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 (toxic alcohols, salicylates)
    • Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found

Pathophysiology

  • 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

Evaluation

  • 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

Management

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

Disposition

  • 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

References

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