TREATMENT OF DIABETIC-KETOACIDOSIS AND NONKETOTIC HYPEROSMOLAR DIABETIC COMA

Although mortality of diabetic ketoacidosis (KA) has decreased during the past 20yr to 1-2%, hyperosmolar non-ketotic coma (HNC) is still lethal in 20-30% of cases due to severe underlying conditions or to complications. The most frequent causes of death are infections and thromboembolic disorders. The strategies of initial treatment of KA and HNC are similar; in KA, insulin, fluid and electrolyte replacement have first priority. In HNC, rehydration and electrolyte administration are of primary importance. It is now generally recognized that insulin therapy is best performed using low doses (4-8 units/h); after institution of insulin treatment and rehydration there are rapid changes of fluid and electrolytes from the extra- into the intravascular space. In this situation it is a major therapeutic challenge to avoid complications due to hypokalaemia, hypophosphataemia, hypomagnesiaemia and hypovolaemia. These complications should be avoided by adequate replacement, and particularly by regular clinical and laboratory monitoring. When blood glucose concentrations decrease below 14 mmol/l, blood glucose concentrations should initially be maintained at this level because rapid lowering below this level may increase the risk of brain oedema. Too-vigorous fluid replacement with crystalline solutions also increases the risk that brian oedema or complications like the adult respiratory distress syndrome will develop. If hypovolaemia persists in spite of adequate crystalloid solutions, colloid-containing fluids such as albumin should be administered. It is not established whether replacements of phosphate and magnesium have clinical benefits. Nevertheless, it is probably justified to administer phosphate and magnesium when their serum concentrations are below the normal range, particularly if the clinical situation is critical. Mortality from diabetic coma in industrialized countries may only be decreased by prophylaxis, i.e. by education of all diabetic patients and physicians to detect metabolic decompensation early. © 1992 Baillière Tindall.