Delayed-onset hepatic encephalopathy induced by zolpidem: a case report

Hepatic encephalopathy (HE) is a complex neuropsychiatric disorder associated with either hepatocellular insufficiency and/or the presence of porto-systemic shunts. It is thought to be induced by altered neurotransmission mediated by enhanced gamma-aminobutyric acid (GABA)-induced inhibitory tone.1–3 The use of benzodiazepines are generally avoided in patients with advanced chronic liver disease (CLD) because they enhance GABA-mediated neurotransmission. Zolpidem is a non-benzodiazepine hypnotic that selectively binds to the omega-1 GABA-benzodiazepine receptor complex. Although it theoretically has the same propensity to induce HE, its shorter half-life when compared to commonly prescribed benzodiazepines like diazepam, alprazolam and clonazepan, makes it a reasonable choice for subjects with CLD.4 We report a patient with CLD with a rapidly induced grade IV HE attributed to zolpidem that was promptly reversed by flumazenil.