Description
A young man was admitted to the emergency department after consuming zinc phosphide, with severe drug refractory hypotension. ECG (refer figure 1) revealed ST segment elevation involving anterior, lateral and inferior leads. Serum levels of potassium, calcium, magnesium and phosphorous were normal; serum troponin-T was 1126 ng/nL (upper limit of normal 14 ng/nL), with associated metabolic acidosis. Echocardiogram revealed severe left ventricular systolic dysfunction. Severe myocardial depression with histopathological evidence of myocyte vacuolation and myocytolysis has been occasionally described with aluminium phosphide toxicity, primarily mediated by phosphine. The absence of an antidote makes the mortality high, once refractory shock ensues. Our patient succumbed to this condition. Zinc phosphide toxicity mediated by phosphine can have similar multisystem involvement, though dramatic electrocardiographic changes are uncommon.1 2 However, as evidenced by our report, ST segment elevation involving multiple leads on the ECG, though rare, maybe a hazardous manifestation...
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