Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment.

Diabetic ketoacidosis: new concepts and trends in pathogenesis and treatment.
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DOI:
10.7326/0003-4819-88-5-681
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发表时间:
1978-05
影响因子:
39.2
通讯作者:
R. Kreisberg
R. Kreisberg
中科院分区:
医学1区
文献类型:
--
作者:
R. Kreisberg

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综述了糖尿病酮症酸中毒发病机制和治疗的新概念。总结了肝内酶过程对酮生成的调节以及胰岛素缺乏或胰高血糖素或其他反调节激素过量的作用。主要重点是分析使用低剂量胰岛素治疗酮症酸中毒的方案。大多数糖尿病酮症酸中毒患者会对低剂量、每小时、静脉注射或肌内注射常规胰岛素有反应。低剂量的胰岛素与高剂量的胰岛素一样有效,并且低血糖和低钾血症的相关并发症较少。磷缺乏在糖尿病酮症酸中毒中很常见,低磷血症通常在开始治疗后 4 至 12 小时内变得明显。现在普遍建议补充磷来补充红细胞2,3-二磷酸甘油酸并改善组织的氧输送。共存且具有生化意义的乳酸性酸中毒是糖尿病酮症酸中毒相对罕见的并发症,如果出现,通常是由于与组织灌注不良相关的潜在疾病所致。
New concepts concerning the pathogenesis and therapy of diabetic ketoacidosis are reviewed. The regulation of ketogenesis by intrahepatic enzymic processes and the roles of insulin deficiency or glucagon or other counterregulatory hormone excess are summarized. Major emphasis is placed on an analysis of the use of low-dose insulin regimens for the treatment of ketoacidosis. Most patients with diabetic ketoacidosis will respond to low-dose, hourly, intravenous or intramuscular regular insulin. Low doses of insulin are as effective as high doses and have fewer associated complications of hypoglycemia and hypokalemia. Phosphorus deficiency is common in diabetic ketoacidosis and hypophosphatemia usually becomes manifest within 4 to 12 h of institution of therapy. Phosphorus supplementation is now generally recommended to replete erythrocyte 2,3-diphosphoglycerate and improve oxygen delivery to tissues. Coexistent and biochemically significant lactic acidosis is a relatively infrequent complication of diabetic ketoacidosis and when present is usually due to underlying disorders associated with poor tissue perfusion.