Diabetic ketoacidosis insulin therapy

Hypersensitivity to sulfonylureas diabetes complicated by ketoacidosis, with or without coma sole therapy of type 1 (insulin-dependent) diabetes mellitus diabetes when complicated by pregnancy. 

For persons with type 1 diabetes, insulin replacement therapy is necessary to sustain life. Pharmacologic insulin is administered by injection into the subcutaneous tissue using a manual injection device or an insulin pump that continuously infuses insulin under the skin. Interruption of the insulin replacement therapy can be life-threatening and can result in diabetic ketoacidosis or death. Diabetic ketoacidosis is caused by insufficient or absent insulin and results from excess release of fatty acids and subsequent formation of toxic levels of ketoacids. 

However, short-acting, regular soluble insulin is the only type that should be administered intravenously because the dilution causes the hexameric insulin to immediately dissociate into monomers. It is particularly useful for intravenous therapy in the management of diabetic ketoacidosis and when the insulin requirement is changing rapidly, such as after surgery or during acute infections. 

Takaike H, Uchigata Y, Iwasaki N, Iwamoto Y. Transient elevation of liver transaminase after starting insulin therapy for diabetic acidosis or ketoacidosis in newly diagnosed type 1 diabetes mellitus. Diabetes Res Clin Pract 2004 64 27-32. 

Correct answer = C. Protamine complexes with insulin to form an insoluble complex that is slowly absorbed. Insulin is not administered orally because it is destroyed by proteases in the Gl tract. Diet therapy and/or sulfonylureas are often effective without additional insulin In the therapy of Type II diabetics. Ketoacidosis is the most life-threatening consequence of Type I diabetics and requires adequate treatment with insuiin, not sulfonylureas. Insulin acts by binding to specific receptors in the cell membrane, not in the nucleus. 

Wagner A, Risse A, Brill HL, et al. Therapy of severe diabetic ketoacidosis zero-mortality under very-low-dose insulin application. Diabetes Care 22 674-677,1999. 

CM was started on intravenous insulin, fluids, and electrolyte replenishment. Her nausea and vomiting resolved and, although initially, she required 60-70 units of insulin intravenously per day to attain glycaemic control, her blood glucose dropped to 7.4 mmol/L after 4 days of intensive care. However, despite treatment of her diabetic ketoacidosis, including significant rehydration therapy, CM was still found to have an elevated but stable serum creatinine of 246 micromol/L, and so she was transferred from the intensive care unit to the renal unit for further management. 

Rovira A, Cordido F, Vecilla C, Bernacer M, Valverde I, Herrera Pombo JL. Study of beta-cell function and erythrocyte insulin receptors in a patient with diabetic ketoacidosis associated with L-asparaginase therapy. Acta Paediatr Scand 1986 75(4) 670-1. 

Treatment is by correction of the cause of the acidosis (e.g., insulin administration in diabetic ketoacidosis) and neutralization of the acid with NaHCOs, sodium lactate, or TRIS [tris(hydroxymethyl)aminomethane] buffer. Problems that may occur following alkali replacement therapy include development of respiratory alkalosis, particularly if the low CO2 tension persists, and further decline in the pH of CSF, which may decrease consciousness. The alkaline overshoot results from resumption of oxidation of organic anions (e.g., lactate, acetoacetate) with resultant production of bicarbonate from CO2. Severe acidosis should be corrected slowly over several hours. Potassium replacement therapy frequently is needed because of the shift of intracellular K" " to extracellular fluid and loss of K+ in the urine. 

D-Fructose is the sweetest natural sugar. Its use as a natural sweetener is, therefore, increasing rapidly. It is absorbed slowly from the intestine, and thus does not cause abrupt changes in the serum levels of carbohydrates. It has little, if any, effect on insulin secretion. Thus, it exerts beneficial effects as a component of diets for mild and well-balanced diabetes, but should be taken within caloric restriction,445 as obesity impairs D-glucose tolerance and increases the insulin resistance of peripheral tissue.446 Use of D-fructose in the direct treatment of diabetic ketoacidosis does not offer advantages over routine, fluid therapy, and may even be dangerous on the basis that rapid infusion of large amounts of D-fructose may cause lactate acidosis. 

Keywords Diabetic ketoacidosis, hyperosmolar hyperglycemia, ketone bodies, glucose, insulin, fluid and electrolyte therapy. 

In three middle-aged patients, diabetes was diagnosed after 3-7 months of treatment with interferon alfa-2b and ribavirin, and two presented with severe ketoacidosis (534,535). There was a family history of diabetes in one patient and two had high titers of glutamic acid decarboxylase antibodies before treatment. One patient never had diabetes-related serum autoantibodies before or after interferon alfa therapy. All three required permanent insulin treatment despite withdrawal of interferon alfa. 

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