Introduction

Eclampsia refers to the occurrence of one or more generalized convulsions and/or coma in the setting of pre-eclampsia and in the absence of other neurologic conditions. Pre-eclampsia is a multisystem disorder of pregnancy and the puerperium, complicating approximately 6–8% of all pregnancies (ACOG, 1996, 2002). Pre-eclampsia is characterized by new onset hypertension (sitting blood pressure ≥140/90), proteinuria (≥2+ in a random urine sample or ≥300 mg in a 24-h collection) with or without non-dependent edema after 20 weeks' gestation. Eclampsia was at one time thought to be the end result of pre-eclampsia, hence the nomenclature. It is now clear, however, that seizures are but one clinical manifestation of “severe” pre-eclampsia. Other manifestations include, among others, HELLP syndrome (Hemolysis, Elevated Liver enzymes and Low Platelets), disseminated intravascular coagulopathy (DIC), renal failure, hepatocellular damage, pancreatitis, congestive cardiac failure, pulmonary edema and fetal intrauterine growth restriction.

The pathophysiology of pre-eclampsia is poorly understood. It is a disease of human pregnancy; more precisely, it is a disease of the placenta since it is also described in pregnancies where there is trophoblast but no fetal tissue (complete molar pregnancies) (Goldstein and Berkowitz, 1994). The blueprint for the development of pre-eclampsia is laid down early in pregnancy. The pathologic hallmark of pre-eclampsia appears to be a failure of the second wave of trophoblast invasion from 8 to 18 weeks' gestation, a process that is responsible for destruction of the muscularis layer of the spiral arterioles and, as such, establishment of the definitive uteroplacental circulation (Brosens et al., 1972; Cross et al., 1994; Meekins et al., 1994).