Alcoholic ketoacidosis

Revision as of 00:20, 28 September 2011 by Jswartz (talk | contribs)

Background

  • Anion gap met acidosis a/w acute cessation of ETOH consumption after chronic abuse
  • Pathophysiology
    • Ethanol metabolism depletes NAD stores
      • Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
      • 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

Clinical Features

  • Nausea (75%)
  • Vomiting (73%)
  • Abdominal pain (62%)

Diagnosis

  • 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

DDX

  1. Isopropyl alcohol
    1. Results in ketosis
  2. Methanol, ethylene glycol
    1. Do not produce ketosis
  3. Sepsis
  4. Salicylate ingestion
  5. DKA
  6. Starvation ketosis
  7. Uremia

Treatment

  1. Thiamine 100mg IV
  2. D5NS
    1. Glucose stimulates insulin which stops lipolysis
  3. Electrolyte repletion

Disposition

  • Discharge home if resolution of acidosis and pt is able to tolerate PO

Source

Tintinalli