Handbook of Obstetric Anaesthesia

Handbook of Obstetric Anaesthesia
The Simpson Handbook of

Obstetric Anaesthesia
Dr A S Buchan and Dr G H Sharwood-Smith
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Viewed apart, and in an isolated light, the degree of
actual pain (of labour) is as great if not greater than
that attendant upon most surgical operations ...
Sir James Young Simpson, March 1847
Copyright A.S.Buchan and G.H.Sharwood-Smith 1999 all rights reserved. Published by the Royal College of Surgeons of Edinburgh
Updated on August1 2002
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INDEX
INDEX
Acute renal failure Induction of general anaesthesia

Alveolar ventilation Inferior vena cava (IVC)
Amniotic fluid embolus Infiltration and field block anaesthesia for caesarean section
Anaesthesia for:- Inhalational analgesia
cervical suture Intrathecal opioids, (multiple refs) Ref1 Ref2
cord prolapse Intravenous PCA in labour
emergency caesarean section
instrumental delivery Links to other obstetric anaesthetic sites
major obstetric haemorrhage Loss of bladder sensation
manual removal of placenta Lower oesophageal sphincter (LOS)
placenta praevia
post partum evacuation of uterus Magnesium sulphate, (multiple refs) Ref1 Ref2 Ref3 Ref4
the pregnant patient Maintenance of general anaesthesia
Anaphylactic shock Major obstetric haemorrhage management
Antepartum haemorrhage (APH) Malignant hyperpyrexia
Anticoagulant therapy Manual removal of placenta
Aortocaval compression Meconium aspiration syndrome
Apgar score Mendelson's Syndrome
Assessment of the neonate Mobile epidural, (multiple refs)Ref1 Ref2
Audit of epidural analgesia Multiple pregnancy
Awareness under general anaesthesia
Neonatal resuscitation
Blood and circulatory changes in pregnancy Neonatal resuscitation chart 1
Blood products Neonatal resuscitation chart 2
Bloody tap Neurological damage after epidural or spinals
Breast feeding and anaesthetic related drugs Normal delivery of infant
Caesarean section under regional anaesthesia Obesity
Cardiac disorders Obstetric haemorrhage
Cardiac Output Oliguria, (multiple refs) Ref1 Ref2
Cardiopulmonary resuscitation (CPR) Oxy-haemoglobin dissociation curve
Cauda equina syndrome
Caudal analgesia Pain in labour
Central venous pressure, (multiple refs) Ref1 Ref2 Pain pathways
Cervical suture Paracervical block
Checklist prior to delivery of infant Patient controlled epidural analgesia (PCEA)
Clonidine Phenylephrine
Coagulation, (multiple refs) Ref1 Ref2 Ref3 Ref4 Ref5 Physiological changes at birth
Coagulation problems during pregnancy Psychological factors
Colloid solutions Placenta accreta
Combined spinal and epidural (CSE) Placenta praevia
Complications of pregnancy Placental abruption
Continuous spinal analgesia Plasma volume
Contraindications for epidural analgesia Positive intravenous test dose
Convulsions Post partum haemorrhage (PPH)
Cord prolapse Postoperative pain management
CPR algorithm Pre-eclampsia, (multiple refs) Ref1 Ref2 Ref3 Ref4
Cricoid pressure , (multiple refs) Ref1 Ref2 Ref3 Preface
Preparation for general anaesthesia
Dermatome chart Preterm delivery
Diabetes mellitus Problems with epidural analgesia
Difficult intubation Pudendal block
Disseminated intravascular coagulation (DIC) Pulmonary aspiration syndrome
Dopamine,(multiple refs) Ref1 Ref2 Ref3 Ref4 Pulmonary embolism
Drugs for epidural analgesia Pulmonary oedema, (multiple refs) Ref1 Ref2 Ref3 Ref4
Dural blood patch
Dural puncture, (multiple refs) Ref1 Ref2 Ref3 Ref4 Regurgitation,(multiple refs) Ref1 Ref2
Renal changes in pregnancy
Eclampsia Respiratory changes in pregnancy
Entonox, (multiple refs) Ref1 Ref2 Respiratory disorders
Ephedrine, (multiple refs) Ref1 Ref2 Ref3 Ref4 Ref5 Resuscitation drug doses
Epidural abscess
Epidural anaesthesia for Caesarean section Segmental nerve supply to the perineum
Epidural analgesia Serum cholinesterase
Epidural catheter difficulties Spinal anaesthesia for Caesarean section
Epidural infusion Spinal analgesia
Epidural infusion regimens Spinal curves
Epidural vein catheterisation Spinal headache, (multiple refs) Ref1 Ref2
Ergometrine, (multiple refs) Ref1 Ref2 Spinal solutions
Spinal or epidural haematoma
Failed intubation drill Spiral arteries, (multiple refs) Ref1 Ref2
Failure to thread epidural catheter Steroid treatment regimens
Fetal haemoglobin Subdural block
Fetal heart rate (FHR) monitoring Suggested technique for epidural analgesia
Fibrinogen, (multiple refs) Ref1 Ref2 Supine hypotensive syndrome
Systemic analgesia
Gastrointestinal changes in pregnancy
General Anaesthesia Total spinal block
Glyceryl Trinitrate (GTN) Toxic reaction to local anaesthetic
Transcutaneous electrical nerve stimulation (TENS)
HELLP syndrome
Heparin,(multiple refs) Ref1 Ref2 Uterine atony
Hepatic changes in pregnancy Uterine hypertonus
Hypertension, (multiple refs) Ref1 Ref2 Uterine relaxation with glyceryl trinitrate
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INDEX
Hypotension, (multiple refs) Ref1 Ref2 Ref3 Ref4 Ref5

Venous air embolus
Inadequate epidural block Venous thromboembolus
Inadvertent dural puncture Ventilatory parameters
Indications for epidural analgesia
Indications and management of the apnoeic baby
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Preface
ABOUT THE SIMPSON HANDBOOK OF OBSTETRIC ANAESTHESIA
A sound practical and theoretical knowledge of the basic procedures is required to deal with the challenge posed by labour ward
emergencies. This handbook which is based on a manual for a large maternity hospital is designed to meet this need. Recent
advances in electronic publication have opened up new and exciting opportunities for distributing and updating the handbook. While
the approach remains essentially didactic it is now possible to provide an up to date reference base with online links to Medline
and revised clinical guidelines in accordance with current practice. Feedback from our readers will play a welcome and
essential part in developing the content and technical aspects of the book. We hope that all labour ward staff (medical and
midwifery) will find it a useful resource. It should also be a useful revision guide for postgraduate examinations. Hypertext links to
obstetric and anaesthetic WWW resources will be developed further as they become available.
ACKNOWLEDGEMENTS
Several of our anaesthetic and medical colleagues have given their valuable advice in the preparation of the book. We would
particularly like to thank the following obstetric anaesthetists: Professor Felicity Reynolds, Dr Vicki Clark, Dr John McClure and Dr
Anne McCrae. Mrs Glynis Omond has given us invaluable secretarial assistance.
We would also like to acknowledge receipt of a grant from Astra Pharmaceuticals Ltd. towards the costs of multimedia authoring.
LEGAL MATTERS AND DISCLAIMER
Every effort has been made to ensure that the material in this book conforms to current guidelines and practice in obstetric
anaesthesia. Before instituting treatment all dosage schedules should be checked with manufacturers recommendations. Treatment
protocols are not intended to be recommendations for a particular patient. Practitioners should always refer to local practice and
guidelines before instituting treatment. The publisher, editors and authors can not therefore accept any liability arising from the
treatment of any particular patient.
A.S. BUCHAN, G.H. SHARWOOD-SMITH December 1999
While publication has been made possible by the support of advertisers the authors wish to emphasise their complete
independence in deciding the content of the book
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In addition to the normal hypertext features seen in this publication items such as colour pictures, sound, video and live references
to items on the World Wide Web / discussion groups we hope that virtual 3D simulations will soon be included and will be
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CHAPTER 1
Copyright A. S. Buchan and G.H. Sharwood- Smith 1999 all rights reserved. Published by the Royal College of Surgeons of Edinburgh
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Chapter 1
1 PHYSIOLOGICAL CHANGES IN PREGNANCY
Chapter contents
Blood and circulatory changes

Respiratory changes
Gastrointestinal changes
Renal changes
Hepatic changes
The following alterations occur in order to meet the increasing metabolic demands of the fetus and prepare the mother for delivery.
BLOOD AND CIRCULATORY CHANGES
Coagulation
During pregnancy - there is increased activation of the coagulation system affecting the normal balance of intravascular coagulation
and fibrinolysis. Platelet activity and consumption are increased but there is also a compensatory rise in production. The
concentration of most coagulation factors including fibrinogen VII,VIII, IX, X and XII are significantly increased. By contrast factor XIII
(fibrin stabilising factor) decreases. Increased levels of antithrombin III, an increase in fibrin degradation products and increased
plasminogen concentrations reflect enhanced fibrinolysis. These changes are not detected in a routine coagulation screen which is
usually reported as 'normal'
At delivery - placental separation prompts a further shift to increased coagulation but a fall in fibrinolysis. The risk of postpartum
haemorrhage is reduced but this change is also linked to an increased risk of postpartum thromboembolism. Uterine contraction
leading to closure of open placental vessels is also essential in reducing blood loss.
Blood volume - plasma volume increases by 45% while the red cell mass increases by only 20%. This results in the physiological
anaemia of pregnancy (the haemoglobin falling from 15 g/dl to 12 g/dl at 34 weeks). The blood volume returns to normal 10 - 14
days post partum (Fig 1.1).
Haemodynamic changes - progesterone induced vasodilatation causes a 20% decrease in peripheral vascular resistance by term;
consequently there is a fall in systolic and diastolic blood pressures. In the last trimester changes in posture may exert significant
effects on cardiac output and blood pressure. Cardiac output rises to 50% above the non pregnant level during the third trimester;
heart rate and stroke volume both rise by 25%. The central venous pressure, reflecting right ventricular filling pressure, shows no
change during normal pregnancy - left ventricular hypertrophy and dilatation accounting for the increased cardiac output. During
labour cardiac output rises by a further 15% in the latent phase, 30% in the active phase and up to 45% in the expulsive phase.
Fig 1.1 Changes in cardiac output, plasma volume and red blood cell (RBC) volume during pregnancy and the puerperium
(modified from Obstetric Analgesia and Anesthesia: 1980 Bonica JJ. World Federation of Anaesthesiologists, Amsterdam.)
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Chapter 1
Aortocaval compression
After 24 weeks the gravid uterus may compress the inferior vena cava when the patient lies supine thus reducing venous return
and maternal cardiac output. Two compensatory mechanisms exist:
An increase in sympathetic tone leading to venous and arterial constriction (this includes the utero-placental circulation) and
an increase in heart rate.
A collateral circulation allows blood from the lower limbs to flow through the vertebral venous plexus and reach the right side
of the heart via the azygos veins.
In 10% of mothers these mechanisms are inadequate to maintain a normal blood pressure when supine (supine hypotensive
syndrome). If the blood pressure fall is severe, consciousness may be lost. Turning the patient onto her side allows the cardiac
output and blood pressure to return to normal as the IVC is decompressed. Falls in maternal cardiac output and blood pressure lead
to a reduced placental flow with the risk of fetal hypoxia. By contrast the thicker walled aorta is less prone to compression; however,
should it occur blood flow to the kidneys, uterus, placenta and the lower limbs may decrease - inadequate placental perfusion and
fetal hypoxia may also follow. During labour uterine contractions displace most of the blood from the uterus and placenta into the
azygos system; important consequences of this include intermittent increases in epidural venous pressure and cardiac output.
Significance to the anaesthetist
Anaesthesia - The induction of general anaesthesia or the institution of epidural or spinal blockade reduce sympathetic tone
and may unmask aortocaval compression; as a result there is likely to be a fall in maternal cardiac output, blood pressure
and placental perfusion. A left lateral tilt should be maintained by appropriately wedging the mother's pelvis.
Labour and delivery - The mother should be prevented from lying completely supine. This is especially important during
fetal blood sampling or instrumental delivery.

Venous distension - Distension of epidural veins increases the chance of vascular damage during performance of regional
blocks. It also reduces the volume of the epidural and intrathecal spaces therefore a reduced dose of local anaesthetic is
required at term.
Resuscitation - During external cardiac massage tilting the patient is essential to allow refilling of the right side of the heart.
Immediate delivery also improves venous return and offers the best chance of survival for both mother and baby.
Blood loss
During vaginal delivery this averages 300 ml, in Caesarean section 750 ml; normally this is well tolerated because of the
increased blood volume
Cardiac output
Venous return increases immediately after delivery due to an autotransfusion secondary to uterine emptying and the removal
of IVC occlusion. Normally this additional volume is accommodated by vasodilatation and an increase in cardiac output;
however cardiac failure with pulmonary oedema may be precipitated in the following conditions: systemic or pulmonary
hypertension, severe cardiac disease and the use of vasopressors including ergometrine.
Regional analgesia reduces the large increase in cardiac output which occur during labour and following delivery. It may be
of value in patients such as those above with a limited cardiac output
Utero-placental circulation

Chapter 1
Fig 1.2 Diagram of the maternal blood supply to the human placenta
As pregnancy advances a fibrin matrix replaces the elastic lamina and smooth muscle of the spiral arteries ( Fig. 1.2). Consequently
vascular resistance falls and placental blood flow increases. At term the uterine blood flow is around 700 ml/minute (10% of cardiac
output); some 80% of this flows via the maternal spiral arteries into the intervillous space where exchange of gases and nutrients
occurs between the villi containing the fetal capillaries and the maternal blood. Any reduction in uterine blood flow is therefore
detrimental to the fetus.
Uterine blood flow = (uterine arterial pressure - uterine venous pressure)

uterine vascular resistance
An increase in uterine vascular resistance causes a reduction in uterine blood flow. The uterine vascular resistance and venous
pressure rise with each contraction. The bigger the contraction the more profound the drop in uterine perfusion. When the intra-
amniotic pressure rises above 50 - 60 mmHg intervillous perfusion ceases. Hence uterine hypertonus is clearly undesirable.
Likely causes of reduced uterine blood flow are -
Hypotension:- aortocaval compression, blood loss, sympathetic block

Hypertension:- essential or pregnancy-induced elevation of blood pressure
Uterine Hypertonus:- excess oxytocin, placental abruption, high concentrations of local anaesthetic, ketamine in doses > 1.5
mg/kg, cocaine abuse
Vasoconstriction:-sympathetic overactivity due to fear/anxiety or extreme hypoxia, sympathomimetic drugs (a1 adrenergic)
with the exception of ephedrine (mainly ß1 adrenergic),
Fall in cardiac output: - this is not necessarily accompanied by a fall in blood pressure - for example in pre-eclampsia
RESPIRATORY CHANGES
Anatomy - Capillary engorgement affects all the airways. In particular the false cords and arytenoids may be oedematous. There is
a progesterone induced increase in ventilation with tracheal and bronchial dilatation. Although the uterus displaces the diaphragm
upwards inspiration is still predominantly due to diaphragmatic contraction. There is a compensatory increase in both the
anteroposterior and transverse diameters of the rib cage.

Chapter 1
Fig 1.3 Changes in ventilatory parameters during pregnancy (modified from Obstetric Analgesia and Anesthesia: 1980
Bonica JJ. World Federation of Anaesthesiologists, Amsterdam.)
Lung volumes: A 20% reduction in functional residual capacity is present in the third trimester; this is due to a reduction in both
expiratory reserve volume and residual volume. Inspiratory capacity increases and vital capacity is unchanged.
Ventilation and blood gases during pregnancy
Alveolar ventilation - increases by 70% during the second to third month of gestation. This is mainly due to an
increase in tidal volume.
Oxygen consumption and carbon dioxide production - both increase progressively to reach 60% above non pregnant
levels at term.
Pa CO 2 - falls and stabilizes at 4.1 kPa (31 mmHg) by the end of the first trimester; this is due to rising progesterone
levels which reset the sensitivity of the respiratory centre to Pa CO 2
Pa O 2 - rises to 14 kPa (105 mmHg) during the third trimester in the erect position; this is due to the fall in Pa CO 2
plus a reduced arteriovenous oxygen difference. The Pa O 2 declines slightly by term - the rise in cardiac output does
not keep pace with to the increased oxygen consumption and arteriovenous oxygen difference increases. In the
supine position a fall in cardiac output and, in some patients, closure of dependant airways may lead to a fall in
Pa O 2 to <13.5 kPa (100 mm Hg)
Ventilation during labour: Pain and anxiety during labour may induce significant further changes to some of the above values.
Table 1.1 Ventilatory data for pregnancy and labour.
Pregnancy Labour
Respiratory rate /min 15 22 - 70
Tidal volume ml 480 - 680 650 - 2000
Minute ventilation l/min 7.5 - 10.5 9 - 30
Pa CO 2 kPa 4.1 (31 mmHg) 2 - 2.7 (15 - 20 mmHg)
Pa O 2 kPa 14 (105 mmHg) 13.5 -14.4 (100-108 mmHg)
Airway obstruction at induction of general anaesthesia leads to a more rapid fall in oxygen saturation than in the non-
pregnant patient because:
oxygen consumption is increased at term; functional residual capacity is reduced - there is a reduced oxygen reservoir
in the lungs, a fall in cardiac output and sometimes closure of dependant airways.
The reduced functional residual capacity has other important consequences:
during preoxygenation before induction of general anaesthesia (important in delaying the onset of hypoxia) the time for
denitrogenation is reduced: 2-3 minutes is required
during anaesthesia with volatile agents the alveolar anaesthetic concentration rises relatively rapidly to approach the
inspired concentration.
Airway obstruction is more likely to occur during sedation and anaesthesia. The airway mucosa is easily traumatised and may
bleed profusely. A smaller endotracheal tube may be required especially if the larynx is oedematous (pre-eclampsia)
There may be difficulty with laryngoscopy and tracheal intubation. Failed intubation rates of 1:280 compared to 1:2200 in the
non pregnant population have been reported.
Materno-fetal respiratory gas exchange

Chapter 1
Fig 1.4 Oxygen dissociation curves for human maternal and fetal blood, indicating the physiologic range of PO2 and O 2 for
mother and fetus. (Modified from Towell ME: Fetal respiratory physiology in Perinatal Medicine.1976 Edited by JW
Goodwin, GW Chance: Longman; Toronto, Canada.)
Although fetal partial pressure of oxygen is much lower, the saturation is relatively higher than in the adult. This is because fetal
haemoglobin (75% - 80% of the haemoglobin at birth) has a greater affinity for oxygen than adult haemoglobin. The fetal oxy-
haemoglobin dissociation curve is displaced to the left (see fig 1.4).
Important shifts of the dissociation curves take place in the placenta. The maternal blood gains CO 2 , the pH falls and the curve
shifts to the right releasing additional oxygen. On the fetal side of the placenta CO 2 is lost, the pH rises and the curve shifts to the
left allowing additional oxygen uptake (double Bohr effect).
Other important factors in delivery of oxygen to the fetal tissues are:
A high maternal intervillous blood flow (almost double the fetal placental flow)
The high fetal haemoglobin (16 - 17 g/dl)
The high fetal cardiac output
The fetal metabolic acidosis which shifts the curve to the right and thus aids delivery of oxygen to the tissues.
The high oxygen affinity of fetal blood could limit oxygen unloading to the tissues although this is minimised by the steepness
of the curve.
An effective epidural block in labour may largely reverse the following detrimental, metabolic and respiratory changes:
Maternal hyperventilation causes respiratory alkalosis and hypocapnia, causing cerebral and placental vasoconstriction.
The oxyhaemoglobin dissociation curve is shifted to the left. This increases the affinity of maternal haemoglobin for
oxygen and reduces the amount of oxygen available for transfer to the fetus.
During a long labour with painful contractions an opposing change may also occur: there is an increase in the
metabolic rate and oxygen consumption with a tendency to lactic acidosis thus causing a right shift of the curve and
reducing maternal oxygen uptake.
GASTRO-INTESTINAL CHANGES
As pregnancy progresses the intra abdominal pressure increases and the axis of the stomach is altered. The competence of the
lower oesophageal sphincter (LOS) is reduced due to the relaxant effect of progesterone on smooth muscle; most pregnant
women suffer from heartburn and some 80% have gastric reflux at term. There is no evidence of delayed gastric emptying during
pregnancy. By contrast prolonged labour is associated with impaired gastric emptying and increased gastric volume. The
administration of opioids aggravates these changes, and also reduce the tone of the LOS. These physiological changes can be
expected to return to normal within 24 - 48 hours of delivery.
The upper oesophageal sphincter (UOS) is formed mainly from the striated cricopharyngeus muscle. Its pressure varies from 40
mmHg when awake to 8 mmHg during deep sleep. Regurgitation will occur when this pressure falls below that of the oesophageal

Chapter 1
contents. The UOS may retain sufficient tone to prevent regurgitation of oesophageal contents during general anaesthesia with
volatile agents in the absence of neuromuscular blockade: however this cannot be relied upon.
Pulmonary aspiration of gastric acid with a pH of less than 2.5 and a volume of between 25 - 50 ml may lead to the
development of a severe aspiration pneumonitis (Mendelson’s Syndrome).
Obesity, multiple pregnancy, hydramnios and the lithotomy position increase the likelihood of gastric reflux and possible
pulmonary aspiration
Neutralisation of gastric acid and a technique of rapid sequence induction of general anaesthesia are mandatory because of
these changes
The application of cricoid pressure compensates for the reduction in UOS pressure which occurs during induction of general
anaesthesia
The evidence suggests that 24 - 48 hours after delivery and during early pregnancy the above precautionary techniques are
unnecessary unless the woman has symptomatic reflux or severe obesity
RENAL CHANGES
Glomerular filtration rate and renal plasma flow increase rapidly in the first trimester. There is an increase in urine production and
frequency of micturition. The clearances of urea, creatinine and urate are correspondingly increased and serum levels are below non
pregnant levels (table 1.2).
Table 1.2 Pregnant and non pregnant parameters of renal function
Investigation Pregnant Non Pregnant

Plasma creatinine µmol/l 50 - 73 73
Plasma urea mmol/l 2.3 - 4.3 4.3
Plasma urate mmol/l 0.15 - 0.35 0.2 - 0.35
Plasma bicarbonate mmol/l 18 - 26 22 - 26
Aldosterone, progesterone and renin-angiotensin activity increase and there is a rise in total body water and sodium. The
reabsorptive capacity for glucose and lactose is reduced (glycosuria is present in 40% of pregnancies). Progesterone causes
ureteric dilatation; the associated urinary stasis may precipitate infection.
Renal problems are usually encountered with pre-eclampsia. Proteinuria occurs due to glomerular damage. Oliguria may be a
consequence of arteriolar damage and spasm which may lead to acute tubular necrosis.
Non-steroidal anti-inflammatory drugs (NSAID) may be used as tocolytics and for post delivery pain relief. They are
prostaglandin synthetase inhibitors and may reduce renal blood flow when renal function is compromised e.g. pre-eclampsia
or following major blood loss.
Increased doses of renally excreted drugs may be required to obtain adequate therapeutic levels.
HEPATIC CHANGES
Slight elevations in aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and alkaline phosphatase occur during
pregnancy. Serum cholinesterase activity is reduced by 25% at term and by 33% three days postpartum. This appears to be due to
haemodilution rather than decreased synthesis. In practice the duration of action of suxamethonium is increased by 2-3 minutes in
the first week postpartum; this is not a clinical problem.
FURTHER READING
Bonica JJ. Maternal Anatomic and Physiological Alterations during Pregnancy and Parturition. In: Bonica JJ, McDonald JS eds.
Principles and Practice of Obstetric Analgesia. Baltimore:Williams & Wilkins, 1995;45-83.
Conclin KA. Physiologic changes of pregnancy. In:Chestnut DH ed. Obstetric Anesthesia.St Louis: Mosby,1994;17-76.

Chapter 1
Chamberlain G and Pipkin B.F. Clinical Physiology in Obstetrics; Blackwell Science, 1998.
Bourne T, Ogilvy AJ, Vickers R, Williamson K. Nocturnal hypoxaemia in late pregnancy. British Journal of Anaesthesia 1995;75:
678-682.Click here for Medline link
Bassell GM and Marx GF. Optimisation of fetal oxygenation. International Journal of Obstetric Anesthesia 1995;4:238-243.
Pilkington S, Carli F, Dakin MJ, Romney M, Dewitt KA, Dore CJ, Cormack RS. Increase in Mallampati score during pregnancy.
British Journal of Anaesthesia 1995; 74: 638-642.Click here for Medline link
Vanner RG. Mechanisms of regurgitation and its prevention with cricoid pressure. International Journal of Obstetric Anesthesia 1993;
4:207-215.
NEXT CHAPTER

Chapter 2
2. ANALGESIA
Chapter contents
Pain in labour
Pain pathways
Psychological factors
TENS
Systemic opioid analgesia
Inhalational analgesia
Paracervical block (T10 - L1)
Pudendal block (S234)
Caudal analgesia
Spinal analgesia
PAIN IN LABOUR
Unrelieved pain during labour may lead to fetal acidosis and hypoxia in the following situations:
Prolonged labour - causing maternal metabolic acidosis
Maternal hyperventilation - leading to:
increased maternal oxygen consumption

hypocapnia - this may cause constriction of the utero-placental vessels and shift the
oxyhaemoglobin dissociation curve to the left reducing the amount of oxygen available for
transfer to the fetus
Maternal anxiety - leading to increased catecholamine release - a reduction in utero-placental flow may follow; (uterine
contractions may also be inhibited).
PAIN PATHWAYS
Labour pain
This pain is due to cervical and lower uterine segment dilatation, uterine contraction and distension of the structures surrounding the
vagina and pelvic outlet. Initially the pain is felt in the lower abdomen but as labour progresses the distension of the birth canal by
the descending fetal part causes back, perineal and thigh pain.
Fig 2.1 Pain pathways during labour and delivery
Uterus and cervix - afferent impulses are transmitted via the Aδ and C fibres which travel with sympathetic nerves via the
hypogastric plexus to enter the lumbar and lower thoracic parts of the sympathetic chain. Central connection to the spinal cord is via
the dorsal root ganglion and lateral division of the posterior roots of T10-L1. Labour pains are therefore referred to the areas of skin
supplied by these nerves i.e. the lower abdomen, loins and lumbo-sacral region.

Chapter 2
Vagina and pelvic outlet - afferent transmission is also via Aδ and C fibres but with the parasympathetic bundle in the pudendal
nerves (S2,3,4). There is also a minor contribution from the ilio-inguinal, genito-femoral and the perforating branch of the posterior
cutaneous nerve of thigh.
It is important to appreciate that pain sensitive structures in the pelvis are also involved, i.e. the adnexi, the pelvic parietal
peritoneum, bladder, urethra, rectum and the roots of the lumbar plexus. Therefore L2 to S5 must be blocked. There is an overlap
and pain relief is not a simple matter of blocking T10 to L1 for the first stage and S2, 3, 4 for the second stage of labour.
PSYCHOLOGICAL FACTORS
The amount of pain relief does not necessarily equate with maternal satisfaction, the concept of coping with pain is important. Every
mother is different and the degree of discomfort and pain that each is prepared to tolerate varies considerably. Antenatal preparation
in the parenthood classes plays an important role in pain management. Education should be offered in the basic physiology of
pregnancy and labour and there should be an emphasis on choice of analgesic methods. Relaxation and breathing exercises help
the patient to control her response to pain. It is most important that the patient is not made to feel a failure if she eventually
requests epidural analgesia.
Anaesthetic interventions can be made easier and safer by reinforcing what has been taught in the parenthood classes.
TENS
Transcutaneous Electrical Nerve Stimulation (TENS) is a popular method of analgesia that is entirely patient controlled. Two sacral
and two lumbar silicone rubber carbon electrodes are applied by the patient or partner; the amplitude and frequency are set to just
above the sensory threshold, this may require some experimentation. At the onset of a contraction the patient can deliver a boost
using a hand control. The method may be used as sole analgesia throughout labour and delivery but additional or alternative
analgesia is usually required as labour progresses. Full analgesia may not be achieved for twenty minutes or so. The range of
controls is typically:- current 0 - 50 mA, frequency 0 - 100 Hz and pulse width 0.1 - 0.5 milli seconds.
SYSTEMIC OPIOID ANALGESIA
All analgesic drugs cross the placenta freely; narcotic drugs significantly affect respiration and neurobehavioural responses in the
neonate for up to 48 hours. Pethidine is the most widely used analgesic. The dose is 50 - 150 mg i.m. and lasts for 2 - 3 hours.
Respiratory depression in the neonate is maximal when delivery occurs 3 hours following administration. Unfortunately ineffective
analgesia, sedation, nausea and dysphoria are frequent complaints. Morphine 10 - 15 mg and diamorphine 5 - 10 mg are believed
to be more effective and longer acting. They have a greater potential for neonatal respiratory depression but are most useful in the
primigravid patient when a longer labour is anticipated. The request for a second dose is an opportunity to consider the
establishment of an epidural block. The problem of delayed gastric emptying is an important maternal side effect with this group of
drugs. The agonist-antagonist group (pentazocine, butorphanol and nalbuphine) have the advantage of a ceiling effect for respiratory
depression but ineffective analgesia, nausea and dysphoria are disadvantages. Nausea can be relieved by intramuscular cyclizine
50 mg or metoclopramide 10 mg.
A further option is a patient controlled analgesia system (PCAS) in which the anaesthetist can preset the incremental dose and
minimum interdose interval. The drugs most commonly used are pethidine, fentanyl and remifentanil.
Table 2.1 Doses used for intravenous PCA in labour
Pethidine Fentanyl Remifentanil

Initial loading/starting dose 50 - 75 mg 50 µg 35 µg
Bolus 20 - 25 mg 25 - 30 µg 50 - 75 µg
Lock-out period 5 minutes 5 minutes 2 - 3 minutes
Suggested 4 h dose limit 300 mg 400 µg
I t is important that patients are taught how to use PCA so that they do not press the button every time they have a contraction with
pethidine and fentanyl. Remifentanil has a peak plasma to peak pharmacodynamic effect time of 1 - 2 minutes, a bolus dose given
even at the very onset of contraction is always likely to have its peak effect after the height of the contraction. Unfortunately in
practice PCA does not work as well in labour as it does in the post-operative period where the experience of pain is entirely
different. A limit must be set on the total dose of drug given. Analgesic requirements must be reappraised after the first
four hours.

Chapter 2
Anxiety is best managed with the sympathetic support of the partner and the midwifery and medical staff.
INHALATIONAL ANALGESIA
Premixed 50% nitrous oxide in oxygen (Entonox) is self-administered from a piped or cylinder supply by facemask or mouthpiece
with a demand valve. It can be used either as a supplement to parenteral analgesia or alone from the onset of painful contractions
in the first stage until the end of the second stage. Correct use is important and often neglected. The mask should be used with
deep but slow respiration at the onset of a contraction and before pain is experienced. Entonox is not inspired between contractions.
It has a rapid onset and is non-cumulative due to the low blood gas solubility of nitrous oxide. Self-administration prevents excessive
sedation. To avoid separation of the pre-mixed nitrous oxide and oxygen, cylinders should not be exposed to cold. If it is suspected
that the storage temperature has fallen below -7°C the cylinder should be warmed to a safe temperature and inverted three times.
PARACERVICAL BLOCK (T10 - L1)
This technique can produce complete pain relief in the first stage of labour in up to 80% of patients but requires repeated doses. A
sheathed paracervical needle is used and 10 ml of 1% lidocaine or 0.25% bupivacaine are injected into each lateral fornix. Obstetric
applications are limited by the risk of fetal bradycardia and acidosis - the fetal head is close to the site of injection. The main use is
in outpatient gynaecological procedures.
Fig 2.2 Paracervical block
PUDENDAL BLOCK (S234)
Fig 2.3 Pudendal block
This provides anaesthesia for episiotomy and low forceps delivery. It is not adequate on its own for rotational forceps delivery but
may be combined with Entonox. The vaginal approach is usually preferred and each pudendal nerve is blocked as it passes under
and slightly posterior to the ischial spine.
Perineal analgesia may not be complete because overlap can occur from the genital branch of the genito-femoral nerve and also the

Chapter 2
perforating branch of the posterior cutaneous nerve of thigh.
CAUDAL ANALGESIA
Indications
Forceps delivery
Pain relief in labour
Perineal suture
There may be a place for caudal block in the presence of scoliosis or after spinal fusion. Veins in the caudal epidural space are
engorged during pregnancy and the dose must be reduced accordingly e.g. a volume of 30 ml 0.25% bupivacaine may easily reach
T9.
Continuous caudal analgesia requires large doses of drug to obtain pain relief in the first stage of labour. The catheter is in a
potentially dirty area and infection is a hazard. Caudal blockade is difficult in pregnancy because the sacral hiatus is frequently
obscured with a pad of fat. A useful method of ensuring that the needle is in the epidural space, after aspiration, is to inject a small
volume of air (1-2 ml) and listen with a stethoscope over the lumbar area. A crackling sound will be heard if the needle is in the
correct position. In the second stage of labour a volume of 15 - 20 ml 0.25% bupivacaine provides excellent pain relief.
The incidence of dural puncture is similar to that found in the lumbar epidural approach (1%). Important cautionary factors are the
risk of intravascular injection and reports of penetration of the fetal head.
SPINAL ANALGESIA
Spinal blockade is used mainly for surgery (i.e. spinal anaesthesia) and more rarely for analgesia in labour. Pencil point needles
have reduced to the incidence of headache to < 2%; dural fibres are parted rather than torn, minimising any CSF leak.
Indications
Pain relief (analgesia)
Mobile epidural. A combined spinal/epidural technique (CSE ) is used to achieve a walking epidural.
Continuous spinal analgesia. This is not in general use but can be a valuable technique following accidental
dural puncture with an epidural needle .
Intrathecal opioids. These are useful when local anaesthetic drugs are contraindicated; they provide analgesia
without motor block.
Obstetric procedures (anaesthesia)
Cervical suture (T10 - S5)

Instrumental delivery (T10 - S5)
Caesarean section (T4 - S5)
Manual removal of placenta (T6 - S5)
Perineal suture (S1 - S5)
Other surgery, especially during the first trimester as there is minimal exposure to drugs
Advantages
Rapid onset and predictable spread of block

Excellent analgesia with muscle relaxation (local anaesthetic drugs)
Minimum drug dosage and placental transfer
Disadvantages
Hypotension with high block

Headache - but should be < 2% of all spinals administered
A one shot technique unless a spinal catheter is used

Chapter 2
The dura is breached - there is a theoretical risk of infection, neural trauma and chemical damage
Spread of spinal solutions
Baricity is the most important factor in the spread of solution due to the shape of the spinal curves (Figure 2.4). Engorgement of
epidural veins which decreases the volume of the spinal subarachnoid space is also important. The spread of solution can be
enhanced by sudden increases in intra-abdominal pressure (during bearing down) and also active efforts to reposition the patient in
her bed which may cause waves or eddies in the CSF. Barbotage and rapid injection may also increase the height of block but are
not recommended.
Fig.2.4 Spinal curves
Spinal solutions available
Heavy bupivacaine 0.5% in 8% glucose - this is hyperbaric with a specific gravity of 1,020 at 37°C. If the patient is left in a laterally
tilted supine position a block up to T4 can confidently be expected with volumes of 1-3 ml. The greater the mass of drug the longer
the duration of block. Bupivacaine 12 -15 mg normally allows 90 -120 minutes of surgery. To induce a saddle block the patient can
be left in the sitting position for 5 minutes.
Plain bupivacaine 0.5% - this is slightly hypobaric ( 0,999 at 37°C) and has a less predictable spread than the hyperbaric solution.
The dose for Caesarean section is 3 ml in the supine or lateral position. Because it is slightly hypobaric it is possible that high
blocks may occur in the sitting position particularly in association with sudden alterations in posture.
Plain lidocaine 2% - this is used for short procedures, 3 - 4 ml will block to T10 with a duration of 1 hour. There are reports of
transient neurological symptoms (TNS) using 2% plain lidocaine (although not as frequently as with 5% lidocaine which should
never be used).
Plain prilocaine 2% - similar dosage and duration to 2% plain lidocaine, TNS have been reported but infrequently.
Continuous spinal analgesia
This technique is still being evaluated as a primary analgesic technique in labour.There have been reports of cauda equina
syndrome in non pregnant patients with lidocaine. This is thought to be due to the combination of maldistribution and a relatively
high dose of hyperbaric lidocaine pooling in the sacral curve. To reduce the potential for neurotoxicity it is suggested that the
catheter should be inserted just far enough to confirm the presence of CSF on aspiration. The lowest effective concentration of local
anaesthetic should be selected. Inadequate blockade should be managed by altering the patient’s position, using a different baricity
(isobaric is recommended), or abandoning the procedure. There have been no reports of this problem with bupivacaine.
Causes of failure of spinal block
Failure to obtain CSF - the needle is not in the midline, it has gone through the dural sac or has not reached the dural sac.
Subdural injection may occur.
Needle movement may occur out of the subarachnoid space during injection. The aperture of a pencil point needle may
straddle the dura, this can be resolved by pushing the pencil point needle a little further into the subarachnoid space once
CSF is obtained.
Loculation in the subarachnoid space.
Complications of spinal block.

Chapter 2
Hypotension
Total spinal block with cessation of respiration and hypotension - usually a complication of a misplaced epidural
Post dural puncture headache
Neurological problems including TNS, nerve root damage by direct needle trauma, arachnoiditis, cauda equina syndrome,
paraplegia and meningitis. Recent reports of cord damage are related to h needle insertion above L 3.
Intrathecal opioids in labour
Diamorphine - doses up to 2.5 mg have been used. The duration of analgesia averages 5 hours but this may not be sufficient
for the whole of labour. Pruritus and nausea may be a problem. The pruritus can usually be controlled by intravenous
naloxone without loss of analgesia. The technique requires further evaluation and is not recommended for routine use.
Fentanyl is used in the CSE mobile epidural technique.
FURTHER READING
Olofsson C, Ekblom A, Ekman-Ordeberg G, Hjelm A, Irested TL. Lack of analgesic effect of systemically administered morphine or
pethidine on labour pain. British Journal of Obstetrics and Gynaecology 1996; 103: 968-972..Click here for Medline link
Meltram I, and Wee M. Update on Pain Relief in Labour. Current Anaesthesia and Critical Care 1995; 6: 206-211.
Kangas-Saarela T, Kangas-Karki K. Pain and pain relief in labour; parturients' experiences. International Journal of Obstetric
Anesthesia 1994; 2: 67-74. Click here for IJOA link
Pain and its relief in Childbirth; Report of the 1990 NBT Survey. Edinburgh: Churchill Livingstone 1993.
Reynolds F, ed. Effects on the Baby of Maternal Analgesia and Anaesthesia. London: WB Saunders 1993.
Gamlin FMC, Lyons G. Intrathecal opioids International Journal of Obstetric Anesthesia 1997:6;161-172.
NEXT CHAPTER

Chapter 3
3. EPIDURAL ANALGESIA IN LABOUR
Chapter contents
Indications
Contraindications
Drugs
Suggested basic technique
Problems
Bloody tap; Positive intravenous test dose; Toxic reaction to local anaesthetic; Failure to thread epidural catheter; Inadequate
block; Obesity ;Hypotension; Loss of bladder sensation; Inadvertent dural puncture; Management of spinal headache; Subdural
block; Total spinal block; Epidural catheter difficulties; Spinal/epidural haematoma; Epidural abscess
Maintenance of epidural analgesia
Intermittent bolus doses; Epidural infusion; Patient Controlled Epidural Analgesia (PCEA); Mobile epidura l
Audit of epidural analgesia
INDICATIONS
Maternal request
Prolonged and painful labour (often in primiparous patients)
Malpresentation
Anticipated or actual instrument delivery
Trial of labour
Pre-eclampsia
Diabetes
Uncoordinated uterus managed by oxytocin infusion
Multiple pregnancy
Cardiac and respiratory disease
Epidural analgesia should be administered with caution if any of the following apply:
Previous Caesarean section - Sudden analgesic failure may be due to uterine rupture. A dense sensory blockade must be avoided
in order to demonstrate this important sign.
Central nervous system disorders - In multiple sclerosis there is no evidence that demyelination can be provoked by epidural
analgesia. In cerebrovascular accident, porphyria and other rare conditions the pathophysiology should be discussed with a senior
colleague and if necessary the relevant specialist before a decision is made.
Spinal deformity - Technical difficulty may increase the risk of dural puncture and failure, the caudal route may be the preferred
option.
CONTRAINDICATIONS
Full anticoagulant therapy

Coagulopathy. Platelet count must be greater than 80 x 10 9 /l
Hypovolaemic shock
Local or systemic sepsis
Refusal by patient
Raised intracranial pressure
Fixed cardiac output
Lack of appropriately trained staff
DRUGS
The three most commonly used drugs are all amide local anaesthetics. They differ in important respects: rate of onset, duration,
potency, degree of motor blockade, cardiac and neurotoxicity. In labour it is generally desirable to minimise motor blockade in order
to increase maternal mobility and hopefully reduce the rate of instrumental delivery. This can be achieved by the correct choice of
drug, concentration, volume and sometimes by the addition of an opioid e.g. fentanyl.

Chapter 3
Lidocaine is generally administered in a concentration of 2%, has a rapid onset (10-15 minutes) and a relatively short duration (45
min). Inadvertent intravenous injection carries the lowest incidence of toxic effects.
Bupivacaine 0.1-0.5% has a slower onset (20 minutes for maximal effect) than lidocaine but a longer duration. It has four times the
potency of lidocaine and is relatively more cardiotoxic. Used in the correct dosage it is generally without problem; with accidental i.v.
injection there is a risk of delayed cardiac conduction leading to bradycardia, heart block and ultimately a potentially irreversible
ventricular fibrillation. Cardiac toxicity is usually preceded by signs of major CNS toxicity i.e. convulsions.
Ropivacaine 0.1-0.5% has a similar onset and duration to bupivacaine but it is less cardiotoxic and may produce relatively less
motor blockade.
SUGGESTED BASIC TECHNIQUE
A description of technique cannot replace practical experience with a senior colleague. A safe method should be selected and
adhered to until confident and competent.
Establish the indications for epidural anaesthesia and review the patient’s relevant obstetric, medical and anaesthetic history.
Explain the procedure and obtain the patient’s informed verbal consent.
Set up a reliable intravenous infusion of saline or Ringer Lactate with, at least, a 17 gauge intravenous cannula.
Check that an ampoule of ephedrine 30 mg is immediately available.
Record the baseline blood pressure and pulse.
Arrange the patient either in the left lateral or sitting position according to preference.
Put on a face mask, scrub, glove and gown up.
Apply a suitable topical antiseptic solution to the skin and underlying tissues
Site the epidural in the L2/3 or nearest convenient interspace using a saline or air loss of resistance technique.
Measure the epidural space-skin distance using the cm graduations on the Tuohy epidural needle
Insert the catheter 5 - 6 cm into the epidural space, withdraw the needle and then withdraw the catheter to leave 3 - 4 cm in
the space or until the meniscus in the catheter falls.
Ensure that blood or cerebrospinal fluid (CSF) does not flow back either by capillary action or direct aspiration.
Administer an epidural test dose e.g. 4 ml of 2% lidocaine. Inadvertent intravenous injection rapidly produces tinnitus and
facial paraesthesia - maintain verbal contact; ask about any symptoms in a non specific way to avoid suggestion.
After 5 min record pulse and blood pressure and check for evidence of intrathecal placement (established sensory and motor
blockade) - if in doubt wait and reassess after a further 5 min.
If the test dose is negative and blood pressure and fetal heart rate are stable administer a bolus dose of 5 - 8 ml of 0.25%
bupivacaine. (see alternative maintenance regimes)
Progress over the next three contractions should indicate the efficacy of the block. An increase in skin temperature over the
feet and legs is a useful sign and demonstrates the onset of an autonomic block.
Continue with top-ups or an epidural infusion according to preference.
Monitoring the block
The following information should be monitored and recorded:
Maternal blood pressure and pulse - these should be recorded every five minutes for twenty minutes following a top up and
at least half hourly thereafter
Fetal heart rate
Extent of block
Sensory: it is important to record the upper and lower segmental sensory limits of the block bilaterally. These may be
identified by testing with a cotton wool ball (light touch), blunt needle (pinprick) or ethyl chloride (cold sensation).
Starting from an area of skin with an established block the patient will report light touch, pinprick and cold sensation in
sequence as the unblocked area is approached. This progression usually spans three segmental levels. In practice it is
sufficient to select and continue with a single method of testing.
Motor: this can be assessed on the following practical scale which is based on straight leg raising -
0 = full power

1 = able to lift but a little weak
2 = able to lift but very weak

Chapter 3
3 = unable to lift straight leg
Site and severity of any persisting pain

Mode of administration of local analgesia i.e. top ups, infusion or PCEA
Details of maintenance doses prescribed and when actually administered

PROBLEMS
Bloody tap - This is caused by puncture of a distended epidural vein by the needle or the catheter and may lead to inadvertent
intravenous injection of local anaesthetic or to the formation of an epidural haematoma. In order to minimise this risk the epidural
needle or catheter should not be advanced during a uterine contraction. Management is as for positive intravenous test dose
Positive intravenous test dose - The test dose should always be given after gentle aspiration and if positive then the catheter
should be withdrawn and resited in an adjacent interspace.
Toxic reaction to local anaesthetic - rarely this may occur despite a negative test dose. Early central nervous system signs are
slurred speech and tinnitus; with increasing toxicity there may be muscle twitching followed by convulsions. Circulatory signs include
hypotension, bradycardia and possibly cardiac arrest.
Failure to thread epidural catheter
Inject additional saline or lidocaine (3 - 6 ml) down the needle in an attempt to open up the epidural space.
Carefully rotate the Tuohy needle through 180° (risk of dural tear). Do not withdraw the catheter through the needle (risk of
dividing catheter).
Ask the patient to straighten her back by slowly extending her hips.
If associated with marked paraesthesia or failure of the above methods, resite in an adjacent interspace.
Inadequate block - This may be caused by the catheter entering the paravertebral space via an intervertebral foramen which results
in a unilateral lumbar plexus block. Occasionally connective tissue appears to sub-divide the epidural space causing a unilateral
block. Additionally there may be persistent low backache with rectal or sacral pain.
Use posture and the effect of gravity to help the spread of additional local anaesthetic.
The addition of fentanyl 50 mg or clonidine 100 - 150 mg may be of value.
If all these fail the catheter should be resited at an early stage.
Obesity
Explain that the procedure may be difficult.

Use the sitting position.
Ask patient to point to the midline of her back.
Identify and mark the midline by initially palpating the upper thoracic spines.
Palpate the iliac crest and draw a line bisecting the midline.
Infiltrate subcutaneously for 5 cm above and below this point using 1% lidocaine.
Use a suitable needle to probe and mark the midline and a spine and interspace.
If necessary use a long (15 cm) Tuohy needle to reach the epidural space.
Hypotension - Initial symptoms are often due to the rate of fall rather than the absolute level of blood pressure. The complaint is of
nausea, dizziness or sleepiness. Turn the patient onto her side (preferably left) to avoid aortocaval compression. Give 250 ml saline
or Ringer Lactate rapidly and elevate the foot of the bed. In the absence of a rapid response ephedrine is administered
intravenously in 6 mg increments until stability is restored.
Loss of bladder sensation - blockade of sacral roots may result in a failure of the patient to sense bladder distension. The patient
should be encouraged to empty her bladder two hourly or before top ups. If the bladder becomes distended it is necessary to pass
a urinary catheter. Neglect may result in retention of urine and post partum bladder atony .
Inadvertent dural puncture

Chapter 3
There are two alternative strategies
1. Resite the epidural in an adjacent space. Be cautious with the first dose of local anaesthetic as the tip of the catheter may be
adjacent to the dural puncture site and allow some solution to enter the subarachnoid space. The anaesthetist must always give
this dose. Provided a normal initial response is obtained the epidural may be conducted in the usual fashion but with an awareness
of the potential for high blockade.
If the patient is able to deliver spontaneously, then this should be allowed. A long period of strenuous pushing
should be avoided as this may increase the rate of CSF loss.
After delivery, an epidural infusion of Ringer lactate should be set up via the epidural catheter and filter, aiming
to run in one and a half litres over twenty-four hours.
The patient should remain in bed while the infusion is in progress, thereafter she should be allowed to mobilise
normally.
2. The needle tip is left in the subarachnoid space and an end-hole catheter inserted two cm only. The catheter must be clearly
marked as being in the subarachnoid space. All top ups should be given by the anaesthetist. Care should be taken to avoid
excessive loss of CSF.
With the patient in the lateral or supine wedged position, give 1 ml of 0.125% plain bupivacaine followed by 0.5ml increments of
0.125% or 0.25% bupivacaine until satisfactory analgesia is achieved. Consider adding an opioid e.g. 12.5 mg fentanyl. It is
important to appreciate that plain bupivacaine is slightly hypobaric at body temperature and that sudden movements of the patient
may cause displacement of the local anaesthetic in the CSF leading to a high block.
For Caesarean section, manual removal and rotational forceps delivery, 0.5% hyperbaric bupivacaine should be used, administered
in 0.5 to 1ml increments, until adequate anaesthesia is achieved.
Management of spinal headache
Development of a spinal headache is characterised by severe, disabling fronto-occipital pain with radiation to the neck and
shoulders. There may be neck stiffness. In the upright position the brain becomes unsupported by CSF within the cranium. This
results in traction on meninges, venous sinuses and cerebral vessels. A compensatory dilatation of blood vessels takes place with
an increase in cerebral blood flow. The pain may be completely relieved by lying supine. It is very important to discuss the nature of
the problem and the management options with the patient.
Conservative treatment of spinal headache
Bedrest
Encourage the patient to take oral fluids.
Paracetamol, dihydrocodeine or similar analgesia at regular intervals.
Consider sumatriptan. It is a serotonin agonist and may relieve pain due to cerebral vasodilatation.
Reassure the patient that symptoms should resolve within 3 - 7days.
Dural blood patch
A Tuohy needle is sited in the epidural space overlying the puncture site or the space below using a standard epidural
technique.
An assistant scrubs and gloves up to take 20 ml of the patient's blood under sterile conditions.
15 - 20 ml is injected slowly into the epidural space, stopping if it becomes uncomfortable.
The patient lies flat for an hour and then slowly mobilises.
The blood patch can be expected to be successful in 85% of cases. If ineffective it may be repeated after 24 hours.
In the following circumstances a blood patch may be contraindicated:
Patient refusal.
Bleeding diathesis.
Infection and pyrexia

Chapter 3
Persistent headache - If headache persists for more than 7 days the patient should be encouraged to reconsider a blood patch or
have it repeated if already given. Reversible cranial nerve lesions may rarely complicate persistent leakage of CSF (typically VI
nerve palsy). A subdural intracranial haematoma secondary to traction and tearing of small blood vessels may cause raised
intracranial pressure; medullary coning has been reported. A thorough neurological examination, including fundoscopy, is mandatory
if the headache persists. A CT scan or MRI may also be required.
Subdural block - the features are:
Negative epidural test dose.

5 - 15 min after the main dose of local anaesthetic an extensive (to C7 or higher) patchy sensory block will occur. Motor
block is minimal or absent, hypotension is also unusual.
It must be distinguished from spinal block - sacral sensation is usually retained.
Because the subdural space extends intracranially, apnoea and loss of consciousness can occur, intubation and resuscitation
may then be necessary.
If the block regresses before delivery then resite the epidural because there is a risk of intrathecal penetration of the catheter
and subsequent subarachnoid block.
Subdural catheter placement can be confirmed by the injection of radio-opaque dye in the postpartum period when the
classic "tramline" appearance will be seen on x-ray.
Total spinal block
This is the subarachnoid injection of a large (epidural) dose of local anaesthetic. It may result in severe hypotension, bradycardia
with loss of consciousness and apnoea. All resuscitation equipment must be immediately available.
Position patient on left side, administer oxygen with bag and mask if apnoeic
Call immediately for senior anaesthetic and obstetric staff.
An assistant performs cricoid pressure.
Give 500-1000 ml saline or Ringer lactate rapidly intravenously.
Give ephedrine 15 mg intravenously and repeat as necessary.
Intubate the trachea and ventilate if there is apnoea.
Monitor the patient’s pulse, blood pressure and saturation.
Maintain blood pressure with ephedrine; other vasopressors such as phenylephrine may be necessary in bolus doses of 40 -
100 µg
Continually reassure the patient and relatives
Pass orogastric tube, empty stomach and instil 30 ml 0.3 molar sodium citrate.
In the event of fetal distress delivery can take place once the patient is stabilised
Epidural catheter difficulties
The broken epidural catheter - occasionally the tip of the catheter may be sheared by incorrectly withdrawing it through the needle
when the needle is in the epidural space. If this happens it is probably not worth exploring the epidural space or subcutaneous
tissues for the missing tip. The material is relatively inert and should cause no problems unless fibrosis occurs adjacent to nerve
roots. It is essential that the patient be informed and the event documented.
The stuck epidural catheter - after delivery the catheter is normally removed without any difficulty. If the catheter is stuck then
positioning the patient in flexion, extension and lateral rotation should all be tried.
Spinal/epidural haematoma - this rare complication should be recognised as an emergency requiring immediate investigation and
treatment. Predisposing factors are:
Coagulopathy
Anticoagulant therapy
Previous spinal or epidural analgesia
Vascular malformations
Spinal tumour
Combination of the above factors
Effects - spinal cord compression and ischaemia

Chapter 3
Signs/Symptoms - severe localised back pain, sensory loss, paraplegia, bladder and bowel dysfunction
Investigation - immediate MRI or CT scan
Treatment - emergency laminectomy and decompression of spinal cord
Epidural abscess - the space occupying effects are the same as those in spinal/epidural haematoma. Additionally pyrexia and
leukocytosis are likely. Investigations and treatment follow that for spinal haematoma apart from the need for specific treatment of
the infection. Infection in the epidural space may be due to poor aseptic technique, direct spread from an adjacent infected area or
haematogenous spread with bacteraemia. When an unrelated source of infection has been identified and adequately treated there is
no absolute contraindication to siting an epidural and the potential risks need to be weighed against the benefit in a particular
situation.
MAINTENANCE OF EPIDURAL ANALGESIA
The choice lies between intermittent bolus doses, a continuous infusion or a combination technique.
Intermittent bolus doses
This is the basic technique. 15 ml boluses of 0.1% bupivacaine are generally adequate in early labour with minimal motor block; the
addition of 2 µg fentanyl/ml provides additional analgesia . Increasing pain as the presenting part descends may be an indication for
increasing the concentration to 0.25% or occasionally 0.5% bupivacaine in 10 ml boluses. Top ups are not usually needed more
frequently than hourly.
Epidural infusion
Advantages: analgesia is more continuous, hypotension is less likely and the need for top ups is minimised.
Disadvantages: an infusion maintained for several hours may lead to a block with wide segmental sensory and motor spread. The
increased motor block may be associated with a higher instrumental delivery rate than with the bolus technique. (There is evidence
that the frequency of low and outlet forceps delivery may be increased by epidural analgesia).
A 0.125% solution of bupivacaine run at 10-15 ml/h gives good analgesia. An 0.08% solution run at 20 ml/h gives a more
extensive segmental spread with less motor block. The addition of fentanyl to the infusion improves the quality of analgesia. A
solution of 0.1% bupivacaine with 2 mg/ml fentanyl is now available commercially in the UK.
Recommended monitoring should include half-hourly blood pressure recordings, respiratory rate and upper sensory level testing.
The infusion should be stopped and the anaesthetist informed if:
Systolic blood pressure falls below 100 mm Hg.

Skin numbness extends above the xiphisternum.
Patient is unable to bend her knees or the weakness is getting worse.
Infused volume differs from that prescribed.
Respiratory rate falls below 9/min
Click here for methods of making up an infusion.
Patient controlled epidural analgesia (PCEA)
A loading dose of 10 ml of 0.125% bupivacaine is given. A background infusion of 0.1% bupivacaine plus 2 µg fentanyl/ml may then
be set-up and the patient allowed to self administer bolus doses of 5 ml (5 mg bupivacaine + 10 µg fentanyl) with a lock-out time of
10 min. The advantage of the method is the satisfaction afforded to the mother by having some control over the density and spread
of her epidural block. A disadvantage is that due to a lack of supervision of top-ups the mother’s position may not always be optimal
for achieving an effective block.
Mobile epidural
The intention is to provide pain relief while retaining mobility. The combined spinal /epidural (CSE) involves a loading subarachnoid
dose of 2.5 mg of plain bupivacaine (1 ml), 25 mg fentanyl (0.5 ml) made up to a total volume of 2 ml with the addition of 0.5 ml

Chapter 3
saline. This will produce a very rapid onset of analgesia and should allow almost complete motor sparing thus allowing the patient to
mobilise with the assistance of two midwives. The epidural catheter, which is inserted at the same time, is used for subsequent top-
ups. These consist of 0.1% plain bupivacaine plus 2 µg fentanyl/ml in a dose of 10 ml. The CSE technique has been associated
with reports of aseptic meningitis.
Alternative methods are based on the infusion or intermittent injection of very low concentrations of plain bupivacaine plus fentanyl,
e.g. 0.06% bupivacaine plus 2.5 µg fentanyl/ml or 0.1% bupivacaine plus 2µg fentanyl/ml. If the test dose is used as the initial dose
i.e. 15mg of bupivacaine as 15ml of 0.1% bupivacaine plus 50 µg of fentanyl the motor block can be minimal. This block can then
be continued by infusion, intermittent injection or patient controlled analgesia.
AUDIT OF EPIDURAL ANALGESIA
It is important to visit all patients who have received epidural analgesia on the first postpartum day. The following aspects of their
experience should be the subject of enquiry:
Efficacy of the block - An initial failure rate of < 10% falling to < 5% after measures to improve the block is a reasonable
target.
Headache - due to inadvertent dural puncture. The overall rate should be < 1% of all epidurals given. A headache may follow
an apparently uneventful epidural.
Backache - It is important to take a history and examine the patient to determine the cause. Multiple punctures, damage to
ligaments or periosteum cause localised pain which normally settles after 3 or 4 days. Most cases are associated with pre-
existing backache, which may worsen during pregnancy.
Prolonged analgesia and motor Block - The area affected should be mapped and recorded daily. If an epidural infusion
has been running for many hours the block may persist in localised areas for up to 24 hours. If skin analgesia persists for
longer and there is a history of rotational forceps delivery or a prolonged second stage of labour then a lumbar plexus
neurapraxia at the pelvic brim is the likely cause. There may also be a temporary foot drop or other features of motor
weakness. Close liaison with obstetric staff and an obstetric physiotherapist is essential in the management of these cases.
Persistent analgesia and motor block related to a single dermatome may be due to nerve root neurapraxia at the time of
epidural cannula insertion. The patient may have reported marked paraesthesia at the moment of insertion. The outcome is
generally favourable and resolution can be expected within a few weeks. A neurological opinion may be helpful. Outpatient
follow-up with physiotherapy and liaison with the general practitioner and obstetrician are an essential part of the
management. (Neurological damage following spinal/epidural block).
FURTHER READING
Covino BG, and Scott DB. Handbook of Epidural Anaesthesia and Analgesia. Copenhagen: Schultz,1985.
Checketts MR and Wildsmith JAW. Accidental i.v. injection of local anaesthetics: an avoidable event? Editorial 11. British Journal of
Anaesthesia 1998; 80: 710-711. Click here for Medline link
McClure JH. Ropivacaine. British Journal of Anaesthesia 1996; 76: 300-307.Click here for Medline link
Miller AC. The effects of epidural analgesia on uterine activity and labor. International Journal of Obstetric Anesthesia 1997; 6: 2-18.
Collier CB. Why epidurals fail: a study of epidurograms. International Journal of Obstetric Anesthesia 1996; 5: 19-31. Click here for
IJOA link
Savolaine ER, Pandya JB, Greenblatt SH, Conover SR. Anatomy of the human lumbar epidural space: new insights using CT-
epidurography. Anesthesiology 1988; 68: 217-20.
McCrae AF, Whitfield A and McClure JH. Repeated unilateral blockade. Anaesthesia 1992; 47: 859. Click here for Medline link.
Beards SC, Jackson A, Griffiths AG, Horsman EL. Magnetic resonance imaging of extradural blood patches: appearances from 30
mins to 18 hours. British Journal of Anaesthesia 1993; 71: 182-188.Click here for Medline link
Reynolds F. Dural puncture and headache. British Medical Journal 1993; 306: 874-876.Click here for Medline link
Vakharia SB, Thomas P S, Rosenbaum AE, Wasenko JJ, Fellows DG. Magnetic resonance imaging of cerebrospinal fluid leak and

Chapter 3
tamponade effect of blood patch in postdural puncture headache. Anesthesia and Analgesia 1997; 84: 585-590.Click here for
Medline link
Seeberger MD, Kaufmann M, Staender S, Schneider M, Scheidegger D. Repeated dural punctures increase the incidence of
postdural puncture headache. Anesthesia and Analgesia 1996; 82: 302-305.Click here for Medline link
Carson D, Wildsmith JAW. The risk of extradural abscess. British Journal of Anaesthesia 1995; 75: 20-521.Click here for Medline
link
Paech M. Patient controlled epidural analgesia in obstetrics. International Journal of Obstetric Anesthesia 1996; 5: 115-125.
Elton CD, Ali P, Mushambi MC. Walking extradurals in labour: a step forward? British Journal of Anaesthesia 1997; 79: 551-
553.Click here for Medline link
Russell R, Quinlan J, Reynolds F. Motor block during epidural infusions for nulliparous women in labour. International Journal of
Obstetric Anesthesia 1995; 4: 82-88.
McGrady EM. Extradural analgesia: does it affect progress and outcome of labour? British Journal of Anaesthesia 1997; 78: 115-
Collis RE, Baxandall ML, Srikantharajah ID, Edge G, Kadim MY, Morgan BM. Combined spinal epidural (CSE) analgesia: technique
management and outcome of 300 mothers. International Journal of Obstetric Anesthesia 1993; 3: 75-81.
Harding SA, Collis RE, Morgan BM. Meningitis after combined spinal-extradural anaesthesia in obstetrics. British Journal of
Anaesthesia 1994; 73: 545-547.Click here for Medline link
Paech M, Godkin R, Webster S. Complications of obstetric analgesia and anaesthesia: a prospective analysis of 10995 cases.
International Journal of Obstetric Anesthesia 1998; 7: 5-11. Click here for IJOA link
MacArthur C, Lewis M. Anaesthetic characteristics and long-term backache after obstetric anaesthesia. International Journal of
Reynolds F. Maternal sequelae of childbirth. British Journal of Anaesthesia 1995; 75: 515-517.Click here for Medline link
Russell R, Dundas R, Reynolds F. Long-term backache after childbirth: prospective search for causative factors. British Medical
Journal 1996; 312: 1384-1388.Click here for Medline link
Reynolds F. Auditing complications of regional analgesia in obstetrics. International Journal of Obstetric Anesthesia 1998; 7: 1-4.
NEXT CHAPTER

Chapter 4
4. CAESAREAN SECTION UNDER REGIONAL ANAESTHESIA
Chapter contents:
Contraindications
Advantages
Disadvantages
Spinal anaesthesia
Epidural anaesthesia
Combined spinal epidural
Uterine relaxation with glyceryl trinitrate
Infiltration and field block anaesthesia
Postoperative pain management
There are four methods of administering regional anaesthesia for Caesarean section.
Spinal
Epidural
Combined spinal epidural (CSE)
Local infiltration / field block
No local anaesthetic technique is guaranteed to be totally reliable. Inadequate block or prolonged surgery is always a possibility .
Because of this it is essential not only to explain the local technique to the patient but also to prepare her for a general anaesthetic
should this become necessary. Above all she should be reassured that although she may be aware of surgical activity she should be
pain-free and that any problems will be dealt with immediately.
Contraindications to Caesarean section under spinal or epidural block
Patient refusal.
Severe maternal hypovolaemia.
Coagulation disorders.
Active bacteraemia, sepsis or localised infection over the injection site.
Certain neurological disorders.
Severe congenital or acquired heart disease.
Advantages
The avoidance of general anaesthesia

Maternal and paternal participation in the birth.
No drug-induced neonatal depression.
Good post operative pain relief.
Improved bonding between mother and baby with early breast feeding.
Disadvantages
Inadequate blockade.
Maternal hypotension.
Headache following dural puncture (< 2% after spinal)
Length of time until onset of block (epidural).
SPINAL ANAESTHESIA FOR CAESAREAN SECTION
Spinal anaesthesia is the technique of choice for elective and some emergency Caesarean sections. It has a rapid onset, reliable
block and with a pencil point needle the incidence of spinal headache is low.
Basic technique.

Chapter 4
Anaesthetic agent - heavy 0.5% bupivacaine (10 -15 mg) gives a more reliable and predictable block than plain 0.5% bupivacaine
Spinal needle - Sprotte 24 gauge or Whitacre 25 gauge pencil point needles.
Position/height of block - Once the spinal has been sited the initial sitting or lateral position is changed to supine with left uterine
displacement using a wedge. This allows spread of solution with a resulting block up to the required level. Surgery should not begin
until either absence of touch at T6, analgesia to pinprick at T5 or loss of temperature sensation (ice or ethyl chloride) at T4.
Management of hypotension - this is associated with rapid onset of the block, frequently accompanied by pallor, nausea and
vomiting. Systolic blood pressure should be maintained at above 90 mmHg to avoid fetal asphyxia.
Position - Effective wedging is vitally important in order to prevent aortocaval compression. If hypotension persists the patient
should be turned completely into the left lateral position.
Fluids - Ringer Lactate, 500 -1000 ml may be administered while the block is being sited. There is evidence that intravenous
fluids have only a minor role in preventing hypotension. Colloids should be avoided because of the rare occurrence of an
anaphylactic reaction and ensuing fetal hypoxia.
Vasopressors:- these are the most effective way of managing hypotension.
Ephedrine - is drawn up and ready for immediate or prophylactic use. The incremental dose is 6 mg. Alternatively an
ephedrine infusion may be preferred (30 mg in 500 ml Ringer Lactate). Blood pressure is raised by an increase in
cardiac output (ß1 adrenergic effect) and peripheral vasoconstriction ( a1 effect). It acts partly by indirect action so
tachyphylaxis may become a problem.
Phenylephrine - in incremental doses of 20 -100 µg, is a more effective vasopressor (direct a1 adrenergic agonist)
but reflex bradycardia may require the administration of atropine 600 µg. Incremental doses greater than 100 µg may
be associated with placental vasoconstriction.
Intrathecal opioids
Fentanyl - a dose of 12.5 - 25 µg improves the quality of the block intra-operatively.

Diamorphine - a dose of 300 µg enhances block quality and also provides excellent postoperative analgesia for 8 -14hours.
Morphine - a dose of 300 - 500 µg provides analgesia for 12 - 20 hours. Delayed respiratory depression may occur especially
with morphine and all patients receiving intrathecal opioids must have close monitoring of their conscious level and
respiration.
Pethidine - a dose of 1 mg/kg in an equal volume of 10% dextrose can provide complete surgical anaesthesia for Caesarean
section (duration - 60 minutes). It may be indicated in cases of allergy to local anaesthetic drugs or in patients with severe
cardiac disease in order to minimise the risk of hypotension and shunt reversal.
Itching can occur with all these opioids. It is usually not severe and can be minimised with naloxone 0.1 - 0.4 mg iv.
Management of the patient during the operation - key points
A high inspired oxygen is given until the delivery of the infant

Monitoring must include blood pressure, pulse oximetry and ECG,
It is essential that a good rapport be established with the patient and a positive attitude taken.
Hypotension is treated with incremental doses of ephedrine or an ephedrine infusion
Aortocaval compression must be avoided.
Inadequate analgesia may occur despite an apparently good block before surgery. If pain occurs early in the procedure
general anaesthesia is usually indicated. If it occurs later e.g. during wound closure local infiltration with lidocaine together
with an intravenous opioid may be adequate.
Following delivery oxytocin 5 - 10 units is given iv or 20 units added to the infusion. The wedge is removed and the oxygen
may be discontinued. (Ergometrine should be avoided. It may lead to nausea and vomiting; it is also an a 1 adrenergic
agonist and may cause hypertension and pulmonary oedema)
High spinal block
An attempt to extend an existing epidural for Caesarean section may not produce the required height of block. When a spinal is
subsequently inserted a standard dose of 10-15 mg of bupivacaine may lead to a high block with apnoea and profound hypotension.

Chapter 4
This is due to the decrease in CSF volume caused by the solution in the epidural space; it is also possible for local anaesthetic in
the epidural space to enter the CSF via the dural puncture hole. In these cases it is wise to reduce the dose of spinal to less than 2
ml.
Occasionally a high block occurs unexpectedly following a standard spinal anaesthetic or when a large (epidural) dose of local
anaesthetic is given inadvertently into the subarachnoid space.
Signs - paraesthaesiae in fingers and hand (C5-7) is a warning of a high block. Bradycardia, nasal congestion or a Horner’s
syndrome (cervical sympathetic block) may progress to respiratory difficulty or arrest.
Management - the patient should be reassured that the block will regress, hypotension is managed as above, progress to apnoea is
managed as in "total spinal block".
Continuous spinal for Caesarean section
Incremental 2.5 mg doses of plain bupivacaine may be used.
Advantages - the problems of sudden hypotension and unexpectedly high spread may be avoided by placing a subarachnoid
catheter. Additional doses can be administered to prolong the anaesthetic. It may be useful in the morbidly obese.
Disadvantages - the presence of a catheter may increase the risk of meningitis. There is a risk of spinal nerve root trauma and
cauda equina syndrome.
EPIDURAL ANAESTHESIA FOR CAESAREAN SECTION
This is now rarely performed for elective surgery. It takes longer to establish and the frequency of inadequate blockade is a
problem. A different situation occurs when a patient in labour has a working epidural; it can be intensified to produce anaesthesia for
surgery with minimal delay. An epidural extended in this way is more effective for surgery than a ‘de novo’ epidural.
Emergency Caesarean section
Anaesthetic agent - 2% lidocaine with 1:200,000 epinephrine acts rapidly and the patient should be ready for Caesarean section
within 5 - 10 minutes.
Height of Block - 15-20 ml should be adequate to obtain a good block to T4.
Hypotension - This is uncommon if an epidural has been in situ for several hours. Factors here include physiological adaptation to
the sympathetic block and an autotransfusion with each contraction.
Elective epidural Caesarean section (de-novo epidural block)
Anaesthetic agent - the choice lies between 2% lidocaine + 1:200,000 epinephrine, 0.5% bupivacaine +/- 1:200,000 epinephrine or
0.75% ropivacaine. A volume of 20-25 ml is generally adequate. The onset time of lidocaine and epinephrine is the most rapid but
its duration is the shortest (1½ hours). Addition of an opioid e.g. fentanyl 50 - 100 µg intensifies the block.
Incremental technique - this relies on the injection of small volumes of solution, i.e. 5 - 7 ml. If preferred the injection may be made
with the patient sitting and then lying down and moved from side to side. It results in a large total dose with an increase in the risk
of toxicity.
Large bolus technique - a single large volume dose results in a better spread of local anaesthetic but carries the hazard of a large
inadvertent intravenous injection; convulsions and maternal death are a potential risk, even following a negative test dose. This risk
can be minimised if the injection is given through the needle, patient contact maintained and the injection made slowly.
Hypotension - hypotension is less common than with spinal anaesthesia because of the slower onset of the block. Management is
similar to that of spinal anaesthesia. Up to one litre of Ringer Lactate is administered while the block is being sited and incremental
ephedrine is given as required.
Management of inadequate block
Minimise the incidence of inadequate block by an accurate assessment of block height and the addition of opioid with the

Chapter 4
local anaesthetic.
Give plenty of reassurance
Administer nitrous oxide/oxygen - (Entonox)
Extend and intensify the block by topping up when necessary
Administer an intravenous opioid
Ask the surgeon to give supplementary local anaesthesia - the surgeon may inject or spray 0.5 - 1% lidocaine onto the
peritoneum
Induce general anaesthesia - this should not be delayed if the above measures are ineffective or the patient is distresed.
COMBINED SPINAL EPIDURAL
This is a method for elective or emergency Caesarean section. It provides the opportunity to top up and extend a block when
necessary. In addition the epidural catheter can be used for postoperative pain relief. The needle through needle technique is the
most commonly used method. An epidural needle is first positioned in the epidural space. A spinal needle at least an extra 11 mm
in length is then passed through the epidural needle. The local anaesthetic is given through this spinal needle before it is withdrawn
and the epidural catheter passed. There are certain objections to this procedure: -
Metallic fragments may in theory be introduced into the subarachnoid space. Some needle combinations have been designed
to avoid this problem. - the spinal needle takes a direct route and exits through a hole in the curve of the Tuohy needle.
The patient may be unable to warn the anaesthetist of any pain or discomfort when the catheter is passed after the spinal
dose has been given. A two injection technique avoids this problem as the spinal and epidural are sited at different levels.
The epidural catheter is passed before the spinal dose is given.
A test dose cannot exclude subarachnoid placement of the catheter once the initial spinal dose has taken effect therefore
this should be deferred until the spinal dose has worn off.
There have been reports of meningitis following the combined technique
UTERINE RELAXATION WITH GLYCERYL TRINITRATE (GTN)
Urgent uterine relaxation is occasionally necessary to allow obstetric manoeuvres at the time of either vaginal or Caesarean delivery.
If the patient has a general anaesthetic volatile agents are used. With local anaesthesia glyceryl trinitrate can provide uterine
relaxation. An aerosol sublingual spray is an effective method of delivery, which delivers a metered dose of 0.4 mg. The
recommended dose is 0.8 mg. The onset time is 40 seconds, peak effect at 120 seconds, with a duration of 5 minutes. Hypotension
is unlikely to be a problem with this technique of administration.
INFILTRATION AND FIELD BLOCK ANAESTHESIA FOR CAESAREAN SECTION
This may be necessary if there are complex anaesthetic difficulties, no anaesthetist or massive haemorrhage.
Basic technique
Direct local infiltration of the anterior abdominal wall with local anaesthetic layer by layer.
Intercostal block and/or rectus sheath block combined with direct infiltration of the incision line. Particular attention should be
paid to blockade of the iliohypogastric nerve on both sides.
The visceral reflexes can also be obtunded to some degree by injection of local anaesthetic around the utero-vesico fold and
paracervical area.
Up to 100 ml of 0.5% lidocaine with 1 in 200,00 epinephrine may be used
POSTOPERATIVE PAIN MANAGEMENT
Intramuscular opioids - morphine in a dose of 200 µg/kg im and repeated at 3 hour intervals if necessary.
PCA - a solution of morphine 1 mg/ml with bolus doses of 2 mg and a lockout time of 5 min
Non-steroidal anti-inflammatory drugs (NSAIDs) - these reduce the requirement for opioids. They exert an anti-inflammatory effect at
the incision site and also reduce uterine cramp pains due to a depressant effect on uterine contractility. There is no need to withhold
NSAIDs, if they are indicated, in asthmatic patients who are not known to be sensitive to them. Sensitivity to aspirin and NSAIDs
affects only 5 - 10% of adult asthmatics. The oral and rectal route are commonly used:-
A diclofenac 100 mg suppository at the end of surgery followed by either 50 mg orally 8 hourly or ibuprofen 400 mg 8 hourly.

Chapter 4
Epidural opioids - diamorphine 2.5 mg in 5 ml saline. The addition of clonidine 75 mcg may increase the duration.
Spinal opioids - diamorphine 300 µg at the time of intrathecal injection of local anaesthetic will provide 8 - 12 hours analgesia.
Morphine 200 - 500 µg has longer duration but more potential for respiratory depression, pruritus and nausea.
Epidural infusion - 0.1% bupivacaine with fentanyl 2 µg/ml. Sensory and motor block height, blood pressure, conscious level and
repiratory rate are monitored in a properly staffed environment.
Local anaesthetic blocks - bilateral ilio-inguinal/ilio-hypogastric nerve blocks (L1) have been used. Iliac crest blocks where T12 is
also blocked are much more effective. A dose of 10 - 15 ml of 0.25% bupivacaine is used on each side.
Local infiltration of Caesarean section wound - with 25 ml of 0.5% or 50 ml of 0.25% bupivacaine The muscle layers should be
infiltrated after closure of the aponeurosis and the subcutaneous tissue should be infiltrated within 1 - 1½ cm of the cut edge.
FURTHER READING
Rocke DA, Rout CC. Volume preloading, spinal hypotension and Caesarean section. British Journal of Anaesthesia 1995; 75: 257-
Hall PA, Bennett A, Wilkes MP, Lewis M. Spinal anaesthesia for Caesarean section: comparison of infusions of phenylephrine and
ephedrine. British Journal of Anaesthesia 1994; 73: 471-474.Click here for Medline link
Capogna G, Celleno D. Improving epidural anaesthesia during Caesarean section: Causes of maternal discomfort or pain during
surgery. International Journal of Obstetric Anesthesia 1994; 3: 149-152
Husaini SW, Russel IF. Volume preload: lack of effect in the prevention of spinal-induced hypotension at Caesarean section.
International Journal of Obstetric Anesthesia 1998; 7: 76-82 Click here for IJOA link
Burton A, Camann. Electrocardiographic changes seen during cesarean section: a review. International Journal of Obstetric
Graham D, Russell IF. A double blind assessment of the analgesic sparing effect of intrathecal diamorphine (0.3mg) with spinal
anaesthesia for elective Caesarean section. International Journal of Obstetric Anesthesia 1997; 6: 224-230. Click here for IJOA link
NEXT CHAPTER

Chapter 5
5. GENERAL ANAESTHESIA IN OBSTETRICS
Chapter contents
Preparation for general anaesthesia

Induction of general anaesthesia
Maintenance of general anaesthesia
Difficult intubation
Failed intubation drill
Pulmonary aspiration syndrome
Awareness
Indications for general anaesthesia; Emergency Caesarean section: fetal distress, cord prolapse,
hypovolaemic shock ; Placenta praevia; Instrumental delivery; Manual removal of placenta; Evacuation of
retained products; Cervical suture
Incidental surgery during pregnancy
Occupational exposure to anaesthetic agents during pregnancy
Mothers present particular difficulties because of:
The presence of fetus and placenta

Reflux and possible aspiration of gastric contents
Intubation difficulties
Increased oxygen consumption
PREPARATION FOR GENERAL ANAESTHESIA
A suggested antacid regimen
Elective Case
Ranitidine 150 mg orally 2 hours preoperatively

Local anaesthetic cream applied to the intravenous site 1 hours preoperatively
Sodium citrate 30 ml orally in the anaesthetic room
Emergency cases - Identify those at risk
Severe pre-eclampsia
Abnormal presentation
Multiple birth
Antepartum haemorrhage
Previous Caesarean section
Trial of labour
Fetal distress
If blood taken and sent for blood group and screen
A standing order will allow the midwife to administer ranitidine 50 mg i.m. or 150 mg orally to these patients.
If not ranitidine has not been given within 4 hours then immediately the decision to operate is made, the following regimen
should be followed:
Ranitidine 50 mg (diluted in a volume of 20ml of saline) is given i.v., slowly over 3 minutes.
Sodium citrate 30 ml orally is administered in the anaesthetic room.
Essential equipment to be carefully checked and laid out before induction of anaesthesia
Macintosh laryngoscopes: 1 standard blade, 1 long blade and 1 polio blade or short handle
McCoy levering laryngoscope

Chapter 5
Endotracheal tubes (ETT) with a range of sizes 6 - 8

Oral and nasopharyngeal airways
Malleable introducer
Gum elastic bougie
Laryngeal mask airway (LMA) and ProSeal laryngeal mask
Cricothyroidotomy set
Wedge for prevention of aortocaval compression
Anaesthetic suction machine
McCoy laryngoscope ProSeal laryngeal mask
Fig 5.1
Monitoring equipment
Electrocardiogram (ECG), non-invasive blood pressure, end tidal CO 2 , inspired and expired oxygen, inspired and expired
anaesthetic agents, pulse oximeter and peripheral nerve stimulator
Drugs
Syringes of thiopentone 500 mg and suxamethonium 100 mg are prepared together with other essential drugs daily, dated and
stored in the fridge. An intravenous infusion is prepared daily and run through ready for immediate use. All drugs and intubation
equipment must be renewed and checked by the anaesthetist who last used them in readiness for the next emergency.
Assistance
Two properly trained assistants should be present, one to perform cricoid pressure and the other to assist the anaesthetist with
intubation.
Wedge
A left lateral tilt is essential to prevent aortocaval compression. A suitable wedge is inserted under the pelvis.
Cricoid pressure
Compression of the cricoid cartilage against the fifth cervical vertebra will close the oesophagus and prevent regurgitation of gastric
contents. It is useful to mark the anatomy on the neck before induction of anaesthesia. A force of up to 30 Newton's (3 kg) is
necessary to obtain closure. Pressure is applied (1kg ) with the patient awake and increased (3kg) as consciousness is lost; it is
maintained until the trachea is intubated and sealed with an inflatable cuff. A skilled assistant performs the manoeuvre using thumb
and two fingers to apply pressure while supporting the cervical spine with the other hand. If pressure is applied before loss of
consciousness the patient may become distressed. There is also a risk of oesophageal rupture if vomiting occurs at this time.
Incorrectly applied pressure, especially with a lateral force, may cause distortion of laryngeal anatomy. This can cause difficulty with
inserting the laryngoscope and failure to visualise the glottis. In this case the assistant should be asked briefly to ease the
pressure and then re-apply it correctly.

Chapter 5
Fig 5.2 Cricoid pressure
INDUCTION OF GENERAL ANAESTHESIA
ENSURE THAT TWO SKILLED ASSISTANTS ARE PRESENT
Give 0.3 molar sodium citrate 30 ml orally

Wedge the patient to allow uterine displacement
Switch on suction and place under pillow
Preoxygenate with 10 l/minute for at least 3 minutes
Administer thiopentone 250 - 350 mg (5-7 mg/kg) followed by suxamethonium 100 mg
Cricoid pressure is applied as consciousness is lost and maintained until the trachea is intubated, the cuff inflated and found
to be leak free.
CHECK POSITION OF ENDOTRACHEAL TUBE (ETT)
Chest movement, stethoscope, end tidal CO 2 monitor, oesophageal detector device
Administer 50% nitrous oxide 50% oxygen with a volatile agent.
MAINTENANCE OF GENERAL ANAESTHESIA
50% nitrous oxide: 50% oxygen is given with a volatile agent - either 0.5% halothane, 0.75% isoflurane, 1% enflurane, which
should be continued to the end of procedure.
Administer a non-depolarising muscle relaxant, e.g., atracurium 25 - 30 mg once the suxamethonium wears off. If surgery is
rapid then intermittent suxamethonium can be used after intravenous atropine has been given to prevent bradycardia.
A peripheral nerve stimulator should be used to assess neuromuscular blockade
Monitor the inspired and expired CO 2 , oxygen and anaesthetic agent concentrations.
At delivery administer oxytocin 5 units i.v. as a bolus and 10 - 20 units may be added to the infusion and administered over 4
hours. Deepen anaesthesia with an opioid drug, e.g. 10 mg morphine i.v.; reduce the inspired oxygen concentration to 33%
and remove the wedge. The risk of aspiration will be reduced by emptying the stomach before extubation.
Reverse any residual neuromuscular block, administer 100% oxygen, extubate the patient on her side and awake after
thorough suction of the pharynx.
Move the patient to the recovery area
DIFFICULT INTUBATION
The airway must always be assessed before elective or emergency surgery. An inability to visualise the uvula or fauceal pillars,
obesity, a short neck, receding mandible and protuberant maxillary incisors are all important warning signs of potential difficulty with
intubation. The following tests can be easily and quickly performed - a combination of adverse findings indicates a significantly
increased risk of difficulty.
Table 5.1 Assessment of the airway
TEST ADVERSE FINDINGS

Mouth opening < 4 cm (< two fingers)

Chapter 5
Extension at the atlanto-occipital joint - in the

Little detectable movement at the atlanto-occipital
standard intubating position gentle manipulation
joint
may reveal up to 30 degrees of movement
Mallampati view of the pharynx with mouth open
grade III or more (uvula not seen)
and tongue maximally protruded
Thyromental distance measured with the head fully
< 6 cm (<three fingers)
extended and mouth closed
If there are two or more adverse findings regional anaesthesia should be considered. If general anaesthesia is essential an
awake fibreoptic intubation under local anaesthesia is likely to be the safest technique. Retrograde catheterisation via the
cricothyroid membrane is an alternative method of guiding the ETT into position. Nasal intubation should be avoided, if possible, as
mucosal hyperaemia may cause bleeding.
If intubation is difficult one or more of the following basic steps should be effective:
Ensure that cricoid pressure is applied correctly.

Try with an alternative laryngoscope blade
Insert a gum elastic bougie into the trachea and use it as a guide to railroad the ETT (Macintosh technique)
Try a smaller size of ETT
As a general rule:
Limit suxamethonium to one dose unless the larynx can be seen and an adequate airway maintained with a facemask
There should normally be a maximum of 3 attempts before proceeding to a failed intubation drill
FAILED INTUBATION DRILL
Every anaesthetist MUST have a drill to follow should intubation fail (see fig 5.3). Oxygenation is of prime importance - it is better to
have a live patient with pulmonary aspiration than a patient dead from a hypoxic cardiac arrest.
Decide on the urgency of delivery. Most cases can be allowed to wake up before the administration of a spinal or epidural.
Maintenance of cricoid pressure and ventilation with 100% oxygen are essential.
If mask ventilation is impossible then an LMA should be inserted. The ProSeal laryngeal mask may provide a better seal and
allow venting of the stomach. If ventilation is still impossible a cricothyroidotomy must be done without delay.
If mask ventilation is easy then anaesthesia can be continued either using the facemask or by substituting a laryngeal mask
airway. Cricoid pressure should be continuously applied provided that this does not obstruct the airway. Anaesthesia can be
maintained by spontaneous ventilation with nitrous oxide, oxygen and a volatile agent. This may provide relatively safe
conditions for managing the immediate problem. However if it is thought necessary to intubate the trachea a 6.0 mm
endotracheal tube may be passed down a size 3 or 4 LMA - preferably under direct vision using a fibreoptic endoscope. If
prolonged ventilation is required a larger endotracheal tube may be substituted later on by using an airway exchange
catheter. If possible the stomach should be emptied with a large diameter tube.
Fig 5.3 Failed intubation flow chart

Chapter 5
When there is difficulty with intubation the patient must be informed. Details should be noted in the records for future
reference. The patient is advised to carry MedicAlert identification. More detailed information on problem airways may be
entered and/or obtained from the UK National Difficult Airway Database.
PULMONARY ASPIRATION SYNDROME
The presentation may vary from unexplained bronchospasm during the anaesthetic to postoperative tachypnoea, cyanosis,
respiratory distress and tachycardia. The chest X-ray may be normal initially but usually progresses to patchy pulmonary infiltration
and then, in severe cases, to gross pulmonary oedema. The blood gases will show a deterioration in oxygenation with a metabolic
acidosis.
Prophylaxis
Avoid general anaesthesia by using a regional technique

Avoid excessive sedation during a regional block
Administer H 2 receptor antagonists to reduce acid production and oral 0.3 molar sodium citrate to neutralise acid already in
the stomach.
Consider giving metoclopramide to increase gastric emptying and tone in the lower oesophageal sphincter.
Cricoid pressure should be correctly applied as part of a rapid sequence induction technique.
Pre-oxygenation not only provides a reserve of oxygen in the lungs but also eliminates the risk of gastric distension during
face mask IPPV.
Perform skilled and rapid intubation of the trachea with cuff inflation.
If necessary, attempt to empty the stomach with a tube prior to extubation.
Turn the patient on her side at the end of operation, allow protective reflexes to return and then extubate the patient.
Treatment of aspiration pneumonitis

Chapter 5
If suspected treatment must be vigorous and immediate. The first step is to aspirate the airways and remove any gastric fluid.
Subsequently the management is as follows:
Acute bronchospasm is treated with salbutamol 250 µg i.v. or aminophylline 250 mg i.v.
Increase the inspired oxygen concentration to maintain an adequate SpO 2
Support the circulation with inotropes e.g. dopamine if necessary
There is no evidence that bronchial lavage with saline, or the administration of steroids or antibiotics is of any immediate
value.
Postoperatively the patient is managed in a high dependency or intensive care unit as a case of adult respiratory distress
syndrome. This includes oxygen administration, chest physiotherapy and, if necessary, intermittent positive pressure
ventilation (IPPV). The addition of positive end expiratory pressure may improve oxygenation by minimising intrapulmonary
shunting and preventing atelectasis. Antibiotics may be necessary if there is proven infection. The extent of pulmonary
damage depends on the volume and pH of the aspirate. More than 25 ml of gastric contents with a pH of <2.5 are considered
to be critical factors. Particulate aspiration may lead to granuloma formation and subsequent pulmonary fibrosis. Despite full
intensive care measures some patients may not survive.
AWARENESS
Obstetric patients undergoing Caesarean section under general anaesthesia are particularly at risk of awareness. This is for a
number of reasons -
High inspired oxygen concentrations may be used because of fetal distress.

Sedative premedication is not used for elective Caesarean section.
Respiratory depressant drugs including opioids and volatile agents are either avoided or used in relatively small doses to
avoid depression of the infant at the time of birth.
Volatile agents are given in inadequate concentration for fear of excessive uterine relaxation.
The extent of awareness varies: there may be dreams, amnesic wakefulness (awareness at the time but without subsequent recall),
recall of sounds or complete wakefulness during the procedure with all the concomitant pain and discomfort. Because these patients
are paralysed, they cannot signal to the anaesthetist and may undergo very severe emotional distress. This frequently leads to a
post traumatic stress disorder after delivery. This is characterised by flashbacks, unpleasant dreams, insomnia and mood changes
including depression. An additional problem is the increase in catecholamine release during surgery which may adversely effect
utero-placental flow. Awareness is therefore to be avoided at all costs.
Awareness may be avoided by:
Using a large enough induction dose of thiopentone - 4 mg/kg is not adequate. If there is delay in intubation additional doses
of thiopentone must be given.
Careful observation of the mother for lacrimation, sweating, tachycardia and hypertension.
The addition of sufficient volatile agent to a 50% mixture of nitrous oxide/oxygen. The minimum recommended concentrations
are - 0.5% halothane, 1% enflurane and 0.75% isoflurane. The use of overpressure will result in these concentrations being
rapidly reached. Above these concentrations hypotension is more common and myometrial relaxation occurs. If it is obvious
that the mother is very lightly anaesthetised then the concentration of volatile agent should be increased until consciousness
is lost. After delivery of the infant an opioid should be given to deepen anaesthesia. The volatile agent should be continued to
the end of surgery and the nitrous oxide concentration increased.
If the mother does complain of awareness, dreaming or recall then it is absolutely essential that these memories be acknowledged
and discussed fully so that the patient is allowed to verbalise her fears and anxieties. Monitoring of the volatile agent and the
inspired oxygen concentrations should detect empty vaporisers and leaks in the circuit.
INDICATIONS FOR GENERAL ANAESTHESIA
Fetal distress - All patients are given 100% oxygen by facemask and transported to theatre in the lateral position to prevent further
aortocaval compression and subsequent fetal hypoxia. If an effective epidural is in situ a top up with 15-20 ml of 2% lidocaine with
1:200,000 epinephrine (+/- fentanyl 50 µg) to provide anaesthesia up to T4 will ensure anaesthesia for surgery within 5 - 10 min.
Otherwise a spinal anaesthetic is given. Only very rarely should a patient with an adequate analgesic level be given general
anaesthesia for Caesarean section.

Chapter 5
Cord prolapse - The umbilical vessels may be compressed or go into spasm leading to asphyxia of the infant. Immediate delivery is
essential, the presenting part is elevated by the obstetrician, oxygen administered and aortocaval compression avoided. General
anaesthesia, with a rapid sequence induction technique, is indicated.
Hypovoloemic shock - in dire emergencies general anaesthesia may be necessary before the patient is fully resuscitated. Etomidate
(100 µg/kg) for induction causes little hypotension. Ketamine 1.5 mg/kg may be used to allow 100% oxygen to be given until
delivery.
Placenta praevia
Massive haemorrhage is a recognised complication of placenta praevia; effective uterine contraction is prevented if the placenta is in
the lower uterine segment and an anterior placenta may be divided during surgery. Placenta praevia is associated with placenta
accreta in 5% of cases, rising to 15% if a previous Caesarean section has been performed - these patients are at particular risk of
massive haemorrhage and should be given a general anaesthetic. When the placenta is not encroaching on the anterior wall a
regional technique may be used but these cases must be discussed with senior staff.
Instrumental delivery
General anaesthesia is only required when, exceptionally, a regional block can not be given. In this situation a rapid sequence
induction is required. Normally the delivery is managed under regional anaesthesia either with continuous epidural or spinal block;T5
to S5 segments should be blocked. If a trial of forceps is planned this should be done in theatre and the patient must be blocked up
to T4 so that Caesarean section can proceed immediately if required.
Manual removal of placenta
General and regional anaesthesia are both options. If significant volume depletion has occurred due to blood loss or is expected to
occur during the procedure then regional anaesthesia is contraindicated. If an effective epidural is in situ then a top-up to provide
analgesia to T5 is all that is required. Alternatively spinal anaesthesia can be used. If general anaesthesia is necessary then a rapid
sequence induction is used and excessive concentrations of volatile agents avoided because they may cause myometrial relaxation
and further blood loss. Occasionally it is necessary to give the patient a high dose of volatile halogenated agent to relax the uterus
and allow the obstetrician access through the cervix to the placental bed.
Evacuation of retained products
Most patients present at least a week after delivery for evacuation of remaining uterine contents. A spinal anaesthetic can be used; if
general anaesthesia is preferred it is safe to use a facemask rather than intubate as gastric emptying is normal and the risk of reflux
is minimal at this time.
Cervical suture
Cervical suture is performed between 12 and 18 weeks gestation. Spinal anaesthesia is the technique of choice as exposure of the
developing fetus to drugs is minimal. General anaesthesia may be used quite safely with either a volatile agent or short acting opioid
drugs, e.g. fentanyl or alfentanil.
INCIDENTAL SURGERY DURING PREGNANCY
The administration of nitrous oxide in early pregnancy has given two causes for concern. There is inhibition of the methionine
synthase reaction in the DNA metabolic pathway. Vitamin B12 , a co-factor in this reaction, is oxidised by nitrous oxide. Although
there is evidence for teratogenesis in some animals this not been proven in humans. The deficient metabolites can be restored by
the administration of folinic acid though this is only required after prolonged exposure and following haematological advice. The
second concern is that nitrous oxide may enhance adrenergic tone leading to vasoconstriction. In practice hypocarbia, hypercarbia
and hypotension are the most important risk factors; they may cause reduced placental perfusion and fetal hypoxia and should be
carefully avoided. Additionally the administration of halogenated agents may prevent vasoconstriction.
Spontaneous abortion: There is an increased risk of spontaneous abortion in patients who undergo surgery under general
anaesthesia during the first or second trimester. It is believed that it is the surgical procedure which has the significant effect,
particularly when it involves the reproductive organs. Any adverse outcome may also be primarily due to the underlying condition
e.g. appendicitis.

Chapter 5
Practical recommendations
Only emergency surgery should be performed during pregnancy.

Drug exposure should be minimised
A regional technique, usually a spinal, is preferred specially during the first trimester
If general anaesthesia has to be administered nitrous oxide should not be given for long periods or in high concentrations. In
the second and third trimester antacids are administered and aortocaval compression prevented. A rapid sequence induction
technique is used. If ketamine is used as the sole induction agent the dose should be less than 2 mg/kg in order to prevent
uterine hypertonus.
Avoid hypotension and hyperventilation.
Continuous monitoring of the fetal heart is recommended during surgery
The obstetrician may recommend prophylactic tocolysis; suppositories of indomethacin or diclofenac are most commonly used
OCCUPATIONAL EXPOSURE TO ANAESTHETIC AGENTS DURING PREGNANCY
There is inadequate evidence to conclude that occupational exposure to anaesthetic agents in the operating room causes any health
hazards during pregnancy. Cocaine is the only anaesthetic agent that has been shown to be teratogenic in humans.
FURTHER READING
Vanner RG and Asai T. Safe use of cricoid pressure. Anaesthesia 1999; 54: 1-3 Click here for Medline link
Lawlor M, Johnson C, Weiner M. Airway management in obstetric anaesthesia. International Journal of Obstetric Anesthesia 1993;
2: 225-233.
American Society of Anesthesiologists (ASA) Practice guidelines for management of the difficult airway. Click here for web link
Brimacombe J, Berry A. The laryngeal mask airway for obstetric anaesthesia and neonatal resuscitation. International Journal of
Harmer M. Difficult and failed intubation in obstetrics. International Journal of Obstetric Anesthesia 1997; 6: 25-31.
Bogod DG. The postpartum stomach – when is it safe? Anaesthesia 1994; 49: 1-2. Click here for Medline link
MedicAlert Foundation (Registered Charity) Click here for Web link
NEXT CHAPTER

Chapter 6
6. COMPLICATIONS OF PREGNANCY
Chapter contents
Pre-term delivery
Pre-eclampsia
Eclampsia
Multiple pregnancy
Placenta praevia
Placental abruption
Diabetes mellitus
Respiratory disorders
Cardiac disorders
PRE-TERM DELIVERY
Definition: Delivery before 37 weeks gestation.
Pre-term delivery, operative or by induction, may be indicated in intra-uterine growth retardation (IUGR), diabetes, pre-eclampsia or
eclampsia. Pre-term labour may also be spontaneous.
Fetal immaturity, particularly of hepatic enzyme systems, means that regional blockade is preferable to opioids or general
anaesthesia. An epidural established early in labour will facilitate a forceps delivery and can be extended if necessary for a
Caesarean section. The larger fluctuations in maternal blood pressure associated with the induction of spinal anaesthesia may
prejudice placental flow and great care should be taken if this technique is chosen.
Tocolytic therapy
There is no clear evidence of its effect on perinatal mortality or serious morbidity. The women most likely to benefit from tocolysis
are those in early pregnancy, those needing transfer to a hospital providing neonatal intensive care , or those who have not yet
completed a full course of corticosteroids.
Reduction of intracellular free calcium inhibits myometrial function by one of the following means:
Calcium channel blockade - nifedipine

Atosiban - an oxytocin receptor antagonist
Adenyl cyclase activation - an adrenergic b2 receptor agonist e.g. ritodrine, terbutaline, fenoterol
Membrane binding and calcium channel blockade - magnesium sulphate
Inhibition of prostaglandin synthesis - indomethacin
Nitric oxide donors - glyceryl trinitrate
In the acute situation a b2 agonist is frequently chosen and there are potentially important cardiovascular and metabolic side effects.
As the dose is increased b1 effects may become a problem, especially tachycardia and arrhythmia. Unwanted b2 effects include
vasodilatation, hyperglycaemia, hyperinsulinaemia, hypokalaemia and increased renin activity. The net impact on the circulation may
result in a rise of up to 50% in cardiac output, hypertension and pulmonary oedema. Regional and general anaesthesia should if
possible be avoided until maternal heart rate and blood pressure have been restored to baseline values. The half-life of b2 agonists
varies from approximately 2 hours (ritodrine) to 15 hours (terbutaline).
For tocolytic therapy on a longer-term basis a NSAID such as indomethacin may be chosen. The main side effect is premature
closure of the fetal ductus arteriosus.
PRE-ECLAMPSIA
This is a multi-system disorder of pregnancy affecting 6.2% of all pregnancies in the UK of which most are primigravida
Classical presentation

Chapter 6
1. Onset after 20 weeks gestation in a previously normotensive, non-proteinuric woman.
2. One or both of the following two features -
Hypertension as defined by a diastolic blood pressure >110 mm Hg on any one occasion or a diastolic blood pressure >90
mm Hg on two or more occasions at least four hours apart
Proteinuria as defined by albuminuria of >300 mg in 24 hours, on reagent test strip 2+ or more. (Oedema is often a feature
but is not essential for the diagnosis.)
Patho-physiology
Placenta
There is incomplete trophoblastic invasion of the spiral arteries leading to a reduction in maternal placental flow.
Cardiovascular system
Vascular endothelium: There is dysfunction of endothelial cells, vasospasm and increased sensitivity to angiotensin 2. Increased
platelet reactivity, elevated von Willebrand factor and an imbalance of the prostacyclin - thromboxane ratio, which may lead to
disseminated intravascular coagulation. This condition may develop acutely or more gradually over the course of several days.
Haemodynamics: The normal expansion of plasma volume does not take place, cardiac output may be reduced. The following
changes may precipitate pulmonary oedema, hypoalbuminaemia, increased capillary permeability, oliguria, intravenous fluid overload
and cardiomyopathy in the face of increased systemic vascular resistance. Central venous pressure does not reliably reflect left
atrial pressure.
Kidney
Glomerular capillary endotheliosis leads to proteinuria and to diminished perfusion and filtration. Effects range from a mild elevation
of serum creatinine through to oliguria or anuria. Acute tubular necrosis is a rare complication and generally has a good prognosis.
The main problem is the predisposition to fluid retention and pulmonary oedema. Any drugs known to interfere with renal function,
especially NSAIDs should be avoided.
Liver
There may be hepatocellular damage secondary to vascular damage. Liver enzymes may be elevated. Rarely subcapsular
haemorrhage leads to hepatic rupture.
Brain
In severe cases there may be cerebral oedema, vasospasm, microinfarcts and haemorrhages. These complications may lead to the
development of eclamptic convulsions.
HELLP syndrome
The multi-system nature of the disorder is such that some patients may present atypically with malaise and an acutely tender and
palpable liver. Investigations reveal Haemolysis, Elevated Liver enzymes and a Low Platelet count. The condition is a manifestation
of severe pre-eclampsia.
Severe pre-eclampsia
To prevent complications it is essential to identify progress to severe pre-eclampsia at an early stage. A diagnosis may be made
when one of the following conditions apply:
Diastolic blood pressure consistently >110 mmHg

Diastolic blood pressure consistently >100 mmHg plus proteinuria ++
Diastolic blood pressure not >100 mmHg but the presence of two or more of the following: severe headache, visual
disturbance, hyper-reflexia with clonus, epigastric pain and coagulopathy especially when associated with a progressive
thrombocytopenia

Chapter 6
It is essential to exclude other, non-pregnancy-related causes of hypertension.
Aims of management:
1. To control and if possible prevent the complications listed above

2. To achieve an optimally timed delivery for both mother and fetus.
Investigations
Haematology: haemoglobin, serial haematocrit (as an index of intravascular volume), haptoglobin (lowered if there is haemolysis)
Coagulation - platelets. If platelets fall below 80 x 10 9 /l a full coagulation screen should be performed
Clinical chemistry - plasma urea, urate, creatinine, electrolytes, plasma proteins, liver function tests.
A useful early sign of deterioration is a raised plasma urate >0.35 mmol/l. A late sign in severe disease is a rising plasma creatinine.
Monitoring
Blood pressure: NIBP devices should periodically be cross-checked manually. The Korotkov 4 sound is the most reliable as an
indication of diastolic pressure. The insertion of a radial arterial line may be indicated in the following circumstances: the
administration of intravenous hypotensive drugs, the development of pulmonary oedema, complicating major haemorrhage.
Central venous pressure: This is useful in the management of severe blood loss. The response to a fluid challenge may give some
indication as to circulatory filling. Caution in interpreting the CVP should be exercised as absolute values give little indication of the
development of pulmonary oedema, trends in response to a fluid challenge can be helpful. If the patient has a coagulopathy it is
probably wise to avoid using the internal jugular route.
Pulse oximetry: in addition to routine observations the SpO 2 should be recorded two hourly after a stable reading has been
reached with supplementary oxygen temporarily removed. This is a useful measurement as a downward trend may be a valuable
early warning of pulmonary oedema which should be confirmed by X-ray.
Fluid balance: accurate input and output charts are essential. Intake should be restricted to 80 ml/h plus additional losses.
Oliguria: after delivery urine output may remain at <30 ml/h for several hours. A diuresis may be expected to follow within 6-8
hours. There is no need to intervene within this period unless plasma potassium, urea and creatinine begin to rise or pulmonary
oedema is a problem. When a decision is taken to resort to active treatment the first step is to try the effect of giving 20 - 40 mg of
frusemide. If circulatory underfilling is suspected a challenge of 250 ml synthetic colloid should be administered. If the CVP rises and
there is no diuresis the renal unit should be contacted. The use of calcium resonium for hyperkalaemia and the administration of
dopamine 2-5 mg/kg / min to improve renal blood flow should be considered.
Antihypertensive therapy
Oral drugs
Aims:
1. Over a period of days or weeks to allow the fetus to mature. The object is to minimise the risk of hypertensive complications
by maintaining placental function and maternal organ perfusion.
2. To control blood pressure before or after delivery when intravenous drugs are not required.
Methyldopa: in a dose of 1 g gradually rising to a maximum of 3 g daily in divided doses.

Labetalol: in a dose of 100 mg rising to a maximum of 200 mg six-hourly.
Hydralazine: in a dose of 25 mg rising to 75 mg six-hourly given alone or with methyldopa or labetalol.
Nifedipine: initially in a dose of 10 mg eight hourly. It may be useful to give nifedipine 10 mg sublingually for its
rapid onset (10-15 minutes) and repeat the dose after one hour if required.
Angiotensin converting enzyme (ACE) inhibitors should not be given due to the risk of fetal toxicity
Diuretics are generally not indicated before delivery since plasma volume is already reduced

Chapter 6
Intravenous drugs
When oral therapy becomes ineffective intravenous drugs are required. The target blood pressure is generally a diastolic of <100
mm Hg. In order to avoid cerebral or placental ischaemia it is important not to exceed a fall of more than 25% of mean arterial
pressure initially. It may be beneficial to use more than one antihypertensive drug, for example, a regular sublingual maintenance
dose of nifedipine may be given if required in addition to hydralazine or labetalol.
Hydralazine - Start at 2.5 mg/h and double every half hour to a maximum of 10 mg/h or until the target blood pressure is reached.
Side effects sometimes causing problems include allergy, maternal tachycardia, headaches and flushing. If labetalol has already
been given there is a risk of severe hypotension and the management should be discussed with experienced medical staff.
Labetalol - Start at a rate of 20 mg/h and double every 30 min to a maximum of 80 mg/h until the target blood pressure is achieved
when the rate is kept constant. If bradycardia develops give atropine 600 mcg and repeat as required. Asthma, known allergy and
atrio-ventricular block are contraindications. The alpha:beta receptor blocking ratio is 1:3 when given orally and 1:7 intravenously.
There is always a risk of the beta blocking component precipitating pulmonary oedema by depressing myocardial contractility.
Rapid blood pressure reduction - an intravenous loading dose may be required before initiating maintenance treatment as above.
This is most likely to occur in severe hypertension when oral medication has not been given first. Hydralazine 10 mg is given
intravenously over 2 min with 2 minute recordings of blood pressure for 10 min reducing stepwise to half-hourly after one hour.
Alternatively labetalol 50 mg is given intravenously over 2 min with blood pressure monitoring as for hydralazine.
Decision to deliver
It is essential to investigate the coagulation status before selecting an appropriate anaesthetic technique.
Vaginal delivery: consider an epidural if platelets are normal. If <100x10 9 /l or rapidly falling a full coagulation screen should
be performed and if abnormal a regional technique should not be used.
Caesarean section: if coagulation is normal a regional technique may be used. The abnormal circulatory physiology
generally protects the patient from a hypotensive response to regional anaesthesia and a spinal can be perfectly safe and
effective. Pre-loading with 250 ml normal saline is normally quite adequate. When eclampsia is thought to be imminent a
general anaesthetic should be given.
General anaesthesia
All precautions and methods employed in standard obstetric anaesthesia are used. There is an added risk of difficult intubation due
to laryngeal oedema. It may be beneficial to give up to 1.0 mg alfentanil or an increment of labetalol on induction in order to reduce
the pressor response to intubation. For maintenance the vasodilating properties of isoflurane make it the preferred volatile agent with
halothane as an alternative. The stomach should be emptied with a nasogastric tube if a prolonged period of sedation is planned
postoperatively.
Guidelines for the management of severe pre-eclampsia from the Report on Confidential Enquiries into Maternal Deaths in
UK 1997-1999
can be accessed here
ECLAMPSIA
Eclampsia is the occurrence of one or more seizures in association with pre-eclampsia. The incidence in the UK is 1:2000
deliveries. Labour Ward staff should be alert to the prodromal signs of impending eclampsia; 20% of eclamptics do not have
hypertension as defined for severe pre-eclampsia. Subtle alterations in consciousness, for example impaired concentration and
amnesia may be present for one or more days and be followed by severe headaches, epigastric pain, vomiting, visual disturbance
and photophobia. The objective signs of clonus and hyper-reflexia indicate central nervous system irritability and /or cerebral
oedema.
Treatment of eclampsia
Secure airway: maintain ventilation give supplementary oxygen

Control convulsions: initially with diazepam 2.5 - 20 mg intravenously. If this fails, thiopentone may be given in 25 mg
increments intravenously followed if necessary by intubation facilitated by suxamethonium.

Chapter 6
Establish monitoring: blood pressure, pulse oximetry and fluid balance as for severe pre-eclampsia
Prevent further convulsions: give an intravenous-loading dose of 4 g magnesium sulphate over 10 - 15 minutes. Continue
with a maintenance infusion as per protocol
Fluid balance: should be restricted to 80 ml per hour plus losses as for severe pre-eclampsia.
Treat cerebral oedema: consider intravenous frusemide 20 - 40 mg, dexamethasone 8 mg, and mannitol (risk of pulmonary
oedema), IPPV and sedation may be required for 12 - 24 hours especially when more than one seizure has occurred
Exclude other causes of seizures: consider Computerised Axial Tomography (CAT) or Magnetic Resonance Imaging
(MRI) when the patient is stable
MULTIPLE PREGNANCY
Twins
An effective epidural should be established early in labour. The anaesthetist should be in the labour ward during the second stage
and the epidural should be topped up so that a Caesarean section may be performed urgently if required. Equipment should also be
fully prepared for the administration of a general anaesthetic. Problems are most likely to occur with the delivery of the second twin
and the aim should be for any instrumental or other obstetric manipulations or urgent Caesarean section to be conducted under an
extension of the epidural block.
Triplets or quadruplets
These are normally delivered by Caesarean section.There is an increased risk of supine hypotension and regurgitation with
aspiration due to the large uterus. The large placental site may lead to a major haemorrhage; blood should be immediately available.
Prematurity and pre-eclampsia are other hazards. Limitation of spinal flexion may cause technical difficulties in siting a spinal or
epidural, otherwise the management will be the same as for twins. Adequate equipment and staff will be required to resuscitate all
the infants.
PLACENTA PRAEVIA
Placenta praevia is a condition in which the placenta attaches to the uterine wall in the lower portion of the uterus and covers all or
part of the cervix. It is much more common in early pregnancy than at term. During routine second-trimester ultrasound, the
placenta is observed to cover the cervix in 5 to 20% of pregnancies. However, because of the growth of the uterus throughout
pregnancy, more than 90% of early placenta praevias convert to a normal location by the time of delivery. There is painless bleeding
with a relaxed non tender uterus in the second half of pregnancy. Abnormal fetal presentation is observed in up to 30% of cases.
Diagnosis is made with vaginal ultrasound and this does not appear to increase the risk of bleeding in placenta praevia.
Occasionally the obstetrician may wish to do a vaginal examination to exclude laceration as a source of bleeding. This must be
performed in theatre where the patient and anaesthetist should be fully prepared for the immediate administration of general
anaesthesia in the event of a haemorrhage.
When there is a definite ultrasound diagnosis of placenta praevia an elective Caesarean section is performed at about 38 weeks
gestation. The choice of regional or general anaesthesia will depend on the grade of placenta praevia and position - anterior or
posterior and the risk of haemorrhage at delivery. If there has been a previous Caesarean section there is a serious risk of placenta
accreta. In this situation there is a significant risk of major haemorrhage and a coagulopathy. Blood must be cross-matched and the
laboratory should be alerted about the possible need for clotting factors. (Chapter 7)
The incidence of placenta praevia at term is approximately 1 in 200.
PLACENTAL ABRUPTION
There is abdominal pain, bleeding, and uterine irritability or tenderness. Management is determined by the clinical severity of the
abruption. The condition may be complicated by a coagulopathy. The full extent of haemorrhage may not be revealed and if
maternal hypovalaemic shock is present the management is that of major obstetric haemorrhage. When haemodynamic stability has
been established Caesarean section is performed under general anaesthesia.
DIABETES MELLITUS
The obstetric complications of diabetes mellitus include: polyhydramnios, macrosomia, pre-eclampsia and intra-uterine death. The
neonate is at risk of hypoglycaemia. These problems have been reduced by tight antenatal control of maternal blood glucose.
Antenatal monitoring of mother and fetus determines time and mode of delivery. An otherwise uncomplicated pregnancy with good
glycaemic control will result in vaginal delivery at or near term. Oral hypoglycaemic drugs are not given in pregnancy. Intravenous

Chapter 6
insulin is used in Type 1 diabetes and also in type 2 and gestational diabetics if blood glucose exceeds 10 mmol/l during labour.
The diabetic physician and obstetrician manage the antenatal diabetic control aiming at a blood sugar level of 5-7 mmol/l. However
if a Caesarean section is needed there must be close co-ordination with anaesthetic requirements. The anaesthetist must be able to
take over diabetic management in the absence of a physician.
Caesarean section
Gestational diabetics not receiving insulin do not require any special management in labour. Insulin requirements are based on
hourly blood glucose test strip estimations.
Intravenous insulin is best administered with a syringe driver. Add 50 units soluble insulin (Actrapid) to 50 ml NaCl 0.9%
in a 50ml syringe ( 1unit per 1 ml)
An infusion of 500 ml of 5% glucose with 10 mmol potassium chloride is run at 125 ml/h and insulin is administered by a
separate infusion pump typically at a rate of 0 - 3 units/h to maintain a blood glucose level at 4 - 9 mmol/l. (Sliding scale)
Alternatively, the insulin can be added directly to the 5% glucose infusion - this is less physiological but may be safer if there
is concern about the risk of separate infusions.
The patient should be encouraged to have epidural analgesia for vaginal delivery or spinal anaesthesia for Caesarean
section. This technique provides optimum conditions for the infant since opioids and other anaesthetic drugs will not be
administered before delivery.
An independent infusion should be sited for electrolytes, colloids or blood. (Ringer lactate should be avoided as it complicates
the estimation of maternal carbohydrate load.)
Following placental delivery there is a rapid reduction in insulin requirement. The insulin infusion should be stopped and 5%
glucose with 10 mmol potassium chloride continued at 125 ml/h until the blood glucose rises to 11 mmol/l. Insulin can then be
restarted to maintain the desired blood glucose level, normally at 0 - 3 units/h.
In this situation the management depends on the current blood sugar level and the timing of the last insulin injection. If insulin has
already been given and the patient is being starved 10% glucose is administered to give the equivalent in calories to the meal that
is being omitted. If insulin is due then an infusion is set up as above.
Induction of labour
The following regimen has proved satisfactory. The usual insulin is given the previous night and the usual breakfast is taken after
only the short-acting insulin. A prostaglandin pessary is inserted in the morning and the situation reviewed at lunchtime. If labour is
likely to become established lunch is omitted and an infusion of 5% glucose with 10 mmol potassium chloride is started and insulin is
given according to the following sliding scale:
Table 6.1 Sliding scale for insulin
Blood glucose test strip: (mmol/l) Insulin infusion (unit/h)

3.5 - 4.9 0.5
5 - 6.9 1
7 - 8.9 2
9 - 9.9 3
10 - 12.9 4
13 - 15.9 5
>16 6

Chapter 6
A small number of patients may be insulin resistant, when up to 100 units/day may be required.
When labour is not likely to become established within the next 6 h lunch is taken and covered by short-acting insulin given
subcutaneously.
Spontaneous vaginal delivery
As in the case of emergency Caesarean section the glucose and insulin requirements will be determined by the timing of the last
meal and subcutaneous insulin administration.
RESPIRATORY DISORDERS
The normal maternal physiological changes that occur are required to maintain feto-maternal blood gases and hence fetal growth.
Only severe maternal obstructive or restrictive disorders interfere with fetal oxygenation. In the case of restrictive disease a vital
capacity of <1litre may presage respiratory insufficiency.
Sympathomimetic bronchodilators and inhaled steroids are administered in the normal way. If systemic steroids are required,
additional cover will be necessary for both vaginal and operative delivery. If it is necessary to monitor progress closely antenatal
respiratory function tests including blood gases should be monitored.
Epidural analgesia is nearly always the technique of choice for obstructive or restrictive disorders. Severe scoliosis may present
technical difficulties which should be anticipated; the caudal approach may be useful.
CARDIAC DISORDERS
Cardiac disorders were the second commonest cause of maternal death in the Confidential Enquiries into Maternal Deaths 1997-
1999. The highest levels of mortality were associated with the following pathologies:
Congenital
Aortic valve disease
Ventricular septal defect (VSD)
Eisenmenger syndrome
Primary pulmonary hypertension
Acquired
Aneurysm of thoracic aorta and branches
puerperal cardiomyopathy
cardiomyopathy and myocarditis
myocardial infarction
There are some other important features to note:
Endocarditis as an important cause of maternal mortality and morbidity - antibiotic prophylaxis should be administered
according to protocol.
Central chest pain during pregnancy may be due to myocardial infarction or aortic aneurysm ( precipitated by the normal
vascular wall changes of pregnancy in a susceptible patient e.g. Marfan's syndrome)
Post cardiac transplant patients increasingly present for anaesthesia and analgesia.
Rheumatic heart disease, especially mitral stenosis/incompetence, has declined in incidence over the past twenty years.
In cyanotic heart disease, Eisenmenger syndrome and severe pulmonary hypertension pregnancy has a high mortality risk
and should normally be discouraged
Management
Teamwork, involving early and close communication between anaesthetist, cardiologist and obstetrician is essential for success.
Some of the disorders are rarely seen by any of these specialties - therefore the following key features must be addressed and
agreed well in advance of delivery:
an understanding of the normal cardiovascular changes in pregnancy

the detailed pathology of the cardiac problem:

Chapter 6
the haemodynamic effects including any maternal compensation already present (e.g. ventricular hypertrophy).
the goals of management and the means of achieving them:
the effect of pregnancy on the cardiac disorder
the effect of the cardiac disorder on the pregnancy
the optimum time for delivery
if corrective surgery is required - can it be deferred until the post partum period?
the choice of anaesthetic and analgesic techniques available and their haemodynamic effects
the need for and interpretation of invasive monitoring e.g. central venous, left atrial pressure, arterial pressure, cardiac
output
the need for pre and postoperative high dependency or intensive care
the management plan for delivery should be clearly written in the patients case record - it should include provision for
alternative delivery modes if relevant and it must be updated frequently
there are no controlled trials involving alternative anaesthetic management strategies - knowledge is based on clinical
experience, case reports and a small number of retrospective series.
Investigations: following a detailed history and clinical examination Chest X-ray, ECG and echocardiography are the basic
investigations. Repeated investigations must be performed to monitor progress and pick up any deterioration without delay. Ejection
fraction analysis requires a knowledge of the physiological changes of pregnancy together with the likely haemodynamic effects of
the lesion concerned.
Rather than attempt to detail the management of every conceivable cardiac condition - it is more useful to illustrate the above
principles when applied to aortic and mitral valve disease in patients presenting for delivery.
Aortic Stenosis
The risk of mortality is greatly increased when the valve area <0.7 cm 2 and pressure gradient >50mmHg -
though pressure gradient may be difficult to interpret due to the haemodynamic changes of pregnancy. This
degree of severity may present unexpectedly during pregnancy when the cardiovascular stress precipitates
symptoms e.g. cardiac failure with pulmonary oedema and syncope. The additional pressure load on the left
ventricle results in massive left ventricular hypertrophy. The stiff hypertrophied ventricle has poor diastolic
compliance and coronary perfusion pressure may fall critically. Afterload reduction (systemic vasodilatation) and
tachycardia may further reduce coronary filling which takes place in diastole.
An adequate preload, given with central venous monitoring, must be given to fill the stiff ventricle.
Hypotension should be managed aggressively with a vasopressor that avoids tachycardia e.g. phenylephrine in
40µg increments.
Single shot spinal anaesthesia should not be given but incremental epidural or spinal anaesthesia may be safe
if meticulous attention is given to blood pressure control.
General anaesthetic techniques should involve the same constraints i.e. avoiding hypotension and tachycardia.
Oxytocic drugs should be either avoided or administered very slowly to avoid critical hypotension.
Aortic Incompetence
The main problem is ventricular volume overload.

The compensatory mechanisms are ventricular hypertrophy plus dilatation.
The goal is to maintain forward flow for which tachycardia is preferable to bradycardia - bradycardia may
aggravate ventricular overfilling leading to increased regurgitation.
Afterload reduction may also increase forward flow by decreasing regurgitation - vasoconstriction may therefore
be detrimental.
Epidural analgesia and anaesthesia are usually beneficial - if a vasopressor is required ephedrine, rather than
a pure α 1 agonist, should be given to maintain or increase heart rate.
If general anaesthesia is required the same considerations apply to the choice of technique i.e. avoid
bradycardia and vasoconstriction.
Mitral Stenosis
Diagnosis is often made during pregnancy when the cardiovascular stress of a valve area <1.5 cm 2
precipitates symptoms. Pure stenosis (without incompetence) is unusual. The left ventricle is under filled. The

Chapter 6
left atrium is distended and the pressure raised - there is pulmonary venous congestion. Pulmonary
hypertension and right heart failure may follow.
Tachycardia should be avoided as diastolic filling is compromised - this may require the administration of a
beta-blocking drug
Hypotension is detrimental as cardiac output can not rise in compensation.
Epidural analgesia or anaesthesia or general anaesthesia may be used as long as hypotension is managed
aggressively with a vasopressor such as phenylephrine in 40µg increments.
Mitral Incompetence
Patients with regurgitant valve disease do well even when the leak is severe, but there is always the risk of
atrial fibrillation with sudden pulmonary oedema if the valve disease is rheumatic in origin.
Epidural analgesia and anaesthesia are beneficial as reducing pain avoid increases in systemic vascular
resistance thus minimising risk of pulmonary congestion.
Venous return must be maintained to allow ventricular filling
Ephedrine is good as patients benefit from its chronotrophic effect if a vasopressor is required.
Heparin therapy should be stopped before delivery and a coagulation screen should be normal before establishing an epidural.
FURTHER READING
Mushambi MC, Halligan AW, Williamson K. Recent developments in the pathophysiology and management of pre-eclampsia. British
Journal of Anaesthesia 1996; 76: 133-148. Click here for Medline link
Sharwood-Smith G, Clark V, Watson E. Regional anaesthesia for caesarean section in severe pre-eclampsia: spinal anaesthesia is
the preferred choice. International Journal of Obstetric Anesthesia 1999; 8, 85-89. Click here for IJOA link
Santos AC. Spinal anesthesia in severely preeclamptic women when is it safe? Editorial. Anesthesiology 1999; 90 1243-1254. Click
here for Medline link
Hood DD, Curry R. Spinal vs epidural for cesarean section in severely preeclamptic patients. Anesthesiology 1999; 90: 1276-1282.
Click here for Medline link
Roberts JM. Magnesium for preeclampsia and eclampsia. New England Journal of Medicine 1995; 333: 250-251. Click here for
Medline link
The Eclampsia Trial Collaborative Group. Which anticonvulsant for women with eclampsia? Evidence from the Collaborative
Eclampsia Trial. Lancet 1995; 345: 1445-1463. Click here for Medline link
Idama TO, Lindow SW. Magnesium Sulphate: A Review of Clinical Pharmacology applied to obstetrics. British Journal of Obstetrics
and Gynaecology 1998; 105: 260-268. Click here for Medline link
MacAnulty JH. Heart and Other Circulatory Diseases. In: Bonica JJ, MacDonald JS, eds. Principles and Practices of Obstetric
Analgesia and Anesthesia., Baltimore Williams & Wilkins 1995; 1013-1039.
American College of Cardiology Guidelines for the Management of Patients with Valvular Heart Disease
Suntharalingam G, Dob D and Yentis SM. Obstetric epidural analgesia in aortic stenosis: a low dose technique for labour and
instrumental delivery. International; Journal of Obstetric Anesthesia 2001; 10: 129-134.
Brighouse D. Anaesthesia for caesarean section in patients with aortic stenosis: the case for regional anaesthesia. Editorial.
Whitfield A, Holdcroft A. Anaesthesia for caesarean section in patients with aortic stenosis: the case for general anaesthesia.
Editorial. Anaesthesia 1988; 53: 109-111. Click here for Medline link
Rigg CD, Bythell, Bryson MR, Halshaw J and Davidson JM. Caesarean section in patients with heart-lung transplants: a report of
three cases and a review. International; Journal of Obstetric Anesthesia 2000; 9: 125-132. Click here for IJOA link

Chapter 6
NEXT CHAPTER

Chapter 7
7. OBSTETRIC HAEMORRHAGE
Chapter contents
The principles of managing acute haemorrhage

Postpartum haemorrhage
Management of major obstetric haemorrhage
Anaesthesia in cases of major obstetric haemorrhage
Acute renal failure
Coagulation problems during pregnancy
Disseminated intravascular coagulation (DIC)
Use of anticoagulant therapy during pregnancy and the puerperium

Typical blood volume changes in normal pregnancy

Non pregnant Pregnant at term % Increase
Plasma volume ml 2700 4200 55
Red cell volume ml 1400 2800 (on iron) 50
Blood volume ml 4000 5800 45

Cardiac output increases up to 6-7 litres/min BEFORE LABOUR
Blood loss at vaginal delivery averages 500 ml and at caesarean section 800 ml

American College of Surgeons blood loss classification
15 % loss - minimal effect

15-30% loss – tachycardia and restlessness
30-40% loss – tachycardia, tachypnoea, systolic hypotension
Young healthy patients with a 30-40% loss are treated adequately with crystalloids.
A 1500ml loss is approximately 25% of blood volume at term
Carefully estimate the volume of blood lost using the following clinical signs
peripheral perfusion
heart rate
blood pressure
Peripheral vasoconstriction and a tachycardia of >100 indicate significant blood loss and initial physiological
compensation - when this is followed by a fall in systolic blood pressure to <100 mm Hg (and there is no other cause)
a blood loss of at least 25% of maternal blood volume is likely - follow the guidelines for management of major
haemorrhage
Define the cause - arrest the source of bleeding, immediately if possible, or plan an appropriate strategy with obstetric staff
Restore circulating blood volume
ANTEPARTUM HAEMORRHAGE (APH)
Principal causes
Placenta praevia - 22%

Placental abruption - 31%
Coagulopathy
Uterine rupture
Vasa praevia

Chapter 7
Management This depends on the cause and state of mother and fetus. In severe cases the cornerstone of
management is immediate delivery to empty the uterus. In vasa praevia rupture of the membranes may tear a fetal
vessel leading to fetal exsanguination (the fetal blood volume is approximately 250 ml). It is a fetal rather than maternal
emergency and is managed by immediate delivery.
POSTPARTUM HAEMORRHAGE (PPH) -
Principal causes
Uterine atony - 90%

Retained placenta
Trauma to the birth canal
Coagulopathy
Placenta accreta - an abnormally firm attachment of the placenta to the wall of the uterus. Separation of the placenta from
the uterine wall at the time of delivery can cause severe bleeding that often necessitates hysterectomy. Placenta accreta is a
potential complication in all women with placenta praevia, particularly those with previous caesarean sections. It may be
possible to diagnose placenta accreta with ultrasound.
Uterine rupture
Uterine inversion - may result during vaginal delivery from placenta accreta
Management
Bimanual compression of the uterus may be life-saving.

Oxytocin is given up to a maximum recommended total dose of 50 units
Ergometrine 500 µg i.v. bolus
Carboprost (important side effects) - Prostaglandin F2 a (PGF 2 a ) 250 µg i.m. or intramyometrially at intervals of no less than
15 minutes, maximum total dose is 2 mg.
Embolisation techniques
Surgical intervention under general anaesthesia - Haemostatic suturing (B-Lynch), ligation of uterine or internal iliac arteries
or, if all else fails, a hysterectomy
Management of uterine inversion
Replacement of the uterus - relaxation of the myometrium by the administration of a general anaesthetic including a volatile
agent is usually required. Glyceryl trinitrate should also be considered.
MANAGEMENT OF MAJOR OBSTETRIC HAEMORRHAGE >1500 ml
Identify patients at risk

CALL FOR HELP - summon senior help and extra staff.
Alert haematology and blood transfusion staff
Anticipate coagulation problems
Stop haemorrhage at source
Administer oxygen by face mask
Insert 2 peripheral lines with large bore intravenous cannulae (14 gauge)
Take 20 ml blood for grouping, cross-matching and coagulation studies. Order 10 units of blood.
Infuse fluid rapidly with a high flow pressure infuser and heating coil. Avoid blood filters.
Consider establishing a CVP line and direct arterial pressure measurement
The SIGN postpartum haemorrhage flow chart can be accessed here:
Fluid therapy
Start with crystalloid and colloid solutions up to 3.5 litres until blood is available. Of the colloids, gelofusine, haemaccel or
pentastarch are preferable; dextran 70 should be avoided since it interferes with coagulation screening. Human albumin
solution (4.5%) is only used if there is an allergy to synthetic colloids.

Chapter 7
Blood of the patient’s own group is preferable. All labour wards should store two units of O Rh negative blood - this will be
compatible in 99% of patients not already known to have specific antibodies. Most blood is available as a supplemented red
cell concentrate; almost no plasma is present so additional intravenous colloid is essential.
Fresh frozen plasma (FFP), platelet concentrate and cyroprecipitate should not be given until at least 6 units of stored blood
have been infused after which further blood loss may lead to a dilutional coagulopathy. FFP and platelet concentrate contain
all coagulation components; cryoprecipitate is used when a more concentrated source of fibrinogen is required.
Further management
Specific action should be taken to reduce heat loss including the use of a warming blanket.
Monitor - heart rate, blood pressure, pulse oximetry, ECG, respiration, CVP - aim for 4-8 mmHg, urine output, temperature
and blood gases. Serial haemoglobin or haematocrit are performed aiming for optimal oxygen delivery with a haematocrit of
25 - 30%.
Continue to monitor coagulation and give further treatment as advised by the haematologist
Give oxygen by facemask or by IPPV to maintain an adequate SpO 2
Consider calcium, bicarbonate and inotropes e.g. dopamine 2.5 µg/kg/min.
Prevent renal failure
Intensive care nursing
Treatment of adult respiratory distress syndrome
Further investigations
Urea and electrolytes, serum calcium, and acid base balance should be monitored regularly.
ANAESTHESIA IN CASES OF MAJOR OBSTETRIC HAEMORRHAGE
Vigorous resuscitation should begin before induction of anaesthesia but in many cases it may be necessary to induce anaesthesia
while resuscitation is in progress.
A rapid sequence induction is used with minimal doses of thiopentone; etomidate (100 µg/kg) or ketamine (1-2 mg/kg) may be
preferred if there is severe hypovalaemia.
Postoperative care - the patient should be transferred to a high dependency or intensive care unit until fully stabilised. Monitoring
should continue as above. ARDS may develop in which case a period of IPPV will be required.
ACUTE RENAL FAILURE
Diagnosis Oliguria < 20 ml/h.
Special considerations apply to oliguria in severe pre-eclampsia
Pre-renal causes: pre-renal causes of acute renal failure include hypotension and/or hypovolaemia, e.g. obstetric
haemorrhage or hyperemesis. The renal response is to retain maximum amounts of fluid and sodium. The urine is:-
concentrated - the specific gravity is >1020, urine osmolality is high at >700 mmol/kg.
low in sodium - the urine sodium concentration is <15 mmol/l.
high in urea - the urinary urea concentration is >250 mmol/l.
Intrinsic renal causes - Acute renal failure may result from failure to correct pre-renal factors and may be complicated by
exposure to nephrotoxins, e.g., bacteraemia, incompatible blood transfusion, disseminated intravascular coagulation, amniotic
fluid embolus, cephalosporin and amino-glycoside antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs) and hepatic
failure. The kidney fails to concentrate urine effectively. The urine is:
dilute - the specific gravity is <1010, urine osmolality is low at <300 mmol/kg i.e. close to that of plasma
high in sodium - the urine sodium concentration is >60 mmol/l.
low in urea - the urinary urea concentration is <160 mmol/l.
Management of oliguria
Catheterise the bladder, measure hourly volumes, measure the urinary osmolality and sodium concentrations, obtain a
specimen for culture and sensitivity.

Chapter 7
Monitor the CVP

Correct hypovolaemia.
Avoid nephrotoxins.
Check electrolytes, full blood count and coagulation
If oliguria persists despite correcting pre-renal factors, then frusemide 40 - 80 mg is given i.v. and repeated as necessary. A
low dose dopamine infusion may be indicated (2 - 5 µg/kg/min).
Contact the Renal Unit.
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
In DIC normal control of the balance of coagulation and fibrinolysis is lost. Blood is exposed to a large excess of thromboplastin or
other active tissue substance. Coagulation factors are consumed and the fibrinolytic system is activated; the process often continues
until haemostasis is no longer possible. A progressively falling platelet count suggests a chronic DIC which may continue and
progress for several days; DIC can also arise abruptly - sometimes catastrophically.
Laboratory tests are essential to monitor the progress of the condition and any response to treatment. The D-dimer test is specific
for breakdown of the fibrin polymer and is the most useful test of fibrinolytic activity. The Thromboelastogram (TEG) is a whole blood
viscoelastic test that gives information on platelet function and can be used at the bedside.
The causes are as follows:
placental abruption
severe pre-eclampsia
placenta accreta and percreta
retained dead fetus
amniotic fluid embolus
septic shock
incompatible blood transfusion
The treatment is:
Contact the haematology department for advice

If one of the above high risk conditions is present and bleeding cannot be surgically controlled it may be
necessary, or even life saving, to give FFP, cryoprecipitate and platelets before the results of a coagulation
screen are available - otherwise manage as a case of major obstetric haemorrhage
Remove the cause as quickly as possible
Table 7.1 Coagulation values after 30 weeks of normal pregnancy and with DIC
NORMAL (>30/52) DIC

Fibrinogen (g/l ) 4.0 - 6.0 < 0.15
Platelets (x 10 9 /l) 150 - 400 < 50
Prothrombin time (s) 12 - 14 > 100
APPT (s) 35 - 40 > 100
FDP (µg/l) < 16 > 200
D-dimer (mg/l) < 0.25 >8
Bleeding time (min) < 10.5 prolonged
USE OF ANTICOAGULANT THERAPY DURING PREGNANCY AND THE PUERPERIUM
In general the risk of venous thrombosis is greater in the days and weeks after delivery than it is during pregnancy.
Indications for full anticoagulant therapy

Chapter 7
Deep venous thrombosis (DVT) prophylaxis - (heparin).
DVT treatment - (heparin and warfarin)
Prosthetic heart valve - (warfarin)
Thrombophilia e.g. antithrombin III, proteins C and S deficiency, Factor V Leiden polymorphism - (heparin).
Indications for low dose heparin therapy and alternative methods
(Adapted from) PROPHYLAXIS AGAINST THROMBOEMBOLISM IN CAESAREAN SECTION

(1998 RCOG Working Party Report on Prophylaxis against thromboembolism)
Risk assessment profile for thromboembolism in Caesarean section
LOW RISK - early mobilisation and hydration
Elective Caesarean section - uncomplicated pregnancy and no other risk factors
MODERATE RISK - Consider heparin prophylaxis +/- leg stockings
Age >35 years

Obesity (>80Kg)
Para 4 or more
Labour 12hours or more
Gross varicose veins
Current infection
Pre-eclampsia
Immobility before surgery ( >4days)
Major current illness e.g. heart disease, cancer, inflammatory bowel disease, nephrotic
syndrome
Emergency Caesarean section in labour
HIGH RISK - Heparin prophylaxis + leg stockings
A patient with three or more risk factors from above

Extended major pelvic or abdominal surgery, e.g. Caesarean hysterectomy
Patients with a personal or family history of DVT, pulmonary embolism or thrombophilia
Paralysis of lower limbs
Patients with antiphospholipid antibody (cardiolipin antibody or lupus anticoagulant).
The heparin regimen should consist of 7,500 units of subcutaneous standard heparin 12 hourly or enoxaparin (LMWH) 40
mg daily.
Anticoagulant drugs
Vitamin K antagonists - phenindione, warfarin. Warfarin has a low molecular weight, is lipid soluble and crosses the placenta; it is
teratogenic and may cause placental or fetal bleeding. This group of drugs should be avoided in pregnancy if possible; treatment
during the first and third trimesters presents the greatest risk. If the balance of risk results in administration during the middle
trimester (e.g. for a prosthetic heart valve) a change to heparin is normally made at least 4 weeks before delivery. The prothrombin
time, reported as the international normalised ratio (INR), is monitored; the therapeutic range is 2 - 5:1. Excessive anticoagulation or
haemorrhage may require intravenous phytomenadione ( Vitamin K), plus FFP if life threatening; close liaison with the haematologist
is essential.
Unfractionated heparin (UHF) - this is a mucopolysaccharide with a high molecular weight and protein binding capacity, which does
not cross the placenta. Coagulation is inhibited by a number of steps including the potentiation of antithrombin III and alterations in
platelet function. The activated partial thromboplastin time (APTT) is monitored and the therapeutic range is 1.5 - 2.5:1. If
haemorrhage occurs withdrawal of heparin may be sufficient, otherwise protamine is given. When heparin is given in low dose by
subcutaneous injection laboratory monitoring is not required.

Chapter 7
Low molecular weight heparin (LMWH) - heparin is fractionated to produce LMWH which inhibits activated factors II and X with little
effect on platelet function; a longer action means that only a single daily subcutaneous dose is required e.g. enoxaparin. Factor Xa
activity is not normally monitored.
Aspirin - this inhibits cyclo-oxygenase which is required for prostacyclin production (vasodilator, decreased platelet aggregation) and
thromboxane A2 production (vasoconstriction, increased platelet aggregation) in platelets and the vascular endothelium. Suppression
of thromboxane A2 is greater and of longer duration than that of prostacyclin - so the net effect is vasodilatation and decreased
platelet aggregation. Aspirin shows very limited efficacy in preventing DVT. It has been used in an attempt to improve fetal outcome
in pre-eclampsia but published evidence has not been favourable.
Anticoagulants with epidurals and spinals
Full anticoagulation with warfarin or heparin is a contraindication to spinal and epidural techniques.
Haematoma in the vertebral canal is rare and can arise spontaneously. The risk of this complication is slightly increased when
spinal or epidural analgesia is performed in a patient to whom low dose subcutaneous heparin, including LMWH, is being
administered. The risk appears to be greatest for epidural catheterisation. The increase in cases associated with LMWH recently
reported from America may be related to the larger doses given there.
The risk may be minimised by applying a few basic precautions:
Weigh the small increased risk against the benefits of an epidural in the situation presenting and discuss the
matter fully with the patient
Use a skilful atraumatic technique
Before performing a central nerve block: -
4 hours should be allowed after the last dose and 1 hour before the next dose of UHF
10-12 hours should be allowed after the last dose and 4 hours before the next dose of LMWH
Continue to monitor the patient for signs of cord compression for the entire duration of anticoagulant therapy.
Aspirin therapy interferes with platelet function, an effect which may persist for 7 days after stopping treatment. The risk of
haematoma formation appears to be very slight if the coagulation screen is normal. Extra care when inserting and removing the
catheter is a sensible precaution.
FURTHER READING
Lechner RB. Hematologic and coagulation disorders. In: Chestnut DH ed. Obstetric Anesthesia. St Louis: Mosby, 1994; 815-845.
Howell CJ, Clowes NWB. The management of major obstetric haemorrhage. Current Anaesthesia and Critical Care 1995; 6: 218-
223.
Scottish Obstetric Guidelines and Audit Project . The Management of Postpartum Haemorrhage. 1998; click here for WWW link
Harmer M. Maternal mortality – is it still relevant? Anaesthesia 1997; 52: 99-100.Click here for Medline link
Donaldson MDJ, Seaman MJ, Park GR. Massive Blood Transfusion. British Journal of Anaesthesia 1992; 69: 621-630.Click here for
Medline link
Bell K. Blood transfusion in the critically ill: coagulopathy and hypoalbuminaemia. British Journal of Intensive Care 1996; 6:10-15.
Bell K. Blood transfusion in the critically ill: volume replacement and transfusion of red cells. British Journal of Intensive Care 1995;
6: 218-273.
Checketts MR and Wildsmith JAW. Central nerve block and thromboprophylaxis - is there a problem? British Journal of Anaesthesia
1999; 82:164-167.Click here for Medline link
NEXT CHAPTER

Chapter 7

Chapter 8
8. MATERNAL RESUSCITATION
Chapter contents
Cardio-pulmonary resuscitation
CPR Algorithm
Resuscitation drug dosages
Convulsions
Anaphylactic shock
Pulmonary embolism
Venous thromboembolus: Amniotic fluid embolus: Venous Air Embolus
Pulmonary oedema
Malignant hyperpyrexia
CARDIO-PULMONARY RESUSCITATION (CPR)
Cardiac arrest is rare with an incidence of 1:30,000 pregnancies. The survival of mother and fetus depends on prompt recognition
and treatment.
Main causes of cardiac arrest
Anaesthetic Problems
Failed intubation
Aspiration of gastric contents
Total spinal anaesthesia
Drug induced reactions
Local anaesthetic toxicity
Obstetric Problems
Massive haemorrhage
Amniotic fluid embolism
Venous and/or air embolism
Intracranial haemorrhage
Magnesium toxicity
After 26 weeks of pregnancy aortocaval compression is likely. If cardiac arrest occurs the complete absence of any vascular tone
leads to a reduction in venous return to the right side of the heart. External cardiac compression may therefore be ineffective, as the
heart is empty. The patient must be tilted to at least a 30° angle. This is best achieved using a specially wedged board, although it
is possible to use a "human wedge".
Fig 8.1 Wedged board Human wedge
If CPR is not effective (15:2 ratio) in generating a powerful pulse (100/min) or adequate perfusion within 3 - 4 minutes and there is

Chapter 8
no other obvious remediable cause, e.g. massive haemorrhage, bilateral tension pneumothorax or pulmonary embolus, the fetus
must be delivered while CPR is continuing; effective cardiac filling and output should then occur. Early delivery may also save the
baby (the fetus is more resistant to hypoxia than the mother).
THE CHAIN OF SURVIVAL

Early ® Early ®
Early ® Defibrillation Early
Access Basic Life Support
Advanced Life Support
For every minute that elapses following the onset of a shockable arrhythmia, there is 5-10% less chance of survival. Early
defibrillation is critical; therefore it should not be delayed if available and appropriate. Administration of 200, 200 and 360 joule
shocks, given in sequence if required with a monophasic defibrillator, should not take any longer than 30 seconds. As soon as the
shocks have been delivered, B.L.S must be restarted immediately. Available data suggests that defibrillation is safe in all phases of
pregnancy and labour as only a small amount of current penetrates the uterus. Biphasic defibrillators are effective at lower energy
levels e.g. 200 J. They reverse current flow during defibrillation and are as effective or better than monophasic defibrillators.
ADVANCED LIFE SUPPORT ALGORITHM FOR THE MANAGEMENT OF CARDIAC ARREST IN ADULTS
Note: each successive step is based on the assumption that the one before has been unsuccessful
Resuscitation Council UK.
Table 8.1 Resuscitation drug doses

Chapter 8
TRACHEAL
DRUGS
made up in a
all doses based on INTRAVENOUS COMMENT
volume of 10
a 70 kg woman
ml saline
Epinephrine a and ß receptor stimulant
1:10,000 0.1-1 mg 2 mg Infusion 5 mg:500 ml saline
10 ml = 1 mg (10 µg/ml)
Atropine
1 mg 2 mg Increases heart rate
0.6 mg/ml
Completely blocks the vagus nerve,
3 mg used in asystole
300 mg
Amiodarone in 20 Used in refractory fibrillation.
ml 5% dextrose
second dose Consider as early as fourth shock
150 mg
Bretylium tosylate
50 mg/ml
500 mg Used in refractory fibrillation
Mexiletine Membrane stabilisation, reduces

25 mg/ml
150 mg bolus tendency to tachyarrythmias
Calcium gluconate
10% 10 ml Inotropic action
(0.225 mmol Ca/ml)
Infusion 1.5 g:500 ml
Lidocaine 2% 100 mg 200 mg
3 mg/ml
Adenosine 6 mg then 12 mg x 3 every 2 min
Sodium bicarbonate Not as routine, only refractory cases, pH
8.4%
50 ml to be measured as soon as possible
Metoprolol ß-blocker used for supraventricular
(1 mg/ml)
5 mg arrythmias (SVT)
Any effects of these drugs on the fetus can be addressed after delivery, resuscitation of the mother is the prime consideration.
Algorithms for treatment of Periarrest Arrhythmias can be accessed here
BRADYCARDIA
BROAD COMPLEX TACHYCARDIA
NARROW COMPLEX TACHYCARDIA
CONVULSIONS
Main causes
Eclampsia, epilepsy and local anaesthetic toxicity. Consider all obstetric convulsions eclamptic in origin despite a normal blood
pressure until proved otherwise.
Premonitory signs
Eclampsia - May be NONE: severe frontal headache with visual disturbance, photophobia, nausea and vomiting, right upper
quadrant pain.
Epilepsy - Aura, history of epilepsy, anticonvulsant therapy.
Local anaesthesia - Numbness of the tongue and circumoral tissues, light-headedness, dizziness, difficulty focusing, tinnitus, slurred
speech, shivering and muscle twitching.

Chapter 8
Management
Turn the patient on her side to avoid aortocaval compression. Maintain and protect the airway, administer 100% oxygen. Ensure
fetal monitoring. Follow one of the two regimes:-
Diazepam 5 - 20 mg i.v. (more than 30 mg may cause neonatal hypotonia)
Intravenous thiopentone 50 mg increments - suxamethonium, cricoid pressure and intubation may be required. If eclampsia is
suspected once convulsions have ceased then the magnesium sulphate protocol is followed.
ANAPHYLACTIC SHOCK
Common labour ward causes:- antibiotics, suxamethonium, latex, oxytocin, NSAIDs and colloids.
An anaphylactic reaction is where previous sensitisation has occurred and vasoactive substances e.g. histamine, serotonin are
released from mast cells in response to an IgE antibody mediated reaction.
An anaphylactoid reaction is where there is no antibody mediation in mast cell release.
Management
Stop the administration of all suspected drugs and curtail surgery if appropriate.
Maintain the airway, give 100% oxygen, and avoid aortocaval compression.
Give epinephrine 1:10,000 (1 mg:10 ml saline) i.v. as 0.5 - 1 ml boluses, titrate as necessary for hypotension and
bronchospasm.
Start rapid intravascular volume expansion with crystalloid or colloid.
Specific measures
Hypotension - Elevate the legs, establish monitoring with ECG and possibly CVP and arterial line. Circulatory support with
catecholamines.
Bronchospasm
aminophylline 250 - 500 mg i.v. slowly

salbutamol 250 µg i.v. slowly
2.5 - 5 mg nebulised in 3 ml saline
Antihistamines
chlorpheniramine 10 - 20 mg i.v.
Steroids
hydrocortisone 100 - 200 mg i.v.
Anaphylaxis algorithm can be accessed here:-
Investigation
Immediate - mast cell tryptase, the principle protein content of mast cell granules is released with histamine and other amines
in anaphylactic and anaphylactoid reactions. Plasma concentration is raised 1 - 6 h after a reaction.
Normal level 0.8 - 1.5 ng/ml Anaphylactic reactions occur at concentrations >20ng/ml

Chapter 8
Long term - referral to allergist for skin testing and specific IgE antibody detection by radio-allergosorbent test (RAST)
PULMONARY EMBOLISM
This is the commonest cause of maternal death in the United Kingdom. Emboli may be thrombus, amniotic fluid or air. The
physiological changes that occur depend on the degree of obstruction to blood flow through the pulmonary artery and the increase
in dead space ventilation. These may lead to pulmonary hypertension, right ventricular strain and cardiac failure. During anaesthesia
an early sign is an abrupt fall in end tidal PCO 2
Venous thromboembolus
The risk of venous thrombosis is increased in pregnancy due to the relatively hypercoagulable state, particularly in the postpartum
period. The presentation includes retrosternal discomfort, dyspnoea, pleuritic pain, haemoptysis, profound collapse, raised central
venous pressure and cardiac arrest. The ECG shows:-
S1 Q 3 T3 pattern with prominent S wave in lead I, Q wave and inverted T in lead III
Sinus tachycardia
T wave inversion in leads V1 -V3
Right bundle branch block
Low amplitude deflection
A ventilation perfusion scan will show normal ventilation with a segmental perfusion defect. Pulmonary angiography may
demonstrate an intraluminal filling defect and/or the abrupt termination of a branch vessel.
Management of minor thromboembolism
Heparinisation - 5,000 -10,000 i/u i.v. followed by a continuous infusion of 1,000-2,000 i/u per hour. Monitored with the APPT
- therapeutic range 1.5-2.5.
Antenatally heparin is given sc - 12,000 i/u 12 hourly.
Postnatally oral warfarin is started at the same time as i.v. heparin - 10 mg/day for 2days. Subsequent dosage depends on
the INR - therapeutic range 2-3.
Management of massive thromboembolism
Oxygen therapy, cardiac massage and intermittent positive pressure ventilation (IPPV)
An intravenous bolus of heparin - 15,000 i/u should be given.
Cardiovascular support with a norepinephrine infusion 4 mg in 500 ml of saline
A pulmonary angiogram should be obtained immediately: if this is not available thrombolytic therapy must be started with
streptokinase in a loading dose of 600,000 units with a maintenance dose of 100,000 u/h for 24 hours. The thrombin time
should be maintained at a level of 1½ times the control value.
Amniotic fluid embolus (Anaphylactoid Syndrome of Pregnancy)
The incidence is 1 in 30,000 pregnancies with a maternal mortality rate approaching 85%, It can occur during labour (70%), after
Caesarean delivery (19%), or after vaginal delivery (11%).
The presenting features are
Sudden collapse
Excessive bleeding in labour or post partum
Seizures
Dyspnoea
Fetal bradycardia
There is a history in 41% of mothers of atopy (asthma, eczema, hay fever) or allergy, often to drugs.

Chapter 8
There is a biphasic response to the presence of amniotic fluid (or meconium) in the maternal circulation causing release of
substances that produce pulmonary vascular spasm, pulmonary hypertension, hypoxic injury to the pulmonary capillaries and heart.
This leads to left ventricular failure and subsequent adult respiratory distress syndrome. Coagulopathy may be related to the
presence of a factor X activator in amniotic fluid.
Diagnosis is made on clinical grounds. The presence of fetal cells in the maternal blood is NOT pathognomonic and they are
commonly detected in normal patients. In primates it has been shown that infusions of large amounts of amniotic fluid do NOT cause
the syndrome. Minor degrees of the syndrome are probably quite common.
Management
Cardiopulmonary resuscitation with the patient wedged if the fetus is still in utero
Deliver the fetus and placenta as soon as possible
Insert 2 large peripheral cannulae, CVP line, urinary catheter, arterial line and if possible a pulmonary artery catheter
Aspirate blood from the right side of the heart
Monitor ECG, pulse, blood pressure, CVP and pulmonary artery wedge pressure
Cardiovascular support with dopamine and epinephrine
DIC management in consultation with the Haematology Department
Venous air embolus
This can occur during Caesarean section particularly at the time of uterine incision and placental separation. It has been shown that
subclinical venous air embolism occurs in up to 50% of patients at this time; the risk is increased when the uterus is exteriorised
and the patient is head down. A head up tilt has been advocated during surgery for Caesarean section. A patent foramen ovale is
present in 20 - 25 % of patients and paradoxical air embolism is possible although very rare in clinical practice. Large air embolism
will result in frothing of blood in the right ventricle causing an air lock and cardiac arrest. The diagnosis is made with a precordial or
oesophageal Doppler probe. A mill wheel murmur is accompanied by hypotension, a fall in SpO 2 , end tidal PE CO 2 and an increase
in central venous pressure.
Management
100% oxygen must be given

Stop the nitrous oxide to reduce the air bubble size
Replace the uterus if exteriorised
Flood the wound with fluid to prevent further aspiration of air.
Place the patient in a head down position on the left side to allow any air to collect in the apex of the right ventricle
Aspirate air from the right atrium via a central venous line.
Provide cardio-respiratory support as necessary. Internal cardiac massage may be required - access to the great vessels will
permit direct aspiration of air (or amniotic fluid) .
PULMONARY OEDEMA
Maternal pulmonary oedema is associated with:
Pre-eclampsia - capillary permeability is increased and colloid osmotic pressure falls due to proteinuria. There may also be
an element of left ventricular failure secondary to severe hypertension. Antihypertensive therapy with ß-blockers may
contribute to this.
Fluid overload - due to over-treatment of severe haemorrhage, or fluid challenges in pre-eclamptic patients.
Myocardial disease - e.g. cardiomyopathy of pregnancy or myocardial ischaemia.
The use of tocolytic therapy for premature labour with ß-adrenergic agonists, e.g., ritodrine, isoxuprine, salbutamol.
Tachycardia is a prominent feature. Steroid therapy for fetal lung maturation may be a contributory factor
It presents with tachycardia, tachypnoea, hypoxia and cyanosis. An early sign is a fall in oxygen saturation. On auscultation of the
chest, basal crepitations and rhonchi are heard. Chest x-ray shows fluffy shadowing or the more extensive butterfly wing
appearance.
Management

Chapter 8
Oxygen
Sedation with i.v. morphine to relieve agitation / anxiety and reduce the pre-load by venodilatation.
Diuretic therapy with frusemide 40 - 80 mg i.v., repeated as necessary. Dopamine 2 - 5 µg/kg / min may be required i.v..
Intubation and IPPV may be necessary with positive end expiratory pressure (PEEP)
Treatment of the underlying cause
MALIGNANT HYPERPYREXIA (MH)
The incidence is 1:30,000 of all general anaesthetic administered. Not every patient with a genetic predisposition developes a MH
crisis during exposure to triggering agents which include all volatile anaesthetics and depolarising muscle relaxants.
MH presents with the following signs:
Unexplained tachycardia
Tachypnoea
A rise in body temperature which increases by more than 2° C/h
An abnormal reaction to suxamethonium - trismus is an early sign of this
Cyanosis
Muscular rigidity developing later during the anaesthetic
Increased oozing is usually a sign of DIC
A fall in SpO 2 , a rise in PE CO 2 , metabolic acidosis and hyperkalaemia
A diagnosis of MH should be assumed if suspicions are aroused.
Management
Discontinue inhalational agents, terminate surgery CALL FOR HELP.

Hyperventilate with 100% oxygen 2 - 3 times the predicted minute volume
Give dantrolene 2 mg/kg i.v.. Repeat as necessary up to a total of 10 mg/kg
Cool with 1 - 2 litres iced saline i.v., apply surface cooling over the major vessels, and lavage to the pleural or peritoneal
cavities. Consider cardiopulmonary bypass via femoro-femoral circulation
Correct metabolic acidosis with sodium bicarbonate, monitor blood gases and pH and correct hyperkalaemia. Treat
arrhythmias if severe.
Establish the following monitoring: SpO 2 , ECG, arterial cannulation, a muscle temperature probe, central venous cannulation,
urinary catheter, blood pressure and a fluid balance chart.
Investigations should include the following: blood gases, haemoglobin, urea, electrolytes, clotting screens and CPK level
Admit to the intensive care unit
Late management must include screening of the patient and her family for MH susceptibility
In the management of known MH or MH susceptible patients, the technique of choice is regional anaesthesia. The administration of
general anaesthesia requires the following conditions:-
A clean anaesthetic machine with disposable tubing and no vaporisers

The circuit which has been flushed with 10 litres of oxygen for at least 20 minutes before use
A cooling blanket on the operating table,
Dantrolene and ice must be available.
Only 'safe' drugs must be used
SAFE UNSAFE
Diazepam, thiopentone, propofol,
Succinylcholine
methohexitone.
Halothane, enflurane, isoflurane,
Nitrous oxide
desflurane, sevoflurane
Atracurium, pancuronium, vecuronium,
mivacurium,, rocuronium


Chapter 8
Local anaesthetic drugs

Oxytocin, PGF2 a, ergometrine
Nitroglycerine, magnesium sulphate
Ephedrine, epinephrine, norepinephrine
FURTHER READING
The American Heart Association in Collaboration with the International Liaison Committee on Resuscitation (ILCOR) Guidelines 2000
for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - An International Consensus on Science. Resuscitation
2000; 46: 1-448
The 1998 European Resuscitation Council Guidelines for Adult Advanced Life Support. In: Bossaert L (ed.). European Resuscitation
Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 36-37.
The 1998 European Resuscitation Council Guidelines for the management of the airway and ventilation during resuscitation. In:
Bossaert L (ed.). European Resuscitation Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 129-158.
Kudenchuk PJ, Cobb LA, Copass MK et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular
fibrillation. New England Journal of Medicine 1999; 341: 871-878.Click here for Medline link
The Association of Anaesthetists of Great Britain and Ireland and The British Association of Allergy and Immunology. Suspected
anaphylactic reactions associated with anaesthesia. Published by: The Association of Anaesthetists of Great Britain and Ireland
1995. MedicAlert Foundation (Registered Charity)
Fletcher SJ, Parr MJA. Amniotic fluid embolism: a case report and review. Resuscitation 2000: 43;141-146 Click here for Medline
link
Halsall P, Ellis FR. Malignant hyperthermia. Current Anaesthesia and Critical Care 1996; 7; 3: 158-166.
NEXT CHAPTER

Chapter 9
9. NEONATAL RESUSCITATION
Chapter contents
Physiological changes
Checklist before delivery
Normal delivery
Assessment of the neonate
Indications for positive pressure ventilation
Resuscitation chart 1
PHYSIOLOGICAL CHANGES AT BIRTH
The infant’s first breath expands the lungs and reduces pulmonary vascular resistance, thus allowing increased pulmonary blood
flow. Clamping the umbilical cord increases systemic vascular resistance and these changes together with a rising arterial PO2
result in closure of the foramen ovale and ductus arteriosis to establish a pulmonary and systemic circulation. The arterial PO2
slowly increases and may take up to six weeks to reach adult values, due to intrapulmonary shunting of venous blood which may be
as high as 20% in the first few days of life. As the lungs expand surfactant function becomes well established and less negative
pressure is required to allow air entry. Each subsequent breath therefore requires less effort.
Blood from the umbilical vessels has the following values -
Table 9.1
Umbilical vein (UV) Umbilical artery (UA)

pH 7.24 - 7.49 7.15 - 7.43
PaCO 2 kPa 3.0 - 6.5 (23 -49 mmHg) 4.0 - 10 (31 - 74 mmHg)
PaO 2 kPa 2.0 - 6.4 (15 - 48 mmHg) 0.5 - 4.5 (4 - 34 mmHg)
Base excess mmol /l - 9.0 to - 3 .5 -11.2 to - 6.2
Some degree of acidosis is common at birth. Cerebral palsy is unlikely to be related to intrapartum hypoxia unless cord pH at birth is
< 7.00. Most infants with a pH as low as this develop normally. Umbilical arterial samples are a better reflection of fetal status than
venous.
Normal acid base status is achieved after 1 - 2 hours.
CHECKLIST BEFORE DELIVERY
Switch on radiant warmer.

Check oxygen supply, connections and self inflating bag.
Maximum pressure control blow-off is set at 25 cm water.
Suction apparatus, oral mucus extractor and fine suction catheters, laryngoscopes, endotracheal tubes
Dry and warm towels
Drugs -
naloxone 400 µg/ml

epinephrine 100 µg/ml or 1/10,000 concentration
dextrose 5-10% solutions
sodium bicarbonate 0.5 mmol/ml or 4.2% concentration
NORMAL DELIVERY

Chapter 9
The mouth and oropharynx are always aspirated first as stimulation of the nose may cause the neonate to gasp and inhale any
pharyngeal contents. The suction catheter must not be passed too far into the mouth as stimulation of the hypopharynx can cause
laryngospasm and bradycardia.
As neonates have poor thermoregulation they should be dried and wrapped in warm towels. Most newborn babies do not need any
resuscitation and after they have been dried they can be returned to their mothers.
ASSESSMENT OF THE NEONATE
Apgar score
The Apgar scoring system at 1 minute and 5 minutes is in common use and gives information about the severity and prognosis of
asphyxia. In pre-term infants the score is more likely to be affected by gestational age than by asphyxia.
Table 9.2 Apgar scoring system
Clinical Sign Apgar Score

0 1 2
A: Appearance (colour) Blue, pale Body pink, extremities blue Completely pink
P: Pulse Absent Less than 100 More than 100
G: Grimace (reflex irritability) No response Grimaces Cries
A: Activity (muscle tone) Limp Some flexion of extremities Active, well flexed
R: Respiratory effort Absent Weak cry or shallow Good strong cry
Score 10 = optimal condition
Score 6 or less = depression, resuscitative measures required
Heart rate
This is a reliable indicator of the newborn’s degree of distress. It can be evaluated by palpation of the pulse at the base of the
umbilical cord or auscultation of apical heart sounds. If the heart rate is greater than 100 beats/min and spontaneous respirations
are present assessment continues. If the heart beat is less than 100 beats/min positive pressure ventilation with 100% oxygen
should be started immediately. If the heart rate is less than 60 beats/ min and not increasing despite effective ventilation with 100%
oxygen, chest compression should be initiated.
Colour
The infant may be cyanotic despite adequate ventilation and a heart rate greater than 100 beats/min. It has been suggested that an
Apgar minus colour score (A-C) is of better prognostic value as colour does not correlate well with the acid base state of the infant
at birth.
INDICATIONS FOR POSITIVE PRESSURE VENTILATION
Apnoea
Heart rate less than 100 beats/min
Persistent central cyanosis despite the administration of 100% oxygen
Effective ventilation can usually be provided with a bag and mask; the infant should be positioned with neck slightly extended (rolled
towel 2.5 cm thick placed under the shoulders). Initial inflation pressures may need to be as high as 50 cmH2 0, the first five or six
breaths require that inspiration is held for 1-2 seconds to establish an adequate functional residual capacity for continued
spontaneous ventilation. If adequate ventilation as indicated by effective chest movement is not achieved then immediate intubation
of the trachea and ventilation are performed. The time taken from birth to the baby’s first gasp and to the onset of regular respiration
should be recorded. Assisted ventilation should be at a rate of 40 - 60 breaths/min, and chest compression at a rate of 120/min (i.e.
a ratio of 3:1).
There is evidence that air is as effective as 100% oxygen in term babies. !00% oxygen has little advantage and may increase
oxygen free radical damage. If gas mixing facilities are available 40% oxygen is recommended.

Chapter 9
Factors affecting resuscitation
Maternal sedation
Meconium stained amniotic fluid
Fetal heart rate abnormalities during labour
Operative delivery
Prolapsed cord
Prolonged labour
Infection
Maternal health problems e.g. pre-eclampsia, diabetes mellitus, antepartum haemorrhage
Naloxone is used if apnoea is due to maternal opioid sedation. The recommended dose is 100 µg kg-1 i.m.
The indications and management of the apnoeic baby are illustrated in figs 9.1& 9.2.
Fig 9.1 Resuscitation chart 1
Note: if there is particulate meconium and the baby is unresponsive, proceed at once to fig 9.2
MECONIUM ASPIRATION SYNDROME
If the liquor is meconium stained during delivery then the pharynx must be aspirated before the first breath, the trachea intubated
and any remaining meconium aspirated by direct suction. The indications and management of meconium aspiration can be seen in
fig 9.2
CIRCULATION
Lack of improvement in the heart rate is usually due to inadequate ventilation. Check face mask seal or tracheal tube
position.
If the newborn fails to respond to ventilation then chest compression must commence at a rate of 120/min, ventilation
occurring every third compression.
Epinephrine 10-30 µg kg-1 i.v. (0.1-0.3 ml kg-1 of 1:10,000 solution) via the umbilical venous catheter flushed with saline 2ml
and repeated as necessary with a third dose of 100 µg kg-1 .
If there is no response or evidence of severe acidosis sodium bicarbonate 1-2 mmol kg-1 i.v. is given slowly over 2-3 minutes

Chapter 9
Hypovolaemia requires active volume replacement which is indicated when:-
1. Evidence of acute fetal loss

2. Pallor persisting after oxygenation
3. Faint pulses with a good heart rate but poor response to resuscitation including adequate ventilation
Fluid replacement 10-20 ml kg-1 is given with 4.5% albumin, whole blood or plasma.
(a) Consider while preparing for (b) ± (c) depending on local policy.
* may vary with individual circumstances and local guidelines
Figs 9.1 and 9.2 from Guidelines for resuscitation of babies at birth; Royal College of Paediatrics and Child Health
and Royal College of Obstetricians and Gynaecologists 1997. BMJ Publishing Group, London.
FURTHER READING
Zideman DA. Resuscitation. British Journal of Anaesthesia; 83: 157-168.1999 Click here for Medline link

Chapter 9
Resuscitation Council (UK). Newborn Life Support; Resuscitation Guidelines 2000.
Paediatric Life Support: (including the recommendations for resuscitation of babies at birth). European Resuscitation Council.
Resuscitation; 37(2): 95 - 96. 1998 Click here for Medline linkThe 1998 European Resuscitation Council Guidelines. Resuscitation
of babies at birth.
APPENDICES

APPENDICES
APPENDICES
Normal female clinical chemistry and haematology values

Composition of colloid solutions and blood products
Epidural infusion regimens for labour
Catecholamine infusions
Fetal heart rate (FHR) monitoring
Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1991-1993 & 1994-1996
Guidelines for the management of severe pre-eclampsia from the Report on Confidential Enquiries into Maternal
Deaths in UK 1997-1999
Breast feeding and anaesthetic related drugs
Side effects of drugs associated with obstetric anaesthesia
Dermatome chart and segmental nerve supply to the perineum
Magnesium sulphate in the management of eclampsia
Neurological damage following epidural/spinal blockade after delivery
Steroid treatment regimens
Links to other obstetric anaesthetic sites
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Chapter 8
8. MATERNAL RESUSCITATION
Chapter contents
Cardio-pulmonary resuscitation
CPR Algorithm
Resuscitation drug dosages
Convulsions
Anaphylactic shock
Pulmonary embolism
Venous thromboembolus: Amniotic fluid embolus: Venous Air Embolus
Pulmonary oedema
Malignant hyperpyrexia
CARDIO-PULMONARY RESUSCITATION (CPR)
Cardiac arrest is rare with an incidence of 1:30,000 pregnancies. The survival of mother and fetus depends on prompt recognition
and treatment.
Main causes of cardiac arrest
Anaesthetic Problems
Failed intubation
Aspiration of gastric contents
Total spinal anaesthesia
Drug induced reactions
Local anaesthetic toxicity
Obstetric Problems
Massive haemorrhage
Amniotic fluid embolism
Venous and/or air embolism
Intracranial haemorrhage
Magnesium toxicity
After 26 weeks of pregnancy aortocaval compression is likely. If cardiac arrest occurs the complete absence of any vascular tone
leads to a reduction in venous return to the right side of the heart. External cardiac compression may therefore be ineffective, as the
heart is empty. The patient must be tilted to at least a 30° angle. This is best achieved using a specially wedged board, although it
is possible to use a "human wedge".
Fig 8.1 Wedged board Human wedge
If CPR is not effective (15:2 ratio) in generating a powerful pulse (100/min) or adequate perfusion within 3 - 4 minutes and there is
file:///C|/Users/Administrator/Downloads/shoa%20current%20MASTER/CHPT8.HTM[20/1/2011 6:58:27 pµ]

Chapter 8
no other obvious remediable cause, e.g. massive haemorrhage, bilateral tension pneumothorax or pulmonary embolus, the fetus
must be delivered while CPR is continuing; effective cardiac filling and output should then occur. Early delivery may also save the
baby (the fetus is more resistant to hypoxia than the mother).
THE CHAIN OF SURVIVAL

Early ® Early ®
Early ® Defibrillation Early
Access Basic Life Support
Advanced Life Support
For every minute that elapses following the onset of a shockable arrhythmia, there is 5-10% less chance of survival. Early
defibrillation is critical; therefore it should not be delayed if available and appropriate. Administration of 200, 200 and 360 joule
shocks, given in sequence if required with a monophasic defibrillator, should not take any longer than 30 seconds. As soon as the
shocks have been delivered, B.L.S must be restarted immediately. Available data suggests that defibrillation is safe in all phases of
pregnancy and labour as only a small amount of current penetrates the uterus. Biphasic defibrillators are effective at lower energy
levels e.g. 200 J. They reverse current flow during defibrillation and are as effective or better than monophasic defibrillators.
ADVANCED LIFE SUPPORT ALGORITHM FOR THE MANAGEMENT OF CARDIAC ARREST IN ADULTS
Note: each successive step is based on the assumption that the one before has been unsuccessful
Resuscitation Council UK.
Table 8.1 Resuscitation drug doses

Chapter 8
TRACHEAL
DRUGS
made up in a
all doses based on INTRAVENOUS COMMENT
volume of 10
a 70 kg woman
ml saline
Epinephrine a and ß receptor stimulant
1:10,000 0.1-1 mg 2 mg Infusion 5 mg:500 ml saline
10 ml = 1 mg (10 µg/ml)
Atropine
1 mg 2 mg Increases heart rate
0.6 mg/ml
Completely blocks the vagus nerve,
3 mg used in asystole
300 mg
Amiodarone in 20 Used in refractory fibrillation.
ml 5% dextrose
second dose Consider as early as fourth shock
150 mg
Bretylium tosylate
50 mg/ml
500 mg Used in refractory fibrillation
Mexiletine Membrane stabilisation, reduces

25 mg/ml
150 mg bolus tendency to tachyarrythmias
Calcium gluconate
10% 10 ml Inotropic action
(0.225 mmol Ca/ml)
Infusion 1.5 g:500 ml
Lidocaine 2% 100 mg 200 mg
3 mg/ml
Adenosine 6 mg then 12 mg x 3 every 2 min
Sodium bicarbonate Not as routine, only refractory cases, pH
8.4%
50 ml to be measured as soon as possible
Metoprolol ß-blocker used for supraventricular
(1 mg/ml)
5 mg arrythmias (SVT)
Any effects of these drugs on the fetus can be addressed after delivery, resuscitation of the mother is the prime consideration.
Algorithms for treatment of Periarrest Arrhythmias can be accessed here
BRADYCARDIA
BROAD COMPLEX TACHYCARDIA
NARROW COMPLEX TACHYCARDIA
CONVULSIONS
Main causes
Eclampsia, epilepsy and local anaesthetic toxicity. Consider all obstetric convulsions eclamptic in origin despite a normal blood
pressure until proved otherwise.
Premonitory signs
Eclampsia - May be NONE: severe frontal headache with visual disturbance, photophobia, nausea and vomiting, right upper
quadrant pain.
Epilepsy - Aura, history of epilepsy, anticonvulsant therapy.
Local anaesthesia - Numbness of the tongue and circumoral tissues, light-headedness, dizziness, difficulty focusing, tinnitus, slurred
speech, shivering and muscle twitching.

Chapter 8
Management
Turn the patient on her side to avoid aortocaval compression. Maintain and protect the airway, administer 100% oxygen. Ensure
fetal monitoring. Follow one of the two regimes:-
Diazepam 5 - 20 mg i.v. (more than 30 mg may cause neonatal hypotonia)
Intravenous thiopentone 50 mg increments - suxamethonium, cricoid pressure and intubation may be required. If eclampsia is
suspected once convulsions have ceased then the magnesium sulphate protocol is followed.
ANAPHYLACTIC SHOCK
Common labour ward causes:- antibiotics, suxamethonium, latex, oxytocin, NSAIDs and colloids.
An anaphylactic reaction is where previous sensitisation has occurred and vasoactive substances e.g. histamine, serotonin are
released from mast cells in response to an IgE antibody mediated reaction.
An anaphylactoid reaction is where there is no antibody mediation in mast cell release.
Management
Stop the administration of all suspected drugs and curtail surgery if appropriate.
Maintain the airway, give 100% oxygen, and avoid aortocaval compression.
Give epinephrine 1:10,000 (1 mg:10 ml saline) i.v. as 0.5 - 1 ml boluses, titrate as necessary for hypotension and
bronchospasm.
Start rapid intravascular volume expansion with crystalloid or colloid.
Specific measures
Hypotension - Elevate the legs, establish monitoring with ECG and possibly CVP and arterial line. Circulatory support with
catecholamines.
Bronchospasm
aminophylline 250 - 500 mg i.v. slowly

salbutamol 250 µg i.v. slowly
2.5 - 5 mg nebulised in 3 ml saline
Antihistamines
chlorpheniramine 10 - 20 mg i.v.
Steroids
hydrocortisone 100 - 200 mg i.v.
Anaphylaxis algorithm can be accessed here:-
Investigation
Immediate - mast cell tryptase, the principle protein content of mast cell granules is released with histamine and other amines
in anaphylactic and anaphylactoid reactions. Plasma concentration is raised 1 - 6 h after a reaction.
Normal level 0.8 - 1.5 ng/ml Anaphylactic reactions occur at concentrations >20ng/ml

Chapter 8
Long term - referral to allergist for skin testing and specific IgE antibody detection by radio-allergosorbent test (RAST)
PULMONARY EMBOLISM
This is the commonest cause of maternal death in the United Kingdom. Emboli may be thrombus, amniotic fluid or air. The
physiological changes that occur depend on the degree of obstruction to blood flow through the pulmonary artery and the increase
in dead space ventilation. These may lead to pulmonary hypertension, right ventricular strain and cardiac failure. During anaesthesia
an early sign is an abrupt fall in end tidal PCO 2
Venous thromboembolus
The risk of venous thrombosis is increased in pregnancy due to the relatively hypercoagulable state, particularly in the postpartum
period. The presentation includes retrosternal discomfort, dyspnoea, pleuritic pain, haemoptysis, profound collapse, raised central
venous pressure and cardiac arrest. The ECG shows:-
S1 Q 3 T3 pattern with prominent S wave in lead I, Q wave and inverted T in lead III
Sinus tachycardia
T wave inversion in leads V1 -V3
Right bundle branch block
Low amplitude deflection
A ventilation perfusion scan will show normal ventilation with a segmental perfusion defect. Pulmonary angiography may
demonstrate an intraluminal filling defect and/or the abrupt termination of a branch vessel.
Management of minor thromboembolism
Heparinisation - 5,000 -10,000 i/u i.v. followed by a continuous infusion of 1,000-2,000 i/u per hour. Monitored with the APPT
- therapeutic range 1.5-2.5.
Antenatally heparin is given sc - 12,000 i/u 12 hourly.
Postnatally oral warfarin is started at the same time as i.v. heparin - 10 mg/day for 2days. Subsequent dosage depends on
the INR - therapeutic range 2-3.
Management of massive thromboembolism
Oxygen therapy, cardiac massage and intermittent positive pressure ventilation (IPPV)
An intravenous bolus of heparin - 15,000 i/u should be given.
Cardiovascular support with a norepinephrine infusion 4 mg in 500 ml of saline
A pulmonary angiogram should be obtained immediately: if this is not available thrombolytic therapy must be started with
streptokinase in a loading dose of 600,000 units with a maintenance dose of 100,000 u/h for 24 hours. The thrombin time
should be maintained at a level of 1½ times the control value.
Amniotic fluid embolus (Anaphylactoid Syndrome of Pregnancy)
The incidence is 1 in 30,000 pregnancies with a maternal mortality rate approaching 85%, It can occur during labour (70%), after
Caesarean delivery (19%), or after vaginal delivery (11%).
The presenting features are
Sudden collapse
Excessive bleeding in labour or post partum
Seizures
Dyspnoea
Fetal bradycardia
There is a history in 41% of mothers of atopy (asthma, eczema, hay fever) or allergy, often to drugs.

Chapter 8
There is a biphasic response to the presence of amniotic fluid (or meconium) in the maternal circulation causing release of
substances that produce pulmonary vascular spasm, pulmonary hypertension, hypoxic injury to the pulmonary capillaries and heart.
This leads to left ventricular failure and subsequent adult respiratory distress syndrome. Coagulopathy may be related to the
presence of a factor X activator in amniotic fluid.
Diagnosis is made on clinical grounds. The presence of fetal cells in the maternal blood is NOT pathognomonic and they are
commonly detected in normal patients. In primates it has been shown that infusions of large amounts of amniotic fluid do NOT cause
the syndrome. Minor degrees of the syndrome are probably quite common.
Management
Cardiopulmonary resuscitation with the patient wedged if the fetus is still in utero
Deliver the fetus and placenta as soon as possible
Insert 2 large peripheral cannulae, CVP line, urinary catheter, arterial line and if possible a pulmonary artery catheter
Aspirate blood from the right side of the heart
Monitor ECG, pulse, blood pressure, CVP and pulmonary artery wedge pressure
Cardiovascular support with dopamine and epinephrine
DIC management in consultation with the Haematology Department
Venous air embolus
This can occur during Caesarean section particularly at the time of uterine incision and placental separation. It has been shown that
subclinical venous air embolism occurs in up to 50% of patients at this time; the risk is increased when the uterus is exteriorised
and the patient is head down. A head up tilt has been advocated during surgery for Caesarean section. A patent foramen ovale is
present in 20 - 25 % of patients and paradoxical air embolism is possible although very rare in clinical practice. Large air embolism
will result in frothing of blood in the right ventricle causing an air lock and cardiac arrest. The diagnosis is made with a precordial or
oesophageal Doppler probe. A mill wheel murmur is accompanied by hypotension, a fall in SpO 2 , end tidal PE CO 2 and an increase
in central venous pressure.
Management
100% oxygen must be given

Stop the nitrous oxide to reduce the air bubble size
Replace the uterus if exteriorised
Flood the wound with fluid to prevent further aspiration of air.
Place the patient in a head down position on the left side to allow any air to collect in the apex of the right ventricle
Aspirate air from the right atrium via a central venous line.
Provide cardio-respiratory support as necessary. Internal cardiac massage may be required - access to the great vessels will
permit direct aspiration of air (or amniotic fluid) .
PULMONARY OEDEMA
Maternal pulmonary oedema is associated with:
Pre-eclampsia - capillary permeability is increased and colloid osmotic pressure falls due to proteinuria. There may also be
an element of left ventricular failure secondary to severe hypertension. Antihypertensive therapy with ß-blockers may
contribute to this.
Fluid overload - due to over-treatment of severe haemorrhage, or fluid challenges in pre-eclamptic patients.
Myocardial disease - e.g. cardiomyopathy of pregnancy or myocardial ischaemia.
The use of tocolytic therapy for premature labour with ß-adrenergic agonists, e.g., ritodrine, isoxuprine, salbutamol.
Tachycardia is a prominent feature. Steroid therapy for fetal lung maturation may be a contributory factor
It presents with tachycardia, tachypnoea, hypoxia and cyanosis. An early sign is a fall in oxygen saturation. On auscultation of the
chest, basal crepitations and rhonchi are heard. Chest x-ray shows fluffy shadowing or the more extensive butterfly wing
appearance.
Management

Chapter 8
Oxygen
Sedation with i.v. morphine to relieve agitation / anxiety and reduce the pre-load by venodilatation.
Diuretic therapy with frusemide 40 - 80 mg i.v., repeated as necessary. Dopamine 2 - 5 µg/kg / min may be required i.v..
Intubation and IPPV may be necessary with positive end expiratory pressure (PEEP)
Treatment of the underlying cause
MALIGNANT HYPERPYREXIA (MH)
The incidence is 1:30,000 of all general anaesthetic administered. Not every patient with a genetic predisposition developes a MH
crisis during exposure to triggering agents which include all volatile anaesthetics and depolarising muscle relaxants.
MH presents with the following signs:
Unexplained tachycardia
Tachypnoea
A rise in body temperature which increases by more than 2° C/h
An abnormal reaction to suxamethonium - trismus is an early sign of this
Cyanosis
Muscular rigidity developing later during the anaesthetic
Increased oozing is usually a sign of DIC
A fall in SpO 2 , a rise in PE CO 2 , metabolic acidosis and hyperkalaemia
A diagnosis of MH should be assumed if suspicions are aroused.
Management
Discontinue inhalational agents, terminate surgery CALL FOR HELP.

Hyperventilate with 100% oxygen 2 - 3 times the predicted minute volume
Give dantrolene 2 mg/kg i.v.. Repeat as necessary up to a total of 10 mg/kg
Cool with 1 - 2 litres iced saline i.v., apply surface cooling over the major vessels, and lavage to the pleural or peritoneal
cavities. Consider cardiopulmonary bypass via femoro-femoral circulation
Correct metabolic acidosis with sodium bicarbonate, monitor blood gases and pH and correct hyperkalaemia. Treat
arrhythmias if severe.
Establish the following monitoring: SpO 2 , ECG, arterial cannulation, a muscle temperature probe, central venous cannulation,
urinary catheter, blood pressure and a fluid balance chart.
Investigations should include the following: blood gases, haemoglobin, urea, electrolytes, clotting screens and CPK level
Admit to the intensive care unit
Late management must include screening of the patient and her family for MH susceptibility
In the management of known MH or MH susceptible patients, the technique of choice is regional anaesthesia. The administration of
general anaesthesia requires the following conditions:-
A clean anaesthetic machine with disposable tubing and no vaporisers

The circuit which has been flushed with 10 litres of oxygen for at least 20 minutes before use
A cooling blanket on the operating table,
Dantrolene and ice must be available.
Only 'safe' drugs must be used
SAFE UNSAFE
Diazepam, thiopentone, propofol,
Succinylcholine
methohexitone.
Halothane, enflurane, isoflurane,
Nitrous oxide
desflurane, sevoflurane
Atracurium, pancuronium, vecuronium,
mivacurium,, rocuronium


Chapter 8
Local anaesthetic drugs

Oxytocin, PGF2 a, ergometrine
Nitroglycerine, magnesium sulphate
Ephedrine, epinephrine, norepinephrine
FURTHER READING
The American Heart Association in Collaboration with the International Liaison Committee on Resuscitation (ILCOR) Guidelines 2000
for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - An International Consensus on Science. Resuscitation
2000; 46: 1-448
The 1998 European Resuscitation Council Guidelines for Adult Advanced Life Support. In: Bossaert L (ed.). European Resuscitation
Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 36-37.
The 1998 European Resuscitation Council Guidelines for the management of the airway and ventilation during resuscitation. In:
Bossaert L (ed.). European Resuscitation Council Guidelines for Resuscitation. Amsterdam: Elsevier, 1998; 129-158.
Kudenchuk PJ, Cobb LA, Copass MK et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular
fibrillation. New England Journal of Medicine 1999; 341: 871-878.Click here for Medline link
The Association of Anaesthetists of Great Britain and Ireland and The British Association of Allergy and Immunology. Suspected
anaphylactic reactions associated with anaesthesia. Published by: The Association of Anaesthetists of Great Britain and Ireland
1995. MedicAlert Foundation (Registered Charity)
Fletcher SJ, Parr MJA. Amniotic fluid embolism: a case report and review. Resuscitation 2000: 43;141-146 Click here for Medline
link
Halsall P, Ellis FR. Malignant hyperthermia. Current Anaesthesia and Critical Care 1996; 7; 3: 158-166.
NEXT CHAPTER

COMPOSITION OF COLLOID SOLUTIONS AND BLOOD PRODUCTS
COMPOSITION OF COLLOID SOLUTIONS AND BLOOD PRODUCTS
COLLOID SOLUTIONS
Colloid Fluid Composition Molecular Plasma Half Life Allergic Remarks

Weight Reaction
Gelofusin succinylated 35,000 4 hours 0.38%
gelatine
Haemaccel polygelin 30,000 2-4 hours 0.38% Contains 10 times more Ca and K than
(urea-linked) gelofusin. This may lead to clotting in
heating coils when mixed with citrated
blood or FFP
Pentastarch hydroxyethyl starch 250,000 12-16 hours 0.0014% Taken up by the reticuleondothial
system, final elimination from body very
slow. Long term effect of this is unknown
Dextran 70 glucose polymer 70,000 12 hours 0.008% Inhibits platelet aggregation and renders
fibrin more susceptible to fibrinolytic
enzymes. Take blood sample before use.
Maximum volume I litre
Plasma Protein 4.5% protein (85% 70,000 > 24 hours 0.003% 1998 controversial meta-analysis
Solution (PPS) albumin in saline) suggested relatively increased mortality
COMPOSITION OF BLOOD PRODUCTS
Blood Products Pack Volume Contents Remarks

Red cells in additive solution 300 ml Red cells after removal of almost all Must be ABO +Rh (D) compatible
plasma made up with saline, adenine, Haematocrit is 0.55-0.65
dextrose +/- mannitol Flows like blood.
Fresh frozen plasma 300 ml All clotting factors except platelets ABO compatibility preferred
Cryoprecipitate 10 - 20 ml Fibrinogen, fibrinectin, Von Transfuse when fibrinogen < 1gm

Willebrand factor, factors VIII & Xlll
Platelet concentrate 50 - 60 ml Platelets Must be ABO + Rh(D) compatible
Transfuse when < 50,000
FURTHER READING
Cochrane Injuries Group Albumin Reviewers. Human albumin administration in critically ill patients: systematic review of randomised
controlled trials. British Medical Journal 1998; 317: 235-40. Click here for Medline link
file:///C|/Users/Administrator/Downloads/shoa%20current%20MASTER/composition_of_colloid_solutions.htm[20/1/2011 6:58:29 pµ]

Chapter 3
3. EPIDURAL ANALGESIA IN LABOUR
Chapter contents
Indications
Contraindications
Drugs
Suggested basic technique
Problems
Bloody tap; Positive intravenous test dose; Toxic reaction to local anaesthetic; Failure to thread epidural catheter; Inadequate
block; Obesity ;Hypotension; Loss of bladder sensation; Inadvertent dural puncture; Management of spinal headache; Subdural
block; Total spinal block; Epidural catheter difficulties; Spinal/epidural haematoma; Epidural abscess
Maintenance of epidural analgesia
Intermittent bolus doses; Epidural infusion; Patient Controlled Epidural Analgesia (PCEA); Mobile epidura l
Audit of epidural analgesia
INDICATIONS
Maternal request
Prolonged and painful labour (often in primiparous patients)
Malpresentation
Anticipated or actual instrument delivery
Trial of labour
Pre-eclampsia
Diabetes
Uncoordinated uterus managed by oxytocin infusion
Multiple pregnancy
Cardiac and respiratory disease
Epidural analgesia should be administered with caution if any of the following apply:
Previous Caesarean section - Sudden analgesic failure may be due to uterine rupture. A dense sensory blockade must be avoided
in order to demonstrate this important sign.
Central nervous system disorders - In multiple sclerosis there is no evidence that demyelination can be provoked by epidural
analgesia. In cerebrovascular accident, porphyria and other rare conditions the pathophysiology should be discussed with a senior
colleague and if necessary the relevant specialist before a decision is made.
Spinal deformity - Technical difficulty may increase the risk of dural puncture and failure, the caudal route may be the preferred
option.
CONTRAINDICATIONS
Full anticoagulant therapy

Coagulopathy. Platelet count must be greater than 80 x 10 9 /l
Hypovolaemic shock
Local or systemic sepsis
Refusal by patient
Raised intracranial pressure
Fixed cardiac output
Lack of appropriately trained staff
DRUGS
The three most commonly used drugs are all amide local anaesthetics. They differ in important respects: rate of onset, duration,
potency, degree of motor blockade, cardiac and neurotoxicity. In labour it is generally desirable to minimise motor blockade in order
to increase maternal mobility and hopefully reduce the rate of instrumental delivery. This can be achieved by the correct choice of
drug, concentration, volume and sometimes by the addition of an opioid e.g. fentanyl.

Chapter 3
Lidocaine is generally administered in a concentration of 2%, has a rapid onset (10-15 minutes) and a relatively short duration (45
min). Inadvertent intravenous injection carries the lowest incidence of toxic effects.
Bupivacaine 0.1-0.5% has a slower onset (20 minutes for maximal effect) than lidocaine but a longer duration. It has four times the
potency of lidocaine and is relatively more cardiotoxic. Used in the correct dosage it is generally without problem; with accidental i.v.
injection there is a risk of delayed cardiac conduction leading to bradycardia, heart block and ultimately a potentially irreversible
ventricular fibrillation. Cardiac toxicity is usually preceded by signs of major CNS toxicity i.e. convulsions.
Ropivacaine 0.1-0.5% has a similar onset and duration to bupivacaine but it is less cardiotoxic and may produce relatively less
motor blockade.
SUGGESTED BASIC TECHNIQUE
A description of technique cannot replace practical experience with a senior colleague. A safe method should be selected and
adhered to until confident and competent.
Establish the indications for epidural anaesthesia and review the patient’s relevant obstetric, medical and anaesthetic history.
Explain the procedure and obtain the patient’s informed verbal consent.
Set up a reliable intravenous infusion of saline or Ringer Lactate with, at least, a 17 gauge intravenous cannula.
Check that an ampoule of ephedrine 30 mg is immediately available.
Record the baseline blood pressure and pulse.
Arrange the patient either in the left lateral or sitting position according to preference.
Put on a face mask, scrub, glove and gown up.
Apply a suitable topical antiseptic solution to the skin and underlying tissues
Site the epidural in the L2/3 or nearest convenient interspace using a saline or air loss of resistance technique.
Measure the epidural space-skin distance using the cm graduations on the Tuohy epidural needle
Insert the catheter 5 - 6 cm into the epidural space, withdraw the needle and then withdraw the catheter to leave 3 - 4 cm in
the space or until the meniscus in the catheter falls.
Ensure that blood or cerebrospinal fluid (CSF) does not flow back either by capillary action or direct aspiration.
Administer an epidural test dose e.g. 4 ml of 2% lidocaine. Inadvertent intravenous injection rapidly produces tinnitus and
facial paraesthesia - maintain verbal contact; ask about any symptoms in a non specific way to avoid suggestion.
After 5 min record pulse and blood pressure and check for evidence of intrathecal placement (established sensory and motor
blockade) - if in doubt wait and reassess after a further 5 min.
If the test dose is negative and blood pressure and fetal heart rate are stable administer a bolus dose of 5 - 8 ml of 0.25%
bupivacaine. (see alternative maintenance regimes)
Progress over the next three contractions should indicate the efficacy of the block. An increase in skin temperature over the
feet and legs is a useful sign and demonstrates the onset of an autonomic block.
Continue with top-ups or an epidural infusion according to preference.
Monitoring the block
The following information should be monitored and recorded:
Maternal blood pressure and pulse - these should be recorded every five minutes for twenty minutes following a top up and
at least half hourly thereafter
Fetal heart rate
Extent of block
Sensory: it is important to record the upper and lower segmental sensory limits of the block bilaterally. These may be
identified by testing with a cotton wool ball (light touch), blunt needle (pinprick) or ethyl chloride (cold sensation).
Starting from an area of skin with an established block the patient will report light touch, pinprick and cold sensation in
sequence as the unblocked area is approached. This progression usually spans three segmental levels. In practice it is
sufficient to select and continue with a single method of testing.
Motor: this can be assessed on the following practical scale which is based on straight leg raising -
0 = full power

1 = able to lift but a little weak
2 = able to lift but very weak

Chapter 3
3 = unable to lift straight leg
Site and severity of any persisting pain

Mode of administration of local analgesia i.e. top ups, infusion or PCEA
Details of maintenance doses prescribed and when actually administered

PROBLEMS
Bloody tap - This is caused by puncture of a distended epidural vein by the needle or the catheter and may lead to inadvertent
intravenous injection of local anaesthetic or to the formation of an epidural haematoma. In order to minimise this risk the epidural
needle or catheter should not be advanced during a uterine contraction. Management is as for positive intravenous test dose
Positive intravenous test dose - The test dose should always be given after gentle aspiration and if positive then the catheter
should be withdrawn and resited in an adjacent interspace.
Toxic reaction to local anaesthetic - rarely this may occur despite a negative test dose. Early central nervous system signs are
slurred speech and tinnitus; with increasing toxicity there may be muscle twitching followed by convulsions. Circulatory signs include
hypotension, bradycardia and possibly cardiac arrest.
Failure to thread epidural catheter
Inject additional saline or lidocaine (3 - 6 ml) down the needle in an attempt to open up the epidural space.
Carefully rotate the Tuohy needle through 180° (risk of dural tear). Do not withdraw the catheter through the needle (risk of
dividing catheter).
Ask the patient to straighten her back by slowly extending her hips.
If associated with marked paraesthesia or failure of the above methods, resite in an adjacent interspace.
Inadequate block - This may be caused by the catheter entering the paravertebral space via an intervertebral foramen which results
in a unilateral lumbar plexus block. Occasionally connective tissue appears to sub-divide the epidural space causing a unilateral
block. Additionally there may be persistent low backache with rectal or sacral pain.
Use posture and the effect of gravity to help the spread of additional local anaesthetic.
The addition of fentanyl 50 mg or clonidine 100 - 150 mg may be of value.
If all these fail the catheter should be resited at an early stage.
Obesity
Explain that the procedure may be difficult.

Use the sitting position.
Ask patient to point to the midline of her back.
Identify and mark the midline by initially palpating the upper thoracic spines.
Palpate the iliac crest and draw a line bisecting the midline.
Infiltrate subcutaneously for 5 cm above and below this point using 1% lidocaine.
Use a suitable needle to probe and mark the midline and a spine and interspace.
If necessary use a long (15 cm) Tuohy needle to reach the epidural space.
Hypotension - Initial symptoms are often due to the rate of fall rather than the absolute level of blood pressure. The complaint is of
nausea, dizziness or sleepiness. Turn the patient onto her side (preferably left) to avoid aortocaval compression. Give 250 ml saline
or Ringer Lactate rapidly and elevate the foot of the bed. In the absence of a rapid response ephedrine is administered
intravenously in 6 mg increments until stability is restored.
Loss of bladder sensation - blockade of sacral roots may result in a failure of the patient to sense bladder distension. The patient
should be encouraged to empty her bladder two hourly or before top ups. If the bladder becomes distended it is necessary to pass
a urinary catheter. Neglect may result in retention of urine and post partum bladder atony .
Inadvertent dural puncture

Chapter 3
There are two alternative strategies
1. Resite the epidural in an adjacent space. Be cautious with the first dose of local anaesthetic as the tip of the catheter may be
adjacent to the dural puncture site and allow some solution to enter the subarachnoid space. The anaesthetist must always give
this dose. Provided a normal initial response is obtained the epidural may be conducted in the usual fashion but with an awareness
of the potential for high blockade.
If the patient is able to deliver spontaneously, then this should be allowed. A long period of strenuous pushing
should be avoided as this may increase the rate of CSF loss.
After delivery, an epidural infusion of Ringer lactate should be set up via the epidural catheter and filter, aiming
to run in one and a half litres over twenty-four hours.
The patient should remain in bed while the infusion is in progress, thereafter she should be allowed to mobilise
normally.
2. The needle tip is left in the subarachnoid space and an end-hole catheter inserted two cm only. The catheter must be clearly
marked as being in the subarachnoid space. All top ups should be given by the anaesthetist. Care should be taken to avoid
excessive loss of CSF.
With the patient in the lateral or supine wedged position, give 1 ml of 0.125% plain bupivacaine followed by 0.5ml increments of
0.125% or 0.25% bupivacaine until satisfactory analgesia is achieved. Consider adding an opioid e.g. 12.5 mg fentanyl. It is
important to appreciate that plain bupivacaine is slightly hypobaric at body temperature and that sudden movements of the patient
may cause displacement of the local anaesthetic in the CSF leading to a high block.
For Caesarean section, manual removal and rotational forceps delivery, 0.5% hyperbaric bupivacaine should be used, administered
in 0.5 to 1ml increments, until adequate anaesthesia is achieved.
Management of spinal headache
Development of a spinal headache is characterised by severe, disabling fronto-occipital pain with radiation to the neck and
shoulders. There may be neck stiffness. In the upright position the brain becomes unsupported by CSF within the cranium. This
results in traction on meninges, venous sinuses and cerebral vessels. A compensatory dilatation of blood vessels takes place with
an increase in cerebral blood flow. The pain may be completely relieved by lying supine. It is very important to discuss the nature of
the problem and the management options with the patient.
Conservative treatment of spinal headache
Bedrest
Encourage the patient to take oral fluids.
Paracetamol, dihydrocodeine or similar analgesia at regular intervals.
Consider sumatriptan. It is a serotonin agonist and may relieve pain due to cerebral vasodilatation.
Reassure the patient that symptoms should resolve within 3 - 7days.
Dural blood patch
A Tuohy needle is sited in the epidural space overlying the puncture site or the space below using a standard epidural
technique.
An assistant scrubs and gloves up to take 20 ml of the patient's blood under sterile conditions.
15 - 20 ml is injected slowly into the epidural space, stopping if it becomes uncomfortable.
The patient lies flat for an hour and then slowly mobilises.
The blood patch can be expected to be successful in 85% of cases. If ineffective it may be repeated after 24 hours.
In the following circumstances a blood patch may be contraindicated:
Patient refusal.
Bleeding diathesis.
Infection and pyrexia

Chapter 3
Persistent headache - If headache persists for more than 7 days the patient should be encouraged to reconsider a blood patch or
have it repeated if already given. Reversible cranial nerve lesions may rarely complicate persistent leakage of CSF (typically VI
nerve palsy). A subdural intracranial haematoma secondary to traction and tearing of small blood vessels may cause raised
intracranial pressure; medullary coning has been reported. A thorough neurological examination, including fundoscopy, is mandatory
if the headache persists. A CT scan or MRI may also be required.
Subdural block - the features are:
Negative epidural test dose.

5 - 15 min after the main dose of local anaesthetic an extensive (to C7 or higher) patchy sensory block will occur. Motor
block is minimal or absent, hypotension is also unusual.
It must be distinguished from spinal block - sacral sensation is usually retained.
Because the subdural space extends intracranially, apnoea and loss of consciousness can occur, intubation and resuscitation
may then be necessary.
If the block regresses before delivery then resite the epidural because there is a risk of intrathecal penetration of the catheter
and subsequent subarachnoid block.
Subdural catheter placement can be confirmed by the injection of radio-opaque dye in the postpartum period when the
classic "tramline" appearance will be seen on x-ray.
Total spinal block
This is the subarachnoid injection of a large (epidural) dose of local anaesthetic. It may result in severe hypotension, bradycardia
with loss of consciousness and apnoea. All resuscitation equipment must be immediately available.
Position patient on left side, administer oxygen with bag and mask if apnoeic
Call immediately for senior anaesthetic and obstetric staff.
An assistant performs cricoid pressure.
Give 500-1000 ml saline or Ringer lactate rapidly intravenously.
Give ephedrine 15 mg intravenously and repeat as necessary.
Intubate the trachea and ventilate if there is apnoea.
Monitor the patient’s pulse, blood pressure and saturation.
Maintain blood pressure with ephedrine; other vasopressors such as phenylephrine may be necessary in bolus doses of 40 -
100 µg
Continually reassure the patient and relatives
Pass orogastric tube, empty stomach and instil 30 ml 0.3 molar sodium citrate.
In the event of fetal distress delivery can take place once the patient is stabilised
Epidural catheter difficulties
The broken epidural catheter - occasionally the tip of the catheter may be sheared by incorrectly withdrawing it through the needle
when the needle is in the epidural space. If this happens it is probably not worth exploring the epidural space or subcutaneous
tissues for the missing tip. The material is relatively inert and should cause no problems unless fibrosis occurs adjacent to nerve
roots. It is essential that the patient be informed and the event documented.
The stuck epidural catheter - after delivery the catheter is normally removed without any difficulty. If the catheter is stuck then
positioning the patient in flexion, extension and lateral rotation should all be tried.
Spinal/epidural haematoma - this rare complication should be recognised as an emergency requiring immediate investigation and
treatment. Predisposing factors are:
Coagulopathy
Anticoagulant therapy
Previous spinal or epidural analgesia
Vascular malformations
Spinal tumour
Combination of the above factors
Effects - spinal cord compression and ischaemia

Chapter 3
Signs/Symptoms - severe localised back pain, sensory loss, paraplegia, bladder and bowel dysfunction
Investigation - immediate MRI or CT scan
Treatment - emergency laminectomy and decompression of spinal cord
Epidural abscess - the space occupying effects are the same as those in spinal/epidural haematoma. Additionally pyrexia and
leukocytosis are likely. Investigations and treatment follow that for spinal haematoma apart from the need for specific treatment of
the infection. Infection in the epidural space may be due to poor aseptic technique, direct spread from an adjacent infected area or
haematogenous spread with bacteraemia. When an unrelated source of infection has been identified and adequately treated there is
no absolute contraindication to siting an epidural and the potential risks need to be weighed against the benefit in a particular
situation.
MAINTENANCE OF EPIDURAL ANALGESIA
The choice lies between intermittent bolus doses, a continuous infusion or a combination technique.
Intermittent bolus doses
This is the basic technique. 15 ml boluses of 0.1% bupivacaine are generally adequate in early labour with minimal motor block; the
addition of 2 µg fentanyl/ml provides additional analgesia . Increasing pain as the presenting part descends may be an indication for
increasing the concentration to 0.25% or occasionally 0.5% bupivacaine in 10 ml boluses. Top ups are not usually needed more
frequently than hourly.
Epidural infusion
Advantages: analgesia is more continuous, hypotension is less likely and the need for top ups is minimised.
Disadvantages: an infusion maintained for several hours may lead to a block with wide segmental sensory and motor spread. The
increased motor block may be associated with a higher instrumental delivery rate than with the bolus technique. (There is evidence
that the frequency of low and outlet forceps delivery may be increased by epidural analgesia).
A 0.125% solution of bupivacaine run at 10-15 ml/h gives good analgesia. An 0.08% solution run at 20 ml/h gives a more
extensive segmental spread with less motor block. The addition of fentanyl to the infusion improves the quality of analgesia. A
solution of 0.1% bupivacaine with 2 mg/ml fentanyl is now available commercially in the UK.
Recommended monitoring should include half-hourly blood pressure recordings, respiratory rate and upper sensory level testing.
The infusion should be stopped and the anaesthetist informed if:
Systolic blood pressure falls below 100 mm Hg.

Skin numbness extends above the xiphisternum.
Patient is unable to bend her knees or the weakness is getting worse.
Infused volume differs from that prescribed.
Respiratory rate falls below 9/min
Click here for methods of making up an infusion.
Patient controlled epidural analgesia (PCEA)
A loading dose of 10 ml of 0.125% bupivacaine is given. A background infusion of 0.1% bupivacaine plus 2 µg fentanyl/ml may then
be set-up and the patient allowed to self administer bolus doses of 5 ml (5 mg bupivacaine + 10 µg fentanyl) with a lock-out time of
10 min. The advantage of the method is the satisfaction afforded to the mother by having some control over the density and spread
of her epidural block. A disadvantage is that due to a lack of supervision of top-ups the mother’s position may not always be optimal
for achieving an effective block.
Mobile epidural
The intention is to provide pain relief while retaining mobility. The combined spinal /epidural (CSE) involves a loading subarachnoid
dose of 2.5 mg of plain bupivacaine (1 ml), 25 mg fentanyl (0.5 ml) made up to a total volume of 2 ml with the addition of 0.5 ml

Chapter 3
saline. This will produce a very rapid onset of analgesia and should allow almost complete motor sparing thus allowing the patient to
mobilise with the assistance of two midwives. The epidural catheter, which is inserted at the same time, is used for subsequent top-
ups. These consist of 0.1% plain bupivacaine plus 2 µg fentanyl/ml in a dose of 10 ml. The CSE technique has been associated
with reports of aseptic meningitis.
Alternative methods are based on the infusion or intermittent injection of very low concentrations of plain bupivacaine plus fentanyl,
e.g. 0.06% bupivacaine plus 2.5 µg fentanyl/ml or 0.1% bupivacaine plus 2µg fentanyl/ml. If the test dose is used as the initial dose
i.e. 15mg of bupivacaine as 15ml of 0.1% bupivacaine plus 50 µg of fentanyl the motor block can be minimal. This block can then
be continued by infusion, intermittent injection or patient controlled analgesia.
AUDIT OF EPIDURAL ANALGESIA
It is important to visit all patients who have received epidural analgesia on the first postpartum day. The following aspects of their
experience should be the subject of enquiry:
Efficacy of the block - An initial failure rate of < 10% falling to < 5% after measures to improve the block is a reasonable
target.
Headache - due to inadvertent dural puncture. The overall rate should be < 1% of all epidurals given. A headache may follow
an apparently uneventful epidural.
Backache - It is important to take a history and examine the patient to determine the cause. Multiple punctures, damage to
ligaments or periosteum cause localised pain which normally settles after 3 or 4 days. Most cases are associated with pre-
existing backache, which may worsen during pregnancy.
Prolonged analgesia and motor Block - The area affected should be mapped and recorded daily. If an epidural infusion
has been running for many hours the block may persist in localised areas for up to 24 hours. If skin analgesia persists for
longer and there is a history of rotational forceps delivery or a prolonged second stage of labour then a lumbar plexus
neurapraxia at the pelvic brim is the likely cause. There may also be a temporary foot drop or other features of motor
weakness. Close liaison with obstetric staff and an obstetric physiotherapist is essential in the management of these cases.
Persistent analgesia and motor block related to a single dermatome may be due to nerve root neurapraxia at the time of
epidural cannula insertion. The patient may have reported marked paraesthesia at the moment of insertion. The outcome is
generally favourable and resolution can be expected within a few weeks. A neurological opinion may be helpful. Outpatient
follow-up with physiotherapy and liaison with the general practitioner and obstetrician are an essential part of the
management. (Neurological damage following spinal/epidural block).
FURTHER READING
Covino BG, and Scott DB. Handbook of Epidural Anaesthesia and Analgesia. Copenhagen: Schultz,1985.
Checketts MR and Wildsmith JAW. Accidental i.v. injection of local anaesthetics: an avoidable event? Editorial 11. British Journal of
McClure JH. Ropivacaine. British Journal of Anaesthesia 1996; 76: 300-307.Click here for Medline link
Miller AC. The effects of epidural analgesia on uterine activity and labor. International Journal of Obstetric Anesthesia 1997; 6: 2-18.
Collier CB. Why epidurals fail: a study of epidurograms. International Journal of Obstetric Anesthesia 1996; 5: 19-31. Click here for
IJOA link
Savolaine ER, Pandya JB, Greenblatt SH, Conover SR. Anatomy of the human lumbar epidural space: new insights using CT-
epidurography. Anesthesiology 1988; 68: 217-20.
McCrae AF, Whitfield A and McClure JH. Repeated unilateral blockade. Anaesthesia 1992; 47: 859. Click here for Medline link.
Beards SC, Jackson A, Griffiths AG, Horsman EL. Magnetic resonance imaging of extradural blood patches: appearances from 30
mins to 18 hours. British Journal of Anaesthesia 1993; 71: 182-188.Click here for Medline link
Reynolds F. Dural puncture and headache. British Medical Journal 1993; 306: 874-876.Click here for Medline link
Vakharia SB, Thomas P S, Rosenbaum AE, Wasenko JJ, Fellows DG. Magnetic resonance imaging of cerebrospinal fluid leak and

Chapter 3
tamponade effect of blood patch in postdural puncture headache. Anesthesia and Analgesia 1997; 84: 585-590.Click here for
Medline link
Seeberger MD, Kaufmann M, Staender S, Schneider M, Scheidegger D. Repeated dural punctures increase the incidence of
postdural puncture headache. Anesthesia and Analgesia 1996; 82: 302-305.Click here for Medline link
Carson D, Wildsmith JAW. The risk of extradural abscess. British Journal of Anaesthesia 1995; 75: 20-521.Click here for Medline
link
Paech M. Patient controlled epidural analgesia in obstetrics. International Journal of Obstetric Anesthesia 1996; 5: 115-125.
Elton CD, Ali P, Mushambi MC. Walking extradurals in labour: a step forward? British Journal of Anaesthesia 1997; 79: 551-
Russell R, Quinlan J, Reynolds F. Motor block during epidural infusions for nulliparous women in labour. International Journal of
McGrady EM. Extradural analgesia: does it affect progress and outcome of labour? British Journal of Anaesthesia 1997; 78: 115-
Collis RE, Baxandall ML, Srikantharajah ID, Edge G, Kadim MY, Morgan BM. Combined spinal epidural (CSE) analgesia: technique
management and outcome of 300 mothers. International Journal of Obstetric Anesthesia 1993; 3: 75-81.
Harding SA, Collis RE, Morgan BM. Meningitis after combined spinal-extradural anaesthesia in obstetrics. British Journal of
Anaesthesia 1994; 73: 545-547.Click here for Medline link
Paech M, Godkin R, Webster S. Complications of obstetric analgesia and anaesthesia: a prospective analysis of 10995 cases.
International Journal of Obstetric Anesthesia 1998; 7: 5-11. Click here for IJOA link
MacArthur C, Lewis M. Anaesthetic characteristics and long-term backache after obstetric anaesthesia. International Journal of
Reynolds F. Maternal sequelae of childbirth. British Journal of Anaesthesia 1995; 75: 515-517.Click here for Medline link
Russell R, Dundas R, Reynolds F. Long-term backache after childbirth: prospective search for causative factors. British Medical
Journal 1996; 312: 1384-1388.Click here for Medline link
Reynolds F. Auditing complications of regional analgesia in obstetrics. International Journal of Obstetric Anesthesia 1998; 7: 1-4.
NEXT CHAPTER

BREASTFEEDING AND ANAESTHETIC RELATED DRUGS
BREASTFEEDING AND ANAESTHETIC RELATED DRUGS
Most drugs will be excreted into the milk in amounts too small to effect the baby. The amount of drug which passes from the
plasma into the milk depends on the extent to which it is bound to plasma proteins and also its lipid solubility. If these are high
there is less drug in the plasma therefore less available for transfer. If possible mother should feed infant before next dose is due.
Drug Group Safe Contraindicated Effects on Infant

Thiopentone, Propofol,
Halothane, Enflurane,
Anaesthetic Agents/Drugs Isoflurane, Sevoflurane
muscle relaxants, atropine,
neostigmine
Tetracycline, Teeth discoloration
Antibiotics Chloramphenicol Blood dyscrasias
Heparin and Warfarin
Increases prothrombin time and
Anticoagulants Phenindione
APPT in infant

Some doubts as to the effects
Metoclopramide, Cyclizine, on the infants nervous system.
Anti-emetics
Prochlorperazine, Ondansetron
Use with caution where
indicated
Salbutamol, Terbutaline - best Prednisolone in doses over 40 No evidence that high dose
Bronchodilators
administered by inhaler mg prednisolone is safe
Lorazepam, Midazolam,
Benzodiazepines Diazepam Lethargy and weight loss
Temazapam
Cimetidine, Ranitidine, Significant amount crosses but
Histamine H 2 antagonists no ill effects yet seen
Famotidine Less significant transfer
Local Anaesthetics Lidocaine, Bupivacaine Cocaine Infant intoxication
Paracetamol, Ibuprofen,
Non opioid analgesics Aspirin Reye’s Syndrome
Indomethacin, Diclofenac
Neuro-behavioural depression,
Morphine, Codeine Fentanyl,
Opioids Pethidine as PCA norpethidine has a long
Sufentanil, Alfentanil
duration
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Chapter 4
Chapter contents:
Contraindications
Advantages
Disadvantages
Spinal anaesthesia
Spinal
Epidural
Patient refusal.
Advantages

Disadvantages
Basic technique.

Chapter 4
Intrathecal opioids

respiration.

High spinal block

Chapter 4
ml.
of toxicity.

Chapter 4
local anaesthetic.
peritoneum
Basic technique
paracervical area.

Chapter 4
FURTHER READING
NEXT CHAPTER

Chapter 2
2. ANALGESIA
Chapter contents
Pain in labour
Pain pathways
TENS
Caudal analgesia
Spinal analgesia
PAIN IN LABOUR

PAIN PATHWAYS
Labour pain

Chapter 2
TENS

Bolus 20 - 25 mg 25 - 30 µg 50 - 75 µg
four hours.

Chapter 2

Chapter 2
CAUDAL ANALGESIA
Indications
Forceps delivery
Perineal suture
T9.
SPINAL ANALGESIA
Indications

Advantages

Disadvantages


Chapter 2
not recommended.
never be used).
CSF is obtained.

Chapter 2
Hypotension
FURTHER READING
NEXT CHAPTER

DERMATOME CHART AND SEGMENTAL NERVE SUPPLY TO THE PERINEUM
DERMATOME CHART AND SEGMENTAL NERVE SUPPLY TO THE PERINEUM
Skin area supplied by the dorsal nerve roots

(Dermatomes) on the ventral surface of the body.
Showing ophthalmic V1, maxillary V2, and
mandibular V3 divisions of the trigeminal nerve, the
cervical, thoracic, lumbar and sacral nerves down
to S3.
Fig A.3 Dermatomal Chart
Showing the skin area supplied by the sacral

nerves 2-5 and the coccygeal nerve.
Fig A.4 Segmental nerve supply to the perineum
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CATECHOLAMINE INFUSIONS
CATECHOLAMINE INFUSIONS
DOPAMINE
To make up a solution for a 66 kg woman
Take one ampoule of 200 mg dopamine and add it to 5% dextrose to make a total volume of 50 ml. Run through an infusion pump,
the setting of ml/h will equal dosage at rate of µg/kg/min.
Alternatively - Multiply the body weight in kg by 3 to obtain the dopamine dose, then add it to 5% dextrose to a total volume of 50
ml. Run through an infusion pump, the setting of ml/h will equal dosage at rate of µg/kg/min.
Different dosage regimens exert different effects -
2-5 µg/kg/min - predominantly renal effects. - at a rate of 2-5 ml/h
5-10 µg/kg/min - predominantly ß effects . - at a rate of 5-10 ml/h
>10 µg/kg/min - predominantly a effects. - at a rate of >10 ml/h
EPINEPHRINE
5 mg in 500 ml saline (10 µg/ml) - at a rate of 10-85 ml/h.
NOREPINEPHRINE
4 mg in 500 ml saline (8 µg/ml) - at a rate of 25-100 ml/h
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EPIDURAL INFUSION REGIMENS FOR LABOUR
EPIDURAL INFUSION REGIMENS FOR LABOUR
0.1% bupivacaine + 2µg/ml fentanyl
Remove 24 ml from 100 ml 0.9% saline

Add 20 ml 0.5% bupivacaine (100mg) and 4ml (200 µg) fentanyl
0.08% bupivacaine
Add 20 ml 0.5% bupivacaine to 100 ml of 0.9% saline, making a total volume of 120 ml.
To obtain 2 µg/ml fentanyl Add 5 ml (250 µg) to 115 ml of solution.
0.0625% bupivacaine + fentanyl 2.5 µg/ml
Add 15 ml of 0.5% plain bupivacaine to 100ml saline making a total volume of 115 ml.
To obtain 2.5 µg/ml fentanyl, add 6 ml (300 µg) to 115 ml of solution.
Establish epidural block and Infuse initially at 12 m/h. If block inadequate 10 ml of solution or 5 ml boluses of 0.25% bupivacaine
are given until analgesia is achieved, infusion increased by 2 ml/h.
If block above T8 then reduce infusion by 2 ml/h.
Commercial solutions containing bupivacaine and fentanyl, e.g., 0.1% bupivacaine + fentanyl 2 µg/ml are available.
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Chapter 1
Chapter contents

Respiratory changes
Renal changes
Hepatic changes
Coagulation

Chapter 1

required at term.
Blood loss
Cardiac output

Chapter 1


RESPIRATORY CHANGES

Chapter 1
levels at term.
Pa O 2 to <13.5 kPa (100 mm Hg)
Pregnancy Labour
Tidal volume ml 480 - 680 650 - 2000
Pa O 2 kPa 14 (105 mmHg) 13.5 -14.4 (100-108 mmHg)

Chapter 1
of the curve.

Chapter 1
these changes
anaesthesia
RENAL CHANGES

HEPATIC CHANGES
FURTHER READING

Chapter 1
4:207-215.
NEXT CHAPTER

FETAL HEART RATE
FETAL HEART RATE (FHR) MONITORING
CLASSIFICATION
Normal
1. Baseline 110-160 bpm

2. Baseline variability > 5 bpm
3. No change or an acceleration in FHR during a contraction
4. For early decelerations amplitude does not normally exceed 40 bpm and recovery to the baseline occurs by the end of the
contraction. If uncomplicated, the most likely cause is fetal head compression.
Borderline
1. Baseline bradycardia (100-110 bpm) and tachycardia (160-180 bpm) may indicate fetal hypoxia.
2. Variable decelerations. The amplitude, duration and relationships to contractions vary from one contraction to the next.
Variable decelerations are usually attributed to umbilical cord compression (baroreceptor reflex) and may be associated
with fetal hypoxia. More likely with oligohydramnios
Abnormal
1. Loss of baseline variability (a "flat" tracing).

2. Late decelerations, there is a consistent delay between the peak of the contraction and the trough.
3. Complicated patterns. A combination of the above features of abnormality usually indicates significant fetal hypoxia, e.g.
tachycardia with late decelerations and loss of baseline variability
Decelerations should be described according to the terms used above. Use of "type I" and "type II" is discouraged. The
interpretation of abnormal fetal heart rate tracings does require experience.
Identification of a significant abnormality will lead to fetal blood sampling or often to immediate delivery by Caesarean section or
forceps.
A = Deceleration Duration
B = Deceleration Amplitude
C = Lag time
D = Peak pressure
E = Duration
F = Basal tone
G = Loss of beat to beat variation
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FETAL HEART RATE
Fig A.1 Terms used in the study of continuous records of FHR
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LINKS TO OTHER OBSTETRIC ANAESTHETIC SITES
LINKS TO OTHER OBSTETRIC ANAESTHETIC SITES
Hypertextbook of Regional Anaesthesia for Obstetrics
Obstetric Anaesthetists Association (OAA)
Society for Obstetric Anesthesia and Perinatology (SOAP)
Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1994-1996. (Why Mothers Die)
The Scottish Obstetric Guideline Audit Project (SOGAP)
Cochrane Pregnancy and Childbirth Group (Abstracts of Cochrane Reviews)
Resuscitation Council (UK)
Scottish Intercollegiate Guidelines Network (SIGN)
American Searchable Resource of Available Guidelines
Centre for Evidence Based Medicine (UK)
UK Difficult Airway Society Conferencing Server (National Difficult Airway Database and Links)
Medline
British Journal Of Anaesthesia CEPD reviews
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MAGNESIUM SULPHATE
MAGNESIUM SULPHATE IN THE MANAGEMENT OF ECLAMPSIA
In women who have had an eclamptic seizure magnesium sulphate significantly reduces the risk of recurrent convulsions. In this
respect it is superior to phenytoin or diazepam.
Magnesium sulphate decreases smooth muscle activity by several mechanisms. It is a physiological calcium antagonist, and in
particular an endogenous calcium channel blocker which inhibits the release of acetyl choline into the neural synapse. This results
in several important effects:-
Cerebral vasodilatation
Systemic hypotension
Tocolysis
Respiratory depression
Myocardial depression
Muscular weakness
There is also evidence for an antagonist action at central NMDA receptors; this may result in anti-convulsant activity.
MAGNESIUM SULPHATE - ECLAMPTIC PROTOCOL
Each labour ward should have a detailed protocol for the administration of magnesium sulphate including guidelines for clinical and
laboratory monitoring. The following details give the principles on which a protocol may be based.
Loading dose is 4 g i.v. of 20% magnesium sulphate given over 20 min.
Maintenance dose is 3 g i.v. infusion of 20% magnesium sulphate over the first hour and then 2 g/h subsequently.
The following are monitored-
Respiratory rate
Hourly urine volume
Confirm that patellar or forearm reflex is present every 5-10 min for first 2 hours and thereafter every 15 min for the duration
of the treatment.
Therapeutic levels: 2-4 mmol/litre.
Management of overdose - 10 ml i.v.10% calcium gluconate is given i.v. every 10 min.
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Chapter 9
9. NEONATAL RESUSCITATION
Chapter contents
Physiological changes
Checklist before delivery
Normal delivery
Assessment of the neonate
Indications for positive pressure ventilation
PHYSIOLOGICAL CHANGES AT BIRTH
The infant’s first breath expands the lungs and reduces pulmonary vascular resistance, thus allowing increased pulmonary blood
flow. Clamping the umbilical cord increases systemic vascular resistance and these changes together with a rising arterial PO2
result in closure of the foramen ovale and ductus arteriosis to establish a pulmonary and systemic circulation. The arterial PO2
slowly increases and may take up to six weeks to reach adult values, due to intrapulmonary shunting of venous blood which may be
as high as 20% in the first few days of life. As the lungs expand surfactant function becomes well established and less negative
pressure is required to allow air entry. Each subsequent breath therefore requires less effort.
Blood from the umbilical vessels has the following values -
Table 9.1
Umbilical vein (UV) Umbilical artery (UA)

pH 7.24 - 7.49 7.15 - 7.43
PaCO 2 kPa 3.0 - 6.5 (23 -49 mmHg) 4.0 - 10 (31 - 74 mmHg)
PaO 2 kPa 2.0 - 6.4 (15 - 48 mmHg) 0.5 - 4.5 (4 - 34 mmHg)
Base excess mmol /l - 9.0 to - 3 .5 -11.2 to - 6.2
Some degree of acidosis is common at birth. Cerebral palsy is unlikely to be related to intrapartum hypoxia unless cord pH at birth is
< 7.00. Most infants with a pH as low as this develop normally. Umbilical arterial samples are a better reflection of fetal status than
venous.
Normal acid base status is achieved after 1 - 2 hours.
CHECKLIST BEFORE DELIVERY
Switch on radiant warmer.

Check oxygen supply, connections and self inflating bag.
Maximum pressure control blow-off is set at 25 cm water.
Suction apparatus, oral mucus extractor and fine suction catheters, laryngoscopes, endotracheal tubes
Dry and warm towels
Drugs -
naloxone 400 µg/ml

epinephrine 100 µg/ml or 1/10,000 concentration
dextrose 5-10% solutions
sodium bicarbonate 0.5 mmol/ml or 4.2% concentration
NORMAL DELIVERY

Chapter 9
The mouth and oropharynx are always aspirated first as stimulation of the nose may cause the neonate to gasp and inhale any
pharyngeal contents. The suction catheter must not be passed too far into the mouth as stimulation of the hypopharynx can cause
laryngospasm and bradycardia.
As neonates have poor thermoregulation they should be dried and wrapped in warm towels. Most newborn babies do not need any
resuscitation and after they have been dried they can be returned to their mothers.
ASSESSMENT OF THE NEONATE
Apgar score
The Apgar scoring system at 1 minute and 5 minutes is in common use and gives information about the severity and prognosis of
asphyxia. In pre-term infants the score is more likely to be affected by gestational age than by asphyxia.
Table 9.2 Apgar scoring system
Clinical Sign Apgar Score

0 1 2
A: Appearance (colour) Blue, pale Body pink, extremities blue Completely pink
P: Pulse Absent Less than 100 More than 100
G: Grimace (reflex irritability) No response Grimaces Cries
A: Activity (muscle tone) Limp Some flexion of extremities Active, well flexed
R: Respiratory effort Absent Weak cry or shallow Good strong cry
Score 10 = optimal condition
Score 6 or less = depression, resuscitative measures required
Heart rate
This is a reliable indicator of the newborn’s degree of distress. It can be evaluated by palpation of the pulse at the base of the
umbilical cord or auscultation of apical heart sounds. If the heart rate is greater than 100 beats/min and spontaneous respirations
are present assessment continues. If the heart beat is less than 100 beats/min positive pressure ventilation with 100% oxygen
should be started immediately. If the heart rate is less than 60 beats/ min and not increasing despite effective ventilation with 100%
oxygen, chest compression should be initiated.
Colour
The infant may be cyanotic despite adequate ventilation and a heart rate greater than 100 beats/min. It has been suggested that an
Apgar minus colour score (A-C) is of better prognostic value as colour does not correlate well with the acid base state of the infant
at birth.
INDICATIONS FOR POSITIVE PRESSURE VENTILATION
Apnoea
Heart rate less than 100 beats/min
Persistent central cyanosis despite the administration of 100% oxygen
Effective ventilation can usually be provided with a bag and mask; the infant should be positioned with neck slightly extended (rolled
towel 2.5 cm thick placed under the shoulders). Initial inflation pressures may need to be as high as 50 cmH2 0, the first five or six
breaths require that inspiration is held for 1-2 seconds to establish an adequate functional residual capacity for continued
spontaneous ventilation. If adequate ventilation as indicated by effective chest movement is not achieved then immediate intubation
of the trachea and ventilation are performed. The time taken from birth to the baby’s first gasp and to the onset of regular respiration
should be recorded. Assisted ventilation should be at a rate of 40 - 60 breaths/min, and chest compression at a rate of 120/min (i.e.
a ratio of 3:1).
There is evidence that air is as effective as 100% oxygen in term babies. !00% oxygen has little advantage and may increase
oxygen free radical damage. If gas mixing facilities are available 40% oxygen is recommended.

Chapter 9
Factors affecting resuscitation
Maternal sedation
Meconium stained amniotic fluid
Fetal heart rate abnormalities during labour
Operative delivery
Prolapsed cord
Prolonged labour
Infection
Maternal health problems e.g. pre-eclampsia, diabetes mellitus, antepartum haemorrhage
Naloxone is used if apnoea is due to maternal opioid sedation. The recommended dose is 100 µg kg-1 i.m.
The indications and management of the apnoeic baby are illustrated in figs 9.1& 9.2.
Note: if there is particulate meconium and the baby is unresponsive, proceed at once to fig 9.2
MECONIUM ASPIRATION SYNDROME
If the liquor is meconium stained during delivery then the pharynx must be aspirated before the first breath, the trachea intubated
and any remaining meconium aspirated by direct suction. The indications and management of meconium aspiration can be seen in
fig 9.2
CIRCULATION
Lack of improvement in the heart rate is usually due to inadequate ventilation. Check face mask seal or tracheal tube
position.
If the newborn fails to respond to ventilation then chest compression must commence at a rate of 120/min, ventilation
occurring every third compression.
Epinephrine 10-30 µg kg-1 i.v. (0.1-0.3 ml kg-1 of 1:10,000 solution) via the umbilical venous catheter flushed with saline 2ml
and repeated as necessary with a third dose of 100 µg kg-1 .
If there is no response or evidence of severe acidosis sodium bicarbonate 1-2 mmol kg-1 i.v. is given slowly over 2-3 minutes

Chapter 9
Hypovolaemia requires active volume replacement which is indicated when:-
1. Evidence of acute fetal loss

2. Pallor persisting after oxygenation
3. Faint pulses with a good heart rate but poor response to resuscitation including adequate ventilation
Fluid replacement 10-20 ml kg-1 is given with 4.5% albumin, whole blood or plasma.
(a) Consider while preparing for (b) ± (c) depending on local policy.
* may vary with individual circumstances and local guidelines
Figs 9.1 and 9.2 from Guidelines for resuscitation of babies at birth; Royal College of Paediatrics and Child Health
and Royal College of Obstetricians and Gynaecologists 1997. BMJ Publishing Group, London.
FURTHER READING
Zideman DA. Resuscitation. British Journal of Anaesthesia; 83: 157-168.1999 Click here for Medline link

Chapter 9
Resuscitation Council (UK). Newborn Life Support; Resuscitation Guidelines 2000.
Paediatric Life Support: (including the recommendations for resuscitation of babies at birth). European Resuscitation Council.
Resuscitation; 37(2): 95 - 96. 1998 Click here for Medline linkThe 1998 European Resuscitation Council Guidelines. Resuscitation
of babies at birth.
APPENDICES

NEUROLOGICAL DAMAGE FOLLOWING OBSTETRIC EPIDURAL
NEUROLOGICAL DAMAGE FOLLOWING OBSTETRIC EPIDURAL/SPINAL BLOCKADE AFTER DELIVERY
Pathology Cause Onset Clinical Feature Outcome

Peripheral nerve Compression of nerves by In hours Sensory and or motor loss in Recovery 1 - 24
palsies fetal head, instrumentation the distribution of affected weeks
(Obstetric nerve and poor positioning peripheral nerve, e.g. foot drop
palsies)
Spinal nerve Trauma (needle or 0 - 2 days Pain during insertion, pain on Recovery 1 - 24
neuropathy catheter). Spinals have an injection , paraesthesia, pain weeks
incidence of 7% and numbness over distribution
paraesthesiae of spinal nerve
Anterior spinal artery Hypotension Immediate Post-operative painless Painless paraplegia
syndrome paraplegia. Posterior columns
are preserved
Adhesive arachnoiditis Irritant injectate 0 - 7 days but May be pain on injection. A Severe disability with
may be much variable degree of neurological pain and paralysis
longer defect often with progressive
pain and paraplegia
Space occupying Coagulation defects 0 - 2 days Severe backache Requires immediate
lesion (haematoma or postoperatively with progressive surgery otherwise
abscess) Bacteraemia paraplegia permanent
paraplegia
Chemical neurotoxicity hyperbaric 5% lidocaine 0-3 days Cauda equina syndrome. Disability variable but
Bladder and anal sphincter usually permanent
preservatives dysfunction with perineal
sensory loss and motor
weakness in legs
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Preface
ABOUT THE SIMPSON HANDBOOK OF OBSTETRIC ANAESTHESIA
A sound practical and theoretical knowledge of the basic procedures is required to deal with the challenge posed by labour ward
emergencies. This handbook which is based on a manual for a large maternity hospital is designed to meet this need. Recent
advances in electronic publication have opened up new and exciting opportunities for distributing and updating the handbook. While
the approach remains essentially didactic it is now possible to provide an up to date reference base with online links to Medline
and revised clinical guidelines in accordance with current practice. Feedback from our readers will play a welcome and
essential part in developing the content and technical aspects of the book. We hope that all labour ward staff (medical and
midwifery) will find it a useful resource. It should also be a useful revision guide for postgraduate examinations. Hypertext links to
obstetric and anaesthetic WWW resources will be developed further as they become available.
ACKNOWLEDGEMENTS
Several of our anaesthetic and medical colleagues have given their valuable advice in the preparation of the book. We would
particularly like to thank the following obstetric anaesthetists: Professor Felicity Reynolds, Dr Vicki Clark, Dr John McClure and Dr
Anne McCrae. Mrs Glynis Omond has given us invaluable secretarial assistance.
We would also like to acknowledge receipt of a grant from Astra Pharmaceuticals Ltd. towards the costs of multimedia authoring.
LEGAL MATTERS AND DISCLAIMER
Every effort has been made to ensure that the material in this book conforms to current guidelines and practice in obstetric
anaesthesia. Before instituting treatment all dosage schedules should be checked with manufacturers recommendations. Treatment
protocols are not intended to be recommendations for a particular patient. Practitioners should always refer to local practice and
guidelines before instituting treatment. The publisher, editors and authors can not therefore accept any liability arising from the
treatment of any particular patient.
A.S. BUCHAN, G.H. SHARWOOD-SMITH December 1999
While publication has been made possible by the support of advertisers the authors wish to emphasise their complete
independence in deciding the content of the book
ABOUT THE TECHNOLOGY OF THIS PUBLICATION
This Book has been specially prepared in HTML format for conventional online viewing, or alternatively for email transmission or
Web download as a self installing Windows 95/98/NT program. This program permanently stores the publication on your hard disk
as a mini Web site; a single click of the mouse will then run your existing Web browser and allow you read the publication. If you
have an intranet then the book can be copied direct to the server (assuming you have the appropriate license). For those who do
not use the Windows operating system a zipfile version of the book is available although you will have to manually install it on your
machine.
This architecture results in maximum compatibility with existing trends in intranet/internet information delivery whilst allowing
transfer of publications to machines without a network connection using floppy disks. Optimised compression techniques ensure
very small file sizes for publications. There are substantial savings in publication costs and many extra facilities, particularly the
ability to send further partial or complete updates by email or download. If the book is installed on an individual PC or Intranet then
readers will not suffer from the slowness or expense of online connections although online references are automatically retrieved
when necessary. The subscriber also has tangible "ownership" of their publication in that it resides on their own computer. The
familiar interface of the subscribers Web browser helps to reduce the learning curve.
In addition to the normal hypertext features seen in this publication items such as colour pictures, sound, video and live references
to items on the World Wide Web / discussion groups we hope that virtual 3D simulations will soon be included and will be
developed in future versions.
CHAPTER 1
Copyright A. S. Buchan and G.H. Sharwood- Smith 1999 all rights reserved. Published by the Royal College of Surgeons of Edinburgh
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STEROID TREATMENT REGIMENS
STEROID TREATMENT REGIMENS
Patients on steroids Assume normal HPA* Additional steroid cover not required
<10mg/day response
>10mg/day Minor surgery 25mg hydrocortisone @ induction
Intermediate surgery Usual pre-op steroids + 25 mg hydrocortisone @

induction + 100 mg/day for 24h
Usual pre-op steroids + 25 mg hydrocortisone @

Major surgery induction + 100 mg/day for 24 - 72h
High-dose immunosuppression Give usual immunosuppressive doses during peri-operative period
Patients stopped steroids < 3 months Treat as if on steroids
> 3 months No peri-op steroids necessary
* HPA:- hypothalamic-pituitary-adrenal
Nicholson G, Burrin JM.Hall GM. Peri-operative steroid supplementation. Anaesthesia 1998; 53: 1091-1105. Click here for Medline
link
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APPENDICES
APPENDICES

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Handbook of Obstetric Anaesthesia
The Simpson Handbook of

Obstetric Anaesthesia
Dr A S Buchan and Dr G H Sharwood-Smith
Click the headings at the left to read the
book
Research Assistant: Dr Pamela Johnston
Illustration: Rachel Ellaway
Authoring: Janet Lindsey
Concept & Software Development: Leon Lindsey and Andrew Lamb -
Faculty of Medical Informatics RCSEd
This publication is sponsored as a service to anaesthesia by
This publication is delivered using Microsoft® technology and we recommend

that it is read using Microsoft Internet Explorer at a screen resolution of 800
by 600 in at least 256 colours.
Viewed apart, and in an isolated light, the degree of
actual pain (of labour) is as great if not greater than
that attendant upon most surgical operations ...
Sir James Young Simpson, March 1847
Copyright A.S.Buchan and G.H.Sharwood-Smith 1999 all rights reserved. Published by the Royal College of Surgeons of Edinburgh
Updated on August1 2002
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Chapter 1
Chapter contents

Respiratory changes
Renal changes
Hepatic changes
Coagulation
file:///C|/Users/Administrator/Downloads/shoa%20current%20MASTER/Chpt1.htm[20/1/2011 6:58:49 pµ]

Chapter 1

required at term.
Blood loss
Cardiac output

Chapter 1


RESPIRATORY CHANGES

Chapter 1
levels at term.
Pa O 2 to <13.5 kPa (100 mm Hg)
Pregnancy Labour
Tidal volume ml 480 - 680 650 - 2000
Pa O 2 kPa 14 (105 mmHg) 13.5 -14.4 (100-108 mmHg)

Chapter 1
of the curve.

Chapter 1
these changes
anaesthesia
RENAL CHANGES

HEPATIC CHANGES
FURTHER READING

Chapter 1
4:207-215.
NEXT CHAPTER

Chapter 2
2. ANALGESIA
Chapter contents
Pain in labour
Pain pathways
TENS
Caudal analgesia
Spinal analgesia
PAIN IN LABOUR

PAIN PATHWAYS
Labour pain

Chapter 2
TENS

Bolus 20 - 25 mg 25 - 30 µg 50 - 75 µg
four hours.

Chapter 2

Chapter 2
CAUDAL ANALGESIA
Indications
Forceps delivery
Perineal suture
T9.
SPINAL ANALGESIA
Indications

Advantages

Disadvantages


Chapter 2
not recommended.
never be used).
CSF is obtained.

Chapter 2
Hypotension
FURTHER READING
NEXT CHAPTER

SIDE EFFECTS OF DRUGS ASSOCIATED WITH OBSTETRIC ANAESTHESIA
Drugs Effect
Diuretics
Ethacrynic acid Neonatal deafness
Thiazides Neonatal thrombocytopenia
Intra uterine growth retardation (IUGR), neonatal hypoglycaemia,
ß -Adrenoceptor blockers
bradycardia
Oxytocic drugs
Bolus dose can cause maternal hypotension due to
Oxytocin vasodilatation. Excess may cause uterine hypertonia and fetal
asphyxia
Ergometrine Vasoconstriction, hypertension, pulmonary oedema
Bronchospasm, nausea, vomiting, hyperthermia, flushing,
Carboprost - Prostaglandin F2 a
hypertension, cardiovascular collapse.
Tocolytics
Maternal tachycardia, hyperglycaemia, hypokalaemia, congestive
Ritodrine (ß agonist)
cardiac failure and pulmonary oedema (especially with steroids)
nausea, vomiting, tachycardia, hypotension, headache,
Atosiban - an oxytocin receptor antagonist dizziness, hot flushes, hyperglycaemia, injection site reaction;
less commonly pruritus, rash, fever, insomnia
Nifedipine fewer side effects than ß agonists
Indomethacin (prostaglandin inhibitor) Premature ductus arteriosus closure
Antihypertensive drugs
Diazoxide }
Nifedipine } All may inhibit uterine activity
Verapamil }
Angiotensin converting enzyme inhibitors (ACE) IUGR, oligohydramnios, neonatal anuria
Sodium nitroprusside Cyanide intoxication

Anticoagulants
Teratogenic, especially during the first trimester. High incidence
Warfarin of haemorrhagic complications to mother and fetus. Do not use
after 36 weeks
Heparin Does not cross the placenta - and is therefore safe
Barbiturates
Thiopentone Neonatal depression
Benzodiazepines
Neonatal depression, hypotonia, hypothermia (bilirubin
Diazepam
displacement from albumin by preservative sodium benzoate)
Intrauterine growth retardation with chronic abuse, intrauterine
Narcotic analgesics death with maternal withdrawal. Neonatal depression
Decrease in gastric emptying in labour
Non-steroidal anti-Inflammatory drugs (NSAID)
Inhibition of pre-term labour

Indomethacin (prostaglandin inhibitor)
Premature ductus arteriosus closure
Prolongation of labour, increased incidence of haemorrhage in
Aspirin
large doses
Ethacrynic acid Neonatal deafness
Thiazides Neonatal thrombocytopenia
Anticonvulsants
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Magnesium Sulphate Muscle weakness, respiratory depression, interaction with

muscle relaxant drugs
Phenytoin Congenital malformations. Enzyme induction leads to lowered
Carbamazepine vitamin K levels, neonatal bleeding tendency. Vitamin K1 should
Phenobarbitone be given to the mother at 36 weeks
Inhalation anaesthetics
Halothane Dose related neonatal depression and myometrial relaxation,
Enflurane hypotension but no evidence of teratogenicity
Isoflurane
Nitrous oxide May interfere with DNA synthesis
Local anaesthetics
Prilocaine Methaemoglobinaemia > 600 mg (8 mg/kg)
Large doses may cause maternal and neonatal depression
Lidocaine
especially after epidurals.
Fetal bradycardia a feature after paracervical block. Minimal
Bupivacaine
neurobehavioural effects
Quaternary ammonium compounds do not cross the placenta in
Muscle relaxants
clinically significant amounts
Anticholinergics
Fetal tachycardia and loss of beat to beat variation in large
Atropine
doses
Glycopyrrolate Quaternary ammonium compound does not cross the placenta
High doses cause maternal and neonatal adrenal suppression.
Corticosteroids
Cover required during labour
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Chapter 4
Chapter contents:
Contraindications
Advantages
Disadvantages
Spinal anaesthesia
Spinal
Epidural
Patient refusal.
Advantages

Disadvantages
Basic technique.

Chapter 4
Intrathecal opioids

respiration.

High spinal block

Chapter 4
ml.
of toxicity.

Chapter 4
local anaesthetic.
peritoneum
Basic technique
paracervical area.

Chapter 4
FURTHER READING
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Guidelines for the management of severe pre
GUIDELINES FOR THE MANAGEMENT OF SEVERE PRE-ECLAMPSIA FROM THE REPORT ON CONFIDENTIAL ENQUIRIES
INTO MATERNAL DEATHS IN UK 1997-1999
Eclampsia and pre-eclampsia continue to be a leading cause of maternal mortality and morbidity.1 Eclampsia is a rare occurrence,
with a UK incidence of 4.9/10,000 maternities. Almost half of the seizures (44%) occur in the postnatal period, with over one-third
(38%) occurring antenatally and 18% occurring in the intrapartum period.2 The incidence of pre-eclampsia is unknown. The
Collaborative Eclampsia Trial (1995)3 established that magnesium sulphate is more effective in preventing recurrent seizures
following eclampsia than either phenytoin or diazepam.
The aim of the guidelines is to increase the safety and stability of the woman although, if the fetus is still in utero, constant
monitoring of fetal well-being should be an integral part of management protocol.
Criteria for inclusion
Any woman with severe proteinuric hypertension where the decision has been made to deliver and with one of the following criteria
(either 1, 2 or 3).
1. Hypertension ( > 140/90 mmHg) with proteinuria (> 0.3 g/day or > 2+) and at least one of the following:
i) Headache, visual disturbance, epigastric pain
ii) Clonus (> 3 beats)
iii) Platelet count less than 100 x 10 9 , ALT (alanine aminotransferase) > 50 iu/l
iv) Creatinine greater than 100 or creatinine clearance less than 80.
2. Severe hypertension (systolic > 160 mmHg or diastolic > 110 mmHg) with proteinuria (> 0.5 g/day or > 2+)
3. Eclampsia
4. Clinical discretion should be used to include women who present with atypical symptoms.
Key personnel to be contacted
Obstetric registrar on call
Anaesthetic registrar on call
Senior labour-ward midwife
Consultant obstetrician on call
Consultant anaesthetist on call.
Maternal observations and investigations
All maternal observations should be recorded on a specialised pregnancy-induced hypertension chart or an ICU chart.
Oxygen saturation should be continuously monitored.
Blood-pressure recordings should be made every 15–20 minutes.
Maternal temperature should be recorded hourly.
A Foley catheter should be in situ and hourly urinary output measured.
Routine blood samples should be taken every 12–24 hours, including full blood count, urea and electrolytes,
creatinine and liver function tests.
Fetal observations
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Minimum assessment of fetal well-being should include the following:
Growth assessment scan
Liquor volume assessment
Continuous external fetal monitoring
Umbilical cord Doppler if the woman’s condition allows.
Management of seizures
All women with eclampsia should be treated with magnesium sulphate as the first-line drug of choice. The
intravenous (IV) route is preferable. A loading dose of 4 g magnesium sulphate should be given over 5–10 minutes,
followed by a maintenance infusion of 1–2g/hour IV at the discretion of the consultant in charge, continued for at least
24 hours after the last seizure. Recurrent seizures should be treated by a further bolus of 2 g magnesium sulphate.
Diazepam may be administered if fits continue, at the discretion of the consultant in charge.
Magnesium levels should be monitored when repeat fitting occurs or renal compromise is evident (therapeutic range
2–4 mmol/litre).
Deep tendon reflexes should be monitored hourly when magnesium therapy is commenced. If reflexes are absent, or
respirations are less than 14 per minute, or SaO2 less than 95%, magnesium therapy should be stopped.
If the fits continue, it is important to exclude other causes of fits and a CT scan should be considered.
Management of hypertension
Severe hypertension is defined as greater than 160/110 mmHg or mean arterial pressure (MAP) greater than 125
mmHg.
Hydralazine is the first-line drug of choice for management of severe hypertension titrated against blood pressure,
except in the presence of tachycardia (greater than120 bpm). The agreed dose is 5 mg IV repeated every 20
minutes, to a maximum cumulative dose of 20 mg.
Labetalol should be used as a second choice, given 20 mg IV followed at ten-minute intervals by 40 mg, 80 mg and
80 mg, up to a cumulative dose of 300 mg.
Prophylactic H2 antagonists should be given until the woman is transferred to normal postnatal care.
Fluid balance management
Fluid intake should be restricted to 85 ml/hour.
Urinary output should be measured hourly.
500 ml human albumin solution (HAS) should be considered:
– prior to hydralazine therapy
– prior to caesarean section
– if oliguria is evident (defined as urinary output less than 100 ml in a consecutive four-hour period)
– prior to the administration of regional anaesthesia.
If HAS has previously been administered, the insertion of a central venous pressure (CVP) line should be considered.
If further complications occur, especially oliguria, after the administration of HAS, a line is recommended.
Although the success rate of the subclavian vein route is greater than the antecubital fossa route, clinicians should
use the route with which they are more familiar.
If the central venous pressure value is greater than 10 mmHg, 20 mg frusemide should be considered.

If the central venous pressure value is less than 10 mmHg, HAS 500 ml should be considered.
A further dose of 20–40 mg frusemide should be considered if there is persistent oliguria.
Informing ICU personnel
There should be locally agreed criteria regarding the physical transfer of women to the adult ICU.
ICU is not a place, it is a service.
Effective communications are of the utmost importance.
The labour ward may be the most appropriate place to care for pregnant women.
Non pregnancy-related problems such as cerebral vascular accident and pulmonary oedema need to be considered.

Chapter 7
Chapter contents

Acute renal failure





heart rate
blood pressure
haemorrhage
Principal causes

Coagulopathy
Uterine rupture
Vasa praevia

Chapter 7
Principal causes
Uterine atony - 90%

Retained placenta
Coagulopathy
Uterine rupture
Management


Fluid therapy

Chapter 7
Further management
25 - 30%.
ACUTE RENAL FAILURE

Chapter 7
Monitor the CVP

Avoid nephrotoxins.
placental abruption
retained dead fetus
septic shock
The treatment is:

NORMAL (>30/52) DIC

Fibrinogen (g/l ) 4.0 - 6.0 < 0.15
Platelets (x 10 9 /l) 150 - 400 < 50
APPT (s) 35 - 40 > 100
FDP (µg/l) < 16 > 200
D-dimer (mg/l) < 0.25 >8

Chapter 7

Age >35 years

Obesity (>80Kg)
Para 4 or more
Current infection
Pre-eclampsia
syndrome

mg daily.
Anticoagulant drugs
is essential.

Chapter 7
FURTHER READING
223.
Medline link
6: 218-273.
NEXT CHAPTER

Chapter 7

REPORT ON CONFIDENTIAL ENQUIRIES INTO MATERNAL DEATHS IN THE UNITED KINGDOM 1991
REPORT ON CONFIDENTIAL ENQUIRIES INTO MATERNAL DEATHS IN THE UNITED KINGDOM 1997-1999
Major causes of maternal death, rates per million maternities, United Kingdom 1997-99. The deaths due to cardiac disease and
suicide are classed as indirect, the others are direct deaths. Data from Why Mothers Die 1997-1999. The Confidential Enquiry into
Maternal Deaths in the United Kingdom. London: RCOG Press, 2001
Anaesthesia was directly responsible for 2.8 % of maternal deaths between 1997-1999
The main recommendations were:
Dedicated obstetric anaesthesia services should be available in all consultant obstetric units. These services should be capable of taking
responsibility for regional analgesia, anaesthesia, recovery from anaesthesia and the management and monitoring of intravenous
fluidreplacement therapy.

Adequate advance notice of elective high-risk cases must be given to the obstetric anaesthetic service. The notice must be sufficient to
allow the consultation, investigation and assembly of resources needed for these cases to take place.

When presented with problem cases requiring special skills or investigations, obstetric anaesthetists should not hesitate to call on the
assistance of anaesthetic colleagues in other subspecialties, as well as colleagues in other disciplines.

Invasive central venous and arterial pressure measurement can provide vital information about the cardiovascular system which can be life
saving. Invasive monitoring via appropriate routes should be used particularly when the cardiovascular system is compromised by
haemorrhage or disease.

Care of women at high risk of maternal haemorrhage must involve consultant obstetric anaesthetists at the earliest possible time.

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REPORT ON CONFIDENTIAL ENQUIRIES INTO MATERNAL DEATHS IN THE UNITED KINGDOM 1991
Anaesthetists have a responsibility, as do all medical practitioners, to ensure that drugs are given in the correct dose, at the correct rate, by
the correct route and by the most accurate means.

It seems not to be widely appreciated that Syntocinon® (Alliance) can cause profound, fatal hypotension, especially in the presence of
cardiovascular compromise. Administration should follow the guidance in the British National Formulary, Martindale and other standard
formularies. When given as an intravenous bolus the drug should be given slowly in a dose of not more than 5 iu.
Why Mothers Die: Report on Confidential Enquiries into maternal deaths in the United Kingdom 1997-1999. Click here for web link
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Chapter 7
Chapter contents

Acute renal failure





heart rate
blood pressure
haemorrhage
Principal causes

Coagulopathy
Uterine rupture
Vasa praevia

Chapter 7
Principal causes
Uterine atony - 90%

Retained placenta
Coagulopathy
Uterine rupture
Management


Fluid therapy

Chapter 7
Further management
25 - 30%.
ACUTE RENAL FAILURE

Chapter 7
Monitor the CVP

Avoid nephrotoxins.
placental abruption
retained dead fetus
septic shock
The treatment is:

NORMAL (>30/52) DIC

Fibrinogen (g/l ) 4.0 - 6.0 < 0.15
Platelets (x 10 9 /l) 150 - 400 < 50
APPT (s) 35 - 40 > 100
FDP (µg/l) < 16 > 200
D-dimer (mg/l) < 0.25 >8

Chapter 7

Age >35 years

Obesity (>80Kg)
Para 4 or more
Current infection
Pre-eclampsia
syndrome

mg daily.
Anticoagulant drugs
is essential.

Chapter 7
FURTHER READING
223.
Medline link
6: 218-273.
NEXT CHAPTER

Chapter 7

SCOTTISH OBSTETRIC GUIDELINES
THE MANAGEMENT OF POSTPARTUM HAEMORRHAGE

QUICK REFERENCE GUIDE
PERCEIVED BLOOD LOSS 500-1000 ml, NO CLINICAL SHOCK: BASIC MEASURES
Cross-match 2 units
Full blood count
Clotting screen
IV access with 14 G cannula (Hartmann’s infusion)
Clinical vigilance
PERCEIVED BLOOD LOSS >1000 ml OR ANY CLINICAL SIGNS OF SHOCK: FULL PROTOCOL:
SIMULTANEOUSLY: COMMUNICATE, RESUSCITATE, MONITOR / INVESTIGATE, STOP THE BLEEDING:
COMMUNICATE: RESUSCITATE:
IV access with 14 G cannula X 2
Head down tilt
Call experienced midwife Oxygen by mask, 8 litres / min.
Call obstetric registrar & alert consultant Transfuse cross-matched blood ASAP. Until blood arrives, infuse as rapidly
as required:
Call anaesthetic registrar & alert consultant
Crystalloid (eg Hartmann’s)
Alert haematologist
Colloid (eg Gelofusine)
Alert Blood Transfusion Service
If no cross-matched blood available once 3.5 litres infused, GIVE ‘O
Call porters for delivery of specimens / blood NEG’
or uncross-matched own-group blood, as available.
Use a warming device
Use a compression cuff
Do not use a blood filter
Do not give dextrans
Give up to 1 litre Fresh Frozen Plasma and 10 units cryoprecipitate if

clinically indicated
MONITOR / INVESTIGATE: STOP THE BLEEDING:
Cross-match 6 units Exclude causes of bleeding other than uterine atony

Full blood count Ensure bladder empty
Clotting screen Uterine compression
Continuous pulse / BP / ECG / Oximeter IV syntocinon 10 units
Foley catheter: urine output IV ergometrine 500 mg
CVP monitoring Syntocinon infusion (30 units in 500 ml)
Discuss transfer to ITU IM Carboprost (500 mg)
Clinical vigilance Surgery earlier rather than late
Hysterectomy early rather than late

SCOTTISH OBSTETRIC GUIDELINES & AUDIT PROJECT prepared June 1998
A Guideline development project initiated by the Scottish Executive Committee of the RCOG, funded by the Clinical Resource & Audit Group of the SODoH and working to
the methodology of the Scottish Intercollegiate Guidelines Network
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SCOTTISH OBSTETRIC GUIDELINES
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APPENDICES
APPENDICES

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NORMAL FEMALE CLINICAL CHEMISTRY VALUES
NORMAL FEMALE CLINICAL CHEMISTRY VALUES (non pregnant)
Investigation Reference Values

Blood
Hydrogen ion nmol/l 36 - 44
PaCO 2 kPa 4.4 - 6.1
PaO 2 kPa 12 -15
plasma bicarbonate mmol/l 21.0 - 27.5
base excess mmol/l - 4 to + 4
Aspartate aminotransferase (AST) u/l 10 - 35
Calcium mmol/l 2.12 - 2.62
Chloride mmol/l 95 - 107
Cholinesterase u/l 600 -1400
Dibucaine no 77- 83
Fluoride no 50 - 68
Creatine kinase (CK) u/l 30 -150
Creatinine mmol/l 55 -150
Sodium mmol/l 132 -144
Potassium mmol/l 3.6 - 5.1
Total CO 2 mmol/l 24 - 30
Urea mmol/l 2.5 - 6.6
Glucose mmol/l 3.6 - 5.8
Alanine aminotransferase u/l 10 - 40
Albumin g/l 36 - 47
Alkaline phosphatase u/l 40 - 125
values in excess of 100 u/l are
often observed in childhood and
adolescence and during pregnancy
Bilirubin, total mmol/l 2 - 17
g -Glutamyl transferase (GGT) u/l 5 - 35
Protein (total) g/l 60 - 80
Magnesium mmol/l 0.75 - 1.0
Osmolality mmol/kg 280 - 290
Phosphate mmol/l 0.8 - 1.4 (fasting specimen)
Urate mmol/l 0.12 - 0.36
Urea-stable lactate dehydrogenase 100 - 300
(USLD) u/l
Cerebrospinal Fluid
Glucose mmol/l 2.5 - 4.0
Protein mg/l 100 - 400
Urine
Potassium mmol/24 h 25 - 100
Sodium mmol/24 h 100 - 200
Urea mmol/24 h 170 - 600
Renal pregnancy changes are described in chapter 1
NORMAL HAEMATOLOGY VALUES
Investigation Full-Term Infants Adult Female Adult Female (pregnant)

White cell count (x10 9 /l) 9 - 30 4.0 – 11.0 4.0 – 9.0
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NORMAL FEMALE CLINICAL CHEMISTRY VALUES
Red cell count (x10 12 /l) 5.0 - 6.0 3.5 - 5.8 3.7 - 4.2
Haemoglobin (g/l) 145 - 195 115 – 165 100 – 120
Haematocrit 0.44 - 0.64 0.35 – 0.47 0.31 – 0.42
Mean corpuscular volume (fl) 94 - 118 76 – 100 76 – 100
Reticulocytes (x10 9 /l) 150 mean 25 – 85 25 – 85
Platelets (x10 9 /l) 100 - 260 150 – 350 150 – 350
Blood and circulatory pregnancy changes are described in chapter 1
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Handbook of Obstetric Anaesthesia

The Simpson Handbook of

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Acute renal failure Induction of general anaesthesia

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Hypotension, (multiple refs) Ref1 Ref2 Ref3 Ref4 Ref5

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ABOUT THE SIMPSON HANDBOOK OF OBSTETRIC ANAESTHESIA

LEGAL MATTERS AND DISCLAIMER

A.S. BUCHAN, G.H. SHARWOOD-SMITH December 1999

ABOUT THE TECHNOLOGY OF THIS PUBLICATION

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1 PHYSIOLOGICAL CHANGES IN PREGNANCY

Blood and circulatory changes

BLOOD AND CIRCULATORY CHANGES

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Significance to the anaesthetist

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Uterine blood flow = (uterine arterial pressure - uterine venous pressure)

Likely causes of reduced uterine blood flow are -

Hypotension:- aortocaval compression, blood loss, sympathetic block

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Ventilation and blood gases during pregnancy

Table 1.1 Ventilatory data for pregnancy and labour.

Significance to the anaesthetist

Materno-fetal respiratory gas exchange

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Other important factors in delivery of oxygen to the fetal tissues are:

Significance to the anaesthetist

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Significance to the anaesthetist

Table 1.2 Pregnant and non pregnant parameters of renal function

Investigation Pregnant Non Pregnant

Significance to the anaesthetist

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Prolonged labour - causing maternal metabolic acidosis

Maternal hyperventilation - leading to:

increased maternal oxygen consumption

Fig 2.1 Pain pathways during labour and delivery

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SYSTEMIC OPIOID ANALGESIA

Table 2.1 Doses used for intravenous PCA in labour

Pethidine Fentanyl Remifentanil

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PARACERVICAL BLOCK (T10 - L1)

Fig 2.2 Paracervical block

PUDENDAL BLOCK (S234)

Fig 2.3 Pudendal block

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perforating branch of the posterior cutaneous nerve of thigh.

Pain relief (analgesia)

Obstetric procedures (anaesthesia)

Cervical suture (T10 - S5)

Rapid onset and predictable spread of block

Hypotension with high block

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Spread of spinal solutions

Fig.2.4 Spinal curves

Spinal solutions available

Continuous spinal analgesia