Status Epilepticus

Introduction

Status epilepticus (SE) is any seizure lasting more than 30 minutes, whether or not consciousness is impaired, or recurrent seizures without an intervening period of consciousness. SE is a medical emergency, and aggressive treatment of seizures that last 5 minutes or more is strongly recommended.

• Seizure initiation is likely caused by an imbalance between excitatory (eg, glutamate, calcium, sodium, substance P, and neurokinin B) and inhibitory (γ-aminobutyric acid [GABA], adenosine, potassium, neuropeptide Y, opioid peptides, and galanin) neurotransmission.
• Seizure maintenance is largely caused by glutamate acting on postsynaptic N-methyld-aspartate (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptors. Sustained depolarization can result in neuronal death.
• GABAA receptors may become less responsive to endogenous GABA and GABA antagonists.
• During phase I of GCSE, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, hypotension, shock, rhabdomyolysis, and secondary hyperkalemia, and acute tubular necrosis may ensue.
• In phase II, beginning 30 minutes into the seizure, the patient begins to decompensate and may become hypotensive with compromised cerebral blood flow. Serum glucose may be normal or decreased, and hyperthermia, respiratory deterioration, hypoxia, and ventilatory failure may develop.
• In prolonged seizures, motor activity may cease, but electrical seizures may persist.

Morbidity And Mortality

• Younger children, the elderly, and those with preexisting epilepsy have a higher propensity for sequelae.
• Recent estimates suggest a mortality rate up to 16% in children, 20% in adults, and 38% in the elderly. Neonates have a higher mortality and more neurologic sequelae.
• Variables affecting outcome are (1) the time between onset of GCSE and the initiation of treatment and (2) the duration of the seizure. The mortality rate is 2.6%, 19%, and 32% for those with seizures lasting 10 to 29 minutes, longer than 30 minutes, and longer than 60 minutes, respectively.

Clinical Presentation

Symptoms: impaired consciousness (e.g., ranging from lethargy to coma); disorientation (once GCSE is controlled); and pain associated with injuries.

• Early signs: generalized convulsions; acute injuries or central nervous system (CNS) insults that cause extensor or flexor posturing; hypothermia or fever suggestive of intercurrent illnesses (e.g., sepsis or meningitis); incontinence; normal blood pressure or hypotension; and respiratory compromise.
• Late signs: clinical seizures may or may not be apparent; pulmonary edema with respiratory failure; cardiac failure (dysrhythmias, arrest, or cardiogenic shock); hypotension or hypertension; disseminated intravascular coagulation or multi-system organ failure; rhabdomyolysis; and hyperpyrexia

Diagnosis

Assess: language; cognitive abilities; motor, sensory, and reflex abnormalities; pupillary response; injuries; asymmetry; and posturing.

• Initial laboratory tests: complete blood count (CBC) with differential; serum chemistry profile (e.g., electrolytes, calcium, magnesium, glucose, serum creatinine, alanine aminotransferase [ALT], and aspartate aminotransferase [AST]); urine drug/alcohol screen; albumin, hepatic function; renal function; blood cultures; arterial blood gases (ABGs); and serum drug concentrations if previous anticonvulsant use is suspected or known.
• Other potential diagnostic tests: spinal tap if CNS infection suspected; electroencephalograph (EEG) should be obtained immediately and once clinical seizures are controlled; computed tomography (CT) with and without contrast; magnetic resonance imaging (MRI); and radiograph if indicated to diagnose fractures.

Treatment

Goals of Treatment: 1) identify GCSE subtype and precipitating factors; 2) terminate clinical and electrical seizure activity as soon as possible and preserve cardiorespiratory function, 3) minimize side effects, 4) prevent recurrent seizures, and 5) avoid pharmacoresistant epilepsy and/or neurologic sequelae.

• For any tonic-clonic seizure that does not stop automatically or when doubt exists regarding the diagnosis, treatment of GCSE should begin during the diagnostic workup.

Dosing of Medications Used in the Initial Treatment of GCSE

Diazepam (IV) (Valium)

Adult 0.25 mg/kg

Pediatric 0.25–0.5 mg/kg

Lorazepam (IV) (Ativan)

Adult 4 mg, Pediatric 0.1 mg/kg

Phenytoin (IV) (Dilantin) Adult 20–25 mg/kg, Pediatric 20–25 mg/kg.