Chapter 130. Alcoholic Ketoacidosis

Alcoholic ketoacidosis (AKA) results from heavy alcohol intake, either acute or chronic, and lack of food intake. Glycogen stores are depleted. Alcohol consumption along with the body's fat metabolism generatesketoacids, with a resultant anion gap metabolic acidosis.

The patient typically presents with nausea, vomiting, orthostasis, and abdominal pain 24 to 72 hours after the last alcohol intake. On examination, the patient appears acutely ill and dehydrated. Abdominal tenderness is diffuse and nonspecific or is the result of other causes related to alcohol, such as gastritis, hepatitis, or pancreatitis.

Laboratory investigation reveals an anion gap metabolic acidosis. However, the serum pH may vary as these patients often have mixed acid-basedisorders such as a metabolic acidosis from AKA and a metabolic alkalosis from vomiting and dehydration. Blood glucose is low to mildly elevated. The alcohol level is usually low or 0 as symptoms limit intake. Serum ketones, acetoacetate, and β-hydroxybutyrate, are elevated. If the nitroprusside test is used to measure serum and urine ketones, acetoacetate is detected but not β-hydroxybutyrate. The redox state may be such that most or all acetoacetate is reduced to β-hydroxybutyrate, which may result in a false negative or falsely low result.

Diagnostic criteria for AKA are listed in Table 130-1. The differential diagnosis of an anion gap metabolic acidosis is listed in Table 130-2.

1. Administer D5NS. The isotonic crystalloid solution restores intravascular volume. The glucose stimulates the patient's endogenous insulin release, which inhibits ketosis. Unlike treatment for DKA, insulin administration is not necessary.

2. Thiamine 100 milligrams IV before glucose administration may prevent precipitation of Wernicke disease.

3. Supplement other electrolytes and vitamins as warranted.

4. Continue treatment until the acidosis clears, which is usually within 12 to 24 hours.