Berger W
Abteilung Endokrinologie, Kantonsspital Basel.
Praxis (Bern 1994). 1997 Feb 18;86(8):308-13.
Based on case reports pathogenesis and treatment of the following diabetic emergencies were discussed: 1. The hyperosmolar non-ketotic coma without or with only modest ketosis occurring mainly in type II diabetics and the severe ketoacidosis with or without disturbed consciousness occurring mainly in type I diabetics are the two forms of severe metabolic decompensation of diabetes mellitus. 2. Severe hypoglycaemia may be caused by treatment with sulfonylureas and insulin. 3. The most dangerous life threatening adverse effect of biguanides is lactic acidosis. The incidence of ketoacidosis is about 1-5% in type I diabetics with a mortality of 3-9%. Mortality rates of hyperosmolar non-ketotic comas are much higher, approaching 20-40%, and are explained by severe concomitant complications and older age. The most important triggering factors of diabetic coma are infections, insulin dispensing errors and non-compliance. Carefully instructing patients about the risks of loosing appetite and vomiting as early signs of ketoacidosis is essential. Adequate replacement of fluid, electrolyte and water are the most important therapeutical aspects of ketoacidosis and hyperosmolar non-ketotic coma. Early diagnosis and appropriate treatment of infection by antibiotics are important. Complication of therapy (hypokalemia, hypovolemia and rapid full of oncotic pressure) should be avoided by clinical and laboratory monitoring. Treatment of acidosis with bicarbonate has been found more dangerous than useful. Severe hypoglycaemia is the most important and most dangerous side effect of sulfonylurea and insulin. The incidence of severe hypoglycaemia under glibenclamide ist 3-5 fold higher than under treatment with tolbutamide or glibornurid. Glibenclamide should not be recommended anymore. Longterm experience of the therapeutic security of new sulfonylurea derivates like glimepirid is lacking. Blood-glucose-measurements in the afternoon are important for recognizing disposition to sulfonylurea hypoglycaemia, because at this time the blood-glucose-values tend to be lower than in the morning fasting state. Under insulin treatment the following risk factors for severe hypoglycaemia need to be considered: metabolic control in the near normal range, intensified treatment with rapidly decreasing HbA1c-levels, impaired renal function, unawareness o hypoglycaemia. When the renal function is impaired, biguanide treatment is not indicated because of the risk of lactic acidosis. Most of the diabetic emergency situations are avoidable by proper education of the patients.
基于病例报告,讨论了以下糖尿病急症的发病机制和治疗方法:1. 高渗非酮症昏迷,无酮症或仅有轻度酮症,主要发生于II型糖尿病患者;严重酮症酸中毒,伴有或不伴有意识障碍,主要发生于I型糖尿病患者,这是糖尿病严重代谢失代偿的两种形式。2. 严重低血糖可能由磺脲类药物和胰岛素治疗引起。3. 双胍类药物最危险的危及生命的不良反应是乳酸性酸中毒。I型糖尿病患者酮症酸中毒的发生率约为1 - 5%,死亡率为3 - 9%。高渗非酮症昏迷的死亡率要高得多,接近20 - 40%,这是由严重的伴随并发症和患者年龄较大所致。糖尿病昏迷最重要的触发因素是感染、胰岛素给药错误和不遵医嘱。仔细告知患者食欲不振和呕吐作为酮症酸中毒早期症状的风险至关重要。充分补充液体、电解质和水分是酮症酸中毒和高渗非酮症昏迷最重要的治疗方面。早期用抗生素诊断和适当治疗感染很重要。应通过临床和实验室监测避免治疗并发症(低钾血症、低血容量和快速充盈胶体渗透压)。用碳酸氢盐治疗酸中毒已被发现弊大于利。严重低血糖是磺脲类药物和胰岛素最重要、最危险的副作用。使用格列本脲时严重低血糖的发生率比使用甲苯磺丁脲或格列波脲治疗时高3 - 5倍。不应再推荐使用格列本脲。缺乏关于新的磺脲类衍生物如格列美脲治疗安全性的长期经验。下午测量血糖对于识别磺脲类药物低血糖倾向很重要,因为此时血糖值往往低于早晨空腹状态。在胰岛素治疗下,需要考虑以下严重低血糖的危险因素:代谢控制接近正常范围、强化治疗导致糖化血红蛋白水平快速下降、肾功能受损、低血糖无意识。当肾功能受损时,由于存在乳酸性酸中毒风险,不建议使用双胍类药物治疗。通过对患者进行适当教育,大多数糖尿病急症情况是可以避免的。