Snapshot A 56-year-old man is brought to the emergency department after being found in the park in a lethargic state. The patient has a history of multiple hospital visits for pain management of acute pancreatitis. Medical history is significant for alcohol use disorder. On physical exam, the patient has slurred speech, nystagmus, and unsteady gait. Laboratory testing is significant for an elevated blood alcohol level. Urine and serum toxicology is negative for illicit drugs. He is started on intravenous thiamine and glucose. Approximately 6 hours after admission the patient becomes nauseous, anxious, tremulous, and develops palpitations. He is subsequently started on intravenous lorazepam. (Alcohol withdrawal) Introduction Medications short-acting benzodiazepines alprazolam triazolam oxazepam midazolam longer-acting benzodiazepines flurazepam chlordiazepoxide lorazepam diazepam Mechanism of action ↑ the frequency of Cl- channel opening and thus facilitating GABAA action via its binding to the α and γ subunit of the GABAA receptor this in turn ↓ neuron firing Metabolism oxazepam, temazepam, and lorazepam is not dependent on liver metabolism Adverse reaction dependence can have an additive CNS depressive effect with other CNS depressants (e.g., alcohol and barbiturates) the antidote to benzodiazepine overdose is flumazenil a competitive benzodiazepine receptor antagonist can provoke seizures in chronic benzodiazepine users Clinical use anxiety and panic disorder status epilepticus alcohol withdrawal anesthesia premedication sleep walking and other parasomnias skeletal muscle relaxation insomnia