Alcoholic ketoacidosis

Revision as of 11:11, 1 September 2019 by Beren85 (talk | contribs) (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 (toxic alcohols, salicylates)
    • Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found


  • Ethanol metabolism depletes NAD stores[1]
    • Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
    • Suppresses gluconeogenesis and may result in hypoglycemia
    • 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
AKA crashingpatient.JPG

Clinical Features

Differential Diagnosis

Ethanol related disease processes


  • 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
  • Typically normal osmolal gap
  • Alcohol level usually zero or not considerably high


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


  • 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


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