Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android


Alcoholic ketoacidosis (AKA) results from heavy alcohol intake, either acute or chronic. Glycogen stores are depleted, activating lipolysis to supply energy. Lipolysis and alcohol metabolism generate ketoacids, causing an anion gap metabolic acidosis.


The patient typically presents with nausea, vomiting, and abdominal pain after heavy alcohol intake. The patient appears acutely ill, dehydrated, and has abdominal tenderness that is nonspecific or is the result of other causes related to alcohol, such as gastritis, hepatitis, or pancreatitis.


Laboratory investigation reveals an anion gap metabolic acidosis. However, the serum pH may vary as these patients often have mixed acid–base disorders such as a metabolic acidosis from AKA and a metabolic alkalosis from vomiting and dehydration. Blood glucose is low to mildly elevated. The alcohol level is usually low or undetected as symptoms limit intake. Serum ketones, acetoacetate, and its reduced form, beta-hydroxybutyrate, are elevated. If the nitroprusside test is used to measure serum and urine ketones, acetoacetate is detected, but beta-hydroxybutyrate is not. The redox state may be such that most, or all, acetoacetate is reduced to beta-hydroxybutyrate resulting in a falsely low- or false-negative result, respectively.

Diagnostic criteria for AKA are listed in Table 130-1. The differential diagnosis of an anion gap metabolic acidosis is listed in Table 130-2.

Table 130-1

Diagnostic Criteria for Alcoholic Ketoacidosis*

Table 130-2

The Differential Diagnosis of an Anion Gap Metabolic Acidosis Is Recalled by the Acronym MUDPILES


  1. Administer D5NS IV till rehydrated, then D5 0.45NS IV for maintenance. The isotonic crystalloid solution restores intravascular volume. The glucose stimulates the patient's endogenous insulin release, which inhibits ketosis (insulin is not administered, unlike treatment for DKA).

  2. Thiamine 100 mg IV before glucose administration may prevent precipitation of Wernicke's disease.

  3. Supplement electrolytes and other vitamins as indicated.

  4. Continue treatment until the acidosis clears and oral intake is tolerated.

  5. Consider other causes of an anion gap acidosis if the gap does not close with treatment.

  6. Consider sodium bicarbonate if, despite treatment, the pH remains <7.0.


Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.