10/7/2017 Eclampsia - UpToDate

Author: Errol R Norwitz, MD, PhD, MBA

Section Editors: Charles J Lockwood, MD, MHCM, Timothy A Pedley, MD
Deputy Editor: Vanessa A Barss, MD, FACOG

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2017. | This topic last updated: Jul 06, 2017.

INTRODUCTION — Eclampsia refers to the occurrence of new-onset, generalized, tonic-clonic seizures or

coma in a woman with preeclampsia. It is the convulsive manifestation of preeclampsia and one of several
clinical manifestations at the severe end of the preeclampsia spectrum (table 1). Despite advances in
detection and management, preeclampsia/eclampsia remains a common cause of maternal morbidity and
death.

The clinical manifestations, diagnosis, and management of eclampsia will be reviewed here. Issues related
to preeclampsia are discussed separately:

● (See "Preeclampsia: Pathogenesis".)

● (See "Preeclampsia: Clinical features and diagnosis".)
● (See "Preeclampsia: Management and prognosis".)
● (See "Preeclampsia: Prevention".)
● (See "Expectant management of preeclampsia with severe features".)

INCIDENCE AND EPIDEMIOLOGY — Eclampsia occurs in 2 to 3 percent of women with severe features of
preeclampsia not receiving anti-seizure prophylaxis and up to 0.6 percent of women with preeclampsia
without severe features (previously referred to as “mild” preeclampsia) [1]. The incidence of eclampsia has
been stable at 1.5 to 10 cases per 10,000 deliveries in developed countries [2-8]. In developing countries,
however, the incidence varies widely: from 6 to 157 cases per 10,000 deliveries [9-11].

Risk factors for eclampsia are similar to those for preeclampsia (table 2). Women at highest risk of
developing eclampsia are nonwhite, nulliparous, and from lower socioeconomic backgrounds. The peak
incidence is in adolescence and the early twenties but is also increased in women over age 35.

PATHOGENESIS OF SEIZURES — The precise cause of seizures in preeclamptic women is not clearly
understood. Two models have been proposed, based on the central role of hypertension. According to the
first model, hypertension causes a breakdown of the autoregulatory system of the cerebral circulation,
leading to hyperperfusion, endothelial dysfunction, and vasogenic and/or cytotoxic edema. In the second
model, hypertension causes activation of the autoregulatory system, leading to vasoconstriction of cerebral
vessels leading to hypoperfusion, localized ischemia, endothelial dysfunction, and vasogenic and/or
cytotoxic edema [12]. Cerebral inflammation may also play a role [13].

The pathogenesis of preeclampsia is reviewed elsewhere. (See "Preeclampsia: Pathogenesis".)

CLINICAL PRESENTATION AND FINDINGS — Most women have premonitory signs/symptoms in the
hours before the initial seizure. In a systematic review including 59 studies involving over 21,000 women
with eclampsia from 26 countries, the most common antecedent signs/symptoms and percent of women
with the sign/symptom were [14]:

● Hypertension (75 percent)

● Headache (persistent frontal or occipital headaches or thunderclap headaches) (66 percent)

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● Visual disturbances (scotomata, loss of vision [cortical blindness], blurred vision, diplopia, visual field
defects [eg, homonymous hemianopsia], photophobia) (27 percent)

● Right upper quadrant or epigastric pain (25 percent)

● Asymptomatic (25 percent)

Ankle clonus is also a common finding [15].

Eclampsia is generally manifested by a generalized tonic-clonic seizure or coma. At onset, there is an

abrupt loss of consciousness, often associated with a scream or shriek. The muscles of the arms, legs,
chest, and back then become stiff. The woman may begin to appear cyanotic during this tonic phase. After
approximately one minute, the muscles begin to jerk and twitch for an additional one to two minutes. During
this clonic phase, the tongue may be bitten and frothy and bloody sputum may come out of the mouth. The
postictal phase begins once the twitching movements end. The woman is initially in a deep sleep, breathing
deeply, and then gradually wakes up, often complaining of a headache (table 3). Most patients begin to
recover responsiveness within 10 to 20 minutes after the generalized convulsion. Focal neurologic deficits
are generally absent.

Fetal bradycardia for at least three to five minutes is a common finding during and immediately after the
seizure. Resolution of maternal seizure activity is associated with fetal tachycardia and loss of heart rate
variability, sometimes with transient decelerations [16]. The fetal heart rate pattern generally improves with
maternal and fetal therapeutic interventions (see 'Management' below). A nonreassuring pattern with
frequent, recurrent decelerations for more than 10 to 15 minutes despite maternal and fetal resuscitative
interventions suggests the possibility of an occult abruption [17].

On physical examination, neurologic findings may include memory deficits, increased deep tendon reflexes,
visual perception deficits, visual processing deficits, altered mental status, and cranial nerve deficits [18].

Timing — Eclampsia occurs preterm in approximately 50 percent of women and between 20 and 30 weeks
of gestation in approximately 20 percent [2,19]. In the systematic review described above, 59 percent of
eclampsia occurred antepartum, 20 percent occurred intrapartum, and 21 percent occurred postpartum [14].
Approximately 90 percent of postpartum seizures occur within one week of delivery [20-24]. Antecedent
symptoms were similar to those with antepartum and intrapartum eclampsia. In a series of women
discharged and later readmitted with eclampsia more than two days but less than six weeks after delivery,
the most common presenting symptom was headache, which occurred in about 70 percent [24]. Other
prodromal symptoms included shortness of breath, blurry vision, nausea or vomiting, edema, neurological
deficit, and epigastric pain. Many women did not have hypertension during the antecedent pregnancy.

Other findings

Electroencephalography — There is limited information on electroencephalography (EEG) in

eclampsia. A literature review reported postictal EEG abnormalities were common in eclamptic women, and
the EEG became normal with prolonged postpartum follow-up [25]. The studies were of low methodologic
quality and all but one were published between 1955 and 1984; findings using modern equipment and
practices have not been reported. (See "Electroencephalography (EEG) in the diagnosis of seizures and
epilepsy".)

Neuroimaging — Neuroimaging findings similar to those seen with reversible posterior

leukoencephalopathy syndrome (RPLS; also called posterior reversible encephalopathy syndrome [PRES])
are the hallmark of eclampsia, found in over 90 percent of patients in small series [26,27]. The most
common findings of RPLS on magnetic resonance imaging (MRI) are patchy T2/FLAIR hyperintensity in the
subcortical white matter and adjacent gray matter of the parietal and occipital lobes. (See "Reversible
posterior leukoencephalopathy syndrome", section on 'Neuroimaging'.)

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Neurologic histopathology — A classic report described neurologic histopathology in eclamptic women

autopsied shortly after death [28]. Over 50 percent of women who died within two days of seizures had
cerebral hemorrhages. Petechial cortical hemorrhages were most common, especially involving the occipital
lobe. Diffuse cerebral edema and gross hemorrhage occurred less frequently. Cerebral venous thrombosis
was common in women who developed eclampsia postpartum.

DIAGNOSIS — Eclampsia is a clinical diagnosis typically based upon the occurrence of new-onset
generalized tonic-clonic seizures in a woman with preeclampsia [29].

In a pregnant woman with seizures, the typical clinical and neuroimaging findings of RPLS (headache,
confusion, visual symptoms, seizures, vasogenic edema predominantly localized to the posterior cerebral
hemispheres) are indicative of eclampsia, even when features of preeclampsia (hypertension with or without
proteinuria) are absent [30,31]. Preeclamptic women with neurologic symptoms may also be diagnosed with
RPLS [31]. (See "Reversible posterior leukoencephalopathy syndrome".)

Diagnostic evaluation — Women with preeclampsia who develop a generalized tonic-clonic seizure
without persistent neurologic deficit require no diagnostic evaluation beyond that for preeclampsia [32]. (See
"Preeclampsia: Clinical features and diagnosis".)

Atypical cases, such as women who do not meet criteria for diagnosis of preeclampsia (table 4) or who
have persistent neurologic deficits, prolonged loss of consciousness, onset of seizures >48 hours after
delivery, onset of seizures before 20 weeks of gestation, or seizures despite adequate magnesium sulfate
therapy should be evaluated for other causes of seizures. A neuroimaging study should be performed in
these patients to evaluate for a culprit structural brain abnormality. (See 'Differential diagnosis' below.)

Differential diagnosis — The differential diagnosis of new-onset seizures in a pregnant woman involves
determining whether the seizure was mostly incidental to the pregnant state (eg, brain tumor, ruptured
aneurysm), exacerbated by the pregnant state (eg, thrombotic thrombocytopenic purpura [TTP], hemolytic
uremic syndrome [HUS], cerebral venous thrombosis), or unique to the pregnant state (eg, eclampsia). The
following issues should be considered in differential diagnosis:

● The occurrence of preeclampsia/eclampsia before 20 weeks of gestation is rare and should raise the
possibility of an underlying molar pregnancy or a cause of seizure unrelated to pregnancy. Complete
molar pregnancy can be detected by ultrasound examination. (See "Hydatidiform mole: Epidemiology,
clinical features, and diagnosis", section on 'Pelvic ultrasound' and "Evaluation and management of the
first seizure in adults".)

● Persistent neurologic deficits suggest an anatomic abnormality, whether or not the woman has
eclampsia. Causes of neurologic symptoms developing suddenly include: stroke, intracranial
hemorrhage, brain mass lesion, toxic and metabolic encephalopathies, reversible cerebral
vasoconstriction syndrome, thrombotic thrombocytopenic purpura, and central nervous system infection
[33]. The assessment and differential diagnosis of a first seizure in adults with neurologic deficits is
described separately. (See "Evaluation and management of the first seizure in adults".)

● Seizures without neurologic deficits (see 'Diagnostic evaluation' above) may be triggered by metabolic
abnormalities (eg, hypocalcemia, hyponatremia, hypoglycemia), toxins (drug or alcohol withdrawal,
drug intoxication), infection (meningitis, encephalitis, sepsis), or recent head trauma. History, physical
examination, and laboratory studies can help distinguish these disorders from eclampsia. Laboratory
tests appropriate for the evaluation of a first seizure include electrolytes, glucose, calcium, magnesium,
hematology studies, renal function tests, liver function tests, and toxicology screens, although the
likelihood of finding a relevant abnormality in unselected patients is low. The absence of neurologic
deficits does not exclude an anatomic abnormality within the brain. Neuroimaging when the patient is
clinically stable may be valuable in select cases. (See "Evaluation and management of the first seizure
in adults".)

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● Pregnancy is a precipitating factor for some disorders associated with seizure activity, such as TTP or
HUS. TTP and HUS may be indistinguishable from eclampsia occurring in a woman with HELLP
syndrome (hemolysis, elevated liver enzymes, low platelets) (table 5) and approximately 10 to 20
percent of women with preeclampsia/eclampsia have laboratory findings of HELLP syndrome.
Eclampsia and HELLP improve after delivery, but delivery does not affect the course of TTP and HUS.
(See "HELLP syndrome", section on 'Differential diagnosis' and "Approach to the patient with suspected
TTP, HUS, or other thrombotic microangiopathy (TMA)".)

MANAGEMENT

Key principles — If the seizure is witnessed, maintaining airway patency and preventing aspiration are the
initial priority. The woman should be rolled onto her left side. The immediate issues include:

● Prevention of maternal hypoxia and trauma

● Treatment of severe hypertension, if present
● Prevention of recurrent seizures
● Evaluation for prompt delivery

Women who do not improve promptly following control of hypertension and seizures and those who develop
localizing neurologic signs should be evaluated by a neurologist.

Maternal oxygenation and protection from trauma — The patient is placed in a lateral position, if
possible. Supplemental oxygen (8 to 10 L/min) is administered via a nonrebreather face mask to treat
hypoxemia from hypoventilation during the seizure [17]. Raised, padded bedrails provide protection from
trauma.

Treatment of hypertension — Antihypertensive therapy (table 6) is administered to prevent stroke, which

accounts for 15 to 20 percent of deaths from eclampsia. A common threshold for initiating antihypertensive
therapy is sustained diastolic pressures greater than 105 to 110 mmHg or systolic blood pressures ≥160
mmHg, although the validity of these thresholds has not been tested prospectively. The risk of stroke
correlates with the degree of elevation in systolic and diastolic pressures and maternal age [34], but it is not
clear whether there is a threshold pressure above which emergent therapy should be started in pregnant
hypertensive women [35]. The cerebral vasculature of women with underlying chronic hypertension can
probably tolerate higher systolic pressures without injury, while adolescents with normally low blood
pressures may benefit from starting treatment at lower blood pressure levels.

The indications for treatment of hypertension, drug choice and dose, and target blood pressure are the
same as in preeclampsia and reviewed in detail separately. (See "Management of hypertension in pregnant
and postpartum women", section on 'Preeclampsia'.)

Prevention of recurrent seizures — The anticonvulsive drug of choice is magnesium sulfate. Treatment is
primarily directed at prevention of recurrent seizures rather than control of the initial seizure since the initial
seizure is usually of short duration and may occur in a setting where intravenous access and drugs are not
readily available.

Approximately 10 percent of eclamptic women will have repeated seizures if managed expectantly [36].
There is universal agreement that women with eclampsia require anticonvulsant therapy to prevent
recurrent seizures and the possible complications of repeated seizure activity: neuronal death,
rhabdomyolysis, metabolic acidosis, aspiration pneumonitis, neurogenic pulmonary edema, and respiratory
failure. Magnesium sulfate is the drug of choice based on randomized trials demonstrating that it reduces
the rate of recurrent seizures by one-half to two-thirds (relative risk [RR] 0.44, 95% CI 0.32-0.51) and the
rate of maternal death by one-third (RR 0.62, 95% CI 0.39-0.99) [1].

A series of systematic reviews reported magnesium sulfate was safer and more effective than phenytoin,
diazepam, or lytic cocktail (ie, chlorpromazine, promethazine and pethidine) for prevention of recurrent

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seizures in eclampsia [37-39]. Additional advantages of magnesium sulfate therapy were its low cost, ease
of administration (eg, cardiac monitoring is not required), and lack of sedation. In utero exposure to
magnesium sulfate therapy decreases the risk of cerebral palsy and severe motor dysfunction in offspring
born prematurely. (See "Neuroprotective effects of in utero exposure to magnesium sulfate".)

The Eclampsia Trial Collaborative Group conducted the seminal trial establishing the effectiveness of
magnesium sulfate therapy in eclampsia [40]. In two international multicenter trials, 905 eclamptic women
were randomly assigned to receive either magnesium or diazepam and another 775 eclamptic women were
randomly assigned to receive either magnesium or phenytoin. The primary outcome measures were the
rates of recurrent seizures and maternal death. Magnesium sulfate was significantly more effective than
either diazepam or phenytoin:

● Women allocated to magnesium sulfate therapy had one-half the rate of recurrent seizures of those
allocated to diazepam (13 and 28 percent, respectively). There were no other significant differences in
maternal or perinatal mortality and/or morbidity between the two groups.

● Women allocated to magnesium sulfate therapy had one-third the rate of recurrent seizures of those
allocated to phenytoin (6 versus 17 percent). In this arm of the study, women who received magnesium
sulfate were less likely to be admitted to an intensive care facility (17 versus 25 percent), less likely to
require ventilatory support (15 versus 23 percent), and less likely to develop pneumonia (4 versus 9
percent) compared with women who were given phenytoin. There were no other significant differences
in maternal mortality or perinatal outcome between the two groups.

Administration of magnesium sulfate

● Loading dose – We administer a loading dose of magnesium sulfate 6 g intravenously over 15 to 20

minutes. This dose quickly and consistently achieves a therapeutic level. Loading doses of 4 to 6 g
intravenously are commonly used [1]. An alternative dose/route is magnesium sulfate 5 g
intramuscularly into each buttock for a total of 10 g; however, the onset of a therapeutic effect will be
slower and intramuscular injection is painful. These loading doses may be given safely to patients with
renal insufficiency.

● Maintenance dose – We administer a maintenance dose of magnesium sulfate 2 g/hour as a

continuous intravenous infusion to women with good renal function. Maintenance doses of 1 to 3 g/hour
are commonly used. Alternatively, magnesium sulfate 5 g can be given intramuscularly every four
hours. The maintenance phase is given only if a patellar reflex is present (loss of deep tendon reflexes
is the first manifestation of symptomatic hypermagnesemia), respirations are greater than 12 per
minute, and urine output is over 100 mL in four hours. Following serum magnesium levels is not
required in women with good renal function if the woman's clinical status is closely monitored and
shows no evidence of potential magnesium toxicity.

In patients with renal insufficiency, maintenance dosing should be lower and dosed in consultation with
a nephrologist or pharmacologist and magnesium levels should be monitored. The author generally
holds the maintenance infusion if the serum creatinine is >1.5 mg/dL (133 micromol/L) or if the urine
output is <20 mL per hour and rechecks the magnesium level in six hours. If the serum creatinine is 1.0
to 1.5 mg/dL (88 to 133 micromol/L) and the urine output is adequate, the maintenance infusion is
reduced by half to 1 g /hour and a magnesium level is rechecked in six hours.

A clear threshold magnesium concentration for insuring the prevention of seizures has not been
established, but a range of 4.8 to 8.4 mg/dL (1.9 to 3.5 mmol/L) is recommended if serum levels are
checked because of recurrent seizures or concerns about toxicity [41]. The dose should be adjusted
according to the clinical response of individual patients.

Calcium gluconate (1 g intravenously) may be administered to counteract magnesium toxicity, if necessary.

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Concurrent use of magnesium sulfate with calcium channel blockers may result in hypotension, but the risk
appears to be minimal. Magnesium sulfate is contraindicated in women with myasthenia gravis since it can
precipitate a severe myasthenic crisis.

Additional information on complications and side effects of magnesium sulfate therapy, dosing, and possible
mechanisms of action can be found separately. (See "Preeclampsia: Management and prognosis", section
on 'Toxicity' and "Preeclampsia: Management and prognosis", section on 'Dosing' and "Preeclampsia:
Management and prognosis", section on 'Drug of choice: Magnesium sulfate'.)

Management of persistent seizures — Recurrent seizures in patients on maintenance magnesium

sulfate therapy can be treated with an additional bolus of 2 g magnesium sulfate over 5 to 10 minutes, with
frequent monitoring for signs of magnesium toxicity (eg, loss of patellar reflex, respirations <12 per minute)
[40,42]. If two such boluses do not control seizures, then other drugs should be given. Diazepam or
lorazepam is a common choice.

● Diazepam – 5 to 10 mg intravenously every 5 to 10 minutes at a rate ≤5 mg/minute and maximum dose

30 mg. Diazepam will control seizures within 5 minutes in over 80 percent of patients [43]. A diazepam
gel 0.2 mg/kg is available for rectal administration.

Some experts recommend avoiding benzodiazepines for management of eclamptic seizures because
of potentially profound depressant effects on the fetus and mother. This effect becomes clinically
significant when the total maternal dose of diazepam exceeds 30 mg. Because of subsequent
redistribution of the drug into adipose tissue, the duration of diazepam's acute anticonvulsant effect is
typically less than 20 minutes.

● Lorazepam – 4 mg intravenously at maximum rate 2 mg/minute. Lorazepam is as effective as

diazepam for terminating seizures, but the time from its injection to its maximum effect against seizures
is as long as two minutes. The clinical advantage of lorazepam is that the effective duration of
protection from additional seizures is as long as four to six hours because of its less-pronounced
redistribution into adipose tissue.

● Midazolam – 1 to 2 mg bolus given intravenously at a rate of 2 mg/min. Additional boluses can be given
every five minutes until seizures stop (up to a maximum of 2 mg/kg). An advantage of midazolam is its
short duration of action, which may minimize maternal postictal confusion and fetal effects.

Treatment of status epilepticus is discussed in detail separately. (See "Convulsive status epilepticus in
adults: Treatment and prognosis".)

Response to therapy — Women who do not improve within 10 to 20 minutes following control of
hypertension and seizures and those with neurologic deficits should be evaluated by a neurologist as they
may have ongoing nonconvulsive seizures or underlying structural pathology, such as hemorrhage. (See
"Evaluation and management of the first seizure in adults".)

There is no role for mannitol in the routine care of women with eclampsia [44]. It can be harmful because it
can enter the brain through a damaged blood-brain barrier and reverse the osmotic gradient, thus
increasing intracranial pressure. A neurologist should be consulted for management of women with
signs/symptoms potentially related to increased intracranial pressure (eg, depressed consciousness,
papilledema, respiratory depression). (See "Evaluation and management of elevated intracranial pressure in
adults".)

Fetal resuscitation — Fetal bradycardia lasting at least three to five minutes is a common finding during
and immediately after an eclamptic seizure and does not necessitate emergent cesarean delivery.
Stabilizing the mother by administering anticonvulsant drugs and oxygen and treating severe hypertension
(if present) can help the fetus recover in utero from the effects of maternal hypoxia, hypercarbia, and uterine
tachysystole. However, if the fetal heart rate tracing does not improve within 10 to 15 minutes despite

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maternal and fetal resuscitative interventions, then the possibility of an occult abruption should be
considered and emergent delivery may be indicated [17].

Evaluation for prompt delivery — Eclampsia is usually considered an absolute contraindication to

expectant management, although this has been attempted [45]. The definitive treatment for eclampsia is
prompt delivery; however, this does not necessarily preclude induction and a trial of labor [29,46]. After
maternal stabilization, factors to consider in determining the mode of delivery are gestational age, cervical
status, whether the patient is in labor, and fetal condition and position.

We believe that induction is a reasonable option for pregnancies at least 32 to 34 weeks of gestation and for
earlier gestations with a favorable Bishop score (table 7). Cervical ripening agents can be used to improve
the Bishop score; however, in our opinion, long inductions should be avoided and a clear endpoint for
delivery planned (eg, within 24 hours) (see "Induction of labor with oxytocin"). In a trial that randomly
assigned 200 rural Indian women at ≥34 weeks with eclampsia to cesarean delivery or induction after initial
stabilization, planned cesarean delivery did not significantly reduce the rate of adverse maternal or fetal
outcomes, and almost three-quarters of women in the planned vaginal delivery group succeeded in
delivering vaginally [47]. This trial provides support for induction of labor, although it had several limitations:
the number of adverse events was small, leading to wide confidence intervals, and the population was not
representative of women and intrapartum care in higher resource settings.

In contrast, we would not induce eclamptic women less than 32 to 34 weeks of gestation with an
unfavorable cervix. In United States studies, less than one-third of women with severe
preeclampsia/eclampsia successfully delivered vaginally after induction of labor [36,48,49]. Cesarean
delivery is a reasonable option for these women. Because the fetus benefits from in utero resuscitation
before delivery, we wait 15 to 20 minutes and until the mother and fetus show signs of recovery (control of
seizures; mother oriented to name, time, and place; fetal heart rate reassuring) before proceeding to
surgery, if possible.

Anesthesia — Anesthesia issues are the same as for women with preeclampsia. (See "Preeclampsia:
Management and prognosis", section on 'Analgesia and anesthesia'.)

POSTPARTUM CARE — The postpartum care of women with eclampsia is described below, and not
altered by neuroimaging findings similar to those seen with reversible posterior leukoencephalopathy
syndrome (RPLS; also called posterior reversible encephalopathy syndrome [PRES]).

Duration of magnesium sulfate therapy — Seizures due to eclampsia always resolve postpartum,
generally within a few hours to days. Diuresis (greater than 4 L/day) is believed to be the most accurate
clinical indicator of resolution of preeclampsia/eclampsia but is not a guarantee against the development of
seizures [50].

The optimal duration of magnesium sulfate therapy has not been determined. When begun before delivery,
we continue magnesium sulfate for 24 to 48 hours postpartum, when the risk of recurrent seizures is low.
When begun for postpartum eclampsia, we maintain therapy for 24 to 48 hours. In either case, therapy is
continued in women whose disease has not started to improve and discontinued in women who are clearly
improving clinically (eg, diuresis of ≥100 mL/hour for two consecutive hours and the absence of symptoms).
Decisions regarding maternal activity, oral intake, and infant care while on magnesium sulfate therapy
should be made on a case-by-case basis.

Treatment of postpartum hypertension — Antihypertensive therapy is administered to prevent stroke.

Medications similar to those used before delivery (table 6) are often used postpartum, since most are
compatible with breastfeeding. Target blood pressure is also the same. (See "Management of hypertension
in pregnant and postpartum women", section on 'Choice of drug and dose' and "Management of
hypertension in pregnant and postpartum women", section on 'Target blood pressure'.)

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If prepregnancy blood pressure was normal and the patient is not hypertensive on medication, it is
reasonable to stop the antihypertensive agent after three weeks and monitor blood pressure to assess
whether further treatment is indicated. (See "Management of hypertension in pregnant and postpartum
women", section on 'Postpartum hypertension'.)

Driving — Many healthcare professionals caring for women with peripartum seizures have not considered
issues relating to fitness to drive after an eclamptic seizure [51]. States vary widely in driver-licensing
requirements for patients with seizures and in the responsibilities of physicians to notify state authorities.
Most, but not all, specify a seizure-free interval that is required for patients to meet prior to licensure and
driving. Some licensing bureaus include mention of mitigating factors such as an acute symptomatic
seizure, but most do not. This topic is discussed in detail elsewhere. (See "Driving restrictions for patients
with seizures and epilepsy", section on 'Acute symptomatic seizure'.)

PREGNANCY OUTCOME

Maternal — Maternal complications occur in up to 70 percent of women with eclampsia. The types and
frequencies of complications of eclampsia from one review are summarized in the table (table 8). Additional
complications include intracerebral hemorrhage, transient blindness, and cardiorespiratory arrest [36].
Hepatocellular damage, renal dysfunction, coagulopathy, hypertension, and neurologic abnormalities
typically resolve in the hours and days following delivery. However, brain damage from hemorrhage or
ischemia may result in permanent neurologic sequelae and is the most common cause of death in eclamptic
women [52,53].

Maternal mortality rates of 0 to 14 percent have been reported over the past few decades [2,4,8,54,55].
Maternal mortality and severe morbidity rates are lowest among women receiving regular prenatal care who
are managed by experienced physicians in tertiary centers (maternal mortality 0 to 1.8 percent) [4,17,36,56-
58]. The highest mortality rates are in low-income countries where prenatal, intrapartum, and neonatal care
are compromised by limited resources [55,59]. These relationships are illustrated by the following large
series:

● A population-based cohort study from Canada including 1481 cases of eclampsia from 2003 to 2009
reported a case mortality rate of 0.34 percent (5/1481) [5]. Severe morbidity included acute renal
failure, need for assisted ventilation, embolism, shock, and adult respiratory distress syndrome.

● A retrospective analysis of 990 cases of eclampsia in Mexico before 1992 reported a case mortality
rate of 13.9 percent (138/990) [55]. The subgroup of women with eclampsia prior to 28 weeks of
gestation had the highest risk of maternal death (12/54 [22 percent]). Multiple seizures occurring
outside of the hospital setting was a common risk factor for maternal death.

Fetal and neonatal — Premature delivery, abruptio placenta, and intrauterine asphyxia are the primary
causes of perinatal death in eclamptic pregnancies. A population-based cohort study from Canada reported
fetal death rates in eclamptic and noneclamptic pregnancies of 10.8 and 4.1 per 1000 total births,
respectively; neonatal death rates were 7.5 and 2.2 per 1000 live births, respectively [5]. However, perinatal
mortality is closely related to gestational age, and eclamptic pregnancies had a five- to sevenfold increased
risk of preterm birth in this study.

Perinatal morbidity is also increased in eclamptic pregnancies and closely related to gestational age. In
addition, there is a two- to threefold increased risk of delivery of a small for gestational age infant [5].

LONG-TERM PROGNOSIS

Recurrence risk — Recurrent eclampsia occurs in 2 percent of subsequent pregnancies [60,61]. The risk
appears to be reduced by close maternal monitoring and timely intervention if preeclampsia develops [62].
Preeclampsia, however, cannot be prevented in most cases. (See "Preeclampsia: Prevention".)

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The risk of recurrence was illustrated by a study that followed 159 nulliparous women with a history of
eclampsia and no preexisting hypertension through 334 subsequent pregnancies [63]. The incidence of
preeclampsia without severe features, preeclampsia with severe features, and eclampsia in these
pregnancies was 13, 9, and 2 percent, respectively. The risk for preeclampsia but not eclampsia was higher
for the subset of women whose eclampsia occurred at ≤30 weeks of gestation in the index pregnancy:
preeclampsia without severe features, preeclampsia with severe features, and eclampsia 17, 25, and 2
percent, respectively.

Outcome of future pregnancies — In addition to preeclampsia/eclampsia, women with a history of severe

preeclampsia/eclampsia are at increased risk of obstetric complications in subsequent pregnancies
compared with women with no such history. These problems include [60,61,63,64]:

● Abruptio placenta (2.5 to 6.5 versus 0.4 to 1.3 percent of the general obstetrical population)
● Preterm delivery (15 to 21 versus 12 percent)
● Intrauterine growth restriction (12 to 23 versus 10 percent)
● Perinatal mortality (4.6 to 16.5 versus 1 percent)

Women with a history of preeclampsia/eclampsia remote from term (less than 28 weeks of gestation) are at
highest risk of developing these complications as well as recurrent preeclampsia/eclampsia [63,64]. This
risk appears to be the same whether they had severe preeclampsia or eclampsia.

Long-term maternal health — Chronic hypertension develops in 0 to 78 percent (mean 24 percent) of

women with a history of preeclampsia/eclampsia [60,61,63-65]. The wide range reported in the literature is
due to factors such as differences in maternal age and duration of follow-up (the increased risk of
subsequent hypertension only becomes apparent after an average follow-up of 10 years [61]). The risk
appears to be highest in the subgroup of women who have subsequent pregnancies complicated by
hypertension, multiparas with eclampsia, and women with eclampsia remote from term [60,61,63].

In a study of 39 women with a history of eclampsia, magnetic resonance imaging performed an average of
6.4 years following the index pregnancy revealed that these women had a higher prevalence of white matter
lesions than matched controls with normotensive uncomplicated pregnancies (odds ratio [OR] 3.3, 95% CI
1.05-10.6) [66]. About 15 percent of women in each group were currently hypertensive or on
antihypertensive therapy. The source and significance of these lesions are unclear; affected women do not
appear to have increased functional impairment as may be seen in other patients with white matter lesions.
A study of eclamptic women reported no objective cognitive impairment as compared with controls when
evaluated 2 to 20 years after delivery [67]. (See "Etiology, clinical manifestations, and diagnosis of vascular
dementia", section on 'White matter lesions'.)

Both preeclamptic and eclamptic women are at increased risk of developing cardiovascular and
cerebrovascular disease and diabetes later in life. These data are discussed elsewhere. (See
"Preeclampsia: Management and prognosis", section on 'Prognosis'.)

CAN ECLAMPSIA BE PREDICTED AND PREVENTED? — In women who have been diagnosed with
preeclampsia, prophylactic administration of magnesium sulfate can usually prevent seizures (see
"Preeclampsia: Management and prognosis", section on 'Seizure prophylaxis'). However, seizures may not
be preventable with preeclampsia of abrupt onset, onset early in pregnancy, or onset after postpartum
hospital discharge. In one review of 179 consecutive cases of eclampsia, factors identified to be at least
partially responsible for failure to prevent seizures were: physician error (36 percent), lack of prenatal care
(19 percent), abrupt onset (18 percent), magnesium failure (13 percent), late postpartum onset (12 percent),
and early onset before 21 weeks (3 percent) [68].

The majority of eclamptic women have one or more antecedent symptoms in the hours prior to an eclamptic
seizure, thus pregnant women should be educated to call their healthcare provider if these symptoms

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develop (see 'Clinical presentation and findings' above). However, up to 40 percent of eclamptic seizures
are not preceded by premonitory signs and symptoms [2,68-71].

The relationship between hypertension, signs and symptoms of cortical irritability (eg, headache that is
usually severe or persistent, visual disturbances, nausea, vomiting, fever, hyperreflexia) and seizures
remains unclear. The magnitude of blood pressure elevation does not appear to be predictive of eclampsia,
although it correlates well with the incidence of stroke (figure 1). Twenty to 38 percent of eclamptic patients
have a maximal blood pressure less than 140/90 prior to their seizure and about 20 percent have no
evidence of proteinuria [2,54,56]. While antihypertensive treatment is recommended in women with blood
pressures ≥160/105 to 110 mmHg, the use of antihypertensive drugs to control mildly elevated blood
pressure in the setting of preeclampsia/eclampsia does not alter the course of the disease or diminish
perinatal morbidity or mortality. Pharmacologic treatment of mild hypertension is not recommended, as
neither maternal nor fetal benefits have been demonstrated. (See "Management of hypertension in pregnant
and postpartum women".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected
countries and regions around the world are provided separately. (See "Society guideline links: Hypertensive
disorders of pregnancy".)

SUMMARY AND RECOMMENDATIONS

● Eclampsia is a clinical diagnosis based upon the occurrence of new-onset generalized tonic-clonic
seizures in a woman with preeclampsia. (See 'Diagnosis' above.)

● An eclamptic seizure occurs in 2 to 3 percent of women with severe features of preeclampsia who are
not receiving anti-seizure prophylaxis and between 0 and 0.6 percent in women with preeclampsia
without severe features. (See 'Incidence and epidemiology' above.)

● Most women have premonitory signs/symptoms in the hours before their initial seizure, such as
hypertension and proteinuria, headache, visual disturbances, and/or right upper quadrant or epigastric
pain. (See 'Clinical presentation and findings' above.)

● Eclampsia occurs before term in approximately 50 percent of women. Thirty-eight to 55 percent of

eclampsia occurs antepartum, 13 to 36 percent occurs intrapartum, 5 to 39 percent occurs ≤48 hours
postpartum, and 5 to 17 percent occurs >48 hours postpartum. Approximately 90 percent of postpartum
seizures occur within one week of delivery. (See 'Clinical presentation and findings' above.)

● Fetal bradycardia lasting at least three to five minutes is a common finding during and immediately after
an eclamptic seizure. Emergent cesarean delivery is not needed unless the fetal heart rate tracing does
not improve within 10 to 15 minutes of maternal and fetal resuscitative interventions. (See 'Fetal
resuscitation' above.)

● Key management issues are: prevention of maternal hypoxia and trauma, treatment of severe
hypertension (if present), prevention of recurrent seizures with magnesium sulfate, and evaluation for
prompt delivery. (See 'Key principles' above.)

● For women with eclampsia, we recommend treatment with magnesium sulfate rather than other
anticonvulsants (Grade 1A). Compared with phenytoin and diazepam, magnesium sulfate reduces the
rate of recurrent seizures by one-half to two-thirds and reduces the rate of maternal death by one-third.
(See 'Prevention of recurrent seizures' above.)

● We suggest using an intravascular magnesium sulfate regimen rather than an intramuscular regimen
(Grade 2C). We use a 6 gram loading dose over 15 to 20 minutes, followed by 2 grams/hour as a
continuous intravenous infusion. Loading doses of 4 or 5 grams are also reasonable and a lower or
higher maintenance dose (1 or 3 g/hour) is sometimes required.

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The maintenance phase is given only if a patellar reflex is present (loss of deep tendon reflexes is the
first manifestation of symptomatic hypermagnesemia), respirations are greater than 12 per minute, and
urine output is over 100 mL in four hours.

The loading dose may be given safely in renal insufficiency, but the maintenance dose in these patients
should be omitted or reduced in consultation with a nephrologist or pharmacologist. Magnesium levels
should be monitored in patients with renal insufficiency. (See 'Administration of magnesium sulfate'
above.)

● A common threshold for initiating antihypertensive therapy is sustained diastolic pressures greater than
105 to 110 mmHg or systolic blood pressures ≥160 mmHg. (See 'Treatment of hypertension' above.)

● Delivery is the only curative treatment, but this does not preclude induction of labor. Cesarean delivery
is a reasonable option for women less than 32 to 34 weeks of gestation with an unfavorable cervix.
After a seizure, in the absence of fetal bradycardia, we suggest waiting 15 to 20 minutes and until the
mother and fetus show signs of recovery (control of seizures; mother oriented to name, time, and place;
fetal heart rate reassuring) before proceeding to surgery, if possible. (See 'Evaluation for prompt
delivery' above.)

● Seizures due to eclampsia always resolve postpartum, generally within a few hours to days. Diuresis
(greater than 4 L/day) is believed to be the most accurate clinical indicator of resolution of
preeclampsia/eclampsia but is not a guarantee against the development of seizures. When begun
before delivery, we continue magnesium sulfate for 24 to 48 hours postpartum. When begun for
postpartum eclampsia, we maintain therapy for 24 to 48 hours. (See 'Duration of magnesium sulfate
therapy' above.)

● The risk of recurrent eclampsia in a future pregnancy is 2 percent. (See 'Recurrence risk' above.)

● In addition to preeclampsia/eclampsia, women with a history of severe preeclampsia/eclampsia are at

increased risk of obstetric complications in subsequent pregnancies. They are also at increased risk of
cardiovascular disease, cerebrovascular disease, and diabetes later in life. (See 'Long-term maternal
health' above.)

● Eclampsia may not be preventable when of abrupt onset, onset early in pregnancy, or onset after
postpartum hospital discharge. (See 'Can eclampsia be predicted and prevented?' above.)

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