Diagnosis is made in the appropriate clinical setting and is based on laboratory evaluation. Laboratory evaluation should include CBC; electrolyte panel with calcium, phosphate, and magnesium; ethanol, methanol, and isopropyl alcohol levels; hepatic enzymes; lipase; and serum ketones. Determination of serum lactic acid level and serum osmolality also may be helpful. Diagnosis is made by the criteria listed in Table 221-1, with metabolic acidosis, positive serum ketones, elevated anion gap, and a low or mildly elevated serum glucose level. Patients frequently have hypophosphatemia, hyponatremia, and/or hypokalemia. Most patients also will have elevated bilirubin and liver enzyme levels due to liver disease from a long history of chronic ethanol use. BUN levels frequently are elevated due to relative volume depletion. The nitroprusside reagent used to measure urine and serum ketones measures acetoacetate. Acetone is weakly reactive, and βHB is not detected at all. So, the initial ketone levels may be low or negative in alcoholic ketoacidosis. With recovery, acetoacetate increases and assays become positive.1 A small to moderate anion gap is invariable in alcoholic ketoacidosis. Without routine evaluation of the anion gap in every patient at risk for alcoholic ketoacidosis, the diagnosis can be easily missed. The anion gap is usually 16 to 33, with a mean of 21,2 and is due to ketonemia, primarily from βHB. The osmolal gap may be slightly elevated because acetone and its metabolites cause an osmolal gap (<20 mmol/kg).1 Consider co-ingestions or other causes of anion gap acidosis if the anion gap fails to close with ongoing treatment. Mild lactic acidosis may be present due to a shift to pyruvate metabolism toward lactate1.