Seen in patients with recent history of binge drinking with little/no nutritional intake
Anion gap metabolic acidosis associated with acute cessation of EtOH consumption after chronic abuse
Characterized by high serum ketone levels and an elevated AG
Consider other causes of elevated AG, as well as co-ingestants (toxic alcohols, salicylates)
Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found
Consider other causes of elevated AG, as well as co-ingestants (toxic alcohols, salicylates)
Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis, so a normal blood pH may be found
Ethanol metabolism depletes NAD stores
Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
Suppresses gluconeogenesis and may result in hypoglycemia
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
Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation
Suppresses gluconeogenesis and may result in hypoglycemia
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
Lactate higher than normal but not as high as in shock or sepsis
Alcoholic ketoacidosis
Isopropyl Alcohol
Diabetic ketoacidosis 
Results in ketosis
Diabetic ketoacidosis
Methanol, Ethylene Glycol
Starvation ketoacidosis
Do not produce ketosis