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.

Management. Early detection, close surveillance, and timely delivery are the requirements for the management of preeclampsia. Delivery is the ultimate cure, and although always appropriate for the mother, it may not be best for the fetus.

Although some experts advocate hospital admission for all preeclamptic patients, reliable women with mild disease who are remote from term may safely be managed as outpatients. Bed rest is a traditional management strategy for hypertension in pregnancy and is generally employed. Although bed rest does help control blood pressure, it does not change maternal or fetal outcome. Neither sodium nor fluid restriction is indicated. Weekly evaluation of kidney, liver, and coagulation function is important. Weekly or twice-weekly antepartum fetal surveillance is required to ensure adequate placental function. Serial ultrasound evaluation of fetal growth is also used. Evidence of significant intrauterine growth retardation is an indication for delivery. If maternal and fetal conditions are stable, delivery near term or with biochemical evidence of fetal lung maturity before 37 weeks is advisable.

Severe preeclampsia or eclampsia requires delivery. Patients should be treated with magnesium sulfate, 4 to 8 grams, given intravenously over 10 to 20 minutes until normal or diminished deep tendon reflexes are achieved. Continuous intravenous administration of magnesium sulfate, 2 to 3 grams per hour, is usually required to maintain diminished reflexes and serum magnesium levels in the therapeutic range of 6 to 8 mEq per liter. Respiratory depression can occur rapidly with intravenous infusion and may be reversed by slow intravenous administration of 10 ml of 10% calcium gluconate. Respiratory depression may be aggravated by concurrent use of narcotics or benzodiazepines. Oliguria decreases magnesium excretion, increasing the possibility of respiratory depression. Magnesium sulfate treatment should continue for at least 24 hours postpartum.

Arterial blood pressure of 180/110 mm Hg or higher requires treatment. Hydralazine is most often effective when administered in an intravenous bolus of 5 mg. Boluses may be repeated every 15 to 30 minutes if diastolic blood pressure remains at 110 mm Hg, up to a cumulative dose of 20 mg. Diastolic blood pressures below 90 mm Hg are undesirable because of the negative impact on uterine and placental blood flow. If blood pressure control is not achieved, labetalol, 20 mg intravenous bolus, or nifedipine, 10 mg orally, may be necessary to lower diastolic blood pressure.

Recurrence of seizures in a preeclamptic patient requires administration of 10 mg of diazepam, followed by loading and maintenance infusions of magnesium sulfate as outlined earlier. Experience with phenytoin in preeclamptic seizures has been limited.

Vaginal delivery is usually possible once the patient with severe preeclampsia is stabilized. Prostaglandin cervical ripening and oxytocin induction can be used to achieve delivery even in patients with an unfavorable cervix. With rare exceptions, attempts at vaginal delivery should be made in most patients with severe preeclampsia or eclampsia. The majority of patients spontaneously begin diuresis within 24 to 36 hours after delivery. Swan-Ganz catheterization and hemodynamic monitoring are rarely required postpartum unless severe oliguria is encountered. Total fluid intake should be maintained at 2000 to 2500 ml per 24 hours.

Most preeclamptic primigravidas become normotensive shortly after delivery, although elevated blood pressure can persist in a minority of patients for up to 6 weeks. Hypertension that persists 12 weeks postpartum should be considered chronic and should be appropriately evaluated.