Alcoholic ketoacidosis - AKA



Background

  • Mobilisation of free fatty acids in association with ↑ liver capacity to convert these to ketones.
  • Two types ketones produced - acetoacetate and ß-hydroxybutyrate.
  • With alcohol metabolism there is an overall decrease in available NAD.
  • In AKA - NAD dependent hepatic oxidation of free fatty acids is switched to ketone formation.
  • Associated fall in Insulin, rise in cortisol, growth hormone, glucagon and epinephrine.

Beware

Our urinary dip sticks only measure acetoacetate (in reaction with nitroprusside on stick).

Dip stick may be negative for ketones in.

  • Alcoholic ketoacidosis
  • Severely shocked DKA( no peripheral conversion of ß-hydroxybutyrate to acetoacetate.

Clinical

History

  • Binge drinking & reduced food intake for days
  • Nausea & vomiting
  • Abdominal pain

Clinical findings

  • Most patients alert (rarely coma).
  • Tachypnoeic.
  • Possible concurrent sepsis etc.
  • Blood alcohol undetectable.
  • ABGs show a high anion gap acidosis (DDx).
  • Glucosuria absent.

Differential Dx

  • High anion gap acidosis (link)
  • Very unwell DKA

Treatment

  • Thiamine ( ? Wernicke Korsakoff).
  • Salin.e
  • Glucose
    • Glucose stimulates insulin release, inhibiting lipolysis and so stops ketone production.

Content by Dr Íomhar O' Sullivan 14/10/2002. Reviewed by Dr ÍOS 18/05/2005, 22/05/2006, 21/03/2007. Last review Dr. ÍOS 19/09/14.