Introduction
The scale of the problem
Definitions
Chronic hypertension
Gestational hypertension, pre-eclampsia and eclampsia
HELLP syndrome
Introduction
The term ‘gestational hypertension’ suggests a disorder of blood pressure that arises because of the presence of pregnancy. Such a simple view detracts from the fundamental pathological process that underlies this condition: gestational hypertension, pre-eclampsia and its variants are part of a multisystem disorder that can affect every organ system in the body and collectively are a major direct cause of maternal deaths in the UK.
Although pre-eclampsia is associated with abnormal trophoblast invasion in the first half of pregnancy, it is not until later in the pregnancy that the clinical syndrome of pre-eclampsia is seen. The mechanisms by which the abnormal placentation and subsequent impaired placental perfusion cause the widespread vascular endothelial dysfunction that characterizes pre-eclampsia are not fully understood.
Pre-eclampsia is defined as hypertension with proteinuria. It is, however, a very heterogeneous condition such that the timing of onset and the clinical course are unpredictable. In some, hypertension and proteinuria are the only manifestation, while others may present with severe renal or liver impairment, and in yet others the most prominent feature might be fetal growth restriction secondary to placental disease.
Eclampsia is a generalized seizure that occurs during pregnancy in association with the features of pre-eclampsia. In a proportion of women with eclampsia, however, the features of pre-eclampsia are not evident at the time of the first seizure. The only cure for these conditions is delivery.
The scale of the problem
Hypertension is the commonest medical problem encountered in pregnancy, complicating 10–15% of pregnancies. Pre-eclampsia affects 3–5% of pregnancies in total and up to 10% of pregnancies in nulliparous women. The incidence of severe pre-eclampsia is approximately 1%.
Although in recent years, the rate of eclampsia in the UK appears to have fallen, hypertension in pregnancy remains one of the leading causes of maternal death in the UK, accounting for approximately five or six deaths per year. Severe pre-eclampsia is responsible for 40% of severe obstetric morbidity. Eclampsia occurs in 1 in 3000 pregnancies in the UK (0.03%) but in some developing countries, the incidence of eclampsia is 1%. One-third of the women who die from pre-eclampsia have eclamptic seizures.
Hypertensive disorders also carry a risk for the baby including fetal growth restriction and stillbirth. Pre-eclampsia is the commonest cause of iatrogenic prematurity.
There are long-term implications for women who suffer from hypertensive conditions in pregnancy: an increased risk of chronic hypertension and increase in lifetime risk of cardiovascular disease.
Definitions
Chronic hypertension – otherwise known as essential hypertension; presents at booking or before 20 weeks’ gestation. The woman may already be taking antihypertensive medication at her booking appointment
Gestational hypertension – sometimes also referred to as pregnancy induced hypertension (PIH); new hypertension presenting after 20 weeks (hypertension only, no proteinuria)
Pre-eclampsia – hypertension and proteinuria (± multisystem involvement)
Eclampsia – a convulsive condition associated with pre-eclampsia
HELLP syndrome – a syndrome of haemolysis, elevated liver enzymes and low platelet count.
Hypertension
In normal pregnancy, the maternal blood pressure falls slightly during the first trimester, predominantly as a consequence of reduced systemic vascular resistance. Maternal blood pressure continues to fall during the second trimester and reaches a nadir at approximately 22–24 weeks’ gestation. Thereafter, maternal blood pressure steadily increases during the third trimester to reach pre-pregnancy levels. Maternal blood pressure falls immediately after delivery of the baby, but then rises and peaks on the 4th postnatal day.
Maternal blood pressure should be measured in the sitting position with an appropriate-sized cuff that is placed on the upper arm at the level of the heart (Fig. 36.1). Phase V Korotkoff sounds (i.e. ‘disappearance’ rather than ‘muffling’) should be used when measuring the diastolic blood pressure. Some automated machines for measuring blood pressure have been found to consistently underestimate true blood pressure and the use of a mercury sphygmomanometer is preferred. It is important to use an appropriate cuff size; a cuff that is too small will give an overestimate of true blood pressure.
FIG. 36.1Early detection of pre-eclampsia is important.
(A) Measurement of blood pressure (reproduced with permission). (B) Testing for urinary protein.
Hypertension in pregnancy is defined as a blood pressure of ≥ 140/90 mmHg on two occasions more than 4 h apart.
A diastolic blood pressure of ≥ 110 mmHg on any one occasion or a systolic blood pressure of ≥ 150 mmHg on any one occasion is also significant hypertension.
Another useful measure is the mean arterial pressure (MAP). This is the diastolic blood pressure + 
(systolic blood pressure – diastolic blood pressure). MAP should be maintained at < 125 mmHg.
Hypertension in pregnancy may be pre-existing or related to pregnancy (gestational hypertension or pre-eclampsia). An increased maternal blood pressure in early pregnancy (before 20 weeks’ gestation) is usually due to pre-existing hypertension, most commonly essential hypertension. In a young woman with pre-existing hypertension, efforts should be made to identify the rare secondary causes of hypertension such as renal disease, cardiac disease, phaeochromocytoma and endocrine disorders such as Cushing and Conn syndromes. The diagnosis of essential hypertension may be made retrospectively, if the maternal blood pressure has not returned to normal within 3 months of delivery of the baby.
Gestational hypertension and pre-eclampsia rarely occur before 20 weeks’ gestation unless associated with trophoblastic disease or fetal triploidy. The hypertension associated with pre-eclampsia usually resolves within 6 weeks of delivery.
Proteinuria
Significant proteinuria is defined as a urinary protein:creatinine ratio of > 30 mg/mmol or a validated 24-h urine collection result of > 300 mg of protein. An automated reagent-strip reading device or a spot urinary protein:creatinine ratio should be used for estimating proteinuria. If an automated reagent-strip reading for proteinuria gives a result of 1 + or more, a spot urinary protein:creatinine ratio or 24-h urine collection is indicated to quantify proteinuria.
Chronic hypertension
Essential hypertension is more common in older women and the prognosis for pregnancy is generally good; the main risk is from superimposed pre-eclampsia. Women with essential hypertension are also at increased risk of placental abruption and fetal growth restriction. Some women taking antihypertensive drugs may be able to discontinue their medication during pregnancy, particularly during the first and second trimesters. Drugs that are commonly used for the treatment of essential hypertension during pregnancy include methyldopa, labetalol and nifedipine. Diuretics and angiotensin-converting enzyme (ACE) inhibitors are contraindicated in pregnancy but may be used for the management of hypertension during the puerperium.
Gestational hypertension, pre-eclampsia and eclampsia
Pathophysiology
Recognized risk factors for gestational hypertension and pre-eclampsia are shown in Box 36.1.
Box 36.1
Predisposing factors for developing gestational hypertension/pre-eclampsia
First pregnancy
Family history – mother/sister
Extremes of maternal age
Obesity
Medical factors:
– pre-existing hypertension
– renal disease
– acquired thrombophilia – antiphospholipid antibodies
– inherited thrombophilia
– connective tissue disease (e.g. systemic lupus erythematosus)
– diabetes mellitus
Obstetric factors:
– multiple pregnancy
– previous pre-eclampsia
– hydatidiform mole
– triploidy
– hydrops fetalis (immune and non-immune)
– inter-pregnancy interval of > 10 years
The precise aetiology and pathophysiology of gestational hypertension and pre-eclampsia remain unclear. It is established, however, that women who develop pre-eclampsia have a genetic or phenotypic susceptibility and that there are two distinct phases to the condition’s development: first, there is inadequate trophoblast invasion during early pregnancy and second, in later pregnancy, there is reduced placental perfusion and uteroplacental ischaemia, which in turn gives rise to the clinical syndrome.
The precise mechanism by which this abnormal placentation causes the multisystem disorder that characterizes pre-eclampsia is not known. It has been suggested that there is a trigger which promotes widespread vascular endothelial dysfunction in response to the reduced placental perfusion. This endothelial dysfunction subsequently causes metabolic changes, an exaggerated maternal inflammatory response and reduced organ perfusion.
Maternal susceptibility
The evidence for genotypic susceptibility to developing pre-eclampsia is strong. Large epidemiological studies demonstrate a three- to five-fold increased risk of pre-eclampsia in the first-degree relatives of affected women. While it is possible that a single maternal gene in some families may be important, no single gene has been identified. It may be that multiple genes (maternal, paternal and fetal) interact, and that environmental factors may affect their expression.
Certain phenotypes are also more susceptible. Women with insulin resistance and central obesity are at increased risk of developing pre-eclampsia, possibly on account of an exaggerated metabolic response. Those with connective tissue disease, such as systemic lupus erythematosus, are also at increased risk, possibly because of an exaggerated immune response. In addition, those with an inherited thrombophilia are more likely to develop pre-eclampsia. These associations suggest that the pathophysiology of pre-eclampsia involves a significant interaction between metabolic, immunological and coagulation processes, possibly mediated through vascular endothelial dysfunction and damage.
Phase 1: abnormal placentation
In normal pregnancy, placentation occurs between 6 and 18 weeks’ gestation. During normal placental development, major structural alterations of the spiral arteries occur, allowing an increase in blood supply to the placenta. Trophoblast invasion of the maternal spiral arteries causes the diameter of these arteries to increase approximately five-fold, converting a high-resistance, low-flow system to one with a low resistance and high flow. In women who develop pre-eclampsia, adequate trophoblast invasion does not seem to occur, or the trophoblast invasion is limited to the decidual portions of the vessels. The result is inadequate placental perfusion. This type of abnormal placentation is also associated with fetal growth restriction that occurs independently of pre-eclampsia.
During early pregnancy, trophoblast invasion is regulated at the maternal decidual barrier by the action of factors expressed within the decidua and on the trophoblast cells. These regulatory factors include cell adhesion molecules (CAMs) and the extracellular matrix (ECM), proteinases and their inhibitors, growth factors and cytokines. Abnormalities in any one of these factors may lead to inadequate trophoblast invasion and subsequent pre-eclampsia.
It has been suggested that the primary factor in the aetiology of pre-eclampsia is immunological in origin. Abnormal placentation may be the result of maternal immune rejection of paternal antigens expressed by the fetus. HLA-G is a class 1B major histocompatibility antigen that is expressed by extra-villous trophoblast and may protect cells from natural killer cell lysis. Women who develop pre-eclampsia appear to have extra-villous trophoblast that does not express HLA-G. The predominance of pre-eclampsia in first pregnancies and the protective effect of parity further support an immunological mechanism for the condition.
Phase 2: endothelial dysfunction
The second phase of pre-eclampsia is characterized by widespread endothelial damage and dysfunction. Women with pre-eclampsia have increased circulating levels of markers of endothelial dysfunction. Endothelial damage promotes platelet adhesion and thrombosis, and disturbs the normal physiological modulation of vascular tone, further amplifying the response.
The underlying pathophysiology of this second phase of pre-eclampsia is characterized by an exaggerated maternal systemic inflammatory response, with associated activation of leucocytes, platelets and the coagulation system. Pre-eclampsia is also associated with other markers of inflammation. Features of oxidative stress and dyslipidaemia are also evident and the overall effect is reduced organ perfusion.
Normal pregnancy is a state of systemic inflammation. In normal pregnancy there is a leucocytosis and an increase in leucocyte activation. Women with pre-eclampsia appear to have an excessive inflammatory response to pregnancy. Animal models have demonstrated that the administration of endotoxin during pregnancy can cause hypertension and proteinuria.
It has been suggested that the exaggerated maternal inflammatory response that is seen in pre-eclampsia may lead to endothelial dysfunction and damage. Other systemic metabolic changes that are associated with pre-eclampsia include hypertriglyceridaemia and a significant increase in free fatty acids. This atherogenic lipid profile may also be a contributor to endothelial dysfunction in women with pre-eclampsia.
Many of the features of the second phase of pre-eclampsia are the result of reduced organ perfusion caused by vasoconstriction, activation of the coagulation system and reduction of plasma volume. The resulting organ damage caused by hypoperfusion gives rise to the clinical features of pre-eclampsia, eclampsia and HELLP syndrome (see later and Table 36.1).
Table 36.1
Potential secondary effects of the metabolic, inflammatory endothelial alterations in pre-eclampsia
|
CVS |
Increased peripheral resistance leading to hypertension |
|
Lungs |
Laryngeal and pulmonary oedema |
|
Renal |
Glomerular damage leading to proteinuria, hypoproteinaemia and reduced oncotic pressure which further exacerbates the hypovolaemia |
|
Clotting |
Hypercoagulability, with increased fibrin formation and increased fibrinolysis, i.e. disseminated intravascular coagulation |
|
Liver |
HELLP syndrome |
|
CNS |
Thrombosis and fibrinoid necrosis of the cerebral arterioles |
|
Fetus |
Impaired uteroplacental circulation, potentially leading to FGR, hypoxaemia and intrauterine death |
CVS, cardiovascular system; CNS, central nervous system; FGR, fetal growth restriction.
Normal pregnancy is associated with an increase in angiotensin II levels. Angiotensin II is a potent vasoconstrictor. However, during normal pregnancy, despite increased angiotensin II levels, peripheral vascular resistance falls. This appears to be because normal pregnant women are resistant to the effects of angiotensin II, a phenomenon that seems to be lost in women who develop gestational hypertension and pre-eclampsia. This suggests that abnormalities in the renin–angiotensin–aldosterone system may play a role in the pathogenesis of the condition. Women with pre-eclampsia are also more responsive to other vasoconstrictors such as vasopressin and noradrenaline and appear to be less responsive to vasodilators such as nitric oxide and prostacyclin (PGI2).
In pre-eclampsia, organ perfusion is further compromised by activation of the coagulation cascade. Altered platelet function is seen in most women with pre-eclampsia. In normal pregnancy, there is increased biosynthesis of eicosanoids, particularly prostacyclin and thromboxane A2. Prostacyclin is a vasodilator with platelet-inhibitory properties and thromboxane A2 is a vasoconstrictor with a tendency to promote platelet aggregation. Prostacyclin and thromboxane A2 usually increase in proportion to one another and consequently there is a net neutralization, and homeostasis is maintained. In women with pre-eclampsia, this homeostasis is disrupted due to a relative deficiency of prostacyclin. This occurs either because of a reduction in prostacyclin synthesis or because of an increased production of thromboxane A2. This imbalance leads to platelet stimulation and also vasoconstriction and hypertension.
In pre-eclampsia, plasma volume is reduced as a consequence of increased capillary permeability. This further reduces organ perfusion.
Linking phase 1 and phase 2
It has been suggested that the reduced placental perfusion that is a feature of the first phase of pre-eclampsia is associated with oxidative stress. Women who develop pre-eclampsia have reduced levels of the antioxidant ascorbic acid, as well as increased levels of markers of oxidative stress. Furthermore, women who develop pre-eclampsia have increased cytotrophoblast levels of xanthine oxidase, a superoxide-generating enzyme. The oxidative stress that is associated with placental hypoperfusion may lead to leucocyte activation and/or cytokine production and subsequently the production of free radicals. Oxidative stress may also cause placental apoptosis and result in the shedding of placental debris into the maternal circulation. This debris, along with the free radicals produced by oxidative stress, may then lead to vascular endothelial damage that characterizes the maternal syndrome of the second phase of pre-eclampsia.
Screening and detection
Pre-eclampsia is an unpredictable condition and extremely variable in its manner of presentation. The aim of antenatal screening is to detect pre-eclampsia early enough to prevent disease progression, and hence both maternal and fetal complications, by timely delivery of the baby.
An important component of routine antenatal care for all pregnant women is directed towards screening for hypertension and proteinuria. Risk factors for pre-eclampsia can be identified at the booking visit. A number of additional screening tests for predicting pre-eclampsia have been proposed, but most are of limited clinical use. Abnormalities of the maternal uterine artery Doppler waveform between 18 and 24 weeks’ gestation may identify a group of women at increased risk of developing severe pre-eclampsia (Fig. 36.2). Abnormalities of the maternal uterine artery Doppler waveform appear to be more significant if they are bilateral and if they persist into the third trimester of pregnancy.
FIG. 36.2Uterine artery Doppler notching at 24 weeks is predictive of pre-eclampsia and fetal growth restriction in high-risk mothers.
Angiogenic factors such as placental growth factor (PlGF) are reduced in the early second trimester in pregnancies destined to develop pre-eclampsia. Antiangiogenic factors, e.g. soluble fms-like tyrosine kinase (sFlt) are increased approximately 5 weeks before the onset of pre-eclampsia. sFlt:PlGF ratios may be of value in the prediction of pre-eclampsia. Further studies are needed but near-patient testing for PlGF may develop into a diagnostic test for pre-eclampsia.
In PIH and pre-eclampsia there are many non-specific symptoms and signs that are important indicators of widespread multisystem involvement and these symptoms may herald the onset of severe pre-eclampsia (Box 36.2).
Box 36.2
Symptoms and signs of impending eclampsia
1. Unusual headaches, typically frontal
2. Visual disturbances (blurring of vision, diplopia, scotomas or flashes of light)
3. Restlessness or agitation
4. Epigastric pain, nausea and vomiting
5. Sudden severe hypertension and proteinuria
6. Fluid retention with reduced urine output
7. Hyperreflexia or ankle clonus
8. Retinal oedema, haemorrhages or papilloedema
Clinical management of hypertension in pregnancy without proteinuria
If the maternal blood pressure is found to be elevated, measurement should be repeated after 10–20 min. If it settles, no further action is needed; if still elevated, further assessment is required, ideally at an antenatal day care unit. The woman should be asked about the symptoms of pre-eclampsia (headaches, visual disturbance, epigastric pain, oedema), and the fetal size and well-being should be assessed clinically. Ultrasound can be used to assess fetal size, amniotic fluid volume and fetal umbilical artery Doppler waveform. Serum urate (which rises with pre-eclampsia), urea and electrolytes (U&Es), liver enzymes and platelets (which fall with pre-eclampsia) should also be checked (Table 36.2).
Table 36.2
Investigations in PIH and pre-eclampsia
FBC, full blood count.
In the absence of severe hypertension (≥ 150/110), significant proteinuria or symptoms of pre-eclampsia, and if the biochemistry and haematology results are normal, then the woman can usually be managed as an outpatient. She should be seen at least twice weekly, for blood pressure and urinalysis checks. Serum biochemistry and haematology should also be repeated at least once a week. The woman should be advised to return to hospital if she feels unwell, or if there is any headache, visual disturbance or epigastric pain.
Treatment of the mother with antihypertensive drugs controls the hypertension but does not alter the course of pre-eclampsia. Treatment of hypertension may allow prolongation of the pregnancy and thereby may indirectly improve fetal outcome. Antihypertensive treatment is appropriate with consistent recordings of ≥ 150/100.
Clinical management of pre-eclampsia
In a woman with pre-eclampsia, it is important to consider the overall picture, rather than make decisions on the basis of a single parameter. Progression of the disease is not consistent and further management should be tailored to the individual woman.
Indications for admission to hospital include:
blood pressure > 150/110 mmHg or > 140/90 mmHg with 2 + proteinuria
significant symptoms (headaches, visual disturbance, epigastric pain, oedema)
abnormal biochemistry or haematology results
significant proteinuria
the need for antihypertensive treatment
signs of fetal compromise.
The aim should be to prolong the pregnancy in order to reduce the risk to the baby, but this must be balanced against the risks to the mother. The only true ‘cure’ for pre-eclampsia is delivery of the fetus and placenta, but the timing of this will significantly influence the outcome for both the mother and the baby.
The decision to deliver and the method of delivery are dependent on many factors. There are usually fetal advantages to conservative management before 34 weeks if the blood pressure, laboratory values and fetal condition are stable.
The principles of management of pre-eclampsia:
To control the maternal blood pressure. Reduce the diastolic blood pressure to < 100 mmHg using labetalol, nifedipine, hydralazine or methyldopa (Table 36.3). Effective control of hypertension is essential to prevent the woman having a cerebrovascular accident.
Table 36.3
Drug treatment of hypertension in pregnancy
To assess maternal fluid balance. Pre-eclampsia is associated with an increased vascular permeability and a reduced intravascular compartment. In women with pre-eclampsia, administering too little fluid risks maternal renal failure and giving too much fluid may cause pulmonary oedema. Fluid input and urine output should therefore be monitored. In severe pre-eclampsia, the maternal oxygen saturation (SaO2) should also be monitored, along with serum U&Es, urate, LFTs, haemoglobin, haematocrit, platelets and coagulation. If there is marked oliguria, central venous pressure monitoring may be helpful to differentiate intravascular volume depletion from renal impairment.
To prevent seizures (eclampsia). The use of magnesium sulphate in severe pre-eclampsia halves the risk of subsequent eclampsia, and may reduce the risk of maternal death. Magnesium sulphate, given to those who have had an eclamptic seizure, also prevents further seizures.
To consider delivery. The timing of this depends on the maternal condition, the fetal condition and the gestational age. If preterm delivery is being considered, corticosteroids should be administered to the mother to reduce the risks associated with prematurity (Fig. 36.3).
FIG. 36.3This baby, born at 36 weeks to a mother with severe pre-eclampsia, weighed 1.6 kg.
(Usual weight at 36 weeks: 2.2–3.3 kg.)
Women with pre-eclampsia who remain hypertensive in the initial postpartum period are still at risk of pre-eclampsia related complications, particularly for the initial 72 h following delivery. Continued vigilance is advisable during this period, as an inpatient if necessary.
Management of eclampsia
Eclampsia occurs when there is a tonic–clonic convulsion in association with the features of pre-eclampsia (the word ‘eclampsia’ means ‘lightning’). In the UK, the incidence of eclampsia is 1 in 3000 pregnancies, with 38% of eclamptic seizures occurring antepartum, 18% intrapartum and 44% postpartum. Over one-third of eclamptic seizures occur before proteinuria and hypertension have been documented. In the UK, the maternal mortality associated with eclampsia is 0.22 per 100 000 maternities. In less-developed countries, incidences of up to 80 per 10 000 maternities have been reported, with maternal death occurring in approximately 10% of cases.
The treatment of eclampsia is outlined in Box 36.3.
Box 36.3
Treatment of eclampsia
The patient should be turned onto her left side to avoid aortocaval compression. The airway should be secured and high-flow oxygen should be administered
Magnesium sulphate (MgSO4) should be administered intravenously to terminate the seizure and then by intravenous infusion to reduce the chance of further convulsions. The infusion should be continued for at least 24 h following delivery or after the last seizure. MgSO4 can depress neuromuscular transmission and the patient should be monitored for signs of toxicity. The respiratory rate and patellar reflexes should be monitored (reduced patellar reflexes usually precede respiratory depression). If there is significant respiratory depression, calcium gluconate can be used to reverse the effects of MgSO4 and consideration given to ventilation
Urgent delivery is necessary if the seizure has occurred antenatally or intrapartum
Paralysis and ventilation should be considered if the seizures are prolonged or recurrent
Prevention
Various preventive strategies have been employed in women considered to be at risk of developing pre-eclampsia. The estimated value of these interventions is shown in Box 36.4.
Box 36.4
Prevention of pre-eclampsia
Proven to be of value
Low-dose aspirin
Possibly of value
Calcium supplementation
Not of value
Diet with high protein content
Restriction of salt in diet
Restriction of weight gain
Vitamins C and E
Aspirin inhibits prostaglandin synthesis via cyclooxygenase and the dose of aspirin required to inhibit thromboxane synthesis is less than that required for prostacyclin inhibition. Low-dose aspirin should reduce the vascular and prothrombotic effects of thromboxane A2 in women at risk of developing pre-eclampsia. Taking 75 mg aspirin daily from the first trimester of pregnancy leads to a 15% reduction in the incidence of pre-eclampsia. It should be offered to those women at high risk of developing pre-eclampsia and should be commenced at 12 weeks’ gestation.
The use of antioxidants such as vitamin C and E is not useful for the prevention of pre-eclampsia. Likewise, restriction of salt intake and limiting weight gain during pregnancy are not useful in this regard.
HELLP syndrome
HELLP is the acronym for haemolysis, elevated liver enzymes (particularly transaminases) and low platelets. It is a variant of pre-eclampsia, and affects up to 12% of those with pre-eclampsia/eclampsia. HELLP syndrome is more common in multiparous women experiencing pre-eclampsia. Women with HELLP syndrome may present with epigastric pain, nausea and vomiting, and right upper quadrant tenderness may be evident on examination. Aspartate transaminase (AST) rises first, followed by a rise in lactate dehydrogenase (LDH). A blood film may show burr cells and polychromasia consistent with haemolysis, although frank anaemia is uncommon. Platelet transfusion is only rarely required. HELLP syndrome is also associated with acute renal failure and disseminated intravascular coagulation (DIC), and there is also an increased incidence of placental abruption.
The management of HELLP syndrome is to stabilize the mother, correct any coagulation disorder, assess fetal well-being and assess the need for delivery. It is generally considered that delivery is appropriate for moderate or severe cases, but management may be more conservative (with close monitoring) if the condition is mild. Vigilance is required for at least 48 h postpartum, as deterioration in the maternal condition may occur. The risk of recurrence of HELLP syndrome in subsequent pregnancies is approximately 20%.
Key points
• Pre-eclampsia is a multisystem disorder, and is a major cause of maternal and perinatal morbidity and mortality.
• There are two phases: phase 1 is associated with abnormal placentation and phase 2 is characterized by an exaggerated maternal inflammatory response, endothelial dysfunction and reduced organ perfusion.
• The cure for pre-eclampsia is delivery of the fetus. Antihypertensive therapy does not fundamentally alter the progress of the condition.
• HELLP syndrome is a variant of pre-eclampsia; HELLP is an acronym for haemolysis, elevated liver enzymes and low platelets.