Major advances in the treatment of diabetic ketoacidosis have been made since the institution of insulin therapy, but mortality remains high, 5-10%, because of associated medical conditions. Both insulin deficiency and insulin resistance contribute to the decompensated metabolic state. Increased circulating levels of counterregulatory hormones (epinephrine, norepinephrine, glucagon, cortisol, growth hormone) and substrates (free fatty acids, amino acids) electrolyte depletion, hypertonicity, and metabolic acidosis, all contribute to the defect in insulin action. Hyperglycemia and hyperketonemia are related to the marked stimulation of hepatic glucose production and ketogenesis, respectively, in the presence of impaired glucose and ketone uptake by peripheral tissues. The clinical manifestations in patients with diabetic ketoacidosis are related to the marked osmotic diuresis that results in major electrolyte and fluid losses, intracellular dehydration secondary to hyperglycemia, and metabolic acidosis. The cornerstone of medical management remains insulin in combination with appropriate fluid, sodium, and potassium replacement. Routine parenteral bicarbonate and phosphate therapy are not indicated and specific indications for their use are discussed.
|Original language||English (US)|
|Number of pages||30|
|State||Published - Jan 1 1994|
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism