Pathogenesis

Evidence from epidemiological data and animal experiments implicate the placenta as the origin of pre-eclampsia. Poor placental perfusion causes the release of blood borne products from the fetoplacental unit which result in endothelial cell dysfunction. There is an increased sensitivity to normal circulating pressor agents, increased intracellular coagulation and increased fluid loss from the intravascular compartment.

Evidence for the role of the placenta in pre-eclampsia comes from many observations including:

• pre-eclampsia is uniquely a disease of pregnancy - by 6 months post partum, the observed pathophysiological changes have reverted to normal
• pre-eclampsia may occur in abdominal pregnancy - so the uterus is unlikely to be involved
• pre-eclampsia may occur with a hydatidiform mole - so a foetus is not always necessary

Causes of a poorly perfused placenta include:

• abnormal trophoblast implantation and spiral artery atherosis
• microvascular disease - pre-existing hypertension, diabetes, collagen vascular diseases
• a large placenta - multiple pregnancy, hydatidiform mole, a fetus with a hydropic placenta