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Preeclampsia is
pregnancy-induced hypertension plus proteinuria. Eclampsia is
unexplained generalized seizures in patients with preeclampsia.
Preeclampsia and eclampsia develop between 20 wk gestation and the
end of the 1st wk postpartum. Diagnosis is clinical and by urine
protein measurement. Treatment is with IV Mg sulfate and usually
rapid delivery.
Preeclampsia affects 3 to 7% of pregnant women, usually primigravidas and women with preexisting hypertension (see Pregnancy Complicated by Disease: Hypertension in Pregnancy) or vascular disorders (eg, renal disorders, diabetic vasculopathy). Other risk factors may include maternal age < 20, a family history of preeclampsia, preeclampsia or poor outcome in previous pregnancies, multifetal pregnancy, obesity, and thrombotic disorders (eg, antiphospholipid antibody syndrome—see Thrombotic Disorders: Antiphospholipid Antibody Syndrome).
Preeclampsia develops during pregnancy and eclampsia usually does, but 25% of eclampsia cases develop postpartum, most often in the 1st 4 days. 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
Cause and pathophysiology of preeclampsia and eclampsia are unknown. Factors may include poorly developed uterine placental spiral arterioles (which decrease uteroplacental blood flow in late pregnancy) and placental ischemia or infarction. Fetal growth restriction may result. Diffuse or multifocal vasospasm can result in ischemia, eventually damaging multiple organs, particularly the brain, kidneys, and liver. Contributors to vasospasm may 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).
Lipid peroxidation of cell membranes induced by free radicals may contribute to preeclampsia. The coagulation system is activated, possibly secondary to endothelial cell dysfunction, leading to platelet activation. However, frank coagulopathy is rare unless abruptio placentae is also present.
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. Other signs may include increased reflex reactivity, indicating neuromuscular irritability, which can progress to seizures (eclampsia). Petechiae may reflect a bleeding tendency. 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 enlargement), nausea, vomiting, shortness of breath or dyspnea (reflecting pulmonary edema or acute respiratory distress syndrome [ARDS]), and oliguria (reflecting decreased plasma volume or ischemic acute tubular necrosis).
Diagnosis
Diagnosis is suggested by symptoms or presence of hypertension. Tests include urinalysis, CBC, platelet count, urate, liver function tests, and measurement of serum electrolytes, BUN, creatinine, creatine clearance, and 24-h urine protein. Preeclampsia is diagnosed when pregnant women have new-onset hypertension (BP ≥ 140/90 mm Hg) plus unexplained proteinuria of ≥ 1+ on dipstick on 2 occasions at least 4 h apart after 20 wk. Occasionally, tests detect the HELLP syndrome (hemolysis, elevated liver function tests, and low platelets).
Preeclampsia is classified as severe based on symptoms; other evidence of organ damage; presence of fetal growth restriction; and laboratory tests, including results that indicate HELLP syndrome, BP ≥ 160/110 mm Hg on 2 occasions ≥ 6 h apart, urine protein ≥ 5 g in a 24-h collection or ≥ 3+ in 2 samples obtained ≥ 4 h apart, and urine output < 500 mL in 24 h.
Treatment
Definitive treatment is delivery. For term pregnancy, immediate delivery after maternal stabilization is safest. For pregnancies < 37 wk, risk of early delivery is balanced against severity of the preeclampsia and response to treatment. Treatment aims to optimize maternal health, which usually optimizes fetal health. If preeclampsia is mild, outpatient treatment is possible; it includes strict bed rest, lying on the left side whenever possible, a normal salt intake, increased fluid intake, and evaluation every 2 or 3 days.
Patients with mild eclampsia that does not immediately abate, severe preeclampsia, or eclampsia require hospitalization; a few hours of stabilizing medical treatment to lower BP to 140 to 155/90 to 105 mm Hg, and to resolve seizures and reduce reflex reactivity; and then delivery. Exceptions include advanced prematurity when mild preeclampsia does not progress and severe preeclampsia that improves with hospitalization. Whether patients with mild preeclampsia always require Mg sulfate before delivery is controversial. Patients with severe preeclampsia require Mg sulfate as soon as diagnosis is made. When delivery is delayed before about 32 to 34 wk in patients who are not clinically deteriorating, corticosteroids are given for 48 h. Delivery is mandated at 34 wk or when deterioration of maternal or fetal status or documentation of fetal lung maturity occurs. Eclampsia always requires delivery after seizures and severe hypertension have been controlled. All hospitalized patients are checked frequently for seizures, symptoms of severe preeclampsia, and vaginal bleeding. BP, reflexes, and fetal heart rate are monitored continuously or several times a day.
Patients with severe preeclampsia or with eclampsia are often admitted to the ICU. Continued management by the obstetrician is mandatory. As part of stabilization, these patients are given IV Ringer's lactate or 0.9% normal saline solution at about 125 mL/h (to increase urine output) and IV Mg sulfate (to stop or prevent seizures and reduce reflex reactivity and BP). Mg sulfate 4 g IV over 20 min is 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.
If Mg therapy is ineffective, phenytoin or valium can be given to stop seizures, and IV hydralazine or labetalol is given in a titrated dose to lower BP to 140 to 155/90 to 105 mm Hg. 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 Swan-Ganz catheter may be considered. Anuric patients with normovolemia may require renal vasodilators or dialysis.
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, delivery by cesarean section is indicated. Preeclampsia and eclampsia, if not resolved before delivery, usually resolve rapidly afterward, beginning within 6 to 12 h. As patients gradually improve, ambulation is allowed. Patients should be evaluated every 1 to 2 wk postpartum with periodic BP measurement. If BP remains high after 8 wk postpartum, chronic hypertension should be considered.
Last full review/revision November 2005
Content last modified November 2005
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