HAEMODYNAMIC CONTRIBUTIONS TO THE PATHOGENESIS OF PREECLAMPSIA AND ECLAMPSIA

Abstract

Current hypotheses regarding the origins of preeclampsia have focused on the “Two stage model”. This model suggests that the primary steps in the pathophysiologic sequence of preeclampsia are initiated by abnormal placentation including the classic finding of abnormal trophoblast invasion of maternal decidual spiral arteries. The second stage of the sequence includes the elaboration of a single or multiple substances from these disordered placentas which contribute to the generalized maternal systemic illness, eventually manifesting as endothelial injury, hypertension and proteinuria. Recent studies have focused on the role of pro and anti-angiogenic peptides as potential placentally derived aetiologic agents in this pathophysiologic sequence, although other placental products have been highlighted in recent research. Despite the fact that this modeling of preeclampsia has widespread support significant limitations to this hypothesis can be identified.