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Pre-eclampsia is usually defined as hypertension and proteinuria that develops after 20 weeks' gestation in a previously normotensive and non-proteinuric woman (oedema is now omitted from the definition, although it is often present).

It is possible to develop non-proteinuric pre-eclampsia and also to have eclamptic seizures with minimal or even no hypertension. Pre-eclampsia occurs in 5-6% of pregnancies overall (up to 25% in patients with pre-existing hypertension).

Pre-eclampsia/eclampsia is a major direct cause of maternal death worldwide. Pre-eclampsia is a multisystem disease with a variable clinical presentation. The pathophysiology of pre-eclampsia is still only partially understood, but it is known that failure of placentation occurs early in pregnancy and this leads to vascular endothelial cell damage and dysfunction. The endothelial cell damage is thought to lead to release of vasoactive substances, which promote generalised vasoconstriction and reduced organ perfusion. This is exacerbated by the increased sensitivity to circulating catecholamines found in the pre-eclamptic patient. Pre-eclamptic women demonstrate an imbalance of the normal thromboxane/ prostacyclin ratio and increased free radical activity.

Pre-eclampsia encompasses HELLP (haemolysis, elevated liver enzymes and low platelets) syndrome, eclampsia and possibly acute fatty liver of pregnancy. Although the disease is progressive, a mother may be asymptomatic until she presents with an eclamptic fit, and although pre-eclampsia is a disease of pregnancy, terminated only by delivery, pre-eclampsia, HELLP syndrome and eclampsia may all present only after delivery.

There have been many attempts to prevent development of pre-eclampsia, e.g. with dietary vitamins, antioxidants and minerals, with no clear benefit found. The large international CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) trial failed to show universal benefit from low-dose aspirin, suggesting instead that aspirin may be beneficial in selected high-risk women.

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