This review summarizes the current therapeutic approach to diabetic ketoacidosis and hyperosmolar coma. The focus is on emergency treatment and intensive care management, particularly with regard to volume substitution, insulin therapy and potassium replacement. The basic concepts of low and very low insulin therapy are presented, with special emphasis on the pathogenesis and avoidance of the disequilibrium syndrome. Furthermore, the indications for bicarbonate therapy as well as phosphate and magnesium replacement in diabetic ketoacidosis are discussed.
Until the introduction of substitution therapy with insulin in the 1920s, the diabetic coma was the inevitable cause of death for all patients with type 1 diabetes mellitus and for many patients with type 2 diabetes. During the following decades, high-dose insulin therapy was wide-spread. Today, therapy of diabetic ketoacidosis is differentiated with the combination of low dose of insulin and avoidance of disequilibrium syndrome by limited and controlled reconciliation of electrolytes and fluid.
Katsch (1) gave the first recommendation for a differentiated application of a smaller dose of insulin, which has been the standard therapy in many countries for about the last 30 years (2). The association of the development of early recognition with controlled management has greatly reduced mortality.
In general, one can see the incidence of coma diabeticum as an indicator for the quality of early recognition and quality of diabetes therapy in our countries. In Germany about 5 to 12.5 per 1000 patients with diabetes mellitus (type 1 and type 2) are admitted to the hospital because of coma diabeticum (3).
In a review of more than 100 childrens hospitals in Germany, about 19% of patients had a first manifestation of type 1 diabetes with diabetic ketoacidosis (4). Besides coma as a clinical manifestation of disease, specific situations can be a trigger, which are summarized in Table 1.
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