Abstract
Acute pulmonary edema due to scorpion toxins has been attributed to acute left ventricular failure resulting from massive catecholamine release or myocardial damage induced by the venom. 1–3 It has been proposed that pulmonary edema could also result from increased pulmonary vascular permeability produced by vasoactive substances that may be released by the venom. 4 This report presents radiologic, electrocardiographic, enzymatic, echocardiographic and histopathologic evidence that support both cardiogenic and noncardiogenic factors in the pathogenesis of acute pulmonary edema after Tityus serrulatus scorpion sting in children.
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