Murthy K Radha Krishna
Department of Physiology, Santhiram Medical College & Santhiram General Hospital, Nandyal.
J Indian Med Assoc. 2013 Apr;111(4):254-9.
Scorpion envenoming syndrome results in a severe autonomic storm with a massive release of catecholamines, increased levels of angiotensin II, an increase in glucagon, cortisol, thyroid hormones; either suppressed insulin levels or hyperinsulinaemia (insulin resistance), hyperglycaemia; increased circulating free fatty acid levels. These hormonal alterations could be responsible for the pathogenesis of a variety of clinical manifestations. Under these conditions, scorpion envenoming syndrome with myocardial damage, cardiovascular disturbances, peripheral circulatory failure, respiratory and cardiac pulmonary oedema, and many other clinical manifestations resulting in a syndrome of fuel-energy deficits and an inability to use the existing metabolic substrates by vital organs causing multisystem organ failure and death. Based on 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 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. The mordality of treatment is continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1g/kg body weight/hour, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance is required. This treatment should be given at the earliest on admission and continued for the next 48-72 hours. Antiscorpion serum could also be given independently or along with insulin-glucose infusion.
蝎螫伤综合征会引发严重的自主神经风暴,伴有儿茶酚胺大量释放、血管紧张素II水平升高、胰高血糖素、皮质醇、甲状腺激素增加;胰岛素水平要么被抑制,要么出现高胰岛素血症(胰岛素抵抗)、高血糖;循环中游离脂肪酸水平升高。这些激素变化可能是多种临床表现发病机制的原因。在这些情况下,蝎螫伤综合征会导致心肌损伤、心血管紊乱、外周循环衰竭、呼吸和心源性肺水肿以及许多其他临床表现,进而引发能量燃料缺乏综合征,重要器官无法利用现有的代谢底物,导致多系统器官衰竭和死亡。基于动物实验(其中胰岛素给药可逆转蝎螫伤诱导的代谢和心电图变化)以及用胰岛素治疗有毒蝎螫伤受害者的情况,我们认为胰岛素在预防和逆转蝎螫伤引起的心血管、血流动力学、神经学表现及肺水肿方面具有主要的代谢作用。对蝎螫伤受害者输注胰岛素 - 葡萄糖似乎是控制代谢反应的生理基础,而此时代谢反应已成为生存的决定因素。治疗方式是按0.3 U/g葡萄糖的速率持续输注正规结晶胰岛素,按0.1g/kg体重/小时的速率输注葡萄糖,根据需要补充钾,并维持液体、电解质和酸碱平衡。这种治疗应在入院后尽早开始,并持续48 - 72小时。抗蝎毒血清也可单独使用或与胰岛素 - 葡萄糖输注联合使用。