Acute complications of preeclampsia.

Preeclampsia is an idiopathic multisystem disorder specific to human pregnancy and the puerperium. More precisely, it is a disease of the placenta, because it has also been described in pregnancies where there is trophoblast but no fetal tissue (complete molar pregnancies). Although the pathophysiology of preeclampsia is poorly understood, it is clear that the blueprint for its development is laid down early in pregnancy. It has been suggested that the pathologic hallmark is a complete or partial failure of the second wave of trophoblast invasion from 16 to 20 weeks’ gestation, which is responsible in normal pregnancies for destruction of the muscularis layer of the spiral arterioles. As pregnancy progresses, the metabolic demands of the fetoplacental unit increase. However, because of the abnormally shallow invasion of the placenta, the spiral arterioles are unable to dilate to accommodate the required increase in blood flow, resulting in “placental dysfunction” that manifests clinically as preeclampsia. Although attractive, this hypothesis remains to be validated. Preeclampsia is a clinical diagnosis. The classic definition of preeclampsia encompasses three elements: new-onset hypertension (defined as a sustained sitting blood pressure !140/90 mm Hg in a previously normotensive woman); new-onset proteinuria (defined as >300 mg/24 hours or !2+ on a clean-catch urinalysis in the absence of urinary tract infection); and new-onset significant nondependent edema. However, more recent consensus reports have suggested eliminating edema as a criterion for the diagnosis. A more extensive synopsis of preeclampsia is beyond the scope of this discussion. This monograph serves to review in detail the diagnosis and management of several acute maternal complications of preeclampsia: eclampsia, HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome, liver rupture, pulmonary edema, renal failure, disseminated intravascular coagulopathy (DIC), hypertensive emergency, and hypertensive encephalopathy and cortical blindness. Correspondence: Errol R. Norwitz, MD, PhD, Department of Obstetrics & Gynecology, Brigham & Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115. E-mail: [email protected] PROD. # GRF20214