eMedicine Specialties > Obstetrics and Gynecology > Obstetrical Complications

Eclampsia

Michael G Ross, MD, MPH, Professor of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles; Professor, Department of Community Health Sciences, University of California at Los Angeles School of Public Health; Chair, Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center

Updated: Apr 1, 2009

Introduction

Background

Eclampsia is commonly defined as new onset of grand mal seizure activity and/or unexplained coma during pregnancy or postpartum in a woman with signs or symptoms of preeclampsia. Nonetheless, eclampsia in the absence of hypertension with proteinuria has been demonstrated to occur in 38% of cases reported in the United Kingdom.¹ Similarly, hypertension was absent in 16% of cases reviewed in the United States.²

Most cases of eclampsia present in the third trimester of pregnancy, with about 80% of eclamptic seizures occurring intrapartum or within the first 48 hours following delivery. Rare cases have been reported prior to 20 weeks' gestation or as late as 23 days’ postpartum. Other than early detection of preeclampsia, no reliable test or symptom complex predicts the development of eclampsia. In developed countries, most of recent reported cases have been classified as unpreventable.

Pathophysiology

Many investigators have proposed factors relating to genetics, immunology, endocrinology, nutrition, and infection as possible etiologies leading to the development of preeclampsia/eclampsia. Despite extensive research, no definitive cause for preeclampsia has been identified (see eMedicine article Preeclampsia). The pathogenesis of eclamptic seizures may include mechanisms of cerebral vasoconstriction, hypertensive encephalopathy, cerebral edema, hemorrhage, and infarction. Whether these findings are causes or results of seizure activity is unclear.

Preeclampsia/eclampsia produces multiple systemic derangements that can involve a diversity of organ systems including hematologic, hepatic, renal, and cardiovascular systems as well as the central nervous system. The severity of these derangements often correlates with maternal medical (eg, pre-existing renal or vascular pathology) or obstetric factors (eg, multifetal gestations or molar pregnancy).

Systemic derangements associated with eclampsia can include the following:

• Cardiovascular 
  • Generalized vasospasm
  • Increased peripheral vascular resistance
  • Increased left ventricular stroke work index
  • Decreased central venous pressure
  • Decreased pulmonary wedge pressure
• Hematologic
  • Decreased plasma volume
  • Increased blood viscosity
  • Hemoconcentration
  • Coagulopathy
• Renal
  • Decreased glomerular filtration rate
  • Decreased renal plasma flow
  • Decreased uric acid clearance
• Hepatic
  • Periportal necrosis
  • Hepatocellular damage
  • Sub capsular hematoma
• Central nervous system
  • Cerebral over perfusion due to loss of autoregulation
  • Cerebral edema
  • Cerebral hemorrhage

Frequency

United States

Primigravid and multifetal pregnancies as well as pregnancies in women without access to prenatal care have been identified as having an increased frequency of eclampsia. In the United States, some studies have identified an increased frequency in African Americans and in women with pre-existing cardiovascular or renal complications.³

International

The incidence of eclampsia varies between and within countries. Overall, the rate of eclampsia is higher in developing countries. The highest rate was reported in Columbia (8.1/1000) and the lowest rate was reported in the United Kingdom (0.49/1000 deliveries).⁴ In the developed world, the reported incidence of eclampsia ranges from 1 in 1,000 to 1 in 3,448 pregnancies.^1,3

Mortality/Morbidity

Eclampsia accounts for approximately 50,000 maternal deaths worldwide annually. In developed countries, the maternal death rate has been reported as 0-1.8%. A CDC study found an overall preeclampsia-eclampsia case-fatality rate of 6.4 per 10,000 cases at delivery with a rate twice as high for black women compared with white women. This same study found an increased risk of death among women older than 30 years and those with no prenatal care. The highest risk for maternal death was found in pregnancies at 28 weeks’ gestation or less. The maternal mortality rate is as high as 14% in developing countries.⁵ The perinatal mortality rate from eclampsia in recent reviews in the United States and Great Briton ranges from 5.6-11.8%.^1,6

Maternal complications of eclampsia may include permanent CNS damage from recurrent seizures or intracranial bleeds, disseminated intravascular coagulopathy, renal insufficiency, pulmonary edema, and cardiopulmonary arrest.

Race

Ethnic or racial predilections are unclear. A higher incidence of this condition may exist in African Americans.

Sex

Only females are affected.

Age

Recent reviews confirm both an increase in frequency of preeclampsia/eclampsia and severity of complications (including an increased mortality) risk in older gravidas, especially women aged 40 years or older. Previously reported increased risk in younger women has not been found in recent reviews.

Clinical

History

• Eclampsia is defined by tonic-clonic seizure activity (focal or generalized) or unexplained coma.
• Frequency of signs or symptoms prior to seizure include the following:
  • Headache (83%)
  • Hyperactive reflexes (80%)
  • Marked proteinuria (52%)
  • Generalized edema (49%)
  • Visual disturbances (44%)
  • Right upper quadrant pain or epigastric pain (19%)
• Absence of signs or symptoms prior to seizure include the following:
  • Lack of edema (39%)
  • Absence of proteinuria (21%)
  • Normal reflexes (20%)
• Relation to delivery
  • More than 70% occur prior to delivery.
  • 25% occur before labor (antepartum).
  • 50% occur during labor (intrapartum).
  • 25% occur after delivery (postpartum).
• Patients with severe preeclampsia are at greater risk to develop seizures.
• 25% of patients have symptoms consistent with mild preeclampsia prior to the seizures.

Physical

• Eclamptic seizure
  • One or more seizures may occur.
  • Seizures generally last 60-75 seconds.
  • The face initially may become distorted with protrusion of the eyes.
  • Foaming at the mouth may occur.
  • Respiration ceases for the duration of the seizure.
• The seizure may be divided into 2 phases:
  • Phase 1 lasts 15-20 seconds and begins with facial twitching. The body becomes rigid, leading to generalized muscular contractions.
  • Phase 2 lasts about 60 seconds. It starts in the jaw, moves to the muscles of the face and eyelids, and then spreads throughout the body. The muscles begin alternating between contracting and relaxing in rapid sequence.
• A coma or a period of unconsciousness follows phase 2.
  • Unconsciousness lasts for a variable period.
  • Following the coma phase, the patient may regain some consciousness.
  • The patient may become combative and very agitated.
  • The patient has no recollection of the seizure.
• A period of hyperventilation occurs after the tonic-clonic seizure. This compensates for the respiratory and lactic acidosis that develops during the apneic phase.
• Seizure-induced complications may include tongue biting, head trauma, broken bones, or aspiration.

Causes

The cause of the seizures is not clear, although several processes have been implicated in their development.

• Areas of cerebral vasospasm may be severe enough to cause focal ischemia, which may in turn lead to seizures.
• Pathologic alterations in cerebral blood flow and tissue edema induced by vasospasm may result in headaches, visual disturbances, and hypertensive encephalopathy, resulting in a seizure.

Differential Diagnoses

Workup

Laboratory Studies

• No single laboratory test or set of laboratory determinations is useful in predicting maternal or neonatal outcome in women with eclampsia.
• Laboratory studies that should be ordered include the following:
  • Complete blood cell count
  • Platelet count
  • Blood type and screen
  • Urinalysis for proteinuria
  • Electrolytes, serum calcium and magnesium
  • Liver function tests (ie, lactate dehydrogenase [LDH], aspartate aminotransferase [AST])
  • Serum glucose
  • Pulse oximetry
• The most common hematologic abnormality is thrombocytopenia, which occurs in 17% of patients with eclampsia.
• Disseminated intravascular coagulation (DIC) is uncommon in patients with eclampsia.

Imaging Studies

Imaging studies may be indicated after initial stabilization especially if there is doubt about the diagnosis or possible injuries secondary to seizure activity .

• CT scan of the head, with or without contrast can exclude cerebral venous thrombosis, intracranial hemorrhage, and central nervous system lesions, all of which can occur in pregnancy and present with seizures.
  • Consider CT in patients who (1) have been involved in trauma, (2) are refractory to magnesium sulfate therapy, or (3) have atypical presentations (eg, seizures >24 h after delivery).
  • Although obtaining a CT scan in eclampsia is not routine, abnormalities have been observed in up to 50% of women imaged.
  • Characteristic CT findings include cortical hypodense areas, particularly in the occipital lobes, and diffuse cerebral edema, which is believed to correspond to petechial hemorrhages and diffuse edema noted in postmortem studies.
  • CT findings may include the following:
    • Cerebral edema
    • Diffuse white matter low-density areas
    • Patchy area of low density
    • Occipital white matter edema
    • Loss of normal cortical sulci
    • Reduced ventricular size
    • Cerebral hemorrhage
    • Intraventricular hemorrhage
    • Parenchymal hemorrhage (high density)
    • Cerebral infarction
    • Low attenuation areas
    • Basal ganglia infarctions
• Magnetic resonance imaging of the head
  • Abnormal findings have been reported in up to 90% of women imaged.
  • MRI findings  
    • Increased signal at the grey-white matter junction on T2-weighted images
    • Cortical edema and hemorrhage

Other Tests

EEG and cerebral spinal fluid studies are rarely useful in management; however, they may be indicated if epilepsy or meningitis is considered in the diagnosis.

Treatment

Medical Care

Eclamptic convulsions are life-threatening emergencies and require the proper treatment to decrease maternal morbidity and mortality.  

• The first priority is to prevent maternal injury and to provide respiratory and cardiovascular support.
  • Supplemental oxygen should be administered
  • Place patient in the left lateral position. This positioning decreases the risk of aspiration and will help to improve uterine blood flow by relieving obstruction of the vena cava by the gravid uterus.
  • Protect patient against injury during the seizure by padding and raising guardrails, using a padded tongue blade between the teeth, and suctioning the oral secretions as needed.
• Establish intravenous access: After the seizure has ended, a 16- to 18-gauge intravenous line should be established for drawing specimens and administering fluids and medications. Intravenous fluids should be limited to isotonic solutions to replace urine output plus about 700 mL/d to replace insensible losses.
• Control of the seizure
  • No attempt to shorten or abolish the initial seizure is generally needed.
  • Magnesium sulfate is administered to prevent and treat subsequent seizures in women with eclampsia. Give intravenously as a loading dose of 4-6 g over 20 minutes followed by a maintenance dose of 1-2 g/h as a continuous intravenous infusion.
  • Recurrent seizures: About 10% of women with eclampsia will have an additional seizure after receiving magnesium sulfate. Another 2 g bolus of magnesium may be given in these cases. For the rare patient who continues to have seizure activity while receiving adequate magnesium therapy, seizures may be treated with sodium amobarbital, 250 mg intravenously over 3-5 minutes.⁵ More commonly, lorazepam (Ativan) 4 mg IV over 2-5 minutes (may repeat in 5-15 min to maximum of 8 mg in 12 hours or diazepam (Valium), 5-10 mg IV slowly (may be repeated every 15 min up to 30 mg) both as per protocol for status epilepticus.
• Control hypertension: Blood pressure should be assessed with the goal of maintaining diastolic blood pressure less than 110 mm Hg with administration of antihypertensive medications as needed (eg, hydralazine, labetalol).
• Monitoring
  • Regularly check neurologic status for signs of increased intracranial pressure or bleeding (eg, fundiscopic examination, cranial nerves)
  • Monitor fluid intake and urine output, maternal respiratory rate, and oxygenation, as indicated.
  • Continuously monitor fetal status.
  • Invasive monitoring: Pulmonary arterial pressure monitoring is rarely indicated but may be helpful in patients who have evidence of pulmonary edema or oliguria/anuria.
• Assessment for other coexisting medical conditions: Once the seizure is controlled and the patient has regained consciousness, the general medical condition should be assessed to identify any other causes for seizures.
• Induction of labor may be initiated when the patient is stable.
• Delivery (antepartum or intrapartum eclampsia)
  • Delivery is the treatment for eclampsia after the patient has been stabilized. No attempt should be made to deliver the infant either vaginally or by cesarean delivery until the acute phase of the seizure or coma has passed. The mode of delivery should be based on obstetric indications but should be chosen with an awareness of the fact that vaginal delivery is preferable from a maternal standpoint.
  • Adequate maternal pain relief for labor and delivery is vital and may be provided with either systemic opioids or epidural anesthesia.
  • In the absence of fetal malpresentation or fetal distress, oxytocin or prostaglandins may be initiated to induce labor.
  • Cesarean delivery may be considered in patients with an unfavorable cervix and a gestational age of 30 weeks or less, as induction under these circumstances may result in a prolonged intrapartum course and is frequently unsuccessful in avoiding cesarean section given the high rate of intrapartum complications.³
  • Intrapartum complications include the following:
    • Fetal growth retardation (30%)
    • Nonreassuring fetal heart rate patterns (30%)
    • Placental abruption (23%)
  • Irrespective of gestational age, a prolonged induction with clinically significant worsening of maternal cardiovascular, hematologic, renal, hepatic, and/or neural status is generally an indication for cesarean delivery when the anticipated delivery time is remote. 
• The highest maternal mortality rate associated with preeclampsia and eclampsia occurs in pregnancies 28 weeks’ gestation or less.⁷
• Fetal monitoring
  • Fetal heart rate and uterine contractions should be continuously monitored. Fetal bradycardia is common following the eclamptic seizure and has been reported to last from 30 seconds to 9 minutes. The interval from the onset of the seizure to the fall in the fetal heart rate is typically 5 minutes or less. Transitory fetal tachycardia may occur following the bradycardia.
  • After the initial bradycardia, during the recovery phase, the fetal heart rate tracing may reveal a loss of short- and long-term variability and the presence of late decelerations. These abnormalities are most likely due to the decrease in uterine blood flow caused by the intense vasospasm and uterine hyperactivity during the convulsion. If the fetal heart tracing does not improve following a seizure, further evaluation should be undertaken. Growth restricted and preterm fetuses may take longer to recover following a seizure. Placental abruption may be present if uterine hyperactivity remains and fetal bradycardia persists.

Surgical Care

• Cesarean delivery may be necessary for obstetric indications or deteriorating maternal condition.
• The patient should be stabilized with respect to seizures, oxygenation, and hemodynamic status before initiating cesarean delivery. Blood pressure should be controlled and coagulopathies monitored or corrected.  
• An anesthesiology consultation may be obtained. Early evaluation is recommended to assist with cardiopulmonary stabilization and prepare for a possible operative delivery or endotracheal intubation.
• For nonemergency cesarean delivery, epidural or combined techniques of regional anesthesia are preferred. Regional anesthesia is contraindicated in the presence of coagulopathy or severe thrombocytopenia (<50,000). General anesthesia in women with eclampsia increases the risk of aspiration and airway edema may make intubation difficult. It also can produce significant increases in systemic and cerebral pressures during intubation and extubation.
• The use of spinal anesthesia requires caution because of the possibility of total sympathetic blockade, resulting in maternal hypotension and uteroplacental insufficiency.

Consultations

• An experienced obstetrician or maternal-fetal medicine specialist may be consulted.
• Transport to a tertiary care site after stabilization may be in the best interest of the fetus or mother.
• In the event of premature delivery or fetal compromise, a pediatrician or neonatologist should be consulted.

Diet

Keep nothing by mouth (including medications) until the patient is medically stabilized or delivered as she is at risk of aspiration when postictal and may have recurrent seizures.

Activity

• Strict bedrest (Use thromboprophylaxis as indicated.)
• Maintain in lateral position to relieve the uterine pressure on the inferior vena cava and thereby improve uterine blood flow to the fetus and venous return to the mother.

Medication

Pharmacotherapy goals are to reduce morbidity, prevent complications, and correct eclampsia. The drug of choice to treat and prevent eclampsia is magnesium sulfate.⁸ Familiarity with second-line medications phenytoin and diazepam/lorazepam is required for cases in which magnesium sulfate may be contraindicated (eg, myasthenia gravis) or ineffective. Control of hypertension is essential to prevent further morbidity or possible mortality. The most commonly used antihypertensive agents are hydralazine, labetalol, and nifedipine. These vital medications are described below.

Anticonvulsants

Prevent seizure recurrence and terminate clinical and electrical seizure activity.

Magnesium sulfate

Several studies have revealed that magnesium sulfate is the drug of choice for treating eclamptic seizures. Magnesium sulfate is successful in controlling seizures in >95% of cases. The agent has physiologic advantages to the fetus by increasing uterine blood flow.
The mechanism of action of magnesium sulfate therapy is that it inhibits the release of acetylcholine at the motor endplate. In addition, magnesium has a direct effect on skeletal muscle by virtue of its competitive antagonistic effects with calcium.
Magnesium sulfate is excreted exclusively by the kidneys and has little antihypertensive effect. It is an effective anticonvulsant and helps prevent recurrent seizures and maintain uterine and fetal blood flow.
It can be administered both IV and IM. The intravenous route is preferred over the IM route because administration is more easily controlled and time to therapeutic levels is shorter. Intramuscular administration of magnesium sulfate tends to be more painful and less convenient. If IV access is unavailable, IM administration may be considered.
The goals of magnesium therapy are to terminate ongoing seizures and prevent further seizures. The patient should be evaluated approximately every 1 h to assure that deep tendon reflexes are present, respirations are at least 12 bpm, and urine output is at least 100 mL during the preceding 4 h. When using magnesium sulfate, close monitoring of the patient and fetus is necessary.
Magnesium therapy is usually continued for 12-24 h following delivery and may be stopped depending upon the clinical situation (eg, hypertension resolution, adequate urine output). Renally compromised patients should be monitored with magnesium levels, with adjustments made to facilitate levels at 6-8 mg/dL. Patients with increased urine output may need maintenance dose increased to 3 g/h to maintain therapeutic levels. Monitor patient for signs of worsening condition and magnesium toxicity.

Dosing

Adult

Initial: 4-6 g bolus IV over 15-20 min; if seizure occurs in first 20 min after loading dose, convulsion is usually short and no additional treatment indicated
If seizure occurs >20 min after loading dose, may administer additional 2-4 g of magnesium
Approximately 10-15% of patients will have another convulsion after loading dose
Maintenance: 1-2 g/h IV maintenance drip
If magnesium level is >8 mg/dL at 4 h after initial bolus, decrease maintenance dose

Pediatric

Administer as in adults

Interactions

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine

Contraindications

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis; or myasthenia gravis

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Always monitor for loss of reflexes, respiratory depression, and decreased urine output; magnesium infusion should be stopped for evidence of hypermagnesemia, and patient may require assisted ventilation; maternal dose-related adverse effects at various serum levels include CNS depression at 6-8 mg/dL, loss of deep tendon reflexes at 8-10 mg/dL, respiratory depression at 12-17 mg/dL, coma at 13-17 mg/dL, and cardiac arrest 19-20 mg/dL; calcium gluconate 1 g IV may be administered slowly for evidence of magnesium toxicity

Phenytoin (Dilantin)

Although phenytoin is not as effective as magnesium for prophylaxis or treatment of eclampsia, it can be safely and successfully used when magnesium is inappropriate, such as in women with myasthenia gravis or markedly compromised renal function.
Some benefits to using phenytoin are that it can be continued orally for several days until the risk of eclamptic seizures has subsided, it has established therapeutic levels that are easily tested, and no known neonatal adverse effects are associated with short-term usage. Nonetheless, phenytoin does have potential severe adverse effects that may be magnified by the rarity of its use in the obstetric setting. Cardiac monitoring is often required with IV loading.

Dosing

Adult

10 mg/kg loading dose IV infused no faster than 50 mg/min, followed by maintenance dose started 2 h later at 5 mg/kg

Pediatric

Administer as in adults

Interactions

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid

Contraindications

Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform blood counts and urinalyses when therapy is begun and at monthly intervals for several months thereafter (if chronic use) to monitor for blood dyscrasias; discontinue use if a skin rash appears and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugars); discontinue use if hepatic dysfunction occurs

Diazepam (Valium)

Freely crosses placenta and accumulates in fetal circulation with newborn levels 1-3 times maternal serum concentrations. Moreover, plasma half-life in newborn is increased due to decreased clearance and there are significant fetal CNS depressant effects. Nonetheless, diazepam (if not the shorter acting benzodiazepine lorazepam) may be necessary to treat recurrent seizure activity in patients already adequately treated with magnesium.
Should not be administered to stop or shorten the initial seizure, especially if IV access or the ability to rapidly intubate the patient is not readily available.

Dosing

Adult

5-10 mg IV slowly (may be repeated q15min up to 30 mg)

Pediatric

Administer as in adults

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohol, and MAOIs

Contraindications

Documented hypersensitivity; narrow-angle glaucoma; hepatic or renal failure

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Intra-arterial injection can cause gangrene; may cause maternal apnea and cardiac arrest if infused too quickly; neonatal adverse effects include respiratory depression, hypotonia, and poor feeding (floppy infant syndrome); sodium benzoate preservative competes with bilirubin for albumin binding, thus predisposing the infant to kernicterus

Lorazepam (Ativan)

Benzodiazepine indicated for treatment of status epilepticus and used for recurrent seizures in patients already receiving therapeutic magnesium. Lorazepam crosses placenta, achieving cord levels similar to maternal serum concentrations. Placental transfer is slower than that of diazepam and it is cleared less slowly in the neonate. For these reasons, it is commonly preferred over diazepam. Nonetheless, at high IV doses, lorazepam may also produce floppy infant syndrome (see diazepam for description).

Dosing

Adult

4 mg IV over 5 min; may repeat in 5-15 min to max dose 8 mg in 12h

Pediatric

Administer as in adults

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohol, and MAOIs

Contraindications

Documented hypersensitivity; narrow-angle glaucoma; hepatic or renal failure

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Intra-arterial injection can cause gangrene; may cause maternal apnea and cardiac arrest if infused too quickly; neonatal adverse effects include respiratory depression, hypotonia, and poor feeding (floppy infant syndrome); sodium benzoate preservative competes with bilirubin for albumin binding, thus predisposing the infant to kernicterus

Antihypertensives

Hypertension associated with eclampsia is often adequately controlled by stopping the seizure.

Antihypertensive medications are used to maintain diastolic blood pressure <110 mm Hg.

Antihypertensive therapy has 2 main goals: (1) reducing maternal morbidity and mortality associated with seizures, strokes, and pulmonary embolism, and (2) potentially reducing fetal morbidity and mortality secondary to intrauterine growth restriction, placental abruption, and infarcts.

Uterine hypoperfusion may result if blood pressure is lowered too quickly. Uterine vasculature is generally maximally vasodilated; thus a decrease in maternal systemic blood pressure tends to decrease uteroplacental perfusion.

Although total body water in patients with eclampsia is excessive, intravascular volume is contracted and women with eclampsia are very sensitive to further volume changes. Hypovolemia results in decreased uterine perfusion. Therefore, diuretics generally should be avoided in eclampsia, unless indicated for maternal symptoms (eg, pulmonary edema).

Drugs used most commonly for hypertension in pregnancy are hydralazine and labetalol. Nifedipine has also been used to control hypertension, but less commonly as it cannot be given intravenously.

Hydralazine (Apresoline)

Drug is a direct arteriolar vasodilator that causes a secondary baroreceptor-mediated sympathetic discharge resulting in tachycardia and increased cardiac output.
Hydralazine helps to maintain uterine blood flow and blunts the hypotensive response.
Hydralazine is metabolized in the liver.
Controls hypertension in up to 95% of patients with eclampsia.

Dosing

Adult

5-10 mg IV q15-20min as needed to keep diastolic blood pressure <110 mm Hg
Onset of action 15 min; peak effect 30-60 min; duration of action 4-6 h

Pediatric

Administer as in adults

Interactions

MAOIs and beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin

Contraindications

Documented hypersensitivity; mitral valve rheumatic heart disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Implicated in myocardial infarction; caution in suspected coronary artery disease; adverse effects include flushing, headache, dizziness, palpitations, angina, and an idiosyncratic lupus-like syndrome (dose-related as well as chronic use)

Labetalol (Normodyne, Trandate)

Nonselective beta-blocker.
Available in IV and PO preparations. Used as an alternative to hydralazine in eclampsia. Uteroplacental blood flow appears to be unaffected by IV labetalol.

Dosing

Adult

IV dosing q10min in a step-wise fashion
20 mg initial dose; second dose is increased to 40 mg; subsequent doses are administered at 80 mg to a maximum cumulative dose of 300 mg; may be administered as a constant infusion; onset of action 5 min; peak effect 10-20 min; duration of action 45 min to 6 h

Pediatric

Administer as in adults

Interactions

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes

Contraindications

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction are present; in elderly patients, a lower response rate and higher incidence of toxicity may be observed

Nifedipine (Adalat, Procardia)

Produces calcium channel blockade, causing powerful arteriolar vasodilation.
Only available in PO form.

Dosing

Adult

10 mg PO tid; may increase to maximum dose of 120 mg/d

Pediatric

Administer as in adults

Interactions

Caution with coadministration of any agent that can lower BP, including beta-blockers and opioids; H2 blockers (cimetidine) may increase toxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause lower extremity edema; allergic hepatitis has occurred but is rare; the main problem with nifedipine is profound hypotension; hypotension usually responds to the administration of calcium; best to avoid in growth restricted pregnancies or in patients with abnormal fetal heart rate tracings; not well used in the setting of eclampsia

Follow-up

Further Inpatient Care

Continue to monitor blood pressure, neurologic status, and urine output until the patient is stable after delivery. Patients may require antihypertensive therapy after delivery and hospital discharge.

Further Outpatient Care

Follow up 1-2 weeks after delivery to evaluate for blood pressure control and any residual deficits from the eclamptic seizure. Patients with persistent hypertension past 8 weeks' puerperium or neurologic changes may need medical referral.

Inpatient & Outpatient Medications

This disease is treated on an inpatient basis, as described above. Outpatient care plays no role in management.

Transfer

Eclampsia clearly poses a risk of considerable maternal and neonatal morbidity and mortality. Patients with eclampsia may benefit from management at a tertiary care center.

Deterrence/Prevention

• Routine prenatal care
• Early diagnosis and aggressive management of preeclampsia

Complications

• As many as 56% of patients with eclampsia may have transient deficits, including cortical blindness.
• Studies have failed to demonstrate evidence of persisting neurologic deficits after uncomplicated eclamptic seizures during the follow-up period.⁶
• Maternal, as well as fetal, death can be a consequence of eclampsia and its complications.

Prognosis

• About 25% of women with eclampsia have hypertension in subsequent pregnancies.
• 5% of patients with hypertension develop severe preeclampsia.
• About 2% of women with eclampsia develop eclampsia with future pregnancies.
• Multiparous women with eclampsia have the following:
  • A higher risk for development of essential hypertension
  • A higher mortality rate in subsequent pregnancies as compared with primiparous women

Patient Education

• The patient should be advised and educated on the course of the disease and any residual problems.
• The patient should be educated on the importance of adequate prenatal care in subsequent pregnancies.
• If the patient has preexisting hypertension, she should have good control prior to conception and throughout pregnancy. Her case should be followed for recognition and treatment of preeclampsia.

Miscellaneous

Medicolegal Pitfalls

• The mode of delivery should be based on obstetric indications, with the understanding that vaginal delivery is preferable from a maternal standpoint.
• When emergent cesarean delivery is indicated, substantiating the absence of DIC prior to the procedure is important.
• Fetal bradycardia is common following an eclamptic seizure and usually resolves within 10 minutes. Consider placental abruption if uterine hyperactivity remains and fetal bradycardia persists.
• Cervical examination should not be overlooked. The delivery mode may be largely dependent on the cervical status.
• Fluid management is critical in patients with eclampsia.
• Avoid the use of multiple agents, unless necessary, to abate eclamptic seizures.
• Ruling out eclampsia in an obstetrical patient who has been involved in an unexplained trauma is important.

Special Concerns

• Do not overlook other neurologic causes, particularly if the seizure occurs more than 24 hours after delivery.
• When preeclampsia occurs in the early second trimester (ie, 14-20 weeks' gestation), the diagnosis of hydatiform mole or choriocarcinoma should be considered.
• Eclampsia always should be considered in a pregnant patient with a seizure episode.
• A pregnant patient who has been involved in an unexplained trauma (such as a single-vehicle auto accident) and has exhibited seizure activity should be evaluated for eclampsia.

References

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2. Mattar, F, Sibai BM. Eclampsia. VIII. Risk Factors for maternal morbidity. Am J Obstet Gynecol. 1990;163:1049-55.

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Keywords

eclampsia, seizures in pregnancy, toxemia of pregnancy, coma in pregnancy, preeclampsia, cerebral vasospasm, focal ischemia, hypertensive encephalopathy

Contributor Information and Disclosures

Author

Michael G Ross, MD, MPH, Professor of Obstetrics and Gynecology, David Geffen School of Medicine, University of California at Los Angeles; Professor, Department of Community Health Sciences, University of California at Los Angeles School of Public Health; Chair, Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center
Michael G Ross, MD, MPH is a member of the following medical societies: American Association for the Advancement of Science, American College of Obstetricians and Gynecologists, American Federation for Clinical Research, American Gynecological and Obstetrical Society, American Physiological Society, American Public Health Association, Association of Professors of Gynecology and Obstetrics, Perinatal Research Society, Phi Beta Kappa, Society for Gynecologic Investigation, Society for Maternal-Fetal Medicine, and Society for Neuroscience
Disclosure: Nothing to disclose.

Medical Editor

Bruce A Meyer, MD, MBA, Vice President for Medical Affairs, Associate Dean for Health System Affairs and Director of the Faculty Practice Plan, Professor, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School
Bruce A Meyer, MD, MBA is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Physician Executives, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Medical Group Management Association, and Society for Maternal-Fetal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Antonio V Sison, MD, Medical Director, Ob/Gyn Group, Robert Wood Johnson University Hospital at Hamilton
Antonio V Sison, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists and Association of Professors of Gynecology and Obstetrics
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

David Chelmow, MD, Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Program Director, Tufts University Affiliated Hospitals OB/GYN Residency Program; Chair, Tufts University Health Sciences Campus Institutional Review Board; Vice Chair for Research and Education, Dept of OB/GYN, Tufts Medical Center
David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical Decision Making
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Stephanie R Fugate, DO and coauthor Gregory E Chow, MD to the development and writing of this article.

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