Effective therapeutic interventions for post-anoxic status epilepticus (PASE) are lacking. Vigabatrin (VGB) could be an attractive adjunct drug in PASE by increasing GABA availability in inhibitory synapses; however, enteral malabsorption in the post-cardiac arrest (CA) period and difficulty enrolling in the FDA mandatory registry could hinder its use in this setting.  We hypothesize that CA survivors absorb VGB despite vasopressor use, concurrent enteral feeding, and regardless of gastric or post-pyloric drug delivery.  

We administered a single load 1125-4500 mg VGB (based on creatinine clearance; CrCl) in adults with non-traumatic CA, with electrographic SE and gastric or duodenal access. Plasma samples were collected at 0, 0.5, 1, 2, 3, 6, 12, 24, 48, 72 and 168 hours.   

Interim results from a cohort of 6 subjects comprised of 67% male (4 of 6), 83% White (5 of 6), with a median age 62 years (22-68), median BMI 30 Kg/m2 (20-53), and median CrCl 44cc/min (22-186) are presented.  

All subjects received VGB within 48h window; median VGB dose was 2250 mg (1125-4500). The median time to peak (Tmax) was 2 h (1-3); median peak concentration (Cmax) was 38.1 mcg/ml (16.7 -91.8). Median 24h VGB concentration (C24) was 9.4 mcg/ml (3.4-14.2) and half-life (T1/2) was 16 h (10-24). The AUC 0-24 value was 318 mcg*h/ml (262-1012). No significant association was found between sex or BMI and Cmax. Three out of six patients achieved EEG response following VGB load; no association with dose or concentration was noted.