ACEM Fellowship
Alcoholic ketoacidosis

Alcoholic ketoacidosis

Introduction

  • HAGMA usually seen within 1-3 days of acute alcohol cessation on the background of chronic alcoholism
  • Often present with nausea, vomiting and GI complaints with dehydration
  • Alcohol metabolism in the absence of glycogen reserves results in ketonaemia

Pathophysiology

  • EtOH – Acetaldehyde – Acetate – AcetylCoA – Ketones/FFA/Krebs cycle
    • Requires NAD to NADH for first 2 steps
    • Requires Alcohol dehydrogenase for first step
    • Requires acetaldehyde dehydrogenase for second step
  • Thus, ethanol metabolism results in NAD depletion with high NADH:NAD ratio
  • Counter-regulatory hormones released in setting of glycogen depletion and concurrent illness
    • Inhibits aerobic metabolism and favors anaerobic metabolism and lipolysis, converting AcetylCoA to ketone bodies
  • NAD is used for conversion of beta-hydroxbutyrate to acetoacetate. Given NAD depletion, get predominance of betaHB (not picked up on urine ketostix)
  • Once NADH:NAD ratio returns to normal, lactate levels reduce and acetoacetate is increased
  • Acetoacetate is converted to acetone and can cause an osmolar gap
  • Ketone production also stimulated by malnourished, vomiting and hypophosphataemia (all seen in alcoholics)

Diagnosis

  • Criteria
    • Low, normal or slightly elevated glucose
    • Binge drinking ending in nausea, vomiting and decreased intake
    • Positive serum ketones (although absence on nitroprusside test may miss beta-hydroxbutyrate, which predominates)
    • HAGMA without alternative explanation
  • Always look for underlying precipitant illness
  • Almost always normal conscious state (if not, consider alternative diagnosis)

DDx

  • Lactic acidosis – Sepsis, hypotension, ethanol, methanol, isopropyl alcohol
  • Uraemia
  • Diabetic ketoacidosis
  • Starvation ketosis

Treatment

  • Thiamine 300mg IV BEFORE GLUCOSE
  • 5% dextrose in N/S
    • Glucose triggers insulin release and inhibits lipolysis to cease ketone production
    • Glucose increases oxidation of NADH to NAD, further stopping ketone formation
  • Cerebral oedema of little concern as not hyperosmolar
  • Insulin is of no proven benefit and may be dangerous given normal or low glucose levels and lack of glycogen stores in case of hypoglycaemia
  • Monitor phosphate levels
  • Consider multivitamins and magnesium supplementation

Last Updated on October 8, 2021 by Andrew Crofton