Acute Complications of Preeclampsia ERROL R. NORWITZ, MD, PhD,* CHAUR-DONG HSU, MD, MPH,† and JOHN T. REPKE, MD† Departments of Obstetrics & Gynecology, *Brigham & Women’s Hospital, Harvard Medical School, Boston, Massachusetts, and †University of Nebraska Medical Center, University of Nebraska Medical School, Omaha, Nebraska Preeclampsia is an idiopathic multisystem disorder specific to human pregnancy and the puerperium. 1 More precisely, it is a dis- ease of the placenta, because it has also been described in pregnancies where there is tro- phoblast but no fetal tissue (complete molar pregnancies). Although the pathophysiol- ogy 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. 2 As pregnancy progresses, the metabolic de- mands of the fetoplacental unit increase. However, because of the abnormally shal- low invasion of the placenta, the spiral arte- rioles are unable to dilate to accommodate the required increase in blood flow, result- ing in “placental dysfunction” that manifests clinically as preeclampsia. Although attrac- tive, this hypothesis remains to be validated. Preeclampsia is a clinical diagnosis. The classic definition of preeclampsia encom- passes three elements: new-onset hyperten- sion (defined as a sustained sitting blood pressure 140/90 mm Hg in a previously normotensive woman); new-onset protein- uria (defined as >300 mg/24 hours or 2+ on a clean-catch urinalysis in the absence of urinary tract infection); and new-onset sig- nificant nondependent edema. 1 However, more recent consensus reports have sug- gested eliminating edema as a criterion for the diagnosis. 3 A more extensive synopsis of preeclamp- sia is beyond the scope of this discussion. This monograph serves to review in detail the diagnosis and management of several acute maternal complications of preeclamp- sia: eclampsia, HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome, liver rupture, pulmonary edema, renal fail- ure, disseminated intravascular coagulopa- thy (DIC), hypertensive emergency, and hy- pertensive encephalopathy and cortical blindness. Correspondence: Errol R. Norwitz, MD, PhD, Depart- ment of Obstetrics & Gynecology, Brigham & Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115. E-mail: enorwitz@partners.org CLINICAL OBSTETRICS AND GYNECOLOGY Volume 45, Number 2, 308–329 © 2002, Lippincott Williams & Wilkins, Inc. CLINICAL OBSTETRICS AND GYNECOLOGY / VOLUME 45 / NUMBER 2 / JUNE 2002 308