Preeclampsia and Eclampsia

Diagnosis. Preeclampsia is a multiorgan disease unique to pregnancy. The condition is characterized by the development of elevated blood pressure, proteinuria, and generalized edema. The condition may also be recognized by visual changes, headache, hyperreflexia, fundoscopic changes, and the presence of hyperuricemia. Eclampsia is the presence of generalized seizures or coma in a patient with preeclampsia. Preeclampsia usually occurs after 20 weeks' gestation and before the seventh postpartum day. The vast majority of women who develop preeclampsia are nulliparous and frequently at the extremes of their childbearing years. Other identified risk factors for preeclampsia include family history of preeclampsia, history of preeclampsia in a previous pregnancy, multiple gestation, and hydatidiform mole. Chronic hypertension and underlying vascular disease increase the likelihood that superimposed preeclampsia will develop. Pregnant women with diastolic blood pressure consistently greater than 75 mm Hg in the second trimester or greater than 85 mm Hg in the third trimester should be observed closely for signs of preeclampsia.

It is clinically useful to separate preeclampsia into mild and severe disease. In most cases the development of severe preeclampsia requires delivery, regardless of gestational age. Box 372-2 lists criteria frequently used to indicate severe disease if any are present. Even in mild disease, careful frequent evaluation is necessary because of the possibility of rapid deterioration and the development of eclampsia. Nearly 25% of eclamptics experience their first seizure with "mild" disease.

A subset of severe preeclamptic patients develop hemolysis (H), elevated liver enzymes (EL), and low platelets (LP), or the "HELLP syndrome." The majority of cases occur between the twenty-seventh and thirty-sixth week of gestation, but approximately one third occur postpartum, with peak laboratory abnormalities on the day or two following delivery. Presenting symptoms in women with the HELLP syndrome include right upper quadrant or epigastric pain, malaise, nausea or vomiting, and headache. Physical examination may reveal right upper quadrant tenderness, edema, and weight gain, but hypertension and proteinuria may be absent. Maternal mortality is about 1% to 3% in tertiary care settings, but rates as high as 25% have been reported in community hospitals. Complications of the HELLP syndrome include disseminated intravascular coagulation, abruptio placenta, acute renal failure, and pulmonary edema.

Pathophysiology. Systemic alteration in vascular endothelial function leading to reduced organ perfusion appears to be the basic pathologic mechanism in preeclampsia. This abnormality is the result of a cascade of events that begins with an abnormal immunologic reaction to placental implantation that prevents trophoblastic invasion of the uterine spiral arteries. The arteries reach only about 40% of the diameter achieved in normal pregnancy, and the placenta, in turn, becomes chronically hypoperfused. This hypoperfusion leads to the elaboration of toxic mediators, which may then cause endothelial dysfunction. The end result is hypoperfusion of vital organs and activation of the clotting cascade.