Dexmedetomidine for Alcohol Withdrawal: Looks Can Be Deceiving

Alcohol is a gamma-aminobutyric acid (GABA) receptor agonist and an N-methyl-D-aspartate (NMDA) receptor antagonist. Although benzodiazepines and barbiturates are the standard treatments for alcohol withdrawal, there is some recent interest in adding dexmedetomidine. We report cases of two patients with severe alcohol withdrawal to highlight some limitations of dexmedetomidine therapy. The first case was of a 58-year-old man who presented with severe alcohol withdrawal. He received chlordiazepoxide, diazepam, and phenobarbital with resolution of his symptoms. He was later started on dexmedetomidine (0.2 mcg/kg/hr), with no other therapy, during which time he appeared sedated with a heart rate (HR) of 80 beats/minute, blood pressure (BP) of 126/80 mmHg, and respiratory rate (RR) of 18 breaths/minute. Seven hours after stopping the infusion, he said that he "had been lying in bed staring at the ceiling feeling like hell… felt extremely agitated in my head". The second patient was a 41-year-old man who developed alcohol withdrawal and required intubation seven hours after presentation. Maximal sedation was 50 mcg/kg/min of propofol and 14 mg/hr of midazolam. On hospital day 3, the team stopped propofol, decreased midazolam to 10 mg/hour, and added dexmedetomidine 0.2 mg/kg/hr. Forty minutes later, the toxicology team observed the patient unresponsive with left gaze deviation and rhythmic eye movements. Video EEG was consistent with a seizure. The patient's EEG rapidly improved with a midazolam bolus. Although dexmedetomidine controls the autonomic instability and behavior associated with alcohol withdrawal, it does not address the underlying pathophysiology, leaving patients to suffer the psychological effects of withdrawal. The role of dexmedetomidine remains to be determined, with studies that address cognitive and long-term outcomes of alcohol withdrawal rather than just vital signs, behavior, and doses of other medications used.