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Prof Maddury Jyotsna, Hyderabad 06 January 2018

Placenta plays a central role in the pathogenesis of pre-eclampsia. The reduced uteroplacental perfusion, which develops as a result of abnormal cytotrophoblast invasion of spiral arterioles, triggers the cascade of events leading to the maternal disorder. Placental ischemia leads to release of soluble placental factors, many of which are classified as anti-angiogenic or pro-inflammatory. Once these ischemic placental factors reach the maternal circulation, they cause widespread activation and dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin-1 and superoxide, increased vascular sensitivity to angiotensin II and decreased formation of vasodilators such as nitric oxide.
Current therapy does not ameliorate the placental pathology nor alter the pathophysiology or natural history of pre-eclampsia. Treatment of HT in pregnancy does not cure pre-eclampsia but is intended to prevent cerebral hemorrhage and eclampsia and perhaps delay progression of proteinuria. Delivery is the definitive management and is followed by resolution, generally over a few days but sometimes much longer.
A team approach, involving obstetrician, midwife, neonatologist, anesthetist and physician provides the best chance of achieving a successful outcome for mother and baby. Regular and ongoing reassessment of both the maternal and fetal condition is required.

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