Alcoholic Ketoacidosis

In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration.[1, 2]

Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages. Patients typically have a recent history of binge drinking, little or no food intake, and persistent vomiting.[3, 4, 5] A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup).[6]

Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are:

Extracellular fluid volume depletion
Glycogen depletion
An elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+)
This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment).