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Eclampsia

Eclampsia
Literature review current through: May 2024.
This topic last updated: Feb 05, 2024.

INTRODUCTION — Eclampsia refers to the occurrence of new-onset, generalized, tonic-clonic seizures or coma in a patient with preeclampsia or gestational hypertension (in those cases where, in retrospect, a diagnosis of gestational hypertension was given before the patient 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 areas.

The clinical manifestations, diagnosis, and management of eclampsia will be reviewed here. Issues related to preeclampsia and HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome are discussed separately:

(See "Preeclampsia: Pathogenesis".)

(See "Preeclampsia: Clinical features and diagnosis".)

(See "Preeclampsia: Antepartum management and timing of delivery".)

(See "Preeclampsia: Prevention".)

(See "Preeclampsia with severe features: Delaying delivery in pregnancies remote from term".)

(See "HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets)".)

EPIDEMIOLOGY — High-resource countries have a low incidence of eclampsia and the incidence has been 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 patients 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 limited [9].

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

PATHOGENESIS OF SEIZURES — The precise cause of eclamptic seizures is not clearly understood. Two models have been proposed, based on the effect of hypertension on the vasculature of the brain. 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. This is typical of a barotrauma injury. In the second model, hypertension causes activation of the autoregulatory system, leading to constriction 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 most often in patients with known preeclampsia, but may sometimes be the presenting feature of the disorder. Most patients have premonitory signs/symptoms in the minutes or hours before the initial seizure. In a systematic review including 59 studies involving over 21,000 patients with eclampsia from 26 countries, the most common antecedent signs/symptoms and percent of patients 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), deficits in visual perception and processing, altered mental status/memory deficits, and cranial nerve deficits [13,14].

Characteristics of eclamptic seizures — Eclampsia is generally manifested by a self-limited generalized tonic-clonic seizure. The initial tonic phase is characterized by an abrupt loss of consciousness and stiffening of the muscles of the arms, legs, chest, and back. The patient may begin to appear cyanotic. After approximately one minute, the clonic phase begins as 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 seizure typically resolves spontaneously within a few minutes. Other manifestations include focal or multifocal seizures or coma, but these are less common.

The postictal phase begins once the twitching movements end. The patient initially appears as if sleeping, breathing deeply, and then gradually regaining consciousness, often complaining of a headache (table 3). Most patients begin to recover responsiveness within 10 to 20 minutes after the generalized convulsion. Focal neurologic deficits are generally absent.

Fetal 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. 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]. (See 'Management' below and 'Fetal resuscitation' below.)

Time of presentation

Approximately 50 percent of eclampsia cases occur preterm and approximately 20 percent occur between 20 and 30 weeks of gestation [1,17].

Approximately 60 percent of eclampsia cases occur antepartum, 20 percent occur intrapartum, and 20 percent occur postpartum [12].

Among postpartum cases, approximately 90 percent occur within one week of delivery [18-22]. Antecedent symptoms are similar to those with antepartum and intrapartum eclampsia. In a series of patients discharged and later readmitted with eclampsia more than two days but less than six weeks after giving birth, the most common presenting symptom was headache, which occurred in approximately 70 percent of patients [22]. Other prodromal symptoms included shortness of breath, blurry vision, nausea or vomiting, edema, neurological deficit, and epigastric pain. Of note, many patients did not have hypertension during the antecedent pregnancy.

Neuroimaging — In over 90 percent of patients with eclampsia 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'.)

A prospective study reported that transcranial Doppler examinations after delivery showed depressed dynamic cerebral autoregulation and increased cerebral perfusion pressure in patients with eclampsia compared with other groups [25]. Cerebral perfusion pressure was similar for those with eclampsia and those with preeclampsia with severe features.

Electroencephalography — Information on electroencephalography (EEG) in eclampsia is limited. A literature review reported postictal EEG abnormalities were common in patients with eclampsia, and the EEG became normal with prolonged postpartum follow-up [26]. The studies were of low methodologic quality and all but one were published between 1955 and 1984; findings using contemporary equipment and practices have not been published. (See "Electroencephalography (EEG) in the diagnosis of seizures and epilepsy".)

Neurohistopathology — A classic report from 1973 described neurohistopathology in patients with eclampsia who underwent autopsy shortly after death [27]. In this series, >50 percent of those who died within two days of seizing 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 patients 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) [28]. 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.

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 patient with a hypertensive disorder of pregnancy (preeclampsia, HELLP syndrome, gestational hypertension) (table 4) [29]. 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 person with seizures who has the typical clinical and neuroimaging findings of reversible posterior leukoencephalopathy syndrome (RPLS; headache, confusion, visual symptoms, vasogenic edema predominantly localized to the posterior cerebral hemispheres) [30,31]. (See "Reversible posterior leukoencephalopathy syndrome".)

Differential diagnosis — The differential diagnosis of new-onset seizures in a pregnant patient 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). There are many causes of postpartum seizures (table 5). 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, with or without coexistent eclampsia. Causes of sudden development of neurologic symptoms include stroke, intracranial hemorrhage, brain mass lesion, toxic and metabolic encephalopathies, reversible cerebral vasoconstriction syndrome, 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, kidney 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 in 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 HUS. TTP and HUS may be indistinguishable from eclampsia that occurs in a patient with HELLP syndrome (table 6) and approximately 10 to 20 percent of patients 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 "Diagnostic approach to suspected TTP, HUS, or other thrombotic microangiopathy (TMA)".)

POSTICTAL EVALUATION — Patients with preeclampsia who develop a generalized tonic-clonic seizure without persistent neurologic deficit require no diagnostic evaluation beyond that for preeclampsia [33]. (See "Preeclampsia: Clinical features and diagnosis".)

Atypical cases should be evaluated for other causes of seizures, preferably by a neurologist. These patients include pregnant individuals who do not meet criteria for diagnosis of preeclampsia (table 7), HELLP syndrome, or gestational hypertension or who have persistent neurologic deficits, prolonged loss of consciousness, onset of seizures >48 hours after giving birth, onset of seizures before 20 weeks of gestation, or seizures despite adequate magnesium sulfate therapy. A neuroimaging study should be performed in these patients to evaluate for a culprit structural brain abnormality.

MANAGEMENT

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

Prevention of maternal hypoxia and trauma

Treatment of severe hypertension, if present

Terminating the seizure, if necessary

Prevention of recurrent seizures

Evaluation for delivery

Persistent seizures (status epilepticus), focal neurological signs, or seizure recurrence (particularly when magnesium levels are "therapeutic") should raise concerns about an intracranial lesion/stroke. A neurology consultation and head imaging are generally indicated in this setting, in addition to antiseizure therapy. (See "Convulsive status epilepticus in adults: Management" and "Evaluation and management of the first seizure in adults".)

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 8) is administered to prevent stroke, which accounts for 15 to 20 percent of deaths in patients with eclampsia. A common threshold for initiating antihypertensive therapy is a diastolic pressure ≥110 mmHg or systolic blood pressure ≥160 mmHg on repeated measurements, although the validity of these thresholds has not been tested prospectively. The risk of stroke correlates with the degree of elevation in systolic and diastolic pressures and maternal age [34]. The cerebral vasculature of patients 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 patients", section on 'Acute therapy of severe hypertension'.)

Antiseizure medication

Persistent seizure activity — The tonic-clonic phase of an eclamptic seizure usually resolves within two to three minutes (table 3), at which time magnesium sulfate can be initiated for prevention of recurrent seizures (see 'Magnesium sulfate prophylaxis' below). However, if the patient is actively seizing for >5 minutes, we consider initiating treatment to terminate the seizure:

Lorazepam 4 mg IV at a maximum rate of 2 mg/minute; may repeat at three to five minutes if the seizure continues.

If IV access has not been established, midazolam 10 mg intramuscularly is usually effective. Two IV lines should be placed as soon as possible.

This approach is similar to the treatment of status epilepticus in nonpregnant adults with new-onset seizures, except valproate is avoided in pregnancy [35,36]. Treatment is reviewed in detail separately. (See "Convulsive status epilepticus in adults: Classification, clinical features, and diagnosis", section on 'Treatment'.)

Complications of prolonged maternal seizure activity may include hypoventilation and hypoxia, fever, and aspiration pneumonitis. Physiologically, deleterious neurologic effects of status epilepticus worsen after approximately 30 minutes. (See "Convulsive status epilepticus in adults: Classification, clinical features, and diagnosis", section on 'Complications and outcome'.)

Prevention of recurrent seizures

Magnesium sulfate prophylaxis — Magnesium sulfate is the antiseizure medication of choice in the setting of preeclampsia/eclampsia. Treatment is primarily directed at prevention of recurrent seizures (prophylaxis) 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 patients with eclampsia will have repeated seizures if managed expectantly [37]. There is universal agreement that patients with eclampsia require antiseizure medication 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 antiseizure medication 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 meperidine) for prevention of recurrent seizures in eclampsia [38-40]. Other 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 before 32 to 34 weeks of gestation. (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 [41]. In two international multicenter trial arms, 905 patients with eclampsia were randomly assigned to receive either magnesium sulfate or diazepam and another 775 patients 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:

Patients allocated to magnesium sulfate therapy had one-half the rate of recurrent seizures of those allocated to diazepam (13 and 28 percent, respectively).

Patients 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. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Drug of choice: Magnesium sulfate'.)

Dosing and toxicity — Our approach is described below and shown in the algorithm (algorithm 1). The superiority of any one specific magnesium regimen over another has not been established [42].

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 [9,43]. Using a loading dose at the lower end of this range (4 to 5 g) may be prolong the duration of time to achieve peak levels, especially in patients with obesity [44,45].

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. Mixing the medication with 1 mL of lidocaine 2% solution reduces pain.

These loading doses may be given safely to patients with impaired kidney function. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Dosing'.)

Maintenance dose – We administer a maintenance dose of magnesium sulfate 2 g/hour as a continuous IV infusion to patients with good kidney function. Maintenance doses of 1 to 2 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 resource-limited areas [46-48].

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 patients with good kidney function if the patient's clinical status is closely monitored and shows no evidence of potential magnesium toxicity. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Clinical assessment and adjusting maintenance therapy'.)

In patients with impaired kidney function, maintenance dosing should be lower and dosed in consultation with a nephrologist or pharmacist and magnesium levels should be monitored. The author of this topic 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. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Dosing'.)

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 [49]. The dose should be adjusted according to the clinical response of individual patients.

Toxicity, 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 patients with myasthenia gravis since it can precipitate a severe myasthenic crisis.

Additional information on complications and side effects of magnesium sulfate therapy can be found separately. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Maternal side effects' and "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Contraindications' and "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Fetal and neonatal effects from magnesium sulfate' and "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Drug interactions'.)

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

There is no role for mannitol in the routine care of patients with eclampsia [50]. It can be harmful because it can enter the brain and reverse the osmotic gradient, thus increasing intracranial pressure. A neurologist should be consulted for management of patients 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 despite therapy — In patients with recurrent seizures on maintenance magnesium therapy, a magnesium level should be obtained. These patients 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) [11,41,51]. If kidney function is normal, magnesium sulfate maintenance doses of 2 to 3 g/hour are commonly used. The author of this topic administers a 4 g magnesium sulfate bolus and 3 g/hour maintenance infusion to patients with recurrent seizures and normal kidney function.

If more than two recurrences occur after these measures, we suggest discontinuing magnesium sulfate, administering fosphenytoin 20 mg PE/kg at 100 to 150 mg PE/min IV or phenytoin 20 mg/kg IV at a rate of up to 50 mg/minute (cardiac monitoring and frequent vital signs are required during these infusions), and obtaining an urgent consultation from the neurology service. (Note: Fosphenytoin is prescribed as phenytoin sodium equivalents (mg PE) and 1 mg PE is equivalent to 1 mg phenytoin sodium). (See "Convulsive status epilepticus in adults: Management".)

Fetal resuscitation — Fetal bradycardia lasting at several minutes is a common finding during and immediately after an eclamptic seizure and does not necessitate emergency cesarean birth. In a series of 34 intrapartum eclamptic seizures, a prolonged fetal heart rate deceleration was documented in 79 percent of cases, and the mean duration of bradycardia was 5.8 minutes [52]. Fetal heart rate decelerations occurred a mean 2.7 minutes after the onset of the seizure. Half of the fetuses with fetal heart rate changes subsequently developed fetal tachycardia and variability was minimal in 48 percent of cases.

Stabilizing the mother by administering antiseizure medications 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]. In the previously mentioned case series, 4 of 31 patients underwent emergency cesarean birth, two of whom had suspected abruption, and there were no perinatal deaths [52]. (See "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences" and "Acute placental abruption: Management and long-term prognosis".)

Delivery timing and route — Eclampsia is considered an absolute contraindication to continued expectant management. The definitive treatment for eclampsia is prompt delivery; however, this does not necessarily preclude induction and a trial of labor [29,53]. 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 9). 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 patients in rural India at ≥34 weeks with eclampsia to cesarean birth or induction after initial stabilization, planned cesarean did not significantly reduce the rate of adverse maternal or fetal outcomes, and almost three-quarters of patients in the planned vaginal birth group succeeded in giving birth vaginally [54]. 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 patients and intrapartum care in higher resource settings.

By contrast, we would not induce patients 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 patients with severe preeclampsia/eclampsia remote from term successfully gave birth vaginally after induction of labor [37,55,56]. Thus, cesarean birth is a reasonable option for these patients. 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 patients with preeclampsia. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Analgesia and anesthesia'.)

POSTPARTUM CARE — The postpartum care of patients 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 [57].

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 similarly maintain therapy for 24 to 48 hours. In either case, therapy may be continued in patients in whom signs and symptoms of preeclampsia have not started to improve and discontinued in those 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 newborn 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 maternal stroke. Medications similar to those used before delivery (table 8) 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 patients", section on 'Acute therapy of severe hypertension' and "Treatment of hypertension in pregnant and postpartum patients", 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 to four weeks and monitor blood pressure to assess whether further treatment is indicated. (See "Treatment of hypertension in pregnant and postpartum patients", section on 'Postpartum hypertension'.)

Driving — Many health care professionals caring for patients with peripartum seizures have not considered issues relating to fitness to drive after an eclamptic seizure [58]. 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 should have follow-up with a neurologist. These include patients who do not meet criteria for diagnosis of preeclampsia (table 7), gestational hypertension, or HELLP syndrome or who have persistent neurologic deficits, prolonged loss of consciousness, onset of seizures >48 hours after giving birth, onset of seizures before 20 weeks of gestation, or seizures despite adequate magnesium sulfate therapy.

PREGNANCY OUTCOME

Maternal — Maternal complications occur in up to 70 percent of patients with eclampsia. The types and frequencies of complications from one review are summarized in the table (table 10). Additional complications include intracerebral hemorrhage, transient cortical blindness, and cardiorespiratory arrest [37]. 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 patients with eclampsia [59,60].

Maternal mortality rates of 0 to 14 percent have been reported over the past few decades [1,6,8,61-63]. Maternal mortality and severe morbidity rates are lowest among patients receiving regular prenatal care who are managed by experienced physicians in tertiary centers (maternal mortality 0 to 1.8 percent) [16,37,61,64-66]. The highest mortality rates are in low-resource countries where prenatal, intrapartum, and neonatal care are compromised by limited resources [8,63,67]. 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 patients 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 birth, placental abruption, 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 patients 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 newborns were small for gestational age.

LONG-TERM PROGNOSIS

Recurrence risk — Recurrent eclampsia occurs in 2 percent of subsequent pregnancies [68,69]. The risk of developing preeclampsia in subsequent pregnancies can be reduced by the daily administration of low-dose aspirin, beginning at ≥12 weeks of gestation and ideally prior to 16 weeks (see "Preeclampsia: Prevention"). If preeclampsia develops, the risk of eclampsia appears to be reduced by close maternal monitoring and timely intervention [70].

The risk of recurrence was illustrated by a study that followed 159 nulliparous patients with a history of eclampsia and no preexisting hypertension through 334 subsequent pregnancies in the era before low-dose aspirin prophylaxis [71]. 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 patients whose eclampsia occurred at ≤30 weeks of gestation in the index pregnancy. In these patients, 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, patients with a history of severe preeclampsia/eclampsia are at increased risk of obstetric complications in subsequent pregnancies compared with patients with no such history. These problems include [68,69,71,72]:

Placental abruption (2.5 to 6.5 versus 0.4 to 1.3 percent of the general obstetric population)

Preterm birth (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)

Patients 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 [71,72]. This risk appears to be the same whether they had eclampsia or another manifestation of preeclampsia with severe features.

Long-term maternal health

Future cardiovascular disease – Both preeclampsia and eclampsia are associated with an increased risk for development of cardiovascular and cerebrovascular disease and diabetes later in life. These data are discussed elsewhere. (See "Preeclampsia: Intrapartum and postpartum management and long-term prognosis", section on 'Prognosis'.)

Chronic hypertension develops in 0 to 78 percent (mean 24 percent) of patients with a history of preeclampsia/eclampsia [68,69,71-73]. 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 [69]). The risk appears to be highest in the subgroup of patients who have subsequent pregnancies complicated by hypertension, parous patients with eclampsia, and patients with eclampsia remote from term [68,69,71].

Future seizure disorder – Patients with eclampsia may be at higher risk of a future seizure, but the absolute risk is small. In a retrospective study that included 1615 patients 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 [74]. The authors did not distinguish patients who had one subsequent seizure from those who had recurrent seizures.

Other – In a study of 39 patients with a history of eclampsia, magnetic resonance imaging performed an average of 6.4 years following the index pregnancy revealed that these patients 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) [75]. Approximately 15 percent of patients in each group were currently hypertensive or on antihypertensive therapy. The source and significance of these lesions are unclear; affected individuals do not appear to have increased functional impairment as may be seen in other patients with white matter lesions. Another study of patients with eclampsia reported no objective cognitive impairment as compared with controls when evaluated 2 to 20 years after delivery [76].

CAN ECLAMPSIA BE PREDICTED AND PREVENTED? — In patients who have been diagnosed with preeclampsia with severe features, prophylactic administration of magnesium sulfate can usually prevent seizures (see "Preeclampsia: Intrapartum and postpartum management and long-term 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) [77].

The majority of patients with eclampsia have one or more antecedent symptoms in the hours prior to an eclamptic seizure, thus pregnant patients 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 [1,77-80]. In a systematic review, the most commonly reported symptoms (visual disturbances, epigastric pain, and headache) neither accurately predicted, nor ruled out, imminent eclampsia [81].

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 [1,62,64]. While antihypertensive treatment is recommended for patients with blood pressures ≥160/110 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 patients".)

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

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) in a patient with a hypertensive disorder of pregnancy (preeclampsia, gestational hypertension, HELLP syndrome [hemolysis, elevated liver enzymes, low platelets] (table 4 and algorithm 2)). Some patients present with focal or multifocal seizures or coma. (See 'Diagnosis' above.)

Differential diagnosis – Pregnancy is a precipitating factor for some disorders associated with seizure activity, such as thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS). TTP and HUS may be indistinguishable from eclampsia that occurs in a patient with HELLP syndrome (table 6) and approximately 10 to 20 percent of patients with preeclampsia/eclampsia have laboratory findings of HELLP syndrome. (See 'Differential diagnosis' above.)

Incidence – In patients not receiving antiseizure prophylaxis, an eclamptic seizure occurs in 2 to 3 percent of patients diagnosed with preeclampsia with severe features and in 0 to 0.6 percent of those with preeclampsia without severe features. (See 'Epidemiology' above.)

Clinical features

Maternal signs/symptoms – Eclampsia is manifested by a generalized tonic-clonic seizure (table 3). Most patients 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.)

Fetal heart rate – Fetal bradycardia lasting at least three to five minutes is a common finding during and immediately after an eclamptic seizure. Emergency cesarean birth 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.)

Gestational age at occurrence – Eclampsia occurs before term in approximately 50 percent of patients. 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.)

Prediction/prevention – The majority of patients with eclampsia have one or more antecedent symptoms in the hours prior to an eclamptic seizure; however, the most commonly reported symptoms (visual disturbances, epigastric pain, and headache) neither accurately predicted, nor ruled out, imminent eclampsia. Eclampsia may not be preventable with magnesium sulfate when onset is abrupt, early in pregnancy, or after postpartum hospital discharge. (See 'Can eclampsia be predicted and prevented?' above.)

Management – Our approach is described in the algorithm (algorithm 1). Key management issues are: prevent maternal hypoxia and trauma, treat severe hypertension (if present), treat prolonged seizure activity if present, prevent recurrent seizures with magnesium sulfate, and evaluate for delivery. (See 'Key principles' above.)

Termination of prolonged acute seizure activity – The tonic-clonic phase of an eclamptic seizure usually resolves within two to three minutes, at which time magnesium sulfate can be initiated for prevention of recurrent seizures. If the patient is actively seizing for >5 minutes, we consider administering:

-Lorazepam 4 mg IV at a maximum rate of 2 mg/minute; may repeat at three to five minutes if the seizure continues.

-If IV access has not been established, midazolam 10 mg intramuscularly is usually effective. Two IV lines should be placed as soon as possible.

Magnesium sulfate prophylaxis – For patients with eclampsia, we recommend prophylaxis 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 'Dosing and toxicity' above.)

Antihypertensive therapy – A common threshold for initiating antihypertensive therapy is sustained diastolic pressures greater than 110 mmHg or systolic blood pressures ≥160 mmHg. Drugs options are described in the table (table 8). (See 'Treatment of hypertension' above.)

Recurrent seizures – In patients with recurrent seizures on maintenance magnesium therapy, a magnesium level should be obtained. The author administers a 4 g magnesium sulfate bolus and 3 g/hour maintenance infusion to patients with recurrent seizures and normal renal function. (See 'Management of recurrent seizures despite therapy' above.)

Neurology consultation – Persistent seizures (status epilepticus), recurrent seizures while on magnesium seizure prophylaxis, focal neurological signs, or seizure occurrence when magnesium levels are “therapeutic” should raise concerns about an intracranial lesion/stroke. A neurology consultation and head imaging are generally indicated in this setting, in addition to antiseizure therapy. (See 'Management of recurrent seizures despite therapy' above.)

Delivery – 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 timing and route' above.)

Postpartum care and course – 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 similarly maintain therapy for 24 to 48 hours. (See 'Duration of magnesium sulfate therapy' above.)

Pregnancy outcome – The types and frequencies of complications from one review are summarized in the table (table 10). (See 'Pregnancy outcome' above.)

Long-term prognosis

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

In addition to preeclampsia/eclampsia, patients 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.)

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References

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