Alcoholic Ketoacidosis (AKA)

Epidemiology

  • Heavy ETOH use with minimal food intake

Etiology

  • ETOH ingestion

Physiology

  • Accumulation of Mostly ß-Hydroxybutyrate: which is eventually converted to acetoacetic acid

Diagnosis

Ethanol Level

  • xxxx

  • Anion Gap: usually >20
    Osmolal Gap: increased
    Serum Ketones: positive

Acetest/Ketostix (Nitroprusside reaction only detects acetoacetic acid and acetone): may be negative or only weakly positive

Serum Potassium: normal
-NOTE: ketoacidosis (unlike inorganic acidoses) does not cause hyperkalemia


Clinical Manifestations

Neurologic Manifestations

  • Depressed Mental Status (see Coma-Obtundation, [[Coma-Obtundation]])
  • Normal Mental Status

Renal Manifestations

Anion Gap Metabolic Acidosis (AGMA) (see Metabolic Acidosis-Elevated Anion Gap, [[Metabolic Acidosis-Elevated Anion Gap]])

  • Physiology:
  • Clinical
    • Delta Gap/Delta Bicarbonate Ratio: around 1.1

Ketosis

  • Diagnosis
    • ß-Hydroxybutyrate: detected

Elevated Osmolal Gap (see Serum Osmolality, [[Serum Osmolality]])

  • Physiology
    • Presence of the low molecular weight osmotically-active solute, ethanol
    • Persistence of osmotically-active acetone after ethanol is metabolized
  • Clinical: may produce a large osmolal gap (>20 mOsm/L)

Other Manifestations

  • xxxx

Treatment

  • Supportive Care

References

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