Alcoholic ketoacidosis

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Background

  • Seen in patients with recent history of binge drinking with little/no nutritional intake
  • Anion gap metabolic acidosis associated with acute cessation of ETOH consumption after chronic abuse
  • Characterized by high serum ketone levels and an elevated AG
    • Consider other causes of elevated AG, as well as co-ingestants
    • Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis

Pathophysiology

  • Ethanol metabolism depletes NAD stores[1]
    • Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
    • High NADH:NAD also results in increased lactate production
      • Lactate higher than normal but not as high as in shock or sepsis
    • Acetoacetate is metabolized to acetone so elevated osmolal gap may also be seen
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Clinical Features

Differential Diagnosis

Ethanol related disease processes

Evaluation

  • Binge drinking ending in nausea, vomiting, and decreased intake
  • Wide anion gap metabolic acidosis (ketonemia, lactic acidosis)
  • Positive serum ketones
  • Wide anion gap metabolic acidosis without alternate explanation
  • Urine ketones may be falsely negative or low
    • Lab measured ketone is acetoacetate
    • May miss beta-hydroxybutyrate

Management

Consider associated diseases (ie pancreatitis, rhabdomyolysis, hepatitis, infections)

Disposition

  • Discharge home after treatment if able to tolerate POs and acidosis resolved
  • Consider admission for those with severe volume depletion and/or acidosis
  • Hypoglycemia is poor prognostic feature, indicating depleted glycogen stores

See Also

References

  1. McGuire LC, Cruickshank AM, Munro PT. Alcoholic ketoacidosis. Emerg Med J. 2006 Jun;23(6):417-20.