Obstetric disorders

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Chapter8

Obstetric disorders

Henry G. Murray

Hypertensive disorders of pregnancy

Hypertensive disorders remain the commonest complication of pregnancy in the developed world, and are consistently one of the three main causes of maternal death. The incidence varies substantially in different countries and is influenced by a number of factors, including parity, ethnic group and dietary intake. In the UK the condition occurs in 10–15% of all pregnancies and 4–13% of the population will develop pre-eclampsia, i.e. both hypertension and proteinuria. While most episodes of hypertension are specifically related to the pregnancy and will resolve when the pregnancy is completed, some women who suffer from other forms of hypertension, e.g. essential hypertension or that due to renal disease, will also conceive. These diseases may influence the outcome of the pregnancy and the progress of the disease may be influenced by the pregnancy.

In its mildest form, hypertension alone arising in late pregnancy appears to be of minimal risk to mother or child.

In its most severe form, the condition is associated with placental abruption, convulsions, proteinuria, severe hypertension and oedema, and may result in cerebral haemorrhage, renal and hepatic failure as well as disseminated intravascular coagulopathy. This may lead to fetal and maternal death.

The association between convulsions and pregnancy was described in ancient Greek and Egyptian writings. The first description of eclampsia, with the occurrence of convulsions, hypertension and proteinuria, was given by Vasquez in 1897.

Blood pressure is determined by cardiac output (stroke volume × heart rate) and peripheral vascular resistance. Cardiac output increases substantially in normal pregnancy, but blood pressure actually falls in the mid-trimester. Thus the most important regulatory factor is the loss of peripheral resistance that occurs in pregnancy. Without this effect, all pregnant women would presumably become hypertensive!

As sympathetic tone appears to remain unchanged, peripheral resistance is determined by the balance between humoral vasodilators and vasoconstrictors. There is a specific loss of sensitivity to angiotensin II, which is associated with locally active vasodilator prostaglandins. Thus factors that increase the activity of the renin–angiotensin system or reduce the activity of tissue prostaglandins will result in raising of the blood pressure.

In the pre-eclamptic woman there is evidence of a reduced sensitivity to infused angiotensin II associated with downregulation of vascular and platelet AII receptors, and there is evidence that platelet AII receptors are increased.

Current evidence also suggests that pre-eclampsia is a disease of endothelial dysfunction. Nitric oxide (NO) or endothelial-derived relaxing factor (EDRF) is a potent vasodilator. In pre-eclampsia, NO synthesis is reduced, possibly by the inhibition of NO synthetase activity.

A further area of consideration is the damaging effect of lipid peroxides on the endothelium. Normally, the production of antioxidants limits these effects but, in pre-eclampsia, antioxidant activity is decreased and endothelial damage occurs throughout the body resulting in fluid loss from the intravascular space. All these changes occur in the 2nd trimester long before a rise in blood pressure is measurable in the mother.

Once vasoconstriction occurs in the placental bed, it results in placental damage and the release of trophoblastic material into the peripheral circulation. This trophoblastic material is rich in thromboplastins, which precipitate variable degrees of disseminated intravascular coagulation. This process gives rise to the pathological lesions most notably in the kidney, liver and placental bed. The renal lesion results in sodium and water retention, with most of this fluid accumulated in the extracellular space. In fact, the intravascular space is reduced in severe pre-eclampsia as plasma volume diminishes. At the same time, increased sodium retention results in increased vascular sensitivity to vasoconstrictor influences, and therefore promotes further vasoconstriction and tissue damage in a vicious circle of events that may ultimately result in acute renal failure with tubular or cortical necrosis, hepatic failure with periportal necrosis, acute cardiac failure and pulmonary oedema, and even cerebral haemorrhage as blood pressure becomes uncontrolled.

As the disease progresses, the placenta becomes grossly infarcted and this results in intrauterine growth restriction, increased risk of abruption and sometimes fetal death.

Why do some women develop pre-eclampsia and others do not? Is there a genetic predisposition in some women? The answer to this question is almost certainly yes. Longitudinal studies in the US, Iceland and Scotland have shown that the daughters of women who have suffered from pre-eclampsia or eclampsia have themselves a 1 in 4 chance of developing the disease, a risk that is 2.5 times higher than in the daughters-in-law of such women. The data suggests that a single recessive maternal gene is associated with pre-eclampsia. However, the data could also support a hypothetical model of dominant inheritance with partial penetrance. Although various gene loci have been proposed, there are further long-term studies ongoing to try and identify the correct candidate gene. It is in fact unlikely that there is a single pre-eclampsia gene; it is probable that there are interactions between several genes with external environmental factors enhancing this predisposition. These factors include autoimmune conditions, diseases that increase venous and arterial thromboembolic disease (thrombophilias) and the existence of underlying chronic renal disease or essential hypertension. Dietary intake may also be a factor.

The renal lesion

The renal lesion is, histologically, the most specific feature of pre-eclampsia (Fig. 8.3). The features are:

Fig. 8.3 Renal changes in pre-eclampsia include endothelial swelling (E), apparent avascularity of the glomerulus and fibrin deposition (arrow) under the basement membrane.

• Swelling and proliferation of endothelial cells to such a point that the capillary vessels are obstructed.

• Hypertrophy and hyperplasia of the intercapillary or mesangial cells.

• Fibrillary material (profibrin) deposition on the basement membrane and between and within the endothelial cells.

The characteristic appearance is therefore one of increased capillary cellularity and reduced vascularity. The lesion is found in 71% of primigravid women who develop pre-eclampsia but in only 29% of multiparous women. There is a much higher incidence of women with chronic renal disease in multiparous women.

The glomerular lesion is always associated with proteinuria and with reduced glomerular filtration resulting in a raised serum creatinine. Decreased renal blood flow and proximal tubular changes result in impaired uric acid secretion, leading to hyperuricaemia.

Placental pathology

Placental infarcts occur in normal pregnancy but are considerably more extensive in pre-eclampsia. The characteristic features in the placenta (Fig. 8.4) include:

Fig. 8.4 Placental changes in pre-eclampsia include an increase in syncytial knots, proliferation of cytotrophoblast and thickening of trophoblastic basement membrane.

• increased syncytial knots or sprouts

• increased loss of syncytium

• proliferation of cytotrophoblast

• thickening of the trophoblastic basement membrane

• villous necrosis.

In the uteroplacental bed, the normal invasion of extravillous cytotrophoblast along the luminal surface of the maternal spiral arterioles does not occur beyond the deciduomyometrial junction and there is apparent constriction of the vessels between the radial artery and the decidual portion (Fig. 8.5). These changes result in reduced uteroplacental blood flow and results in placental hypoxia.

Fig. 8.5 Trophoblast invasion of the spiral arterioles results in dilatation of these vessels. This process is defective in pre-eclampsia.

Disseminated intravascular coagulation (DIC)

In severe pre-eclampsia and eclampsia, thrombosis can be seen in the capillary bed of many organs. Multiple platelet and fibrin thrombi can be identified in the brain. Similar changes are seen in the periportal zones of the liver and in the spleen and the adrenal cortex. Thrombocytopenia may occur in some cases, but in only 10% of eclamptic women does the platelet count fall below 100 000/mL. There is an increase in fibrin deposition and in circulating fibrin degradation products as a result of increased fibrin production and impaired fibrinolysis. There seems to be little doubt that, while these changes are not the cause of pre-eclampsia, they do play an important role in the pathology of the disease.

Other associations with pregnancy hypertension

It has been postulated that pre-eclampsia may be due to an abnormality of the fetomaternal host response. There is a lower incidence of pre-eclampsia in consanguineous marriages and an increased incidence of hypertension in first pregnancies of second marriages. Levels of human leukocyte antigen (HLA)-G are altered in pre-eclamptic women.

Indices of cell-mediated immune response have also been shown to be altered in severe pre-eclampsia. However, there are many other factors that operate independently from any potential immunological factors, such as race, climatic conditions and the genetic or familial factors. One of these includes raised free fatty acids found in pre-eclampsia and their causative role in the increased incidence of pre-eclampsia in women with diabetes and obesity.

The HELLP syndrome

A severe manifestation of pre-eclampsia occurs in a variant known as the HELLP syndrome. In this syndrome, there is a triad of manifestations that include haemolysis (H), elevated levels of liver enzymes (EL) and a low platelet count (LP). This manifestation is an extension of the DIC causing the haemolysis and low platelets, and the endothelial dysfunction/hypoxia in the liver resulting in release of liver transaminases especially the alanine aminotransferase (ALT).

The thrombocytopenia is often rapidly progressive and if left to become severe may result in haemorrhage into the brain and the liver. The syndrome demands intervention and termination of the pregnancy as soon as any acute manifestations like hypertension are controlled.

Management of gestational hypertension and pre-eclampsia

The object of management is to prevent the development of eclampsia and to minimize the risks of the condition to both the mother and the fetus. The achievement of these objectives depends on careful scrutiny of the condition of both the mother and the fetus and timely intervention to terminate the pregnancy when the risks of continuation outweigh the risks of intervention.

Blood pressure measurement

A rise in blood pressure (BP) is usually the first sign to be noted at the antenatal visit. Blood pressure should be recorded in a constant position at each visit, as it is posture-dependent. The most comfortable position is seated, with a mercury sphygmomanometer and a cuff of an appropriate size applied to the right upper arm. Automated blood pressure machines can be unreliable in measuring BP in pregnancy.

If the pressure is elevated, the measurement should be repeated after a short period of rest. If the blood pressure remains elevated, then continuing close observation is essential. This may be achieved by hospital admission if significant pre-eclampsia is suspected, a visit to a ‘day ward’ for hypertension of uncertain significance, or by careful scrutiny at home by a visiting midwife or doctor for the possibility of white coat hypertension. The woman should be advised to rest. However, although bed rest improves renal blood flow and uteroplacental flow and commonly results in a diuresis and improvement in the blood pressure, it has not been shown to improve overall outcomes in the mother or the fetus.

The development of more than 1+ proteinuria or a spot urinary/creatinine ratio of more than 30 mg/mmol is an absolute indication for hospital admission as this change constitutes the dividing line between minimal risk and significant risk to both mother and baby.

If the hypertension persists or worsens, and the mother is at or close to term the fetus should be delivered. If it is considered that the fetus would benefit from further time in utero and there is no maternal contraindication, treatment with antihypertensive drugs should be considered. It must be remembered that prolonging the pregnancy in pre-eclampsia is solely for the benefit of the fetus.

Antihypertensive drug therapy

In the presence of an acute hypertensive crisis, controlling the blood pressure is essential but, in the case of mild gestational hypertension and moderate pre-eclampsia, their role is more contentious. There is, however, convincing evidence that the treatment of mild or moderate chronic hypertension in pregnancy reduces the risk of developing severe hypertension and the need for hospital admission.

In women with gestational hypertension, treatment with antihypertensive drugs should be confined to those women who fail to respond to conservative management including stopping work if that is possible. Early treatment possibly reduces the risk of progression to proteinuric hypertension. Management is based on the principle of minimizing both maternal and fetal morbidity and mortality. Blood pressures of more the 170 mmHg systolic or 110 mmHg diastolic must be treated as a matter of urgency to lower the risk of intracerebral haemorrhage and eclampsia. Until recently it was believed that if blood pressure stays above 160/100, antihypertensive treatment is essential as there is a risk of maternal cerebral haemorrhage. Data from the UK maternal death enquiry 2011 clearly shows that treatment is warranted at levels above 150/100.

The drugs most commonly used are:

• methyldopa (oral)

• hydralazine (oral and IV)

• combined alpha- and beta-blockers such as labetalol (oral or IV)

• alpha-blocker such as prazosin (oral)

• calcium channel blockers such as nifedipine (oral).

Note: angiotensin-converting-enzyme (ACE) inhibitors are contraindicated in pregnancy.

Where acute control is required, an intravenous bolus of hydralazine 5 mg or labetalol 20 mg should be administered. Oral medications can take a variable time to control blood pressure.

Steroids: where a woman is less than 34 weeks gestation and her hypertensive disease is severe enough that early delivery is contemplated, betamethazone 11.4 mg IM, 2 doses 12–24 hours apart should be given to minimize neonatal consequences of prematurity like respiratory distress syndrome (RDS), intraventricular haemorrhage and necrotizing enterocolitis.

Maternal investigations

The most important investigations for monitoring the mother are:

• The 4-hourly measurement of blood pressure until such time that the blood pressure has returned to normal.

• Regular urine checks for proteinuria. Initially, screening is done with dipsticks or spot urinary protein/creatinine ratio but, once proteinuria is established, 24-hour urine samples should be collected. Values in excess of 0.3 g/L over 24 hours are abnormal.

• Maternal serum screening for pre-eclampsia.

Laboratory investigations

• Full blood count with particular reference to platelet count.

• Tests for renal and liver function.

• Uric acid measurements: a useful indicator of progression in the disease.

• Clotting studies where there is severe pre-eclampsia.

• Catecholamine measurements in the presence of severe hypertension, particularly where there is no proteinuria to rule out phaeochromocytoma.

Case study

Mrs F was pregnant with her first child after a long history of subfertility. She had been admitted to hospital before her pregnancy for tubal evaluation by dye laparoscopy, but at no time then or subsequently during her pregnancy had she shown any evidence of hypertension. At 32 weeks gestation, she was admitted to hospital at 10 pm with acute headache and severe hypertension, with a blood pressure reading of 220/140. There was no proteinuria and no hyper-reflexia. There was no evidence of fetal growth restriction. Despite initial attempts to control her blood pressure with hydralazine and labetalol, her hypertension remained severe and uncontrollable and she went into high-output cardiac failure and died at 7 am the following morning. Autopsy revealed a large phaeochromocytoma in the right adrenal gland.

This is an extremely rare form of hypertension in pregnancy. It has an appalling prognosis unless it is detected early. In this case it presented late. All other antenatal recordings of blood pressure had been normal. Although it would not have helped in this case, where hypertension is severe and presents antenatally it is always worth checking urinary catecholamines.

Fetoplacental investigations

Pre-eclampsia is an important cause of fetal growth restriction and prenatal death and it is therefore essential to monitor fetal wellbeing using the following methods:

• Serial ultrasounds for:

Measurements of fetal growth every 2 weeks. Parameters measured are fetal biparietal diameter, head circumference, abdominal circumference and femur length.

Measurements of liquor volume up to twice weekly.

• Doppler flow studies up to twice weekly. The use of serial Doppler waveform measurements in the fetal umbilical artery and the maternal uterine artery makes it possible to assess increasing vascular resistance and hence impairment of uteroplacental blood flow typical of pre-eclampsia. In the second trimester poor diastolic flow in the uterine artery waveform warns of an increased risk of pre-eclampsia and fetal growth restriction later in pregnancy. In the third trimester, an increase in the systolic/diastole flow ratio in the fetal umbilical artery due to a progressive diminution of flow in diastole warns of worsening placental vascular disease. Absent or reverse flow in diastole indicates severe vessel disease, probable fetal compromise and delivery of the fetus must be considered if the cardiotocography (CTG) is abnormal.

• Antenatal CTG: Used in conjunction with Doppler assessment, the measurement of fetal heart rate in relation to uterine activity provides a useful, but by no means infallible indication of fetal wellbeing. The presence of episodes of fetal deceleration and the loss of baseline variability may indicate fetal hypoxia.

A summary of the various management strategies is shown in Figure 8.6. This flow diagram shows the various pathways of progression and their management. An initial presentation of mild hypertension may get better with conservative management or it may progress rapidly to the severe forms of pre-eclampsia and ultimately eclampsia.

Fig. 8.6 Flow diagram of the management of gestational hypertension and pre-eclampsia. BP, blood pressure; CVP, central venous pressure; PCWP, pulmonary capillary wedge pressure.

Prevention of pre-eclampsia

There is no doubt that careful management and anticipation can largely prevent the occurrence of eclampsia, but preventing pre-eclampsia is much more difficult.

There is some evidence that calcium supplements may reduce the risk but only in populations that have dietary deficiency. Low dose aspirin acts as an inhibitor of cyclooxygenase activity, thromboxane synthesis and of platelet aggregation. Clinical trials show that low-dose aspirin (60–100 mg/day) has moderate benefits when used for prevention of pre-eclampsia and its consequences, especially in women where there is a history of severe early onset disease. In these women, a thrombophilia screen should be undertaken, as there is an incidence of underlying thrombotic tendencies that may also benefit from low-molecular weight heparin therapy.

Symptoms of pre-eclampsia and eclampsia

Pre-eclampsia is commonly an asymptomatic condition. However, there are symptoms that must not be overlooked and these include frontal headache, blurring of vision, sudden onset of vomiting and right epigastric pain. Of these symptoms, the most important is the development of epigastric pain – either during pregnancy or in the immediate puerperium (Fig. 8.7).

Fig. 8.7 Presenting signs of impending eclampsia.

The occurrence of epigastric pain is commonly misdiagnosed or overlooked as a feature of severe pre-eclampsia and impending eclampsia. Presenting often in the late second trimester, an erroneous diagnosis of indigestion, heartburn or gallstones is made and, unless the blood pressure is recorded and the urine checked for protein, the significance of the pain is overlooked until the woman presents with fitting.

Induction of labour

A pregnancy complicated by hypertensive disease should be terminated for maternal or fetal/placental reasons:

• maternal

gestation > 37 weeks

uncontrollable blood pressure

HELLP syndrome

– rising liver dysfunction

– falling platelets

– falling haemoglobin due to haemolysis

deteriorating renal function (creatinine > 90 mmol/L)

eclampsia

acute pulmonary oedema

• fetal/placental

fetal compromise on CTG tracing

absent or reversal of end diastolic flow in the umbilical artery

no fetal growth over more than 2 weeks

placental abruption.

If the decision has been made to proceed to delivery, the choice will rest with either the induction of labour or delivery by caesarean section. Antenatal steroids should be given for gestations of less than 34 weeks to minimize neonatal morbidity.

If the cervix is unsuitable for surgical induction (Bishop score of less than 7), it can often be ripened by the introduction of a prostaglandin E preparation into the posterior fornix or the use of a mechanical balloon catheter (Foley catheter) through the cervix.

If the cervix is ripe, labour is induced by artificial rupture of membranes and oxytocin infusion (see Chapter 11).

Complications

Complications can be grouped as follows:

• fetal

growth restriction, hypoxia, death

• maternal

severe pre-eclampsia is associated with a fall in blood flow to various vital organs. If the mother is inadequately treated/the fetus is not delivered in a timely manner, complications include renal failure (raised creatinine/oliguria/anuria), hepatic failure, intrahepatic haemorrhage, seizures, DIC, adult RDS (ARDS), cerebral infarction, heart failure

• placental

infarction, abruption.

Eclampsia

The onset of convulsions in a pregnancy complicated by pre-eclampsia denotes the onset of eclampsia. Eclampsia is a preventable condition and its occurrence often denotes a failure to recognize the early worsening signs of pre-eclampsia. Although it is more common in primigravid women, it can occur in any pregnancy during the antepartum, intrapartum or postpartum period. It carries serious risks of intrauterine death for the fetus and of maternal death from cerebral haemorrhage and renal and hepatic failure.

All cases must be managed in hospital and preferably in hospitals with appropriate intensive care facilities. Any woman admitted to hospital with convulsions during the course of pregnancy, or who is admitted in a coma associated with hypertension, should be considered to be suffering from eclampsia until proved otherwise.

Case study

Not all women admitted with fitting in pregnancy are eclamptic. Marilyn D was a single mother who was brought into an accident and emergency department by two friends with a statement that she had fitted on two occasions. She was booked for confinement at the same hospital and her antenatal records showed that her pregnancy had so far been uncomplicated. She was 34 weeks pregnant and on admission her blood pressure was 140/90. There was a trace of protein in the urine. She was brought into hospital on a Saturday night and her friends stated that they had stopped the car on the way in to hospital and laid Marilyn down on the pavement by the roadside because of the violence of her fits.

After careful assessment and normal biochemical testing, it was decided to proceed with observation and, within 24 hours, there were no further fits. Further discussion with Marilyn revealed that she had taken a mixture of illicit drugs including amphetamines: a diagnosis that was suggested by one of the medical students!

Management of eclampsia

The three basic guidelines for management of eclampsia are:

• control the fits

• control the blood pressure

• deliver the infant.

Control of fits

In the past various drugs were used to control the fits:

• Eclamptic seizures are usually self-limiting. Acute management is to ensure patient safety and protecting the airway

• Magnesium sulphate is the drug of choice for the control of fits thereafter. The drug is effective in suppressing convulsions and inhibiting muscular activity. It also reduces platelet aggregation and minimizes the effects of disseminated intravascular coagulation. Treatment is started with a bolus dose of 4 g given over 20 minutes as 20 mL of a 20% solution. Thereafter blood levels of magnesium are maintained by giving a maintenance dose of 1 g/h administered as a solution with 5 g/500 mL and run at 100 mL/h. The blood level of magnesium should only by measured if there is significant renal failure or seizures recur. The therapeutic range is 2–4 mmol/L. A level of more than 5 mmol/L causes loss of patellar reflexes and a value of more than 6 mmol/L causes respiratory depression. Magnesium sulphate can be given by intramuscular injection but the injection is often painful and sometimes leads to abscess formation. The preferred route is by intravenous administration.

It is not always possible to monitor the blood levels of magnesium. It is, however, important to avoid toxic levels of magnesium as they may result in complete respiratory arrest. Eclampsia is associated with hyper-reflexia and, on occasions, with clonus, so a guide to the levels of magnesium can be obtained by regular checks on the patellar reflexes. If patellar reflexes are absent magnesium should be stopped. In the event of the suppression of respiration, the effects can be reversed by the administration of 10 mL of 10% calcium gluconate given intravenously over 2–3 minutes.

It is important to ensure that further fits are prevented, blood pressure is well controlled, fluid balance is strictly monitored, and urine output is maintained at 0.5 to 1.0 mL/kg/h. To this end, the patient should be managed jointly with staff in an intensive care/high dependency unit. Constant nursing attendance is essential by staff accustomed to managing patients with airway problems. As a general principle, total fluid input should be restricted to 100 mL/h. If the urine flow falls to below 30 mL/h, a central venous pressure measurement should be considered. Fluid overload in these women may induce pulmonary oedema and adult respiratory distress syndrome with lethal consequences.

Control of blood pressure

It is essential to control the blood pressure to minimize the risk of maternal cerebral haemorrhage. Hydralazine is a useful drug in acute management and is given intravenously as 5 mg bolus over an interval of 5 minutes and repeated after 15 minutes if the blood pressure is not controlled. If the mother is still pregnant it is important not to drop the blood pressure below a diastolic BP of 90 mmHg in order not to compromise the uterine/placental blood flow.

An alternative is to use intravenous labetalol, starting with a bolus of 20 mg followed by further doses of 40 mg and 80 mg to a total of 200 mg.

Subsequent blood pressure control can be maintained with a continuous infusion of hydralazine at 5–40 mg/h or labetalol 20–160 mg/h.

Epidural analgesia relieves the pain of labour and also helps to control the blood pressure by causing vasodilatation in the lower extremities. It also reduces the tendency to fit by relieving pain in labour. However, it is essential to perform clotting studies before inserting an epidural catheter because of the risk of causing bleeding into the epidural space if there is a coagulopathy.

Delivery of the infant

A diagnosis of severe pre-eclampsia/eclampsia indicates that the risk to both the mother and the infant of continuing the pregnancy will exceed the risk of delivery. Where the gestation is less than 28 weeks, serious neonatal morbidity associated with prematurity and an increased risk for the requirement of a classical caesarean section necessitates that the decision to deliver includes consultation with neonatal and maternofetal medicine specialists.

It is essential to establish reasonable control of the blood pressure before embarking on any procedures to expedite delivery as the intervention itself may precipitate a hypertensive crisis.

If the cervix is sufficiently dilated to enable artificial rupture of the membranes, labour should be induced by forewater rupture and an oxytocin infusion. If this is not possible, then it is best to proceed to delivery by caesarean section, which requires early consultation with an anaesthetic colleague.

Management after delivery

The risks of eclampsia do not stop with delivery, and the management of pre-eclampsia and eclampsia continues for up to 7 days after delivery although, after 48 hours, if fitting occurs for the first time, alternative diagnoses such as epilepsy or intracranial pathology such as cortical vein thrombosis must be considered. Up to 45% of eclamptic fits occur after delivery, including 12% after 48 hours.

The following points of management should be observed:

• Maintain the patient in a quiet environment under constant observation.

• Maintain appropriate levels of sedation. If she has been treated with magnesium sulphate, continue the infusion for 24 hours after the last fit.

• Continue antihypertensive therapy until the blood pressure has returned to normal. This will usually involve transferring to oral medication and, although there is usually significant improvement after the first week, hypertension may persist for the next 6 weeks.

Case study

Mrs T was a 28-year-old primigravida and the wife of one of the junior medical staff. Her pregnancy was uneventful until 37 weeks, when she developed hypertension and was admitted to hospital for bed rest. Her blood pressure stayed around 140/90 and there was a trace of protein in the urine. At 38 weeks gestation, labour was induced and she had a normal delivery of a healthy male infant. The following day she was fully mobile but complained to the midwifery staff that she had a frontal headache and indigestion, with epigastric discomfort. She was given aspirin and an antacid but the symptoms persisted. Her hypertension also persisted and later that day she fitted. Unfortunately, she fell against the side of her bed and fractured her zygoma. Although she had not fitted before delivery, it is important to remember that such symptoms in a pre-eclamptic woman are as significant after delivery as they are antenatally.

• Strict fluid balance charts should be kept and blood pressure and urine output observed on an hourly basis. Biochemical and haematological indices should be made on a daily basis until the values have stabilized or started to return to normal.

Although most mothers who have suffered from pre-eclampsia or eclampsia will completely recover and return to normal, it is important to review all such women at 6 weeks after delivery. If the hypertension or proteinuria persist at this stage, then they should be investigated for other factors such as underlying renal disease. Women should also be investigated for the possibility of an autoimmune, thrombophilic or antiphospholipid cause of her disease.

Antepartum haemorrhage

The definition of antepartum haemorrhage varies from country to country. The WHO definition, accepted by many countries including the UK, is haemorrhage from the vagina after the 24th week of gestation. In other countries, including Australia, the defined gestation is 20 weeks, however a few use 28 weeks. The factors that cause antepartum haemorrhage may be present before 20 weeks, but the distinction between a threatened miscarriage and an antepartum haemorrhage is based on whether the fetus is considered potentially viabile. Antepartum bleeding remains a significant cause of perinatal and maternal morbidity and mortality.

Vaginal bleeding may be due to:

• Haemorrhage from the placental site and uterus: placenta praevia, placental abruption, uterine rupture.

• Lesions of the lower genital tract: heavy show/onset of labour (bleed from cervical epithelium), cervical ectropion/carcinoma, cervicitis, polyps, vulval varices, trauma, infection.

• Bleeding from fetal vessels, including vasa praevia.

The rate of antepartum haemorrhage is generally increased in women who smoke or who are from the lower socioeconomic classes. The rate therefore varies from 2–5% depending upon the population studied. For any woman admitted with bleeding, the cause is often not immediately obvious. In any large obstetric unit the diagnoses after admission are approximately:

• unclassified/uncertain cause 50%

• placenta praevia 30%

• placental abruption 20%

• vasa praevia (rare).

Placenta praevia

The placenta is said to be praevia when all or part of the placenta implants in the lower uterine segment and therefore lies beside or in front of the presenting part (Fig. 8.8).

Incidence

Approximately 1% of all pregnancies are complicated by clinical evidence of a placenta praevia. Unlike the incidence of placental abruption, which varies according to social and nutritional factors, the incidence of placenta praevia is remarkably constant.

Placenta praevia is more common in multiparous women, in the presence of multiple pregnancy and where there has been a previous caesarean section.

Aetiology

Placenta praevia is due to delay in implantation of the blastocyst so that this occurs in the lower part of the uterus.

Classification

Placenta praevia is diagnosed using ultrasound. Given that the lower segment forms at 26–28 weeks of pregnancy, a diagnosis of placenta praevia cannot be made before that gestation. If a placenta is detected to be within 2 cm of the cervix before 26 weeks it is called ‘low lying’, with 95% of such placentas ending well clear of the cervix after the lower segment develops.

There are numerous classifications of placenta praevia. The classification that affords the best anatomical description and clinical information is based on grades. Grade I being defined by the placenta encroaching on the lower segment but not on the internal cervical os; grade II when the placenta reaches the internal os; grade III when the placenta is covering the cervical os with some placental tissue also being in the upper segment; and grade IV when all the placenta is in the lower segment with the central portion close to the cervical os (see Fig. 8.8). Women with a grade I or grade II placenta on the anterior wall of the uterus will commonly achieve a normal vaginal delivery without excess blood loss. A posterior grade II placenta praevia where the placental mass in front of the maternal sacrum prevents the descent of the fetal head into the pelvis, along with a grade III and IV placenta praevia will require delivery by caesarean section, either urgently if labour or significant bleeding commences preterm, or electively at term.

Bleeding in placenta praevia results from separation of the placenta as the formation of the lower segment occurs and the cervix effaces. This blood loss occurs from the venous sinuses in the wall of the uterine lower segment. Very occasionally, fetal blood loss may occur at the time of maternal bleeding, if the placenta is disrupted. This will result in anomalies on the CTG record, so close fetal monitoring must be undertaken during any bleeding.

Symptoms and signs

The main symptom of placenta praevia is painless vaginal bleeding. There may sometimes be lower abdominal discomfort where there are minor degrees of associated placental separation (abruption).

The signs of placenta praevia are:

• vaginal bleeding

• malpresentation of the fetus

• normal uterine tone.

The bleeding is unpredictable and may vary from minor – common with the initial bleed – to massive and life-endangering haemorrhage.

Case study

Jane T was admitted to hospital at 28 weeks gestation with a painless vaginal haemorrhage of approximately 100 mL in her first pregnancy. The presenting part was high, but central and the uterine tone was soft. A diagnosis of a grade III anterior placenta praevia was made on ultrasound and the fetus showed no sign of compromise. Given the site of the placenta and the risk of a further and more substantial bleed, Jane was advised to stay in hospital under observation until delivery. The bleeding settled and, at 32 weeks gestation, she asked to go home to marry her partner. As this necessitated a 1-hour flight, she was strongly advised against this action so her partner flew to Janet instead and the wedding was arranged in a church close to the hospital. At the wedding, Janet had a further substantial bleed as she walked down the aisle and was rushed back into hospital. On admission the bleeding was found to be settling and the fetus was not compromised. Given the gestation was less than 35 weeks, management was to observe and attempt to prolong the gestation to improve neonatal outcome. At 35 weeks gestation Janet had a massive haemorrhage in the ward to the extent that blood soaked her bed linen and flowed over the side of the bed. The resident staff inserted two intravenous lines and she was rushed to theatre. She was shocked and hypotensive and it was extremely difficult to maintain her blood pressure. The fetal heart showed hypoxic decelerations and finally a bradycardia associated with poor placental perfusion. A ‘crash section’ was performed and the diagnosis of grade III placenta praevia was confirmed. A healthy male infant was delivered. Janet was resuscitated with over 10 units of blood and blood product. Had Janet been at home, it is possible that neither she nor her baby would have survived.

Diagnosis

Clinical findings

Painless bleeding occurs suddenly and tends to be recurrent. If labour starts and the cervix dilates, profuse haemorrhage may occur. Where there is a grade I anterior or lateral placental praevia, rupture of the membranes may assist the descent of the head and slow the blood loss.

Abdominal examination

• Displacement of the presenting part: The finding of painless vaginal bleeding with a high central presenting part, a transverse or an oblique lie strongly suggests the possibility of placenta praevia. Although a speculum examination may be undertaken by a skilled obstetrician in these cases to check for the site of the bleeding, a digital vaginal examination must not be undertaken until an ultrasound has been performed. A digital examination may disrupt the placenta and cause excessive bleeding.

• Normal uterine tone: Unlike with abruption, the uterine muscle tone is usually normal and the fetal parts are easy to palpate.

Diagnostic procedures

• Ultrasound scanning: Transabdominal and, for posterior placentas, transvaginal ultrasound is used to localize the placenta where there is a suggestion of placenta praevia. Anteriorly, the bladder provides an important landmark for the lower segment and diagnosis is more accurate. When the placenta is on the posterior wall, the sacral promontory is used to define the lower segment, however if this cannot be seen with transabdominal scanning, a transvaginal scan is used to determine the distance from the cervical os to the lower margin of the placenta. Localization of the placental site in early pregnancy may result in inaccurate diagnosis, as development of the lower segment will lead to an apparent upward displacement of the placenta by 30 weeks.

• Magnetic resonance imaging: This is used when the placenta is implanted on the lower uterine segment over an old caesarean scar. It may help to determine if the placental tissue has migrated through the scar (placenta percreta) or even into the bladder tissue.

Management

When antepartum haemorrhage of any type occurs, the diagnosis of placenta praevia should be suspected and hospital admission advised. An IV line should be established and the mother resuscitated as necessary after blood has been taken for full blood count and cross match. A CTG should be performed to determine fetal status. A cause for the bleeding should be sought by ultrasound imaging, remembering that in up to 50% of cases no obvious cause will be seen. In the acute setting, a vaginal examination should be performed only in an operating theatre prepared for caesarean section, with blood cross-matched. Anti-D immunoglobulin needs to be given if the mother is Rhesus negative and blood taken for Kleihauer-Betke test to determine the extent of fetomaternal transfusion to determine the adequacy of the dose. There is only one indication for performing a vaginal examination:

• When there is serious doubt about the diagnosis due to inadequate ultrasound facilities and labour appears to have commenced. First the examination has to be through the fornices to feel whether the presenting part can be felt easily. If there is difficulty in palapating or a boggy mass is felt then it is likely to be placenta. If the presenting part is felt via the fornices, careful digital examination can be done via the cervix with the intention of rupturing the membranes. Blood should be in the theatre and anaesthetist and theatre staff ready for caesarean section should there be a torrential haemorrhage.

It is, in fact, often difficult to establish a diagnosis of placentae praevia by vaginal examination where the placenta is lateral, and there is a serious risk of precipitating massive haemorrhage if the placenta is central. If the placenta is lateral, then it may be possible to rupture the membranes and allow spontaneous vaginal delivery if the head of the baby is in the pelvis.

Conservative management of placenta praevia should always be considered in the preterm situation and where the bleeding is not life threatening. This involves keeping the mother in hospital with blood cross-matched until fetal maturity is adequate, and then delivering the child by caesarean section. Blood loss should be treated by oral iron, or transfusion where necessary, so that an adequate haemoglobin concentration is maintained.

Postpartum haemorrhage is also a hazard of the low-lying placenta, as contraction of the lower segment is less effective than contraction of the upper segment.

There is an increased risk of placenta accreta/increta/precreta where placental implantation occurs over the site of a previous uterine scar.

Placenta praevia accreta is one of the most lethal conditions in obstetrics. It commonly occurs where the placenta is implanted over a previous section scar. The trophoblast grows into the scar tissue, making it impossible to separate the placenta from the uterine wall and, as a consequence, massive bleeding may occur. The only way this bleeding can be controlled is by hysterectomy. If not predicted and prepared for, the condition may carry a high mortality rate. The important management issue is to be prepared. Caesarean section associated with an anterior implantation of a placenta praevia over previous section scar is best performed by an experienced obstetric surgeon with the assistance of a vascular surgeon/gynaecological oncologist, and with the aid of interventional radiology to occlude blood flow into the internal iliac arteries if excessive loss occurs. Ample supplies of blood and blood product should be on standby.

Abruptio placentae

Abruptio placentae or accidental haemorrhage is defined as haemorrhage resulting from premature separation of the placenta. The term ‘accidental’ implies separation as the result of trauma, but most cases do not involve trauma and occur spontaneously.

Aetiology

The incidence of placental abruption varies from 0.6–7.0%, the rate depending on the population studied. It occurs more frequently under conditions of social deprivation in association with dietary deficiencies, especially folate deficiency, and tobacco use. It is also associated with hypertensive disease, maternal thrombophilia, fetal growth restriction and a male fetus. Although motor vehicle accidents, falls, serious domestic violence, and blows to the abdomen in later pregnancy are commonly associated with placental separation, trauma is a relatively uncommon cause of abruption. In the majority of cases no specific predisposing factor can be identified for a particular episode. There is a high recurrence rate both within a pregnancy and in subsequent pregnancies.

The main fetal effect is a high perinatal mortality rate. In one study of 7.5 million pregnancies in the US, the incidence of placental abruption has been recorded as 6.5/1000 births with a perinatal mortality in associated cases of 119/1000 births. Fetal prognosis is worst with maternal tobacco use.

Whatever factors predispose to placental abruption, they are well-established before the abruption occurs.

Case study

Mandy, a 23-year-old primigravida, was admitted to hospital at 35 weeks gestation with a complaint that she had developed severe abdominal pain followed by substantial vaginal bleeding. On examination, she was restless and in obvious pain. Her blood pressure was 150/90 and the uterus was rigid and tender. Her pulse rate was 100 beats/min and she looked pale and tense. The uterine fundus was palpable at the level of the xiphisternum. The fetal lie was longitudinal, with the head presenting. The fetal heart beat could not be detected. An intravenous line was established and blood cross-matched as a matter of urgency. Mandy was given pain relief and her blood picture and clotting profile were examined. Vaginal examination showed that the cervix was effaced and 3 cm dilated and the membranes were bulging through the os. A forewater rupture was performed and blood-stained amniotic fluid was released. Labour ensued and Mandy was delivered 3 hours later of a stillborn male infant. A large amount of clot was delivered with the placenta, and some 50% of the placenta appeared to have been avulsed from the uterine wall.

Clinical types and presentation

Although three types of abruption have been described, i.e. revealed, concealed or mixed (Fig. 8.9), this classification is not clinically helpful. Commonly the classification is made after delivery when the concealed clot is discovered.

Unlike placenta praevia, placental abruption presents with pain, vaginal bleeding of variable amounts, and increased uterine activity.

Haemorrhage

Abruption involves separation of the placenta from the uterine wall and subsequent haemorrhage. The amount of haemorrhage revealed will depend on the site of the abruption. A bleed from the lower edge of the placenta will pass more easily through the cervical os than a bleed from the upper margin. Blood within the uterus causes an increase in the resting tone and possibly the onset of contractions. The increased tone and blood clot may make palpation of the fetus and auscultation of the fetal heart difficult. The retained blood clot may also lead to abnormal consumption of maternal clotting factors and profuse bleeding.

It is important to realize that any pregnant woman presenting after 20 weeks with the sudden onset of abdominal pain, and/or uterine contractions with or without significant bleeding may have suffered a placental abruption. Urgent assessment of the mothers’ blood pressure, pulse and oxygenation is warranted as she may have a large concealed bleed. If her pulse rate is above the measure of her systolic blood pressure, e.g. pulse is 110 and systolic BP 80, she could have lost 1 L, or more, of blood. If she bleeds further she will become shocked with the development of marked tachycardia, hypotension and oliguria. She requires IV fluids, blood for full blood count and cross matching, fetal CTG and/or ultrasound assessment of fetal welfare and placental status and possible visualization of blood in the uterus. However, in abruption action should be taken based on clinical findings. Ultrasound examination should not delay clinical management and it may not show any diagnostic features.

In some severe cases, haemorrhage penetrates through the uterine wall and the uterus appears bruised. This is described as a Couvelaire uterus. On clinical examination the uterus will be tense and hard and the uterine fundus will be higher than is normal for the gestational age. With this severe form of abruption the mother will often be in labour and in approximately 30% of cases the fetal heart sounds will be absent and the fetus will be stillborn.

The prognosis for the fetus in any abruption is dependent on the extent of placental separation, and is inversely proportional to the interval between onset of the abruption and delivery of the baby. This means that early assessment and delivery in cases with fetal compromise is essential.

Clinical assessment/differential diagnosis

The diagnosis of abruption is made on the history of vaginal bleeding, abdominal pain, increased uterine tonus and, commonly, the presence of a longitudinal lie of the fetus. The condition of the mother may be worse than the revealed blood would indicate. This must be distinguished from placenta praevia, where the haemorrhage is painless, the lie unstable with the uterus having a normal tone, and the amount of blood loss relates to maternal condition. Occasionally, however, some manifestations of placental abruption may arise where there is a low-lying placenta. In other words, placental abruption can arise where there is low placental implantation and, on these occasions, the diagnosis can only really be clarified by ultrasound location of the placenta.

The diagnosis should also be differentiated from other acute emergencies such as acute hydramnios, where the uterus is enlarged, tender and tense but there is no haemorrhage. Other acute abdominal emergencies such as perforated ulcer, volvulus of the bowel and strangulated inguinal hernia may simulate concealed placental abruption, but these problems are rare during pregnancy.

Management

The patient must be admitted to hospital and the diagnosis established on the basis of the history, examination findings (Fig. 8.10) and ultrasound findings. In preterm pregnancy, mild cases (mother stable and CTG normal) may be treated conservatively. An ultrasound examination should be used to assess fetal growth and wellbeing, and the placental site should be localized to confirm the diagnosis. If the fetus is preterm, the aim of management is to prolong the pregnancy if the maternal and fetal condition allow. Conditions that are associated with abruption, e.g. hypertension, should be managed appropriately. If the haemorrhage is severe, resuscitation of the mother is the first prerequisite, following which fetal condition can be addressed.

It is often difficult to assess the amount of blood loss accurately and intravenous infusion should be started with normal saline, Hartmann’s solution or blood substitutes until blood is cross-matched and transfusion can be commenced. A urinary catheter is essential to monitor the urine output.

If the fetus is alive, close to term and there are no clinical signs of fetal compromise, or if the fetus is dead, surgical induction of labour is performed as soon as possible and, where necessary, uterine activity is stimulated with a syntocinon infusion. The fetal heart should be monitored and caesarean section should be performed if signs of fetal compromise develop. If induction is not possible because the cervix is closed, maternal condition is unstable due to ongoing bleeding, or a maternal coagulopathy develops, delivery should be effected by caesarean section with senior obstetric and anaesthetic staff present. Pain relief is achieved by the use of opiates. Epidural anaesthesia should not be used until a clotting screen is available.

If the fetus is preterm and maternal and fetal condition are stable, the mother should be admitted and monitored until all signs of bleeding and pain have settled. Most units subsequently will induce labour at 37–38 weeks due to the increased risk of a further abruption.

Complications

The complications of placental abruption are summarized in Figure 8.11.

Afibrinogenaemia

Afibrinogenaemia occurs when the clot from a severe placental abruption causes the release of thromboplastin into the maternal circulation. This in turn may lead to a disseminated intravascular coagulation, the consumption of coagulation factors including platelets, with the development of hypo- and afibrinogenaemia. The condition may be treated by the infusion of fresh frozen plasma, platelet transfusion and fibrinogen transfusion after delivering the fetus. It may lead to abnormal bleeding at operative delivery or uncontrolled postpartum haemorrhage unless the clotting defect has been corrected. Replacing products with the placenta in place may worsen the outcome as can be rapidly consumed, with a resultant increase in degradation product and clotting dysfunction.

Renal tubular or cortical necrosis

This is a complication of undertreated hypovolaemia and disseminated intravascular coagulation. A careful assessment of urinary output is essential. Anuria in a pregnant woman must be urgently and aggressively managed. If it is not, it may, on occasion, necessitate haemodialysis or peritoneal dialysis, but it is becoming increasingly rare.

Other causes of antepartum haemorrhage

These are summarized in Figure 8.12.

Fig. 8.12 Non-placental causes of antepartum haemorrhage.

Vasa praevia

Vasa praevia is a very rare condition where one of the branches of the fetal umbilical vessels lies in the membranes and across the cervical os. This occurs when there is a membranous insertion of the cord and the vessels course through the membranes to the placenta, or if there is succenturiate lobe of the placenta and the vessels in the membrane connect the main placental mass and the separate lobe. Rupture of the membranes over the cervical os may cause a tear in the vessels which will result in the rapid exsanguination of the fetus. Vasa praevia can be diagnosed with colour Doppler ultrasound at the fetal anatomy scan.

Unexplained antepartum haemorrhage

In almost 50% of cases of women presenting with vaginal bleeding in pregnancy, it is not possible to make a definite diagnosis of abruption or placenta praevia.

Where the bleeding is confirmed to be coming from the uterine cavity, it is proposed that the cause is bleeding from the edge of the placenta. Whatever the cause, there is a significant increase in perinatal mortality and it is therefore important to monitor placental function and fetal growth for the rest of the pregnancy. The pregnancy should not be allowed to proceed beyond term.

Vaginal infections

Vaginal moniliasis or trichomoniasis may cause blood-stained discharge and, once the diagnosis is established, should be treated with the appropriate therapy.

Cervical lesions

Benign lesions of the cervix such as cervical polyps are treated by removal of the polyp. Cervical erosions are best left untreated.

Carcinoma of the cervix is occasionally found in pregnancy. If the pregnancy is early, termination is indicated followed by staging of the cancer and definitive therapy. If the diagnosis is made late in pregnancy, the diagnosis should be established by biopsy, the baby delivered when mature and the lesion treated according to the staging, including caesarean section and radical hysterectomy for early stage disease.

Multiple pregnancy

Multiple pregnancy is an anomaly in the human with the single cavity uterus, unlike many other species where the mother has a bicornuate uterus that allows for 2 or more offspring to be gestated as the norm. A pregnancy with twins, triplets or higher numbers of embryos is considered a high risk given the increased risk of maternal and fetal morbidity and mortality.

Prevalence

The prevalence of multiple pregnancies varies with race and the use of assisted reproductive techniques. The prevalence of natural twinning is highest in Central Africa, where there are up to 30 twin sets (60 twins) per 1000 live births and lowest in Latin America and South-East Asia where there are only 6–10 twin sets per 1000 live births. North America and Europe have intermediate rates of 5–13 twin sets per 1000 live births. Between 1985 and 2005 there was a more than doubling in the rates of twins due to reproductive technologies. The twins resulted from ovulation induction and the replacement of more than one fertilized embryo in the in vitro fertilization (IVF) cycle. Given the risks of multiple pregnancy the technique of replacing many embryos to enhance the conception rate has been abandoned, resulting in a fall in the rates of twins.

The natural prevalence of triplet pregnancy rate appears to have increased over the past 30 years. In 1985 the rate in the UK was 10.2/100 000, but in 2002–2006 the rate was close to 25/100 000. The cause of this rise is unclear. Higher multiple births such as quadruplets and quintuplets are commonly associated with the use of fertility drugs but, if one excludes this cause, figures for England and Wales suggest a pregnancy rate of 1.7/1 000 000 maternities.

The highest naturally occurring multiple pregnancy recorded so far is nonuplets.

Types of twinning and determination of chorionicity

Any multiple pregnancy may result from the release of one or more ova at the time of ovulation.

Monozygotic multiple pregnancy

If a single ova results in a multiple pregnancy the embryos are called monozygotic, with alternative names of uniovular and identical. The rate of monozygotic twins is approximately 1/280 pregnancies, is unaffected by race, and is increased by reproductive technology for unknown reasons. The zygote divides sometime after conception (Fig. 8.13). If the split postconceptually occurs at:

Fig. 8.13 Types of twinning, indicating the structure of the membranes and placentae. Note that twins of different sexes are always dizygous and those with a single chorion are always monozygous. Dichorionic twins of the same sex can be monozygous or dizygous.

0–4 days there will be 2 embryos, 2 amnions, 2 chorions (as for dizygotic twins): 25–30%

4–8 days there will be 2 embryos, 2 amnions, 1 chorion: 65–70%

9–12 days there will be 2 embryos, 1 amnion and 1 chorion: 1–2%

13+ days there will be conjoint twins, 1 amnion and 1 chorion: <1%

Given that the embryo splits under some unknown influence, monozygotic multiple pregnancy is considered to be an anomaly of reproduction. Occasionally the embryo splits into 3 resulting in monozygotic triplets. In the case of triplets the splitting may occur at the same time or sequentially resulting in conjoint twins with a separate singleton pregnancy all within one chorion!

The determination of monozygocity is performed by early ultrasound preferably before 14 weeks. A pregnancy where the zygote splits after 4 days will show a single thin membrane (monochorionic diamniotic) or no membrane (monochorionic monoamniotic) separating the two embryos and a single placental mass. If the split in the embryo was in the first 4 days there may be two separate placental masses or a single mass with a membrane that is easier to visualize on ultrasound and which has a twin peak sign where the membrane and the placenta intersect. This appearance is the same as that for diamniotic dichorionic twins where there is a single placental mass. Early determination of zygosity is important to plan the management of the pregnancy. Genetic assessment of amniotic fluid, chorionic villous samples, or postnatally cord blood can be used to confirm zygosity. These techniques are seldom used in the face of modern ultrasound technology.

Dizygotic twins

These come from the separate fertilization of separate ova by different sperm. In 50% of such pregnancies the fetuses are male–female, with 25% being male–male and 25% being female–female. All will have either 2 separate placentas on ultrasound or a single placenta with a thick membrane with a ‘twin peak’ sign. The presence of lambda (chorion in between membranes) or T (absence of chorion in between membranes) sign at the site of membrane insertion of the placenta in the first trimester has been valuable to determine whether they are monochorionic diamniotic or dichrionic diamniotic twins (Fig. 8.14). Monochorionic diamniotic twins may have placental vascular anastomosis and may give rise to complications of twin to twin transfusion and its consequent sequelae.

Fig. 8.14 Ultrasound figure demonstrating (A) T and (B) lambda sign.

The rate of dizygotic twins varies with:

• Familial factors: The familial tendency is apparent in dizygotic twinning, but this appears to be on the maternal side only. In a study of records at Salt Lake City, the twinning rates of women who were themselves dizygotic twins was 17.1/1000 maternities compared with 11.6/1000 maternities for the general population, but the rate for males who were themselves dizygotic twins was only 7.9/1000 maternities.

• Parity and maternal age: Studies in Aberdeen have shown that the rate increases from 10.4/1000 in primigravidae to 15.3/1000 in the para 4+ group. There is also a small increase in twinning in older mothers.

• Ovulation induction: Multiple pregnancy is common following the use of drugs to induce ovulation. It is important to note that the use of gonadotrophin therapy can result in twins, triplets or even higher order pregnancies. To some degree this can be avoided by monitoring ovarian follicular development and withholding the injection of human chorionic gonadotrophin if excessive numbers of follicles develop. The use of fertility drugs accounts for 10–15% of all multiple pregnancies and has therefore significantly altered the incidence of multiple pregnancy.

As mentioned earlier the risk of multiple pregnancy as a result of IVF has decreased with the limitation of the number of embryos transferred.

Complications of twin pregnancy

The normal processes of maternal physiological adaptation are exaggerated in multiple pregnancy. Total weight gain is, on average, 3.5 kg greater than in singleton pregnancy. There is an increase in red cell mass. However, this does not match the expansion in plasma volume that exceeds that of a singleton pregnancy by 17% at term, and a relative anaemia develops. Compared with singleton pregnancies, maternal cardiac output was greater by 20% because of an increase in stroke volume by 15%, and heart rate by 3.5%.

It is thus to be expected that the increased strain put on the system by carrying more than one fetus will result in a higher incidence of complications (Table 8.1).

Table 8.1

Risks associated with twin pregnancies

Obstetric complication	Risk*
Anaemia	x2
Pre-eclampsia	x3
Eclampsia	x4
Antepartum haemorrhage	x2
Postpartum haemorrhage	x2
Fetal growth restriction	x3
Preterm delivery	x6
Caesarean section	x2

^*Compared with singleton pregnancies

Complications unrelated to zygosity

Nausea and vomiting

Early onset of nausea and subsequent vomiting is often the sign that points to a twin pregnancy before ultrasound confirmation. The incidence of vomiting in twins is significantly higher compared with that of singletons

Anaemia

Twins are associated with extra metabolic demands on the mother. As a minimum all mothers should consider iron and folate supplements throughout gestation.

Miscarriage

Resorption of a fetus between 6 and 10 weeks occurs in over 15% of twin pregnancies and is referred to as the vanishing twin syndrome. The incidence of threatened and actual miscarriage is higher in twins. Evidence from Aberdeen has shown that threatened miscarriage occurs in 26% of twin pregnancies and 20% of singleton pregnancies, and missed miscarriage between 10 and 14 weeks is twice that of singletons.

Antepartum haemorrhage

The incidence of antepartum haemorrhage as a result of abruption and placenta praevia doubled in twin pregnancies.

Pre-eclampsia

There is an increased incidence of gestational hypertension, pre-eclampsia and eclampsia in twin pregnancies. The rate in primigravida is five times that of singletons and multigravida is ten times.

Intra-uterine growth restriction (IUGR)

In 20% of twins, one fetus is significantly smaller than the other as defined by a difference in the abdominal circumference of more than 20%. Given that this difference is impossible to detect clinically, regular ultrasound screening of growth and fetal wellbeing in twin pregnancies is mandatory.

Preterm labour

The occurrence of preterm labour is the most important complication of twin pregnancy (Table 8.2). The onset of labour before 37 weeks gestation occurs in over 40% of twin pregnancies. The phenomenon appears to be associated with overdistension of the uterus associated with the presence of more than one fetus and is further increased if the amniotic fluid volume is increased.

Table 8.2

Rates of preterm delivery by fetal number

Number of fetuses	<28 weeks
Singleton	0.7%
Twins	4.4%
Triplets	21.8%

Complications related to zygosity

Monozygotic twins have a higher perinatal mortality rate than dizygotic twins. This is due to a higher incidence of congenital abnormalities, preterm delivery and the twin–twin (fetofetal) transfusion syndrome.

Twin-to-twin transfusion syndrome (TTTS)

This syndrome arises in 10–15% of all monochorionic diamniotic twin pregnancies. In this condition, one fetus (the donor) transfuses the other (the recipient) through interlinked vascular channels in the placenta. Presentation occurs in the second trimester. The donor twin is oliguric and growth-restricted with oligohydramnios, and the recipient fetus exhibits polyhydramnios and is at risk of cardiomegaly and hydrops fetalis.

Without treatment, the perinatal mortality exceeds 80%. Treatment options include serial amniocenteses to remove fluid from around the recipient twin, selective feticide, or laser ablation, via a fetoscope, of the communicating vessels. Laser treatment has survival rates of 49–67%. If one twin dies in utero before laser treatment, the other twin also often dies as a result of acute haemodynamic changes.

Monoamniotic and conjoined twinning

Monoamnionicity occurs in 1% of monochorionic twins and cord entanglement by 22 weeks is a common complication, such that survival rates are as low as 50%.

Conjoined twinning occurs in 1.3/100 000 births, with fusion occurring at different sites on the bodies of the fetuses. The prognosis for separation and for a normal life after birth depends on the site of fusion and is determined with tertiary level ultrasound by 18–20 weeks gestation. Where there is a major cardiovascular connection, or a shared organ, perinatal death of at least one twin at separation is almost certain.

Prenatal diagnosis

The risk of structural abnormalities such as anencephaly and congenital heart defects is increased in multiple pregnancies, particularly with monozygotic babies. Determination of chorionicity, prenatal diagnosis, and assessment for impending TTTS is particularly important. Screening for abnormalities presents particular difficulties because of the need to differentiate between the two sacks and therefore all such screening should be referred to a tertiary care centre.

The missed diagnosis of twins and other multiple pregnancies was relatively common before the advent of modern ultrasound screening techniques and still occurs where such facilities are not available on a routine basis. Although the initial clinical diagnosis of twins was always made in the past on the basis of an abnormally enlarged uterus, such assessments were notoriously inaccurate. The real danger of undiagnosed twins is that oxytocic drugs are administered after delivery of the first twin, leading to entrapment of the second twin. This situation cannot be reversed even with the use of tocolytic drugs and often results in the death of or damage to the second twin. If there is any suspicion of undiagnosed twins and ultrasound is not available, do not give oxytocic drugs; palpate the maternal abdomen immediately after delivery of the first twin.

Management of twin pregnancy

Multiple pregnancies exhibit every type of pregnancy complication at a greater frequency than occurs in singleton pregnancy. Early diagnosis is therefore essential and provides a convincing argument for routine early pregnancy ultrasound scanning (Fig. 8.15).

Fig. 8.15 Ultrasound scan of twins early in pregnancy.

The commonest clinical sign of twin pregnancy is the greater size of the uterus, which is easier to detect in early, rather than late, pregnancy. There are, of course, other reasons why the uterus may be abnormally enlarged, such as hydramnios and uterine fibroids.

Treatment of any antenatal complication is the same as in singleton pregnancies, but remember that the onset of complications, particularly preterm labour, tends to be earlier and of greater severity. Routine hospital admission from 28 weeks gestation for bed rest has been advocated in the past, but clinical trials have failed to demonstrate efficacy. However, careful antenatal supervision and ultrasound examinations to detect fetal growth anomaly or TTTS should be undertaken 2–4 weekly. It is important that women with multiple pregnancies are booked for confinement where complications can be readily treated.

Intrauterine growth restriction is common and if detected, early induction of labour should be considered. The overall incidence of IUGR in one or both twins is 29%, involving 42% of monochorionic twins and 25% of dichorionic twins.

Management of labour and delivery

Delivery poses many difficulties in twin pregnancy because of the variety and complexity of presentations and because the second twin is at significantly greater risk from asphyxia due to placental separation and cord prolapse.

Presentation at delivery

There are a number of permutations for presentation in twin pregnancy at delivery, which are partly influenced by the management of the second twin. Rounded-up figures for these presentations are shown in Figure 8.16.

Fig. 8.16 The four major presentations of twin pregnancy. The 5% of other variations are not listed in these major groups.

By far the commonest presentation is cephalic/cephalic (50%), followed by cephalic/breech (25%), breech/cephalic (10%) and breech/breech (10%). The remaining 5% consist of cephalic/transverse, transverse/cephalic, breech/transverse, transverse/breech and transverse/transverse.

Method of delivery

A decision about the method of delivery should preferably be made before the onset of labour.

Caesarean section

Delivery by elective caesarean section is indicated for the same reasons that exist for singleton pregnancies. However, the threshold for intervention is generally lower. Where an additional complication exists, such as a previous caesarean scar, a long history of subfertility, severe pre-eclampsia or diabetes mellitus, most obstetricians will opt for elective caesarean section. Preterm labour between 28 and 34 weeks gestation is an indication for caesarean delivery, as also is malpresentation of the first twin. Furthermore, the presentation does have an important part to play in deciding the best method of delivery. Caesarean section rates for twins increased in the UK from 28% in 1980–1985 to 42% in 1995–1996 and, in general, very few obstetricians now advise vaginal delivery for twin breech presentation or for a breech presentation of the first twin, for fear of locked twins.

Vaginal delivery

When labour is allowed to proceed normally, it is advisable to establish an intravenous line at an early stage. Labour normally lasts the same time as a singleton labour.

The first twin can be monitored with a scalp electrode or by abdominal ultrasound and it is important to monitor both fetuses. When the first twin is delivered, the lie and presentation of the second twin must be immediately checked and the fetal heart rate recorded.

For delivery of the second twin, the membranes should be left intact until the presenting part is well into the pelvis and cord prolapse excluded. If the uterus does not contract within a few minutes, an oxytocin infusion should be started. If fetal heart rate anomalies occur, then delivery should be expedited by forceps delivery or breech extraction. Under very exceptional circumstances, it may be necessary to deliver the second twin by caesarean section. It is important to use oxytocic agents with delivery of the second twin as there is an increased risk of postpartum haemorrhage.

Not all obstetricians advocate immediate stimulation of the uterus after delivery of the first twin. It is reasonable to wait for the spontaneous onset of further contractions without further intervention if the fetal heart rate is normal. However, because of the ever-present risk of placental separation and intrauterine asphyxia in the second twin, an upper limit of 30 minutes between the two deliveries is generally accepted as reasonable practice. The delivery of an asphyxiated second twin after a long birth interval will always lead to the question as to why intervention did not take place at an earlier stage.

Higher-order multiple births such as triplets or quadruplets are now delivered by caesarean section. Under these circumstances, the onset of labour is often preterm, the birth weights are low and the presentations uncertain.

Complications of labour

There are several complications of labour, some of which are associated with malpresentation. Babies may become obstructed, particularly where there is a transverse lie presenting and that is, in fact, an indication for delivery by caesarean section. If caesarean section is performed in the presence of an obstructed transverse lie, it may on occasions be preferable to make a vertical incision in the lower and upper segment rather than a transverse incision because of the possibility of extension of the lower segment incision into the uterine vessels and the broad ligaments, resulting in uncontrollable haemorrhage.

Once the first twin has been delivered, the attendant stabilizes the lie of the second twin via abdominal palpation to ensure it is longitudinal. An oxytocin infusion may then be needed to ensure the uterus contracts to cause the baby to descend into the pelvis. The fetal heart is auscultated throughout this process to ensure fetal welfare. If the baby presents by the vertex, the membranes are ruptured once the head is in the pelvis. If the baby is breech, in the absence of spontaneous descent the attendant may need to hold the fetal foot after placing a hand into the uterus, rupture the membranes with a contraction and guide the foot and breech into the pelvis to effect delivery (if possible the foot can be grasped with intact membranes to avoid cord prolapse). As this can be uncomfortable, many attendants prefer, if the mother is agreeable, to have an epidural cannula in place during the labour of a twin pregnancy so adequate analgesia can be administered if the second stage becomes complicated. Very occasionally, after the delivery of the first twin, the placentae separate and attempt to deliver before the second baby. In this event, or in the event that the second baby cannot be delivered easily, a caesarean section must be urgently performed.

Case study

A 22-year-old woman in her first pregnancy with twins presented at 37 weeks gestation in spontaneous labour. The presentation of both babies was cephalic. An epidural catheter was sited for analgesia and labour progressed uneventfully, with the first twin delivering spontaneously. The presentation of the second twin was confirmed as cephalic with a longitudinal lie. As the presenting part was still above the pelvic brim, a syntocinon infusion was commenced to maintain uterine contractions, and the membranes were left intact awaiting descent of the presenting part. Shortly afterwards, external monitoring of the fetal heartbeat showed a bradycardia of 60 beats/min. Delivery of the second twin was expedited by reaching inside the uterus with the membranes still intact (internal podalic version), locating the feet of the fetus and rotating the fetus to the breech presentation before rupturing the membranes and delivering the infant by breech extraction.

Locked twins

This is a very rare complication, where the first twin is a breech presentation and the second is cephalic. Clinically, as the first twin descends during the delivery, the twins lock chin to chin. The condition is usually not recognized until delivery of part of the first twin has occurred and its survival is unlikely unless an urgent caesarean section is organized. Twins where ultrasound reveals the first is presenting by the breech and the second by the vertex, are often delivered by elective caesarean section.

Conjoined twins

The union of twins results from the incomplete division of the embryo after formation. Union may occur at any site but commonly is head-to-head or thorax-to-thorax. The antenatal assessment of the twins with tertiary level ultrasound before 20 weeks allows for the prognosis to be determined and whether surgical separation may be attempted postnatally.

If the union is recognized by ultrasound before the onset of labour, then the twins should be delivered by caesarean section. If the abnormality is not recognized before the onset of labour, then the labour will usually obstruct.

Perinatal mortality

Approximately 10% of all perinatal mortality is associated with multiple pregnancies. Compared with a singleton pregnancy, the mortality rate increases with the number of fetuses: twins ×4, (monochorionicity ×8, with the second twin vs first twin ×1.5); triplets ×8.

The commonest cause of death in both twins is prematurity. Over 50% of twins and 90% of triplets deliver before 37 weeks. Second-born twins are more likely to die from intrapartum asphyxia with separation of the placenta following delivery of the first twin, or where cord prolapse occurs in association with a malpresentation or a high presenting part when the membranes are ruptured.

Overall, perinatal mortality rates are 27, 52 and 231/1000 live and stillbirths, for twins, triplets, and higher multiple births, respectively. In comparison with singleton births of like gestational age, twins have a relative risk for low-birth weight infants (<2.5 kg) of 4.3.

Perhaps of greater concern is the fact that the risk of producing a child with cerebral palsy is 8 times greater in twins and 47 times greater in triplets compared with singleton pregnancies.

Prolonged pregnancy

The terms ‘prolonged pregnancy’, ‘post-dates pregnancy’ and ‘post-term pregnancy’ are all used to describe any pregnancy that exceeds 294 days from the first day of the last menstrual period in a woman with a regular 28-day cycle.

The term ‘postmaturity’ refers to the condition of the infant and has characteristic features (Box 8.1). These are all indicators of intrauterine malnutrition and may therefore occur at any stage of the pregnancy if there is placental dysfunction. Postmaturity is often associated with oligohydramnios, an increased incidence of meconium in the amniotic fluid and an increased risk of intrauterine aspiration of meconium-stained fluid into the fetal lungs. It is found in 2% of pregnancies at 41 weeks and up to 5% of pregnancies at 42 weeks. Unexpected stillbirth in such prolonged pregnancies is a particular tragedy for the mother, and she and her carer will always live with the knowledge that the child would almost certainly have survived had action to deliver the baby been taken earlier.

The accurate diagnosis of prolonged pregnancy varies with the method of dating. On the basis of the date of the last menstrual period, the incidence is about 10%, but by using accurate ultrasound dating in the first trimester this figure can be reduced to 1%. This provides a strong case for routine ultrasound dating in early pregnancy.

Aetiology

Prolonged pregnancy can be considered as one end of the spectrum of normal pregnancy. However, the condition may be familial and is sometimes associated with abnormalities of the fetal adrenal–pituitary axis, as in anencephaly.

Management

Evidence in many large studies suggest an increase in perinatal mortality after 39 weeks that necessitates a close appraisal of every pregnancy at term to ensure continuation beyond 40 weeks is safe for the fetus. To do this many units employ a postdate service where women present between 40 and 41 weeks for a CTG and amniotic fluid index (AFI) assessment. Those with a low AFI, taken as less than 5 cm are at increased risk of postmaturity syndrome and fetal hypoxic morbidity. They are offered induction after counselling. For those with normal liquor and CTG, large studies have shown that whether a woman is induced at 41–42 weeks or whether the labour is allowed to start spontaneously, the caesarean section rates are the same. Many units will therefore have a policy of offering induction to all women by 41+5 weeks. Those women who decline induction need careful monitoring with frequent CTG and liquor volume assessment until delivery. Management in this form has resulted in reported fetal morbidity of close to zero.

Labour management

Should the decision be made to induce labour, this may in itself prove difficult, as the cervix is often unfavourable, with a Bishop’s score of less than 3. In these circumstances, cervical preparation with prostaglandins or mechanical methods should be attempted. If this fails and the infant is large, it may on occasions be preferable to deliver the child by elective caesarean section.

Careful observation during labour is mandatory, as these are high-risk pregnancies.

Breech presentation

The incidence of breech presentation depends on the gestational age at the time of onset of labour. At 32 weeks, the incidence is 16%, falling to 7% at 36 weeks and 3–5% at term. Thus it is clear that the fetus normally corrects its own presentation and attempts to correct the presentation before 37 weeks are generally unnecessary.

Types of breech presentation

The breech may present in one of three ways (Fig. 8.17):

• Frank breech: The legs lie extended along the fetal trunk and are flexed at the hips and extended at the knees. The buttocks will present at the pelvic inlet. This presentation is also known as an extended breech.

• Flexed breech: The legs are flexed at the hips and the knees with the fetus sitting on its legs so that both feet present to the pelvic inlet.

• Knee or footling presentation: one or both of the lower limbs of the fetus are flexed and breech of the baby is above the maternal pelvis so that a part of the fetal lower limb (usually feet) descends through the cervix into the vagina.

The position of the breech is defined using the fetal sacrum as the denominator. At the onset of labour the breech enters the brim of the true pelvis with the bitrochanteric diameter (less than 10 cm) being the diameter of descent. This diameter is slightly smaller than the biparietal diameter in the full-term fetus. The type of breech presentation has a significant impact on the risk of vaginal breech delivery. The more irregular the presenting part, the greater is the risk of a prolapsed cord or limb. A foot pressing into the vagina below the cervix may stimulate the mother to bear down before the cervix is fully dilated and thus lead to entrapment of the head (Fig. 8.17).

Causation and hazards of breech presentation

Breech presentation is common before 37 weeks gestation, but most infants will turn spontaneously before term (as previously discussed). Breech presentation may, however, be associated with factors such as multiple pregnancy, congenital abnormalities of the maternal uterus, fetal malformation, fetal hypotonia secondary to medication use, and placental location, either placenta praevia or cornual implantation.

There is also evidence to suggest that persistent breech presentation may be associated with the inability of the fetus to kick itself around from breech to vertex and that there may therefore be some neurological impairment of the lower limbs (Box 8.2).

Box 8.2 Causation of breech presentation

• Neurological impairment of the fetal limbs

There is a higher incidence of neurological impairment in breech babies even when delivered by caesarean section, although the overall risk is still less than 1%.

Delivery by the breech carries some specific hazards to the infant as compared with normal vertex presentation, particularly in preterm infants and in infants with a birth weight in excess of 4 kg:

• There is an increased risk of cord compression and cord prolapse because of the irregular nature of the presenting part. This is particularly the case where the legs are flexed or there is a footling presentation.

• Entrapment of the head behind the cervix is a particular risk with the preterm infant, in whom the bitrochanteric diameter of the breech is significantly smaller than the biparietal diameter of the head. This means that the trunk may deliver through an incompletely dilated cervix, resulting in entrapment of the larger head. If the delivery is significantly delayed, the child may be asphyxiated and either die or suffer brain damage.

• The fetal skull does not have time to mould during delivery and therefore, in both preterm and term infants, there is a significant risk of intracranial haemorrhage.

• Trauma to viscera may occur during the delivery process, with rupture of the spleen or gut if the obstetrician handles the fetal abdomen.

Management

Antenatal management

Because of the risks to the fetus of breech birth, the best option is to avoid vaginal breech delivery through accurate diagnosis and the performance of external cephalic version.

External cephalic version (ECV)

Indication

Breech presentation persisting after 36 weeks gestation.

Contraindications

External cephalic version should not be attempted where there is a history of antepartum haemorrhage, where there is placenta praevia, the CTG is abnormal, there is a previous uterine scar or where the pregnancy is multiple. It is also pointless to turn the infant if the intention is to deliver the child by elective caesarean section for some other indication.

Technique

The mother rests supine with the upper body slightly tilted down. The presentation and placental position are confirmed by ultrasound. The fetal heart rate is checked preferably with a small strip of CTG. A tocolytic agent (oral nifedipine or IM terbutaline) is given to relax the uterus as this improves the success rate (Fig. 8.18).

Fig. 8.18 External cephalic version: pressure is applied in the opposite direction to the two fetal poles.

The breech is disimpacted from the pelvic brim and shifted to the lower abdomen and the fetus is gently rotated, keeping the head flexed. The fetal heart rate should be checked during the procedure.

It is essential not to use excessive force and, if there is evidence of fetal bradycardia, the fetus should be returned to the original presentation if the version is not past the halfway point and the fetus monitored with continuous CTG.

Complications

The risks of the procedure are cord entanglement, placental abruption and rupture of the membranes. Persistent fetal bradycardia occurs in approximately 1% and this may necessitate urgent delivery by caesarean section. There is some evidence to suggest that, even where external version is successful, the section rate is higher than normal due to dystocia and fetal compromise. ECV is successful in up to 50% of cases in the best hands.

However, this is not always possible and the important decision to be made relates to the assessment of the size of the fetus and the size and shape of the maternal pelvis.

Although the size and shape of the maternal pelvis can be assessed by pelvic examination or formally using magnetic resonance imaging (MRI), neither technique has been shown to be accurate in determining the possible success of a breech delivery.

Fetal size is difficult to assess but, if fetal gestational age is less than 32 weeks and more than 28 weeks, the birth weight will be less than 2 kg and delivery by caesarean section is the preferred option. If the fetal weight as assessed clinically and by ultrasound is calculated to be in excess of 4 kg, then delivery by section is the preferred option but it must be remembered that such estimates can be unreliable.

Method of delivery

In 1999 the term breech trial was published which suggested that the delivery of the breech presenting fetus was safest by caesarean section. As a result many units now no longer perform vaginal delivery of the breech. Since that time, considerable literature has shown that the trial had methodological issues and the conclusions may not have been justified. Some units are therefore reintroducing vaginal breech delivery as a safe option in selected cases, where obstetricians with the appropriate expertise for assisting delivery are available.

Vaginal breech delivery

The first stage of labour should be no different from labour in a vertex presentation. Epidural analgesia is the preferred method of pain relief but is not essential. The woman should be advised to attend hospital as soon as contractions commence or the membranes rupture and vaginal examination should be performed on admission to exclude cord presentation or prolapsed. The presence of meconium-stained liquor has exactly the same significance as with a vertex presentation except in the second stage of labour when descent of the breech will often result in the passage of meconium.

Technique

When the cervix is fully dilated, and the presenting part is low in the pelvis the mother is encouraged to bear down with her contractions until the fetal buttocks and anus come on view (Fig. 8.19). To minimize soft tissue resistance, an episiotomy should be considered under either local or epidural anaesthesia, unless the pelvic floor is already lax and offers little resistance. The legs are then lifted out of the vagina by flexing the fetal hip and knees. The baby is then expelled with maternal pushing with the obstetrician only touching the upper thighs and then only to ensure that the fetal back remains anterior. Once the trunk has delivered as far as the scapula, the arms can usually be easily delivered one at a time by sliding the fingers over the shoulder and sweeping them downwards across the fetal head. If the arms are extended and pose difficulty in delivering, the body of the fetus is rotated by holding the baby’s pelvis till the posterior arm comes under the symphysis pubis. The arm can then be delivered by flexing at the elbow and the shoulders. The procedure is repeated by rotating the body to deliver the other arm (Loveset’s manouvre). The trunk is then allowed to remain suspended for about 30 seconds to allow the head to enter the pelvis and then the legs are grasped and swung upwards through an arc of 180° until the child’s mouth comes into view. At this point the baby may spontaneously deliver, however a number of techniques including the use of forceps can be used to ensure the safe delivery of the head.