Cardiac Sarcolemmal Defects in Acute Myocarditis Due to Scorpion Envenoming Syndrome


Death due to scorpion envenoming syndrome is a common event in tropical and subtropical countries. Severe scorpion envenoming causes autonomic storm, massive release of catecholamines, counter-regulatory hormones, suppressed insulin/hyperinsulinemia, acute myocarditis, hyperglycemia, increased free fatty Acid levels, acute pancreatitis, disseminated intra-vascular coagulation, acute pulmonary oedema and death. Severe scorpion envenoming causes cardiac sarcolemmal defects displayed by alterations in Na+ - K+ ATPase, Mg++ ATPase and Ca2+ ATPase activities, inhibition of erythrocyte Na+ - K+ ATPase activities, hyperkalemia and may result in death. Based on our animal experiments in which insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming and treating the poisonous scorpion sting victims with insulin, we consider that insulin has a primary metabolic role in preventing and reversing acute myocarditis, the cardiovascular, haemodynamic, and neurological manifestations and pulmonary oedema induced by scorpion envenoming. Administration of insulin-glucose infusion to scorpion sting victims appears to be the physiological basis for the control of the metabolic response when that has become a determinant to survival. Continuous infusion of regular crystalline insulin should be given at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48 - 72 hours, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance. The observation of cardiac sarcolemmal defects and physiological basis of various patho-physiological mechanisms involved in the genesis of scorpion envenoming syndrome and its reversal (in the experimental animals and scorpion sting victims) by administration of insulin are reviewed.

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Murthy, K. (2014) Cardiac Sarcolemmal Defects in Acute Myocarditis Due to Scorpion Envenoming Syndrome. World Journal of Cardiovascular Diseases, 4, 432-454. doi: 10.4236/wjcd.2014.49054.

Conflicts of Interest

The authors declare no conflicts of interest.


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