Preeclampsia is new-onset hypertension and proteinuria after 20 wk gestation. Eclampsia is unexplained generalized seizures in patients with preeclampsia. Diagnosis is clinical and by urine protein measurement. Treatment is usually with IV Mg sulfate and delivery at term.
Preeclampsia affects 3 to 7% of pregnant women. Preeclampsia and eclampsia develop after 20 wk gestation; up to 25% of cases develop postpartum, most often within the first 4 days but sometimes up to 6 wk postpartum.
Untreated preeclampsia usually smolders for a variable time, then suddenly progresses to eclampsia, which occurs in 1/200 patients with preeclampsia. Untreated eclampsia is usually fatal.
Etiology is unknown; however, risk factors include the following:
Pathophysiology of preeclampsia and eclampsia is poorly understood. Factors may include poorly developed uterine placental spiral arterioles (which decrease uteroplacental blood flow during late pregnancy), a genetic abnormality on chromosome 13, immunologic abnormalities, and placental ischemia or infarction. Lipid peroxidation of cell membranes induced by free radicals may contribute to preeclampsia.
Fetal growth restriction may result. Diffuse or multifocal vasospasm can result in ischemia, eventually damaging multiple organs, particularly the brain, kidneys, and liver. Factors that may contribute to vasospasm include decreased prostacyclin (an endothelium-derived vasodilator), increased endothelin (an endothelium-derived vasoconstrictor), and increased soluble Flt-1 (a circulating receptor for vascular endothelial growth factor).
The coagulation system is activated, possibly secondary to endothelial cell dysfunction, leading to platelet activation. The HELLP syndrome (hemolysis, elevated liver function tests, and low platelet count) develops in 10 to 20% of women with severe preeclampsia or eclampsia; this incidence is about 100 times that for all pregnancies (1 to 2/1000).
Symptoms and Signs
Preeclampsia may be asymptomatic or may cause edema or excessive weight gain. Nondependent edema, such as facial or hand swelling (the patient's ring may no longer fit her finger), is more specific than dependent edema. Reflex reactivity may be increased, indicating neuromuscular irritability, which can progress to seizures (eclampsia). Petechiae may develop, as may other signs of bleeding.
Severe preeclampsia may cause organ damage; manifestations may include headache, visual disturbances, confusion, epigastric or right upper quadrant abdominal pain (reflecting hepatic ischemia or capsular distention), nausea, vomiting, dyspnea (reflecting pulmonary edema or acute respiratory distress syndrome [ARDS]), stroke (rarely), and oliguria (reflecting decreased plasma volume or ischemic acute tubular necrosis).
Diagnosis is suggested by symptoms or presence of hypertension, defined as systolic BP > 140 mm Hg, diastolic BP > 90 mm Hg, or both. Except in emergencies, hypertension should be documented in > 2 measurements taken > 6 h apart. Urine protein excretion is measured in a 24-h collection.
The following points help differentiate among hypertensive disorders in pregnant women:
If preeclampsia is diagnosed, tests include urinalysis, CBC, platelet count, uric acid, liver function tests, and measurement of serum electrolytes, BUN, creatinine, and creatine clearance. The fetus is assessed with a nonstress test or biophysical profile.
HELLP syndrome is suggested by microangiopathic findings (eg, schistocytes, helmet cells) on peripheral blood smears, elevated liver enzymes, and a low platelet count.
Severe preeclampsia is differentiated from mild by one or more of the following:
Definitive treatment is delivery. However, risk of early delivery is balanced against severity of preeclampsia and response to other treatments. Usually, immediate delivery after maternal stabilization (eg, controlling seizures, beginning to control BP) is indicated for the following:
Other treatments aim to optimize maternal health, which usually optimizes fetal health. If delivery can be delayed in pregnancies of about 32 to 34 wk, corticosteroids are given for 48 h to accelerate fetal lung maturity.
Most patients are hospitalized. Patients with eclampsia or severe preeclampsia are often admitted to an ICU.
If preeclampsia is mild, outpatient treatment is possible; it includes strict bed rest, lying on the left side whenever possible, BP evaluation and physician visits 2 to 3 times/wk, a normal salt intake, and increased fluid intake.
However, most patients with mild eclampsia require hospitalization; some also need drug treatment for a few hours to stabilize them and to lower systolic BP to 140 to 155 mm Hg and diastolic BP to 90 to 105 mm Hg. Delivery follows unless preeclampsia does not progress and the fetus is very premature.
Outpatients are usually evaluated once every 2 or 3 days for seizures, symptoms of severe preeclampsia, and vaginal bleeding. BP, reflexes, and fetal heart status (with nonstress testing or a biophysical profile) are also checked. Platelet count, serum creatinine, and serum liver enzymes are measured at least weekly. All hospitalized patients are followed by an obstetrician and evaluated as described above but more frequently, particularly patients that are in an ICU.
As soon as eclampsia or severe preeclampsia is diagnosed, Mg sulfate must be given to stop or prevent seizures and reduce reflex reactivity. Whether patients with mild preeclampsia always require Mg sulfate before delivery is controversial.
Mg sulfate 4 g IV over 20 min is given, followed by a constant IV infusion of about 1 to 3 g/h, with supplemental doses as necessary. Dose is adjusted based on the patient's reflexes, BP, and serum Mg levels (therapeutic range, 4 to 7 mEq/L). Patients with excess Mg levels (eg, with Mg levels > 10 mEq/L or a sudden decrease in reflex reactivity) or hypoventilation are treated with Ca gluconate 1 g IV.
IV Mg sulfate may cause lethargy, hypotonia, and transient respiratory depression in neonates. However, serious neonatal complications are uncommon.
Hospitalized patients are given IV Ringer's lactate or 0.9% normal saline solution, beginning at about 125 mL/h (to increase urine output). Persistent oliguria is treated with a fluid challenge, followed by furosemide 10 to 20 mg IV; diuretics are not used otherwise. If fluids plus furosemide are ineffective, determining intravascular volume and cardiac output with a pulmonary artery catheter may be considered. Anuric patients with normovolemia may require renal vasodilators or dialysis.
If seizures occur despite Mg therapy, diazepam or lorazepam can be given IV to stop seizures, and IV hydralazine or labetalol is given in a dose titrated to lower systolic BP to 140 to 155 mm Hg and diastolic BP to 90 to 105 mm Hg.
The most efficient method of delivery should be used. If the cervix is favorable and rapid vaginal delivery seems feasible, a dilute IV infusion of oxytocin is given to accelerate labor; if labor is active, the membranes are ruptured. If the cervix is unfavorable and prompt vaginal delivery is unlikely, cesarean delivery is indicated. Preeclampsia and eclampsia, if not resolved before delivery, usually resolve rapidly afterward, beginning within 6 to 12 h.
All patients are typically given Mg sulfate for 24 h postpartum.
Patients should be evaluated every 1 to 2 wk postpartum with periodic BP measurement. If BP remains high after 6 wk postpartum, patients may have chronic hypertension.
Last full review/revision February 2010 by Antonette T. Dulay, MD
Content last modified February 2010