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 & ↓ food for days
- Nausea & vomiting
- Abdominal pain
Examination
- Most patients alert (rarely coma)
- Tachypnoeic
- Possible concurrent sepsis etc
- Blood alcohol undetectable
- VBGs show a high anion gap acidosis (DDx)
- Glucosuria absent
Differential Dx
- High anion gap acidosis (link)
- DKA
Treatment
- Thiamine ( ? Wernicke Korsakoff)
- Saline
- Glucose - ↑ insulin release, ↓ lipolysis - so ↓ ketone production