
regarding anaesthetic management.
Combined ICP management and regional anaesthesia has been reported using a lumbar drain.
Chiari malformation
The (Arnold) Chiari (type 1) malformation (ACM) consists of descent of the cerebellar tonsils and
medulla through the foramen magnum (with or without syringomyelia). It has an incidence of ~0.7% in
females, being completely asymptomatic in many cases. Classical presentation is with headache and
neck pain, both worse on coughing and on neck extension. Issues of co-ordination, with nausea and
vomiting, may occur. In the presence of syringomyelia, the loss of function in the central cord region
can result in upper limb weakness and dissociative sensory loss with characteristic loss of pain
sensation.
Key points
Dural puncture in a symptomatic, untreated ACM may cause acute tonsillar descent and
coning.
CSFBrain:CSFspinal gradient is unlikely in the asymptomatic patient. Patients who have had
corrective surgery may still have abnormal CSF flow.
Surgical treatment is foramen magnum decompression, with the aim of improving CSF
drainage. The full benefits of surgery may not be achieved for 12 months following surgery.
Successful surgery results in lack of strain-related, or neck extension-related headache.
Syringomyelia is associated with sensitivity to non-depolarizing muscle relaxants and

hyperkalaemia with suxamethonium.
NAP3 did not identify any cases where neurological complications could have been attributed to
undiagnosed ACM Type 1 or 2 in either the obstetric or general population.
Neurovascular pathology
Cerebral aneurysm
Arising from the cerebral arterial vessels, when unruptured, these lesions are usually asymptomatic.
Large aneurysms may cause mass effect with headache and focal neurological signs. Aneurysms of the
posterior communicating artery may cause third nerve palsy. Large aneurysms of the basilar
termination may cause brain stem decompression.
Cerebral aneurysms that are at increased risk of rupture (characterized by size and shape) may
be treated electively.
Commonly held opinion is that neuraxial blockade may increase the gradient across the
aneurysm wall by dropping CSF pressure. However, experience within neurosurgery, where
intentional intrathecal lumbar drains are inserted for aneurysm surgery and CSF drainage is actively
performed at craniotomy, suggests that this does not increase the risk of rupture.
Literature suggests that normal vaginal delivery with shortened second stage may be preferable,
though evidence is lacking. The literature does not exist to give definitive advice regarding
uterotonics. Specialist neurosurgical advice should be taken regarding anaesthetic management.
Cerebral arterio-venous malformations (AVM)

Cerebral AVM may increase in size during pregnancy. Up-to-date evaluation of lesions is necessary
prior to forming an anaesthetic plan. Providing there is no mass effect, there is no evidence for
increased risk of complications with neuraxial anaesthesia.
Cavernomas
Cavernomas can occur in the brain or spinal cord in 1 in 600 persons, of which 50% will be
asymptomatic. Exclude lumbar spinal cavernomas prior to performing neuraxial anaesthesia in those
known to be affected.
Sub-arachnoid haemorrhage
This is defined as the presence of free blood within the sub-arachnoid space, mixed with CSF. The
blood may extend into the brain tissue (intracerebral haemorrhage (ICH)) and into the CSF ventricles
(IVH). Risk of aneurysmal SAH is increased during pregnancy, labour and delivery, but is not
increased by neuraxial anaesthesia.
Use of recreational drugs, e.g. cocaine, can result in both hypertension and vasculitis, both
predisposing to intracranial bleeding. SAH/IVH may be the first presentation of AVM; in the absence
of flow-related aneurysms, the risk of rebleeding is much lower than that of aneurysmal SAH.
Presentation (non-traumatic SAH)

Headache is classically accompanied by photophobia and vomiting. Immediate complications can be
those of hydrocephalus and seizure. Rebleeding in the acute phase is associated with poor outcome.
Alterations in cerebral perfusion may also occur between 221 days post primary bleed; these can be
severe, causing cerebral ischaemia. Non-cranial complications of SAH include cardiac ischaemia,
which may compromise cardiac function. Neurogenic pulmonary oedema may develop.
For differential diagnosis of headache see Chapter 25.
The diagnosis of aneurysmal SAH requires cerebral angiography, performed by CT, MR or
formal angiography.
Treatment involves nimodipine orally/IV for 21 days. Prevention of rebleeding can be achieved
by endovascular techniques or surgical clipping.
Cerebral venous thrombosis (CVT) commonly presents as insidious onset headache though may
cause thunderclap headache in approximately 10% of cases. Symptoms may progress to reduced level
of consciousness, seizures, lateralizing signs and papilloedema. The venous hypertension results in
hypoperfusion and can cause cerebral infarction that commonly undergoes haemorrhagic conversion.
Most CVTs (75%) occur post partum, and are linked with low CSF pressure states (e.g. PDPH).
Presentation during pregnancy shows an initial peak in the first trimester, possibly due to dehydration
resulting from hyperemesis, or related to undiagnosed thrombophilias.
Investigations
CT venogram/MR venogram (gold standard) are diagnostic but be aware, non-contrast CT head may
be negative.
Treatment requires anticoagulation, though haemorrhagic transformation may impact upon the
decision to start this.
Rare vascular conditions of brain and spinal cord, including conditions such as von Hippel
Lindau disease (VHL) and hereditary haemorrhagic telangiectasia (HHT), present the anaesthetist
with craniospinal concerns of mass effect and haemorrhage. Such lesions are seldom solitary.
Vascular lesions (haemangiomata, haemangioblastomata and arteriovenous malformations) of the
cord may result in abnormal venous drainage and increased diameter of the cord within the canal,
hence increasing the perceived risk of cord injury, haemorrhagic trauma to the lesion and increased
risk of venous bleeding. As vascular lesions may increase in size during pregnancy, a detailed up-to-
date evaluation of lumbar spinal anatomy is necessary to evaluate risk of epidural/sub-arachnoid
anaesthesia.
Head injury in the obstetric population

Patients with head injury requiring admission have better outcomes (from the head injury) if they are
treated in a specific neurosurgical centre, so transfer to a centre with co-located neurosurgery and
obstetrics should be considered. It had been thought that the progestogenic and oestrogenic state of
pregnancy would afford neuroprotection; however, a large retrospective review suggests that
outcome is similar to that of non-pregnant women.
Surgical management of traumatic brain injury may involve insertion of an ICP monitor, EVD,
evacuation of haematoma and decompressive craniectomy. Evidence is lacking to suggest that
modification of standard practice is required for management of head injury and neuroanaesthesia in
the pregnant patient.
The neuroanaesthetic principles aim to:
Avoid hypoxia.
Obtain an optimal cerebral blood volume and perfusion. Patients should be ventilated to a
normal PaCO2; this will depend upon the stage of pregnancy.
Optimize CPP (CPP = MAP (mean arterial pressure) ICP). Head up position and loose ET
ties reduce cerebral venous congestion (the CPP target is 6070 mmHg).
Minimize rises in ICP. In the absence of ICP monitoring, an estimate of >20 mmHg should be
assumed in the presence of a reduced level of consciousness. Mannitol is widely used in
neurosurgical practice; however, evidence on outcome is lacking. Doses of 0.52.0 g/kg can
acutely reduce ICP by both increasing CPP and also reducing brain water and hence brain
volume. Furosemide is also used, and appears safe in pregnancy and breastfeeding.
Avoid fluctuations in blood pressure. Preanaesthetic blood pressure can guide target
postinduction blood pressure. Control excess hypertension using magnesium sulfate infusion
rather than cerebral vasodilators, e.g. GTN. Avoid hypotension with its resultant reduced CPP
and increased CBV.
Avoid increasing cerebral metabolic rate (CMR).
Minimize the risk or duration of seizure activity as this will increase cerebral metabolic rate
(CMRO2), particularly post head injury.
Avoid and treat pyrexia.
Avoid hypo/hyperglycaemia.
Epilepsy
Epilepsy is a common neurological disorder characterized by recurrent seizures. Women with
epilepsy account for 0.30.7% of pregnancies in the developed world.
Epilepsy is the commonest cause of seizures during confinement; eclampsia, however, is the
most common precipitant for peripartum seizures. (Local anaesthetic toxicity, metabolic derangement,
amniotic fluid embolism (AFE) and space-occupying lesions must also be excluded.)
Most pregnancies are uneventful in women with epilepsy. However, there is evidence that
parturients taking antiepileptic drugs (AED) are more at risk of developing pre-eclampsia.
Of parturients with epilepsy, 15%37% will experience an increase in seizure frequency during
pregnancy or in the early puerperium. This increase in seizure frequency can perhaps be attributed to
poor treatment compliance, altered AED pharmacokinetics or sleep deprivation.
Of parturients with active epilepsy, 12% will have a tonic-clonic seizure during labour, and a
further 12% within 24 hours post partum. A more profound hypoxia is observed in generalized
tonic-clonic seizures during pregnancy as a result of the increased oxygen demand; this can adversely
impact on the fetus.
There is no evidence that simple focal, complex focal, absence and myoclonic seizures
adversely affect the pregnancy or developing fetus.
When managing AED during pregnancy, the risk of maternal and fetal harm from seizures needs
to be balanced against the risk of harm from AED. NICE 2012 guidelines recommend aiming for
seizure freedom before conception and during pregnancy (particularly for women with generalized
tonic-clonic seizures) by using the lowest effective dose of each AED, avoiding polytherapy where
possible. AED can cause fetal malformations and possible neurodevelopmental impairments. Studies
suggest that valproate is significantly more teratogenic than carbamazepine, and valproate when used
in combination (especially with lamotrigine) is particularly teratogenic.
Altered AED pharmacokinetics are observed in pregnancy: an increase in the clearance and a
decrease in the concentration of lamotrigine, phenytoin and to a lesser extent carbamazepine is
observed; the levels of levetiracetam and the active oxcarbazepine metabolite can also decrease.
Despite this, NICE do not recommend the routine monitoring of AED levels during pregnancy. If
seizures increase or are likely to increase, monitoring AED levels (particularly levels of lamotrigine
and phenytoin) may be useful when making dose adjustments.
Breastfeeding is encouraged in parturients with epilepsy; however, certain AEDs may be
transferred into breast milk in amounts that may be clinically important.
Epidural anaesthesia is a good analgesic option for labour in epileptics, avoiding opiate-
induced CNS depression. Slow establishment of the block limits the plasma concentrations of local
anaesthetic and reduces the risk of seizures. There are no contraindications to spinal anaesthesia or
general anaesthesia.
Migraine
Migraine is a chronic disorder characterized by recurrent moderate to severe headaches, often
unilateral and associated with autonomic nervous system symptoms. For diagnostic criteria refer to
The International Headache Society.
Approximately one-third of women of childbearing age suffer with migraines. New onset
migraines can occur in 1.316.5% pregnancies; these are more likely to occur in the first trimester
and be accompanied by aura.
Between 50 and 75% of migraineurs experience a reduction in the frequency of migraines or
complete cessation of symptoms, normally in their second and third trimesters. This is particularly the
case with parturients whose migraines are perimenstrual or pure menstrual. In such cases, as
pregnancy progresses, remaining migraines show a reduction in pain intensity.
If a migraineur experiences no reduction in frequency or severity by the end of the first trimester
then migraines are likely to continue throughout the peripartum period.
Approximately 8% of migraineurs will experience an increase in frequency and pain intensity of
migraines throughout pregnancy. This is more likely in those who suffer with aura. In general, those
who suffer with aura are less likely to experience an improvement of symptoms.
Postpartum headache occurs in 3040% of all parturients. An increased incidence of headache
immediately following birth and 3 weeks post partum has been observed. This is postulated to be
multifactorial: fatigue, anxiety, hormonal changes and iatrogenic causes at the time of delivery.
Of migraineurs who experience improvement in their symptoms during pregnancy, 50% will
have a recurrence of their normal migraine pattern shortly post partum.
Some studies have concluded that whilst breastfeeding, the stable oestrogen levels preventing
menstruation also offer some protection against migraine recurrence. Other studies have failed to
reproduce these findings. There is no evidence that breastfeeding increases the occurrence of
headaches in the postpartum period.
Some studies suggest that parity does not have an effect on migraine symptoms during pregnancy.
Other studies show that multiparous patients are more likely to have an increase in migraines at the
end of the third trimester and post delivery.
Women with migraine have been shown to have an increased risk of pre-eclampsia and
gestational hypertension in pregnancy. They may also have an increased risk of stroke and cerebral
vasoconstrictive syndrome.
There are no contraindications to any pharmacological or neuraxial analgesia options for
delivery; however, investigation of postpartum headache in migraineurs can be challenging and
complications of neuraxial blockade add to the differential diagnosis.
Multiple sclerosis (MS)

MS is an idiopathic inflammatory disease affecting the central nervous system leading to
demyelination in the brain and spinal cord. It affects more women compared to men and about 70% of
cases present between 20 and 40 years of age. In the UK it is estimated that 20,000 or more women of
childbearing age are affected.
MS typically follows a relapsing remitting course that can present with sensory or motor deficit
of varying severity. The PRIMS study (a large multicentre study of parturients suffering from MS)
demonstrated a significant decrease in the relapse rate during pregnancy with a rebound increase in
the first 3 months post partum.
The fetus, having both paternal and maternal antigens, induces a degree of immunosuppression in
pregnancy that is necessary for its survival. This is achieved by the upregulation of type 2 helper T
cells (Th-2), which encourages a humeral response, while inhibiting type 1 helper T cell (Th-1)
response. As MS is an autoimmune disease mediated by activation of Th-1 cells and proinflammatory
cytokines, these pregnancy-related changes lead to a decrease in MS disease activity.
A recent survey reported that within a 10-year period, 91% of anaesthetists have encountered
<10 cases of MS. Limited case exposure hinders data collection regarding optimal management.
Key anaesthetic issues based on recent available evidence include:
All patients should be reviewed in an antenatal anaesthetic clinic. Disease severity and extent
of pre-existing neurological deficit should be documented. Analgesic and anaesthetic options
for labour and operative intervention should be discussed.
Use of 0.1% bupivacaine with 2 g/mL fentanyl mixture for epidural labour analgesia is
deemed safe. Theoretically, epidural anaesthesia would expose the demyelinated nerves to
lower concentrations of local anaesthetic, although this effect might be negated by the use of
multiple top-ups.
Epidurals can be topped up with a higher concentration of local anaesthetic for an operative
intervention.
The majority of surveyed UK anaesthetists would offer regional anaesthesia, with spinal
anaesthesia being the preferred anaesthetic option, for elective or emergency caesarean
section. Combined spinal-epidural may also be considered on an individual case basis. This
could reduce the amount of local anaesthetic in the sub-arachnoid space.
Due to the upregulation of acetylcholine receptors, it is advisable to avoid succinylcholine, as

this can lead to hyperkalaemia and cardiac arrest.
Dosage of non-depolarizing blocking agents should be guided by neuromuscular function

monitoring. Maintenance of normothermia is also important.
Key points
When caring for parturients with co-existing neurosurgical pathology remember:
A multidisciplinary approach involving obstetricians, neurosurgeons and anaesthetists is

necessary. Neurology and endocrinology input may also be required. Timely antenatal
assessment and risk/benefit discussions are essential for ongoing care during pregnancy,
delivery and post partum.
Conditions can progress during pregnancy and decisions regarding care must be made upon
up-to-date evaluation and imaging.
Non-obstetric causes of headache or neurological deterioration must always be considered.
Acute neurological deterioration requires urgent attention and involvement of specialists.
Transfer of care to a centre with co-located neurosurgery and obstetric facilities may be
appropriate.
Further reading
Drake, E., Drake, M., Bird, J. and Russell, R. (2006). Obstetric regional blocks for women with
multiple sclerosis: a survey of UK experience. Int. J. Obstet. Anaesth., 15(2), 115123.
Griffiths, S. and Durbridge, J. A. (2011). Anaesthetic implications of neurological disease in

pregnancy. Contin. Educ. Anaesth. Crit. Care Pain., 11, 157.
Klein, A. and Loder, E. (2010). Postpartum headache. Int. J. Obstet. Anaesth., 19, 422430.
Kvisvik, E. V., Stovner, L. J., Helde, G., Bovim, G. and Linde, M. (2011). Headache and migraine
during pregnancy and puerperium: the MIGRA-study. Headache Pain, 12, 443451.
Lindsay, K. W. and Bone, I. (2004). Neurology and Neurosurgery, 4th edn. London: Churchill
Livingstone.
Matta, B., Menon, D. and Turner, J. (2000). Textbook of Neuroanaesthesia and Critical Care.
London: Greenwich Medical Media Ltd.
Nolan, J. and Soar, J. (2012). Anaesthesia for Emergency Care. Oxford: Oxford Speciality
Handbooks.
Vukusic, S., Hutchinson, M., Hours, M. et al. (2004). Pregnancy and multiple sclerosis (the PRIMS
study): clinical predictors of post-partum relapse. Brain, 127(6), 13531360.
Chapter 23
Immunology, including testing and management
of allergy during pregnancy

Gareth Kitchen, Tomaz Garcez and Nigel J. N. Harper
Introduction
This chapter focuses on allergic diseases and their relevance to obstetric anaesthesia, with practical
advice on management. Ideally, parturients with suspected allergic disease should be assessed prior
to pregnancy, in order to identify relevant allergens and to confirm a management plan. Parturients
with a history suggestive of adverse drug reaction require further investigation to identify the cause or
to exclude allergy. A previous perioperative or peripartum adverse event necessitates review of
those anaesthetic and medical records. If a patient has experienced a serious adverse reaction, their
notes should be clearly marked with drug allergy information and a hazard-warning bracelet advised.
Pregnancy presents other immunological challenges to the mother and semiallograft fetus. For the
pregnancy to succeed, local and systemic immunological changes are required, including reduction in
cytotoxic adaptive immunity and enhancement of regulation. The systemic impact of the
immunological changes is not clear, but there is an increased risk of atopic and autoimmune
dermatoses in pregnancy. There is no clear evidence to suggest that general atopic diseases are
affected.
Autoimmune diseases can have a significant impact on pregnancy, particularly when
autoantibodies directed against phospholipids, SS-A or SS-B are present. Antiphospholipid
syndrome is associated with increased risk of pregnancy morbidity and loss. The presence of
antibodies directed against SS-A and/or SS-B is associated with neonatal lupus and congenital heart
block. The effect of pregnancy on the course of autoimmune diseases is more variable, with both
improvement and deterioration reported without consistency.
Immunodeficiency syndromes may also present challenges in pregnancy. Patients with antibody
deficiency syndromes will have increased requirements of immunoglobulin replacement in the third
trimester of pregnancy due to active transplacental transfer of immunoglobulin G. Patients with
hereditary angioedema (HAE) may improve, remain stable or deteriorate during pregnancy and
should receive prophylactic treatment before any instrumental delivery or surgical procedure.
Increased vigilance through pregnancy and during delivery is therefore advised for most patients with
pre-existent immunologically mediated diseases.
Allergens relevant to anaesthesia

A perioperative allergic reaction is often attributed to drugs, chlorhexidine or latex exposure.
Taking a clinical history for drug allergy

Type I hypersensitivity (IgE-mediated) is often considered to be true allergy. See Table 23.1.
Table 23.1 Classification of hypersensitivity reactions
Type I Immediate Mediated by IgE, mast cells Allergic anaphylaxis

and basophils
Type II Cytotoxic IgG and IgM antibody ABO incompatibility, drug induced
mediated haemolysis and haemolytic disease of
the newborn
Type III Immune complex Immune complex mediated Rheumatoid arthritis and SLE
Type IV Delayed T-cell mediated Contact sensitivity
Many patients report allergy to medications: 10% of hospital inpatients self-report penicillin
allergy; 90% of patients self-reporting penicillin allergy are able to tolerate penicillin on challenge
without adverse reaction (see Box 23.1 and Figure 23.1). The most significant features are time
course from exposure to onset of symptoms and nature of the symptoms. In many cases, patients are
unable to recall an accurate history, making further assessment challenging. This approach can be
applied to other suspected drug allergies.
Box 23.1 History details required for a drug allergy history
1. Exact drug and route
2. Exact timing of reaction
a. From last dose
b. During course (after which dose)
3. Details of infection/symptoms at the time of exposure (what was the infection)
4. Features of the reaction
a. Itch
b. Rash
i. Flushing
ii. Urticaria
iii. Maculopapular
iv. Morbilliform
v. Bullous/AGEP
vi. Erythema multiforme/SJS/TEN
vii. Desquamation
viii. Mucosal involvement
ix. Fixed drug eruption
c. Angioedema
d. Wheeze
e. GI symptoms
f. Hypotension
g. Fever
h. Abnormal LFT
5. Other medications at the time
6. Treatment and response to treatment
7. Details of reactions on prior exposure to same drug(s)
8. Details of any subsequent exposure to same or similar drug(s).
Key:
AGEP = Acute generalized exanthematous pustulosis
EM = erythema multiforme
SJS = StevensJohnson syndrome
TEN = toxic epidermal necrolysis
LFT = liver function tests
Figure 23.1 Flowchart for management of patients with self-reported penicillin allergy.
Investigations for antibiotic allergy include the use of skin prick (SPT) and intradermal (IDT)
tests. If the skin tests are negative, graded challenge is required to exclude allergy. Allergen-specific
IgE is available for penicillin allergy, but is not sufficiently sensitive to exclude allergy. If either the
skin or blood tests are positive in the context of penicillin allergy, a challenge would not be
performed as the tests are considered to have high specificity. The reliability of skin testing for
non--lactam antibiotics is less well understood, but SPT and IDT are generally carried out prior to
challenge tests, which are the gold standard test for drug allergy.
Cross-sensitization within antibiotics

The most reliable data exists for penicillin-based (-lactam group) antibiotics and local antibiotic
guidelines should detail antibiotics that are considered safe in patients with documented penicillin
allergy. The risk of cross-reactivity or sensitization within the -lactam group varies. A positive skin
test reaction to penicillin infers a 2% risk of reacting on challenge to a cephalosporin and
approximately 1% risk to a carbapenem. The safest approach in confirmed penicillin allergy is to
avoid all -lactam antibiotics, as reactions, although infrequent, can include anaphylaxis.
If patients are selectively allergic to the amoxicillin or ampicillin (aminopenicillins) side chain,
rather than the -lactam ring structure, then cephalosporins with an identical side chain should be
avoided, but other -lactam antibiotics do not need to be avoided. The estimated risk of cross-
reactivity between aminopenicillins and cephalosporins with an identical side chain is around 24%,
but this is based on limited data from a single country. The safest approach in aminopenicillin allergy
is to avoid all -lactam antibiotics unless assessed in an allergy clinic specifically for cross-
reactivity.
Reliable data are not available on cross-reactivity for other antibiotic groups and therefore the
safest advice is to avoid all structurally similar antibiotics.
Reactions to neuromuscular blocking drugs

Anaphylaxis to neuromuscular blocking drugs may be allergic or non-allergic: the clinical features
may be indistinguishable. Mivacurium and atracurium commonly cause degranulation of mast cells.
Mast-cell degranulation in the skin produces the familiar cutaneous flush, but more widespread
degranulation of mast cells and basophils may result in life-threatening bronchospasm, hypotension
and angioedema. Cisatracurium, rocuronium and vecuronium are not characterized by non-allergic
anaphylaxis. Suxamethonium is the anaesthetic drug most likely to cause an allergic anaphylactic
reaction. When a patient reports a previous adverse reaction to suxamethonium, it is often unclear
whether the mechanism was anaphylaxis, a plasma cholinesterase deficiency causing suxamethonium
apnoea, or even malignant hyperthermia (MH). In addition to obtaining copies of the relevant
documentation, it is a relatively easy matter to exclude plasma cholinesterase deficiency with the
appropriate blood test. The majority of MH-susceptible families, in the UK, are known to the MH
Unit at St James Hospital, Leeds. If any uncertainty persists, the avoidance of trigger agents is
straightforward, and rocuronium should be used in preference to suxamethonium to facilitate tracheal
intubation. Sugammadex should be available in all obstetric units as a rescue drug in a cant intubate
cant ventilate (CICV) situation.
Cross-sensitivity between neuromuscular blocking agents (NMBA) is present in a high
proportion of patients who are diagnosed with NMBA-induced anaphylaxis. Contrary to common
belief, cross-sensitivity is not confined within classes of NMBA: for example, a patient who has
experienced allergic anaphylaxis to atracurium may be co-allergic to rocuronium or suxamethonium.
Consequently, a patient with known or suspected allergy to a specific muscle-relaxant drug must not
be exposed to any NMBA unless skin testing has confirmed a suitable alternative to which the patient
is unlikely to be allergic. In practice this necessitates skin prick testing (SPT) followed, if negative,
by intradermal testing (IDT). The sensitivity of IDT for NMBA is high. SPT is performed initially
because, although the sensitivity of the test may be less than IDT, SPT is less likely to induce a
significant reaction if the patient is allergic to the drug. There are no reliable blood tests for NMBA
allergy. The sensitivity of the blood test for specific antibodies to suxamethonium is relatively poor
and this test should not be used to exclude allergy because the consequences of a false-negative result
could be catastrophic. It must be emphasized that skin testing must be performed only in expert
centres with considerable experience of interpreting the results. Pregnancy is not an absolute
contraindication to skin testing, but the decision should be left to the expert centre. The decision
whether to perform skin testing will depend on the suspected allergen, the prior probability of
allergy, the sensitivity and specificity of the test, and the likelihood of a serious reaction occurring if
the patient becomes exposed to the allergen. Intubation of the trachea without muscle relaxants has not
been investigated in the pregnant patient, but avoiding NMBA is associated with a 52% higher
likelihood of difficult intubation in the non-parturient.
Reactions to analgesics
Reported allergy to opioid analgesia is common, which raises the question about management of pain
in labour. A careful, unhurried history of events is important. Nausea and vomiting alone is highly
unlikely to represent allergy. A localized itchy rash after the administration of IV morphine is
characteristic of harmless non-specific histamine release and is not suggestive of allergy. A sensation
of being acutely unwell after taking codeine is likely to be the consequence of ultra-fast metabolism to
morphine as a result of CYP2D6 gene duplication, seen in 1%7% of the population. Allergy to
fentanyl, alfentanil and remifentanil is vanishingly uncommon. There are recent reports of serious
adverse reactions to remifentanil during labour, but these are highly unlikely to be the result of
allergy. Skin tests are not useful for investigating suspected allergy to morphine, diamorphine,
pethidine or codeine because these drugs cause non-specific degranulation of mast cells in the skin. In
contrast, fentanyl, alfentanil and remifentanil are not associated with false-positive skin tests. A
blood test for specific-IgE to morphine is marketed, but its reliability is uncertain and it is not widely
available in UK immunology laboratories.
Gastrointestinal intolerance to NSAIDs is extremely common. They may also be responsible in
some individuals for non-IgE-mediated swelling, rash or bronchospasm. Skin testing is not useful in
making the diagnosis, but avoidance is not problematical. A graded challenge test may be the only
way to confirm the diagnosis, but should be delayed until after delivery.
Local anaesthetic (LA) allergy

Allergy to LA is a real entity, but is extremely uncommon. The issue of supposed LA allergy usually
arises because a patient has experienced unpleasant symptoms during dental treatment. Because LA
drugs are the mainstay of obstetric anaesthesia and analgesia, it is important to investigate these
suspected reactions to reassure the parturient. Exclusion of allergy on history alone is usually
possible; the sensation of palpitations, headache and a feeling of impending catastrophe is
characteristic of the systemic effects of vasoconstrictor agents used in dental surgery. Delayed
swelling after dental treatment often results from tissue oedema, but occasionally represents stress-
induced angioedema. The differential diagnosis includes latex allergy (see below). If allergy to LA
cannot be excluded by taking a careful history, the parturient should be referred to a specialist centre
for skin testing. The investigation pathway comprises SPT, IDT and sub-cutaneous challenge.
Delayed hypersensitivity to prilocaine is sometimes seen after local anaesthetic cream is used to
reduce the discomfort of venepuncture. This is not life-threatening and does not preclude the use of
spinal or epidural analgesia with bupivacaine.
Allergy to chlorhexidine
Anaphylaxis to chlorhexidine appears to be increasing. Features of anaphylaxis may be immediate or
delayed for up to 30 minutes following exposure. Individuals become sensitized by exposure to
chlorhexidine in daily life and subsequent exposure in a healthcare setting may cause a life-
threatening anaphylactic reaction. Severe anaphylaxis appears to be more likely when chlorhexidine
gains access to the circulation during interventional procedures, such as central venous cannulation,
cardiac catheterization, dental surgery and urethral catheterization. The MHRA issued a Medical
Devices Alert (MDA) in July 2012 relating to chlorhexidine-coated central venous lines and
haemodialysis catheters, and a second MDA in October 2012 relating to all medical devices and
medicinal products containing chlorhexidine.
Some patients previously experience symptoms suggestive of chlorhexidine allergy that goes
unrecognized. Increased awareness among healthcare professionals of chlorhexidine allergy might
highlight this possibility and allow the patient to be referred for allergy testing before the occurrence
of life-threatening allergy. Avoidance of chlorhexidine is a considerable undertaking, especially if an
obstetric patient is admitted as an emergency, and therefore efforts to diagnose chlorhexidine allergy
should be made as early as possible in pregnancy so that a management plan can be documented. The
currently available blood test for IgE antibodies specific to chlorhexidine has a relatively high
sensitivity and this should be the first step in the diagnostic pathway in the pregnant patient. If the
specific IgE test is negative, despite a strong clinical history, the patient should be referred to a
specialist allergy clinic so that the relative merits of skin testing can be discussed.
Latex allergy
All healthcare environments should have a documented protocol for managing patients who are
allergic to natural rubber latex (NRL). Allergy to latex is discussed in detail in the AAGBI
guidelines, Suspected Anaphylactic Reactions Associated with Anaesthesia , 2009. Anaphylaxis to
latex is decreasing, probably because non-latex gloves and other equipment are increasingly used in
healthcare. Type 1 latex allergy can usually be identified or excluded on history alone. If a patient can
blow-up a party balloon without experiencing itch or swelling, it is highly unlikely that they are
allergic to latex. If the history is suspicious of latex allergy, a blood test for latex-specific IgE should
be performed, but the sensitivity is less than 85%. If the blood test is positive the prevailing latex-
avoidance protocol should be invoked and the parturient should be offered referral to a specialist
allergy centre for further investigation post partum. If the history is strongly suggestive of latex allergy
and the blood test is negative, the parturient should still be offered referral to a specialist allergy
centre to discuss skin testing. Preparation of the delivery room and operating theatre for a patient who
is allergic to latex does not need to be an onerous undertaking if common sense is applied. All
obstetric units should have a list of equipment that contains latex. It is necessary to remove all latex
gloves and other latex-containing equipment from the room and a notice should be posted on the door.
It is not necessary to remove items of equipment that do not contain latex. Because modern hospital
rooms and operating theatres are equipped with forced ventilation, it is unnecessary to prepare the
room earlier than a couple of hours before admitting a latex-allergic patient. Allergy to latex is not
transmitted from mother to fetus, but the neonatal paediatric team should avoid using equipment that
contains latex if they are present in the same room as the mother.
Allergy to intravenous colloids

Intravenous gelatins are a significant cause of anaphylaxis, although often overlooked. Onset is
usually within minutes of starting an infusion. The reaction is usually IgE-mediated, but the sensitivity
of the blood test for gelatin-specific IgE is very poor; diagnosis requires skin prick testing or
intradermal testing. Intravenous starch solutions are no longer available in the UK.
Allergy to adhesive tape/dressings

Suspected allergy to adhesive dressings results from non-specific irritation of the skin or type 4
delayed hypersensitivity. Patch testing can be performed locally (it does not require special
expertise) with a selection of adhesive tapes and dressings. A positive test produces a raised,
reddened area.
Presentations that may not be allergy

Non-allergic drug reactions
Only a small proportion of drug reactions are allergic in origin. Type A, augmented, reactions are
responsible for the majority of the observed instances of hypotension during anaesthesia (see Table
23.2).
Table 23.2 Non-allergic drug reactions
Type A Augmented. An exaggerated, expected Type B Idiosyncratic. These are unexpected

pharmacodynamic response, for example and unrelated to the dose administered. Allergy
respiratory depression with opioids, or and anaphylaxis belong to this group.
bradycardia with remifentanil. These are
frequent, predictable and dose related.
Type C Continuing. Will occur in most patients Type D Delayed. The adverse effect can be
if the duration of treatment is long enough. seen a significant amount of time after the drug
has been stopped, for example carcinogenicity
and teratogenicity.
Urticaria: hives
Urticaria is a common medical problem affecting 20% of the population at some point in their lives.
Urticaria results from histamine release from mast cells. The majority of urticaria occurs during viral
infections in childhood, often leading to a presumptive diagnosis of antibiotic drug allergy as the
urticaria arises shortly after starting antibiotics for a viral infection. Only 20% of cases of urticaria
are caused by allergy, and in these cases the triggering agent is often obvious to the patient. Many
cases of urticaria remain of unknown cause and are termed idiopathic urticaria. A diagnosis of
chronic idiopathic urticaria is made if urticaria occurs on most days of the week for a 6-week period.
It is thought to be autoimmune in origin, although this theory has not been conclusively confirmed. Of
patients with chronic idiopathic urticaria, 40% also experience angioedema with episodes of
urticaria. Chronic idiopathic urticaria has a prevalence of around 1% and spontaneously remits in
most patients within 2 to 5 years. There are a number of recognized aggravating factors for idiopathic
urticaria including physical factors, alcohol, stress and histamine releasing medications. The physical
and emotional stresses involved in delivery (including instrumental or operative) will contribute to
an increased peripartum risk of an urticarial reaction. The use of various medications including those
known to release histamine from mast cells, such as atracurium, mivacurium, opiates, contrast,
gelatin-based intravenous fluids and non-steroidal anti-inflammatory drugs can increase the
likelihood of an urticarial eruption in susceptible patients. In parturients with a background history of
urticaria the risk of an eruption may be reduced by premedication with antihistamines prior to
exposure to an aggravating factor.
Angioedema: swellings
Angioedema most commonly occurs with urticaria as part of chronic idiopathic urticaria, but may
also occur without urticaria (idiopathic angioedema), as a side effect of angiotensin converting
enzyme inhibitors (ACEi) or due to hereditary or acquired angioedema (HAE or AAE). The
pathogenesis of idiopathic angioedema is not clear. ACEi-related angioedema occurs due to
interference with the kinin system and increased production of bradykinin. Bradykinin is a potent
vasodilatory mediator and excess causes localized oedema. The only intervention required for ACEi
angioedema is to stop the ACEi. HAE is a genetic condition where there is a deficiency of active
complement protein C1 esterase inhibitor, which results in increased levels of bradykinin. The
prevalence of HAE is estimated at 1 per 50,000. Patients with HAE should be managed in
conjunction with a clinical immunologist during pregnancy as their requirements for treatment
including prophylaxis prior to labour will need to be customized based on previous history. In the
case of emergency intervention, administration of C1 esterase inhibitor concentrate should be
provided as soon as possible. The dose of C1 esterase inhibitor concentrate prior to delivery is 500
to 1000 IU. In low-risk pregnancies, where it has been decided not to provide prophylaxis, C1
esterase inhibitor should be available in the delivery room. AAE is a very rare condition where
angioedema presents in the absence of urticaria, but often associated with B-cell malignancies or
autoimmune diseases. The prevalence of AAE is unknown but is far less than HAE (1 AAE patient
per 12 HAE patients in one large angioedema centre). Angioedema occurs secondary to bradykinin
accumulation in AAE, similar to HAE, and the treatment is the same.
Atopic illnesses during pregnancy

Rhinitis
See Chapter 16 for asthma.
Ideally patients with rhinitis should be assessed for allergy prior to pregnancy so appropriate
avoidance advice can be provided. Rhinitis severity can improve during pregnancy, however oedema
of the nasal mucosa can complicate pregnancy and this can worsen or cause rhinitis symptoms.
Rhinitis does not appear to have an adverse impact on the outcomes of pregnancy. Non-
pharmacological management of rhinitis includes saline nasal spray or irrigation, physical exercise,
mechanical airway dilatation with adhesive strips and elevation of the head end of the bed.
Pharmacological measures considered safe in pregnancy include nasal cromoglycate, nasal
corticosteroids and antihistamines. Nasal and systemic decongestants should be avoided if possible.
Immunotherapy for allergic rhinitis can be continued, but is normally not commenced during
pregnancy.
Food allergy is managed as per the non-pregnant population.
Exercise-induced anaphylaxis
Exercise-induced anaphylaxis (EIA) is a rare, but increasingly recognized syndrome of anaphylaxis
developing in the context of exercise. In some cases EIA occurs only if food has been consumed
within a few hours prior to exercise, and often only following specific food (such as wheat-dependent
EIA). The prevalence is largely unknown, but has been estimated at 0.03% in a Japanese adolescent
population. Management focuses on avoidance of known triggers, fasting prior to exercise and
identification of an exercise regimen that does not precipitate symptoms. Pharmacological therapy
includes the use of sodium cromoglycate and antihistamines, but there is limited evidence of
significant efficacy. There are reports of labour precipitating episodes of EIA and anecdotal reports
of early epidural leading to normal labour in parturients at risk. Measures to reduce stress during
labour theoretically should reduce the risk of EIA in susceptible individuals. Emergency facilities
should be available.
Testing for allergy in pregnancy

Testing for allergy involves taking a clinical history and performing allergy skin and/or blood tests. If
the skin and blood tests are negative a provocation challenge is offered as the gold standard test to
exclude allergy. Challenge testing is not required in all cases, but is useful to exclude allergy in cases
of suspected antibiotic allergy. Ideally a diagnosis of allergy should be made prior to pregnancy to
reduce risks and ensure avoidance advice is in place. Parturients are often worried about the risks of
allergy testing. There are no significant risks with allergy blood tests. Skin prick tests are also safe
with only very rare reports of systemic reactions. In most cases allergy skin testing can be delayed
until after delivery, but the parturient can be reassured that the tests are safe if they are required to
exclude latex or drug allergy. Intradermal skin testing and challenge testing potentially carry more
risk of inducing a severe reaction during the testing procedure; these forms of testing are not usually
undertaken in pregnancy unless there is a specific need, such as to exclude penicillin allergy to enable
treatment of syphilis.
Management of atopic presentations in pregnancy

Antihistamines in pregnancy
All drugs should be avoided in the first trimester of pregnancy if possible. Chlorphenamine and
hydroxyzine at standard dose have appropriate safety data during pregnancy and should be the
preferred first-line agents. If chlorphenamine or hydroxyzine are not tolerated due to adverse effects
loratadine or cetirizine are suitable alternatives, without any current evidence of teratogenesis, but
should be avoided in the first trimester if possible.
Management of patients undergoing desensitization

Desensitization (immunotherapy) therapy is used to modify the allergic response and is currently
offered in the UK for respiratory, venom, food and drug allergy. Food and drug desensitization is not
widely offered. Desensitization is not started during pregnancy except for the rare cases of syphilis
infection occurring in penicillin-allergic mothers. Patients already established on desensitization
when they become pregnant do not appear to be at increased risk of pregnancy-related morbidity,
despite continuing desensitization and are therefore advised to continue desensitization unless they
are not deriving any benefit or have experienced frequent systemic reactions during therapy.
Clinical features and management of anaphylaxis in

pregnancy and parturition
Anaphylaxis in pregnancy is rare but may be associated with disastrous consequences for mother and
fetus. The incidence of maternal anaphylaxis in the US appears to be approximately 2.7 per 100,000
deliveries. The most recent CMACE triennial report included a maternal death from anaphylaxis to
co-amoxiclav given intravenously for pyrexia in labour. There was no history of penicillin allergy
nor was there sub-standard care. The report highlighted the importance of immediate medical
response, administration of adrenaline and that anaphylaxis management charts should be immediately
available in all clinical areas. The UK Obstetric Surveillance System (UKOSS) 20122014 report
should provide further incidence data.
The cardinal clinical features of anaphylaxis in pregnancy are the same as in the non-pregnant
individual. However, several additional causes of maternal collapse in the third trimester may
complicate diagnosis (Chapter 25). Amniotic fluid embolism (AFE) may mimic anaphylaxis but the
pattern of clinical features usually enables the clinician to distinguish between them (Table 23.3).
Table 23.3 Distinguishing features of anaphylaxis and amniotic fluid embolism
Feature (frequency +) Anaphylaxis Amniotic Fluid Embolism
Suspected exposure to specific trigger +++

agent
Coagulopathy + ++++
Pulmonary oedema + +++
Rash ++ +
Bronchospasm ++ +
Right ventricular end-diastolic volume Low (reduced venous High (right heart failure)
(echocardiogram) return)
Raised mast cell tryptase +++ +
The management of anaphylaxis is described in the AAGBI Safety Guideline (2009) and the
Resuscitation Council Guideline (2008). Management algorithms differ depending on resuscitation
setting, with additional considerations in pregnancy. Despite the high success rate of maternal
resuscitation, there are several reports of hypoxic neurological damage occurring in the neonate as a
result of maternal anaphylaxis. Adrenaline remains the drug of choice for anaphylaxis treatment with
-adrenergic receptor activity and -adrenergic mast cell stabilizing effects. Limited data exists
concerning alternative vasopressor drugs in anaphylaxis, especially in pregnancy. Phenylephrine is
used commonly in UK practice to maintain blood pressure during neuraxial blockade. This drug is a
suitable vasopressor in anaphylaxis, but only as a second-line drug if the blood pressure fails to
respond to repeated doses of adrenaline. There have been several reports describing the efficacy of
vasopressin in intractable anaphylaxis, but there is no experience of this drug during pregnancy.
Factors determining the decision whether to proceed urgently to deliver the baby in maternal
collapse are discussed in Chapter 25 and the same general principles apply in maternal anaphylaxis
(see Tables 23.4 and 23.5).
Table 23.4 Immediate management of anaphylaxis
ABC approach
Remove potential causative agents if possible (e.g. IV colloids, chlorhexidine, latex)
Call for help, note the time
Maintain a patent airway, high-flow oxygen, intubate the trachea if necessary
If appropriate, immediate cardiopulmonary resuscitation according to ALS Guidelines
IM adrenaline 500 g (0.5 mL 1:1000), repeated if necessary. IV adrenaline if full vital-

signs monitoring available, initial dose 50 g (0.5 mL 1:10,000) repeated if necessary
Rapid IV crystalloid infusion
Displace the gravid uterus to the left (manual displacement or wedge)
Consider immediate delivery of the baby
Do not sit up the patient
Table 23.5 Secondary management of anaphylaxis
Chlorphenamine 10 mg IV (adult dose)
Hydrocortisone 200 mg IV (adult dose)
If the blood pressure does not recover despite an adrenaline infusion, consider IV
metaraminol, phenylephrine or noradrenaline
Treat persistent bronchospasm with a metered-dose inhaler or an IV infusion of salbutamol.

Consider IV aminophylline or magnesium sulfate
If the patient takes -receptor antagonist drugs, consider glucagon IV 15 mg followed by an

infusion at 515 g/min
Blood sample for coagulation profile and blood cross-match
Blood samples for mast cell tryptase (1 h, 2 h, baseline)
Arrange transfer of the patient to the obstetric operating theatre or critical care unit
Key points
1. Ideally parturients with suspected allergic disease should be assessed prior to pregnancy.
2. Although 10% of hospital inpatients self-report penicillin allergy, 90% of these patients are
able to tolerate penicillin on challenge with no adverse reactions.
3. Pregnancy is not an absolute contraindication to skin prick testing.
4. The decision whether to perform skin prick testing during pregnancy depends on the suspected
allergen, probability of allergy, sensitivity and specificity of the test, and the likelihood of a
serious reaction if the woman is exposed to the allergen.
5. Non-allergic drug reactions account for most drug reactions.
6. It is rare to commence desensitization therapy during pregnancy, but women already on a

programme may continue with no increase in pregnancy-related morbidity.
Further reading
Association of Anaesthetists of Great Britain and Ireland (2009). AAGBI Safety Guideline:
Suspected anaphylactic reactions associated with anaesthesia.
http://www.aagbi.org/sites/default/files/anaphylaxis_2009.pdf (accessed May 2015).
Bhole, M. V., Manson, A. L., Seneviratne, S. L. and Misbah, S. A. (2012). IgE-mediated allergy to
local anaesthetics: separating fact from perception: a UK perspective. Br. J. Anaesth. 1, 108,
903911.
Chaudhuri, K., Gonzales, J., Jesurun, C. A., Ambat, M. T. and Mandal-Chaudhuri, S. (2008).
Anaphylactic shock in pregnancy: a case study and review of the literature. Int. J. Obstet. Anesth., 17,
350357.
Gompels, M. M., Lock, R. J., Abinun, M. et al. (2005). C1 inhibitor deficiency: consensus document.
Clin. Exp. Immunol., 139(3), 379394. Erratum: 141: 189190.
Kar, S., Krishnan, A., Preetha, K. and Mohankar, A. (2012). A review of antihistamines used during
pregnancy. J. Pharmacol. Pharmacother., 3: 105108.
Lundstrm, L. H., Mller, A. M., Rosenstock, C. et al. and the Danish Anaesthesia Database (2009).
Avoidance of neuromuscular blocking agents may increase the risk of difficult tracheal intubation: a
cohort study of 103,812 consecutive adult patients recorded in the Danish Anaesthesia Database. Br.
J. Anaesth., 103, 283290.
Nakonechna, A., Dore, P., Dixon, T. et al. (2012). Immediate hypersensitivity to chlorhexidine is
increasingly recognised in the United Kingdom. Allergol. Immunopathol. (Madr.), 42, 4449.
OConnor, K. (2010). Labour complicated by a history of exercise induced anaphylaxis. BJA out of
the blue. http://bja.oxfordjournals.org/forum/topic/brjana_el%3B5485 (accessed May 2015).
Soar, J., Pumphrey, R., Cant, A. et al.; Working Group of the Resuscitation Council (UK). (2008).
Emergency treatment of anaphylactic reactions-Guidelines for healthcare providers. Resuscitation.,
77(2), 157169.
Srensen, M. K., Bretlau, C., Gtke, M. R., Srensen, A.M. and Rasmussen, L. S. (2012). Rapid
sequence induction and intubation with rocuronium-sugammadex compared with succinylcholine: a
randomized trial. Br. J. Anaesth., 108, 682689.
Chapter 24
HIV and infectious disease in pregnancy,
including herpes, syphilis and hepatitis

Jacqueline E. A. K. Bamfo, Matthew D. Phillips, M. Kingston, K. Chan and Ian Clegg
HIV
Introduction
Human immunodeficiency virus (HIV) is a retrovirus acquired by direct inoculation of infected
bodily fluids. This is most often during sexual intimacy, but may also result from contaminated
needles or iatrogenic interventions, such as blood transfusion or surgical procedures with
contaminated products. The infection is lifelong and if untreated significant morbidity and mortality
arise from HIV-associated infections and malignancies; this is termed the acquired immune deficiency
syndrome (AIDS). During infection, HIV enters cells presenting CD4 receptors, the most common
being the CD4+ T lymphocyte. Within the hosting cell, HIV replication, virion release and eventual
cell death occur. The main measurable and prognostic parameters widely used are quantification of
peripheral CD4 cells (the CD4 count), and the level of viraemia (HIV viral load). The likelihood of
AIDS-defining illness developing increases with progressive CD4+ cell depletion, which occurs
steadily over time from infection and more rapidly in individuals with a higher HIV viral load.
The advent of highly active antiretroviral therapy (HAART) in the late 1990s transformed the
management of HIV-positive patients, and the infection is now generally treatable with a good
prognosis, particularly when detected early. In addition to this, effective HAART together with
appropriate obstetric management, infant antiretroviral prophylaxis and avoidance of breastfeeding
has reduced rates of mother-to-child transmission (MTCT) of HIV significantly. Universal screening
for HIV in UK antenatal clinics from 1999 onwards, followed by appropriate management of mothers
and their babies, has resulted in MTCT rates falling from between 2030%, depending on maternal
viral load in the mid-1990s to less than 1% in 2010. Worldwide, of the 34 million people living with
HIV, 69% reside in sub-Saharan Africa, with other high-prevalence areas including Asia, the
Caribbean and Eastern Europe. Many HIV-positive parturients receiving their antenatal care in the
UK have acquired HIV whilst residing in one of the pandemic areas. The estimated UK prevalence in
2009 was 2.2 per 1000 women giving birth; most of these live in urban areas, with London having the
highest rates.
Effect of HIV on pregnancy

HIV infection itself does not cause sub-fertility, although HIV-positive women may have decreased
fertility due to associated conditions such as concurrent infections or illnesses, opiate use and low
weight. HAART itself, particularly protease inhibitors, has been associated with preterm delivery in
some studies, but not in others. Of all the available antiretroviral medications only zidovudine is
licensed for use in pregnancy. Current information from the Antiretroviral Pregnancy Register and the
National Study of HIV in Pregnancy and Childhood indicates that in women taking modern HAART,
there is no increased risk of congenital abnormalities. During pregnancy, several risk factors increase
the risk of MTCT (Table 24.1).
Table 24.1 Risk factors of mother-to-child transmission of HIV during pregnancy
Antenatal risk factors
High HIV RNA PCR (viral load)
Low CD4 lymphocyte count
Co-infection with sexually transmitted infections
Substance use (including cigarette smoking)
Maternal symptomatic HIV disease/AIDS
Intrapartum risk factors
Duration of membrane rupture
Mode of delivery
Obstetric interventions (e.g. fetal scalp monitoring, forceps, vacuum)
Premature delivery prior to 32 weeks of gestation
Chorioamnionitis
Postpartum
Breastfeeding
Effect of pregnancy on HIV

There is no evidence that being pregnant has a deleterious effect on HIV disease or increases the rate
of progression. Complications of antiretroviral medications such as for hepatitis can at times be
difficult to distinguish from pre-eclampsia and obstetric cholestasis. Pregnant women with HIV are at
increased risk of puerperal fever and postpartum complications after caesarean delivery.
Preconception
Couples contemplating a pregnancy where one or both partners are known to be HIV positive should
ideally discuss their plans with their HIV team and, if appropriate, obstetrician. This allows optimal
medical management of the HIV-positive partner. For the parturient, this would include a medication
review to minimize teratogenicity and fetal harm and commencement of prophylaxis required for
opportunistic infections.
Management of HIV in pregnancy
Screening and diagnosis

HIV testing should be offered and encouraged in all pregnancies at booking, and pathways should
exist to facilitate urgent referral of all women following a positive result to specialist HIV services
able to offer information, support and medical treatment. This includes addressing partner notification
and testing existing children, as appropriate.
Antenatal management
This should be by a multidisciplinary team (MDT) consisting of a consultant obstetrician, HIV
physician, specialist nurses and midwives, a paediatrician and, if needed, psychiatric or perinatal
mental health specialists and social services. Women with HIV should undergo the standard routine
first trimester screening tests and can have chorionic villus sampling or amniocentesis if clinically
indicated (only after HIV test results are known and when HIV viral load is suppressed on HAART)
(Table 24.2).
Table 24.2 Antenatal management of the HIV-positive parturient
First trimester
Standard booking tests
Specific tests for HIV-positive women
Hepatitis B (if HBV infection, quantitative HBV DNA, hepatitis A virus (HAV), HCV and
hepatitis delta virus (HDV), liver function tests)
Hepatitis C (if HCV infection, quantitative VL and genotype, liver function tests)
Serology for syphilis, toxoplasmosis, varicella zoster, measles
HIV resistance testing
Monitoring tests for HIV
Baseline CD4 cell count at booking
Frequency of checking CD4 count, plasma viral load and drug levels should be according to
recommendations of HIV physician
Pregnant women on HAART will require a viral load (VL) 24 weeks after commencing
HAART, at least once every trimester, at 36 weeks and at delivery
Full blood count, renal, bone and liver profile tests before starting HAART treatment and at
each antenatal visit
Vaccination of HIV-positive women for hepatitis B, pneumococcus and influenza
Second trimester
Second trimester anomaly scan at 18 + 0 to 20 + 6 weeks gestation
Offer quadruple test between 15 + 0 to 20 + 0 weeks gestation in women that have missed
combined screening test
Offer HIV screening at 28 weeks gestation if previously declined
Screen for genital tract infections at 28 weeks gestation
HIV disease monitoring with plasma viral load and drug toxicities should be performed
according to recommendations of HIV physician
Third trimester
A decision on mode of delivery should be made by 36 weeks gestation
A delivery care plan individualized to the woman should be issued and made available to
all healthcare professionals involved in her care. A copy should be carried by the patient
ECV should be offered to women with a VL <50 copies/mL and breech presentation at >36
weeks gestation in the absence of obstetric contraindications
Women with a plasma VL of <50 HIV RNA copies/mL at 36 weeks gestation and in the
absence of obstetric contraindications should be offered a planned vaginal delivery
Women with a plasma VL of 50399 HIV RNA copies/mL at 36 weeks gestation should be
offered a prelabour planned elective caesarean section at 38 weeks gestation
Delivery by prelabour planned elective caesarean section at 38 weeks gestation is

recommended for women taking zidovudine monotherapy, irrespective of plasma VL at the
time of delivery and for women with VL >400 HIV RNA copies/mL regardless of ART
Delivery by prelabour planned elective caesarean section for obstetric indications or

maternal request should be delayed until after 39 weeks gestation in women with VL <50
HIV RNA copies/mL to reduce the risk of transient tachypnoea of the newborn
Antenatal management aims to optimize maternal health and to prevent MTCT. ART is required
to prevent MTCT. If the parturient is not already taking ART prior to pregnancy then, as per national
guidelines, this should be initiated by week 24 gestation at the latest and earlier if the HIV viral load
is high. Parturients already established on effective HAART prior to pregnancy should continue
treatment with regular monitoring of HIV parameters.
The altered volume of distribution during the third trimester can result in the concentration of
protease inhibitors being reduced and a higher dose being required. Therapeutic drug-level
monitoring (TDM) may be helpful in determining an effective dose and close monitoring of the HIV
viral load is vital. Parturients with a CD4 count of less than 200 require prophylaxis against
opportunistic infections, including Pneumocystis jirovecii pneumonia. Additional prophylaxis is
dependent on the CD4 count and previous exposure to such opportunistic infections. If an antifolate
drug such as co-trimoxazole is used, then 5 mg folic acid should be co-administered.
Zidovudine monotherapy initiated between 20 and 28 weeks is an alternative to HAART and
may be considered for women who do not require HIV treatment for their own health, have a plasma
viral load of less than 10,000 copies/mL and are prepared to be delivered by elective caesarean
section.
Delivery planning
An intrapartum management plan should be formulated by the members of the MDT and the parturient,
ideally by 36 weeks gestation. If the HIV viral load is undetectable (<50 copies/L) and there are no
obstetric contraindications, a vaginal delivery can be planned. A previous caesarean section is not a
contraindication to this. HIV-positive women who are booking late for antenatal care, women with
poor adherence and detectable HIV viraemia or women diagnosed later in pregnancy, or even during
labour, pose particular challenges to the MDT. By using intensive HAART that produces dramatic
falls in HIV viral load, the risk of MTCT can be significantly reduced.
Intrapartum management
In parturients with detectable HIV viraemia, MTCT can be further reduced by administering
intravenous zidovudine either for 4 hours before beginning the caesarean section until the umbilical
cord has been clamped, or for those who elect for a vaginal delivery, during labour. Oral HAART
should be continued and can be intensified in certain situations, including premature rupture of
membranes or if a peripartum HIV diagnosis is made.
For parturients with an undetectable HIV viral load who plan to have a vaginal delivery,
artificial rupture of membrane (ARM) should be avoided unless absolutely necessary. ARM and
oxytocin may be considered for labour augmentation. Fetal scalp electrode or fetal blood sampling
are contraindicated. If instrumental delivery is needed, the instrument of choice is that which will
achieve a safe delivery with minimal maternal and fetal trauma. The most senior obstetrician present
should perform the procedure. An episiotomy should be avoided unless clinically indicated. Early
recourse to caesarean section should be considered if labour is not progressing satisfactorily.
If presenting with threatened or established preterm labour or prelabour rupture of membranes
(PROM), a genital infection screen should be performed and any infection treated. Maternal
corticosteroids should be administered to reduce the risk of respiratory distress of the newborn.
Multidisciplinary team advice (HIV physicians and paediatricians) is essential, particularly for
preterm gestations. In PROM after 34 weeks gestation, delivery should be expedited. In PROM
before 34 weeks gestation, oral erythromycin should be started and broad-spectrum intravenous
antibiotic cover should be considered. The presence of chorioamnionitis and fetal distress necessitate
immediate delivery.
Where diagnosis of HIV occurs during labour, urgent advice from HIV physicians is essential to
facilitate administration of antiretrovirals that produce rapid HIV suppression and that also cross the
placenta and effectively deliver prophylaxis to the fetus. Urgent liaison with neonatal colleagues is
required to ensure timely infant prophylaxis. Delivery should be by caesarean section, if appropriate,
with intravenous zidovudine, if possible.
Healthcare professionals should exercise universal precautions when caring for parturients with
HIV, including double gloving and protective eyewear.
Analgesia and anaesthesia

There may be significant drug interactions between analgesic and anaesthetic agents, notably
benzodiazepines, and antiretrovirals. This is particularly important when protease inhibitors are
being taken as part of the HAART regime, as ritonavir is almost always used as a pharmacological
booster due to its profound inhibiting effect on the CYP P450 liver enzyme system. The University of
Liverpool maintains a comprehensive reference website where interactions can be checked against
all antiretrovirals (http://www.hiv-druginteractions.org/, accessed May 2015).
The choice of anaesthesia for HIV-infected parturients should be based upon the usual obstetric
and anaesthetic considerations. Current evidence suggests that both regional and general anaesthesia
can be safely used. Neither has been found to be associated with worsening of maternal immune
status.
Regional anaesthesia has not been associated with infectious complications or neurologic
changes in the peripartum period. The parturients should be examined for pre-existing neurology prior
to performing neuraxial anaesthesia. HIV infection is not a contraindication to performing epidural
blood patch.
Post partum
Care of mother
Following delivery, cabergoline 1 mg once only is offered to suppress lactation. Measles, mumps and
rubella (MMR) and varicella zoster vaccines should be considered in those susceptible, although in
the very immunosuppressed with CD4 counts less than 200 the MMR should be deferred until after
immune reconstitution as it is a live vaccine. Appropriate contraception should be discussed by the
HIV team, as there are significant drug interactions with hormonal contraception and many
antiretrovirals. The mothers ongoing care will be based on her prepregnancy care or baseline HIV
parameters if she was diagnosed antenatally. Those women who started HAART solely for
prevention of MTCT will have the option to continue on HAART or to cease and continue regular
monitoring. Women who were on HAART prior to their pregnancy will continue as before. Patients
who had their HAART dosages increased in the third trimester, reduce to standard dosages two
weeks after delivery.
Genital herpes
Introduction
Genital herpes infection is caused by herpes simplex virus type 2 (HSV-2). This virus is widely
distributed throughout the population and is usually acquired through sexual contact. It causes painful
vesicular lesions on the skin or mucous membranes of the genital tract; however, women may also be
asymptomatic carriers. The primary infection with HSV-2 often causes a viraemia with symptoms
including fever and headache. More serious complications such as encephalitis, meningitis and
hepatitis can also occur.
Women with primary herpes, or active lesions, at the time of labour should be delivered by
caesarean section as this dramatically lowers the risk of vertical transmission to the baby through
vaginal delivery. Neonatal HSV infection may also occur by ascent of the organism after maternal
membrane rupture. The incidence of neonatal HSV infection is 1:6600 live births in the UK, the
majority being from maternal transmission, with few acquired postnatally. The sequelae of neonatal
HSV infection can be severe. It may appear initially as a cutaneous lesion, but visceral infection can
ensue, carrying a high mortality.
The primary anaesthetic concern is transmission of the virus to the central nervous system from
central neuraxial blockade. Several studies have looked retrospectively at the use of neuraxial
anaesthesia in patients with genital herpes. A summary of their findings is illustrated in Table 24.3.
Table 24.3 The use of neuraxial anaesthesia in patients with genital herpes.
Study author Number of % Active disease % Primary Neurological

patients (all had disease complications
neuraxial
anaesthesia)
Crosby et al. 93 65 0 0
Bader et al. 164 100 3 Transient

postoperative
weakness in one
patient with
primary disease
following spinal
anaesthesia
Ramanathan et al. 43 71 0 0
These results, although limited in number, suggest that it is considered safe to initiate neuraxial
anaesthesia/analgesia in patients with HSV recrudescence. However, the risk of viral translocation
following breech of the dura during a primary infection cannot be quantified. The patient is often
viraemic during the initial infection and spontaneous CNS infection, although rare, can occur. We
would therefore advise caution in performing neuraxial block in those with primary genital herpes.
Viral hepatitis
Hepatitis viruses A, B, C, D and E can cause viral hepatitis. Serology is required in order to confirm
diagnosis. Patients present with fever, nausea, abdominal pain and fatigue akin to flu-like illness
and jaundice may also be present. Thorough evaluation to determine the degree of hepatic impairment
should be undertaken. Blood tests, including full blood count, electrolytes, liver function tests and
prothrombin time should be taken. As with herpes, we would advise caution in performing neuraxial
anaesthesia in patients with viraemic symptoms. An additional precaution would be to ensure that
coagulation studies are within normal limits.
If general anaesthesia is required then drugs with minimal hepatic metabolism should be used.
Isoflurane has been shown to have minimal effect on hepatic circulation and is the agent of choice for
maintenance of anaesthesia.
Syphilis
Syphilis, caused by the organism Treponema pallidum, has increased in incidence 12-fold between
1997 and 2007. It is spread via both sexual contact and placental transfer, with four stages in the
disease process: primary, secondary, latent and tertiary. Antenatal syphilis causes significant risk of
fetal infection via placental transfer, which can occur at any time throughout pregnancy. Effects on the
fetus include preterm delivery, impaired growth and stillbirth. Anaesthetic management of these
patients is largely straightforward, including use of universal precautions, avoiding direct contact
with lesions and using techniques with a low potential for needle stick injury. General anaesthesia
has no specific considerations, with no additional risk to the syphilis patient. Likewise there is no
specific contraindication to regional anaesthesia; however, neurosyphilis may present atypically and
so a full neurological examination should be documented prior to regional blockade.
Key points
1. Antenatal screening for HIV became universal in the UK in 1999.
2. Preconception counselling and specialist antenatal care ensures optimal medical management
with medication review to minimize MTCT, teratogenicity and provide opportunistic infection
prophylaxis.
3. If HIV viral load is <50 copies/mL, vaginal delivery can be considered.
4. MTCT in parturients with detectable HIV viraemia can be decreased by administering 4 hours
of IV zidovudine prior to performing a caesarean section.
5. Both general and regional anaesthesia can be used in women with HIV infection.
6. Breastfeeding is not recommended owing to the risk of MTCT.

Further reading
Brown, Z. A., Wald, A., Morrow, R. A. et al. (2003). Effect of serological status and caesarean
delivery on transmission rates of herpes simplex virus from mother to infant. JAMA, 289, 203209.
Fiore, S., Newell, M. L. and Thorne, C. (2004). Higher rates of post-partum complications in HIV-
infected than in uninfected women irrespective of mode of delivery. AIDS, 18(6), 933938.
Gershon, R. Y. and Manning-Williams, D. (1997). Anesthesia and the HIV infected parturient: a
retrospective study. Int. J. Obstet. Anesth., 6(2), 7681.
Kourtis, A. P., Lee, F. K., Abrams, E. J., Jamieson, D. J. and Bulterys, M. (2006). Mother-to-child
transmission of HIV01: timing and implications for prevention. Lancet Infect. Disease., 6(11),
726732.
Read, J. S. and Newell, M. K. (2005). Efficacy and safety of cesarean delivery for prevention of
mother-to-child transmission of HIV-1. Cochrane Database Syst. Rev., 2005(4):CD005479.
Louzada, R. R., Taleco, T., Ricardo, A.S. et al. (2007). HIV and epidural blood patch: the state of the
art: 312. Reg. Anesth. Pain Med., 32(5 Suppl. 1), 85.
Royal College of Obstetricians and Gynaecologists (2010). Management of HIV in Pregnancy. Green-
top Guideline No. 39. London: RCOG Press.
Taylor, G. P., Clayden, P., Dhar, J. et al. (2012). British HIV Association guidelines for the
management of HIV infection in pregnant women 2012. HIV Med., 13(2), 87157.
Tom, D. J., Gulevich, S. J., Shapiro, H. M., Heaton, R. K. and Grant, I. (1992). Epidural blood patch
in the HIV-positive patient. Review of clinical experience. San Diego HIV Neurobehavioral
Research Center. Anesthesiology, 76(6), 943947.
Williams, I., Churchill, D., Anderson, J. et al. (2012). British HIV Association guidelines for the
treatment of HIV-1-positive adults with antiretroviral therapy 2012. HIV Med., 13(2), 185.
Section 5

Postpartum complications and obstetric

emergencies
Chapter 25
Maternal collapse, including massive obstetric
haemorrhage, amniotic fluid embolism and
cardiac arrest

Kate Grady and Tracey Johnston
Definition
Maternal collapse is defined as an acute event involving the cardiorespiratory systems and/or brain,
resulting in a reduced or absent conscious level (and potentially death), at any stage in pregnancy and
up to 6 weeks after delivery. Although collapse is often unpredicted, early warning scoring systems
can help to identify deterioration and prompt initiation of interventions that can prevent collapse.
Incidence
Accurate figures are not available as this data is not routinely collected, but the incidence of maternal
collapse is estimated to lie between 0.14 and 6/1000 pregnancies. As this is not a commonly
encountered scenario, it is essential that care-givers are skilled in effective initial resuscitation
techniques and investigation and diagnosis of the cause of the collapse, thus enabling appropriate,
directed continuing management. Due to lack of robust data, accurate survival rates following
maternal collapse are not available, but the near-miss to death ratios from two large severe
morbidity studies are 56:1 and 79:1.
The team
In addition to the standard members, the arrest team should also include a senior midwife, an
obstetrician and an obstetric anaesthetist. This ensures that skilled care-givers (who understand the
altered physiology of pregnancy and the impact of this on resuscitation) are able to implement
directed, cause-specific treatment and effect delivery if indicated. Units must ensure there is a robust
system in place for calling the appropriate team. The consultant obstetrician and consultant obstetric
anaesthetist should be alerted and asked to attend. If the collapsed woman is over 22 weeks
gestation, the neonatal team should be alerted and prepared if perimortem delivery is required. In
cases where resuscitation is successful, the critical care team should then be involved in the ongoing
management. Communication and clear definition of roles are essential during the resuscitation
process.
In general, roles are as follows:
Anaesthetist to manage the airway and breathing
Two care-givers to perform chest compressions (rotating every two minutes to avoid fatigue)
Two care-givers for the arms (one each), to insert a wide-bore cannula in each arm. One
care-giver takes the appropriate bloods, labels and sends the samples, and communicates with
laboratories. The other care-giver manages fluid and drug administration
Obstetrician or midwife to manage the uterus (tilt or manual displacement, perimortem CS,
management of postpartum haemorrhage)
One care-giver as scribe
One care-giver as runner to obtain any equipment not immediately available
Porter to take samples to the laboratories and collect blood products
Laboratory staff and the haematologist to be involved if haemorrhage persists.
If collapse occurs in a location without access to the full team e.g. a stand-alone midwifery unit or the
community, basic life support should be implemented and emergency transfer via 999 effected to the
nearest appropriate environment.
Management of maternal collapse

The physiological changes in pregnancy are covered in Chapter 1. The unique problems encountered
by the pregnant woman in a state of cardiorespiratory collapse are secondary to a number of
physiological and physical changes. The key to successful maternal resuscitation is early recognition,
appropriate skilled help and early recourse to emptying the uterus if CPR is initially unsuccessful.
Ongoing success is secondary to identification of the cause of collapse and directed treatment.
Cardiopulmonary resuscitation should follow the British Resuscitation Council approach of airway,
breathing, circulation, with specific adaptations for pregnancy (see Figure 25.1).
Tilt
After 20 weeks gestation, compression of the IVC and aorta by the gravid uterus must be
relieved immediately if resuscitation is to be successful. As the objective of relieving
aortic and IVC compression is to improve the efficacy of chest compressions in terms of
cardiac output, it is essential that the method used to achieve this does not compromise
chest compressions directly. The thorax must be in contact with a rigid surface to ensure
effective chest compression, thus improving cardiac output. This can be achieved either
by employing a left lateral tilt of 1530 on a rigid surface that extends from the
shoulders to the pelvis e.g. tilting theatre table or an appropriate wedge, or by manual
displacement of the uterus to the left whilst supine. If a cardiac output cannot be achieved
after 4 minutes of properly performed CPR, the uterus should be emptied to facilitate
maternal resuscitation (see Perimortem Caesarean Section below).
Airway
The pregnant airway is potentially complicated by the following: capillary engorgement

of the respiratory tract causing swelling of the oropharynx, larynx and trachea, laryngeal
oedema secondary to pre-eclampsia, breast hypertrophy and generalized weight gain
during pregnancy hindering access to the airway. Given the potential for difficult
intubation, careful preparation of airway equipment and a skilled anaesthetist and
assistant are required.
Nasopharyngeal airways are not recommended on account of the risk of bleeding.
Oesophageal sphincter relaxation secondary to progesterone significantly increases the

risk of aspiration, therefore early recourse to cuffed endotracheal intubation using
cricoid pressure is recommended. During bag and mask ventilation, the risk of aspiration
can be reduced by employing cricoid pressure and by performing gentle hand ventilation
to avoid insufflation of the stomach. An oropharyngeal airway can assist in reducing the
required inflation pressure.
Breathing
A reduction in functional residual capacity and an increased oxygen consumption (by up

to 60% at term) can rapidly result in hypoxia during hypoventilation. Irreversible
neurological damage can be sustained within 46 minutes of collapse. High-flow oxygen
should be administered as soon as possible.
Ventilation can be more difficult secondary to diaphragmatic splinting by the gravid

uterus and reduced chest wall compliance secondary to breast hypertrophy.
During CPR, the ratio of chest compressions to ventilation breaths is 30:2. Once
intubated, chest compressions are continuous and ventilation maintained at 10 breaths
per minute. In the case of respiratory arrest alone, maintain ventilation at 10 breaths per
minute.
Circulation
Chest compressions are to be delivered at a rate of 120 per minute. In a left lateral tilt
they are more difficult to perform and the resuscitator will tire more quickly, so it is
important to rotate the resuscitator performing chest compressions every two minutes.
Otherwise healthy mothers can lose up to 35% of their circulating blood volume before
becoming symptomatic. Those with pre-existing anaemia do not tolerate haemorrhage as
well, and clotting is less efficient if there is significant anaemia.
Mothers may compensate for hypovolaemia by reducing fetoplacental blood flow and
therefore maternal signs of hypovolaemia are subtle and late. If bleeding is concealed,
the significance of tachycardia secondary to hypovolaemia can be overlooked or
misinterpreted.
Maternal blood loss can be rapid and dramatic; large-bore venous access must be
secured, haemorrhage controlled and rapid restoration of circulating volume with oxygen
transporting red cells is paramount in order to minimize the risk of hypoxic injury. Fluid
replacement, in women with pre-eclampsia, needs careful consideration.
Drugs and defibrillation
There should be no alteration in the drugs used during resuscitation, or their dose.
Increased doses may be considered in the presence of severe vasodilatation
(hypotension) secondary to a dense spinal or epidural block.
There is no alteration to the defibrillation energy level. Defibrillator pads should be

applied one to the right of the sternum below the clavicle and one in the left mid axillary
line, avoiding breast tissue and placing the electrode vertically to maximize efficiency of
defibrillation. There is no evidence that shocks from a direct current defibrillator have
an adverse effect on the fetus. Fetal and uterine monitoring should be removed prior to
defibrillation.
Figure 25.1 Maternal collapse algorithm.
(Reproduced from Royal College of Obstetricians and Gynaecologists. Maternal Collapse in

Pregnancy and the Puerperium. Green-top Guideline No. 56. London: RCOG; 2011, with the
permission of the Royal College of Obstetricians and Gynaecologists.)
Perimortem caesarean section

As well-performed chest compressions in the non-pregnant situation can achieve only 30% of normal
cardiac output and aortocaval compression further reduces this efficiency to an estimated 10%, there
should be early recourse to emptying the uterus if CPR is unsuccessful. For this reason, from 20
weeks gestation, if there has been no response to appropriately performed CPR by 4 minutes, or if
resuscitation is continuing beyond this time (e.g. following transfer from the community), the uterus
should be emptied to improve the response to CPR. This should be carried out by 5 minutes. This is
done purely in maternal interests, whether the baby is alive or dead (do not waste time checking), but
a neonatologist should be present in a hospital setting for assessment and resuscitation of the baby
after viability (23 weeks onwards). No anaesthetic is required, and it should be performed where
resuscitation is taking place. A fixed blade scalpel should be available on the resuscitation trolley,
and the operator should perform the incision they are most comfortable with, although a classical
incision is marginally faster. In the absence of circulation, blood loss is minimal, but if circulation is
restored, transfer to the theatre environment and anaesthesia should be instigated. Haemorrhage can
be controlled in the short term if indicated by compressing the aorta against the spine with a fist just
above the bifurcation.
The most robust data available regarding maternal outcome following perimortem caesarean
section shows a survival rate of 65% if the cause of collapse is reversible, with survival rates being
improved if the procedure is carried out within 5 minutes of collapse. Neonatal survival is influenced
by rapid delivery, gestational age and delivery in the delivery suite environment or critical care.
The UK Obstetric Surveillance System (UKOSS) is currently studying outcomes following
maternal collapse and will give more current information for the UK.
Postcollapse processes
Accurate, full documentation is essential detailing events, decisions and interventions.
Debriefing must be carried out with the woman (if she survives), the family, and with the staff
involved, to ensure understanding of events, explain actions taken and to provide support for
those in need.
Incident reporting using the local system allows local data collection of frequency of such
events, and should trigger formal event reviews to ensure local and organizational learning,
and to enable feedback where care has been optimal.
All cases of maternal death must be reported to MBRRACE-UK as part of the ongoing
confidential enquiries into maternal deaths.
Causes of maternal collapse

Outside pregnancy, the 4Hs and 4Ts aide memoire of reversible causes is useful, and many have
modified this for the pregnant patient to THE reversible causes of maternal collapse, with the 4Hs
and 4Ts unchanged, and the E added for eclampsia (Chapter 14), including intracranial haemorrhage.
Haemorrhage and thromboembolism are the most common causes of collapse. See Figure 25.2 for
causes of maternal collapse.
Figure 25.2 Causes of maternal collapse.
(Reproduced from Royal College of Obstetricians and Gynaecologists. Maternal Collapse in
Pregnancy and the Puerperium. Green-top Guideline No. 56. London: RCOG; 2011, with the
permission of the Royal College of Obstetricians and Gynaecologists.)
Another useful mnemonic for causes of maternal collapse by Dr Joel Naftalin (Year 6 Specialist
Trainee in Obstetrics and Gynaecology, London Deanery) is SHE CAN DIE:
S
Sepsis
H
Haemorrhage
E
Embolism
C
Cardiac
A
Anaphylaxis
N
Non-pregnant causes (4 Hs and 4 Ts)
D
Drug toxicity
I
Intracranial haemorrhage
E
Eclampsia
Amniotic fluid embolism

Amniotic fluid embolism (AFE), also known as the anaphylactoid syndrome of pregnancy, was first
described in the 1940s after fetal material was found in the pulmonary circulation of women who had
died following maternal collapse in labour. It presents as acute maternal collapse during labour, birth
or the first 60 minutes after delivery. The incidence in the UK is around 2/100,000 maternities, and its
occurrence, in general, is unpredictable. Survival rates have improved significantly over the last 35
years, and are currently around 80%, but with a significant risk of hypoxic neurological damage in the
survivors. If AFE occurs prior to birth, perinatal mortality remains high at 135 per 1000 total births.
Risk factors include induction of labour, caesarean section, abruption, placenta praevia,
eclampsia, advanced maternal age and multiple pregnancy. Clinical features of AFE include sudden
anxiety and agitation, acute hypotension, dyspnoea, cyanosis, respiratory distress, acute hypoxia,
arrhythmias, seizures and cardiac arrest. If it occurs prior to delivery, acute fetal distress is seen. The
exact aetiology remains unclear, but it is thought that fetal material enters the maternal circulation and
is transported to the lungs. Pulmonary hypertension develops acutely, due to vascular occlusion
secondary to vasoconstriction caused by the release of various vasoactive substances, or debris
blocking the pulmonary microvasculature, along with acute right ventricular failure leading to a
marked reduction in cardiac output and acute hypoxia. This is followed by left ventricular dysfunction
or failure. If the mother survives, profound disseminated intravascular coagulation (DIC) occurs
rapidly, which often results in major postpartum haemorrhage. The pathophysiology of AFE has been
likened to anaphylaxis or sepsis, hence the name anaphylactoid syndrome of pregnancy. The diagnosis
is made clinically or at the time of autopsy, but is often a diagnosis of exclusion. Although various
other diagnostic tests are being researched, none have been shown to be clinically useful as yet. As
the diagnosis is often one of exclusion, other causes of collapse must be investigated and excluded. A
useful indicator is a coagulation screen, as if clotting is impaired in the absence of major
haemorrhage and replacement therapy, AFE is likely.
Management is supportive and input from senior staff, including an intensivist, is required.
Aggressive resuscitation is essential, with rapid oxygenation and early recourse to intubation and
ventilation. If AFE occurs antepartum, the baby and placenta should be delivered immediately.
Pharmacological support of the cardiovascular system is often required, and central monitoring of
cardiac output is useful to avoid fluid overload, as this will increase the risk of pulmonary oedema
and acute respiratory distress syndrome (ARDS). Arrhythmias are common, and should be treated as
standard. Major postpartum haemorrhage is likely if the mother survives the initial collapse, and is
secondary to DIC and uterine atony. Both should be treated aggressively (see below). Following
resuscitation, transfer to a critical care setting for ongoing management is indicated, with
multidisciplinary support.
Haemorrhage
This is the commonest cause of maternal collapse, and is responsible for up to 50% of the estimated
500,000 maternal deaths that occur worldwide each year, although in the UK deaths from obstetric
haemorrhage are uncommon (3.9/1,000,000 maternities). It is also the major cause of severe maternal
morbidity in almost all near miss audits, in both developed and developing countries. In many
cases, sub-standard care is identified as a contributing factor.
Haemorrhage can occur antepartum, intrapartum or postpartum, and it is well recognized that
visual blood loss estimation often underestimates actual losses. Major haemorrhage is defined as a
blood loss of greater than 1000 mL. The main causes of major antepartum/intrapartum haemorrhage
are placental abruption and placenta praevia.
Placental abruption
This occurs when part of the placenta separates from the uterus prior to delivery of the baby, with
resultant haemorrhage, which may be revealed, concealed behind the placenta, or a mixture of both
(thus blood loss is often greater than that seen). With large placental abruption, the uterus has a hard
wooden consistency. The diagnosis is a clinical one, as ultrasound is not a reliable method to
diagnose placental abruption. Significant placental abruption carries an increased risk of DIC, and
this should be screened for early. Bleeding can often go unrecognized or underestimated, and it
predisposes to postpartum haemorrhage secondary to atony +/ DIC.
Placenta praevia
This occurs when the placenta lies within the lower uterine segment and partially or completely
covers the internal cervical os. It is now routine practice to document the placental site on the mid-
trimester scan and a quick review of the scan report, if available, will often rule out placenta praevia.
In the absence of knowing the placental site, vaginal examination should not be performed until the
placental site has been identified by ultrasound, to avoid provoking further, potentially catastrophic
haemorrhage in cases of placenta praevia.
The causes of postpartum haemorrhage are easily remembered using the 4 Ts tone, tissue,
trauma and thrombin. Uterine atony accounts for over 70% of cases and can co-exist with the other
causes.
Management of major obstetric haemorrhage

Management should follow the initial resuscitation processes as above, ensuring that all
relevant personnel are involved, i.e. in addition to the arrest team, consultant obstetrician and
consultant anaesthetist asked to attend, laboratory staff informed specifically of major
obstetric haemorrhage, on-call haematologist informed, dedicated porter available to take
samples to laboratories and collect blood products, and dedicated scribe to record timings,
treatments and events. Maternal blood should be sent for FBC, coagulation screen, urea and
electrolytes and cross-match for four units.
If the fetus is not yet delivered and is still alive, delivery should be effected rapidly to enable
control of the bleeding and improve the chances of survival for the baby, but this should not
compromise maternal resuscitation.
If the fetus is dead, delivery should usually be effected vaginally following maternal
resuscitation and stabilization, but occasionally caesarean section will be indicated either as
part of the resuscitation process or to control and arrest haemorrhage rapidly in maternal
interests. This decision should be taken by the consultant obstetrician, in conjunction with the
consultant obstetric anaesthetist. In such cases, general anaesthesia would usually be
employed due to maternal cardiovascular instability and potential DIC.
In cases of postpartum haemorrhage secondary to atony, rubbing up a contraction and

emptying the bladder can be all that is required. In cases where these measures are
ineffective, bimanual compression of the uterus can be lifesaving, while resuscitation is taking
place and cause-specific treatment instigated. This is performed by placing a fist in the vagina
and acutely anteverting the uterus abdominally with the other hand and compressing the uterus
firmly between both hands. This has the dual effect of compressing the open vascular sinuses
in the placental bed, and reducing blood flow through the uterine arteries with the acute
anteversion.
Hypothermia should be avoided by actively warming the woman in order to improve the
function of endogenous and exogenous coagulation factors.
Volume replacement and replacement of oxygen-carrying capacity, i.e. red cells, is

paramount, whilst simultaneously addressing the underlying cause of bleeding. The objective
is to maintain the haemoglobin above 80 g/L, platelets above 75 109/L, APTT less than
1.5 mean control, PTT less than 1.5 mean control and fibrinogen above 1.0 g/L.
Fluid replacement
Commence resuscitation with crystalloids. Colloid can be considered.
Blood, in the form of red cell concentrate, should be rapidly infused. Ideally fully cross-
matched blood should be used. In the absence of this, group-specific blood should be given. In
an emergency, O Rhesus-negative blood can be used until group-specific or cross-matched
blood is available.
Platelets should be administered if the platelet count falls below 50 109/L.
In cases of major haemorrhage causing collapse, the risk of DIC is high and should be actively
prevented if possible. With ongoing haemorrhage, fresh frozen plasma should be given in a
ratio of 1:1 with red cells.
Cryoprecipitate should be given if the fibrinogen falls below 1 g/dL.
Cause-specific treatment
In cases of antepartum or intrapartum haemorrhage, delivery will often resolve the problem, but the
incidence of postpartum haemorrhage is increased and this should be addressed according to cause.
The four main causes of postpartum haemorrhage are uterine atony, retained tissue, genital tract
trauma and DIC. DIC can result from any of the other three if blood loss is sufficient, and both
retained tissue and uterine trauma can lead to atony, so a systematic assessment and exclusion of the
four causes is essential. Often atony can be diagnosed by abdominal palpation, and the act of rubbing
up a contraction can improve uterine tone. There should be a careful exploration of the genital tract
for trauma, which can be difficult if bleeding is heavy and this should be done in theatre. Any retained
tissue should be removed and trauma repaired. Rarer traumatic causes of haemorrhage that will not
be diagnosed by this approach include broad ligament haematoma, hepatic sub-capsular haemorrhage,
ruptured spleen and rupture of splenic artery aneurysm; thus if all other causes of bleeding have been
excluded, abdominal ultrasound, paracentesis or laparotomy may be required.
Management of atonic haemorrhage can be divided into first-line pharmacological management
and mechanical/surgical methods.
Pharmacological methods
Syntocinon this is synthetic oxytocin and is the drug of choice for active management of the
third stage of labour, and many women with postpartum haemorrhage will already have
received up to 10 IU following delivery. It acts within 12 minutes via oxytocin receptors in
the myometrium to cause myometrial contraction, but has a short half-life so does not provide
a sustained contraction. It also has antidiuretic hormone properties and in large doses can
cause water intoxication. In the case of uterine atony, 510 IU of syntocinon by IV injection
(diluted in 10 mL water for injection and given slowly to avoid the risk of profound
hypotension) is the first-line management. This can be repeated after 10 minutes.
Ergometrine this is a potent smooth muscle contractor causing myometrial contraction within
approximately 35 minutes. It has a longer half-life of up to 30 minutes, resulting in a more
sustained contraction of up to three hours. It also causes contraction of vascular smooth
muscle and can result in acute hypertension. It is contraindicated in parturients with
hypertension, cardiac disease, Raynauds disease, AV shunts and peripheral vascular disease.
Another common side effect is vomiting. The dose is 0.5 mg either IM or by slow IV
injection.
Syntometrine this is a premixed combination of 5 IU syntocinon for immediate effect and

0.5 mg of ergometrine for sustained action.
40/40 syntocinon a continuous infusion of syntocinon 40 IU in 36 mL of 0.9% normal saline

infused over 4 hours (10 mL/h) provides prolonged uterine contraction, without the risk of
fluid overload secondary to the antidiuretic effect of the syntocinon.
Carboprost (Hemabate) this is a synthetic prostaglandin F2 analogue which is an effective

uterotonic agent. The dose is 250 g given by IM injection, and repeated every 15 minutes to
a maximum of eight doses. It also acts on the bronchial smooth muscle and is contraindicated
in asthma. It must never be given IV, but can be given directly into the myometrium, ensuring
that it is not injected intravascularly, although it is not licensed for this route of
administration. In cases of hypotension and reduced peripheral perfusion, this method may be
more effective compared to peripheral IM injection (although be aware it may cause localized
myometrial contraction and ischaemia).
Misoprostol this is frequently used in the management of atonic haemorrhage, although the
evidence shows carboprost to be more effective, and systematic reviews have demonstrated
that the optimal route of administration or dose is not known. It can be given rectally in a dose
of 8001000 g. As it has not been demonstrated to have benefits over other more effective
uterotonics, its place in the developed world is limited, but as it is inexpensive, heat stable
and light stable, and does not require injection or infusion, it has been shown to be of benefit
in under-resourced countries.
Recombinant factor VII this is licensed for use in haemophiliacs and has proven to be an
effective haemostatic agent when used in the right conditions. It replaces a missing factor and
actively initiates and promotes coagulation. It binds to tissue factor and activates platelets,
activating factor II to thrombin and X to Xa, providing a local fibrin burst at the site of tissue
damage. Effects occur within around 30 minutes, providing the patient is not hypothermic or
acidotic at the time of administration. Successful effect is also dependent upon adequate
concentration and function of other clotting factors. The platelet count must be above
20 109/L and fibrinogen above 1 g/L before its use is considered. A recent Cochrane review
(2012) of 29 RCTs reported that the effectiveness of rFVIIa as a more general haemostatic
drug, either prophylactically or therapeutically, remains unproven. The results indicate
increased risk of arterial events in patients receiving rFVIIa. The use of rFVIIa outside its
current licensed indications should be restricted to clinical trials. For all these reasons a
consultant haematologist should be involved in the decision to use this agent.
Tranexamic acid 1 g oral or IV can be given three times daily to minimize bleeding. There
are trials currently underway looking at its role in major haemorrhage in both obstetrics and
trauma.
Mechanical/surgical methods
Balloon tamponade this is an established and effective, relatively non-invasive mechanical
method for controlling uterine haemorrhage. Different balloons have been used, the
commonest being Rusch or Bakri balloons. The balloon is inserted into the uterine cavity and
inflated with water on average about 300 mL. In cases where the cervix has been dilated, a
vaginal pack is often required to stop the balloon being expelled. This method has been shown
to be effective in almost 80% of cases, avoiding the need for hysterectomy. The balloon
should be left in for a minimum of 6 hours, and should be removed during the day when
facilities and staff are available should further bleeding occur.
Brace sutures If bimanual compression controls bleeding secondary to atony, then the
insertion of compression sutures to vertically compress the body of the uterus is often
successful.
Stepwise uterine devascularization if bleeding continues, then stepwise devascularization of
the uterus can be considered, starting with bilateral uterine artery ligation, bilateral ovarian
artery ligation and ultimately bilateral internal iliac ligation. Uterine artery ligation is more
successful for controlling haemorrhage from the upper rather than the lower segment. Ligation
of the internal iliac arteries can be technically challenging. It must be remembered that these
techniques will preclude the option of arterial embolization.
Arterial embolization selective arterial occlusion or embolization by interventional

radiology can prevent major blood loss, obviating the need for blood transfusion and
hysterectomy.
Hysterectomy in some cases, the only way to control life-threatening haemorrhage is to

perform hysterectomy. This should not be done too early, as it is associated with a significant
risk of increased transfusion, other organ damage, ITU admission and return to theatre, nor
should it be left too late. It is good practice to involve another consultant in the decision to
perform hysterectomy. Studies show that there is little difference in morbidity between total
and subtotal hysterectomy.
Cardiac disease
Cardiac disease was the most common overall cause of maternal death in the last CEMACH report,
being responsible for 48 maternal deaths. The majority of deaths secondary to cardiac causes occur in
women with no previous history. The main cardiac causes of death are myocardial infarction, aortic
dissection and cardiomyopathy. The incidence of primary cardiac arrest in pregnancy is much rarer at
around 1 in 30,000 maternities, and most cardiac events have preceding signs and symptoms. Aortic
root dissection can present in otherwise healthy women, and signs and symptoms such as central chest
or interscapular pain, a wide pulse pressure, mainly secondary to systolic hypertension, and a new
cardiac murmur must prompt referral to a cardiologist and appropriate imaging. The incidence of
congenital and rheumatic heart disease in pregnancy is increasing secondary to increased survival
rates owing to improved management of congenital heart disease, and increased immigration. These
cases should be managed by an appropriately skilled and experienced multidisciplinary team, usually
in regional centres. Other cardiac causes include dissection of the coronary artery, acute left
ventricular failure, infective endocarditis and pulmonary oedema. With the increasing incidence of
obesity, diabetes and advanced maternal age, acute myocardial infarction is also becoming more
prevalent.
Training
There is good evidence that training in obstetric emergencies improves outcomes. All team members
should undergo specific training in the adaptations and complexities of maternal cardiac arrest and
resuscitation, and nationally based courses are available. Local policies should be in place for annual
training for all staff, and it would appear that integrating clinical teaching with teamwork training in
small groups, with all members of the team training together is the best way. It must, however, be
remembered that delivery of teaching and training does not necessarily equate to learning and
acquisition of skills.
Key points
1. Altered physiology of pregnancy complicates resuscitation in the case of maternal collapse.
2. Senior anaesthetists and obstetricians should be present to guide management.
3. Relieving compression of the IVC and aorta in the supine position is essential for successful
resuscitation.
4. Maternal haemorrhage can be rapid. Maternal compensation for haemorrhage can give a
falsely reassuring blood pressure measurement that can delay diagnosis and management of
hypovolaemia.
5. Consideration of the neonate is required. Ensure a neonatal resuscitation team is present and,
where appropriate, consider early delivery of the neonate to aid both maternal and neonatal
resuscitation.
6. Teams caring for parturients should be trained in the adaptations and complexities of maternal
resuscitation.
Further reading
Centre for Maternal and Child Enquiries (CMACE). (2011). Saving mothers lives: reviewing
into Maternal Deaths in the United Kingdom. Br. J. Obstet. Gynaecol., 118 (1), 1203.
Knight, M. (2007). Peripartum hysterectomy in the UK; management and outcomes of the associated
haemorrhage. BJOG, 114(11), 13801387.
Knight, M., Tuffnell, D., Brocklehurst, P. et al. (2010). Incidence and risk factors for amniotic fluid
embolism. Obstet. Gynecol., 115(5), 910917.
Royal College of Obstetricians and Gynaecologists (2011). Antepartum Haemorrhage. Green Top
Guideline No. 63. London: RCOG Press.
Royal College of Obstetricians and Gynaecologists (2011). Maternal Collapse in Pregnancy and the
Puerperium. Green Top Guideline No. 56. London: RCOG Press.
Royal College of Obstetricians and Gynaecologists (2011). Prevention and Management of

Postpartum Haemorrhage. Green Top Guideline No. 52. London: RCOG Press.
Chapter 26
Postpartum complications, follow-up and
maternal satisfaction

Richard Wadsworth and Kailash Bhatia
Introduction
Over the last three decades, the use of regional anaesthesia has led to a significant decrease in
maternal morbidity and mortality. However, obstetric anaesthesia remains one of the leading causes
of litigation in anaesthesia in the UK. All anaesthetic techniques carry a risk of complication and
potential patient harm. Although complications cannot be entirely eliminated, risks can be reduced
with a combination of:
Appropriate training and supervision
Meticulous technique
Reliable follow-up with vigilance for complications
Sound multidisciplinary communication
Regular audit.
Post dural puncture headache (PDPH)

PDPH is one of the most common complications encountered following neuraxial anaesthesia in
obstetrics. A tear in the dura leads to leakage of cerebrospinal fluid (CSF), which results in reduction
in intracranial pressure and a downward traction on pain-sensitive intracranial structures, including
meninges, veins and cranial nerves. Following CSF loss, compensatory vasodilatation occurs, which
further exacerbates symptoms.
In parturients receiving epidural anaesthesia, the incidence of accidental dural puncture (ADP)
is between 0 and 2.6%. The incidence of PDPH varies: up to 80% of women will have a headache
after an ADP following a labour epidural with a 16G Tuohy needle, 05% following spinal
anaesthesia with a 25G Whitacre needle, whilst a tertiary unit reported an incidence of 0.5%
following 16,000 combined spinal epidurals (CSE).
In addition to the size and type of needle, the incidence of ADP is inversely proportional to the
experience of the person performing the procedure and directly proportional to the number of attempts
at needle insertion. In almost 30% of patients, ADP is not recognized at the time of epidural needle
placement, suggesting that the epidural catheter is responsible.
PDPH is classically described as an occipitofrontal headache, often radiating to the neck and
shoulders with postural features (exacerbated by sitting, standing, coughing and straining, and
alleviated by lying flat). A majority (90%) of patients will report symptoms within 72 hours post
puncture, although both immediate and later presentations have been described. Other features of
PDPH include: nausea, vomiting, neck stiffness, tinnitus and visual disturbances. Rarely, cranial
nerve palsies, convulsions or subdural haematomas have been reported as a result of PDPH. Criteria
for PDPH have been described by The International Classification of Headache Disorders (ICHD)
and are summarized in Table 26.1.
Table 26.1 Diagnostic criteria for PDPH as per ICHD
A Headache that
worsens within
15 min after sitting or
standing, and
improves within
15 min after lying,
with at least one of
the following, and
fulfilling criteria C
and D:
Neck stiffness
Tinnitus
Hyperacusia
Photophobia
Nausea
B Dural puncture has

been performed
C Headache develops
within 5 days after
dural puncture
D Headache resolves
spontaneously either:
Spontaneously
within 1 week
Within 48
hours after
effective
treatment of
CSF leak
(usually by
epidural
blood patch)
The parturient should be reassured, a full explanation given for the signs and symptoms
experienced, and a management plan should be agreed upon.
Initial management includes adequate hydration, simple analgesics including paracetamol and
non-steroidal anti-inflammatory drugs. The pharmacological management of PDPH has recently been
subjected to a Cochrane review, which concluded that caffeine (150300 mg 68 hourly) may
provide symptomatic relief and possibly reduce the need for further interventions. Gabapentin,
sumatriptan, ACTH and steroids have been suggested, but the evidence base for their use is weak.
Therapeutic epidural blood patch (EBP) forms the mainstay of management of PDPH. There is
limited evidence to support the use of prophylactic (before the development of headache) EBP. The
procedure involves injection of autologous blood into the epidural space in a theatre environment.
Contraindications include sepsis, coagulopathy and patient refusal. The risks of EBP include all the
risks associated with epidural, back pain, neck pain, fever, cranial nerve palsy and possible
worsening of headache. The timing of EBP is controversial, but good results have been obtained
when it is performed over 2448 hours after the development of symptoms.
To perform an EBP, a senior anaesthetist locates the epidural space using a loss of resistance
technique, while another anaesthetist takes 20 mL of blood from the patient. This is then slowly
injected into the epidural space.
Strict asepsis is mandatory. The interspace at or below the original puncture is recommended, as
injected blood has been shown to track upwards on MRI scans. The optimal blood volume for
injection is unknown, but general recommendations are 1520 mL. If the patient reports pain during
injection of blood then the procedure should be stopped.
The blood not only seals the dural leak site, but also increases the CSF pressure, leading to an
immediate relief of headache in up to 65% of cases. Parturients in whom the first EBP has failed may
be offered a repeat procedure, which has a 9095% success rate. Maintenance of a supine position
for 24 hours post procedure is recommended. Further follow-up initially via the telephone and later
at the anaesthesia clinic is recommended to confirm resolution of symptoms.
Failure of headache resolution 48 hours after blood patch should raise suspicion of acute
subdural bleeding and haematoma (ASDH), or other causes of postpartum headache (see Table 26.2).
Table 26.2 Differential diagnosis of postpartum headache:
Hypertensive disorders of pregnancy
Migraine
Tension-type headache
Stroke
Subdural haematoma
Subarachnoid haemorrhage
Venous sinus thrombosis
Posterior reversible encephalopathy syndrome
Benign intracranial hypertension
Space-occupying lesion
Others sinusitis, dehydration, drugs
Remain vigilant for any of the following:
1. Focal neurological symptoms
2. Change in mental status
3. Headache of unilateral nature not responding to normal pain killers
4. Sudden uncontrollable vomiting
5. Above symptoms with co-existing medical issues (e.g. bleeding disorder or

immunocompromise).
Presence of any of these signs necessitates neurological referral and consideration of further
investigation, including a computerized tomography (CT) scan/magnetic resonance imaging (MRI).
An obstetric patient with ASDH is best treated in a facility providing both neurosurgery and obstetric
care. ASDH may be treated conservatively; however, the presence of localizing signs or neurological
deterioration will require neurosurgical intervention.
Itching
The use of intrathecal opioids during neuraxial anaesthesia makes itching one of the most common
side effects observed at follow-up. Itching is more pronounced when opioid is administered
intrathecally compared with systemically. The incidence varies from 30100% with neuraxial
anaesthesia. The incidence is highest for intrathecal morphine and lowest with lipophilic drugs such
as fentanyl and sufentanil. The exact causal mechanism for itching is not absolutely clear but one
theory postulates the existence of an itch centre in the lower medulla, including the trigeminal
nucleus. Neuraxial opioids ( receptor and serotonin receptor mediated) seem to remove the
inhibitory effects of pruritis pathways leading to itching, especially along the face and upper thorax.
Less than 1% of patients request treatment for severe itching. Various regimes have been tried.
Propofol in sub-hypnotic doses, droperidol, ondansetron, nalbuphine and naloxone are some of the
common ones. The best results have been obtained with naloxone given sub-cutaneously (50150 g)
or via a low-dose infusion (0.40.6 mg/h), and by using nalbuphine and naltrexone, though higher
doses of these opioid antagonists result in a diminishing quality of analgesia.
Postoperative nausea and vomiting (PONV)

PONV is common in pregnancy; other factors during the peripartum period increase the risk. These
incude the use of neuraxial opioids, intraoperative hypotension associated with sympathetic blockade,
supplementation with systemic opioids, use of ergometrine, exteriorization of uterus (visceral pain),
and pain postoperatively are the chief factors responsible for this side effect. The incidence is higher
during caesarean delivery after spinal anaesthesia (2030%) as compared to general anaesthesia
(10%) with the incidence falling somewhere in between for epidurals. Intrathecal morphine has the
highest incidence of around 5060% compared to the more lipophilic agents like diamorphine (10
30%) and fentanyl (<10%). The incidence of PONV is higher when the dose of intrathecal opioid is
increased.
Several pharmacological and non-pharmacological strategies (oxygen, acupressure at P6 point,
intravenous fluids) have been investigated to prevent this side effect, with variable success.
Prophylactic 5-HT3 antagonists, cyclizine, scopolamine, droperidol, and dexamethasone or a
combination of them have been used and have the best evidence of reducing PONV. A review
emphasized the need to optimize intraoperative care by reducing hypotension with vasopressors,
aiming for adequate block height, giving appropriate doses of neuraxial opioids, minimizing surgical
stimuli and by judicious use of uterotonics. Prophylactic antiemetics should be reserved for high-risk
patients. A Cochrane review 2012 on the interventions for reducing nausea and vomiting during
caesarean section concluded that there was insufficient data to demonstrate any class of intervention
(5HT antagonist, dopamine antagonist, sedative) was superior to another. There were no significant
differences observed in the comparison of combined vs. single interventions.
Awareness
This refers to a state where patients can recall intraoperative events and is caused as a result of
inadequate general anaesthesia. This complication is known to cause significant dissatisfaction,
anxiety, sleep and behavioural disturbances, including post-traumatic stress disorder (PTSD) in a
parturient. The incidence in obstetrics is estimated at 1:2001:350. Factors contributing to this
include: the use of rapid sequence induction, use of thiopentone in inappropriately low doses, use of
muscle relaxants, the concern of exposing the fetus to anaesthetic agents, increased risk of difficult
intubation, obesity, short obstetric gap i.e. time from induction to start of surgery, the effect of
volatile agents on uterine tone, junior staff managing surgery out of hours. The results of the 5th
National Audit Project, Accidental Awareness during General Anaesthesia in UK and Ireland 2014,
made a number of recommendations for obstetric anaesthesia. Anaesthetists should be aware of the
increased risk of awareness in obstetric patients, particularly when undergoing caesarean section.
Appropriate doses of induction agents, nitrous oxide, volatile agents and opioids should be used. If
airway management proves difficult, plans should be in place regarding additional IV anaesthesia or
plans to allow return of consciousness. Failed regional anaesthesia progressing to general anaesthesia
in obstetric surgery is an additional risk factor for awareness.
It has been suggested that parturients having general anaesthesia be warned about this risk. A
minimum alveolar concentration (MAC) of at least 0.71 of volatile agent (monitored with a volatile
agent monitor) has been suggested as the minimum during GA for lower segment caesarean section
(LSCS). Assessing depth of anaesthesia during LSCS is difficult and none of the available monitors
have shown to be superior to monitoring simple vital signs like pulse blood pressure, sweating and
tears (PRST).
A senior anaesthetist should review any patient complaining of awareness. The events
surrounding the event, including the anaesthetic chart, should be reviewed. The patient should be
offered an apology and appropriate counselling and all the conversation and assessments documented
for future reference in case of legal action.
Respiratory depression (RD)

The use of neuraxial opioids in the obstetric anaesthesia setting makes this one of the most feared
complications after an operative intervention. The true incidence is not known though figures ranging
from 0.017% have been quoted in the literature. This large variation is due to the fact that there is
lack of agreement on the definition of the term respiratory depression. The risk is higher with
neuraxial morphine, which exhibits a biphasic response initially RD is caused by intravascular
absorption (3090 min) whilst late RD is caused by rostral spread in cerebrospinal fluid and slow
penetration into the brainstem. RD caused by lipophilic opioids (fentanyl, sufentanil (0.02% or less)
and diamorphine) is rare, though early onset RD has been reported in the literature. Risk factors in
obstetrics include morbid obesity, pre-eclamptics on magnesium sulfate and patients receiving
concomitant doses of opioids via other routes.
It is important that nursing staff monitor the respiratory rate, sedation score and oxygen
saturation, following neuraxial opioid administration for at least 1012 hours if diamorphine has been
used and to at least 24 hours if morphine is used to provide analgesia. Local protocols should exist in
each delivery unit to ensure a swift response to respiratory events noted by staff. These include
administration of naloxone as a bolus and/or an infusion, and if necessary by securing the airway to
prevent hypoxia and aspiration.
Neurological complications
Neurological complications during the peripartum period could be intrinsic to the process of labour
and delivery or could result from an extrinsic intervention such as a neuraxial anaesthetic. Those
resulting from regional anaesthesia are fortunately rare, though it is difficult to ascertain their exact
incidence. Studies from Sweden (over 250,000 obstetric neuraxial blocks) quote an incidence of
1:25,000 and from France quote an incidence of neuropathy of 1:10001:3000 for spinal and 1:5000
1:10,000 for epidural anaesthesia.
A meta-analysis (15 studies, 987,218 patients) reported a calculated rate of transient neurologic
(< 1 y) injury of 2.57/10,000. In the UK, a national audit project (NAP3 January 2009) by the Royal
College of Anaesthetists (RCOA) described an incidence of permanent nerve damage of between 0.2
(optimistically) and 1.2 (pessimistically) in 100,000 of the obstetric population, based on a study of
320,000 regional blocks. One study, looking for postpartum neurological symptoms from anaesthesia
and obstetric factors combined, found the incidence to be much higher almost 1 in 150 patients.
Intrinsic nerve damage

Intrinsic nerve damage (1% incidence) mainly presents as peripheral nerve lesions and is caused as a
result of obstetric and fetal reasons. Rarely the fetal head can compress blood vessels supplying the
trunk, conus medullaris or cauda equina.
Almost all major peripheral nerves of the lower limb can be damaged, with factors ranging from
exaggerated lumbar lordosis, maternal obesity, diabetes, fetal macrosomia, use of forceps, use of
retractors during LSCS and lithotomy position. For the anaesthetist, it is important to know the
functional anatomy to delineate the possible nerves implicated in injury. Lateral cutaneous nerve of
thigh or meralgia paraesthetica, femoral nerve palsy (affecting sensation on the anterior thigh, hip
flexion and knee reflex), obturator nerve palsy (affecting medial thigh and hip adduction) and the
common peroneal or the lumbosacral trunk injury (presenting as foot drop) are the most common
lesions. Fortunately most are neuropraxial in nature and will recover within a few months. Nerve
conduction studies will help in diagnosis and determine whether the lesion is central or peripheral.
Extrinsic nerve damage

This can be caused by a number of factors: traumatic, chemical, ischaemic, infective and others
(caused by CSF leakage and unknown factors):
Nerve root damage this is most likely caused by the needle/catheter whilst establishing a
neuraxial block in the parturient. Pain and/or paraesthesia are often experienced at the time of
instrumentation. The occurrence and site of pain whilst performing the block must always be
documented on the anaesthetic chart. It usually presents as hypoaesthesia or paraesthesia
along the relevant dermatome and very rarely with muscular weakness. Most recover within a
few weeks. The patient should be reassured and if symptoms persist or lead to mobility
issues, a neurological opinion should be sought. Damage to the conus medullaris has been
described following spinal and epidural anaesthesia, and could be caused by a block placed
at a relatively high level in the neuraxis or by abnormally low-lying conus. A lumbar disc
prolapse may cause nerve root damage, and this usually presents as back pain and sciatica
(see Chapter 17).
Chemical this can lead to aseptic meningitis or chronic adhesive arachnoiditis (CAA).
Previously, detergents, contaminants in epidurals, contrast agents and more recently 2%
chlorhexidine have been implicated in CAA, where incidence is not known. Rice et al. have
defined CAA after neuraxial block as: back pain, increasing with activity, leg pain, which
may be bilateral, neurological abnormality on examination, most commonly hyporeflexia and
MRI changes consistent with CAA (Table 26.3). Leg weakness, sphincter disturbances,
paraplegia and hydrocephalus have been described in case reports of CAA. Rarely, aseptic
meningitis has been described following neuraxial blockade, where patients present with
signs and symptoms of meningism, but no organism is isolated from CSF. Fortunately, it has a
self-limiting benign course.
Infective meningitis (Streptococcus viridans) and epidural abscess (Staphylococcus aureus)

have been described following neuraxial anaesthesia, but are fortunately rare in obstetrics.
The NAP3 audit revealed an incidence of epidural abscess of 1 in 300,000. The source of
infection could arise from the skin flora, vaginal flora or the airway of the anaesthetist. Strict
asepsis is mandatory for all procedures. Cases of suspected CNS infection necessitate a
senior anaesthetic review. MRI spine should be performed urgently to confirm epidural
abscess, antibiotics commenced and neurosurgical referral for emergency decompressive
laminectomy if necessary.
Ischaemic anterior spinal artery syndrome has been reported as a result of hypotension and
hypoperfusion of the spinal cord. Spinal/epidural haematoma has been reported in
coagulopathic patients and has a low incidence of 1 in 200,000. In the NAP3 audit no
vertebral canal haematomas were reported.
Others abducens and facial nerve palsy associated with intracranial hypotension have been
reported following ADP and EBP. Transient neurological symptoms (TNS), a benign self-
limiting condition, presents with moderate to severe lower limb pain with no neurological
deficit. It is most commonly attributed to spinal hyperbaric 5% lignocaine. Cauda equina
syndrome as a result of damage to sacral nerve roots (S24) either by needle trauma or due to
the use of spinal microcatheters using 5% lignocaine have been reported. This leads to a
bowel/bladder dysfunction with saddle anaesthesia and varying degrees of lower limb
weakness. Urgent MRI spine to exclude a haematoma or an abscess is mandatory, along with
neurological referral.
Pre-existing neurology should be documented prior to neuraxial anaesthesia. Document any

intraprocedural paraesthesia. Neurological issues raised during follow-up should prompt a full
clinical examination and senior input. Patients presenting with red flags (Table 26.4) should have
appropriate imaging and neurological/neurosurgical referral. Figure 26.1 is an example of a
diagnostic algorithm used in our institute.
Table 26.3 Magnetic resonance imaging criteria for diagnosis of adhesive arachnoiditis
1. Conglomerations of adherent nerve roots residing centrally within the thecal sac
2. Nerve roots adherent peripherally giving the impression of an empty sac
3. Soft tissue mass replacing the sub-arachnoid space
Table 26.4 Red flags on postpartum neurological examination
1. Persistent or progressive neurological deficit
2. Signs and symptoms of meningism
3. Bladder, bowel dysfunction
4. Saddle anaesthesia
5. Any bilateral signs
6. Back pain associated with fever
7. Any back pain in an immunocompromised patient
Figure 26.1 Neuropraxia algorithm.

(Courtesy of Adam Zermansky, Kirsty MacLennan, Peter Sandbach and Rachel Stoeter.)
Follow-up
Anaesthetic contact with the parturient may occur at any time during the antenatal or peripartum
period. Quality of care delivered at each point of contact is important. Patient safety, clinical
effectiveness and patient experience have been highlighted as some of the key attributes of quality.
Without appropriate follow-up of patients postoperatively, the quality of service provided cannot be
evaluated.
The Association of Anaesthetists of Great Britain and Ireland (AAGBI) and The Obstetric
Anaesthesia Association (OAA) in the UK recommend that all women who have received regional
analgesia, anaesthesia or general anaesthesia be reviewed following delivery. The review provides
feedback for the anaesthetic team. This helps to improve the service and maternal satisfaction based
on real patient feedback.
The main aims of follow up are to:
Identify issues regarding anaesthetic management
Determine any side effects of the anaesthetic intervention
Determine the quality of the postoperative care rendered to the parturient
Gauge maternal satisfaction.
Most UK hospitals use a postanaesthetic intervention follow-up questionnaire. An example is

highlighted in Figure 26.2. Follow up should focus on the quality of analgesia provided, any relevant
side effects and whether those could affect the patients daily routine (e.g. PDPH, sensory or motor
symptoms). A recent study by Nguyen et al. highlighted open questions about follow-up (e.g. how are
you feeling?) and specific questioning (do you have any pain at the moment?) might be necessary to
identify pain after surgical intervention. All women should feel able to offer constructive criticism
about the care they received as this can help guide service improvement. Concerns identified warrant
swift senior attention. Clear lines of communication should exist between anaesthetists, obstetricians,
midwifery staff, other specialities, e.g. neurology, and the parturient.
Follow-up Proforma (Please tick all that apply)

1) Anaesthetic Interventions
Single Shot Spinal Epidural CSE

Intrathecal Catheter Remifentanil Patient-Controlled Analgesia (PCA) for Labour
General Anaesthesia Transversus Abdominal Plane Block
2) Mode of Delivery
Vaginal Vaginal Instrumental
LSCS Grade of LSCS: 1 2 3 4
3) Quality of Pain Relief in Labour
In Labour Good Moderate Poor
During Delivery Good Moderate Poor
Problems Identified
1) Unilateral Block 2) Missed Segments 3) Re-sited
4) Intraoperative Discomfort
None Mild Moderate Severe
5) Postoperative Pain Relief Prescription
Paracetamol NSAIDS Oral Opioids (specify) PCA (specify)
6) Postoperative Pain
None Mild Moderate Severe
7) Side Effects
None Sore Throat Nausea Vomiting Itching
Headache
1) Post Dural Puncture Headache
2) Other
Neurological Issues
1) Sensory Symptoms
2) Motor Symptoms
3) Urinary Catheter > 24 hours
Others (e.g.: Myalgia/ Untoward Dreams etc.)
8) Critical Care Admission Required: Yes/No
9)Is anaesthetic follow-up in the clinic required: Yes /No (If yes please discuss with
consultant)
10) Maternal Satisfaction
Very satisfied Satisfied Dissatisfied
Figure 26.2 Suggested questionnaire for follow-up of patients
Most inpatient follow-ups occur 2436 hours after delivery. Telephonic follow-up may be
possible in those discharged early. Community midwives and general practitioners provide support
once the parturient has been discharged.
Parturients experiencing the anaesthetic complications in Table 26.5 should be seen in clinic 6
8 weeks following delivery. This enables explanation of events, time for questions and can lead to a
discussion about how care could be improved. This may help reduce litigation and improve service
delivery.
Table 26.5 Patients to follow up in clinic 68 weeks post-delivery
Pain during LSCS (the most common reason for litigation in the UK)
Traumatic delivery because of failed regional anaesthesia
PDPH EBP
Persistent neurological symptoms

Awareness or unpleasant dreams experienced by the patient
Any critical incident such as wrong drug/wrong route error
Maternal experience
Childbirth is one of the most significant events in a womans life. Maternity services strive to ensure
a positive overall experience irrespective of the mode of delivery.
Most developed nations now publish a survey about womens experience of all aspects of
childbirth, including postnatal care. Examples include, What Mothers Say, Delivered with Care and
Listening to Mothers from Canada, UK and USA. These surveys cover a wide range of information
pertaining to:
Socio-economic and demographic status
Social habits
Antenatal care
Antenatal and peripartum parturient information
Medical interventions
Postpartum health and care including length of stay in hospital
Partner involvement
Infant feeding
Community midwife involvement.
By analysis of regional variations, statistics of perinatal care and review of real-life experiences,
these surveys are able to make recommendations to improve education, quality of care and maternal
satisfaction.
Maternal experience has been assessed as overall maternal satisfaction after birth, which serves
as a marker of quality of care provided by the child birthing team. Salmon et al. introduced the
concept of birth experience as a multidimensional phenomenon defining emotional distress, physical
discomfort and fulfilment in the form of a 20-item, validated questionnaire using a Likert scale.
Studies looking into maternal experience and satisfaction using Salmons questionnaire have found
that women planning caesarean reported a more favourable birth experience than women planning
vaginal birth, due in part to low satisfaction associated with unplanned caesarean. The studies
concluded that maternal satisfaction with childbirth could be improved by efforts to reduce unplanned
caesarean, but also by support for maternal-choice caesarean, a theme that has recently been
supported by the National Institute of Clinical Excellence (NICE) in the UK.
Measuring satisfaction with respect to childbirth is complex as it is influenced by many factors.
A poor maternal or neonatal outcome can result in a negative experience, irrespective of standard of
care. Key factors identified in systematic reviews of maternal satisfaction with childbirth experience
included: personal expectations, sense of control, support from care-givers, quality of care-giver
patient relationship and involvement in decision-making. All other factors, including womans
demographics, childbirth preparation, pain and continuity of care seemed to be less important.
Most anaesthetists use visual analogue or numerical rating scales to measure maternal
satisfaction. Although simple, they are not very objective. Further, we still await a reasonable tool to
measure labour pain experience. Can anaesthetists influence maternal experience and satisfaction
during childbirth, despite the findings in most studies that absence of pain during childbirth does not
equate to satisfaction? The answer is a resounding Yes! Anaesthetists play a major role in many
aspects of maternal care in the peripartum period, including: maternal medicine, managing parturients
with morbid obesity, operative interventions (25% CS rate in UK), maternal high-dependency care on
delivery suite and responding to early warning scores in sick parturients.
For some women, analgesia and anaesthesia can have an enormous impact on maternal
satisfaction. Studies have shown that maternal experience is enhanced if adequate information is
provided about the anaesthetic options and if participation in decision-making is encouraged. For
labour analgesia, using low-dose local anaesthetic/opioid mixtures and mobile epidurals, which
decrease motor block and promote vaginal delivery, enhance a womans feeling of control in labour
and are perceived to encourage satisfaction.
Some of the main factors decreasing parturient satisfaction are:
Poor satisfaction with the anaesthetic procedure (commonly pain or nausea)
Delay in analgesia
Perceived poor co-ordination within healthcare teams
Maternal or neonatal complications.
Negative maternal experience should be explored to identify any deficiencies in care and guide
service improvements.
Key points
1. The risk of developing a PDPH is related to the experience of the operator, the number of
attempts, and the size and type of needle used.
2. When treating a PDPH, 65% of patients will experience immediate relief of headache after a
first EPB, 9095% after a second EBP.
3. Although itching is common following intrathecal opiates, <1% of patients require treatment.
4. Peripartum neurological complication can be caused by intrinsic nerve damage (most

common, due to obstetric causes) or extrinsic nerve damage (less common, including central
neuraxial blocks).
5. Postanaesthetic follow-up allows teams to evaluate and further develop their service.
Further reading
Balki, M. and Carvalho, J. C. (2005). Intraoperative nausea and vomiting during cesarean section
under regional anesthesia. Int. J. Obstet. Anesth., 14, 230241.
Carvalho, B. (2008). Respiratory depression after neuraxial opioids in the obstetric setting. Anesth.
Analg., 107(3), 956961.
Cook, T. M., Counsell, D. and Wildsmith, J. A. W. (2009). Major complications of central neuraxial
block: report on the Third National Audit of The Royal College of Anaesthetists. Br. J. Anaesth.,
102(2), 179190.
Klein, A. M. and Loder, E. (2010). Postpartum headache. Int. J. Obstet. Anesth., 19, 422430.
Paech, M. J., Scott, K. L., Clavisi, O., Chua, S. and McDonnell, N.; ANZCA Trials Group (2008). A
prospective study of awareness and recall associated with general anaesthesia for caesarean section.
Int. J. Obstet. Anesth., 17, 298303.
Robins, K. and Lyons, G. (2009). Intraoperative awareness during general anesthesia for caesarean
delivery. Anesth. Analg., 109, 886890.
Royal College of Anaesthetists and Association of Anaesthetists of Great Britain and Ireland (2014).
Accidental Awareness During General Anaesthesia in UK and Ireland, 5th National Audit Project.
London: RCOA.
Szarvas, S., Harmon, D. and Murphy, D. (2003). Neuraxial opioid-induced pruritus: a review. J.
Clin. Anesth., 15(3), 234239.
Turnbull, D. K. and Shepherd, D. B. (2003). Post dural puncture headache: pathogenesis, prevention
and treatment. Br. J. Anaesth., 91(5), 718729.
Van de Velde, M., Schepers, R., Berends, N., Vandermeersch, E. and De Buck, F. (2008). 10 years of
experience with accidental dural puncture and post dural puncture headache in a tertiary obstetric
anaesthesia department. Int. J. Obstet. Anesth., 17, 329335.
Section 6

Service organization
Chapter 27
Multidisciplinary teaching and training on the
delivery unit

Catherine Robinson and Cathy Armstrong
Introduction
In addition to the central role of training anaesthetic trainees in obstetric anaesthesia, working on the
delivery unit presents many opportunities for the anaesthetist to become involved in education of the
multidisciplinary team. Areas of education particularly pertinent to the skills and expertise of
anaesthetists are:
Training midwives and junior doctors in delivering critical care on the delivery unit and
recognition and management of the sick parturient
Skills/drills or simulation team training for emergencies on the delivery unit
Pain relief for childbirth education for midwives, including regional analgesia/anaesthesia.
One of the main challenges in education provision on the delivery unit is the ability to allocate
adequate time for staff, away from clinical duties, to attend training. It is known that when units are
busy and understaffed, staff are unable to take up scheduled teaching sessions. Anaesthetists should
help champion education needs at management level and also consider strategies to deliver education
in novel ways that can be accessed more flexibly, for example, with e-learning packages or video
podcasts of lectures.
Education on the sick parturient
Care of the sick parturient on the obstetric unit has been closely examined in recent years. Recurrent
themes in the triennial reports from the Centre for Maternal and Child Enquiries (CMACE) have
included:
Late recognition by midwifery and medical staff of the seriously unwell woman
Inadequate and infrequent performance of basic observations
Inappropriate or no action taken in women found to have abnormal observations.
Obstetric anaesthetists should be prominent in the education of midwives and junior doctors in the
recognition and management of the critically ill obstetric patient.
Midwives must be able to accurately measure and record observations, recognize when they are
abnormal and alert the appropriate staff. Many midwives now qualify after a direct-entry degree
course and often have had no prior general nursing exposure. While skilled in many areas of
parturient management, they often lack the experience of caring for sick medical or surgical patients,
and may have an incomplete understanding of the relevance of abnormal physiological observations.
The current undergraduate midwifery courses focus mainly on well women, with less emphasis on
sick patients or those with pre-existing medical conditions. Future curriculum development within
undergraduate midwifery training should aim to address this.
With the 2011 document: Providing equity of critical and maternity care for the critically ill
pregnant or recently pregnant woman (see Further reading), we now have national guidance on the
competencies required for midwifery and medical staff caring for critically ill obstetric patients.
Critically ill parturients should have the same standard of care, whether in a general critical care unit
or a maternity unit. Midwives and medical staff on the delivery unit must have the competencies
outlined in the Department of Health document Competencies for Recognising and Responding to
Acutely Ill Patients in Hospital.
These competencies are wide-ranging and require significant educational input. Courses on
acute illness recognition and management have been developed, which can help units achieve some of
these staff competencies, but to cover all of them requires a co-ordinated educational strategy. These
acute care competencies are not specific to obstetrics, so training on specific obstetric problems and
management of medical illness during pregnancy needs to be incorporated into the training provided.
There are also practical skills outlined in the document which may be best taught and assessed by in-
house hospital training (Table 27.1).
Table 27.1 Suggested minimum acute care practical skill competencies to be undertaken by midwives
(those in italics could be taught to a subgroup of maternal critical care trained midwives)
System Practical skill
Cardiovascular Can set up 3-lead ECG monitoring

Can perform a 12-lead ECG
Successfully completed arterial line competencies including: assisting with
insertion, checking components of arterial line system, checking for
complications, common causes of inaccuracy Taking out arterial lines
Successfully completed central venous line competencies including:
assisting with insertion, checking components of CVP line system, checking for
complications, common causes of inaccuracy. Taking out CVP lines
Respiratory Can set up and administer oxygen via: non-rebreathing mask, MC mask, nasal
cannulae
Can set up and administer nebulized medication
Can set up, check and use suction equipment including portable suction
Can perform peak flow monitoring (PEFR) and act on abnormality
Can set up, check and use equipment for administering humidified oxygen
Renal Can accurately complete fluid balance chart
Neurological Can complete basic neurological observations, including pupillary responses

and conscious level (AVPU or GCS), recognize and act on abnormality
Haematological Completed local blood administration competencies
Communication Gives structured handover of acutely unwell patient, including clear

communication of management plan
The training required for midwifery and medical staff caring for the acutely unwell parturient
can be provided with a combination of the following:
Courses on acute illness recognition and management

Maternal early warning score training
Life support training
Specific obstetric critical care training courses: formal courses available, some with
postgraduate qualification or in-house formal obstetric critical care training
Communication training
Obstetric emergencies training: skills/drills training, simulation training
Practical skills teaching (see Table 27.1).
All midwifery and junior medical staff need to be competent in the recognition and management of the
acutely unwell parturient, management of obstetric emergencies and life support in the pregnant
woman. A subset of midwives should be given further formal training in care of the critically ill
woman on the delivery unit, including competence in caring for women with invasive monitoring.
A designated group of clinicians (obstetric, anaesthetic, midwifery and critical care) need to
take on the role of facilitating this training and ensuring that the competencies are met. Ongoing audit
is essential to identify how many staff have achieved these competencies. The Department of Health
document states that there should be a board-level sponsor for the implementation of these
competencies. Support at senior management level is essential to facilitate the provision of time and
resources for the competencies to be achieved.
Obstetric early warning scores

A top 10 recommendation in the 20032005 CMACE report was to introduce a specific early
warning score system for obstetric patients, in order to aid detection of the patient who is becoming
unwell, and trigger the appropriate response.
Early warning scores (EWS) were introduced over 10 years ago in the non-obstetric setting. It is
known that physiological abnormalities are a marker for clinical deterioration. A track and trigger
early warning score system consists of periodic recording of a set of physiological variables, such as
heart rate, respiratory rate, blood pressure, temperature (track) with pre-defined criteria then
triggering an appropriate response, i.e. the right personnel attending within an agreed time frame.
Non-obstetric EWS are not appropriate for the obstetric population as the normal physiological
changes of pregnancy would result in inappropriate triggering. Scores must also be altered to detect
pathology specific to the parturient, such as pre-eclampsia.
There is potential for any woman to be at risk of physiological deterioration in the peripartum
period, this cannot always be predicted. Equity in Critical Care recommends that all women have
physiological observations done on admission. Following labour and delivery, observations should
be done a minimum of 12-hourly.
Over the last few years, many obstetric units across the UK have independently introduced
modified early warning scores for obstetric patients (MEOWS). This has unfortunately resulted in a
wide variety of charts being used throughout the country some using a colour-coded scheme and
others producing a numerical aggregate score that determines the response triggered. The
physiological variables included also vary: most systems track heart rate, respiratory rate, blood
pressure and temperature. Some also include urine output, oxygen saturations, pain score and
conscious level.
This lack of consistency in early warning systems between hospitals can cause confusion and is
a potential patient safety issue. Movement of staff between hospitals necessitates further education on
the new track and trigger system. This same problem occurred in the non-obstetric setting and resulted
in the development of a National Early Warning Score (NEWS), launched in 2012 (see Further
reading). This means training can be standardized and national education training tools set up the
NEWS e-learning package can be accessed for free.
Most obstetric early warning scores have not yet been validated, but Singh et al. have studied the
validity of the obstetric early warning score system recommended by CEMACH and found that the
system had good sensitivity and reasonable specificity for predicting morbidity in obstetric patients.
Agreement on a national obstetric early warning score would be welcomed. A standardized
training program similar to the NEWS on-line training package would equip staff with transferable
skills and avoid duplication of training if a healthcare professional moves hospital.
MEOWS training for midwives and medical staff needs to include:
How to accurately measure and document observations
Clinical relevance of abnormal physiological observations
How to calculate overall MEOWS score
Ability to trigger an appropriate response, including correct personnel contacted to review in

an appropriate time frame and changes to the frequency of observations if indicated
What to do if MEWS reassuring, but staff member still concerned about patient.
When teaching staff about the track and trigger system it must be emphasized that a full set of
observations must be completed to produce an accurate score and that once the patient has triggered
then a response must be activated.
Early warning scores may help in the early recognition of the sick obstetric patient, but we must
teach the midwives and junior medical staff not to be totally reliant on them. Early warning scores
shouldnt replace thinking about the whole clinical picture. Most pregnant women initially
compensate well physiologically so may have a falsely reassuring early warning score. Women with
any concerning symptoms or signs need full assessment, even if their early warning score is normal.
Multidisciplinary team training in maternity

Organization and delivery of multidisciplinary team training is an important part of curriculum design
when identifying and planning the training needs of a maternity service.
Obstetric emergencies require complex management in a time-constrained, often life-threatening
situation. There is significant pressure on the assembled team, necessitating effective clinical
management and efficient teamwork. The team can be large, consisting of midwives, obstetricians,
anaesthetists, paediatricians, theatre staff and support workers, all with an important role to play.
Traditional healthcare teaching occurs within individual disciplines. For example, obstetricians
attend training programmes separately from anaesthetists and midwives attend training programmes
away from doctors. In an urgent clinical situation all of these disciplines are expected to work
together, often performing multiple complex tasks. While intradisciplinary training is important to
allow individuals to develop expertise within their own field, it is widely agreed that a group of
individual experts does not automatically constitute an expert team.
Multidisciplinary training is nationally recognized as a risk management strategy. In the UK,
evidence of provision of multidisciplinary emergency skills drills is a criterion laid out in the
Clinical Negligence Scheme for Trusts (CNST) document for maternity services. The required
scenario topics are listed in Figure 27.1. Compliance with these standards will impact on the level of
indemnity cover offered to the Trust by the NHS Litigation Authority.
Cord prolapse
Shoulder dystocia
Vaginal breech
Antepartum and postpartum haemorrhage
Eclampsia
Figure 27.1 Clinical scenarios for emergency skills stipulated in CNST criteria
There are various recognized formats for multidisciplinary team training within maternity. These
include:
Workplace-based emergency skills drills on delivery suite
Formal simulation programmes either in-house or within a simulation centre setting.
Whatever the format, simulated multidisciplinary training provides an environment where learners
can make, detect and correct errors without adverse consequences.
Workplace-based emergency skills drills

Workplace-based emergency skills drills involve the organization of an emergency simulation
scenario within the delivery suite or maternity theatre setting. While the organizers, management and
selected clinical staff are informed prior to the exercise, other front-line staff should be unaware that
this is a simulated emergency until they attend.
This form of multidisciplinary team training has many advantages. In particular it can highlight
local logistical issues and potentially identify unexpected training needs. For example, it may
highlight that the defibrillator trolley is located too far from a particular delivery room, or that staff
were not aware of its location.
One major disadvantage, however, is that while these drills may test the logistics and protocols
of the organization as a whole it may not always be tailored towards the individual learner. The
simulation is often run while other clinical activities are taking place, and participants may feel that
their attention is being deflected from actual patient care, thereby devaluing the educational impact
for those learners. The organizers should therefore guarantee patient safety and optimize educational
impact by ensuring that these simulations are not run when the labour ward is busy. Conducting
comprehensive debrief sessions for participants and increasing familiarity by regular simulations will
also help to enhance the learner experience.
Formal multidisciplinary team training simulation programmes

Formal multidisciplinary simulation programmes are those run either in house within the hospital or
in a simulation centre that are not run alongside actual clinical work. They necessitate staff to be
released from their clinical duties for protected study time.
They require a faculty of trainers to run a pre-planned set of scenarios with clearly defined
learning objectives. These should include a mixture of clinical knowledge/skills and
communication/team behaviours. Time should be taken to ensure adequate introduction to the intended
learning objectives and course format. The main body of the course will comprise a selection of
structured simulation scenario cycles (see Figure 27.2 for suggested format). Some programmes will
include elements of didactic teaching to consolidate knowledge further. A wrap-up session to
highlight lessons learned is deemed to be useful.
Briefing
Roles are allocated (as much as possible, participants should perform in their normal roles,
to aid fidelity and relevance)
Facilitator gives some clinical details and sets scene for upcoming scenario
Any procedural queries are answered by facilitator
Scenario
Simulated scenario is commenced
One or more faculty members form part of the multidisciplinary team to ensure smooth
running of the scenario and allow some direction if necessary
Another faculty member operates the mannequin (it is useful to have a communication link
between the mannequin operator and any faculty members participating)
A separate faculty member observes and then facilitates the debrief (use of performance
assessment checklists/tools can be helpful)
Any candidates not participating may observe via cameras/one-way screen from a viewing
room or directly in situ
Debrief
Arguably the most important element which aims to complete the experiential learning
cycle
Faculty members facilitate inclusive debrief discussion encouraging comments from
participants and observers. Aim to identify learning points and desirable/undesirable
behaviours
Use of video debriefing can be a particularly effective demonstration tool.
Figure 27.2 Suggested format of simulation scenario cycle
The main advantage of this formal format over the workplace-based emergency skills drills is
the time taken to consolidate learning for the individual. There are no conflicting workload pressures
and several simulation cycles will be completed allowing repetition and consolidation of many of the
learning points.
An obvious disadvantage is the significant resources required, including expert faculty,
equipment and time away from the workplace.
Components required for successful simulation team training in obstetrics

Planning and implementation of any type of training programme within a healthcare institution is
challenging. Some of the components thought to be required for the success of an obstetric simulation
programme include the following.
Institutional backing
A simulation programme requires significant resources, not just in terms of money for equipment, but
also time. Organizers of emergency drills will require planning time and formal programmes will
require both faculty and participants to be given time away from their clinical duties to attend. It is
vital, therefore, to have enthusiastic support for the programme at both a departmental and Trust level.
Strong leadership
An enthusiastic leader of the program is vital to maintain momentum and keep the programme
continuously updated and relevant. Ideally, obstetric team training should be an ongoing process
rather than a once-only event.
Curriculum design
Outcome-based curriculum design is crucial and it is important to conduct a needs assessment within
your own organization to ensure the course is specifically tailored and fit for purpose. A close
relationship between the faculty and the clinical risk team can allow development of scenarios based
on actual problems experienced in the department and their subsequent solutions to produce highly
relevant local learning.
Setting: in-house versus simulation centre

An in-house programme does offer some obvious advantages in terms of cost, accessible location
for attendance by staff and perhaps more importantly, the ability to tailor the course to local needs.
The in-house course will utilize the equipment, protocols and general set-up that the participants
will be exposed to within their normal working environment, therefore bearing more relevance for
those attending.
The simulation centre setting offers different advantages, including expert simulator facilitators,
often better equipment and debriefing facilities (i.e. video feedback). The learning environment is
away from the workplace, so the staff are far less likely to be affected by workload pressures on the
delivery suite.
Many large healthcare institutions now have their own simulation centres on site.
Equipment
When considering communication/behavioural team training there is no educational benefit in the use
of complex high-fidelity mannequins over low-tech simple mannequins, so a successful team training
programme can be developed without necessarily needing to buy expensive equipment. The key is to
create psychologically realistic high fidelity scenarios. Patient actors and role-play can have an
excellent effect on the fidelity of the scenario. Fidelity can be further increased by the use of a
delivery room with all equipment set out in a familiar way.
High-fidelity mannequins do have a recognized role for some procedural skills within obstetric
simulation. For example, specialized mannequins can allow measurement of pressures applied during
delivery and can aid with training of shoulder dystocia and vaginal breech delivery techniques.
The key is to identify the main aims and objectives of the course during curriculum design,
therefore allowing planning of the equipment required.
Performance assessment tools

Development of tools to assess both clinical and teamwork performance within the scenario is
important, not necessarily just to provide standardized evaluation of performance, but also to
facilitate the feedback discussion in the debrief session and ensure that the intended outcomes are
discussed. These tools often comprise a checklist of desired actions and behaviours that can be used
by faculty members or course participants observing the scenario. Designing performance assessment
tools that are fit for purpose is a challenging task. Skills-based markers can be relatively easy to
highlight within scenario design (e.g. timely administration of magnesium in eclampsia). Desirable
team behaviours are harder to outline. Some suggestions are listed below:
Stating the emergency in specific terms
Management of critical tasks using closed-loop communication
Use of an SBAR style of communication
Reduced number of exits from the room
A leader with high global situational awareness.
It is widely agreed that simulation is a useful educational tool; however, in the literature there is little
robust evidence demonstrating the cost effectiveness and patient safety impact of multidisciplinary
simulation training in obstetrics. It is clear, however, that obstetric emergencies require a skilled and
functional multidisciplinary team. Provision of a controlled environment where team members can
make, detect and correct errors without adverse consequences remains very attractive. The popularity
and development of simulation team training initiatives in obstetrics is likely to continue whilst
awaiting quality research to guide content and design.
Education on pain relief for childbirth for midwives

Anaesthetists have traditionally been key in providing epidural training for midwives, but are also
ideally placed to provide education for all methods of pain relief for labour. Anaesthetic involvement
in this teaching is essential, as new techniques or drugs are introduced onto the labour ward that are
unfamiliar to non-anaesthetists, such as remifentanil patient-controlled analgesia (PCA).
The undergraduate midwifery syllabus does not specify how much time should be given to
learning about analgesia in labour and the time given to this important area of learning can vary
widely between university courses. By getting involved as anaesthetists in providing education for
midwives at the undergraduate level, we can introduce clinically important issues, such as
recognition and management of complications of opioids, epidurals and spinals, which will equip
them well when they qualify and start work on the delivery unit (see Table 27.2).
Table 27.2 Core topics for pain in childbirth education for midwives
Physiology of pain in labour
Non-pharmacological methods of analgesia including TENS transcutaneous electrical nerve

stimulation
Entonox
Opioid analgesia routes of administration: oral, intramuscular, intravenous (PCA systems

including remifentanil), intrathecal, epidural. Monitoring required. Side effects and their
management
Pain management after caesarean section
Regional analgesia (see Table 27.3)
Table 27.3 Recommended topics for midwife teaching on regional analgesia/anaesthesia
Anatomy of the epidural space, dura and intrathecal space
Basic pharmacology of local anaesthetics and opioids
Physiology of pain in labour nerve roots involved in labour pain
Differences between epidurals, spinals and combined spinal-epidurals
Beneficial effects of epidurals
Contraindications to epidurals
Side effects of epidurals
Major complications with epidurals: recognition and management
How to assist anaesthetist for epidural insertion: positioning, equipment
Monitoring the woman with an epidural, including assessment of epidural sensory level and degree
of motor block
How to give a bolus epidural top-up
Practical epidural pump competencies if using continuous epidural infusions/patient-controlled

epidural analgesia
Simple troubleshooting of epidural problems
Documentation
Midwife training on regional analgesia and anaesthesia

Management of epidural analgesia is a significant part of the modern midwifes workload. When the
midwife board agreed in 1970 that midwives could give epidural top-ups independently, it was under
the condition that they were properly instructed in the procedure. As anaesthetists we are ultimately
responsible for all women with ongoing regional anaesthesia in labour. It is vital, therefore, that we
provide robust training for our midwives on the management of women with epidurals or spinals.
National guidance on education for practitioners caring for patients with epidurals has come
from the National Patient Safety Agency (NPSA) Epidural Safety Alert ( 2007) and the OAA/AAGBI
(Obstetric Anaesthetists Association and the Association of Anaesthetists of Great Britain and
Ireland) Guidelines for Obstetric Anaesthetic Services (2013)(see Further reading). The NPSA
recommend that training for new staff should include theoretical and competency-based assessment;
there should also be a programme of continuing education, including regular updates. Both documents
emphasize the need for specific training on potential epidural complications. Although serious
complications with epidurals are rare, they are potentially life-threatening and demand prompt
recognition and effective early management.
In summary, the documents recommend:
Midwives must undergo formal training to an agreed standard in regional analgesia
Training should be competency-based
Anaesthetists need to be involved in midwife education on regional analgesia/anaesthesia
Midwives must be aware of potential epidural complications and their management
Midwives must be able to assess and document sensory block height
Midwives must undergo regular refresher training.

Also, the NPSA specifically recommends that if epidural bolus top-ups are being used, a second
practitioner independently confirms that the correct product and line connection have been selected
and prepared to reduce the risk of wrong route errors. We should ensure that our anaesthetic
trainees are also aware of this, as well as our midwives.
Key points
1. One of the main challenges facing education provision on delivery suite is the allocation of
adequate time for staff training.
2. Obstetric anaesthetists should be prominent in the education of midwives and junior doctors
in the recognition and management of the critically ill obstetric patient.
3. National guidance is available detailing competencies required for midwifery and medical
staff caring for critically ill obstetric patients.
4. Midwifery and medical staff should be trained in interpretation of MEOWS.
5. Multidisciplinary team training is nationally recognized as a risk-management strategy.
6. Anaesthetic involvement in analgesia and anaesthesia training for midwives is essential.
Further reading
Ayres-de-Campos, D., Deering, S. and Siassakos, D. (2011). Sustaining simulation training

programmes experience from maternity care. BJOG, 118, Suppl. 3: 2226.
Centre for Maternal and Child Enquiries (CMACE) (2011). Saving Mothers Lives: reviewing
into Maternal Deaths in the United Kingdom. BJOG, 118, Suppl. 1: 1203.
Department of Health (2008). Competencies for Recognising and Responding to Acutely Ill Patients
in Hospital.
http://webarchive.nationalarchives.gov.uk/+/www.dh.gov.uk/en/Consultations/Closedconsultations/DH
Eppich, W., Howard, V., Vozenilek, J. and Curran, I. (2011). Simulation-based team training in
healthcare. Simul. Healthcare, 6, Suppl. S14S19.
Maternal Critical Care Working Group (2011). Providing equity of critical and maternity care for the
critically ill pregnant or recently pregnant woman. http://www.rcoa.ac.uk/document-store/providing-
equity-of-critical-and-maternity-care-the-critically-ill-pregnant-or (accessed May 2015).
Merien, A. E. R., van de Ven, J., Mol, B. W., Houterman, S. and Oei, S. G. (2010). Multidisciplinary
team training in a simulation setting for acute obstetric emergencies: a systematic review. Obstet.
Gynecol., 115(5), 10211031.
National Patient Safety Agency (2007). Safety Alert 21: Safe practice with epidural injections and
infusions. http://www.nrls.npsa.nhs.uk/resources/?entryid45=59807 (accessed May 2015).
Obstetric Anaesthetists Association and the Association of Anaesthetists of Great Britain and Ireland
(2005). Guidelines for Obstetric Anaesthetic Services. London: OAA/AAGBI.
Royal College of Physicians (2012). National Early Warning Score (NEWS): Standardising the
assessment of acute illness severity in the NHS. Report of a working party. London: Royal College of
Physicians.
Singh, S., McGlennan, A. and England, A. (2012). A validation study of the CEMACH recommended
modified early obstetric warning system (MEOWS). Anaesthesia, 67(1), 1218.
Strachan, B. and Crofts, J. F. (2008). The SaFE study Simulation and Fire-drill Evaluation: Proof
of principle study of the effect of the individual and team drill on the ability of labour ward staff to
manage acute obstetric emergencies Study Report. London: Department of Health.
Chapter 28
Clinical governance and patient safety

Kate OBrien
Introduction: how clinical governance originated

The NHS was established in 1948 and there was no agenda for quality of care. In the early years of
the NHS most doctors rarely looked at their clinical practice or results. In the late 1960s hospital
activity analysis was introduced to provide better patient-based information.
In 1969 the Ely Hospital report was published; this was the first of the modern inquiries into
failure of care: this included cruelty to patients, threatening behaviour, indifference to complaints and
lack of care by the physician superintendent. Subsequently there have been more than 30 reports
highlighting the exact same failings.
The NHS had become a victim of its own success and it had to acknowledge that there had to be
clear financial bounds. The Griffiths report (1983), commissioned by the government, described a
lack of accountability for quality of care at the local level. This led to:
Appointment of managers to lead healthcare units
Medical staff involvement in the management teams
More flexibility in team structures
Introduction of clinical responsibility for quality of the service.
The first government white paper was published in 1997. The New NHS, Modern, Dependable was
the first document to directly address the issues of quality and effectiveness of clinical care and the
introduction of a national framework to drive improvements in NHS performance.
On the back of this paper two new organizations were commissioned:
National Institute for Clinical Excellence (NICE)
To assess treatments using up to date evidence
To provide high-quality national guidelines
The Commission for Health Improvement (CHI)
This body was set up to ensure that high standards of quality and safety for patients and
staff were established and maintained.
In 1998 a white paper was published A First Class Service: Quality in the New NHS. This was the
first paper to mention the concept of clinical governance. The rationale was to have a framework,
which would ensure that high standards of care are achieved. The paper also stated that:
Staff must undertake lifelong learning
Staff must maintain professional standards
The NHS needs to be more open and accountable to the public.
Scally and Donaldson (1998) commented on the fact that quality of care issues had become secondary
to fiscal and activity targets, subsequent to the Griffiths report. The white paper outlined, for the first
time in the NHS:
all health organizations will have a statutory duty to seek quality improvement through
clinical governance.
Clinical governance will provide:
a framework through which NHS organizations are accountable for continually improving the
quality of their services and safeguarding high standards of care by creating an environment in
which excellence in clinical care will flourish.
Clinical governance in the New NHS (1999) provided guidance on how to implement clinical
governance.
The Darzi Report (2009) aimed for high-quality care for all patients, with the emphasis on
moving from centrally set targets to local services focused on quality. This encompassed:
Improved information on clinical performance e.g. Dr Foster

Greater choice and control for patients
Strengthened incentives for providers
New assessment processes to focus on quality of care, patient safety and patient experience.
Background: why good clinical governance processes are

necessary
In the 30 years before The New NHS paper there had been a number of inquiries into the appalling
treatment by staff of patients in certain institutions.
The biggest reforms, however, were as a result of two inquiries; these have resulted in
significant changes to professional regulation and the clinical governance process.
1. The Royal Liverpool Childrens Inquiry (1999)
2. The Bristol Royal Infirmary Inquiry (2001).
The lessons from all these inquiries were strikingly similar:
Inadequate leadership
Systems and process failures
Poor communication
Disempowerment of staff and service users
Organizational or geographic isolation
Lack of internal and external transparency regarding the problems that exist
Ineffective complaints systems.
The Bristol Inquiry (1997) was one of the major catalysts for the introduction of clinical
governance:
An independent expert review (1995), looking at the excess deaths in under one-year-old infants
undergoing complex open-heart surgery, showed that one surgeon had mortality figures fourfold those
of his colleagues performing the same operation. There had been concerns raised by an anaesthetist
about the high death rates as early as 1991. Despite sharing his concerns with colleagues, a senior
medical officer at the hospital and the Department of Health, no action was taken by the Bristol
Healthcare Trust until April 1995.
With the changes implemented in the child cardiac surgery service in Bristol, following the
review in 1995, the mortality had fallen from:
29% (April 1991March 1995)
3% (April 1999March 2002).
The Mid Staffordshire NHS Foundation Trust Public Inquiry final report (2013) was published, and
the root causes were almost identical to all the previous inquiries; however, the report emphasized
poor clinical governance structures as one of the main factors.
Clinical governance in obstetric anaesthesia

The NHS Clinical Governance Support Team was established to support the implementation of
clinical governance.
Clinical effectiveness
This is the efficacy of an intervention and/or treatment provided to a population. The most reliable
evidence comes from large randomized control trials and systematic reviews.
NICE and national service frameworks were put in place to standardize healthcare provision.
For any treatment or intervention the recommendations will also include clinical and cost
effectiveness and efficacy.
Clinical guidelines should contain the best available evidence for the management of a particular
condition. Guidelines reduce variation in management, improve quality of care and are used to set
standards. In anaesthesia we have several professional bodies that provide guidance and standards of
care.
Clinical audit is central to effective clinical governance. The process consists of:
Identifying the problem
Setting criteria and standards, e.g. adherence to a guideline
Data collection
Comparing the performance against the criteria and standards

Implementing change to address deficiencies.
The GMC document Good Medical Practice is explicit in stating that all doctors have a duty to
participate in clinical audit.
An integrated care pathway (ICP) is multidisciplinary, locally agreed practice for a specific
patient group. Documentation is standardized and in one place, this assists team working and
communication.
One example is an ICP for enhanced recovery for elective caesarean section. The pathway starts
at the preoperative visit and finishes at discharge home. All the key stages in the process of an
elective caesarean section are explicitly stated in the multidisciplinary document. There may be
variances from the pathway and these must be documented.
It is essential that ICPs are evaluated and reviewed on a regular basis. This ensures the pathway
is based on the best evidence and is an easy tool to use. Often it is not until the ICP is used clinically
that the problems become apparent. Audit of the ICP should include the process, the content, agreed
targets and outcomes, and non-adherence (variance) to the pathway.
Risk management
Effective risk management is fundamental to governance in any organization. The risks may be at the
patient level or at an organizational level. Healthcare is a vast and complex organization, which will
never be free from error. Risk management is a way of assessing risk awareness, identification,
assessment, controls and assurance.
Risk awareness
This is the recognition of the likelihood of risks, hazards and situations that may result in patient
harm. Being risk aware can modify hazards by putting contingencies in place to mitigate the risk.
A successful patient safety culture is when there is a high awareness of safety issues at all levels
of the organization. There are barriers to developing this culture, and this is seen in the majority of the
national inquiries:
A blame culture
Failure to understand human factors:

Bystander apathy people are less likely to take responsibility if they assume that
someone else will do it
Fixation errors occur because the person is convinced that their first interpretation was
correct
Groupthink usually large groups, fixate on doing things one way; no other options are
explored, often to avoid confrontation and conflict.
Improving risk awareness should be part of the curriculum for all healthcare professionals, this
involves:
Types of patient safety incidents
Human error and human factors
How to report risks and incidents
Mechanisms for learning from error, e.g. root cause analysis
Safety briefings, e.g. WHO Safe Surgery Checklist.
Risk identification
This follows risk awareness in the risk management process. The definition of a patient safety
incident is Any incident which could have or did cause harm, loss or damage to a patient receiving
care in the NHS.
Clinical risks may be identified by many sources:
1. Incident reporting
a. System for submission of reports
b. Need clear indications on what to report; a list of triggers may be available
c. Ease of reporting
d. Confidential reporting
e. Centralized reporting with links to other services, e.g. complaints and claims
f. Needs to be a factual and objective account
g. Needs to be regarded as a positive action

Where there is a culture of incident reporting it helps to identify risk promptly and facilitates the
introduction of preventative measures.
Root cause analysis is a method of looking at the reasons why an incident happened. A
multidisciplinary team is tasked with investigating the incident and then produces an action plan to put
preventative strategies in place. Communicating the lessons learned is an essential part of the action
plan process.
2. Claims and complaints
This is an important source of feedback from our patients. Often with the complaints investigation
there are failings in:
Systems of care delivery
Patient pathways
Facilities
Individual practice
There is a specific timeframe for complaints and it is important that feedback to the patient is prompt.
3. Clinical audit
4. Morbidity and mortality meetings
5. Executive safety walk-rounds
6. Proactive risk assessment, e.g. high-risk injectable medicines
7. National reports and surveys, e.g. confidential enquiries into maternal deaths
8. Patient safety alerts, e.g. MHRA.
Risk assessment
This is the tool that is used to stratify any particular risk; this estimates the likelihood and the
consequence of the risk being realized (Table 28.1).
Table 28.1 Risk assessment tool
The process:
Proactive assessment
Undertaken to prevent a patient safety incident
For example, increasing numbers of deliveries in the unit. Rate of significant postpartum
haemorrhage 1%. The fluid warming devices available were old and inadequate to
manage the potential risk, put on the risk register (Consequence 5 Likelihood 3 = 15).
Two rapid infusors purchased within 6 weeks.
Reactive assessment (Table 28.2)
In response to an incident
Table 28.2 Reactive assessment
Risk control options

The main aim of risk management is to ensure effective controls are in place to mitigate established
risks. As stated before, risks are inevitable in any healthcare system and it is important to understand
that risks cannot be eliminated completely.
The controls put in place target both the elements of the risk and reduce the consequence to the
patient and organization. Measures used to implement controls include: policies, guidelines,
procedures, checks and human factors that are used by the organization. The residual risk must be
regularly monitored and reviewed.
Complaints
Approximately 140,000 are made to the NHS annually. Any complaint about an aspect of treatment or
care can be submitted by the patient or by someone else affected. This has to be within 12 months of
the clinical episode. The patient advice and liaison service (PALS) will often resolve the issue at the
time, if not then they will provide the information to make a formal complaint.
As a clinician, the best way to deal with dissatisfaction is to be honest and open about the
patients concerns. The vast majority of complaints involve poor communication.
Written complaints must be acknowledged within 3 working days, together with an offer to
discuss the matter. A response should be made within 6 months. Complaints should be part of the
agenda at each clinical governance meeting.
Clinical negligence claims

The NHS Litigation Authority (NHSLA) was established in 1995: its purpose was to manage clinical
negligence claims on behalf of the NHS in England.
The Clinical Negligence Scheme for Trusts (CNST) is administered by the NHSLA. The remit
of the organization was to provide indemnity to member trusts and their employees with respect to
clinical negligence claims.
The NHSLA provided a framework of risk management standards to reduce the likelihood of
patient safety incidents. The Maternity CNST standards were related to all aspects of obstetric care.
The assessment relied predominantly on guidelines and audit for each domain. The benefit of the
assessment, if passed, was a reduction in the Trust indemnity payment to the NHSLA. The NHSLA
website stated that assessments provided organizational information, but did not reflect quality of
care or patient outcomes.
From 1st April 2014, there will be no more assessments and no further updates to the standards
from the NHSLA. The standards will be devolved to clinical teams. The agenda will be focused on
patient care, quality and patient safety improvements to reduce harm and provide meaningful outcome
data.
Other aspects of clinical governance

Dashboards
Dashboards can be very useful to monitor changes over time, usually the data per month is collated
and added to the existing data.
The main datasets are:
Bookings, including date of first contact with a midwife
Delivery numbers and types of delivery
Where was the delivery
Caesarean section rate
Staffing levels: sickness is often a surrogate marker of a stressful working environment
Training and education attendance
Maternal morbidity, e.g. postpartum haemorrhage, eclampsia
Risk management: number of SUIs level 4 and 5
Neonatal transfers
Complaints
Infection: MRSA, Clostridium difficile
Teaching and training (Chapter 26)
Research effectiveness.
Patient safety
The protection of patients against harm that results from the efforts or lack of efforts of the
healthcare system.
Patient safety is central to clinical governance. About 10% of inpatients in NHS hospitals have
an adverse event, which impacts on their outcome, and 50% of these are preventable.
The Patient Safety First Campaign (2008):
Patient safety to be the highest priority
Make all avoidable death and harm unacceptable
Trust board leadership. The aim was to have executive accountability for certain strategic
priorities with regards to harm and deliver a patient safety culture.
The campaign was effective in that the patient safety agenda had a much higher profile.
Key points
1. Clinical governance and patient safety is the key to providing a sound basis for quality
improvement in all aspects of care.
2. Assessment of risk is a powerful tool to ensure patient safety. The Royal College of
Anaesthetists and Association of Anaesthetists publish evidence-based standards, which should
be used as evidence if there are resource shortfalls.
Further reading
Department of Health. (1997). The New NHS: Modern, Dependable. London: The Stationery Office.
Department of Health. (1998). A First Class Service Quality in the New NHS. Consultation
Document.
Department of Health (2008). High Quality Care for All: NHS Next Stage Review Final Report:
(Cm7432). London: The Stationery Office.
Francis Inquiry Report (2013). www.midstaffspublicinquiry.com/report
Haynes, A. B., Weiser, T. G., Berry, W. R. et al. (2009). A surgical safety checklist to reduce
morbidity and mortality in a global population. N. Engl. J. Med., 360, 491499.
Higgins, J. (2001). The listening blank. Health Serv. J., 111(5772), 2225.
NHS Litigation Authority www.nhsla.com
The Report of the Public Inquiry into Childrens Heart Surgery at Bristol Royal Infirmary 1984
1995: (Cm 5207) (2001). London: The Stationery Office.
Chapter 29
Ethics, consent and the law

Andrew Heck and Ross Clark
Introduction
Obstetric anaesthesia poses a convergence of all the ethical and consensual dilemmas only
encountered infrequently in other areas of anaesthetic practice. The patient population typically
ranges from teenagers upwards, with varying degrees of capacity to consent, a varying level of
understanding and information provision, but a universally high degree of expectation. Patients can
present in a time-critical manner and the treatment of the mother or the baby may cause risk to one to
save the other. The anaesthetist, however, is well placed to provide a unifying voice of reason in this
difficult arena. Therefore it is incumbent on us to have a good grasp of all the pertinent issues. This
chapter will cover the issues of consent in the obstetric population, the legal background which
underpins our current situation, and finally the ethical controversy that surrounds pregnancy testing in
the under-16s.
Consent
We perform consent for a number of reasons: ethical, legal and regulatory body requirements.
Ethical considerations
Ethically there are a couple of underlying principles which govern our actions in this area. The Select
Committee of Medical Ethics ruled in their report in 1994 that:
Alongside the principle that human life is of special value, the principle is widely held that an
individual should have some measure of autonomy to make choices about his or her life As
the law stands medical treatment may be given to competent adult patients only with their
informed consent, except in an emergency.
Making your own decisions, whether this involves consenting or withholding consent, of itself
promotes welfare. Seeking consent helps to establish trust between the doctor and patient, and
actively involves the patient in their own care. The requirement of consent therefore promotes
individual autonomy and encourages rational decision-making. These derive from the basic principle
of the right to self-determination, complemented by the principle of respect for persons.
Legal considerations
The Department of Health has released the Reference Guide to Consent for Examination or Treatment
(2009), which provides a guide to the legal framework that all health professionals need to take
account of in obtaining valid consent for any examination, treatment or care that they propose to
undertake. It stems from the case law that exists within English law and from Court of Appeal
judgements, as well as the European Court of Human Rights.
The classic legal statement comes from an American case (Schloendroff v Society of New York
Hospital, 1914) where the presiding Judge stated:
Every human being of adult years and sound mind has a right to determine what shall be done
with his own body; and a surgeon who performs an operation without the patients consent
commits an assault.
In English law the concept of informed consent exists in a very limited form in Chatterton v Gerson
(1981) where it was deemed the patient need only be informed in broad terms of the nature of the
procedure. As ethically and legally acceptable consent must always be informed it has been argued
that this phrase represents a tautology, and that valid consent is more appropriate. Valid consent
comprises three main aspects: the voluntary nature of consent, information provision and time for
deliberation, and that the patient must be competent and autonomous. The requirements for valid
consent in UK law were set out in the case highlighted below:
Re. C (Adult: refusal of treatment) [1994] 1 WLR 290, Fam Div. An inpatient at
Broadmoor Hospital for over 30 years due to schizophrenia had developed advanced
gangrene of the foot. He was given an 80% chance of dying despite treatment, but he refused
surgical treatment. The judge acknowledged that although his general capacity was impaired,
he understood the nature, purpose and effect of the proposed treatment; he retained relevant
treatment information and had arrived at a clear choice. This case confirmed the three-stage
test that is now required for valid consent and also that mental disorder per se does not
preclude someone from making a legally competent medical decision.
The three-stage approach to establish capacity to consent

1. Can the patient comprehend and retain the necessary information?
2. Does the patient believe the information?
3. Has the patient weighed the information, balanced the risks and benefits, arrived at a choice
and communicated it?
With the concept of a legal requirement for valid consent in law, to proceed to administer
treatment without consent carries the risks of criminal trespass, any of which could affect the medical
practitioner depending on the circumstances:
Battery. This is non-consensual touching i.e. any act on another person without consent. In
law there is no need for the plaintiff to establish loss and all direct damages are recoverable.
Assault. This is criminal assault and battery and is an offense against the Persons Act and has
a maximum fine of 5000 and/or up to 6 months imprisonment.
Actual bodily harm. This is any hurt or injury calculated to interfere with health or comfort
so anything from a bruise upwards and carries up to 5 years imprisonment.
Medical negligence. The plaintiff needs to establish that the negligence of touching without
consent has led to the injury for which damages are being claimed. There is therefore a need
to establish factual causation in negligence and only foreseeable damages can be recovered.
Gross negligence manslaughter. This charge is attributable when a lawful act is carried out in
a reckless manner leading to the death of a patient.
Murder. Where the death of the patient is intended.

With the legal precedent for valid consent established and the litigious consequences outlined, it
remains to consider what information provision is considered adequate for valid consent. In the
United Kingdom the professional practice standard has been the norm since the Chatterton v Gerson
case mentioned earlier, where the doctor decides what information the patient should be told. Two
contrasting, more recent cases are worth mentioning Sidaway v Board of the Bethlem Royal
hospital and the Maudsley hospital [1985] and Chester v Afshar [2004].
Sidaway v Board of Governors of the Bethlem Royal hospital and the Maudsley hospital
AC 871; [1985] 1 All ER 1018, HL. A patient was consented for spinal surgery, but the
surgeon did not disclose a 12% risk of cord damage. The patient suffered a spinal cord
injury, but the action for negligence failed. The judgement stated that the physician had the
right of therapeutic privilege to withhold information from the patient if they thought that
passing on the information could harm the patient.
Chester v Afshar [2004] UKHL 41. Again a patient was consented for spinal surgery and
the risk of cord damage was not disclosed. The patient suffered a spinal cord injury, but in
this instance the surgeon was found guilty of negligence. The judge concluded that the
necessary causal connection between the negligence and the injury had been established on
the basis that C, if duly warned, would not have undergone surgery as soon as she had, but
would have wished to discuss matters further and explore other options.
Clearly the mandate now is to provide information that the individual in front of you needs to
know to make a decision. This requires two-way communication and may be the most time-consuming
method; nevertheless it is the standard to which we now aspire.
There are situations where the normal consent process may be suspended:
Where the patient is deemed to have incompetent capacity judged by the three-stage rule. This
is covered by the Mental Capacity Act (2005) and Mental Health Act (2007) mentioned
below.
Children <16 years old who are not Gillick competent (see below).
1617 years of age is normally considered competent, but they may not necessarily refuse
treatment under certain circumstances where the illness is very grave or a threat to life and
parents consent to treatment, or where the courts over-rule a parental decision.
Treatment under public health legislation.
The unconscious patient requiring life-saving surgery under the doctrine of necessity. In these
circumstances two requirements must apply: that it is impossible to communicate with the
patient and that what is done is what was necessary to save the persons life.
Under 16 years old

This population group are encountered with reasonable frequency in a busy obstetric unit and have a
number of ethical and legal concerns:
What is the extent of their capacity to consent to treatment? It should not be assumed that
consent to intercourse equates to capacity for competence.
Where under-age sexual intercourse has taken place there may be safeguarding concerns,
especially if the partner is significantly older or where there is any suspicion of coercion or
abuse. The validity of capacity to consent is nearly always questionable in these cases and
should almost always involve the close participation of the safeguarding team. These cases
must be considered on a case by case basis.
Fraser competence or Gillick competence

To be Gillick competent, a child must have sufficient maturity to understand the nature, risks
and purpose of the proposed treatment.
Gillick competence is a sliding scale: the level of competence required to consent to having
a BP check is obviously different to consenting to a bone marrow transplant.
If competent, the child can consent to treatment without parental involvement.
The child may not refuse treatment when consent has been given by a parent or a court.
Patients without capacity

These patients are provided for within law in England and Wales by the Mental Capacity Act (2005)
and the 2007 revision of the Mental Health Act (1983). In Scotland this is provided by Adults with
Incapacity (Scotland) Act 2000.
The Mental Capacity Act 2005
This defined a lack of capacity: a person lacks capacity in relation to a matter if at the
material time he is unable to make a decision for himself in relation to the matter because of
an impairment of, or a disturbance in the functioning of, the mind or brain.
A person lacks capacity if they cannot pass the three-stage assessment.
The Act also sought to promote capacity by ensuring that clinicians:
Provide relevant information, including alternatives
Are aware of specific communication and cognitive problems and communicate in an

appropriate way
Use technology/alternate methods of communication
Are aware of factors undermining capacity and alleviate where possible
Give sufficient time for discussion
New provisions were made for:
The Lasting Power of Attorney (replaced the Enduring Power of Attorney and allowed
those so nominated to make decisions regarding an incapacitated patient, including
withholding life-saving treatments).
Advance directives, which now have a statutory basis. These have direct applicability to
the obstetric situation where blood products may be refused by virtue of an advance
directive. To be valid these must have been made by someone over the age of 18, it must
specify the treatment(s) to be refused, it must not have been modified verbally or in
writing since it has been made; with refusal of life-sustaining treatment it must include
the statement that the decision should stand even if life is at risk, that this is in writing
and has been signed and witnessed. The validity of an advance directive may be
questioned if the patients behaviour is clearly inconsistent with the decision, if the
current situation could not have been anticipated by the patient or if the patient is being
treated under the Mental Health Act.
The Court of Protection, which has the power to make decisions on behalf of individuals
that lack capacity, usually in a one-off situation.
Independent mental capacity advocates. An NHS Trust is now obliged to appoint an
independent advocate for decision-making in serious illness where a patient lacks
capacity and cannot be represented by other means.
Mental Health Act 1983

This legislation is designed to provide legal stature for the detention, assessment and treatment of the
mentally disordered. The umbrella term of what is acceptable medical treatment has been broadened
to include such treatments as caesarean section, provided they can be demonstrated to be therapeutic
in treating the underlying mental illness. One such case within the arena of obstetrics is published and
this will be examined in detail later. It is anticipated that the provisions now made in the Mental
Capacity Act provide a more appropriate tool to guide treatment in those that are mentally
incompetent.
Where patients are deemed to lack capacity then physicians may proceed in a manner consistent
with the patients best interests within the confines of the Bolam principle (that what is done is
considered appropriate by a like-minded body of responsible peers) or under the direction of the
courts, Mental Health Capacity Advocate or Lasting Power of Attorney.
Adults with Incapacity (Scotland) Act 2000

This Act aims to safeguard those without capacity over the age of 16 through mental disorder or some
inability to communicate. It also lays down guidelines in how others may act on their behalf.
Regulatory body requirements

The General Medical Council has laid down guidance in the revised 2008 document Consent:
patients and doctors making decisions together. In summary it reinforces that patient consent should
be patient-centred with the delivery of accurate, appropriate and timely information with valid
alternative therapies and a balanced approach to risk discussion. It also highlights how this should be
documented and under what circumstances it may be considered appropriate to withhold information.
It is worthwhile to note that the GMC requirements exceed the minimum legal requirements in the
United Kingdom.
The obstetric patient

With the underlying principles and stature that guide consent now outlined, it is time to consider how
this translates into the obstetric setting. The capacity to consent may be impaired in the obstetric
setting for a number of reasons. This incorporates patients who have long-term mental impairment, as
well as those in whom capacity to consent would be considered intact in normal circumstances.
These factors are outlined in Table 29.1.
Table 29.1 Factors affecting competence in the obstetric patient
Pain Influence of others
Fear Unrealistic expectations
Drugs Age
Exhaustion Mental incapacity
There are five obstetric cases represented in case law which highlight how these factors have
been dealt with.
Re. S (Adult: refusal of treatment) [1992] A11 ER 671. A 30-year-old women presented
in established labour for her third child, but with a transverse lie with the elbow protruding
through the cervix. The obstetric team recommended a caesarean section for the health of the
mother and fetus as a life and death situation, but the woman refused on the basis of
religious grounds. The court declared to proceed with caesarean section following an 18-
minute hearing.
Tameside and Glossop Acute Services Trust v CH [1996] 1 FLR 762 . A 41-year-old
patient was detained under s.3 of the MHA due to paranoid schizophrenia. A caesarean
section was permitted under s.63 of the 1983 Act as achievement of a successful pregnancy
was a necessary part of the treatment of her psychiatric condition. In addition the doctor
was entitled, if he considered it clinically necessary, to use restraint to the extent reasonably
required to achieve the birth of a healthy baby.
Rochdale NHS Trust v C [1997] 1 FCR 274. The patient arrived at hospital in arrested
labour with clinical suspicion of a rupturing uterus due to a previous caesarean section. The
obstetrician recommended a life-saving caesarean, but the patient refused. An urgent
psychiatric opinion was sought, but unavailable immediately and the obstetrician was of the
opinion the woman had full capacity. After a 2-minute hearing the judge was of the opinion
she lacked capacity: the patient being in the throes of labour with all that involved and who
could speak in terms which accepted the inevitability of her own death and that of the child,
was not a patient who was able to properly weigh-up the considerations that arose so as to
make any valid decision.
Norfolk and Norwich Trust v W [1997] 2 FLR 613. A patient arrived in arrested labour in
the emergency department, but denied she was pregnant. She had a previous history of mental
illness with three previous pregnancies all terminated by caesarean section. A psychiatric
review judged there was no mental disorder, but were unable to say whether she had
capacity. The judge ruled she did not have capacity: although not suffering from a mental
disorder she lacked the mental competence to make a decision about the treatment as she was
incapable of weighing up the considerations involved.
This string of cases led to the Court of Appeal (Butler-Sloss, Saville and Ward, L.JJ.) providing
guidance for future caesarean section refusal cases. This guidance is summarized below:
A mentally competent patient has an absolute right to refuse treatment even if this might lead
to her death.
The only situation in which it is lawful to proceed is if the adult patient did not have the
capacity to decide, the treatment was necessary and what was done was no more than was in
the best interests of the patient.
Panic, indecisiveness and irrationality do not necessarily amount to incompetence. However

they may indicate incompetence and the gravity of the consequences of the decision are
commensurate with the level of competence required to make the decision.
A person could lack the capacity to make a decision by impairment of mental function due to
shock, pain, fatigue, drugs or confusion, but only if the ability to clearly decide is absent as a
result.
Panic induced by fear could influence capacity when extreme, as in the case of Re. MB, but
fear can also be a rational response to surgery, so every case requires careful scrutiny.
The interests of the unborn fetus (i.e. the sanctity of life) do not take precedence over its
mother (i.e. the principle of autonomy and self-determination) unless she is incapable of
making a reasoned choice because of an impairment of mental functioning.
The unborn fetus does not have a legal status until it is born.
It remains to provide some handy tips on what this means on a day to day obstetric unit. This is
summarized in Table 29.2.
Re. MB (Adult: Medical Treatment) [1997] 2 FLR 426, CA. A caesarean section was
recommended for a term breech delivery to which the patient consented. On numerous
attempts the patient refused at the point of anaesthesia due to needle phobia. The court applied
for a compulsory order for section, which was granted on the grounds that at the point of
having her desired treatment her phobia was causing an impairment of her mental functioning,
and she was temporarily incompetent. She appealed the decision but the Court of Appeal
upheld the decision. The following morning she consented to section voluntarily.
Table 29.2 Putting it into practice
Know GMC and Department of Health guidance
Identify potential competency problems early
Provide evidence-based information early
Minimize factors that erode capacity pain, fear, panic
Ensure 24-hour access to translation services
Make use of acute pain protocols
See patients early in labour

Clear documentation of the information provided
When in doubt seek expert opinion
The ethics of pregnancy testing in the under-sixteens

Based on National Statistics from 2010 on the rate of conception in under 16-year-olds and the total
number of procedures performed on females aged 1215, some 200 to 300 young women present for
surgery each year with a wanted pregnancy. The National Institute for Health and Clinical Excellence
and the Health Protection Agency require that the pregnancy status of all reproductive females should
be established prior to any procedure that may harm the mother or fetus. There remain, however,
some ethical and clinical concerns around mandatory pregnancy tests for this age group:
Compulsory testing is increasingly being viewed as unethical and, as a certain number of

these females would be deemed to be Gillick competent, it has the potential to be
discriminatory by not seeking valid consent.
Preprocedure these young persons are frequently seen in the company of parents or guardians
where a sexual history may be embarrassing, and likely uninformative.
Physical examination to establish pregnancy is unreliable and the menstrual history is often
erratic in this age group, making them poor discriminators.
There is concern that not testing for pregnancy may expose a mother and fetus to harm and may
lead to litigious repercussions.
Capacity to consent can be difficult within this age group.
Revelation of active sexual history under the legal age of consent may have implications for
safeguarding, especially where there is coercion, abuse or where the partner is over the age of
18.
Given the extremely low rate of positive pregnancies in the under-15 group, enquiring may
cause undue distress.
Recent guidance has been issued from an expert working group convened by the Royal College of
Paediatrics and Child Health to assist clinicians and institutions in developing local procedures that
strike a balance between minimizing harm and complying with national guidelines. A summary of
some of their key recommendations is presented below:
1. Preadmission information is invaluable in reducing anxiety and allaying fears concerning

questions about sexual activity.
2. The incidence of pregnancy in the under-13 age group is so negligible that this group may be
considered exempt.
3. A key component to establishing trust and complying with guidance is an assessment of

capacity.
4. Privacy and confidentiality is essential to this process.
5. When a sample is positive it should be repeated, together with serum confirmation. A senior
member of the team should be involved and appropriate advice given regarding the risks of
proceeding. Where there is suspicion of coercion, abuse or a partner over the age of 18 then
local safeguarding procedures should be followed.
6. Any positive pregnancy test under the age of 13 should prompt concerns of safeguarding
issues.
7. In the case of clinical emergencies where a sexual history cannot be obtained or competency
cannot be assessed then a balance of risk approach must be taken and documented accordingly.
Key points
1. Obstetric patients may have compromised capacity due to many reasons age, pain, fear,
fatigue, drugs and pre-existing mental illness.
2. Department of Health and GMC guidance on consent exist and should be adhered to.
3. All attempts to minimize the erosion of capacity should be made.
4. The provision of information and the assessment of capacity must be carefully documented.
5. Expert opinion should be sought early where there is doubt.
6. Recent guidelines exist on how to approach the issue of pregnancy testing in the under-16 age
group.
Further reading
General Medical Council. Consent: Patients and Doctors making Decisions Together (online).
http://www.gmc-uk.org/guidance/ethical_guidance/consent_guidance_index.asp (accessed May
2015).
Montgomery, J. (2002). Health Care Law, 2nd edn. Oxford: Oxford University Press.
Royal College of Paediatrics and Child Health (2012). Pre-procedure Pregnancy Checking in Under
16s: Guidance for Clinicians (online). Available:
http://www.rcpch.ac.uk/system/files/protected/page/pregnancy%20checking%20guidance%20final.pdf
Stauch, M., Wheat, K. and Tingle, J (2002). Sourcebook on Medical Law, 2nd edn. London:
Routledge Cavendish Publishing Ltd.
Index
abdominal cerclage 93
abdominal wall, TAP blocks 8790
abortion, spontaneous 5051
absorption of drugs 13
acetaminophen (paracetamol) 20, 70, 153
acidbase balance
fetal acidosis 3637, 38, 50
metabolic acidosis (maternal) 107, 139140
physiology 5
activated protein C 108
actual bodily harm 226
acute coronary syndromes 118, 140, 200
acute kidney injury 149151, 153
acute respiratory distress syndrome (ARDS) 108, 109
acute tubular necrosis 150
Addisons disease 144
adhesive arachnoiditis 205
adhesive dressing allergy 180
adolescents see minors
adrenal gland
disorders 143145
physiology 8, 144
adrenaline (epinephrine) 67, 107, 183
Adults with Incapacity (Scotland) Act (2000) 228
advance directives 227228
adverse effects
allergic reactions 75, 176180
cardiovascular
fetal 20, 50
maternal 14, 17, 50
of Entonox 59
of general anaesthesia 8384
awareness 203204
malignant hyperthermia 129
of local anaesthetics
allergy 179
toxicity 7172, 80
non-allergic drug reactions 180
of opioids see opioids, adverse effects
of regional analgesia see regional analgesia/anaesthesia, adverse effects
of suxamethonium 87, 129, 178
of TAP blocks 8990
teratogenicity 18, 19, 22, 49, 173
AEDs (anti-epileptic drugs) 7, 18, 22, 173
airway management 26, 51, 8384, 179
congenital syndromes 116
diabetic stiff joint syndrome 141
extubation 90, 134135
laryngeal masks 9394
obesity 131, 134135
pre-eclampsia 104
during resuscitation 192
thyroid disease 143
albumin 2, 107
alkaline phosphatase 7
allergy 75, 176180
management 182184
testing 178179, 182
alternative medicine for analgesia 5456
amino acids 11
aminoglycosides 22
amniotic fluid embolism 183, 196
anaemia 1, 152, 155
anaesthetists
antenatal clinics 46, 133
critical care 3334
training role 47, 211
anal sphincter trauma 95
analgesia
non-pharmacological 5456
postoperative 52, 79, 8790
regional see regional analgesia/anaesthesia
systemic 1416, 1920, 5459, 133, 153
see also local anaesthetics; opioids
anaphylactoid syndrome of pregnancy (amniotic fluid embolism) 183, 196
anaphylaxis 177180, 182
management 182184
see also allergy
aneurysm, cerebral 171
angioedema 176, 181
angiogenesis 9899
angiotensin converting enzyme (ACE) inhibitors 139, 181
antenatal assessment
anaesthetic clinics 4447, 133
congenital heart disease 116
obesity 45, 130, 133
antibiotics 22
allergy 176177
prophylaxis
caesarean section 87, 122
cervical cerclage 94
diabetes 141
endocarditis 119
HIV-positive patients 186, 188
MROP 95
in sepsis 106, 107
anticholinesterases 126
anticoagulants 22
antithrombin deficiency 160
diabetes 139
haemodialysis 151
mechanical heart valves 119
obesity 132
PE 124
pre-eclampsia 101102, 103
anticonvulsants 7, 18, 22, 173
antidiuretic hormone (vasopressin) 107, 152, 167
antiemetics 15, 19, 50, 70, 203
antigenic drift/shift in influenza viruses 110
antihistamines 182
antihypertensives 2021, 52, 100101, 102, 103, 139, 147, 151
antihypotensives 20, 52, 69, 7778, 103, 107, 183
antiphospholipid syndrome 149, 161, 176
antiretroviral agents
interactions with anaesthetics/analgesics 188
intrapartum 186187, 188
postpartum 188
in pregnancy 185, 186
antiviral agents 112 see also antiretroviral agents
aortic disease 119120, 199
aortic valve stenosis 119
aortocaval compression 50, 192
arrhythmias 4, 121, 194
arteriovenous malformations, cerebral 171
artificial rupture of membranes (ARM) 94, 187188
aspiration
at extubation 90
pneumonitis 84
premedication for 86, 152
aspirin 99, 139
assault 226
asthma 17, 123
atosiban 16
atracurium 153, 178
atrioseptal defects (ASD) 116117
atrioventriculoseptal defects (AVSD) 117
audit 220
central neuraxial block (NAP3) 77, 204
critical care 2933
failed intubation 26, 8384
maternal morbidity 2728
maternal mortality 2426, 30
autoimmune disease
antiphospholipid syndrome 149, 161, 176
autoimmune thrombocytopenic purpura 157158
lymphocytic hypophysitis 168
multiple sclerosis 174
SLE nephritis 149
autonomy 225
azathioprine 152
back examination 46
back pain 127128
balloon tamponade, uterine 199
barbiturates (thiopentone) 18, 52, 8687
battery (assault) 226
benign intracranial hypertension (BIH) 170
benzodiazepines 18, 49
-adrenoceptor agonists 16
-blockers 2021, 100101, 122, 145
BIH (benign intracranial hypertension) 170
bioavailability of drugs 13
blood pressure
monitoring 66, 100, 134
physiological changes in pregnancy 3
see also hypertension; hypotension
blood tests
coagulation status 159, 161162
microbiological 107
renal function 146
blood transfusions 108, 156, 197
brain
cerebrovascular conditions 171172, 202
mass lesions 165166
see also intracranial pressure
breastfeeding
and drugs 2122, 122, 123, 173
and migraine 173
suppression of lactation 188
breech presentation 4143
external cephalic version 94
head entrapment 4243
twins 41
Bristol Royal Infirmary Inquiry (2001) 220
bupivacaine 14, 63, 70, 153
BurnsMarshall technique 42
C1 esterase inhibitor 181

cabergoline 188
caesarean section
breech presentation 4143
in CAH 144
in cardiac disease 76, 87, 121, 122
in cystic fibrosis 125
general anaesthesia 73, 8390, 103104, 119, 134135
legal cases concerning refusal of treatment 228, 229
and maternal infections
genital herpes 189
HIV 188
maternal satisfaction with 207208
in obese patients 134135
perimortem 194, 197
postoperative care 7981, 8790
in pre-eclampsia 103104
rates 73, 83
regional anaesthesia 7381, 103, 122, 125, 134
top-ups 7678
twins 41
after unsuccessful instrumental delivery 4041
urgency classification 3839, 73
caffeine 22, 201
CAH (congenital adrenal hyperplasia) 144
calcium-channel blockers 16, 21, 100101
calcium ions (Ca2+) 12
capacity for consent 226, 227229
carbon dioxide (CO2) 45, 11, 50
carboprost 17, 121, 198
cardiomyopathy 120121
cardiotocography (CTG)
indications 35, 52, 66
interpretation 3538, 41
twins 41
cardiovascular system, fetal
adverse effects of drugs 20, 50
congenital disease 116
ECG 39
heart rate monitoring 3538, 41, 52, 66
cardiovascular system, maternal
acute coronary syndromes 118, 140, 200
adverse effects of drugs 14, 17
arrhythmias 4, 121, 194
caesarean section 76, 87, 121, 122
cardiac disease intrapartum 4, 121122
cardiac disease in pregnancy 122
acquired 118121
congenital 114, 115118
and diabetes 140
epidemiology 26, 114, 115, 199200
general management 46, 115
and renal disease 152
physiology 34, 52, 114, 132
resuscitation 192194
in sepsis 107
cauda equina syndrome 127128, 205
CAVE assessment 133
cavernoma (cavernous haemangioma) 171
central neuraxial blocks see regional analgesia/anaesthesia
cephalosporins 22, 177
cerebral palsy 21
cerebrospinal fluid (CSF)
BIH 170
hydrocephalus 168170
leaks 165, 201202
cerebrovascular conditions 171172, 202
cervical incisions 4243
Chatterton v Gerson [1981] 225
chest compressions 192
Chester v Afshar [2004] 226
Chiari malformation 170171
chlorhexidine 7475, 179180
cholesterol 11
chronic adhesive arachnoiditis 205
chronic kidney disease (CKD)
causes 147, 148149
definition 146
effect of pregnancy on 146, 147, 149
effect on pregnancy outcome 148
management 152153
systemic manifestations 148
cisatracurium 109, 153, 178
clinical effectiveness 220221
clinical governance 219224
follow-up procedures 80, 81, 207
maternal satisfaction surveys 207209
see also audit; training
clopidogrel 118
coagulation system
assessment 159, 161162
coagulopathy 152, 158160
DIC 159160, 162, 196, 197198
in hypothyroidism 143
physiology 23
in pre-eclampsia 100, 103
recombinant factor VII in PPH 198199
in renal disease 150, 151, 152, 153
in sepsis 108
in SLE 149
thrombophilia 160
acquired 149, 161
congenital 160
see also anticoagulants; thromboembolism
Cochrane Collaboration reports on analgesia in labour 54, 56
codeine 179
cold sensation to check block height 75
colloids 66, 107
allergy 180
combined spinal epidural (CSE)
ARM 94
caesarean section 76, 122, 125, 134
labour 62, 6465, 141
failure 70
needle insertion 67, 76
competence for consent 226, 227229
complaints 221, 223
complementary medicine for analgesia 5456
Comprehensive Critical Care (DoH, 2000) 3031
Confidential Enquiries into Maternal Deaths (UK) 2426, 83, 130, 194
congenital adrenal hyperplasia (CAH) 144
coning 165, 170171
consent 51, 65, 225229, 230
minors 227
contraception 188
conus medullaris 205
coronary heart disease 118, 140, 200
corticosteroids
Addisons disease 144
CAH 144
ITP/ATP 157158
preterm delivery 102
sarcoidosis 124
sepsis 108
thyroid disease 142, 143
transplant patients 152
cortisol 18, 144
Cushings syndrome 145
cranial nerve palsy 205
creatinine 146
cricoid pressure 84
critical care 2934
early warning scores 213
in influenza 112
training 3334, 200, 211212, 213216
Critical Care Minimal Data Set (CCMDS) 29, 31, 33
cryoprecipitate 159, 198
crystalloids 66, 69, 107
CSE see combined spinal epidural
CTG see cardiotocography
Cushings syndrome 145
cyclizine 19
cyclosporin 152
cystic fibrosis 125
cytokines 105106
cytotrophoblast 9
dashboards 223
decelerations in CTG 3738
decision to delivery interval (DDI) 3839, 73
defibrillation 194
desensitization therapy 182
desflurane 19, 59, 87, 153
desmopressin (DDAVP) 158
developing countries, maternal mortality 2627
dexamethasone 102, 144
Di George syndrome 116
diabetes insipidus 167
diabetes mellitus 78, 138141, 145
nephropathy 140, 148
diabetic ketoacidosis 139140
dialysis 109, 151
diamorphine 15, 5657, 133, 204
diet 6, 109, 151
2,3 diphosphoglycerate (2,3-DPG) 1, 6
disseminated intravascular coagulation (DIC) 159160, 162, 196, 197198
diuretics 101, 120
dobutamine 107
documentation
antenatal consultation 4647
maternal collapse 194
dopamine 107
Downs syndrome 117
ductus arteriosus closure 20
dural puncture, inadvertent 67, 71, 134, 201
dural puncture epidural (DPE) 64, 65, 70

Ebsteins anomaly 117
eclampsia 28, 101, 103104
edrophonium 126
Eisenmengers syndrome 116, 118
electrocardiography (ECG)
fetal 39
maternal 34
electrolytes 1, 2, 12
embolism
amniotic fluid 183, 196
pulmonary 124
endocarditis 119
endoglin 99
Entonox/nitrous oxide 16, 19, 59, 87
ephedrine 20, 69, 78, 103
epidural abscess 205
epidural analgesia/anaesthesia see regional analgesia/anaesthesia
epidural blood patches 71, 201202
epilepsy 15, 172173
epinephrine (adrenaline) 67, 107, 183
equipment
critical care 3233
for obese patients 131133
regional analgesia/anaesthesia 6566, 74
used in training 215216
ergometrine 17, 121, 198
erythrocytes 1, 6
erythropoiesis 1
esmolol 2021
ether 54
ethics
consent 225
pregnancy testing in under-16s 229230
etomidate 18, 52, 108
exercise-induced anaphylaxis 182
external cephalic version 94
extubation 90, 134135
facilities
antenatal anaesthetic assessment clinics 46
critical care 3233
surgery during pregnancy 51
factor V Leiden 160
factor VII recombinant 198199
Fallots tetralogy 117
fatty acids 11
fatty liver of pregnancy 150
fentanyl 18, 57, 63, 64, 153, 179, 204
ferritin 2, 155
fetus
acidosis 3637, 38, 50
adverse effects of drugs 20, 4950, 52
regional analgesia 62
teratogenicity 18, 19, 22, 49, 173
congenital heart disease 116
haemophilia 159
head position 3940, 4243
hypoxia 37, 39, 50
IUGR 116, 117
legal status 229
macrosomia 8, 140
maternal CAH 144
maternal surgery 4951
monitoring 3538
blood sampling 38
cardiotocography 3538, 41, 52, 66
ECG 39
in HIV-positive mothers 188
during maternal surgery 52
passive immunity 1112
reduced uteroplacental blood flow 50
syphilis 189
thrombocytopenia 158
thyroid function 142, 143
fever 70, 129
fibrinogen 2, 159, 198
fibrinolysis (postpartum) 3
fluid status/management
ARDS 108
diabetes insipidus 167
hypervolaemia, physiological 12, 3, 7
hypovolaemia can go unrecognized 50, 52, 192194
maternal collapse/haemorrhage 196, 197198
pre-eclampsia 101
regional analgesia 66, 69
renal disease 151, 152, 153
sepsis 107, 108
FMS-like tyrokinase 98
folate 139, 155, 156, 186
Fontan procedure patients 117
forceps deliveries 3941, 188
regional anaesthesia 7381
Fraser competence 227
fresh frozen plasma (FFP) 197198
furosemide 120, 172
GA see general anaesthesia

gastrointestinal system
aspiration of gastric contents 84, 86, 90, 152, 192
gastro-oesophageal reflux 6, 51
physiology 6
reduced gastric motility 6, 15, 141, 152
ulcers 109
general anaesthesia (GA)
caesarean section 73, 8390, 103104, 119, 134135
complications 8384
awareness 203204
induction 1819, 52, 8687, 94, 153
maintenance 19, 87, 189
in myasthenia gravis 126
in neurological disease 165
in obese patients 131, 134135
postpartum procedures 95
in pregnancy 1819, 5152, 9394
premedication 86, 152
preoperative assessment 8486
in renal disease 153
in sickle cell disease 157
in viral hepatitis 189
General Medical Council, on consent 228
genital herpes 188189
gestational diabetes mellitus (GDM) 138, 139
gestational hypertension 97, 140 see also pre-eclampsia
Gillick competence 227
glomerular filtration rate (GFR) 13, 146
glomerulonephritis 149
glucose
blood levels
in diabetes 138, 139, 140
neonatal hypoglycaemia 140
in sepsis 109
in CSF 75
glycosuria 7
metabolism 78, 11
glyceryl trinitrate (GTN) 1617, 21, 93, 95, 120
goitre 141, 143
Graves disease 142
H1N1 influenza (2009 pandemic) 110111

HAART (highly active antiretroviral therapy)
interactions with anaesthetics/analgesics 188
intrapartum 186187, 188
postpartum 188
haematological system 155162
anaemia 1, 152, 155
assessment 159, 161162
haemoglobinopathies 156157
physiology 13, 6
see also coagulation system; thromboembolism
haemodialysis 109, 151
haemoglobin
anaemia 1, 155
fetal 11, 50
haemoglobinopathies 156157
maternal oxygenhaemoglobin dissociation curve 1, 56
in septic shock 108
haemolytic uraemic syndrome (HUS) 150, 158
haemophilia 159
haemorrhage
causes of maternal collapse 196197, 198
intracranial 171, 202
management 197199
maternal compensation/missed diagnosis 2, 50, 52, 192194
perineal tears 40, 95
retained placenta 94
twins 41
halogenated anaesthetics 19, 5960, 87, 153, 189
halothane 19
head injury 172
headache
migraine 173174
post dural puncture 63, 65, 71, 134, 201202
HELLP syndrome 13, 158
heparin 22
diabetes 139
haemodialysis 151
mechanical heart valves 119
obesity 132
PE 124
hepatic system
acute fatty liver of pregnancy 150
drug metabolism 7, 13, 189
physiology 67
pre-eclampsia 100
hepatitis, viral 189
hereditary angioedema 176, 181
herpes, genital (HSV-2) 188189
histamine 178, 181
HIV (human immunodeficiency virus) 185188, 190
hives 178, 181
human placental lactogen (HPL) 78
hydralazine 21, 101
hydrocortisone 108, 144
hydroxycarbamide 156
hypercarbia 50
hyperglycaemia 8, 138
hyperkalaemia 171, 174
hyperosmolar hyperglycaemic state 140
hyperprolactinaemia 167
hypersensitivity reactions see allergy
hypertension
antihypertensives 2021, 52, 100101, 102, 103, 139, 147, 151
classification 9798
in diabetes 140
ergometrine contraindicated in 17, 198
pheochromocytoma 144145
pre-eclampsia see pre-eclampsia
pulmonary 117118, 123124
with pulmonary oedema 120
renal disease 147, 148, 151, 152
hyperthyroidism 141142
hypertrophic cardiomyopathy 120
hypervolaemia, physiological 12, 3, 7
hypocarbia 50
hypoglycaemia 139, 140
neonatal 140
hypotension
causing nausea and vomiting 79
in diabetes 141
regional analgesia 66, 69, 7778
in renal disease 151, 153
septic shock 105, 107
vasopressors 20, 52, 69, 7778, 103, 107, 183
hypothyroidism 142143
hypovolaemia
maternal collapse/haemorrhage 192194, 197198
and regional analgesia 66
unrecognized 50, 52, 192194
hypoxia
fetal 37, 39, 50
maternal 50, 51, 192
hysterectomy 199
ICP see intracranial pressure

immune system 176184
allergy 75, 176180
management 182184
testing 178179, 182
angioedema 176, 181
asthma 17, 123
exercise-induced anaphylaxis 182
passive immunity in the fetus 1112
physiological changes in pregnancy 1, 174
rhinitis 181
sepsis 105106
urticaria 178, 181
see also autoimmune disease
immune thrombocytopenic purpura 157158
immunization
influenza 112
postpartum in HIV-positive patients 188
immunodeficient patients 176
HIV 185188
with influenza 111, 112
transplant recipients 152
incident reporting 221
induction of GA 1819, 52, 8687, 94, 153
infections
epidural abscess 205
sepsis 25, 105109, 112
syphilis 189
see also viral infections
influenza 109112
information provision for consent 133, 226227
informed consent see consent
inhalational anaesthetics 14, 52
nineteenth century 54
halogens 19, 5960, 87, 153, 189
nitrous oxide/Entonox 16, 19, 59, 87
inotropic agents 107
instrumental delivery 3941, 188
insulin, in diabetes 78, 139, 141
integrated care pathways 220221
intervertebral discs 127128
intracranial pressure (ICP)
raised
BIH 170
head injury 172
reduced 205
see also post dural puncture headache
intralipid 72, 80
intrathecal catheters 77
intrauterine growth retardation (IUGR) 116, 117
intravascular injection of local anaesthetics 7172, 80
intravenous catheterization 66
intubation
difficult 131, 141, 179
failure 26, 51, 8384
see also extubation
iron deficiency 2, 155
iron overload 157
isoflurane 19, 59, 153, 189
itching 69, 202203
Kentucky Frontier Nursing Service 24

ketamine 16, 18, 52
ketorolac 20
kidney see renal system
LA see local anaesthetics

labetolol 20, 100101
labour
analgesia 54
inhalational 16, 54, 5960
non-pharmacological 5456
regional 6172, 133134
systemic opioids 1516, 5459
breech delivery 4143, 94
in cardiac disease 114, 121
diabetes 141
fetal monitoring 3538, 39, 41, 66, 188
genital tract/perineal trauma 40, 69, 95, 198
in HIV-positive patients 186188
MROP 9495
obese patients 133134
physiological changes 23, 4, 5
stages 61
timing of delivery 41, 102103, 121
twins 41
see also premature delivery
lactate 106
laparoscopy 51, 93
Lasting Power of Attorney 227
latex allergy 180
legal issues
consent 225229
negligence 223, 226
less developed countries, maternal mortality 2627
leucocytes 1, 2, 106
levobupivacaine 14, 77
lidocaine (lignocaine) 14
lignocaine adrenaline bicarbonate mixture 77
test dose in regional analgesia 67
lipids 2, 11
liver
acute fatty liver of pregnancy 150
drug metabolism 7, 13, 189
physiology 67
pre-eclampsia 100
viral hepatitis 189
living wills (advance directives) 227228
local anaesthetics (LA)
allergy 179
pharmacology 14, 153
in regional analgesia 63, 6768
epidural top-ups 68, 77
in failed analgesia 70
maintenance 68
spinal blocks 75
test dose 67
toxicity (IV injection) 7172, 80
Lovsets manoeuvre 42
low molecular weight heparin (LMWH) see heparin
lower limb, neurological complications 204, 205
lung see respiratory system
lupus nephritis 149
lymphocytic hypophysitis 168
macrosomia 8, 140
magnesium sulfate 17, 21
in eclampsia 101, 103104
in myasthenia gravis 126
malignant hyperthermia 129, 178
malposition 3940
malpresentation see breech presentation
manual removal of placenta (MROP) 9495
Marfans syndrome 114
maternal collapse 191200
causes 194196
anaphylaxis 182183
cardiac disease 199200
haemorrhage 196197, 198
incidence 182, 191
management
caesarean section 194, 197
of haemorrhage 197199
postcollapse 194
resuscitation 183, 191194
training 200
maternal experience of childbirth 207209
maternal monitoring
blood pressure 66, 100, 134
in cardiac disease 121
coagulation status 159, 161162
in obese patients 134
during regional analgesia 66, 69
maternal morbidity 2728
acute kidney injury 149
cardiac disease 114, 118, 120, 199200
in the developing world 2627
hypertension 97, 100
influenza 111
obesity 124, 130131
pulmonary hypertension 117, 118
sepsis 25, 105
thrombosis/PE 26, 124
in the UK 2426, 30, 83
maternal transmission of disease see mother-to-child transmission
MauriceauSmellieViet manoeuvre 42
McDonald sutures 93
Mendelsons syndrome 84
meningioma 166
Mental Capacity Act (2005) 227228
Mental Health Act (1983) 228, 229
MEOWS (modified early warning score for obstetric patients) 213
meperidine (pethidine) 15, 56, 157
for shivering 70, 79
metabolic acidosis 107, 139140
methadone 18
metoclopramide 19, 86
metronidazole 22
midwives, training
critical care 33, 211212
pain relief 216217
migraine 173174
Millennium Development Goals 27
minors
consent 227
maternal mortality 26
safeguarding 227, 230
miscarriage 5051
misoprostol 121, 198
mitral stenosis 118119
mivacurium 178
morphine 15, 57, 153, 179, 204
mortality see maternal mortality
mother-to-child transmission
genital herpes 189
HIV 185, 186, 187188
syphilis 189
MROP (manual removal of placenta) 9495
multidisciplinary care
crash teams 191
in maternal critical care 32, 34
training 200, 213216
multiple pregnancies 41
muscle relaxants 87
anaphylaxis 177179
malignant hyperthermia 129, 178
in multiple sclerosis 174
in myopathies 126
safety 1819, 50, 52
in sepsis 108109
suxamethonium metabolism abnormalities 7, 13
in syringomyelia 171
myasthenia gravis 126
mycophenalate mofentil 152
myocardial infarction 118, 140, 200
myopathies 125126
myotonic dystrophy 125126
naloxone 203
nausea 15, 70, 79
anti-emetics 15, 19, 50, 70, 203
postoperative 203
needle insertion
accidental dural puncture 67, 71, 201
CSE 67, 76
epidural 6667, 134
spinal 75
negligence 223, 226
neonates
cerebral palsy 21
effects of maternal opioids 15, 56, 59
with HIV-positive mothers 188
HSV-2 infection 189
hypoglycaemia 140
premature 92
nephropathy, diabetic 140, 148
neural tube defects 128
neuraxial blocks see regional analgesia/anaesthesia
neurological disease 165174
BIH 170
cerebrovascular 171172, 202
Chiari malformation 170171
complications of general anaesthesia 165
complications of neuraxial blocks 165, 204205 see also post dural puncture headache
diabetic neuropathy 140
eclampsia 101, 103104
epilepsy 172173
head injury 172
intracranial mass lesions 165166
migraine 173174
pituitary apoplexy 167168
syphilis 189
neuromuscular blocking agents see muscle relaxants
nifedipine 16, 21, 100101
nitrate (GTN) 1617, 21, 93, 95, 120
nitroprusside 21
nitrous oxide/Entonox 16, 19, 59, 87
non-allergic drug reactions 180
non-steroidal anti-inflammatory drugs (NSAIDs) 1920, 50, 79, 153, 179
noradrenaline (norepinephrine) 107
Norfolk and Norwich Trust v W [1997] 229
norpethidine 15
nurses, critical care 33
nutrition 6, 109, 151
obesity 130135, 137

antenatal considerations 45, 131133
BIH 170
caesarean section 134135
classification 130
epidemiology 44, 130
labour 133134
physiology 131
postpartum care 135
oedema 2 see also pulmonary oedema
ondansetron 19
opioid antagonists 203
opioids
adverse effects 56, 58
allergy 179
nausea and vomiting 15, 70, 203
non-teratogenic 18
pruritis 69, 202203
respiratory depression 15, 49, 5657, 204
induction of GA 18, 87
in labour 1516, 5459
obese patients 133
regional analgesia 63, 64, 6768
PCA 1516, 5759, 63, 69, 133, 153
for postoperative pain 79
in spinal blocks 75
oral hypoglycaemic agents 139
oseltamivir 112
osmolarity/osmolality of plasma 2, 7
oxygen
physiology 45, 11
therapy
preoxygenation in GA 86, 134
in pulmonary hypertension 117
in sepsis 106, 108
oxygenhaemoglobin dissociation curve
fetal 50
maternal 1, 56
oxytocin 17, 87, 95, 121
oxytocin antagonists 16
pain relief see analgesia

pandemics (influenza) 110
paracetamol (acetaminophen) 20, 70, 153
parturition see labour
patient safety 223224
patient-controlled analgesia (PCA) 1516, 5759, 63, 69, 133, 153
PDPH (post dural puncture headache) 63, 65, 71, 134, 201202
penicillins 22, 176177
peptic ulcers 109
percutaneous coronary intervention (PCI) 118
perineal trauma 40, 95, 198
peripartum cardiomyopathy 120121
peritoneal dialysis 109, 151
pethidine (meperidine) 15, 56, 157
pharmacodynamics 14
pharmacokinetics 13
AEDs 173
antiretroviral drugs 186
and the hepatic system 7, 13, 189
opioids 15, 5657
placental transfer 12, 13
and the renal system 7, 13, 151, 153
suxamethonium abnormalities 7, 13
phenylephrine 20, 52, 69, 7778, 103, 107, 183
physiology 18, 51
anaesthesia-induced derangement 50
cardiovascular 34, 52, 114
obesity 131
placental 1112
renal 1, 7, 146
thyroid 141
pinprick test (block height) 75
pituitary gland lesions 167168
placenta
abruption 196197
anatomy 911
development 9
manual removal 9495
pathogenesis of pre-eclampsia 9899
physiology 1112
see also uteroplacental circulation
placenta praevia 197
platelets 1
assessment of function 161162
in hypothyroidism 143
gestational 1, 157
haemorrhage 197
sepsis 108
TTP/HUS 150, 158
pneumonitis, aspiration 84
polycystic kidney disease 149
positioning of the mother
for GA 86, 131
obese patients 131, 133134
for regional analgesia/anaesthesia 66, 74, 93, 133134
positive end-expiratory pressure (PEEP) 108
post dural puncture headache (PDPH) 63, 65, 71, 134, 201202
postoperative period 52, 7981, 8790
postpartum haemorrhage (PPH)
causes of maternal collapse 196, 197, 198
management 197199
maternal compensation/missed diagnosis 2, 192194
perineal tears 40, 95
retained placenta 94
twins 41
postpartum period
follow-up 80, 81, 207
genital tract/perineal trauma 40, 69, 95, 198
haemorrhage see postpartum haemorrhage
HIV-positive patients 188
maternal satisfaction surveys 207209
MROP 9495
obese patients 135
physiology 3, 4, 5
pre-eclampsia 104
preconception counselling 115, 156, 157, 186
pre-eclampsia 97104
aspirin prophylaxis 99, 139
in congenital heart disease 116
delivery 102104
in diabetes 140
diagnosis 99100
management 100103
pathogenesis 9899
postnatal care 104
and pulmonary oedema 101, 120
renal disease 148
vasopressor use 78, 103
premedication 86, 152
premature delivery 92
in diabetes 140
following surgery 51
in HIV-positive patients 188
steroids 102
prochlorperazine 19, 50
progesterone 1, 45, 6, 7
prolactin 167
propofol 18, 52, 8687, 94
propylthiouracil 142
prostaglandins
in cardiac disease 121
in MROP 95
in PPH/uterine atony 17, 123, 198
protein, plasma 2
drug binding 14
protein C 108, 160
protein S 160
proteinuria 146
in pre-eclampsia 97, 98, 100
proton pump inhibitors 109
Providing equity of critical and maternal care for the critically ill pregnant or recently pregnant
woman (RCOG, 2011) 3133
pruritis 69, 202203
pulmonary embolism (PE) 124
pulmonary oedema
acute 120
in cardiac disease 114, 118
pyelonephritis 149
pyrexia 70, 129
quality of care 25, 207, 219224

maternal experience surveys 207209
ranitidine 86
rapid sequence induction 84
red blood cells 1, 6
referrals for antenatal anaesthetic review 4546, 133
refusal of treatment 226, 227228, 229
regional analgesia/anaesthesia
adjuvants 78
adverse effects 6972, 74, 7779, 201205
failure 70, 7576
fever and shivering 70, 79
high block 7071, 7879
hypotension 69, 7778
LA toxicity 7172, 80
nausea and vomiting 70, 79, 203
neurological 165, 204205
PDPH 63, 65, 71, 134, 201202
pruritis 69, 202203
respiratory depression 204
analgesic choice 63, 64, 6768
artificial rupture of membranes 94
benefits 51, 61, 64, 73
for caesarean section 7381, 103, 122, 125, 134
top-ups 7678
cerebral aneurysm 171
contraindications 52, 6263, 7374
cystic fibrosis 125
diabetes 141
and duration of labour 6162
and the fetus 62, 66
follow-up 81, 207
genital herpes 189
hepatitis 189
HIV-positive patients 188
indications 62, 63, 76, 103
in labour 6172
maintenance 63, 6869
maternal monitoring 66, 69
methods 62, 6367, 7475
assessment of block height 75
intrathecal catheters 77
needle insertion 6667, 75, 76, 134
spinal ultrasonography 135137
test dose 67
MROP 9495
myopathies 126
neurological disease 165, 173, 174
obese patients 133134
perineal repair 95
peripartum interventions 69, 9495
postoperative care 7981
pre-eclampsia 103
renal disease 151, 153
spinal disorders 127, 128
surgery during pregnancy 51, 52, 93
training for midwives 216217
remifentanil 1516, 5759, 87, 133, 153, 179
renal system 146154
acute kidney injury 149151, 153
chronic disease
causes 147, 148149
definition 146
effect of pregnancy on 146, 147, 149
effect on pregnancy outcome 148
management 152153
systemic manifestations 148
dialysis 109, 151
and hypertension 147, 148, 151, 152
pharmacokinetics 7, 13, 151, 153
physiology 1, 7, 146
transplant patients 151152
renin 1
respiratory alkalosis 5
respiratory system
ARDS/sepsis 108, 109
aspiration of gastric contents 84, 86, 90, 152, 192
asthma 17, 123
cystic fibrosis 125
influenza 111
obesity 131, 132, 134135
opioid-induced respiratory depression 15, 49, 5657, 204
physiology 45, 132
pulmonary embolism 124
pulmonary oedema see pulmonary oedema
sarcoidosis 124125
resuscitation
in anaphylaxis 183
in maternal collapse 191194
in sepsis 106107
retinopathy, diabetic 140
rhinitis 181
RIFLE criteria (acute kidney injury) 150
risk management 221223
ritonavir 188
Rochdale NHS Trust v C [1997] 229
rocuronium 87, 153, 178
ropivacaine 14, 77, 153
safeguarding of minors 227, 230

Safer Childbirth: Minimum Standards for the Organization and Delivery of Care in Labour (RCOG,
2007) 31
salbutamol 16
saline, isotonic 107
sarcoidosis 124125
Schloendroff v Society of New York Hospital [1914] 225
scoliosis 126127
Scottish Confidential Audit of Severe Maternal Morbidity (SCASMM) 28
seizures 15, 172173
eclampsia 101, 103104
sepsis 25, 105109, 112
septic shock 105, 107108
serotonin (5-HT3) antagonists 19
service provision
antenatal anaesthetic assessment clinics 4143
in developing countries 27
maternal critical care 3133
shortcomings identified by CEMACH/CMACE 25, 26
sevoflurane 19, 60, 87
sexually transmitted infections 188189
Sheehan syndrome 168
shivering 70, 79
shock
septic 105, 107108
see also hypovolaemia
sickle cell disease 156157
Sidaway v Board of the Bethlem Royal hospital and the Maudsley hospital [1985] 226
simulation programme training 214215
SIRS (systemic inflammatory response syndrome) 25, 105109
definition 105
skin preparation for regional anaesthesia 7475
skin prick test (allergy) 178179, 182
sodium citrate 86
sodium ions (Na+) 1, 12
spinal analgesia/anaesthesia 64
artificial rupture of membranes 94
caesarean section 7475
methods 63, 67
MROP 9495
pre-eclampsia 103
see also combined spinal epidural
spinal blockade, high/total 7071, 7879
spinal disorders
complications of regional analgesia 204205
lumbar pain/nerve compression 127128
scoliosis 126127
spina bifida 128
vascular 172
spinal ultrasonography 135137
spiral arteries 3, 9
spondylithsesis 127
staff
anaesthetic assessment clinics 46
crash teams 191
critical care 32, 3334, 211212
see also training
steroids
physiological changes in pregnancy 1, 45, 6, 7
placental production 11, 12
see also corticosteroids
stiff joint syndrome 140, 141
stress ulcers 109
sub-arachnoid haemorrhage 171
sub-dural bleeding and haematomata 202
sufentanil 64, 204
sugammadex 87, 153, 178
surgery during pregnancy 4953
suxamethonium 87
abnormal metabolism 7, 13
adverse effects 87, 129, 178
in multiple sclerosis 174
in myotonic dystrophy 126
in syringomyelia 171
swine flu (influenza A H1N1) 110111
syncytiotrophoblast 9
syntocinon 17, 121
in uterine atony/PPH 198
syntometrine 17, 103, 198
syphilis 189
syringomyelia 171
Systemic Inflammatory Response Syndrome (SIRS) 25, 105109
definition 105
systemic lupus erythematosus (SLE), nephritis 149
tacrolimus 152
Tameside and Glossop Acute Services Trust v CH [1996] 229
TAP (transverse abdominal plane) blocks 8790
teratogens 18, 19, 22, 49, 173
terbutaline 16
tetracyclines 22
tetralogy of Fallot 117
thalassaemias 157
thiopentone 18, 52, 8687
assessment 161162
gestational 1, 157
haemorrhage 197
sepsis 108
TTP/HUS 150, 158
thromboelastography (TEG) 108, 161162
thromboembolism
cerebral venous thrombosis 172
patients with mechanical heart valves 119
prophylaxis 22
in diabetes 139
obese patients 131
postoperative 81
in sepsis 109
thrombophilia 160, 161
pulmonary embolism 124
thrombolysis 118
thrombophilia 160
acquired 149, 161
congenital 160
thrombotic thrombocytopenic purpura (TTP) 150, 158
thyroid disease 141143, 145
tissue plasminogen activator 118
tocolytic drugs 1617
total intravenous anaesthesia (TIVA) 87
training 211, 217
during antenatal clinics 47
in obstetric emergencies/critical care
for anaesthetists 3334
for midwives 33, 211212
multidisciplinary teams 200, 213216
for obstetricians 33
in pain relief for childbirth, for midwives 216217
performance assessment tools 216
tranexamic acid 199
transfer of patients
for instrumental delivery 40
when critically ill 34
transvaginal cervical cerclage 9394
transverse abdominal plane (TAP) blocks 8790
trauma
genital tract/perineal 40, 69, 95, 198
head injury 172
trisomy 21 (Downs syndrome) 117
twins 41
UK Obstetric Surveillance System (UKOSS) 2728, 8384

ulcers, peptic 109
ultrasonography, spinal 135137
umbilical artery/umbilical vein 1011
umbilical cord prolapse 94
unconscious patients, consent 227
urate 100
urinary tract infections 7, 147
urinary tract obstruction 150151
urticaria 178, 181
uterine arteries 77, 199
uteroplacental circulation 3, 911, 50, 52
uterus
atony 17, 197, 198199
bimanual compression 197
hysterectomy 199
tocolytic agents 1617
vaccination
influenza 112
postpartum in HIV-positive patients 188
vaginal delivery see labour
valid consent see consent
valproate 173
valvular disease
mechanical valves 119
stenosis 118119
vasopressin (antidiuretic hormone) 107, 152, 167
vasopressors 20, 52, 69, 7778, 103, 107, 183
vecuronium 178
vena cava compression 3, 50, 5152, 192
venous thromboembolism see thromboembolism
ventilation 108, 192
ventouse 40, 188
ventriculoseptal defects (VSD) 116
vestibular schwannoma 166
viral infections
genital herpes 188189
hepatitis 189
HIV 185188
influenza 109112
volume of distribution (VD) of drugs 7, 13
vomiting 15, 70, 79
anti-emetics 15, 19, 50, 70, 203
postoperative 203
von Willebrands disease 158159
warfarin 22, 119, 124

white blood cells 1, 2, 106
workplace-based emergency skills training 214
zanamivir 112
zidovudine 185, 186, 187, 188

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CO RE TO PICS IN O BSTETRIC ANAESTHESIA

Cambridge University Press is part of the University of Cambridge.

Information on this title: www.cambridge.org/9781107028494

Cambridge University Press 2015

First published 2015

Printed in the United Kingdom by TJ International Ltd. Padstow Cornwall

Library of Congress Cataloguing in Publication data

Core topics in obstetric anaesthesia / edited by Kirsty MacLennan, Consultant

Obstetric Anaesthetist, St Marys Hospital, Central Manchester, University

Hospitals NHS Trust, Manchester, UK, Katherine OBrien, Consultant Obstetric

Anaesthetist, St Marys Hospital, Central Manchester, University Hospitals NHS

Trust, Manchester, UK, William MacNab, Consultant Obstetric Anaesthetist,

St Marys Hospital, Central Manchester, University Hospitals NHS Trust,

ISBN 978-1-107-02849-4 (hardback)

1. Anesthesia in obstetrics. I. MacLennan, Kirsty. II. OBrien, Katherine,

1962 III. MacNab, William, 1969

ISBN 978-1-107-02849-4 Hardback

3 Pharmacology relevant to pregnancy

4 Maternal morbidity and mortality

6 Obstetrics for the anaesthetist

9 Non-regional analgesia techniques for labour

10 Regional analgesia techniques for labour

11 Regional anaesthesia for operative delivery

15 Sepsis and influenza in pregnancy

16 Cardiac disease in pregnancy

17 Respiratory disease in pregnancy

19 Endocrine disease in pregnancy including diabetes mellitus, thyroid and adrenal

21 Haematologic disease in pregnancy

22 Neurosurgical and neurological disease in pregnancy

23 Immunology, including testing and management of allergy during pregnancy

26 Postpartum complications, follow-up and maternal satisfaction

28 Clinical governance and patient safety

29 Ethics, consent and the law

Basic science, epidemiology and service

N. J. Nirmalan and M. Nirmalan

Table 1.1 The most significant haematological changes in pregnancy

Increased procoagulant factors

The cardiovascular system

Table 1.2 Summary of key cardiovascular changes in pregnancy

Stroke volume +30%

Heart rate +1520%

DBP 1520 mmHg

MAP 1520 mmHg

Cardiac output +5070% (increase is more dramatic in late

The respiratory system

Respiratory rate Unchanged

Minute volume/ventilation Increased by 3050%

Tidal volume Increased by 3050%

Maximum mid-expiratory flow rate (forced expiratory Unchanged

Functional residual volume Decreased by 18%

Changes in the intrapartum and postpartum periods

Acidbase regulation in pregnancy

Oxygenhaemoglobin dissociation curve in pregnancy

The gastrointestinal system

The hepatic system

Table 1.4 Changes in GFR in pregnancy

Normal adult female 106 to 132 mL/min

Trimester one 131 to 166 mL/min

Trimester two 135 to 170 mL/min