Preeclampsia: From Etiopathology to Organ Dysfunction

Abstract

Preeclampsia is a hypertensive disorder of pregnancy affecting 6–12% of the population. There are various risk factors for the development of preeclampsia, ranging from advanced maternal age to genetics. The proposed etiologies for preeclampsia are abnormal placentation, immunological intolerance, endothelial damage, and genetic inheritance. The pathogenesis includes endothelial activation and dysfunction leading to vasospasm. Preeclampsia is divided into two stages: asymptomatic and symptomatic stages. Preeclampsia causes multiple organ involvement, namely central nervous system, respiratory, cardiovascular, hematological dysfunction, HELLP (hemolysis elevated liver enzymes, low platelets) syndrome, endocrine, renal, hepatic, and uteroplacental dysfunction. These organ dysfunctions increase morbidity and mortality in preeclamptic pregnant patients.

Membrane Lesions and Reduced Life Span of Red Blood Cells in Preeclampsia as Evidenced by Atomic Force Microscopy

“…It is one of the leading causes of maternal morbidity, preterm delivery, and fetal compromise. Preeclampsia can cause end organ damage, such as renal or liver impairment, hematological dysfunction, neurological excitability, and fetal growth restriction [ 2 ]. The disease is characterized by dysfunction of vascular endothelium caused by shallow infiltration of cytotrophoblast cells, narrowing arterioles leading to reduced blood flow, and ischemia [ 3 ].…”