Death caused by scorpion envenoming (Buthidae family) is a common event in tropical and subtropical countries. Severe scorpion envenoming causes an autonomic storm resulting in a massive release of catecholamines, angiotensin II, glucagon, cortisol, and changes in insulin secretion. As a consequence of these changes in the hormonal milieu, scorpion envenoming results in a syndrome of fuel energy deficits and an inability of the vital organs to utilize the existing metabolic substrates, which causes myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary oedema, and many other clinical manifestations alone or in combination, producing multi-system-organ-failure (MSOF) and death. Insulin-glucose infusion or antivenom administration through the release of insulin seems to be the physiological basis for the control of the metabolic response when that has become a determinant to survival of scorpion sting victims

The efficacy of insulin-glucose infusion in reversing myocardial damage, haemodynamic changes, peripheral circulatory failure, and pulmonary oedema was evaluated in 25 victims of venomous scorpion stings from the Rayalaseema region in the south of India. Myocardial damage with peripheral circulatory failure was seen in all scorpion sting victims. Ten of these victims also had pulmonary oedema. All the patients received continuous infusion of regular crystalline insulin at the rate of 0.3 U/g of glucose and glucose at the rate of 0.1 g/kg/h with supplementary potassium as needed, inotropic agents, oxygen, as well as maintenance of fluid, electrolytes and acid-base balance. Insulin-glucose infusion was associated with reversal of cardiovascular and haemodynamic changes, and pulmonary oedema in 24 of the 25 victims. One severely envenomed victim admitted 72 hours after the sting died. The scorpion envenoming syndrome with myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary oedema, and many other clinical manifestations may cause multi-system organ failure (MSOF). It is characterised by a massive release of catecholamines, angiotensin II, glucagon, cortisol, and inhibition of insulin secretion. Under these altered conditions in the hormonal milieu, scorpion envenoming essentially results in a syndrome of fuel-energy deficits and an inability to use the existing metabolic substrates by vital organs, causing MSOF and death. 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

Acute myocarditis is produced in rabbits with scorpion (Buthus tamulus) (a common scorpion found in South India) venom. Acute myocarditis is confirmed by changes in the ECG taken before and after venom injection. The atrial and ventricular sarcolemmal Na+-K+ ATPase, Mg++ ATPase, and Ca++ ATPase activities are assayed in control and venom injected rabbits. Atrial and ventricular sarcolemmal ATPase activities are similar in control animals. A significant reduction in atrial Ca++ ATPase activity is seen in venom treated rabbits. Animals injected with 2mg/Kg venom exhibited significant increases in Mg++ ATPase and Ca++ ATPase activities in the ventricular sarcolemma. However, significant reductions in Na+-K+ ATPase and Ca++ ATPase activities are observed in ventricular tissue from rabbits treated with 4mg/ Kg of venom.

Severe envenoming was induced in two groups of experimental dogs after subcutaneous (SQ) injection of venom of the scorpion (Mesobuthus tamulus concanesis, Pocock) (3.0 and 3.5 mg/kg body weight). The circulating levels of blood sugar, insulin, glucagon, and cortisol were assayed at 0, and 30, 60, 90 and 120 min after venom injection. There was an increase in the circulating levels of blood sugar, insulin, glucagon, and cortisol following envenoming. Scorpion envenoming causes an autonomic storm resulting in a massive release of catecholamines, angiotensin II, glucagon, and cortisol accompanied by changes in insulin secretion. The rise in the counter-regulatory hormones (glucagon, cortisol, and catecholamines) oppose the anabolic actions of insulin resulting in a variety of clinical manifestations. These changes may lead to a syndrome of fuel-energy deficits and to an inability of the vital organs to utilise the existing metabolic substrates, ultimately resulting in multisystem organ failure (MSOF) and death

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