Eclampsia

4/5/2014
Eclampsia
Official reprint from UpToDate

www.uptodate.com 2014 UpToDate
Eclampsia
Author
Errol R Norwitz, MD, PhD
Section Editor
Charles J Lockwood, MD
Deputy Editor
Vanessa A Barss, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2014. | This topic last updated: Apr 03, 2014.
INTRODUCTION Eclampsia refers to the occurrence of one or more generalized convulsions and/or coma in
the setting of preeclampsia and in the absence of other neurologic conditions. The clinical manifestations can
appear anytime from the second trimester to the puerperium. In the past, eclampsia was thought to be the end
result of preeclampsia (hence the nomenclature); however, it is now clear that seizures should be considered
merely one of several clinical manifestations of severe preeclampsia (table 1), rather than a separate disease.
Despite advances in detection and management, preeclampsia/eclampsia remains a common cause of
maternal death [1].
The diagnosis and management of eclampsia will be reviewed here. Issues related to preeclampsia are
discussed separately. (See "Pathogenesis of preeclampsia" and "Preeclampsia: Clinical features and
diagnosis" and "Preeclampsia: Management and prognosis" and "Prevention of preeclampsia".)
INCIDENCE AND EPIDEMIOLOGY An eclamptic seizure occurs in 2 to 3 percent of severely preeclamptic
women not receiving anti-seizure prophylaxis; the seizure rate is estimated to be between 0 and 0.6 percent in
women with preeclampsia without severe features (previously referred to as mild preeclampsia) [2]. The
incidence of eclampsia has been relatively stable at 1.6 to 10 cases per 10,000 deliveries in developed countries
[3-8]. In developing countries, however, the incidence varies widely: from 6 to 157 cases per 10,000 deliveries [911].
Risk factors for eclampsia are similar to those for preeclampsia (table 2). Nonwhite, nulliparous women from
lower socioeconomic backgrounds are the group at highest risk of developing eclampsia. Peak incidence is in
the teenage years and low twenties, but there is also an increased incidence in women over 35 years of age.
Timing: antepartum, intrapartum, postpartum Eclampsia prior to 20 weeks of gestation is rare and
should raise the possibility of an underlying molar pregnancy or antiphospholipid syndrome. (See "Gestational
trophoblastic disease: Epidemiology, clinical manifestations and diagnosis" and "Pregnancy in women with
antiphospholipid syndrome".)
Approximately one-half of all cases of eclampsia occur prior to term, with more than one-fifth occurring before 31
weeks of gestation [3]. Just over one-third of cases occur at term, developing intrapartum or within 48 hours of
delivery. Late postpartum eclampsia (ie, eclamptic seizures developing greater than 48 hours, but less than four
weeks postpartum) accounts for the remainder (13 to 16 percent) and represents as many as one-quarter of all
postpartum cases [12-14].
Looked at in another way, the timing and frequency of eclampsia is antepartum (38 to 55 percent), intrapartum
(13 to 36 percent), less than or equal to 48 hours postpartum (5 to 39 percent), and greater than 48 hours
postpartum (5 to 17 percent) [4,15].
PATHOGENESIS OF SEIZURES The exact cause of seizures in women with eclampsia is not known. The
following two hypotheses have been proposed [16]:
Cerebral overregulation in response to high systemic blood pressure results in vasospasm of cerebral
arteries, underperfusion of the brain, localized ischemia/infarction, and cytotoxic (intracellular) edema.
(See "Cerebrovascular disorders complicating pregnancy", section on 'Postpartum angiopathy'.)
Loss of autoregulation of cerebral blood flow in response to high systemic pressure (ie, hypertensive
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encephalopathy) results in hyperperfusion, endothelial damage, and vasogenic (extracellular) edema. (See
"Reversible posterior leukoencephalopathy syndrome", section on 'Eclampsia'.)
A classic report of autopsies performed shortly after death of eclamptic women described the neurological
findings in eclamptic women [17]. The brains of more than 50 percent of the women who died within two days of
seizures displayed cerebral hemorrhages. Petechial cortical hemorrhages were most common, especially
involving the occipital lobe. Diffuse cerebral edema and gross hemorrhage were noted less frequently. Cerebral
venous thrombosis was common in women with postpartum eclampsia.
Additional findings were observed in the largest magnetic resonance imaging study of eclampsia, which involved
27 nulliparous eclamptic women without neurologic deficit [18]. Twenty-five of these women had evidence of
cerebral edema, typically involving the subcortical white and adjacent gray matter in the parieto-occipital lobes.
Six women had restricted diffusion suggestive of infarction and five of the six had persistent imaging
abnormalities six to eight weeks later, but their neurologic examinations remained normal. The authors
hypothesized that hypertensive encephalopathy with hyperperfusion, vasogenic edema, and endothelial damage
caused the eclamptic seizures and that progressive edema, rather than vasospasm, led to focal areas of
cerebral hypoperfusion and, ultimately, infarction in the most severe cases.
The pathogenesis of preeclampsia is reviewed elsewhere. (See "Pathogenesis of preeclampsia".)
CLINICAL MANIFESTATIONS AND DIAGNOSIS
Maternal Eclampsia is a clinical diagnosis based upon evidence of one or more generalized convulsions
and/or coma in a preeclamptic woman and in the absence of other neurologic conditions. Eclamptic seizures
are almost always self-limiting and seldom last longer than three to four minutes (usual duration 60 to 75
seconds). Characteristics of generalized, tonic-clonic seizures are listed in the table (table 3).
Symptoms that may occur in the hours before the seizure include persistent frontal or occipital headaches or
thunderclap headaches, visual disturbances (eg, scotomata, loss of vision, blurred vision, diplopia, homonymous
hemianopsia, photophobia), right upper quadrant or epigastric pain, altered mental status, and shortness of
breath [3].
The relationship between the level of blood pressure elevation and onset of seizures is unclear. The diagnosis of
preeclampsia may not be suspected prior to the development of seizures in women with relative hypertension
(ie, blood pressure elevated compared with patient's baseline, but less than 140/90 mmHg) and no proteinuria
[3,19,20]. (See 'Can eclampsia be predicted?' below.)
In general, women with typical eclamptic seizures who do not have focal neurologic deficits or prolonged coma
do not require diagnostic evaluation with either electroencephalographic or cerebral imaging studies [21]. If
cerebral imaging is performed, magnetic resonance imaging is the optimal study.
Postpartum eclampsia As discussed above, eclampsia can initially present in the postpartum period
and can result in maternal death or severe morbidity [22-24]. (See 'Timing: antepartum, intrapartum, postpartum'
above.) The diagnosis may be delayed because prodromal symptoms are nonspecific and severe signs and
symptoms, such as severe hypertension and severe headache, may be intermittent [24].
A large retrospective cohort study of 152 patients discharged from the hospital postpartum and then readmitted
with preeclampsia/eclampsia more than two days and less than six weeks after delivery observed the following
[25]:
63 percent of the women had no diagnosis of any hypertensive disease during the antecedent pregnancy.
14.5 percent of these patients developed eclampsia. Over 90 percent of the cases of eclampsia occurred
within seven days of delivery.
The most common presenting symptom was headache, which occurred in about 70 percent of patients.
Other prodromal symptoms included shortness of breath, blurry vision, nausea or vomiting, edema,
neurological deficit, and epigastric pain.
Fetal Fetal bradycardia lasting at least three to five minutes is a common finding during and immediately
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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.
Resolution of maternal seizure activity is associated with compensatory fetal tachycardia and loss of variability,
sometimes associated with transient fetal heart rate decelerations [26]. If the fetal heart rate tracing remains
nonreassuring for more than 10 to 15 minutes with no improvement despite maternal and fetal resuscitative
interventions, then the possibility of an occult abruption should be considered and emergent delivery may be
indicated [15].
DIFFERENTIAL DIAGNOSIS Eclamptic seizures are clinically and electroencephalographically
indistinguishable from other generalized tonic-clonic seizures. (See "Electroencephalography (EEG) in the
diagnosis of seizures and epilepsy".)
Clinical conditions other than eclampsia that should be considered when evaluating a pregnant woman who has
had a seizure include:
Reversible posterior leukoencephalopathy syndrome (RPLS), which consists of headaches, seizures,
confusion, and visual disturbances with characteristic neuroimaging findings, is a common clinical
syndrome resulting from a number of different causes that are grouped together because of similar findings
on neuroimaging. Hypertension is usually, but not invariably, present. Some experts suggest that RPLS is
an indicator of eclampsia, even when features of preeclampsia (hypertension, proteinuria) are not present
[27,28]. In a series of 47 patients diagnosed with eclampsia, 46 had RPLS on neuroimaging; the only
patient without RPLS was subsequently found to have an underlying seizure disorder [29].
Blood pressures in pregnant patients who develop RPLS are generally lower than in patients who develop
RPLS in other settings [30,31]. The headache is typically constant, nonlocalized, moderate to severe, and
unresponsive to analgesia, but may be of sudden onset (thunderclap headache). The pathogenesis of
RPLS is unclear, but appears to be related to disordered cerebral autoregulation and endothelial
dysfunction. (See "Reversible posterior leukoencephalopathy syndrome".)
Stroke (hemorrhage, arterial or venous thrombosis). (See "Overview of the evaluation of stroke" and
"Cerebrovascular disorders complicating pregnancy".)
Hypertensive disease (hypertensive encephalopathy, pheochromocytoma). (See "Spontaneous
intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis".)
Space-occupying lesions of the central nervous system (brain tumor, abscess). (See "Clinical presentation
and diagnosis of brain tumors".)
Metabolic disorders (hypoglycemia, uremia, inappropriate antidiuretic hormone secretion resulting in water
intoxication). (See "Manifestations of hyponatremia and hypernatremia" and "Hypoglycemia in adults:
Clinical manifestations, definition, and causes".)
Infection (meningitis, encephalitis). (See "Viral encephalitis in adults" and "Clinical features and diagnosis
of acute bacterial meningitis in adults".)
Thrombotic thrombocytopenic purpura or thrombophilia. (See "Diagnosis of thrombotic thrombocytopenic
purpura-hemolytic uremic syndrome in adults" and "Inherited thrombophilias in pregnancy" and
"Cerebrovascular disorders complicating pregnancy".)
Idiopathic epilepsy. (See "Risks associated with epilepsy and pregnancy".)
Use of illicit drugs (eg, methamphetamine, cocaine).
Cerebral vasculitis. (See "Primary angiitis of the central nervous system in adults" and "Cerebrovascular
disorders complicating pregnancy".)
These etiologies are particularly important in pregnant women who seize in the first half of pregnancy when
eclampsia is rare and in those with focal neurologic deficits, prolonged coma, or atypical eclampsia. The
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approach to evaluation and treatment of noneclamptic seizures is discussed separately. (See "Evaluation of the
first seizure in adults".)
MANAGEMENT A number of management strategies have been developed to prevent maternal and fetal
complications resulting from eclampsia during the peripartum period.
General principles If the seizure is witnessed, maintenance of airway patency and prevention of aspiration
should be the first responsibilities of management. The gravida should be rolled onto her left side. A bed with
raised, padded side rails provides protection from trauma. Supplemental oxygen (8 to 10 L/min) via a face mask
has been recommended to treat hypoxemia due to hypoventilation during the convulsive episode [15].
The immediate issues in caring for an eclamptic woman include:
Prevention of maternal hypoxia and trauma
Management of severe hypertension, if present
Prevention of recurrent seizures
Evaluation for prompt delivery.
The definitive treatment of eclampsia is delivery, irrespective of gestational age, to reduce the risk of maternal
morbidity and mortality from complications of the disease.
Treatment of hypertension Strokes account for 15 to 20 percent of deaths from eclampsia. The general
risk of stroke in the nonpregnant population correlates directly with the degree of elevation in systolic and
diastolic pressures and maternal age [32]. It is not clear whether there is a threshold pressure above which
emergent therapy should be instituted in pregnant hypertensive women [33]. Most experts recommend
aggressive antihypertensive therapy for sustained diastolic pressures greater than 105 to 110 mmHg or systolic
blood pressures 160 mmHg, although the validity of thresholds has not been tested prospectively. 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. (See "Management of hypertension in pregnant and postpartum women".)
Options for initial treatment of hypertensive crisis include:
Hydralazine beginning with 5 mg intravenously, followed by 5 to 10 mg boluses as necessary every 20
minutes, or
Labetalol beginning with 10 or 20 mg intravenously followed by doubling the dose at 10-minute intervals up
to 80 mg for a maximum total cumulative dose of 220 to 230 mg (eg, 20-40-80-80 mg or 10-20-40-80-80
mg)
Although clinical trials have not adequately addressed the question of how aggressively to lower an eclamptic
patient's blood pressure, many experts consider a reasonable goal to be a systolic pressure of 140 to 155
mmHg and diastolic pressure of 90 to 105 mmHg. In women with extremely severe hypertension (180/120
mmHg), a diastolic goal of 100 to 105 mmHg should be achieved within two to six hours, with the maximum
initial (within 10 to 20 minutes) fall in BP not exceeding 25 percent of the presenting value [34,35]. An additional
therapeutic option in these women is nicardipine beginning with 5 mg/hour intravenously and increased by 2.5
mg/hour every 5 to 15 minutes to a maximum dose of 15 mg/hour. Data supporting this recommendation are
provided separately. (See "Management of hypertension in pregnant and postpartum women" and "Malignant
hypertension and hypertensive encephalopathy in adults".)
Women who do not improve rapidly following control of seizures and hypertension, or those who develop
localizing neurologic signs, should be evaluated further. (See "Evaluation of the first seizure in adults".)
The use of antihypertensive agents to control mildly elevated blood pressure in the setting of
preeclampsia/eclampsia has not been shown to alter the course of the disease, nor to diminish perinatal
morbidity or mortality [36-38]. Pharmacologic treatment of mild hypertension is not recommended, as neither
maternal nor fetal benefits have been demonstrated.
Treatment of convulsions The initial convulsion is usually of short duration and often occurs in a setting
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where intravenous access and drugs are not readily available. Therefore, treatment is primarily directed at
prevention of recurrent convulsions rather than control of the initial seizure. The drug of choice is magnesium
sulfate.
An additional benefit of magnesium sulfate therapy is that randomized placebo-controlled trials of maternal
administration of magnesium sulfate in women expected to have a preterm delivery within 24 hours have
consistently demonstrated a decreased risk of cerebral palsy and severe motor dysfunction in offspring. (See
"Neuroprotective effects of in utero exposure to magnesium sulfate".)
Prevention of recurrent convulsions Approximately 10 percent of eclamptic women will have repeated
seizures if managed expectantly [39]. There is universal agreement that women with eclampsia require
anticonvulsant therapy to prevent further seizures and the possible complications of repeated seizure activity:
neuronal death, rhabdomyolysis, metabolic acidosis, aspiration pneumonitis, neurogenic pulmonary edema, and
respiratory failure. However, the choice of agent has been controversial. Obstetricians favor magnesium sulfate
as the drug of choice for prevention of recurrent eclamptic seizures, whereas neurologists tend to favor
anticonvulsants traditionally used in nonpregnant individuals, such as phenytoin or diazepam. The following
evidence appears to have resolved this dispute in favor of magnesium sulfate:
The Eclampsia Trial Collaborative Group conducted two prospective trials in which 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 [40]. 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 convulsions 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 had one-third the rate of recurrent convulsions of those
allocated to phenytoin (6 versus 17 percent). In this arm of the study, women who received
magnesium 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.
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 repeat
seizures in eclamptic women [41-43].
In summary, randomized controlled trials of magnesium sulfate for prevention of recurrent seizures in women
with eclampsia have demonstrated this drug can reduce the rate of recurrent seizures by one-half to two-thirds
(RR 0.44, 95% CI 0.32-0.51) and can reduce the rate of maternal death by one-third (RR 0.62, 95% CI 0.390.99) [2].
Additional advantages of magnesium sulfate therapy include lower cost, ease of administration (eg, cardiac
monitoring is not required), and less sedation than either diazepam or phenytoin. Magnesium also appears to
selectively increase cerebral blood flow and oxygen consumption in women with preeclampsia [44]; this is not
true for phenytoin [45].
Administration of magnesium sulfate The initial dose of magnesium sulfate recommended by experts
varies from 4 to 6 g intravenously over 15 to 20 minutes. We use 6 g. This dose will achieve resolution of an
ongoing convulsion and provide the loading dose prior to maintenance therapy for prevention of recurrences. 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 even in the presence of renal insufficiency. Concurrent use of
magnesium sulfate with calcium channel blockers may result in hypotension. Magnesium sulfate is
contraindicated in women with myasthenia gravis since it can precipitate a severe myasthenic crisis. (See
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"Management of myasthenia gravis in pregnancy", section on 'Treatment issues'.)

The maintenance dose of magnesium sulfate after the initial 6 g loading dose is 1 to 3 g/hour administered as a
continuous intravenous infusion, we use 2 g/hour; alternatively, 5 g can be given intramuscularly every four
hours, but this is painful. 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 if the woman's clinical status is closely monitored for
evidence of potential magnesium toxicity. There does not appear to be a clear threshold magnesium
concentration for insuring the prevention of convulsions, although a range of 4.8 to 8.4 mg/dL has been
recommended [46]. 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.
Management of persistent convulsions Recurrent convulsions occurring in patients on maintenance
magnesium sulfate therapy can be treated with an additional bolus of 2 grams of magnesium sulfate over 15 to
20 minutes, with careful monitoring for signs of magnesium toxicity (see above). If two such boluses do not
control seizures, then other measures should be instituted. A number of options are included below, although
diazepam or lorazepam are used most commonly.
Diazepam Intravenously administered diazepam (0.1 to 0.3 mg/kg over 60 seconds, maximum
cumulative dose 20 mg) rapidly enters the central nervous system, where it achieves anticonvulsant levels
within one minute, and will control seizures in greater than 80 percent of patients within five minutes [47].
A diazepam gel for rectal administration is also available (0.2 mg/kg). 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 0.02 to 0.03 mg/kg intravenously, allowing approximately one minute to assess its effect. If
seizures continue at this point, additional doses of lorazepam (up to a cumulative dose of 0.1 mg/kg) are
infused at a maximum rate of 2 mg/minute for acute treatment. Lorazepam is as effective as diazepam in
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 action against seizures is
as long as four to six hours because of its less pronounced redistribution into adipose tissue.
Sodium amobarbital 250 mg intravenously over three to five minutes [15].
Treatment of status epilepticus is discussed in detail separately. (See "Status epilepticus in adults".)
Delivery Eclampsia is usually considered an absolute contraindication to expectant management, although
this has been attempted [48]. The definitive treatment for eclampsia is prompt delivery; however, this does not
necessarily preclude induction of labor and attempted vaginal delivery [49,50]. After maternal stabilization,
factors to consider in determining the mode of delivery are gestational age, Bishop score, whether the patient is
in labor, and fetal condition and position.
We feel that induction is a reasonable option for women with a favorable cervix at any gestational age or who are
greater than 32 to 34 weeks of gestation. 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 in rural India that randomly assigned 200 eclamptic women at 34 weeks to cesarean
delivery after initial stabilization or to induction, planned cesarean delivery did not lead to a statistically
significant reduction in adverse maternal or fetal events, and almost three-quarters of women in the planned
vaginal delivery group delivered vaginally [51]. This trial provides support for induction of labor, although it had
several limitations: the number of events was small, leading to wide confidence intervals, and the population is
not representative of women and intrapartum care in a higher resource setting. (See "Induction of labor".)
In contrast, we would not induce eclamptic women at less than 32 to 34 weeks of gestation with an unfavorable
cervix. In US studies, fewer than one-third of these women successfully delivered vaginally [39,52,53]. Cesarean
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delivery is a reasonable option for these women. Because the fetus benefits from in utero resuscitation before
delivery, it is desirable to wait 15 to 20 minutes and until the mother and fetus show signs of recovery (control of
convulsions; mother oriented to name, time, and place; fetal heart rate reassuring) before proceeding to surgery,
if possible.
Anesthesia issues are the same as for women with preeclampsia. (See "Preeclampsia: Management and
prognosis", section on 'Anesthesia'.)
Other There is no role for mannitol in the routine care of women with eclampsia. 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.
POSTPARTUM COURSE Maternal vital signs, input, and output should be monitored closely to detect large
changes in blood pressure and fluid imbalance. 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 [13].
Anticonvulsant drugs are generally administered for 24 to 48 hours postpartum, when the risk of recurrent
seizures is low. The optimal duration of therapy has not been determined. Therapy is continued in women
whose disease has not begun to improve postpartum and discontinued in women who are clearly improving
clinically (eg, diuresis of 100 mL/h for two consecutive hours and the absence of symptoms). (See
"Preeclampsia: Management and prognosis", section on 'Magnesium regimen and monitoring'.)
For women receiving magnesium sulfate prophylaxis postpartum, decisions regarding activity, oral intake, and
infant care should be made on a case-by-case basis.
Driving Many healthcare professionals caring for women with peripartum seizures have not considered
issues relating to fitness to drive after an eclamptic seizure [54]. 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'.)
PROGNOSIS A summary of the type and frequency of complications of eclampsia is shown in the table
(table 4).
Maternal outcome Maternal complications occur in up to 70 percent of women with eclampsia and include
abruption placentae, disseminated intravascular coagulopathy, acute renal failure, hepatocellular injury, liver
rupture, intracerebral hemorrhage, transient blindness, cardiorespiratory arrest, aspiration pneumonitis, acute
pulmonary edema, and postpartum hemorrhage [39]. Hepatocellular damage, renal dysfunction, coagulopathy,
hypertension, and neurologic abnormalities typically resolve 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 [55,56]. HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) develops in
approximately 10 to 20 percent of women with preeclampsia/eclampsia.
Maternal mortality rates of 0 to 14 percent have been reported over the past few decades [3,5,19,57]. 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) [5,15,20,39,58,59]. The
highest rates are in developing countries where prenatal, intrapartum, and neonatal care are compromised by
limited resources [57,60]. 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) [6]. 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) [57]. The subgroup of women with eclampsia prior to 28 weeks of gestation had the
highest risk of maternal death (12/54 or 22 percent); multiple seizures outside of the hospital setting was
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another common cause of death.

Perinatal outcome Premature delivery, abruptio placenta, and intrauterine asphyxia are the primary causes
of perinatal death in eclamptic pregnancies. Perinatal mortality ranges from 2 to 23 percent and is closely
related to gestational age [3,6,57]. As an example, perinatal mortality in a series of 54 pregnant women with
eclampsia prior to 28 weeks of gestation was 93 percent [57], but only 9 percent in another study in which the
mean gestational age at birth was 32 weeks [61].
Perinatal morbidity is also closely related to gestational age. In addition, there is a two- to three-fold increased
risk of delivery of a small for gestational age infant [6].
Recurrence risk Recurrent eclampsia occurs in 2 percent of subsequent pregnancies [62,63]. The risk
appears to be reduced by close maternal monitoring and timely intervention if preeclampsia develops [64].
Preeclampsia, however, cannot be prevented in most cases. (See "Prevention of preeclampsia".)
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 [65]. The incidence of mild
preeclampsia, severe preeclampsia, and eclampsia in these pregnancies was 13, 9, and 2 percent, respectively.
The corresponding figures for the subset of women whose eclampsia occurred at 30 weeks of gestation in the
index pregnancy were 17, 25, and 2 percent, respectively.
Subsequent pregnancies in women with a history of severe preeclampsia or eclampsia are also at increased
risk of other obstetric complications compared to women with no such history. These problems include
[62,63,65,66]:
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 [65,66]. This risk appears to
be the same whether they had severe preeclampsia or eclampsia.
Long-term maternal prognosis Chronic hypertension develops in 0 to 78 percent (mean 24 percent) of
women with a history of preeclampsia/eclampsia [62,63,65-67]. The wide range reported in the literature is due
to the influence of variables such as maternal age and duration of follow-up (the increased risk of subsequent
hypertension only becomes apparent after an average follow-up of 10 years [63]). The risk appears to be highest
in the subgroup of women who have subsequent hypertensive pregnancies, multiparas with eclampsia, and
those with eclampsia remote from term [62,63,65].
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 showed these women had a higher prevalence of white matter lesions than
matched controls with normotensive uncomplicated pregnancies (OR 3.3, 95% CI 1.05-10.6) [68]. 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 lesion. (See "Etiology, clinical manifestations, and diagnosis
of vascular dementia", section on 'White matter lesions'.)
Other long-term maternal risks are discussed elsewhere. (See "Preeclampsia: Management and prognosis",
section on 'Prognosis'.)
PREVENTION
Can eclampsia be predicted? 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
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have no evidence of proteinuria [3,19,20].

The majority of eclamptic women have one or more antecedent symptoms in the hours prior to an eclamptic
seizure. A retrospective analysis of 383 cases of eclampsia in the United Kingdom reported that 59 percent of
eclamptic women experienced prodromal headache, visual disturbance (eg, scotomata, amaurosis, blurred
vision, diplopia, homonymous hemianopsia), or epigastric pain [3]. Pregnant women should be aware that they
should call their health care provider if these symptoms develop. However, in a literature review, 20 to 40 percent
of eclamptic seizures were not preceded by premonitory symptoms.
This study also found that eclampsia was the first manifestation of pregnancy-related hypertensive disease in 38
percent of cases [3]. Similar findings were reported in studies from Sweden, Scotland, Tanzania, and the United
States [69-72].
In one review of 179 consecutive cases, factors identified to be at least partially responsible for failure to prevent
eclampsia 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]. Therefore, many cases of eclampsia do not appear to be preventable, even among women receiving regular
prenatal care, or those who are hospitalized.
Prevention of the first eclamptic seizure in preeclamptic women This topic is discussed in detail
separately. (See "Preeclampsia: Management and prognosis", section on 'Seizure prophylaxis'.)
SUMMARY AND RECOMMENDATIONS
Summary
Eclampsia refers to the occurrence of one or more generalized convulsions and/or coma in the setting of
preeclampsia and in the absence of other neurologic conditions. (See 'Introduction' above.)
An eclamptic seizure occurs in 0.5 percent of women with nonsevere preeclampsia and 2 percent of
women with severe disease. The incidence of eclampsia is 4 to 5 cases per 10,000 live births in developed
countries. (See 'Incidence and epidemiology' above.)
Just over one-third of cases occur at term, developing intrapartum or within 48 hours of delivery. (See
'Timing: antepartum, intrapartum, postpartum' above.)
An eclamptic seizure is typically tonic-clonic and lasts 60 to 75 seconds. Symptoms that may occur
before the seizure include persistent frontal or occipital headache, blurred vision, photophobia, right upper
quadrant or epigastric pain, and altered mental status. In up to one-third of cases, there is no proteinuria or
blood pressure is less than 140/90 mmHg prior to the seizure. (See 'Clinical manifestations and diagnosis'
above and 'Can eclampsia be predicted?' above.)
The goals of management are to stabilize the mother, prevent recurrent convulsions, treat severe
hypertension to prevent cerebral hemorrhage, and initiate delivery of the fetus. (See 'Management' above.)
The risk of recurrent eclampsia in a future pregnancy is 2 percent. (See 'Recurrence risk' above.)
Recommendations
For women with eclampsia, we recommend treatment with magnesium sulfate rather than other
anticonvulsants (Grade 1A). Compared to 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
'Treatment of convulsions' above.)
Given that intravascular administration has a faster therapeutic effect and is less painful than intramuscular
administration, we suggest using an intravascular regimen (Grade 2C). We give a loading dose of
magnesium sulfate 6 g intravenously over 15 to 20 minutes, followed by 2 g/hour administered as a
continuous intravenous infusion, but loading doses of 4 or 5 g are reasonable and a lower or higher
maintenance dose (1 or 3 g/hour) is sometimes required.
The loading dose may be given safely in the presence of renal insufficiency, but the maintenance dose
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should be omitted or reduced in this setting. 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. (See
'Administration of magnesium sulfate' above.)
In women with severe hypertension, we administer hydralazine or labetalol to achieve a systolic pressure
of 140 to 155 mmHg and diastolic pressure of 90 to 105 mmHg. (See 'Treatment of hypertension' above.)
Delivery is the only curative treatment, but this does not necessarily preclude induction of labor. Cesarean
delivery is a reasonable option for women less than 32 weeks of gestation who have an unfavorable cervix.
After a seizure, we suggest waiting 15 to 20 minutes and until the mother and fetus show signs of recovery
(control of convulsions; mother oriented to name, time, and place; fetal heart rate reassuring) before
proceeding to surgery, if possible. (See 'Delivery' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
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MacGillivray I, Symonds ED (Eds), University Park Press, Baltimore 1980. p.483.

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Topic 1662 Version 18.0
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GRAPHICS
The presence of one or more of the following criteria are features of
severe preeclamptic disease
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
Altered mental status
Hepatic abnormality:
Severe persistent right upper quadrant or epigastric pain unresponsive to medication and not
accounted for by an alternative diagnosis or serum transaminase concentration twice normal,
or both
Severe blood pressure elevation:

Systolic blood pressure 160 mmHg or diastolic blood pressure 110 mmHg on two occasions at
least four hours apart while the patient is on bedrest (unless the patient is on antihypertensive
therapy)
Thrombocytopenia:
<100,000 platelets/microL
Renal abnormality:
Progressive renal insufficiency (serum creatinine >1.1 mg/dL or doubling of serum creatinine
concentration in the absence of other renal disease)
Pulmonary edema
In contrast to older criteria, the 2013 criteria do not include proteinuria >5 grams/24 hours
and fetal growth restriction as features of severe disease.
Adapted from: Hypertension in pregnancy: Report of the American College of Obstetricians and
Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol 2013; 122:1122.
Graphic 76975 Version 6.0
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Factors 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
Antiphospholipid antibody syndrome or inherited thrombophilia
Vascular or connective tissue disease
Diabetes mellitus (pregestational and gestational)
Multifetal gestation
High body mass index
Black race
Male partner whose mother or previous partner had preeclampsia
Hydrops fetalis
Unexplained fetal growth restriction
Woman herself was small for gestational age
Fetal growth restriction, abruptio placentae, or fetal demise in a previous pregnancy
Prolonged interpregnancy interval
Partner related factors (new partner, limted sperm exposure [eg, previous use of
barrier contraception])
Hydatidiform mole
Susceptibility genes
By comparison, smoking decreases the risk of preeclampsia

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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 which 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
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Summary of maternal and neonatal outcomes

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
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 percent confidence

intervals, 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 agespecific 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).
Data from Prospective Studies Collaboration, Lancet 2002; 360:1903.
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Disclosures
Disclosures: Errol R Norw itz, MD, PhD Consultant/Advisory Boards: Hologic (prediction tests for preterm birth); Natera (prenatal
diagnosis using cell-free DNA). Patent Holder: use of urinary angiogenic factors to predict preeclampsia, purchased by Beyer
(prediction test for preeclampsia). Charles J Lockw ood, MD Nothing to disclose. Vanessa A Barss, MD Employee of UpToDate,
Inc. Equity Ow nership/Stock Options: Merck; Pfizer; Abbvie.
Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are addressed by vetting
through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately
referenced content is required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy
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"Management of myasthenia gravis in pregnancy", section on 'Treatment issues'.)

another common cause of death.

have no evidence of proteinuria [3,19,20].

MacGillivray I, Symonds ED (Eds), University Park Press, Baltimore 1980. p.483.

Severe blood pressure elevation:

Factors associated with an increased risk of developing

By comparison, smoking decreases the risk of preeclampsia

Phases of tonic-clonic seizures

Clonic phase (30 to 90 seconds)

Postictal phase (Minutes to several hours)

Summary of maternal and neonatal outcomes

Disseminated intravascular coagulation

Acute renal failure

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

Stroke mortality related to blood pressure and age

Stroke mortality rate, pictured on a log scale with 95 percent confidence

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