Pre-eclampsia and eclampsia


Essentials

  • 1

    Pre-eclampsia is hypertension with organ-system dysfunction unique to the second half of pregnancy.

  • 2

    Maternal and foetal demise are inevitable and can only be stopped by pregnancy termination.

  • 3

    Early diagnosis is crucial as the rate of deterioration is unpredictable.

  • 4

    Eclampsia is a seizure complicating pre-eclampsia and leads to high maternal and foetal morbidity and mortality.

Introduction

Pre-eclampsia is a hypertensive disorder unique to pregnancy. Maternal and foetal morbidity and mortality are high with pregnancy termination the only definitive treatment. In Australia, severe pre-eclampsia occurs in 1% to 2% of all pregnancies and accounts for 15% of maternal mortality. The perinatal mortality is 10% and accounts for 5% to 10% of pre-term deliveries.

Definitions

The blood pressure (BP) in a normal pregnancy falls in the first trimester, reaching a nadir in the second, and returns to the normal range by the third trimester. Hypertension is a BP of >140/90 mm Hg. A change of >30/15 mm Hg from the preconception level should prompt close monitoring. The four hypertensive disorders in pregnancy are:

  • Chronic hypertension: predates the pregnancy.

  • Gestational hypertension: during pregnancy and resolves within 6 weeks post-partum.

  • Pre-eclampsia: hypertension with organ-system dysfunction occurring at >20 weeks gestation and up to 6 weeks post-partum.

  • Pre-eclampsia superimposed on chronic hypertension.

Pathophysiology

The pathogenesis of pre-eclampsia remains unclear, and some of the current thinking is discussed.

Abnormal placentation

In normal pregnancy, foetal trophoblasts migrate into the endometrial and myometrial spiral arteries, causing their remodelling into low resistance–high capacitance vessels. Trophoblasts in pre-eclamptic pregnancies do not migrate beyond the endometrial spiral arteries. They remain as high resistance vessels that jeopardize the blood supply to the placenta.

Endothelial dysfunction

The systemic effects are thought to result from endothelial dysfunction leading to high systemic vascular resistance. The end result is hypoperfusion of organ-systems. The cause is thought to be an imbalance between angiogenic and antiangiogenic factors.

Immunological cause

An immunological cause without definite evidence has been proposed for the following risk factors: first pregnancy, multiple pregnancy, pregnancy with a different partner or when the inter-pregnancy period is beyond 10 years with the same partner. See Box 19.6.1 for other risk factors.

Box 19.6.1

Age >40 years

BMI >30kg/m 2

Gestational hypertension

Past history of pre-eclampsia

Family history

Antiphospholipid syndrome

Diabetes

Clinical features

Pre-eclampsia causes multiple organ-system dysfunctions that may not be evident on presentation. Checking the BP in patients of >20/40 weeks gestation is an essential component of the assessment. Hypertension detected must trigger the inclusion of preeclampsia in the differential diagnoses. The following are clinical features that may be encountered. More than one organ system may be affected in pre-eclampsia.

Neurological

Neurological features are related to cerebral oedema. Headaches, visual symptoms, confusion and papilloedema should be sought. Stroke may also occur. Seizure, known as eclampsia, is the most time critical complication, with a high maternal and foetal mortality and morbidity.

Eclampsia is a self-limiting seizure that occurs as a complication of preeclampsia. It can occur any time after 20 weeks gestation and up to 6 weeks post-partum. However, it is less common after 24 hours post-partum. It is not always associated with hypertension but more likely to occur with severe preeclampsia with BP of >170/110 mm Hg, which accounts for two-thirds of cases. The rest have a lower BP, including a normal BP. The magnitude of the BP is not a reliable way of predicting eclampsia, and unfortunately, there is no reliable way to detect its imminent onset. Persistent headache, visual disturbances, neurological deficit or hyper-reflexia should trigger preventive measures, as there is a high risk of intracerebral haemorrhage in eclampsia. Eclampsia is the most important differential diagnosis to consider in pre-eclampsia. However, other causes of seizures need to be sought, especially when seizure occurs beyond the first 24 hours post-partum.

Cardiovascular

In normal pregnancy, the fall in the diastolic BP and systemic vascular resistance (SVR) is coupled with a raised cardiac output. In pre-eclamptic pregnancies, the SVR is increased and coupled with a reduced cardiac output. There is left ventricular diastolic dysfunction. In practice, this means that patients are at risk of acute pulmonary oedema with injudicious intravenous fluid therapy.

Gastrointestinal

Pre-eclampsia may present with severe or persistent epigastric or right upper quadrant pain. A transaminitis twice the normal range may be found in isolation or associated with other features of the HELLP syndrome (HELLP stands for haemolysis, elevated liver enzymes and low platelets) discussed below. Biliary tract disease and fatty liver of pregnancy are alternative diagnoses.

The following features of pre-eclampsia need to be sought through investigations.

Renal

Evidence of renal involvement needs to be sought in patients with oedema.

Proteinuria

The current practice is to use a spot urine protein/urine creatinine ratio to quantify the amount of proteinuria. Significant proteinuria is a ratio >30 mg/mol. Replacing the previous criteria of a 24-hour urine sample means early diagnosis can be made in the emergency department (ED).

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