Scorpion-related cardiomyopathy: Clinical characteristics, pathophysiology, and treatment

Context. Scorpion envenomation is a threat to more than 2 billion people worldwide with an annual sting number exceeding one million. Acute heart failure presenting as cardiogenic shock or pulmonary edema, or both is the most severe presentation of scorpion envenomation accounting for 0.27% lethality rate. Objective. The purpose of this review is to characterize the scorpion-related cardiomyopathy, clarify its pathophysiological mechanisms, and describe potentially useful treatments in this particular context. Methods. We searched major databases on observational or interventional studies (whether clinical or experimental) on the cardiorespiratory consequences of scorpion envenomation and their treatment. No limit of age or language was imposed. A critical appraisal of the literature was conducted in order to provide a pathophysiological scheme that reconciles reported patterns of cardiovascular toxicity and hypotheses and assumptions made so far. Results. Early cardiovascular dysfunction is related to the so-called vascular phase of scorpion envenomation, which is related to a profound catecholamine-related vasoconstriction leading to a sharp increase in left ventricular (LV) afterload, thereby impeding LV emptying, and increasing LV filling pressure. Following this vascular phase, a myocardial phase occurs, characterized by a striking alteration in LV contractility (myocardial stunning), low cardiac output, and hypotensive state. The right ventricle involvement is symmetric to that of LV with a profound and reversible alteration in right ventricular performance. This phase is unique in that it is reversible spontaneously or under inotropic treatment. Scorpion myocardiopathy combines the features of takotsubo myocardiopathy (or stress myocardiopathy) which is linked to a massive release in catecholamines leading to myocardial ischemia through coronary vasomotor abnormalities (epicardial coronary spasm and/or increase in coronary microvascular resistance). Treatment of pulmonary edema due to scorpion envenomation follows the same principles as those applied for the treatment of cardiogenic pulmonary edema in general: this begins with oxygen supplementation targeting an oxygen saturation of 92% or more, by oxygen mask, continuous positive airway pressure, noninvasive ventilation, or conventional mechanical ventilation. Dobutamine effectively improves hemodynamic parameters and may reduce mortality in severe scorpion envenomation. Conclusion. Scorpion cardiomyopathy is characterized by a marked and reversible alteration in biventricular performance. Supportive treatment relying on ventilatory support and dobutamine infusion is a bridge toward recovery in the majority of patients.