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Alcoholic ketoacidosis usually occurs in advanced alcoholism when the majority of calories come from alcohol. Ketoacidosis develops due to the combined effects of inadequate carbohydrate intake, ethanol conversion to acetic acid and stimulated lipolysis. Ketoacidosis may be precipitated by decreased intake, pancreatitis, gastrointestinal bleeding, or infection and may be profound. The plasma glucose level is typically normal to low. (Significant elevations suggest concomitant DKA.) It is important to consider other causes of metabolic acidosis in alcoholic patients with acidosis. First, patients with alcoholic ketoacidosis often have concomitant lactic acidosis. Shock and hypoxia should be carefully considered. Lactic acidosis may also occur due to an increase in NADH levels and can be particularly severe in patients with thiamine deficiency. Second, toxic ingestions (methanol, ethylene glycol, or salicylate) should also be considered, especially in patients with a large osmolar gap. (The osmolar gap = measured serum osmolality – calculated serum osmolality. The calculated osmolality = (2 × Na+) + Glucose (mg/dL)/18 + BUN (mg/dL)/2.8) + ETOH (mg/dL)/3.7. A normal osmolar gap < 10 mOsm/kg.) The treatment for alcoholic ketoacidosis should include IV thiamine prior to IV glucose to avoid precipitating Wernicke encephalopathy or Korsakoff syndrome.

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