After studying this chapter you should be able to:
Knowledge criteria
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Describe the pathophysiology, aetiology and presentation of the major antenatal complications of pregnancy:
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hypertension in pregnancy
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antepartum haemorrhage
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multiple pregnancy, breech presentation
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abnormal and unstable lie and prolonged pregnancy
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Clinical competencies
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Plan initial investigations and management of the above obstetric disorders
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Interpret the investigation results of scan, blood and urine tests performed in cases of obstetric disorders
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Explain to the mother and her partner the consequences of the obstetric disorder
Professional skills and attitudes
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Empathize with the woman and her family should an adverse event occur as a result of an obstetric disorder
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.
Definitions
Hypertension in pregnancy is defined as a systolic pressure of at least 140 mmHg or a diastolic pressure of at least 90 mmHg on two or more occasions. Diastolic pressure is taken at the fifth Korotkoff sound. At times in pregnancy there is no fifth sound; in these circumstances it is necessary to use the fourth sound.
Some definitions of hypertension also include reference to a rise in systolic pressure of at least 30 mmHg or a rise in diastolic pressure of at least 15 mmHg. There is no evidence that these women have adverse outcomes, however.
Proteinuria is defined as the presence of urinary protein in concentrations greater than 0.3 g/L in a 24 hour collection or in concentrations greater than 1 g/L on a random sample on two or more occasions at least 6 hours apart.
Oedema is defined as the development of pitting oedema or a weight gain in excess of 2.3 kg in a week. Oedema occurs in the limbs, particularly in the feet and ankles and in the fingers, or in the abdominal wall and face ( Fig. 8.1 ). Oedema is very common in otherwise uncomplicated pregnancies, this is the least useful sign of hypertensive disease. It has therefore been dropped from many classifications.
Classification
The various types of hypertension are classified as follows:
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Gestational hypertension is characterized by the new onset of hypertension without any features of pre-eclampsia after 20 weeks of pregnancy or within the first 24 hours postpartum. Although by definition the blood pressure should return to normal by 12 weeks after pregnancy; it usually returns to normal within 10 days after delivery.
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Pre-eclampsia is the development of hypertension with proteinuria after the 20th week of gestation. It is commonly a disorder of primigravida women.
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Eclampsia is defined as the development of convulsions secondary to pre-eclampsia in the mother.
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Chronic hypertensive disease is the presence of hypertension that has been present before pregnancy and may be due to various pathological causes.
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Superimposed pre-eclampsia or eclampsia is the development of pre-eclampsia in a woman with chronic hypertensive disease or renal disease.
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Unclassified hypertension includes those cases of hypertension arising in pregnancy on a random basis where there is insufficient information for classification.
The critical factor that changes the prognosis for the mother and infant is the development of proteinuria. Those women who develop hypertension alone tend to have normal fetal growth with a good prognosis for the infant, whereas those that develop proteinuria have placental changes that are associated with intrauterine growth restriction and a poorer fetal prognosis. From a management point of view, the final diagnosis can only be made after the pregnancy has been completed so the assumption must be made that any woman who develops hypertension must be considered to be at risk.
Pathogenesis and pathology of pre-eclampsia and eclampsia
The exact nature of the pathogenesis of pre-eclampsia remains uncertain. Nearly every major system in the body is affected by the advanced manifestations of the condition. Therefore every system that is studied appears to show changes without necessarily doing more than manifesting secondary effects.
The pathophysiology of the condition, as outlined in Figure 8.2 , is characterized by the effects of:
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Arteriolar vasoconstriction, particularly in the vascular bed of the uterus, placenta and kidneys.
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Disseminated intravascular coagulation.
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:
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Swelling and proliferation of endothelial cells to such a point that the capillary vessels are obstructed.
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Hypertrophy and hyperplasia of the intercapillary or mesangial cells.
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Fibrillary material (profibrin) deposition on the basement membrane and between and within the endothelial cells.
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:
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increased syncytial knots or sprouts
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increased loss of syncytium
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proliferation of cytotrophoblast
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thickening of the trophoblastic basement membrane
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villous necrosis.
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:
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methyldopa (oral)
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hydralazine (oral and IV)
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combined alpha- and beta-blockers such as labetalol (oral or IV)
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alpha-blocker such as prazosin (oral)
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calcium channel blockers such as nifedipine (oral).
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:
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The 4-hourly measurement of blood pressure until such time that the blood pressure has returned to normal.
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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.
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Maternal serum screening for pre-eclampsia.
Laboratory investigations
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Full blood count with particular reference to platelet count.
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Tests for renal and liver function.
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Uric acid measurements: a useful indicator of progression in the disease.
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Clotting studies where there is severe pre-eclampsia.
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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:
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Serial ultrasounds for:
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Measurements of fetal growth every 2 weeks . Parameters measured are fetal biparietal diameter, head circumference, abdominal circumference and femur length.
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Measurements of liquor volume up to twice weekly.
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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.
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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.
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 ).
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:
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maternal
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gestation > 37 weeks
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uncontrollable blood pressure
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HELLP syndrome
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rising liver dysfunction
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falling platelets
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falling haemoglobin due to haemolysis
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deteriorating renal function (creatinine > 90 mmol/L)
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eclampsia
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acute pulmonary oedema
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fetal/placental
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fetal compromise on CTG tracing
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absent or reversal of end diastolic flow in the umbilical artery
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no fetal growth over more than 2 weeks
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placental abruption.
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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:
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fetal
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growth restriction, hypoxia, death
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maternal
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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
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placental
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infarction, abruption.
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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:
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control the fits
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control the blood pressure
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deliver the infant.
Control of fits
In the past various drugs were used to control the fits:
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Eclamptic seizures are usually self-limiting. Acute management is to ensure patient safety and protecting the airway
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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:
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Maintain the patient in a quiet environment under constant observation.
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Maintain appropriate levels of sedation. If she has been treated with magnesium sulphate, continue the infusion for 24 hours after the last fit.
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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.
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