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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 226-1, 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.
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DIFFERENTIAL DIAGNOSIS
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Table 226-2 and chapter 15, Acid-Base Disorders, list the most important causes of metabolic acidosis that should be excluded to diagnose alcoholic ketoacidosis.
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Alcoholic ketoacidosis should be differentiated from other alcohol ingestions. Methanol and ethylene glycol ingestions do not produce ketosis, and acidosis tends to be severe. Isopropyl alcohol ingestion results in production of ketones. The presence of a large osmolal gap suggests acute isopropyl, ethanol, methanol, or ethylene glycol ingestion. If the blood alcohol level is known, then its contribution to any osmolal gap can be calculated. Each 100 milligrams/dL (21.7 mmol/L) of ethanol raises the osmolal gap by 22. Details of osmolal gap are discussed in chapter 17, Fluids and Electrolytes.
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The presence of a mixed acid-base disturbance suggests a comorbid disorder. Common concurrent illnesses are dehydration and electrolyte disturbances from vomiting and reduced intake, pancreatitis, gastritis or upper GI bleeding, seizures, alcohol withdrawal, pneumonia, sepsis, and hepatitis.
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Starvation ketosis occurs in patients with diminished carbohydrate intake, resulting in lipolysis and ketonuria. Ketone bodies appear after about 3 days of fasting but can appear earlier in the presence of stress and dehydration. Metabolic acidosis and ketonemia are rare in starvation ketosis, but ketonuria is common.7