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English Wikipedia
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Selected developments in the understanding of diabetic ketoacidosis Kandel G; Aberman ACan Med Assoc J 1983[Feb]; 128 (4): 392-7Advances in the understanding of diabetic ketoacidosis have contributed to the recent decrease in the morbidity and mortality associated with this condition. The role of counterregulatory hormones in its pathogenesis is considerable, but insulin deficiency is necessary for diabetic ketoacidosis to develop. Therapy begins with identification and treatment of the factors precipitating ketosis. Isotonic saline is the fluid of choice for initial intravenous therapy; subsequently 0.45% saline is appropriate. Sodium bicarbonate is necessary only if the arterial pH is less than 7.1, and phosphate should be given only when the serum phosphate level is below 0.5 mg/dl (0.16 mmol/l). Factors other than pH are important in causing the hyperkalemia so commonly seen at the time of presentation, but whether or not hyperkalemia is present potassium supplementation is almost always necessary and should be given as long as the urinary output is adequate. Intravenous doses of insulin as low as 5 to 15 U/h are sufficient in most cases, but the occasional patient will require larger amounts. Close clinical and biochemical monitoring is necessary for successful management.|Adult[MESH]|Brain Edema/etiology[MESH]|Child[MESH]|Consciousness Disorders/metabolism[MESH]|Diabetes Mellitus/*metabolism[MESH]|Diabetic Ketoacidosis/complications/*therapy[MESH]|Gastric Dilatation/therapy[MESH]|Glomerular Filtration Rate[MESH]|Humans[MESH]|Hyperglycemia/complications[MESH]|Hyperkalemia/etiology[MESH]|Hyperventilation/etiology[MESH]|Hypophosphatasia/etiology[MESH]|Insulin/therapeutic use[MESH]|Liver/metabolism[MESH]|Mitochondria/metabolism[MESH]|Osmolar Concentration[MESH]|Respiratory Tract Infections/complications[MESH]|Suction[MESH]|Thrombosis/etiology[MESH] |
