Eclampsia is defined as a new onset seizure or coma in a woman with preeclampsia. It is a common cause of maternal and fetal morbidity and mortality. Eclamptic seizures are the result of hypertension in preeclampsia, although the precise mechanism is not well understood.
Essentials
Risk factors for eclampsia are related to those for preeclampsia. The most common signs and symptoms are hypertension, headache, visual disturbances, and right upper quadrant or epigastric pain. However, 25% of affected patients are asymptomatic.
Seizures due to eclampsia are commonly associated with an abrupt loss of consciousness. The seizure generally lasts for a few minutes, followed by a gradual return of consciousness over the following 10-20 minutes. Fetal bradycardia is common after a maternal seizure.
In patients under 20 weeks gestation, eclampsia and preeclampsia are rare; other causes of seizures should be investigated. Consider anatomic abnormalities of cerebral origin in women with persistent neurological deficits. Rule out toxins, infection, and electrolyte disturbances.
Magnesium sulfate is given to prevent a recurrence of seizures rather than to control the initial episode.
Delivery is the definitive treatment for eclampsia.
Additional Treatment Information
Initial assessment should focus on airway protection with adequate oxygenation and ventilation. Position the patient into a left lateral decubitus position and provide high flow supplemental oxygen.
Convey urgently to the nearest hospital. Consider bypass to a hospital with caesarean section capabilities.
General Information
While the pathophysiology of seizures in eclampsia is not well understood, it is believed to result from vasogenic or cytotoxic edema and endothelial dysfunction secondary to abnormal cerebral autoregulation. This results in cerebral hyper- or hypoperfusion stemming from the hypertension.
Cardiac monitoring is required with magnesium administration
Administer the initial dose of 4 to 6 g intravenously over 20 minutes as a loading dose, followed by 1 to 2 g per hour; otherwise, 5 g can be given intramuscularly (use bilateral buttocks) followed by 5 g IM every four hours
If seizures persist following the loading dose of magnesium, up to 4 g IV can be given over five minutes
During long conveyances, check respiratory rate, patellar reflexes, and where possible, urine output; discontinue magnesium if patellar reflex is absent, if respiratory rate falls below 12/minute, or muscle weakness, slurred speech, arrhythmias, or CNS depression develops
Consider calcium chloride for magnesium sulfate overdose if hemodynamic or respiratory instability develops
Myasthenia gravis is a contraindication for magnesium sulfate as it can lead to a severe myasthenic crisis
If the patient is still seizing after 20 minutes, consider MIDAZOLam and other possible causes of seizures
MIDAZOLam crosses the placental barrier and may cause adverse effects on the fetus; however, prolonged seizure activity is life threatening to both the patient and the fetus - MIDAZOLam should remain an option for seizure control in these cases
Critical Care Paramedic (CCP) Interventions
If seizures persist following magnesium administration:
Consider phenytoin IV, 1250 mg IV at a rate of 50 mg/min
Consider antihypertensive to bring diastolic pressure below 110 mmHg and systolic pressure below 160 mmHg:
Labetalol: 20 mg IV over 2 minutes followed by infusion at 1-2 mg/min
Maximum dose of 300 mg; monitor for hypotension and bradycardia; if bradycardia develops but blood pressure remains high, change to hydralazine
Hydralazine: 5 mg IV over 1-2 minutes followed by 5-10 mg IV every 20 minutes until target blood pressure is reached
Maximum dose of 20 mg
Evidence Based Practice
Supportive
Neutral
Against
References
Ambulance Victoria. Clinical Practice Guidelines: Ambulance and MICA Paramedics. 2018. [Link]
Demir BC, et al. Comparison of magnesium sulfate and mannitol in treatment of eclamptic women with posterior reversible encephalopathy syndrome. 2012. [Link]
Marra A, et al. Posterior reversible encephalopathy syndrome: The endothelial hypotheses. 2014. [Link]