Diphenhydramine overdose detected early by integration of toxidrome and electrocardiography and treated with venoarterial extracorporeal membrane oxygenation: a case report

Figures

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  Figure 1.. Initial electrocardiogram on arrival of patient with suspected drug overdose. The electrocardiogram revealed marked sinus tachycardia, QRS widening (250 ms) with a Brugada pattern, right axis deviation, a dominant terminal R wave in lead aVR, and QTc prolongation (496 ms). The mechanism of this cardiotoxicity was speculated to involve the blockage of sodium channels on cells in the His-Purkinje system.

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  Figure 2.. Diagnostic approach in this case. The toxidrome suggested an anticholinergic toxidrome, and the Triage DOA kit results were negative. The electrocardiogram showed a Brugada pattern. The drug that matched all three of these approaches was diphenhydramine, which is an over-the-counter drug without an identification code. AMP, amphetamines; BAR, barbiturates; BZO, benzodiazepines; COC, cocaine; OPI, opiates; PCP, phencyclidine; TCA, tricyclic antidepressants; THC, tetrahydrocannabinol.

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  Figure 3.. Time series of electrocardiographic changes at arrival, 3 hours later, and 24 hours later. The electrocardiogram indicated sinus rhythm after intravenous infusion of sodium bicarbonate and venoarterial extracorporeal cardiopulmonary membrane oxygenation. The high R wave in lead aVR, axial deviation, and intraventricular conduction delay gradually improved, and the normal conduction system was restored after 24 hours.