Abstracts

Rationale: Refractory Status Epilepticus (RSE) is defined as failure of two conventional antiepileptic drugs (AEDs) in controlling seizures. RSE has a high (> 30%) mortality rate. It has been hypothesized that in the late stages of seizures, conventional AEDs acting at gamma aminobutyric acid (GABA) receptors become less effective. N-methyl-D-aspartate (NMDA) antagonists are candidate treatments for RSE. Ketamine is a noncompetitive NMDA receptor antagonist that has shown efficacy in seizure termination in animal studies and in a few case reports. In this study we reviewed our experience with the use of ketamine in RSE. Methods: We reviewed charts for all patients admitted to Allegheny General Hospital with status epilepticus (SE) between the years of 2003-2008. We found 14 patients that were treated with ketamine for RSE. Case records were reviewed for patient characteristics, etiology of RSE, hospital course, and final disposition. Successful treatment of RSE was defined as no clinical or electrographic seizures with no concomitant administration of continuous intravenous (cIV) anesthetic agents. Results: Data were collected from 14 patients (mean age 55.1 yrs, range 22-88 yrs) treated with ketamine for RSE. Low AED levels were noted to be the primary etiology of RSE in 5 patients, whereas systemic infection with underlying structural brain abnormality was the cause of RSE in 4 patients. All patients were treated with at least three AEDs, with one of them being either propofol or a benzodiazepine drip, before initiation of ketamine. Ketamine was introduced because of: failure of the other agents (4 pts); inability to wean cIV anesthetics due to seizure recurrence (2 pts); or significant hypotension requiring vasopressors (8 pts). Thirteen patients received a bolus of ketamine (mean 1.5 mg/kg) that was followed by a continuous drip (mean starting dose 0.56 mg/kg/hr, mean maximum dose 1.45 mg/kg/hr, range 0.12-5.7 mg/kg/hr). In one patient, vasopressors were successfully weaned to discontinuation following the use of ketamine; however, a bolus of ketamine had to be stopped in a septic patient because of worsening systemic hypotension. The average duration of RSE prior to ketamine use was 5.9 days (range 1-20 days). Ketamine successfully suppressed clinical and electrographic seizure ativity in all patients. There was seizure recurrence in 1 patient with weaning of ketamine; this patient was subsequently treated with pentobarbital. We were successful in weaning 13/14 patients from all cIV anesthetic agents. Disposition to home or inpatient rehabilitation was attained in 6 patients, 5 patients were discharged to a skilled nursing facility or a long term acute care facility, and 3 patients died. All deaths occurred after families withdrew care due to significant medical complications. Conclusions: In our case series of 14 patients with RSE, ketamine controlled seizures in all patients and terminated RSE in 12/14 patients. Ketamine was reasonably well tolerated. Future controlled studies are warranted to optimize dosage and timing of administration and to further validate the use of ketamine in RSE.