Etiology

DKA results from insulin deficiency with a relative or absolute increase in glucagon and may be precipitated by inadequate insulin administration, infection (pneumonia, urinary tract infection, gastroenteritis, sepsis), infarction (cerebral, coronary, mesenteric, peripheral), surgery, trauma, drugs (cocaine), or pregnancy. A common clinical scenario is the pt with type 1 DM who erroneously stops administering insulin because of anorexia/lack of food intake caused by a minor illness, followed by lipolysis and progressive ketosis leading to DKA.

Clinical Features

The initial symptoms of DKA include anorexia, nausea, vomiting, polyuria, and thirst. Abdominal pain, altered mental function, or frank coma may ensue. Classic signs of DKA include Kussmaul respirations and an acetone odor on the pt's breath. Volume depletion can lead to dry mucous membranes, tachycardia, and hypotension. Fever and abdominal tenderness may also be present. Laboratory evaluation reveals hyperglycemia, ketosis (β-hydroxybutyrate > acetoacetate), and metabolic acidosis (arterial pH 6.8-7.3) with an increased anion gap (Table 25-1 Laboratory Values in DKA and HHS (Representative Ranges at Presentation)). The fluid deficit is often 3-5 L and can be greater. Despite a total-body potassium deficit, the serum potassium at presentation may be normal or mildly high as a result of acidosis. Similarly, phosphate may be normal at presentation despite total-body phosphate depletion. Leukocytosis, hypertriglyceridemia, and hyperlipoproteinemia are common. Hyperamylasemia is usually of salivary origin but may suggest a diagnosis of pancreatitis. The measured serum sodium is reduced as a consequence of osmotic fluid shifts due to hyperglycemia (1.6-meq reduction for each 5.6-mmol/L [100-mg/dL] rise in the serum glucose).