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Alcoholic Ketoacidosis

Alcoholic ketoacidosis (AKA) principally occurs after the cessation of a drinking binge by a malnourished chronic alcoholic. Increased hepatic ketone formation, active lipolysis, and inadequate peripheral ketone utilization all contribute to the accumulation of ketoacids and the resulting elevated anion gap acidosis that physiologically defines AKA. The diagnosis of AKA is established by the findings of an elevated anion gap acidosis with concurrent ketosis in the absence of a history of diabetes mellitus or a markedly elevated glucose. Co-morbidities such as alcoholic pancreatitis, liver disease, or gastritis that share symptoms and signs with AKA also should be considered.


  • lcoholic patient who has been on a drinking binge suddenly decreases energy intake because of abdominal pain, nausea.
  • AKA is the result of the accumulation of the ketoacids, hydroxybutyric acid, and acetoacetic acid because of the complex interaction caused by alcohol cessation, volume depletion, the metabolic effects of hormonal imbalance.
  • Most cases are related to poor nutritional status due to long-standing alcohol abuse.


  • Anorexia
  • Nausea
  • Vomiting
  • Abdominal pain
  • Orthostatic dizziness


  • Odor of ketones on the breath
  • Tachycardia
  • Orthostatic hypotension
  • Tachypnea, particularly with Kussmaul respirations
  • Diaphoresis
  • The abdomen usually reveals only mild to moderate diffuse tenderness. Marked distention, the absence of bowel sounds, or the presence of peritoneal signs should raise the concern for other concomitant intraabdominal pathologic conditions.
  • Abnormalities in orientation or level of consciousness ++ (may also indicate other pathologic conditions)


Treatment in the hospital with intravenous fluids and frequent blood draws may be necessary to reverse the acidosis. Occasionally patients require intensive care unit stays.

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

    1. extracellular fluid volume depletion
    2. glycogen depletion
    3. an elevated ratio of the reduced form of nicotinamide adenine dinucleotide to nicotinamide adenine dinucleotide.

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