NEUROLOGICALLY INTACT SURVIVAL FOLLOWING CARDIAC ARREST FROM CHLORAL HYDRATE TOXICITY: A SHOWCASE OF MODERN CRITICAL CARE

Chloral hydrate is a sedative and hypnotic agent first introduced in the 19th century, with pharmacological activity mediated through hepatic metabolism into trichloroethanol. Although its clinical use has markedly declined over time, it is still occasionally preferred, particularly in pediatric populations, for pre-procedural sedation in non-invasive interventions. However, the agent’s narrow therapeutic window renders it highly susceptible to dosing errors, predisposing patients to severe cardiovascular and neurological complications. Overdose may result in QTc interval prolongation, torsades de pointes, central nervous system depression, and even sudden cardiac arrest. Moreover, the absence of a specific antidote necessitates that management relies entirely on supportive care. We report a rare case of cardiac arrest and torsades de pointes following ingestion of approximately ten times the recommended oral dose of chloral hydrate intended for procedural sedation. Remarkably, despite the agent’s high cardiotoxic potential and the lack of a specific antidote, complete neurological recovery was achieved, underscoring the critical role of early recognition and multidisciplinary intensive care strategies in the management of such toxicologic emergencies.