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Diabetic ketoacidosis (DKA) is a critical state of hyperglycemia that results in both hyperketonemia and acidosis. Despite elevated serum glucose in DKA, the cells are “starving” due to the lack of insulin to facilitate glucose uptake. Therefore, fatty acids are utilized, which produce ketones and an anion gap ketoacidosis.
Hyperglycemia causes glucose to spill into the urine, resulting in an osmotic diuresis that leads to dehydration and electrolyte derangements. The acidosis causes K+ to shift out of cells, leading to serum hyperkalemia. K+ and bicarbonate are lost in the urine, depleting whole body potassium. The loss of bicarbonate further exacerbates the acidosis.
This chapter discusses the diagnosis, evaluation and management of diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). The classic symptoms of hyperglycemia include polyuria, polydipsia, polyphagia, dizziness, weakness, abdominal pain, nausea, vomiting and altered mental status. Treatment of presumed DKA should begin with rehydration and evaluation for precipitating cause in the setting of a high glucometer reading. Further treatment often awaits laboratory results. HHS is sometimes the result of a precipitating stressor like infection, myocardial infarction, or stroke. In HHS it is believed that the body produces enough insulin to prevent ketoacidosis; however, the state of severe hyperglycemia continues to result in osmotic diuresis, hyperosmolar state, and electrolyte abnormalities. Hypoglycemia can occur as a result of overcorrection of hyperglycemia with insulin drip. Cerebral edema may occur as a result of rapid fluid shifts, particularly in the pediatric population.