• Amar P Jadhav, Maein B Nusair, Apekshe Ingole, and Martin A Alpert.
• Department of Internal Medicine, University of Missouri School of Medicine, Columbia, MO 65212, USA.
• Am J Emerg Med. 2012 May 1;30(4):633.e3-5.

AbstractInhalation or ingestion of aluminum phosphide (AP) generates phosphine gas on exposure to moisture, which, in turn, produces widespread organ toxicity primarily involving the lungs, heart, liver, and kidneys. Cardiac manifestations of AP poisoning include toxic myocarditis, refractory heart failure, bradyarrhythmias, and tachyarrhythmias including ventricular tachycardia (VT). A 19-year-old depressed male farm worker ingested ten 500-mg tablets of Celphos in a suicide attempt. Each Celphos tablet contains 56% AP. Over the course of 10 hours, the patient developed heart failure and respiratory failure associated with a rise in serum troponin level to 12.7 ng/mL. Serum electrolytes (including magnesium) and serum creatinine levels were normal throughout. His course was further complicated by acidemia and hypotension. These hemodynamic and metabolic abnormalities were initially corrected by assisted ventilation and continuous veno-venous hemofiltration. However, he developed hemodynamically stable sustained monomorphic VT, which proved unresponsive to treatment with intravenous magnesium sulfate and intravenous amiodarone therapy. After a decline in blood pressure, 6 attempts at electrocardioversion failed to restore sinus rhythm, and he died. Postmortem histologic examination of myocardium showed contraction band necrosis, early coagulation necrosis, edema, hemorrhage, and pyknosis of cardiac myocyte nuclei. Ventricular tachycardia associated with AP poisoning has been successfully treated with magnesium sulfate, amiodarone, and electrocardioversion. This case report documents failure of all 3 of these therapeutic modalities.

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