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 or death may result. Diffuse or multifocal vasospasm can result in maternal 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). Women who have preeclampsia are at risk of abruptio placentae in the current and in future pregnancies, possibly because both disorders are related to uteroplacental insufficiency.
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). Most pregnant women with this syndrome have hypertension and proteinuria, but some have neither.
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 coagulopathy.
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, acute respiratory distress syndrome [ARDS], or cardiac dysfunction secondary to increased afterload), 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 at least 4 h apart. Urine protein excretion is measured in a 24-h collection. Proteinuria is defined as > 300 mg/24 h. Alternatively, proteinuria is diagnosed based on a protein:creatinine ratio ≥ 0.3 or a dipstick reading of 1+ (used only if other quantitative methods are not available). Absence of proteinuria on less accurate tests (eg, urine dipstick testing, routine urinalysis) does not rule out preeclampsia.
In the absence of proteinuria, preeclampsia is also diagnosed if pregnant women have new-onset hypertension plus new onset of any of the following:
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 using a nonstress test or biophysical profile (including assessment of amniotic fluid volume) and tests that estimate fetal weight.
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 gestational age, 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 a maternal special care unit or an ICU.
If preeclampsia is mild, outpatient treatment is possible; it includes strict bed rest, lying on the left side whenever possible, and BP measurements, laboratory monitoring, and physician visits 2 to 3 times/wk.
However, most patients with mild preeclampsia require hospitalization, at least initially; 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. Hypertension can be treated with oral drugs as needed. As long as no criteria for severe preeclampsia are met, delivery can occur (eg, by induction) at 37 wk.
Outpatients are usually evaluated once every 2 or 3 days for evidence of 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 frequently until stable, then at least weekly.
All hospitalized patients are followed by an obstetrician or a maternal-fetal medicine specialist and evaluated as for outpatients (described above); evaluation is more frequent if severe preeclampsia is diagnosed or if gestational age is < 34 wk.
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. Patients with abnormally high Mg levels (eg, with Mg levels > 10 mEq/L or a sudden decrease in reflex reactivity), cardiac dysfunction (eg, with dyspnea or chest pain), or hypoventilation after treatment with Mg sulfate can be 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 lactate or 0.9% normal saline solution, beginning at about 125 mL/h (to increase urine output). Persistent oliguria is treated with a carefully monitored fluid challenge. Diuretics are usually not used. Monitoring with a pulmonary artery catheter is rarely necessary and, if needed, is done in consultation with a critical care specialist and in an ICU. 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 can be considered. 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 and should be referred to their primary care physician for management.
Last full review/revision January 2014 by Antonette T. Dulay, MD
Content last modified January 2014