Eclampsia is the occurrence of new-onset tonic-clonic, focal, or multifocal seizures in the absence of other causative conditions in pregnant or postpartum women often, but not always, associated with other signs and symptoms of preeclampsia. Atypical eclampsia occurs at <20 wk of gestation or as much as 23 days postpartum.

Toxemia

Seizures of pregnancy

• Seizure often begins as facial twitching which then spreads to a generalized tonic-clonic state, typically lasting 60 to 90 sec, with cessation of respiration followed by a postictal period of amnesia, agitation, and confusion.
• The most common symptoms preceding eclampsia are persistent occipital or frontal headaches (80%), visual disturbance such as blurred vision or photophobia (45%), epigastric pain (20%), and altered mental status.
• Forty percent have severe hypertension, 40% have mild to moderate hypertension, and 20% are normotensive.
• Generalized edema with rapid weight gain (>2 lb/wk) may precede eclampsia.
• Over 17% are completely asymptomatic prior to seizure with no prior documentation of elevated blood pressure or proteinuria.

The proposed common pathway relates to initial abnormal placentation leading to arterial resistance, vasoconstriction, and ischemia, which causes release of mediators of oxidative stress such as free radicals and cytokines. Endothelial damage to the cerebral vasculature ensues in addition to abnormalities in the autoregulation of cerebral blood flow as a result of an imbalance of angiogenic factors. This may involve transient vasospasm, ischemia, cerebral hemorrhage, and edema occurring by a mechanism involving hypertensive encephalopathy, decreased colloid osmotic pressure, and prostaglandin imbalance.

• Preexisting seizure disorder
• Metabolic abnormalities (hypoglycemia, hyponatremia, hypocalcemia)
• Substance abuse
• Head trauma
• Cerebral infection (meningitis, encephalitis)
• Intracranial hemorrhage thrombosis, ischemia, or infarction
• Amniotic fluid embolism
• Space-occupying brain lesions or neoplasms
• Pseudoseizure
• Postdural puncture syndrome
• Hypertensive encephalopathy
• Posterior reversible encephalopathy syndrome (often seen in eclampsia)
• Vasculitis, angiopathy
• Thrombotic thrombocytopenic purpura

Atypical presentations such as prolonged postictal state; status epilepticus; gestational age <20 wk or >48 h postpartum; or signs of meningitis, substance abuse, severe uncontrolled hypertension, or seizures despite therapeutic levels of magnesium sulfate therapy should prompt a search for other seizure etiologies, including but not limited to those listed earlier.

• Laboratory tests
  1. Proteinuria: Severe (49%), mild to moderate (29%), absent (22%)
  2. Hematocrit: Elevated as a result of hemoconcentration
  3. Platelet count: Decreased in HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count)
  4. Liver function tests elevated in HELLP syndrome
  5. Blood urea nitrogen and creatinine: Elevated with renal involvement
• Rule out other causes of seizures during pregnancy:
  1. Serum electrolytes, glucose, calcium
  2. Toxicology profile
  3. Arterial blood gas: Maternal acidemia and hypoxia
  4. Imaging studies: Computed tomography scan or MRI indicated in atypical presentation (suspected intracerebral bleeding or focal neurologic deficit)
  5. Over 90% of patients will have findings consistent with posterior reversible encephalopathy syndrome on MRI
  6. Abnormal findings, including cerebral edema, hemorrhage, and infarction, are apparent in 50% of patients

• Elevate bed side rails, place patient in the lateral decubitus position (physical restraints may be necessary).
• Suction oropharyngeal secretions and vomitus and maintain airway to prevent aspiration.
• Administer adequate oxygenation.
• Obtain intravenous (IV) access.
• Initiate or continue continuous fetal heart monitoring and administer indicated resuscitative maneuvers such as maternal oxygenation and left lateral positioning.
• Magnesium sulfate should be administered. Give magnesium sulfate 6 g IV load over 20 min, then 2 g/h maintenance, for treatment and recurrent seizure prophylaxis. Adjust maintenance dose for renal insufficiency. If there is no IV access, may give 10 g IM (5 g to each buttock). Phenytoin has been used as an alternative in patients in whom magnesium sulfate is contraindicated (e.g., heart block, myasthenia gravis).
• If repeated convulsions, give an additional 2 g IV over 3 to 5 min, as approximately 10% to 15% of patients will have a second seizure after initial loading dose.
• Monitoring parameters required on magnesium include creatinine function, urine output, and deep tendon reflexes. Clinical signs of progressive Mg²⁺ toxicity, such as loss of reflexes, should also be followed. If magnesium toxicity is suspected, check magnesium level (therapeutic range 4 to 7 mEq/L). If serum level >9.6 mg/dl, stop infusion. Respiratory and cardiac arrest occur at extremely high magnesium levels. Antidote for toxicity is IV calcium gluconate 10 ml of 10% solution.
• If persistent seizures despite magnesium treatment, give sodium amobarbital 250 mg IV over 3 min, thiopental, or phenytoin 1250 mg IV over 25 min.
• Treat blood pressure (BP) >160 mm Hg systolic or BP >110 mm Hg diastolic with either hydralazine 5 to 10 mg IV, then 10 mg, then 10 mg every 20 minutes to a maximum of 20 mg; or labetalol hydrochloride 20, 40, 80 mg IV, escalating the dose every 10 minutes to maximum total dose of 300 mg; or nifedipine 10 to 20 mg orally every 20 minutes can be used for acute blood pressure control, if no IV access, to a total dose of 180 mg/day. If maximum dose of one medication is reached, add an additional medication to reach goal of BP 140 to 150/90 to 100 mm Hg.
• Evaluate patient for delivery; if signs of maternal or fetal deterioration are present, urgent or emergent delivery is indicated immediately following maternal stabilization, typically with cesarean delivery (C-section).

• After immediate stabilization of the mother is achieved, the next priority becomes optimization of adequate oxygenation, hemodynamics, and laboratory abnormalities, such as associated coagulopathies.
• Consider delivery timing; important factors include gestational age, labor course, obstetrical history, and fetal presentation in determining mode and urgency of delivery, as eclampsia alone is not an indication for delivery. If greater than 34 wk gestation, timely delivery is warranted once maternal stabilization is achieved. Give antenatal corticosteroids if 24 to 34 wk, and if 34 to 36-6/7 wk or 23-0/7 to 24 wk consider steroids. If unfavorable cervix and <30 wk of gestation, consider cesarean delivery; otherwise, consider induction.
• Controlled epidural is the anesthesia of choice for labor or cesarean delivery.
• Avoid general anesthesia in uncontrolled hypertension to minimize risk of catastrophic cerebral events.
• Continue magnesium sulfate through delivery process and for 24 h postpartum or for at least 24 h after the last convulsion.

• The maternal mortality rate for eclampsia averages 5% to 6%. Morbidity rate is 25%, including placental abruption (10%), disseminated intravascular coagulation, maternal apnea with fetal asphyxia, aspiration pneumonia, pulmonary edema (4%), renal failure, cardiopulmonary arrest, and coma.
• There is an increased risk of fetal death, neonatal death, preterm birth, and small-for-gestational-age birth.
• In patients with eclampsia, the risk of recurrence of eclampsia in a subsequent pregnancy is about 2% and the risk of preeclampsia is about 25%. The use of daily low-dose aspirin initiated at 12 to 16 wk and continuing until delivery may decrease that risk.

Because of the potential for serious permanent maternal and fetal sequelae, all cases should be managed by a team approach of obstetrician, maternal and fetal medicine, neonatologist, and intensivist.

Eclampsia (Patient Information)

HELLP Syndrome (Related Key Topic)

Preeclampsia (Related Key Topic)