4/3/2014

Eclampsia

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Eclampsia
Author: Michael G Ross, MD, MPH; Chief Editor: Ronald M Ramus, MD more...
Updated: Dec 13, 2013

Overview
Ten percent of all pregnancies are complicated by hypertension. Eclampsia and preeclampsia account for about
half of these cases worldwide and have been recognized and described for years despite the general lack of
understanding of the disease.[1] In the fifth century, Hippocrates noted that headaches, convulsions, and
drowsiness were ominous signs associated with pregnancy. In 1619, Varandaeus coined the term eclampsia in a
treatise on gynecology.[2, 3]

Definition
Eclampsia, which is considered a complication of severe preeclampsia, 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.[4] It typically occurs during or after the 20th week of gestation or in the postpartum
period. Nonetheless, eclampsia in the absence of hypertension with proteinuria has been demonstrated to occur in
38% of cases reported in the United Kingdom.[5] Similarly, hypertension was absent in 16% of cases reviewed in
the United States.[4]
The clinical manifestations of maternal preeclampsia are hypertension and proteinuria with or without coexisting
systemic abnormalities involving the kidneys, liver, or blood. There is also a fetal manifestation of preeclampsia
involving fetal growth restriction, reduced amniotic fluid, and abnormal fetal oxygenation.[5] HELLP syndrome is a
severe form of preeclampsia and involves hemolytic anemia, elevated liver function tests (LFTs), and low platelet
count.
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 before 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 , many reported cases have
been classified as unpreventable.

Course of eclamptic seizures

Eclampsia manifests as 1 seizure or more, with each seizure generally lasting 60-75 seconds. The patients face
initially may become distorted, with protrusion of the eyes, and foaming at the mouth may occur. Respiration
ceases for the duration of the seizure.
Eclamptic seizures 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 period of unconsciousness, lasting for a variable period, follows phase 2. After the coma phase, the
patient may regain some consciousness, and she may become combative and very agitated. However, the patient
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will have 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 can include tongue biting, head trauma, broken bones, and aspiration.

Etiologic and Risk Factors for Preeclampsia/Eclampsia

Genetic predisposition, immunology, endocrinology, nutrition, abnormal trophoblastic invasion, coagulation
abnormalities, vascular endothelial damage, cardiovascular maladaptation, dietary deficiencies or excess, and
infection have been proposed as etiologic factors for preeclampsia/eclampsia.[2] Imbalanced prostanoid production
and increased plasma antiphospholipids have also been implicated in eclampsia.[2, 6]

Risk factors for eclampsia

The following are considered risk factors for eclampsia:
Nulliparity
Family history of preeclampsia, previous preeclampsia and eclampsia[2]
Poor outcome of previous pregnancy, including intrauterine growth retardation, abruptio placentae, or fetal
death
Multifetal gestations, hydatid mole, fetal hydrops, primigravida
Teen pregnancy
Primigravida
Patient older than 35 years
Lower socioeconomic status
The following preexisting medical conditions are also considered risk factors [4] :
Obesity
Chronic hypertension
Renal disease
Thrombophilias-antiphospholipid antibody syndrome
Protein C deficiency and protein S deficiency
Antithrombin deficiency
Vascular and connective tissue disorders
Gestational diabetes
Systemic lupus erythematosus

Multiorgan System Effects

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, preexisting renal or vascular pathology)
or obstetric factors (eg, multifetal gestations or molar pregnancy).

Cardiovascular concerns
Eclampsia is associated with cardiovascular derangements such as generalized vasospasm, increased peripheral
vascular resistance, increased left ventricular stroke work index, decreased central venous pressure, and
decreased pulmonary wedge pressure.

Hematologic concerns
Hematologic problems associated with eclampsia can include decreased plasma volume, increased blood
viscosity, hemoconcentration, and coagulopathy.

Renal concerns
Eclampsia-associated renal abnormalities can include decreases in glomerular filtration rate, renal plasma flow,
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and uric acid clearance.

Hepatic concerns
Hepatic derangements associated with eclampsia can include periportal necrosis, hepatocellular damage, and
subcapsular hematoma.

Central nervous system concerns

Eclampsia can result in central nervous system (CNS) abnormalities such as cerebral overperfusion due to loss of
autoregulation, cerebral edema, and cerebral hemorrhage.

Pathophysiology of Eclampsia
Inhibition of uterovascular development
Many uterovascular changes occur when a woman is pregnant. It is believed that these changes are due to the
interaction between fetal and maternal allografts and result in systemic and local vascular changes. It has been
shown that in patients with eclampsia, the development of uteroplacental arteries is hindered.

Hindrance of cerebral blood flow regulation

It is believed that in eclampsia there is abnormal cerebral blood flow in the setting of extreme hypertension. The
regulation of cerebral perfusion is inhibited, vessels become dilated with increased permeability, and cerebral
edema occurs, resulting in ischemia and encephalopathy. In extreme hypertension, normal compensatory
vasoconstriction may become defective. Several autopsy findings support this model and consistently reveal
swelling and fibrinoid necrosis of vessel walls.[2]

Endothelial dysfunction
Factors associated with endothelial dysfunction have been shown to be increased in the systemic circulation of
women suffering from eclampsia. These include the following[1] :
Cellular fibronectin
Von Willebrand factor
Cell adhesion molecules (ie, P-selectin, vascular endothelial adhesion molecule-1 [VCAM-1]
Intercellular adhesion molecule-1 [ICAM-1])
Cytokines (ie, interleukin-6 [IL-6])
Tumor necrosis factor- [TNF-]
In addition, it is believed that antiangiogenic factors, such as placental protein fms-like tyrosine kinase 1 (sFlt-1)
and activin A, antagonize vascular endothelial growth factor (VEGF).[7] Elevated levels of these proteins cause a
reduction of VEGF and induce systemic and local endothelial cell dysfunction.[1]
Leakage of proteins from the circulation and generalized edema are sequelae of the endothelial dysfunction and
thus a defining factor associated with preeclampsia and eclampsia.

Oxidative stress
Evidence indicates that leptin molecules increase in the circulation of women with eclampsia, inducing oxidative
stress, another factor in eclampsia, on cells. (The leptin increase also results in platelet aggregation, most likely
contributing to the coagulopathy associated with eclampsia.)[2, 8]
Oxidative stress has been found to stimulate the production and secretion of the antiangiogenic factor activin A
from placental and endothelial cells.[7] Studies in pregnant mouse models have proposed that there is a
dysregulation in the reactive oxygen species (ROS) signaling pathway.[8, 9]
Studies also suggest that increased systemic leukocyte activity plays a role in the mediation of oxidative stress,
inflammation, and endothelial cell dysfunction. Histochemistry studies indicate that there is predominantly an
increase in neutrophil infiltration of vasculature in patients with eclampsia.[9]
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Evaluation
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. Eclampsia can occur during the antepartum, intrapartum, and postpartum
periods. Ninety percent of eclampsia cases occur after 28 weeks' gestation.[2]
Preeclampsia can quickly develop into eclampsia. The natural progression of the disease is from symptomatic
severe preeclampsia (differentiated from preeclampsia by specific vital signs, symptoms, and laboratory
abnormalities) to seizures.
Features of eclampsia include the following:
Seizure or postictal state (100%)
Headache (80%), usually frontal
Generalized edema (50%)
Vision disturbance (40%), such as blurred vision and photophobia
Right upper quadrant abdominal pain with nausea (20%)
Amnesia and other mental status changes
The incidences of signs or symptoms before 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%)
The absence of signs or symptoms before seizure include the following:
Lack of edema (39%)
Absence of proteinuria (21%)
Normal reflexes (20%)
The relation of seizure to delivery is as follows:
Before delivery (>70%)
Before labor (antepartum) (25%)
During labor (intrapartum) (50%)
After delivery (postpartum) (25%)
Although patients with severe preeclampsia are at greater risk for seizures, 25% of patients have symptoms
consistent with mild preeclampsia before the seizures.
A study by Cooray et al found that the most common symptoms that immediately precede eclamptic seizures are
neurologic symptoms (ie, headache, with or without visual disturbance), regardless of degree of hypertension. This
suggests that closely monitoring patients with these symptoms may provide an early warning for eclampsia.[10]

Physical findings
Most patients with eclampsia present with hypertension and seizures, along with some combination of proteinuria
and edema. Findings at physical examination may include the following:
Sustained systolic BP greater than 160 mm Hg or diastolic BP greater than 110 mm Hg
Tachycardia
Tachypnea
Rales
Mental status changes
Hyperreflexia
Clonus
Papilledema
Oliguria or anuria
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Localizing neurologic deficits

Right upper quadrant or epigastric abdominal tenderness
Generalized edema
Small fundal height for the estimated gestational age
Apprehension
Cervical examination of the patient with eclampsia should not be overlooked, because the delivery mode may
largely depend upon the patients cervical status.

Differential Diagnosis
Adrenal Insufficiency and Adrenal Crisis
Cerebellar Hemorrhage
Cerebral Aneurysms
Cerebral Venous Thrombosis
Encephalopathy, Hypertensive
Encephalitis
Gestational Trophoblastic Neoplasia
Head Trauma
Hyperaldosteronism, Primary
Hypertensive Emergencies
Hypoglycemia
Meningitis
Neoplasms, Brain
Pregnancy, Preeclampsia
Seizures and Epilepsy: Overview and Classification
Shock, Septic
Stroke, Hemorrhagic
Stroke, Ischemic
Subarachnoid Hemorrhage
Systemic Lupus Erythematosus
Thrombotic Thrombocytopenic Purpura
Withdrawal Syndromes
Angiomas
Cerebral Vasculitis
Drug Overdose
Metabolic Disorders
Undiagnosed Brain Tumors

Diagnostic Overview
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Seizures in the first trimester or well into the postpartum period probably are due to CNS pathology and warrant full
evaluation, including computed tomography (CT) scanning of the head, lumbar puncture (if clinical evidence of
meningitis or concern for hemorrhage exists), determination of electrolyte levels, and urine or serum toxicologic
screening. Do not overlook other neurologic causes of seizure, particularly if the seizure occurs more than 24
hours after delivery. In addition, rule out hypoglycemia as cause of seizure or result of seizure, and rule out
hyperglycemia as cause of mental status changes.
When preeclampsia occurs in the early second trimester (ie, 14-20 weeks' gestation), the diagnosis of hydatiform
mole or choriocarcinoma should be considered.
Ruling out eclampsia in an obstetric patient who has been involved in an unexplained trauma is important.
Immediately consult an obstetrician/gynecologist when the diagnosis of eclampsia is being considered.
No single laboratory test or set of laboratory determinations is useful in predicting maternal or neonatal outcome in
women with eclampsia. Imaging studies may be indicated after initial stabilization, especially if there is doubt
about the diagnosis or possible injuries secondary to seizure activity.

Urinalysis and Uric Acid levels

Proteinuria is typically one of the presenting symptoms in patients with eclampsia. A timed collection has been
the criterion standard for urinalysis to detect proteinuria (>300 mg/24 h or >1 g/L). Protein per unit time measured
over 24 hours has been used traditionally; however, 12-hour collections have proved to be as accurate.[11]
Although investigational, Baweja et al suggest that when measuring intact urinary albumin levels using highperformance liquid chromatography in an early and uncomplicated pregnancy, spot urinary albumin:creatinine ratio
(ACR) values are higher. If measured early in the second trimester, an ACR of 35.5 mg/mmol or higher may predict
preeclampsia before symptoms arise.[12]
Uric acid levels may be mildly increased.

Hematologic Studies
A complete blood cell (CBC) count may reveal the following:
Anemia due to microangiopathic hemolysis, hemoconcentration due to third spacing, or physiologic
hemodilution of pregnancy
Peripheral smear (schistocytes, burr cells, echinocytes)
Increased bilirubin (>1.2 mg/dL)
Thrombocytopenia (< 100,000) due to hemolysis and low platelet count associated with HELLP syndrome
(seen in 20-25% of patients with eclampsia)[4]
Low serum haptoglobin levels
Elevated lactate dehydrogenase (LDH) levels (threshold of 180600 U/L)
The coagulation profile may reveal normal prothrombin (PT) and activated partial thromboplastin (aPTT) times, fibrin
split products, and fibrinogen levels. Rule out associated disseminated intravascular coagulation (DIC).

Serum Creatinine level

The serum creatinine level is elevated in eclampsia because of a decreased intravascular volume and a reduced
glomerular filtration rate (GFR). Creatinine clearance (CrCl) may be less than 90 mL/min/1.73 m2 .

Liver Function Tests

Liver function test results may reveal the following (20-25% of patients with eclampsia):
Aspartate aminotransferase (SGOT) level higher than 72 IU/L
Total bilirubin levels higher than 1.2 mg/dL
LDH level higher than 600 IU/L[2]
Elevated levels due to hepatocellular injury and HELLP syndrome

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CT and MRI of the Head

CT scanning 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.
Although obtaining a CT scan in eclampsia is not routine, abnormalities have been observed in up to 50% of
women imaged.
Characteristic CT scan 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 scan 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
Abnormal magnetic resonance imaging (MRI) findings of the head have been reported in up to 90% of women
imaged. These include an increased signal at the gray-white matter junction on T2-weighted images, as well as
cortical edema and hemorrhage. The syndrome of posterior reversible encephalopathy (PRES), indicative of central
vasogenic edema, has been increasingly recognized as a component of eclampsia.[13]
Consider CT or MRI scanning in patients who have been involved in trauma, are refractory to magnesium sulfate
therapy, or have atypical presentations (eg, seizures >24 h after delivery, absence of severe hypertension).

Transabdominal Ultrasonography
Transabdominal ultrasonography is used to estimate gestational age. This may also be used to rule out abruptio
placentae, which can complicate eclampsia.

Electroencephalography and CSF Studies

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

Medical Therapy
Eclamptic convulsions are life-threatening emergencies and require the proper treatment to decrease maternal
morbidity and mortality. Delivery is the only definitive treatment for eclampsia.
The patient should be advised and educated on the course of the disease and any residual problems. She should
also be educated on the importance of adequate prenatal care in subsequent pregnancies.
Several organizations have developed screening, treatment, and prevention guidelines for preeclampsia and
eclampsia.[14, 15]

Consultations and/or Transfer

An experienced obstetrician or maternal-fetal medicine specialist should be consulted. Patients with eclampsia
require immediate obstetric consultation and admission to a labor and delivery unit capable of providing intensive
care until delivery of the neonate. In the event of premature delivery or fetal compromise, a pediatrician or
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neonatologist should be consulted.

When initially evaluating a patient with eclampsia, become familiar with the level of care that the medical center
can offer the patient, as 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, a high-risk obstetric
facility that provides neonatal and maternal intensive care.

Supportive care
Emergency medical services personnel should (1) secure an intravenous (IV) line with a large-bore catheter, (2)
initiate cardiac monitoring and administer oxygen, and (3) transport the patient in the left lateral decubitus position.
Supportive care for eclamptic convulsions includes the following:
Close monitoring (invasive, if clinically indicated)
Airway support
Adequate oxygenation
Anticonvulsant therapy
Blood pressure (BP) control
Place the 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 the 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.
After the seizure has ended, a 16- to 18-gauge IV line should be established for drawing specimens and
administering fluids and medications. (Fluid management is critical in patients with eclampsia.) IV fluids should be
limited to isotonic solutions to replace urine output plus about 700 mL/d to replace insensible losses.

Pharmacologic considerations for convulsions and hypertension

Pharmacotherapy goals are to reduce morbidity, prevent complications, and correct eclampsia. The drug of choice
to treat and prevent eclampsia is magnesium sulfate.[16] 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.
IV magnesium sulfate is the initial drug administered to terminate seizures. Seizures usually terminate after the
loading dose of magnesium. A loading dose of 4-6 g (15-20 min) and a maintenance dose of 1-2 g per hour as a
continuous IV solution should be administered. Alternatively, lorazepam (Ativan; 4 mg IV over 2-5 minutes) or
diazepam (Valium; 5-10 mg IV slowly) can be used to terminate the seizure, after which magnesium sulfate is
administered. Once the seizures terminate, 85% of patients note improved BP control.[17, 15] Note: Magnesium
toxicity can cause coma, and, if mental status changes with these infusion rates, this should be considered.[2]
Benzodiazepines or phenytoin can be used for seizures that are not responsive to magnesium sulfate. Avoid the
use of multiple agents to abate eclamptic seizures, unless necessary.
Severe hypertension must be addressed after magnesium infusions. Hydralazine or labetalol can be administered
IV for BP control. The goal is to maintain systolic BP between 140 and 160 mm Hg and diastolic BP between 90
and 110 mm Hg. An IV bolus of hydralazine (5-10 mg q20min prn) or labetalol (20-40 mg q15min prn) is
recommended. Other potent antihypertensive medications, such as sodium nitroprusside or nitroglycerin, can be
used but are rarely required.[2]
Diuretics are used only in the setting of pulmonary edema.
Care must be taken not to decrease the BP too drastically; an excessive decrease can cause inadequate
uteroplacental perfusion and fetal compromise.[16]
A dose of antenatal steroids may be administered in anticipation of emergent delivery when gestational age is less
than 32 weeks. Betamethasone (12 mg IM q24h 2 doses) or dexamethasone (6 mg IM q12h 4 doses) is
recommended.
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
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receiving adequate magnesium therapy, seizures may be treated with sodium amobarbital, 250 mg IV over 3-5
minutes.[18] Alternatively, lorazepam or diazepam may be administered (as described above) for status epilepticus.
However, these drugs can be associated with prolonged neonatal neurologic depression.
BP should be assessed with the goal of maintaining the diastolic BP at less than 110 mm Hg with administration
of antihypertensive medications as needed (eg, hydralazine, labetalol, nifedipine).
Keep nothing by mouth (including medications) until the patient is medically stabilized or delivered, because she
is at risk for aspiration when postictal and may have recurrent seizures.

Maternal monitoring
Depending on the clinical course, regularly check the patients neurologic status for signs of increased intracranial
pressure or bleeding (eg, funduscopic examination, cranial nerves)
Monitor fluid intake and urine output, maternal respiratory rate, and oxygenation, as indicated, and continuously
monitor fetal status. Pulmonary arterial pressure monitoring is rarely indicated but may be helpful in patients who
have evidence of pulmonary edema or oliguria/anuria.
Once the seizure is controlled and the patient has regained consciousness, the patients general medical
condition should be assessed to identify any other causes for seizures.
Induction of labor may be initiated when the patient is stable.

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. Typically, emergent cesarean delivery is not indicated for this postseizure transient
bradycardia; it spontaneously resolves.
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. Growthrestricted and preterm fetuses may take longer to recover following a seizure. Placental abruption may be present
if uterine hyperactivity remains and fetal bradycardia persists.

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 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 delivery, given the high rate of intrapartum complications. When emergent
cesarean delivery is indicated, substantiating the absence of coagulopathy before the procedure is important. (See
Surgical Therapy.)[19]
Intrapartum complications include the following:
Fetal growth retardation (30%)
Nonreassuring fetal heart rate patterns (30%)
Placental abruption (23%)
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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.

Surgical Therapy
Cesarean delivery may be necessary for obstetric indications or a deteriorating maternal condition. The patient
should be stabilized with respect to seizures, oxygenation, and hemodynamic status before the initiation of
cesarean delivery. BP should be controlled and coagulopathies monitored or corrected.

Anesthesia
An anesthesiology consultation may be obtained. Early evaluation is recommended to assist with cardiopulmonary
stabilization and to 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
platelets/L). 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.

Postpartum Outpatient Monitoring

Follow up 1-2 weeks after delivery to evaluate the patient for BP control and any residual deficits from the
eclamptic seizure. Patients with persistent hypertension past 8 weeks' puerperium or neurologic changes may
need medical referral.
Al-Safi et al suggest that the first week after discharge is the most critical period for the development of
postpartum eclampsia. Discussing the risks and educating patients about the possibility of delayed postpartum
preeclampsia is important, regardless of whether they develop hypertensive disease prior to discharge.[20]

Prevention of Preeclampsia/Eclampsia
Preventing the development of preeclampsia in high-risk patients could theoretically decrease the risk of eclampsia
and its complications later in pregnancy. Aspirin blocks platelet aggregation and vasospasm in preeclampsia, and
it may be effective in preventing preeclampsia. Studies have shown that low-dose aspirin in women at high risk for
preeclampsia can contribute to a decreased risk of preeclampsia, a reduction in preterm delivery rates, and a
reduction in fetal death rates, without increasing the risk of placental abruption. An obstetrician should directly
supervise low-dose aspirin therapy in high-risk patients.
If the patient has preexisting hypertension, she should have good control before conception and throughout her
pregnancy. Her case should be followed for recognition and treatment of preeclampsia.
A study by Vadillo-Ortega et al suggests that in a high-risk population (eg, previous pregnancy complicated by
preeclampsia, preeclampsia in a first-degree relative), supplementation during pregnancy with a special food (eg,
bars) containing L-arginine and antioxidant vitamins may reduce the risk of preeclampsia. Notably, the beneficial
effect was greatest when supplementation was started prior to 24 weeks' gestation. Antioxidant vitamin
supplementation alone did not protect against preeclampsia. More studies performed on low-risk populations are
needed.[21]

Complications of Eclampsia
As many as 56% of patients with eclampsia may have transient deficits, including cortical blindness. However,
studies have failed to demonstrate evidence of persisting neurologic deficits after uncomplicated eclamptic
seizures during the follow-up period.[22] Studies suggest that there is an increased risk for cerebrovascular
accidents (CVAs) and coronary artery disease (CAD) in eclamptic mothers later in life.
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Other potential complications of eclampsia include the following:

Permanent neurologic damage from recurrent seizures or intracranial bleeding
Renal insufficiency and acute renal failure
Fetal changes IUGR, abruptio placentae, oligohydramnios
Hepatic damage and rarely hepatic rupture
Hematologic compromise and DIC
Increased risk of recurrent preeclampsia/eclampsia with subsequent pregnancy
Maternal or fetal death

Outcome
Although the incidence of eclampsia has declined in recent years, mainly due to the improvement of healthcare,
serious adverse outcomes still exist.[23] Five percent of patients with hypertension develop severe preeclampsia,
and about 25% of women with eclampsia have hypertension in subsequent pregnancies. About 2% of women with
eclampsia develop eclampsia with future pregnancies.
Multiparous women with eclampsia have a higher risk for the development of essential hypertension; they also
have a higher mortality rate in subsequent pregnancies than do primiparous women.

Maternal morbidity
Maternal complications from eclampsia include the following:
Permanent CNS damage from recurrent seizures or intracranial bleeds
Disseminated intravascular coagulopathy
Renal insufficiency
Pulmonary edema
Cardiopulmonary arrest
The most significant maternal complication of eclampsia is permanent CNS damage secondary to recurrent
seizures or intracranial bleeding. The maternal mortality rate is 8-36% in these cases.[17]

Maternal mortality
Eclampsia and preeclampsia account for approximately 63,000 maternal deaths annually worldwide.[24] In
developed countries, the maternal death rate is reportedly 0-1.8%. The perinatal mortality rate from eclampsia in
the United States and Great Britain ranges from 5.6% to 11.8%. The maternal mortality rate is as high as 14% in
developing countries.[5, 18, 22]
A study from the US Centers for Disease Control and Prevention (CDC) found an overall preeclampsia/eclampsia
case-fatality rate of 6.4 per 10,000 cases at delivery. The study also found a particularly high risk of maternal
death at 20-28 weeks gestation.[25]
Black woman have twice the risk that white women have for mortality associated with preeclampsia/eclampsia.
This is most likely due to inadequate access to prenatal care among black women, as well as to increased
incidences in black women of genetic diseases associated with circulating antiphospholipids. It has been proven
that patients with elevated antiphospholipid plasma levels have a higher incidence of preeclampsia and eclampsia.
[2] However, whether this is due to the antiphospholipids themselves or to some other underlying process is not
clear.[6]
A majority of women who suffer eclampsia-associated death have concurrent HELLP syndrome.[24]
A report of an international study demonstrated that serious complications among patients with eclampsia
(including maternal mortality) may be predicted by the use of a model that incorporates gestational age, chest
pain or dyspnea, oxygen saturation, platelet count, and creatinine and aspartate transaminase concentrations.
Although clinical use of the model awaits future validation, the identification of the predictive variables may aid in
management decisions.[26]

Fetal/neonatal mortality
The fetal mortality rate varies from 13-30% due to premature delivery and its complications. Placental infarcts,
http://emedicine.medscape.com/article/253960-overview#showall

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