Epidemiology

• Heavy ETOH use with minimal food intake

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Etiology

• ETOH ingestion

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Physiology

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

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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

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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

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Treatment

• Supportive Care

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References

• xxx