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CASE REPORTS
JOURNAL ARTICLE
Fatal diphenhydramine poisoning with increased vascular permeability including late pulmonary congestion refractory to percutaneous cardiovascular support.
Clinical Toxicology 2008 November
BACKGROUND: Fatal adult cases of acute diphenhydramine poisoning are extremely rare.
CASE REPORT: Transiently awakened by a roommate, a 39-year-old man admitted to massive ingestion of an over-the-counter drug containing diphenhydramine salicylate. On admission the patient was semicomatose and developed circulatory collapse with severe dehydration and metabolic acidosis, followed by status epilepticus. Despite extensive life support measures including percutaneous cardiopulmonary support, vascular permeability progressively increased, with pulmonary congestion as well as peripheral vasodilation evident as rubedo. The patient died without improvement of cardiac function. Subsequent diphenhydramine assays in serum specimens obtained at the time of delayed congestive symptoms indicated decreases in drug concentration to a sublethal amount.
DISCUSSION: We suspect that metabolites of diphenhydramine with histamine-agonist actions contributed to the development of fatal delayed symptoms.
CASE REPORT: Transiently awakened by a roommate, a 39-year-old man admitted to massive ingestion of an over-the-counter drug containing diphenhydramine salicylate. On admission the patient was semicomatose and developed circulatory collapse with severe dehydration and metabolic acidosis, followed by status epilepticus. Despite extensive life support measures including percutaneous cardiopulmonary support, vascular permeability progressively increased, with pulmonary congestion as well as peripheral vasodilation evident as rubedo. The patient died without improvement of cardiac function. Subsequent diphenhydramine assays in serum specimens obtained at the time of delayed congestive symptoms indicated decreases in drug concentration to a sublethal amount.
DISCUSSION: We suspect that metabolites of diphenhydramine with histamine-agonist actions contributed to the development of fatal delayed symptoms.
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