Overview

Ten percent of all pregnancies are complicated by hypertension. Eclampsia

and preeclampsia account for about half of these cases worldwide, and these conditions 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, 5] 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. [6] 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. [6] 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. Although there are
numerous studies exploring ultrasound and biomarker prediction of patients at risk of pre-
eclampsia, 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. [37, 38, 39]  
Course of eclamptic seizures

Eclampsia manifests as 1 seizure or more, with each seizure generally lasting 60-75 seconds. The
patient’s 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 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
The mechanism(s) responsible for the development eclampsia remain(s) unclear. [5] 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, 7]  In murine models, placental
ischemia appears to be associated with an increased susceptibility to seizures and cerebrospinal
fluid (CSF) inflammation. [5]

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, and increased left ventricular stroke work
index. Pulmonary capillary wedge pressure (PCWP) may vary from low to elevated. Importantly,
central venous pressure (CVP) may not correlate with PCWP in patients with severe
preeclampsia or eclampsia. [8]  
A prospective observational study by Vaught that included 63 women with pre-eclampsia with
severe features reported higher systolic pressure, higher rates of abnormal diastolic function,
decreased global right ventricular longitudinal systolic strain, increased left-sided chamber
remodeling, and higher rates of peripartum pulmonary edema in these women when compared
with healthy pregnant women. [36]

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, and uric acid clearance as well as proteinuria.

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.
With increasing blood pressure, cerebral autoregulation is impaired  resulting in cerebral regions
of ischemia as well as microhemorrhage, each of which may initiate a seizure focus.  [40] 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-α [TNF-α]
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). [9] 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, 10]
Oxidative stress has been found to stimulate the production and secretion of the antiangiogenic
factor activin A from placental and endothelial cells.  [9] Studies in pregnant mouse models have
proposed that there is a dysregulation in the reactive oxygen species (ROS) signaling
pathway. [10, 11]
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. [11]
Evaluation
Eclampsia always should be considered in a pregnant patient with a seizure episode. Although
trauma-associated cerebral injury must be ruled-out, 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 (i.e., preeclampsia without severe features) 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. [12]
A retrospective study by Nerenberg et al evaluated 1,565,733 births to determine the incidence
rate and relative risk of a seizure disorder after eclampsia. The study reported that eclampsia
exclusively affected 1,615 (0.10%) pregnancies, 17,264 (1.1%) with preeclampsia, 60,863
(3.9%) with gestational hypertension, and 1,485,991 (94.9%) remained unaffected. A future
seizure disorder was more likely after a pregnancy with eclampsia (4.58/10,000 person-years)
than a pregnancy without a hypertensive disorder (0.72/10,000 person-years) however the
absolute risk was low (approximately one seizure/2,200 person-years). [13]

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
 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 patient’s 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
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 a 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.  [14] . In addition, it is now common to rely upon a spot
protein to creatinine ratio to assess proteinuria, instead of a timed collection. The degree of
proteinuria or change in proteinuria is helpful in diagnosing preeclampsia, but does not have any
significant effect on clinical management. 
Although investigational, Baweja et al suggest that when measuring intact urinary albumin levels
using high-performance 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. [15]
Uric acid levels may be mildly to markedly 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 180–600 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). DIC is rare, unless there is an
associated abruption. 

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
 Note that alkaline phosphatase levels are not of value in diagnosing hepatic dysfunction
during pregnancy due to the placental alkaline phosphatase. 

CT Scanning and MRI of the Head

Computed tomography (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. [16]
One should consider CT scanning or MRI 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 and fetal well-being. Poor
fetal growth, oligohydramnios, and/or abnormal umbilical artery Doppler velocimetry may be
seen secondary to the hypertension associated with eclampsia. Ultrasound may also be used to
assess for abruptio placentae, which can complicate eclampsia. However, the sensitivity of
ultrasound to detect an abruption is poor.  

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. [17, 18, 19]  The American College of Obstetricians and Gynecologists
(ACOG) and the Society for Maternal-Fetal Medicine (SMFM) continue to support the short-
term (usually < 48 hours) use of magnesium sulfate in obstetric care for conditions and treatment
durations that include the following [19] :
 For prevention and treatment of seizures in women with preeclampsia or eclampsia
 o Recent recommendations suggest that magnesium sulfate be utilized for seizure
prophylaxis in severe preeclampsia and for controlling seizures in eclampsia, though
magnesium sulfate is not required for preeclampsia without severe features
 For fetal neuroprotection before anticipated early preterm (< 32 weeks of gestation)
delivery
 For short-term prolongation of pregnancy (≤48 hours) to allow for the administration of
antenatal corticosteroids in pregnant women who are at risk of preterm delivery within 7
days

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 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.  [19, 20]  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. For
recurrent seizures or when magnesium is contraindicated, one may use lorazepam (Ativan; 2-4
mg IV over 2-5 minutes) or diazepam (Valium; 5-10 mg IV slowly) can be used to terminate the
seizure. While benzodiazepines can be used to treat the seizures due to eclampsia magnesium
remains the preferred choice. There exist over 50 years of data and experience using magnesium
for this purpose with excellent safety and efficacy. Once the seizures terminate, 85% of patients
note improved BP control. [18, 21] 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 (>160 mm Hg systolic or > 110 mm Hg diastolic)  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 over 2 minutes) or labetalol (initial dose 20 mg) is
recommended. Alternatively, oral nifedipine capsules (10 mg) may be administered. 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 prior to delivery.
Care must be taken not to decrease the BP too drastically; an excessive decrease can cause
inadequate uteroplacental perfusion and fetal compromise. [20]
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 receiving adequate magnesium therapy, seizures may be
treated with sodium amobarbital, 250 mg IV over 3-5 minutes.  [22] 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.
Anjum et al reported that following a loading dose of magnesium sulfate, a reduced duration of
maintenance doses (12 hours vs 24 hours) for women with eclampsia may be effective for
preventing recurrent seizures. [23]  

Maternal monitoring
Depending on the clinical course, regularly check the patient’s 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 patient’s 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. 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.

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.) [24]
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.

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 should 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/µL). 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. [25]
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. 

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.  [27] Studies suggest that there
is an increased risk for cerebrovascular accidents (CVAs) and coronary artery disease (CAD) in
eclamptic mothers later in life.
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: Eclampsia is associated with approximately 13% of maternal
deaths worldwide [5]
Although some women who have had eclampsia or preeclampsia have reported subsequent
cognitive difficulties even years later, a long-term follow-up study by Postma et al utilizing
standardized testing was unable to find objective evidence of such problems. The reported
neurocognitive difficulties have seemingly been associated with concentration and memory, as
well as with vision-related tasks of daily living. In the study, 46 women who had been eclamptic
and 51 who had been preeclamptic were given neurocognitive tests an average of about seven
years following the index pregnancy; 48 controls, who had normotensive pregnancies, were also
involved. [28, 29]
The eclamptic and preeclamptic women in the study did not perform as well as the controls on
motor-function tests. (They also performed more poorly on the Hospital Anxiety and Depression
Scale.) However, they scored similarly to the control subjects with regard to attention, executive
functioning, visual perception, and working and long-term memory. The investigators suggested
that the reported cognitive difficulties in previously eclamptic or preeclamptic women occur
during complex, stressful situations of daily life and may be exacerbated by anxiety and
depression. [28, 29]

Outcome
Although the incidence of eclampsia has declined in recent years, mainly due to the
improvement of healthcare, serious adverse outcomes still exist.  [30] 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. [21]  A loading dose of magnesium sulfate followed by maintenance doses for 12-24 hours
may be effective in preventing recurrent seizures. [23]

Maternal mortality
Eclampsia and preeclampsia account for approximately 63,000 maternal deaths annually
worldwide. [31] 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. [6, 22, 27]
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. [32]
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. [7]
A majority of women who suffer eclampsia-associated death have concurrent HELLP
syndrome. [31]
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. [33]

Fetal/neonatal mortality

The fetal mortality rate varies from 13-30% due to premature delivery and its complications.
Placental infarcts, abruptio placentae, intrauterine growth retardation, and fetal hypoxia also
contribute to fetal demise. [2]