Alcoholic ketoacidosis


  • 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

  • Nausea (75%)
  • Vomiting (73%)
  • Abdominal pain (62%)
  • Typically, history of binge drinking ending in nausea, vomiting, and decreased intake
  • Not hyperosmolar as opposed to DKA

Differential Diagnosis

Ethanol related disease processes


  • Labs
    • Anion gap acidosis
      • Typically wide anion gap
      • Positive serum ketones + lactic acidosis
        • Lab measured ketone is acetoacetate
        • May miss beta-hydroxybutyrate
        • Urine ketones may be falsely negative or low
    • Typically normal osmolal gap
    • Alcohol level usually zero or not considerably high
    • BMP, Mg/phos
  • ECG
    • May show dysrhythmias or QT interval/QRS changes secondary to electrolyte abnormalities
  • Imaging
    • Consider CXR if concern for aspiration pneumonia
    • Consider CT head if presentation associated with trauma


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


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

See Also

External Links


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