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. 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 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.

he 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

athophysiology 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).[8] 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, 9]

Oxidative stress has been found to stimulate the production and secretion of the
antiangiogenic factor activin A from placental and endothelial cells.[8] Studies in pregnant
mouse models have proposed that there is a dysregulation in the reactive oxygen species
(ROS) signaling pathway.[9, 10]

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.[10]

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 (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.[11]

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 patients cervical status.

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.
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.[12]

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.[13]

Uric acid levels may be mildly increased.

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).

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 m 2.

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

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.[15, 16, 17] 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[17] :

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.[17, 18]
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.[16, 19]
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.[18]

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.[20]
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.[21]

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. 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.)[22]

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.

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.

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.[24]

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.[25] 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.[26, 27]

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.[26, 27]

Although the incidence of eclampsia has declined in recent years, mainly due to the
improvement of healthcare, serious adverse outcomes still exist.[28] 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.[19] A loading dose of magnesium sulfate followed by maintenance doses for 12
hours may be effective in preventing recurrent seizures.[21]

Maternal mortality

Eclampsia and preeclampsia account for approximately 63,000 maternal deaths annually
worldwide.[29] 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, 20, 25]

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.[30]

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.[29]

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.[31]

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.