Mechanism[edit]
The presence of a placenta is required, and eclampsia resolves if it is removed.[16] Reduced blood flow to the placenta (placental hypoperfusion) is a key feature of the process. It is accompanied by increased sensitivity of the maternal vasculature to agents which cause constriction of the small arteries, leading to reduced blood flow to multiple organs. Also, an activation of the coagulation cascade may lead to microthrombi formation, which can further impair blood flow. Thirdly, increased vascular permeability results in the shift of extracellular fluid from the blood to the interstitial space, with further reduction in blood flow, and edema. These events lead to hypertension; renal, pulmonary, and hepatic dysfunction; and cerebral edema with cerebral dysfunction and convulsions.[16] Before symptoms appear, increased platelet and endothelial activation[16] may be detected.
Placental hypoperfusion is linked to abnormal modelling of the fetal–maternal placental interface that may be immunologically mediated.[16] The invasion of the trophoblast appears to be incomplete.[17] The placenta produces the potent vasodilator adrenomedullin: it is reduced in pre-eclampsia and eclampsia.[18] Other vasodilators are also reduced, including prostacyclin, thromboxane A2, nitric oxide, and endothelins, also leading to vasoconstriction.[13] Many studies have suggested the importance of a woman's reduced immunological tolerance to her baby's father, whose genes are present in the young fetus and the placenta.[19]
Eclampsia is a form of hypertensive encephalopathy: cerebral vascular resistance is reduced, leading to increased blood flow to the brain, cerebral edema and resultant convulsions.[20] An eclamptic convulsion usually does not cause chronic brain damage unless intracranial haemorrhage occurs