HT during pregnancy: Mechanisms and therapeutic options


Prof Maddury Jyotsna, Hyderabad     03 December 2017

Hypertensive disorders of pregnancy including preeclampsia complicate up to 10 of pregnancies constituting one of the greatest causes of maternal and perinatal morbidity and mortality. Placenta plays a central role in the pathogenesis of preeclampsia. 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 preeclampsia. Treatment of hypertension in pregnancy does not cure preeclampsia 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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