Obstetric Anaesthesia and Analgesia
The obstetric anaesthetist is involved in the care of the parturient as part of a multidisciplinary team, including obstetricians, midwives, health visitors, physicians and intensive care specialists. There are few other areas of anaesthetic practice where communication skills and good record-keeping are so important. Successive reports from the triennial confidential enquiries into maternal mortality currently conducted by the National Perinatal Epidemiology Unit (NPEU), and formerly by the Centre for Maternal and Child Enquiries (CMACE) have highlighted the problems of women with intercurrent medical disease and the importance of the obstetric anaesthetist in their care. This has led to the establishment of obstetric anaesthetic assessment clinics in many hospitals (an Obstetric Anaesthetists’ Association (OAA) survey found that 30% of units in the UK had such clinics in 2005). The education of colleagues, patients and the public about the role of obstetric anaesthetists is essential so that patients are fully informed and hence feel more comfortable about consenting to regional anaesthetic and analgesic techniques when these may be indicated. Information leaflets produced by the OAA on analgesia in labour and caesarean section are available in up to 37 languages.
Many anaesthetists in training approach their obstetric module with trepidation for several possible reasons. All anaesthetists have heard that mothers may die, albeit rarely, as a result of general anaesthesia and that these were previously healthy young women. In addition, they may be aware of the challenge of performing a regional block under the scrutiny of a partner in patients who are awake.
The UK Royal College of Anaesthetists (RCoA) curriculum for anaesthetists in training for obstetric anaesthesia is divided into basic, intermediate, higher and advanced levels. The first three are essential in order to achieve the CCT (Certificate of Completion of Training). An initial assessment of competence in obstetric anaesthesia must also be completed to pass the basic level. Training programmes in other countries have similar objectives.
The basic obstetric module requires the trainee to gain knowledge, skills and experience of the treatment of healthy pregnant women and of the management of common obstetric emergencies. The contents of this chapter are mapped to the RCoA basic curriculum.
An understanding of the physiological changes induced by pregnancy is vital to the clinician involved in the care of pregnant women. The obstetric anaesthetist must understand maternal adaptation to pregnancy in order to manipulate physiological changes following general anaesthesia or regional analgesia and anaesthesia in such a way that the condition of the neonate at delivery is optimized.
The physiological changes of pregnancy are exaggerated in multiple pregnancy. The success of assisted conception means that obstetric anaesthetists now care for more women with twins, triplets and quadruplets.
The hormone progesterone may be considered the most important physiological substance in pregnancy. It is secreted initially in increasing amounts during the second half of the menstrual cycle to prepare the woman for pregnancy. Following conception, the corpus luteum ensures adequate blood concentrations until placental secretion is adequate. The most important physiological role of progesterone is its ability to relax smooth muscle. All other physiological changes stem from this pivotal function (Fig. 35.1).
FIGURE 35.1 Summary of the main actions of progesterone – it establishes the maternal physiological adaptation to pregnancy. PaCO2, arterial carbon dioxide tension; ODC, oxyhaemoglobin dissociation curve; P50, partial pressure of oxygen when haemoglobin is 50% saturated at pH 7.4 and temperature 37°C; bicarbonate.
Blood volume increases from 65–70 to 80–85 mL kg–1 mainly by expansion of plasma volume, which starts shortly after conception and implantation and is maximal at 30–32 weeks (Fig. 35.2). Red cell volume increases linearly but not as much as plasma volume (Table 35.1). Thus, the haematocrit decreases, causing the ‘physiological anaemia’ of pregnancy.
|Haemoglobin||14 g dL–1||12 g dL–1|
|Red cell count||4.2 × 1012 L–1||3.8 × 1012 L–1|
|White cell count||6.0 × 109 L–1||9.0 × 109 L–1|
|Erythrocyte sedimentation rate||10||58–68|
|Platelets||150–400 × 109 L–1||120–400 × 109 L–1|
The increase in blood volume is accompanied by an increase in cardiac output (Fig. 35.3) within the first 10–12 weeks by approximately 1.5 L min–1. By the third trimester, cardiac output has increased by about 40–50% as a result of significant increases in heart rate and stroke volume (Table 35.2). In labour, cardiac output may increase by a further 45%.
|Systolic blood pressure||Decreased||10–15% 2nd trimester|
|Diastolic blood pressure||Decreased|
|Cardiac output||Increased||40–50% by 3rd trimester|
|Systemic vascular resistance||Decreased||20%|
|Central venous pressure||Unchanged|
|Pulmonary vascular resistance||Decreased||30%|
|Pulmonary capillary wedge pressure||Unchanged|
In normal pregnancy, despite the increased blood volume and hyperdynamic circulation, the pulmonary capillary wedge pressure (PCWP) and central venous pressure do not increase, because of the relaxant effect of progesterone on the smooth muscle of arterioles and veins, and dilatation of the left ventricle. Significant decreases in systemic and pulmonary vascular resistance permit the increased blood volume to be accommodated at normal vascular pressures.
Pregnant women who lie supine may suffer from aortocaval compression. Arterial pressure decreases because the gravid uterus compresses the inferior vena cava to reduce venous return and therefore cardiac output. The aorta is also frequently compressed, so that femoral arterial pressure may be lower than brachial arterial pressure; this has been demonstrated to be the main cause of a reduction in uterine blood flow. Compensation for aortocaval compression occurs through sympathetic stimulation and collateral venous return via the vertebral plexus and azygous veins. The effect of aortocaval compression varies from asymptomatic mild hypotension to cardiovascular collapse and is usually prevented/relieved by left tilt/wedging although complete lateral position is required in some cases.
There is a considerable increase in blood flow to the skin, resulting in warm, clammy hands and feet. The purpose of this vasodilatation, together with that in the nasal mucosa, is to dissipate heat from the metabolically active fetoplacental unit.
Respiratory function undergoes several important modifications (Table 35.3), also as a result of the actions of progesterone. The larger airways dilate and airway resistance decreases. There are increases in tidal volume (from 10 to 12 weeks’ gestation) and minute volume (by up to 50%). Progesterone exerts a stimulant action on the respiratory centre and carotid body receptors.
|Tidal volume ↑||450 mL||650 mL|
|Respiratory rate||16 min–1||16 min–1|
|Vital capacity||3200 mL||3200 mL|
|Inspiratory reserve volume||2050 mL||2050 mL|
|Expiratory reserve volume ↓||700 mL||500 mL|
|Functional residual capacity ↓||1600 mL||1300 mL|
|Residual volume ↓||1000 mL||800 mL|
|PaO2 slight ↑||11.3 kPa||12.3 kPa|
|PaCO2 ↓||4.7–5.3 kPa||4 kPa|
|pH slightly ↑||7.40||7.44|
Alveolar hyperventilation leads to a low arterial carbon dioxide tension (PaCO2) during the second and third trimesters. By the 12th week of pregnancy, PaCO2 may be as low as 4.1 kPa (PaCO2 gradually decreases during the premenstrual phase of the menstrual cycle). The respiratory alkalosis is accompanied by a decrease in plasma bicarbonate concentration resulting from renal excretion (base excess decreases from 0 to ‒3.5 mmol L–1). Arterial pH does not change significantly. The oxyhaemoglobin dissociation curve is shifted to the right because the increase in red cell 2,3-diphosphoglycerate (2,3-DPG) concentration outweighs the effects of a low PCO2, which would normally shift the curve to the left. The P50 increases from about 3.5 to 4.0 kPa. The oxyhaemoglobin dissociation curve (ODC) of HbF is to the left of that for HbA. The loading–unloading advantages of HbF are at low oxygen tensions. Placental exchange of oxygen is regulated mainly by a change in oxygen affinities of HbA and HbF caused principally by altered hydrogen ion and carbon dioxide concentrations on both sides of the placenta.
The functional residual capacity (FRC) and residual volume are reduced at term because of the enlarged uterus (Table 35.3). This substantial reduction, combined with the increase in tidal volume, results in large volumes of inspired air mixing with a smaller volume of air in the lungs. The composition of alveolar gas may be altered with unusual rapidity and alveolar and arterial hypoxia develop more quickly than normal during apnoea or airway obstruction. In normal pregnancy, closing volume does not intrude into tidal volume.
Oxygen consumption (Vo2) increases gradually from 200 to 250 mL min–1 at term (up to 500 mL min–1 in labour). Carbon dioxide production parallels oxygen consumption. In the intervillous space, the diffusion gradient for oxygen is approximately 4.0 kPa, and for carbon dioxide is approximately 1.3 kPa.
The incidence of failed intubation in term parturients is approximately 1 in 300 cases, compared with 1 in 2200 in the non-pregnant population. This is caused in part by changes in pregnancy which affect the airway (Table 35.4). These factors increase the difficulty in seeing the larynx and increase the rate at which hypoxaemia develops in an apnoeic patient.
Interstitial oedema of the upper airway, especially in pre-eclampsia
Enlarged tongue and epiglottis
Enlarged, heavy breasts which may impede laryngoscope introduction
Increased oxygen consumption
Restricted diaphragmatic movement, reducing FRC
These changes are shown in Table 35.5. Renal blood flow is increased (Fig. 35.3). By 10–12 weeks, glomerular filtration rate (GFR) has increased by 50% and remains at that level until delivery. Glycosuria often occurs because of decreased tubular reabsorption and the increased load. The renal pelvis, calyces and ureters dilate as a result of the action of progesterone and intermittent obstruction from the uterus, especially on the right.
|Urea (mmol L− 1)||2.5–6.7||2.3–4.3|
|Creatinine (μmol L− 1)||70–150||50–75|
|Urate (μmol L− 1)||200–350||150–350|
|Bicarbonate (mmol L− 1)||22–26||18–26|
|24 hour creatinine clearance||Increased|
A reduction in lower oesophageal sphincter pressure occurs before the enlarging uterus exerts its mechanical effects (an increase in intragastric pressure and a decrease in the gastro-oesophageal angle). These mechanical effects are greater when there is multiple pregnancy, hydramnios or morbid obesity. A history of heartburn denotes a lax gastro-oesophageal sphincter.
Placental gastrin increases gastric acidity. Together with the sphincter pressure changes, this makes regurgitation and inhalation of acid gastric contents more likely to cause pneumonitis in pregnancy.
Gastrointestinal motility decreases but gastric emptying is not delayed during pregnancy. However, it is delayed during labour but returns to normal by 18 h after delivery. Thus women are at risk of regurgitation of gastric contents during this time. Pain, anxiety and systemic opioids (including epidural and subarachnoid administration of opioids) aggravate gastric stasis. Small and large intestinal transit times are increased in pregnancy and may result in constipation.
|Parameter||Change in Pregnancy|
|Alkaline phosphatase||Increased (from placenta)|
Haemoglobin concentration decreases from 14 to 12 g dL–1 (Table 35.1). Cell-mediated immunity is depressed. There is an increase in platelet production but the platelet count falls because of increased activity and consumption. Platelet function remains normal. Haematological changes return to normal by the sixth day after delivery.
Fibrinogen increased from 2.5 (non-pregnant value) to 4.6–6.0 g L–1
Factor II slightly increased
Factor V slightly increased
Factor VII increased 10-fold
Factor VIII increased – twice non-pregnant state
Factor IX increased
Factor X increased
Factor XI decreased 60–70%
Factor XII increased 30–40%
Factor XIII decreased 40–50%
Antithrombin IIIa decreased slightly
Plasminogen activator reduced
Plasminogen inhibitor increased
Fibrinogen-stabilizing factor falls gradually to 50% of non-pregnant value
There is an increase in the majority of clotting factors, a decrease in the quantity of natural anticoagulants and a reduction in fibrinolytic activity. Fibrinolysis decreases due to decreased tissue plasminogen activator (t-PA) activity because of inhibitors produced by the placenta.
Despite these changes, bleeding time, prothrombin time and partial thromboplastin time remain within normal limits. Thromboelastography may be useful to assess platelet function and clot stability but its use in pregnancy is unproven.
The increase in clotting activity is greatest at the time of delivery, with placental expulsion releasing thromboplastic substances. These substances stimulate clot formation to stop maternal blood loss. Coagulation and fibrinolysis generally return to pre-pregnant levels 3–4 weeks postpartum.
The epidural space is the space between the periosteal lining of the vertebral canal and the spinal dura mater. It contains spinal nerve roots, lymphatics, blood vessels and a variable amount of fat (Figs 35.4, 35.5). Its boundaries are as follows:
In the normal adult, the spinal cord begins at the foramen magnum and normally ends at the level of L1 or L2 (though it may end lower); here it becomes the cauda equina. The epidural space is a tube containing the spinal cord, the cerebrospinal fluid (CSF) and the meninges. It is crossed by 32 spinal nerves, each with a dural cuff. The subarachnoid space extends further than the cord, to the level of S2. Below this level, the dura blends with the periosteum of the coccyx. Between the dura and arachnoid is the subdural space, within which local anaesthetic solution may spread extensively.
In pregnancy, the epidural veins are dilated by the action of progesterone. These valveless veins of Batson form collaterals and become engorged as a result of aortocaval compression, during a uterine contraction or secondary to raised intrathoracic or intra-abdominal pressure, e.g. coughing, sneezing or expulsive efforts of parturition. The dose of local anaesthetic for epidural analgesia or epidural/subarachnoid anaesthesia is reduced by about one-third for the following reasons:
Pregnancy itself produces antinociceptive effects. The onset of nerve block is more rapid, and human peripheral nerves have been shown to be more sensitive to lidocaine during pregnancy. Increased plasma and CSF progesterone concentrations may contribute towards the reduced excitability of the nervous system.
During contractions, the pressure in the epidural space may increase by 0.2–0.8 kPa and become very high (2.0–5.9 kPa) in the second stage of labour. Because the spread of local anaesthetic is exaggerated during contractions, top-ups should not be administered at that time.
The CSF pressure increases from about 2.2 to 3.8 kPa during contractions and to 6.9 kPa in the second stage. It is therefore advised not to advance an epidural needle or insert an epidural catheter during contractions due to the increased risk of dural puncture.
Even if precautions are taken to prevent it, intermittent aortocaval compression always occurs in association with maternal movement. Consequently, the epidural veins become intermittently and unpredictably engorged.
The afferent nerve supply of the uterus and cervix is via Aδ and C fibres which accompany the thoracolumbar and sacral sympathetic outflows. The pain of the first stage of labour is referred to the spinal cord segments associated with the uterus and the cervix, namely T10–T12 and L1. Pain of distension of the birth canal and perineum is conveyed via S2–S4 nerves (Fig. 35.6). When anaesthesia is required for caesarean section, all the layers between the skin and the uterus must be anaesthetized. It is important to remember that the most sensitive layer is the peritoneum, and therefore the block should extend up to at least T4 and also include the sacral roots (S1–S5) to cold and T5 to touch.
The placenta is both a barrier and link between the fetal and maternal circulations. It consists of both maternal and fetal tissue – the basal and chorionic plates, separated by the intervillous space.
The two circulations are separated by two layers of cells – the cytotrophoblast and the syncytiotrophoblast. Fetal well-being depends on placental blood flow. Placental blood flow depends on the perfusion pressure across the intervillous space and the resistance of the spiral arteries. The spiral and uterine arteries possess α-adrenergic receptors. Placental perfusion is reduced by a reduction in cardiac output (e.g. haemorrhage) or uterine hypertonicity (e.g. overstimulation with syntocinon)
Hormone Production: Human chorionic gonadotrophin (hCG) is secreted by placental syncytiotrophoblasts and production commences very early in pregnancy and peaks at 8–10 weeks. Its role is to stimulate the corpus luteum to secrete progesterone. hCG levels increase again near term gestation but its role in late pregnancy is unclear.
Placental Transfer of Drugs: The barrier between maternal and fetal blood is a single layer of chorion united with fetal endothelium. The surface area of this is vastly increased by the presence of microvilli. Placental transfer of drugs occurs, therefore, by passive diffusion through cell membranes which are lipophilic. However, this membrane appears to be punctuated by channels which allow transfer of hydrophilic molecules at a rate that is around 100 000 times lower.
Drugs cross the placenta by simple diffusion of unionized lipophilic molecules. Fick’s law of diffusion applies. The rate is directly proportional to the materno-fetal concentration gradient and the area of the placenta available for transfer, and inversely proportional to placental thickness.
Materno-Fetal Concentration Gradient: Drug transfer occurs down a concentration gradient in either direction. The maternal drug concentration depends on the route of administration, dose, volume of distribution, drug clearance and metabolism. The highest concentration is achieved after intravenous administration, although epidural and intramuscular administration result in similar concentrations. Fetal drug concentration depends on the usual factors of redistribution, metabolism and excretion. The fetus eliminates drugs less effectively due to immature enzyme systems. The distribution differs because of the anatomical and physiological organization of the fetal circulation; for example, drugs accumulate in the liver because of the umbilical venous flow to the liver and are metabolized before distribution. The relatively high extracellular fluid volume explains the large volumes of distribution of local anaesthetics and muscle relaxants.
Molecular Weight and Lipid Solubility: The placental membrane is freely permeable to lipid-soluble substances, which undergo flow-dependent transfer. The majority of anaesthetic drugs are small (molecular weights of less than 500 Da) and lipid-soluble and so cross the placenta readily. The main exceptions are the neuromuscular blocking drugs.
Protein Binding: A dynamic equilibrium exists between bound (unavailable) and unbound (available) drug. Reduced albumin concentration increases the proportion of unbound drug. Many basic drugs are bound to α1-glycoprotein, which is present in much lower concentrations in the fetus than in the adult.
Degree of Ionization: The placental membrane carries an electrical charge; ionized molecules with the same charge are repelled, while those with the opposite charge are retained within the membrane. The rate of this permeability-dependent transfer is inversely proportional to molecular size. Size limitation for polar substances begins at molecular weights between 50 and 100 Da. Ions diffuse much more slowly. Factors affecting the degree of ionization alter the rate of transfer.
Maternal and Fetal pH: Changes in maternal or fetal pH alter the degree of ionization and protein binding of a drug, and thus its availability for transfer. This has most significance if the pKa is close to physiological pH (local anaesthetics), and is clinically relevant in the acidotic fetus. Fetal acidosis increases the ionization of the transferred drug, which is then unable to equilibrate with the maternal circulation, resulting in accumulation of the drug. This is known as ion trapping.
Drugs may have a harmful effect on the fetus at any time during pregnancy. In the early stages of pregnancy (at a stage when the woman may be unaware that she is pregnant), the conceptus is a rapidly dividing group of cells and the effect of drugs at that stage tends to be an all-or-nothing phenomenon, either slowing cell division if no harm is done or causing death of the embryo. Drugs may produce congenital malformations (teratogenesis), and the period of greatest risk is from weeks 3 to 11. In the second and third trimesters, drugs may affect the functional development of the fetus or have toxic effects on fetal tissues. Drugs given in labour or near delivery may adversely affect the neonate after delivery. Hence, drugs should be prescribed in pregnancy only if the perceived benefit of the therapy to the mother outweighs the possible detrimental effects on the fetus.
In many studies, the ratio of maternal vein to umbilical vein concentration is used; this indicates the situation at delivery only and gives little information about the effects or distribution of the drug in the neonate.
Neuromuscular blocking drugs, which are quaternary ammonium compounds and ionized fully, cross the placenta very slowly. Only prolonged administration of a muscle relaxant, e.g. in the intensive care unit, might lead to neonatal paralysis. Bolus doses of succinylcholine are safe.
Thiopental is highly lipid-soluble, weakly acidic, 75% protein-bound and less than 50% ionized at physiological pH. It therefore crosses the placenta rapidly, with umbilical vein concentration closely following the relatively rapid decrease in maternal blood concentration. Fetal plasma concentration continues to increase for around 40 min after single exposure. However, because of the relatively large fetal volume of distribution, fetal and neonatal tissue concentrations are lower than maternal. The maintenance of high maternal thiopental concentration by repeated boluses maintains a high diffusion gradient, producing prolonged placental transfer and neonatal sedation. Doses of thiopental greater than 8 mg kg–1 produce neonatal depression, whereas doses of less than 4 mg kg–1 produce no significant neonatal effects provided that the induction to delivery time is less than 5 min. Thiopental in such doses does not affect Apgar score or umbilical cord gas tensions, but may produce subtle changes in the neuroadaptive capacity score (NACS), such as reduction in muscular tone, decreased excitability and a predominant sleep state in the first day of life. A dose of thiopental of 4–7 mg kg–1 is commonly advocated for induction of general anaesthesia because it ensures unconsciousness. Widespread clinical use testifies to the safety of thiopental.
Propofol is highly protein-bound, neutral and lipophilic. Propofol has been used for both induction and maintenance of anaesthesia for caesarean section. There is conflicting evidence concerning the effects of propofol on the neonate. Clearly, if propofol is administered by infusion and uterine blood concentrations are maintained, a high diffusion gradient is maintained across the placenta and there is persistently high transfer of propofol. Induction doses as low as 2–3 mg kg–1 and maintenance doses as low as 5 mg kg–1 h–1 have been shown to cause significant neonatal depression. Neonatal elimination of propofol is slower than that in adults. Unless thiopental is contraindicated, there seems little advantage in using propofol for caesarean section.
Diazepam should be avoided, if possible. It is a non-polar compound which is bound to albumin, but the feto-maternal ratio may reach 2. The neonate may suffer from respiratory depression, hypotonia, poor thermoregulation and raised bilirubin concentrations.
Opioids are mainly weak bases bound to α1-glycoprotein. Pethidine and its metabolite norpethidine depress all aspects of neurobehaviour in the neonate. Feto-maternal ratios increase to exceed 1 after 2–4 h. Neonatal elimination is slow, resulting in prolongation of the effects. Transfer of pethidine is increased in the presence of fetal acidosis. Depressant effects are maximum if administration to delivery time is 2–3 h. Fentanyl is highly lipid-soluble and albumin-bound, and rapidly crosses the placenta. Apgar scores are low after administration of intravenous fentanyl. Epidural administration of fentanyl in doses of less than 200 μg is not associated with any adverse effect on the fetus. Alfentanil is less lipophilic but more protein-bound to α1-glycoprotein. Feto-maternal ratios are low and at caesarean section are more related to feto-maternal α1-glycoprotein concentration. Theoretically, Apgar and neuro-behavioural scores should be less affected.
Remifentanil crosses the placenta readily but appears to have few adverse effects on the fetus/neonate because it is rapidly metabolized. It can be used for patient-controlled analgesia (PCA) in labour (see below).
Women are encouraged to breastfeed. Oestrogen and progesterone stimulate mammary development during pregnancy. These hormones inhibit prolactin. This inhibition ceases at delivery. Suckling triggers lactation and stimulates the release of more prolactin and oxytocin, both of which promote production of milk.
Many women wish to suckle their infant immediately after delivery and are encouraged to do so. The anaesthetist should know, therefore, if the drugs used for obstetric anaesthesia and analgesia are secreted in the milk and, if so, whether they are likely to have an adverse effect either on the process of lactation itself or on the neonate.
The effects of a drug administered to the mother on a breastfeeding neonate are determined by peak plasma concentration of the drug, its transfer into milk, composition of milk, volume ingested, metabolism (including first-pass metabolism by the neonate), pharmacokinetics and action in the neonate. Many studies have relied on assessment of concentration of drug in milk with little consideration of resultant neonatal plasma concentration and the changing composition of breast milk. Human breast milk consists of an isosmotic emulsion of fat in water, with lactose and protein in the aqueous phase. However, its composition varies with time. Colostrum (first milk) contains abundant protein and lactose but no fat. It has a high pH and specific gravity. Over the following 7–10 days, milk has less protein, less lactose and more fat. Colostrum is more likely to be contaminated by water-soluble drugs, whereas lipid-soluble drugs are secreted into mature milk. The volume of colostrum produced is around 10–120 mL, in contrast to ingestion of mature milk by the neonate of 130–180 mL kg–1day–1 (600–1000 mL day–1). Even in mature milk, there is a significant diurnal variation in composition.
The physicochemical properties of a drug which determine transfer into the milk are pKa, the partition coefficient, degree of ionization and molecular weight. The pH of mature human milk is 7.09. Therefore, weak acids are less easily transferred than weak bases.
The total amount of drug contained in the milk depends on binding to milk protein, partition into milk lipid and the quantity which remains unbound in the aqueous phase, e.g. lipid-soluble drugs such as diazepam are concentrated in milk lipid. The dose of drug delivered to the neonate from the milk varies with the volume ingested. The higher gastric pH, different gastrointestinal flora and slow gastrointestinal transit of the neonate influence drug absorption.
The pharmacokinetics of drugs in the neonate may differ markedly from those in adults. Lipophilic and acidic drugs are bound to albumin and may displace unconjugated bilirubin. Metabolic and excretory pathways are immature so elimination may be delayed.
Opioids. Morphine appears safe with conventional administration. PCA may increase maternal plasma concentration. It is transferred readily to breast milk but does not appear to cause neonatal depression, possibly because of first-pass metabolism. Codeine and dihydrocodeine are metabolized to morphine and are not usually associated with neonatal depression. Pethidine is associated with neurobehavioural depression of the neonate. Short-acting opioids such as fentanyl and alfentanil are safe, even by continuous epidural infusion.
Non-steroidal anti-inflammatory drugs. The non-steroidal anti-inflammatory drugs (NSAIDs) ketorolac and diclofenac are safe. The neonate has immature biotransformation and excretory pathways. Aspirin should be avoided because high concentrations have been observed following a single oral dose. Neonates may be at risk of developing Reye’s syndrome.
Syntocinon is a synthetic analogue of the posterior pituitary hormone oxytocin, which is responsible for effective uterine muscle contraction. It is used during labour to augment progress, at delivery to aid placental delivery and closure of uterine vasculature and in the postpartum period to reduce postpartum haemorrhage. For augmentation or induction of labour, Syntocinon is usually administered via a syringe or volumetric pump using an increasing dose. The usual dose at delivery is 5 international units (IU), and 40 IU may be infused over 4 h to maintain myometrial contraction and reduce bleeding.
Syntocinon may cause vasodilatation and tachycardia and so should be administered cautiously in the presence of hypovolaemia and in patients with significant cardiac disease. Syntocinon also has an antidiuretic hormone effect, so care should be taken if infused in dilute dextrose solution, as hyponatraemia may occur.
Carbetocin is a long-acting oxytocin analogue which can be given as a single dose to prevent postpartum haemorrhage as an alternative to an infusion of Syntocinon. The optimal dose is probably 100 μg intravenously at caesarean section. It has a plasma half-life between four and ten times that of Syntocinon.
Ergometrine is also given to stimulate uterine contraction, usually in a dose of 500 μg. Ergometrine causes peripheral vasoconstriction, which may be severe, leading to hypertension and pulmonary oedema; thus it should be avoided in women with hypertensive disease. It can cause nausea and vomiting as a result of its action on other types of smooth muscle and it is usually reserved for more severe cases of uterine atony.
Syntometrine is a combination of ergometrine 500 μg and Syntocinon 5 units. Until recently, it was administered routinely by intramuscular injection at the delivery of the anterior shoulder to assist in placental separation and to reduce postpartum haemorrhage; however, Syntocinon alone is now favoured because of its reduced side-effect profile.
Prostaglandins are a group of endogenous short polypeptides with a wide diversity of physiological functions. Prostaglandins are commonly used to ‘ripen’ the cervix on induction of labour but may cause bronchospasm and hypertension.
Carboprost is prostaglandin F2α. It has an important role in the treatment of severe uterine atony unresponsive to Syntocinon or ergometrine. It is administered intramuscularly (250 μg). It should not be given intravenously or intramyometrially. It may induce bronchospasm and hypertension and should be avoided in asthmatics.
Misoprostol is a prostaglandin E1 analogue. It may be used to induce labour and is given vaginally. It may be given as third or fourth line treatment of postpartum haemorrhage (600 μg p.r.). It produces pyrexia, shivering, nausea and vomiting, and diarrhoea.
Mifepristone is a prostaglandin antagonist which causes luteolysis and trophoblastic separation. It is given orally with prostaglandins to induce labour after intrauterine death of the fetus and when labour is induced for a non-viable fetus. It is associated with headache, dizziness and gastrointestinal upset.
These act on uterine β2-receptors causing relaxation of the myometrium. They can be given orally, subcutaneously or by intravenous infusion for premature labour. The effects should be monitored carefully because severe tachycardia, hypotension, pulmonary oedema, hypokalaemia, and hyperglycaemia may occur.
GTN acts directly on uterine smooth muscle and can be given intravenously (50 μg) or sublingually (200–400 μg) to produce rapid but short-term uterine relaxation. It can be used as part of intrauterine resuscitation, or in cases of uterine hypertonicity, retained placenta and uterine inversion. It causes hypotension and headache.
Initially, the cervix effaces (i.e. becomes thin along its vertical axis and soft in consistency) and then cervical dilatation begins. The rate of cervical dilatation should be about 1 cm h–1 for a nulliparous woman and 2 cm h–1 for a multiparous woman. It is standard practice to examine the woman every 4 h, or more frequently if there is cause for concern. Routine observations are made as per National Institute of Clinical Excellence (NICE) guidelines and these are charted on the partogram (see Fig. 35.7):
The fetal heart may be monitored intermittently by auscultation using a Pinard stethoscope or Doppler ultrasound. Continuous electronic fetal monitoring (EFM) can be performed using a cardiotocograph (CTG). The fetal heart rate may be recorded using either an abdominal transducer or a clip applied to the fetal head. Uterine contractions are also monitored using an abdominal transducer. Radiotelemetry is available in some units and this allows the woman to be mobile while her baby is monitored.
Indications for continuous EFM include insertion of an epidural, meconium-stained liquor, oxytocin for augmentation, abnormal FHR on auscultation, maternal pyrexia, fresh p.v. bleeding and maternal request.
The second stage of labour starts at full dilatation of the cervix and ends at the delivery of the baby. At full dilatation of the cervix, the character of the contractions changes and they become associated with a strong urge to push. In normal labour, Ferguson’s reflex occurs, in which there is an increase in circulating oxytocin secondary to distension of the vagina from the descending presenting part of the fetus, with consequent increased strength of uterine contractions at full dilatation. Epidural analgesia may attenuate the effect of this reflex. The second stage of labour may be classified into passive and active stages and this is particularly relevant when epidural analgesia is used. With epidural analgesia, the labouring woman does not have the normal sensation at the start of the second stage of labour produced by Ferguson’s reflex, and therefore the active stage of pushing should start only when the vertex is visible or the woman has a strong urge to push. If the active second stage is prolonged, the fetus may become acidotic. A diagnosis of delay is made after 2 h in nulliparous women and 1 h in primiparous and multiparous women.
The third stage of labour is the complete delivery of the placenta and membranes, and contraction of the uterus. It is usually managed ‘actively’ by administering an oxytocic (i.m. Syntocinon 5 IU) and early cord clamping but it may also be managed physiologically (no oxytocic and delayed cord clamping). During the third stage of labour, there is redistribution of the former placental blood flow (about 15% of cardiac output). This results in an increase in circulating blood volume which is potentially dangerous to women who have cardiac disease because it may precipitate heart failure immediately postpartum.
Recent developments have made it possible to assess fetal well-being in the antenatal period. An obstetric anaesthetist is often involved when a decision to deliver the baby early is made on the outcome of these assessments. The most commonly used tests are: