10.3 Seizures, Status Epilepticus & Neuromonitoring

Defining Status Epilepticus

A seizure is abnormal, excessive cortical electrical activity. Status epilepticus (SE) is now defined operationally as a single seizure lasting 5 minutes or more, or two or more seizures without full recovery of consciousness between them. The 5-minute threshold matters because prolonged seizures become self-sustaining and progressively pharmacoresistant as GABA receptors internalize; the CCRN expects you to begin treatment at 5 minutes rather than waiting for a seizure to stop on its own. Prolonged convulsive activity also causes hyperthermia, rhabdomyolysis, lactic acidosis, and neuronal injury.

The Time-Based Treatment Ladder

Management follows a strict, escalating timeline:

Benzodiazepines abort the seizure and are the single most important early step. Give IM midazolam when no IV is available. Fosphenytoin requires cardiac monitoring (watch for hypotension and bradycardia during infusion); levetiracetam is often preferred for its favorable interaction and safety profile. Refractory SE almost always requires intubation and continuous EEG to confirm electrographic seizure suppression.

The Glasgow Coma Scale

The Glasgow Coma Scale (GCS) quantifies level of consciousness from 3 (deep coma) to 15 (fully alert) across eye, verbal, and motor responses. Score the best response in each category, add them, and always report the components (for example E3V4M5 = 12), not just the total, because the pattern guides care.

A GCS of 8 or less signals the need for airway protection, and a drop of 2 or more points is a significant deterioration requiring immediate evaluation.

Neuromonitoring

Beyond the bedside neuro exam, ICU neuromonitoring includes: ICP monitors and EVDs; continuous EEG (cEEG) to detect nonconvulsive status epilepticus — critical in comatose patients who stop overt convulsing but keep seizing electrically; brain tissue oxygenation (PbtO2, goal > 20 mmHg); jugular venous oxygen saturation (SjvO2, normal 55-75%); and transcranial Doppler for vasospasm surveillance. The bispectral index (BIS) tracks sedation depth but does not diagnose seizures and is not a substitute for EEG. Any comatose patient who does not wake as expected after a convulsion should prompt consideration of cEEG.

Brain Death Examination Basics

Brain death is the irreversible loss of all brain and brainstem function and is a clinical diagnosis. Prerequisites must be met first: coma of a known, irreversible cause; normothermia; normotension; and exclusion of confounders (sedatives, neuromuscular blockers, severe metabolic or endocrine derangement, alcohol). The exam then demonstrates:

• Coma with no motor response to central pain (spinal reflexes may persist).
• Absent brainstem reflexes: fixed pupils, absent corneal reflex, absent oculocephalic (doll's eyes), absent oculovestibular (cold-caloric) response, and absent gag and cough.
• A positive apnea test: no respiratory effort despite the PaCO2 rising 20 mmHg or more above baseline (or reaching >= 60 mmHg).

Ancillary tests (cerebral angiography showing no intracranial flow, nuclear perfusion scan, EEG, transcranial Doppler) are used only when the clinical exam or apnea test cannot be completed. An isoelectric EEG alone is neither required nor sufficient.

Seizure Causes and Post-Ictal Care

Seizures in the ICU are frequently provoked rather than epileptic: common triggers include hyponatremia, hypoglycemia, hypocalcemia, hypomagnesemia, uremia, hepatic encephalopathy, hypoxia, drug toxicity or withdrawal (alcohol, benzodiazepines), and structural insults (stroke, TBI, tumor, meningitis). Correcting the underlying metabolic cause is as important as giving an antiseizure drug — a patient seizing with a sodium of 112 needs hypertonic saline, not just a benzodiazepine. During any convulsion, protect the airway, turn the patient laterally to reduce aspiration, pad and shield them from injury without restraining the limbs, apply oxygen, and time the event. Afterward expect a post-ictal period of drowsiness and confusion; reorient the patient, monitor the airway, recheck glucose, and perform a focused neuro exam for any new focal deficit (Todd's paralysis is transient, but a persistent deficit suggests a structural cause). Nonconvulsive seizures may present only as unexplained altered mentation, which is why continuous EEG is used liberally in comatose ICU patients.

Related Neuro-Emergencies

Two linked scenarios round out the domain. Bacterial meningitis demands urgent empiric antibiotics (frequently with dexamethasone), droplet precautions, and monitoring for ICP elevation and seizures — antibiotics are given promptly after cultures if obtaining them will not delay therapy; you never withhold them waiting for all results. And TBI or SAH patients may receive short-term seizure prophylaxis (commonly levetiracetam) during the first 7 days, since post-injury seizures spike ICP and worsen secondary brain injury. After a brain-death declaration, the legal time of death is when the confirmatory testing is completed, and the organ procurement organization — not the bedside team — approaches the family about donation to avoid a conflict of interest. Meticulous documentation of each reflex tested, the apnea-test blood gases, and the excluded confounders protects both the patient and the integrity of the determination.