Persistent brain injury after preeclampsia.

Abstract

Preeclampsia, a common hypertensive disorder of pregnancy, contributes substantially to maternal and fetal morbidity and mortality worldwide. While the cause of preeclampsia remains debated, it is clear that there are both placental and maternal causes of preeclampsia, making it a heterogeneous disease.1 Abnormal trophoblast invasion of spiral arteries during placentation leads to placental ischemia and release of placental-derived soluble factors into the maternal circulation.2 These circulating proinflammatory and antiangiogenic factors appear to produce maternal vascular inflammation and cause endothelial dysfunction that underlies hypertension and proteinuria associated with preeclampsia.1,2 However, not all women with preeclampsia have placental dysfunction. In these cases, the physiologic burden of pregnancy, characterized by mild peripheral inflammation, is thought to unmask preexisting maternal vascular dysfunction.1 The presence of both maternal and placental disease leads to the most severe and early-onset form of the disorder.1 Because of this heterogeneity, preeclampsia has been subclassified by clinical severity determined by maternal and fetal characteristics. Preeclampsia is considered severe if it is complicated by fetal growth restriction, which is strongly associated with placental dysfunction and early-onset disease. Subclassification of preeclamptic disease relating to time of delivery has also facilitated understanding the cause and complications of preeclampsia. For example, early-onset preeclampsia is a severe form of the condition involving maternal and placental disease in which delivery occurs ≤34 weeks of gestation, whereas late-onset preeclampsia is typically a more mild form of disease in which delivery occurs >34 weeks of gestation.1