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Ketamine has been the drug du jour for everything from agitation to pain, but status epilepticus?
Looking at the pathophysiology of seizures, they occur due to an imbalance between excitatory mechanisms (through glutamate at the NMDA receptors) and inibitory mechanisms (at GABA receptors). The mainstay for seizure treatment has been mostly potentiation of the inhibitory mechanisms, but why not inhibit the excitatory mechanisms at the NMDA receptors?
Ketamine is the only NMDA antagonist that has been investigated for refractory status epilepticus, mostly in retrospective small series, with only 3 prospective cohort studies, totaling to 162 patients (110 adults and 52 pediatrics). Variable results were recorded, from studies with complete response in all patients to complete treatment failure, with a total of 56.5% of the adult patients having electrographic response. The optimal bolus dose appears to be 1.5-4.5 mg/kg, with an infusion of up to 10 mg/kg/hour.
Bottom Line? Consider using ketamine in patients who are in refractory status - after benzodiazepines, a 2nd line agent (such as fosphenytoin, valproic acid or levetiracetam) and IV anesthetics have failed.
(NMDA: N-methyl-D-aspartate, GABA: -aminobutyric acid)
References
Zeiler FA. Early Use of the NMDA Receptor Antagonist Ketamine in Refractory and Superrefractory Status Epilepticus. Hindawi 2015; 831-60