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Eclampsia
Author: Errol R Norwitz, MD, PhD, MBA
Section Editors: Charles J Lockwood, MD, MHCM, Steven C Schachter, MD
Deputy Editor: Vanessa A Barss, MD, FACOG

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Apr 2021. | This topic last updated: May 22, 2020.

INTRODUCTION

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

or coma in a woman with preeclampsia (including HELLP syndrome [hemolysis,
elevated liver enzymes, low platelets]) or gestational hypertension (in those cases
where, in retrospective, it was a temporary [provisional] diagnosis for a hypertensive
pregnant woman who went on to meet criteria for preeclampsia/eclampsia). (See
"Gestational hypertension".)

Eclampsia 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, especially in resource-limited
regions.

The clinical manifestations, diagnosis, and management of eclampsia will be

reviewed here. Issues related to preeclampsia and HELLP are discussed separately:

● (See "Preeclampsia: Pathogenesis".)

● (See "Preeclampsia: Clinical features and diagnosis".)
● (See "Preeclampsia: Management and prognosis".)
● (See "Preeclampsia: Prevention".)
:
 ● (See "Expectant management of preterm preeclampsia with severe features".)
● (See "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)".)

INCIDENCE AND EPIDEMIOLOGY

In high resource countries, the incidence of eclampsia is low and has been
decreasing or stable at 1.5 to 10 cases per 10,000 deliveries [1-7]. In low and middle
resource countries, however, the incidence varies widely: from 19.6 per 10,000
deliveries in parts of Zambia to 142 per 10,000 deliveries in Sierra Leone [8].

In one review of women who did not receive magnesium sulfate antiseizure
prophylaxis, eclampsia occurred in 2 to 3 percent of those with preeclampsia with
severe features (previously called "severe" preeclampsia) and in 0 to 0.6 percent of
those with preeclampsia without severe features (previously called "mild"
preeclampsia), but data were very limited [9].

Risk factors for eclampsia are similar to those for preeclampsia ( table 2). The
peak incidence is in adolescence and the early twenties, but incidence is also
increased in women over age 35 [8].

PATHOGENESIS OF SEIZURES

The precise cause of eclamptic seizures 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, hypoperfusion, localized ischemia, endothelial dysfunction, and vasogenic
and/or cytotoxic edema [10]. Cerebral inflammation may also play a role [11].

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

Pathogenesis".)
:
 CLINICAL FINDINGS

Clinical presentation — Eclampsia occurs in women with preeclampsia but

sometimes presents before recognition of the underlying disorder. 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 signs/symptoms were [12]:

● Hypertension (75 percent)

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

(66 percent)

● 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)

On physical examination, neurologic findings may include brisk deep tendon

reflexes (clonus), visual perception deficits, visual processing deficits, altered mental
status/memory deficits, and cranial nerve deficits [13,14].

Characteristics of eclamptic seizures — Eclampsia is generally manifested by a

generalized tonic-clonic seizure. 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. The tongue may be bitten; 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.

Other presentations of preeclampsia may include focal or multifocal seizures or

coma, although these manifestations are less common.

Fetal response to eclampsia — 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 fetal heart
rate variability, sometimes with transient decelerations [15]. 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 [16].

Gestational age at onset — Eclampsia occurs preterm in approximately 50 percent

of pregnancies and between 20 and 30 weeks of gestation in approximately 20
percent [1,17].

In the systematic review described above, 59 percent of eclampsia occurred

antepartum, 20 percent occurred intrapartum, and 21 percent occurred postpartum
[12].

Postpartum onset — Approximately 90 percent of postpartum seizures occur

within one week of delivery [18-22]. Antecedent symptoms are 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
approximately 70 percent [22]. Other prodromal symptoms included shortness of
breath, blurry vision, nausea or vomiting, edema, neurological deficit, and epigastric
pain. Of note, many women did not have hypertension during the antecedent
pregnancy.

Neuroimaging — In over 90 percent of eclamptic patients in small series,

neuroimaging findings are similar to those seen with reversible posterior
leukoencephalopathy syndrome (RPLS; also called posterior reversible
encephalopathy syndrome [PRES]) [23,24]. (See "Reversible posterior
:
 leukoencephalopathy syndrome", section on 'Neuroimaging'.)

Neurohistopathology — A classic report from 1973 described neurohistopathology

in eclamptic women autopsied shortly after death [25]. In this series, >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.

A more contemporary series (2003 to 2006) of over 300 maternal deaths in

Mozambique reported the following types and frequencies of brain lesions:
perivascular edema (68 percent), hemorrhage (37 percent), hemosiderin (32
percent), parenchymal necrosis (16 percent), and small vessel thrombosis (11
percent) [26]. Endothelial, histiocytic, and platelet markers suggested capillary injury
in the otherwise intact brain parenchyma, while stains for free radical formation
were positive mostly in areas of tissue injury, with focal positivity in intact
glial/neuronal elements.

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 [27]. 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".)

DIAGNOSIS

In most patients, eclampsia is a clinical diagnosis based upon the occurrence of

new-onset tonic-clonic seizures in the absence of other causative conditions (eg,
epilepsy, cerebral arterial ischemia and infarction, intracranial hemorrhage, drug
use), typically in a woman with a hypertensive disorder of pregnancy (preeclampsia,
HELLP syndrome, gestational hypertension) [28]. Less commonly, focal or multifocal
seizures or coma occurs rather than a tonic-clonic seizure.

Even if criteria for a hypertensive disorder of pregnancy are not met, the diagnosis
:
 can be made in a pregnant woman with seizures who has the typical clinical and
neuroimaging findings of reversible posterior leukoencephalopathy syndrome
(headache, confusion, visual symptoms, vasogenic edema predominantly localized
to the posterior cerebral hemispheres) [29,30]. (See "Reversible posterior
leukoencephalopathy syndrome".)

POSTICTAL EVALUATION

Women with preeclampsia who develop a generalized tonic-clonic seizure without

persistent neurologic deficit require no diagnostic evaluation beyond that for
preeclampsia [31]. (See "Preeclampsia: Clinical features and diagnosis".)

Atypical cases, such as women who do not meet criteria for diagnosis of
preeclampsia ( table 4), HELLP syndrome, or gestational hypertension 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 by a neurologist. A neuroimaging study should be
performed in these patients to evaluate for a culprit structural brain abnormality.

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 factors 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. Molar pregnancy may be suspected based on
the sonographic appearance of the placenta and may occur with a coexistent
normal co-twin. (See "Hydatidiform mole: Epidemiology, clinical features, and
diagnosis" 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 sudden development of neurologic
symptoms include stroke, intracranial hemorrhage, brain mass lesion, toxic and
metabolic encephalopathies, reversible cerebral vasoconstriction syndrome,
thrombotic thrombocytopenic purpura (TTP), and central nervous system
infection [32]. 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 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".)

● Pregnancy is a precipitating factor for some disorders associated with seizure

activity, such as TTP or hemolytic uremic syndrome (HUS). TTP and HUS may be
indistinguishable from eclampsia that occurs in a woman with HELLP syndrome
( table 5) and approximately 10 to 20 percent of women with
preeclampsia/eclampsia have laboratory findings of HELLP syndrome.
Eclampsia and HELLP usually start to quickly improve after delivery, but delivery
does not affect the course of TTP and HUS. (See "HELLP syndrome (hemolysis,
elevated liver enzymes, and low platelets)", section on 'Differential diagnosis'
and "Approach to the patient with suspected TTP, HUS, or other thrombotic
microangiopathy (TMA)".)
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 MANAGEMENT

Key principles — If the seizure is witnessed, maintaining airway patency and

preventing aspiration are the initial priorities. 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 [16]. 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 in
women with 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 [33]. 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 "Treatment of hypertension in pregnant and postpartum women".)
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 Prevention of recurrent seizures — Magnesium sulfate is the anticonvulsive drug
of choice. 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 (IV) access and drugs are not readily
available.

Approximately 10 percent of women with eclampsia will have repeated seizures if

managed expectantly [34]. 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.

Evidence of magnesium sulfate's efficacy — 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) [9].

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 seizures in eclampsia [35-
37]. Additional advantages of magnesium sulfate therapy were its low cost, ease of
administration (eg, cardiac monitoring is unnecessary), and lack of sedation. An
additional benefit is that 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 [38]. In two international
multicenter trials, 905 women with eclampsia were randomly assigned to receive
either magnesium sulfate or diazepam and another 775 women with eclampsia
were randomly assigned to receive either magnesium sulfate or phenytoin. The
primary outcome measures were 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).

● 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, the magnesium sulfate group was 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 the phenytoin group.

There were no other significant differences in maternal or perinatal mortality and/or

morbidity between the two groups.

Administration of magnesium sulfate

● Loading dose – We administer a loading dose of magnesium sulfate 6 g IV over

15 to 20 minutes. This dose quickly and consistently achieves a therapeutic
level. Loading doses of 4 to 6 g IV are commonly used [9].

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 IV 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; a lower dose maintenance regimen (2.5 g intramuscularly every four
hours) may also be effective and more cost effective in low resource areas [39-
41].

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 >100 mL over
:
 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.

● Therapeutic magnesium level – 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 [42]. The dose
should be adjusted according to the clinical response of individual patients.

● Calcium gluconate (1 g IV) may be administered to counteract magnesium

toxicity, if necessary.

● Complications and side effects – 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 'Dosing' and
"Preeclampsia: Management and prognosis", section on 'Drug of choice:
Magnesium sulfate' and "Preeclampsia: Management and prognosis", section
on 'Signs of magnesium toxicity'.)

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 [43]. 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".)

Management of recurrent seizures — Recurrent seizures in patients on

maintenance magnesium sulfate therapy can be treated with an additional bolus of
2 to 4 g magnesium sulfate administered IV over five minutes, with frequent
monitoring for signs of magnesium toxicity (eg, loss of patellar reflex, respirations
<12 per minute) [11,38,44].

In cases refractory to magnesium sulfate (patient is still seizing at 20 minutes after

the bolus or more than two recurrences), a health care provider can administer
sodium amobarbital (250 mg IV over three minutes), thiopental, or phenytoin (1250
mg IV at a rate of 50 mg/minute) [28]. Endotracheal intubation and assisted
ventilation in the intensive care unit are appropriate in these circumstances.

Status epilepticus, as well as recurrent seizures while on magnesium seizure

prophylaxis, should raise concerns about an intracranial lesion/stroke. Although
neurology consultation and head imaging are indicated in this setting, the acute
management of the seizures is similar regardless of the cause of status epilepticus.
(See "Convulsive status epilepticus in adults: Treatment and prognosis".)

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 emergency cesarean delivery. Stabilizing the mother by administering
antiseizure 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 maternal and fetal resuscitative interventions, then the possibility of an
occult abruption should be considered, and emergency delivery may be indicated
[16]. (See "Placental abruption: Pathophysiology, clinical features, diagnosis, and
consequences" and "Placental abruption: Management and long-term prognosis".)

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 [28,46]. 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). In a trial that randomly assigned 200 women
in rural India 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.

By contrast, we would not induce women with eclampsia who are less than 32 to 34
weeks of gestation and have an unfavorable cervix. In United States studies, less
than one-third of women with severe preeclampsia/eclampsia remote from term
successfully delivered vaginally after induction of labor [34,48,49]. 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
because of neuroimaging findings consistent 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, at which time 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 in whom signs and symptoms of preeclampsia have
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 "Treatment of
hypertension in pregnant and postpartum women", section on 'Choice of drug and
dosing' and "Treatment of hypertension in pregnant and postpartum women",
section on 'Target blood pressure'.)

Patients with persistent hypertension may require transition to oral

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

Driving — Many health care 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 mandatory seizure-free interval 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'.)

Neurology follow-up — Atypical cases, such as women who do not meet criteria for
diagnosis of preeclampsia ( table 4), gestational hypertension, or HELLP
syndrome 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 have follow-up with a neurologist.

PREGNANCY OUTCOME

Maternal — Maternal complications occur in up to 70 percent of women with

eclampsia. The types and frequencies of complications from one review are
summarized in the table ( table 8). Additional complications include intracerebral
hemorrhage, transient blindness, and cardiorespiratory arrest [34]. 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 [1,6,8,54-56]. 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) [16,34,54,57-59].
The highest mortality rates are in low-resource countries where prenatal,
intrapartum, and neonatal care are compromised by the limited resources [8,56,60].
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) [3]. Severe morbidity included need for assisted ventilation (53
percent), blood transfusion (24 percent), cardiac failure (10 percent), acute renal
failure (9 percent), embolism (5 percent), sepsis (5 percent), adult respiratory
distress syndrome (5 percent), and shock (4 percent).

● A prospective study including nearly 2700 women with eclampsia in low and
middle resource countries reported maternal mortality in 6.9 percent [8]. The
case fatality rate ranged from 2.1 percent (5/242) in a part of Zambia to 14.4
percent (18/125) in Haiti.

Fetal and neonatal — Preterm delivery, abruptio placentae, 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 [3]. A study
from low and middle resource countries reported that the overall rate of stillbirth or
neonatal mortality in women with eclampsia varied from 41 per 1000 in Malawi to
231 per 1000 in a part of Uganda [8].

Eclamptic pregnancies had a five- to sevenfold increased risk of preterm birth, which
likely accounted for the higher neonatal mortality and high neonatal morbidity (73
percent had respiratory distress syndrome). Twenty-one percent of infants were
small for gestational age.

LONG-TERM PROGNOSIS

Recurrence risk — Recurrent eclampsia occurs in 2 percent of subsequent

pregnancies [61,62]. The risk appears to be reduced by close maternal monitoring
:
 and timely intervention if preeclampsia develops [63]. Preeclampsia, however,
cannot be prevented in most cases. (See "Preeclampsia: Prevention".)

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 [64]. 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. In these women, preeclampsia without severe
features, preeclampsia with severe features, and eclampsia occurred in 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 [61,62,64,65]:

● Abruptio placentae (2.5 to 6.5 versus 0.4 to 1.3 percent of the general obstetric
population)
● Preterm delivery (15 to 21 versus 12 percent)
● Fetal 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 [64,65]. This risk appears to be the same whether
they had preeclampsia with severe features or eclampsia.

Long-term maternal health

● Future cardiovascular disease – 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'.)

Chronic hypertension develops in 0 to 78 percent (mean 24 percent) of women

:
 with a history of preeclampsia/eclampsia [61,62,64-66]. 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 [62]). The risk appears
to be highest in the subgroup of women who have subsequent pregnancies
complicated by hypertension, multiparous women with eclampsia, and women
with eclampsia remote from term [61,62,64].

● Future seizure disorder – Women with eclampsia may be at higher risk of a

future seizure, but the absolute risk is small. In a retrospective study that
included 1615 women with eclampsia, the adjusted hazard ratio for future
seizures was 5.4 (95% CI 2.4-12.1), and the absolute risk was 1 seizure per 2200
person-years [67]. The authors did not distinguish women who had one
subsequent seizure from those who had recurrent seizures.

● Other – 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 3.3, 95% CI 1.05-10.60) [68]. Approximately 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. Another study of eclamptic women reported
no objective cognitive impairment as compared with controls when evaluated 2
to 20 years after delivery [69].

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'). 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) [70].

The majority of eclamptic women have one or more antecedent symptoms in the
hours prior to an eclamptic seizure, thus pregnant women should be counseled to
call their health care provider if these symptoms develop (see 'Clinical findings'
above). However, up to 40 percent of eclamptic seizures are not preceded by
premonitory signs and symptoms [1,70-73]. In a systematic review, the most
commonly reported symptoms (visual disturbances, epigastric pain, and headache)
neither accurately predicted, nor ruled out, imminent eclampsia [74].

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 approximately 20 percent have no evidence of proteinuria [1,55,57].
While antihypertensive treatment is recommended for 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 "Treatment 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

● In most patients, eclampsia is a clinical diagnosis based upon the occurrence of

new-onset tonic-clonic seizures in the absence of other causative conditions (eg,
:
 epilepsy, cerebral arterial ischemia and infarction, intracranial hemorrhage,
drug use) in a woman with a hypertensive disorder of pregnancy (preeclampsia,
gestational hypertension, HELLP syndrome [hemolysis, elevated liver enzymes,
low platelets]). Some patients present with focal or multifocal seizures or coma.
(See 'Diagnosis' above.)

● An eclamptic seizure occurs in 2 to 3 percent of women with severe features of

preeclampsia who are not receiving antiseizure 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 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 findings' above.)

● Fetal bradycardia lasting at least three to five minutes is a common finding

during and immediately after an eclamptic seizure. Emergency 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.

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 'Delivery' above.)

● Seizures due to eclampsia always resolve in the postpartum period, 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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134:677.
Topic 1662 Version 52.0
:
 GRAPHICS

In a patient with preeclampsia, the presence of one or more of the following

indicates a diagnosis of "preeclampsia with severe features"

Severe blood pressure elevation:

Systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg on 2 occasions at least 4 hours
apart while the patient is on bedrest (antihypertensive therapy may be initiated upon confirmation of
severe hypertension, in which case criteria for severe blood pressure elevation can be satisfied without
waiting until 4 hours have elapsed)

Symptoms of central nervous system dysfunction:

New-onset cerebral or visual disturbance, such as:
Photopsia, scotomata, cortical blindness, retinal vasospasm
Severe headache (ie, incapacitating, "the worst headache I've ever had") or headache that persists and
progresses despite analgesic therapy and not accounted for by alternative diagnoses

Hepatic abnormality:
Impaired liver function not accounted for by another diagnosis and characterized by serum transaminase
concentration >2 times the upper limit of the normal range or severe persistent right upper quadrant or
epigastric pain unresponsive to medication and not accounted for by an alternative diagnosis

Thrombocytopenia:
<100,000 platelets/microL

Renal abnormality:
Renal insufficiency (serum creatinine >1.1 mg/dL [97.2 micromol/L] or a doubling of the serum creatinine
concentration in the absence of other renal disease)

Pulmonary edema

Reference:
1. American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin No. 222: Gestational Hypertension and
Preeclampsia. Obstet Gynecol 2020; 135:e237.

Graphic 76975 Version 25.0

:
 Clinical factors that have been associated with an increased risk of developing
preeclampsia

Nulliparity

Preeclampsia in a previous pregnancy

Age >40 years or <18 years

Family history of preeclampsia

Chronic hypertension

Chronic renal disease

Autoimmune disease (eg, antiphospholipid syndrome, systemic lupus erythematosus)

Vascular disease

Diabetes mellitus (pregestational and gestational)

Multifetal gestation

Obesity

Black population

Hydrops fetalis

Poorly controlled hyperthyroidism

Woman herself was small for gestational age

Fetal growth restriction, abruptio placentae, or fetal demise in a previous pregnancy

Prolonged interpregnancy interval if the previous pregnancy was normotensive; if the previous pregnancy was
preeclamptic, a short interpregnancy interval increases the risk of recurrence

Partner-related factors (new partner, limited sperm exposure [eg, previous use of barrier contraception])

In vitro fertilization

Obstructive sleep apnea

Elevated blood lead level

Posttraumatic stress disorder

By comparison, smoking decreases the risk of preeclampsia, and Asian females and Hispanic females have
a lower risk of preeclampsia than White females and a much lower risk than Black females.

Graphic 61266 Version 13.0

:
 Phases of tonic-clonic seizures

Aura (None)

Tonic phase (10 to 20 seconds)

Sudden loss of consciousness

Loss of posture with high risk of self injury depending on activity

Brief flexion of arms, eyes deviated upward

Extension of back, neck, arms, and legs

Involuntary crying out from contraction of respiratory muscles

Shallow respiration, cyanosis may occur

Ends with tremors that gradually slow and merge with clonic phase

Clonic phase (30 to 90 seconds)

Brief, violent, generalized flexor contractions alternating with progressively longer muscle relaxation

Cyanosis

Possible cheek or tongue biting

Foamy salivation

Possible loss of bowel or bladder control

Ends with deep inspiration, sustained muscle relaxation

Postictal phase (Minutes to several hours)

Headache, mild confusion

Muscles sore

Fatigue, patient may sleep and awake refreshed

Other features
Fast heart rate

Elevated blood pressure

Respiratory and metabolic acidosis

Dilated pupils

Risk of vertebral fracture, pneumonia

Graphic 54942 Version 2.0

:
 Criteria for the diagnosis of preeclampsia

Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on at least 2 occasions at
least 4 hours apart after 20 weeks of gestation in a previously normotensive patient AND the new onset
of 1 or more of the following*:

Proteinuria ≥0.3 g in a 24-hour urine specimen or protein/creatinine ratio ≥0.3 (mg/mg) (30 mg/mmol) in
a random urine specimen or dipstick ≥2+ if a quantitative measurement is unavailable

Platelet count <100,000/microL

Serum creatinine >1.1 mg/dL (97.2 micromol/L) or doubling of the creatinine concentration in the
absence of other renal disease

Liver transaminases at least twice the upper limit of the normal concentrations for the local laboratory

Pulmonary edema

New-onset and persistent headache not accounted for by alternative diagnoses and not responding to
usual doses of analgesics ¶

Visual symptoms (eg, blurred vision, flashing lights or sparks, scotomata)

Preeclampsia is considered superimposed when it occurs in a woman with chronic hypertension. It is

characterized by worsening or resistant hypertension (especially acutely), the new onset of proteinuria or a
sudden increase in proteinuria, and/or significant new end-organ dysfunction after 20 weeks of gestation
in a woman with chronic hypertension.

* If systolic blood pressure is ≥160 mmHg or diastolic blood pressure is ≥110 mmHg, confirmation within minutes is
sufficient.
​ ¶ Response to analgesia does not exclude the possibility of preeclampsia.

Adapted from: American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin No. 222: Gestational
Hypertension and Preeclampsia. Obstet Gynecol 2020; 135:e237.

Graphic 79977 Version 36.0

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 Comparison of frequency of signs, symptoms, and laboratory findings in TTP, HUS,
HELLP, and AFLP

TTP HUS HELLP AFLP

Abdominal pain ++ ++ ++ ++

Low ADAMST13 activity +/++ – –/+ ?

Anemia ++ ++ + +

Elevated lactic dehydrogenase ++ very high ++ very high ++ +/++

values values

Elevated transaminases –/+ –/+ ++ ++

Fever + – – +

Headache or visual disturbance ++ – ++ –/+

Hypertension +/++ ++ ++ –

Jaundice – – + +

Nausea and vomiting ++ ++ ++ ++

Proteinuria + and ++ ++ –
hematuria

Thrombocytopenia ++ ++ ++ +

von Willebrand factor ++ ++ – ?

Hypoglycemia – – –/+ ++

TTP: thrombotic thrombocytopenic purpura; HUS: hemolytic uremic syndrome; HELLP: hemolysis, elevated liver
function tests, low platelets; AFLP: acute fatty liver of pregnancy; +: prevalence of finding in affected patients.

Adapted from:​
1. Stella CL, Dacus J, Guzman E, et al. The diagnostic dilemma of thrombotic thrombocytopenic purpura/hemolytic
uremic syndrome in the obstetric triage and emergency department: lessons from 4 tertiary hospitals. Am J Obstet
Gynecol 2009; 200:381. Original Table 4.
2. Pourrat O, Coudroy R, Pierre F. Differentiation between severe HELLP syndrome and thrombotic microangiopathy,
thrombotic thrombocytopenic purpura and other imitators. Eur J Obstet Gynecol Reprod Biol 2015;189:68. Table 1.

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 Antihypertensive agents used for urgent blood pressure control in pregnancy
Drug Initial dose
Labetalol 20 mg IV gradually over 2 minutes.
A continuous IV infusion of 1 to 2
mg/minute can be used instead of
intermittent therapy or started after 20
mg IV dose.
Requires use of programmable infusion
pump and continuous noninvasive
monitoring of blood pressure and heart
rate.
Hydralazine 5 mg IV gradually over 1 to 2 minutes.*
Adequate reduction of blood pressure is
less predictable than with IV labetalol.
Nifedipine 30 mg orally.
extended release
Nicardipine The initial dose is 5 mg/hour IV by infusion
(parenteral) pump and can be increased to a
maximum of 15 mg/hour.
Onset of action is delayed by 5 to 15
minutes; in general, rapid titration is
:
Follow-up
Repeat BP measurement at 10-minute
intervals:
If BP remains above target level at
10 minutes, give 40 mg IV over 2
minutes.
If BP remains above target level at
20 minutes, give 80 mg IV over 2
minutes.
If BP remains above target level at
30 minutes, give 80 mg IV over 2
minutes.
If BP remains above target level at
40 minutes, give 80 mg IV over 2
minutes.
Cumulative maximum dose is 300 mg. If
target BP is not achieved, switch to
another class of agent.
Adjust dose within this range to achieve
target blood pressure.
Cumulative maximum dose is 300 mg. If
target BP is not achieved, switch to
another class of agent.
Repeat BP measurement at 20-minute
intervals:
If BP remains above target level at
20 minutes, give 5 or 10 mg IV over
2 minutes, depending on the initial
response.
If BP remains above target level at
40 minutes, give 10 mg IV over 2
minutes, depending on the previous
response.
Cumulative maximum dose is 30 mg. If
target BP is not achieved, switch to
another class of agent.
If target BP is not achieved in 1 to 2 hours,
another dose can be administered.
If target BP is not achieved, switch to
another class of agent.
Adjust dose within this range to achieve
target BP.
 avoided to minimize risk of overshooting
dose.
Requires use of a programmable infusion
pump and continuous noninvasive
monitoring of blood pressure and heart
rate.

Nifedipine 10 mg orally. Repeat BP measurement at 20-minute

immediate release* May be associated with precipitous drops
in BP in some women, with associated
FHR decelerations for which emergency
cesarean delivery may be indicated. As
such, this regimen is not typically used as
a first-line option and is usually reserved
only for women without IV access. If used,
FHR should be monitored while
administering short-acting nifedipine.
intervals:
If BP remains above target at 20
minutes, give 10 or 20 mg orally,
depending on the initial response.
If BP remains above target at 40
minutes, give 10 or 20 mg orally,
depending on the previous
response.
If target BP is not achieved, switch to
another class of agent.

Labetalol and hydralazine are the preferred drugs.

IV: intravenous; BP: blood pressure; FHR: fetal heart rate.

* We caution against use of immediate-release oral nifedipine, although some obstetric guidelines have endorsed its
use as a first-line option for emergency treatment of acute, severe hypertension in pregnancy or postpartum (other
options were labetalol and hydralazine), particularly when IV access is not in place. In most cases, use of immediate-
release oral nifedipine will be safe and well tolerated; however, there is a risk of an acute, precipitous fall in blood
pressure, which may result in a reduction in uteroplacental perfusion. The immediate-release preparations are also
associated with a higher incidence of headache and tachycardia. In nonpregnant adults, the package insert states
that "nifedipine capsules should not be used for the acute reduction of blood pressure."

Adapted from:​
1. American College of Obstetricians and Gynecologists Committee on Obstetric Practice. Committee Opinion No. 767:
Emergent therapy for acute-onset, severe hypertension during pregnancy and the postpartum period. Obstet
Gynecol 2019.
2. Bernstein PS, Martin JN Jr, Barton JR, et al. National Partnership for Maternal Safety: Consensus Bundle on Severe
Hypertension During Pregnancy and the Postpartum Period. Obstet Gynecol 2017; 130:347.

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 Bishop scoring system [1]

0 1 2 3

Dilation, cm Closed 1 to 2 3 to 4 ≥5 to 6

Effacement, % 0 to 30 40 to 50 60 to 70 ≥80

Station* -3 -2 -1, 0 +1, +2

Cervical consistency Firm Medium Soft

Position of the cervix Posterior Midposition Anterior

* Based on a -3 to +3 scale.

Reference:
1. Bishop EH. Pelvic scoring for elective induction. Obstet Gynecol 1964; 24:266.

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 Summary of maternal and neonatal outcomes in pregnancies complicated by
eclampsia

Outcome Frequency (percent)

Abruption 7 to 10

Disseminated intravascular coagulation 7 to 11

Pulmonary edema 3 to 5

Acute renal failure 5 to 9

Aspiration pneumonia 2 to 3

Cardiopulmonary arrest 2 to 5

Liver hematoma 1

HELLP syndrome 10 to 15

Perinatal death 5.6 to 11.8

Preterm birth 50

Adapted from: Sibai BM. Obstet Gynecol 2005; 105:402.

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 Stroke mortality related to blood pressure and age

Stroke mortality rate, pictured on a log scale with 95% CI, in each decade of age in relation to the
estimated usual systolic and diastolic blood pressure at the start of that decade. Stroke mortality
increases with both higher pressures and older ages. For diastolic pressure, each age-specific
regression line ignores the left-hand point (ie, at slightly less than 75 mmHg) for which the risk
lies significantly above the fitted regression line (as indicated by the broken line below 75 mmHg).

CI: confidence interval.

Data from Prospective Studies Collaboration, Lancet 2002; 360:1903.

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 Contributor Disclosures
Errol R Norwitz, MD, PhD, MBA Grant/Research/Clinical Trial Support: Illumina [Preeclampsia].
Consultant/Advisory Boards: Illumina [Minimally invasive genetic testing for fetal and
pregnancy-related disorders]. Patent Holder: Bayer [Prediction test for preeclampsia]. Equity
Ownership/Stock Options: 1908 Brands/Bundle Organics [Nutritional supplements for
pregnancy]. Charles J Lockwood, MD, MHCM Nothing to disclose Steven C Schachter,
MD Patent Holder: Supernus Pharmaceuticals [Epilepsy]. Grant/Research/Clinical Trial Support:
LivaNova [Epilepsy]. Consultant/Advisory Boards: Supernus Pharmaceuticals [Epilepsy]. Vanessa
A Barss, MD, FACOG Nothing to disclose

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