Preeclampsia, a disease unique to human pregnancy, occurs at or beyond 20 weeks gestation and affects up to 8 percent of pregnancies. Despite increasing awareness, it continues to be a major contributor to maternal and fetal morbidity and mortality in the U.S. and worldwide.1 The placenta instigates changes to endothelial cells that impact vascular function, leading to fetal risks, including growth restriction and preterm delivery. Maternal risks include sequelae of endothelial cell dysfunction and hypertension on various organ systems, most notably pulmonary edema, acute renal insufficiency, impaired liver function, hemorrhagic stroke, seizure and even death. Since the etiology of preeclampsia has not been fully elucidated, the clinical emphasis remains timely recognition and management.
Identified risk factors for the development of preeclampsia include history of preeclampsia, nulliparity, multifetal gestation, assisted reproduction, maternal age >35, diabetes, kidney disease, chronic hypertension and thrombophilia, among others.1
In 2013, the American College of...