Eclampsia
Updated On: July 23, 2026
Anesthesia Implications
The first sixty seconds - Seizures typically run 60-90 seconds. Turn her onto her left side, suction the mouth, protect her from injury, and once the convulsion stops give 8-10 L/min of oxygen by nonrebreather to correct the hypoxemia from hypoventilation during the seizure. Have airway adjuncts open, but do not rush to intubate a seizure that is ending on its own.
Magnesium is the anticonvulsant - Load 4-6 g IV over 15-20 minutes, then run 2 g/hr (1-3 g/hr depending on renal function), and continue at least 24 hours after the last seizure. About 10% seize again on magnesium; an additional 2 g bolus is the answer. IV lorazepam 2 mg over 3-5 minutes is an alternative, and benzodiazepines or barbiturates are reserved for magnesium-refractory seizures. Diazepam and phenytoin are the other listed antiepileptics; in myasthenia gravis use levetiracetam or valproic acid instead, since magnesium and phenytoin worsen muscle weakness.
Bedside magnesium monitoring - Levels every four hours targeting 4-7 mEq/L (5-9 mg/dL), with patellar reflexes, respiratory effort, and urine output followed in between. Absent reflexes, respiratory depression, CNS depression, or PR/QT/QRS prolongation mean toxicity - stop the infusion and give calcium gluconate 1 g IV, repeating as needed since the effect is temporary. Some labels advise holding magnesium two hours before delivery to limit interaction with neuromuscular blockers, but stopping it risks another seizure.
Magnesium changes your relaxants - It competes at voltage-gated calcium channels and blunts acetylcholine release at the neuromuscular junction, so non-depolarizing blockade is potentiated. Cut the dose, use a nerve stimulator with TOF, and confirm recovery before extubation. Magnesium infusion is also a listed risk factor for uterine atony - anticipate postpartum hemorrhage.
Blunt the pressor response if you intubate - She may need an airway after the seizure for a depressed level of consciousness, or for magnesium toxicity causing respiratory paralysis. Laryngoscopy provokes a hypertensive surge that in this patient can produce intracranial hemorrhage, so control the pressure before you touch the airway.
Blood pressure target - IV labetalol is the preferred agent: 20 mg, then 40 mg and 80 mg at 10-15 minute intervals for recalcitrant severe hypertension. Aim for systolic 140-160 and diastolic 90-105 - low enough to protect the brain, high enough to keep the placenta perfused. Hydralazine 5-10 mg IV and oral nifedipine 10 mg are the other first-line options.
Do not cut for the post-ictal strip - Fetal bradycardia lasting 3-5 minutes during and just after the seizure is common and is not by itself an indication for emergency cesarean. Resuscitate the mother instead - stop the seizure, correct hypoxemia and hypercarbia, treat the hypertension - and the strip usually recovers. If it has not improved after 15 minutes of resuscitation, consider occult abruption and go.
Delivery is the definitive treatment - Eclampsia is an absolute contraindication to expectant management. Once mother and fetus are stabilized, deliver; induction is a reasonable route after 32 weeks with a clear endpoint of delivery inside 24 hours. Corticosteroids for lung maturity if under 34 weeks, but delivery is not delayed for them.
Rule out the mimics - A seizure before 20 weeks, or a delayed postpartum seizure, needs non-obstetric causes excluded: electrolyte abnormality, toxin, infection, head trauma, ruptured aneurysm, brain tumor. Persistent neurologic symptoms after the seizure point toward stroke or intracranial hemorrhage and warrant neuroimaging.
Postpartum is not the finish line - Risk is highest in the 48 hours after birth. Magnesium runs 12-24 hours post-delivery, and pressure is treated to keep systolic under 150 and diastolic under 100 on two readings four hours apart, or within an hour if she is above 160/110.
Count the collateral damage after repeat seizures - Recurrent convulsions bring rhabdomyolysis, metabolic acidosis, aspiration pneumonia, and neurogenic pulmonary edema. The underlying preeclampsia adds ARDS, pulmonary edema, renal failure, and hepatic failure - keep fluids tight and watch the oxygenation.
Pathophysiology
Eclampsia is a new-onset generalized tonic-clonic seizure in a patient with preeclampsia (see the Preeclampsia entry for the underlying placental and endothelial disease). It is the severe end of that spectrum: roughly 2-3% of women with severe features who receive no seizure prophylaxis convulse, and up to 0.6% of those without severe features.
Two mechanisms are proposed, both downstream of preeclampsia. Increased blood-brain barrier permeability alters cerebral blood flow through impaired autoregulation, and hypertension-driven autoregulatory failure produces hypoperfusion, endothelial injury, and vasogenic edema - often appearing as posterior reversible encephalopathy syndrome (PRES). About 60% of cases are antepartum, 20% intrapartum, and 20% postpartum, with roughly 90% of postpartum seizures inside the first week. Autopsy series found cerebral hemorrhage in more than half of women who died within two days of a seizure.