In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. The prognosis for alcoholic ketoacidosis is good as long as it’s treated early. However, the long-term prognosis depends on the severity of the underlying alcohol abuse disorder.

BOX 2 BIOCHEMICAL FEATURES OF AKA

If your doctor suspects that you’ve developed this condition, they may order additional tests to rule out other possible conditions. After these test results are in, they can confirm the diagnosis. Detection of acidosis may be complicated by concurrent metabolic alkalosis due to vomiting, resulting in a relatively normal pH; the main clue is the elevated anion gap. If history does not rule out toxic alcohol ingestion as a cause of the elevated anion gap, serum methanol and ethylene glycol levels should be measured.

What causes alcoholic ketoacidosis?

If they can’t use glucose because there’s not enough insulin, your body switches to another method to get energy — breaking down fat cells. Jenkins et al2 suggested that alcohol induced mitochondrial damage might account for AKA. Alcohol produces structural changes in human liver mitochondria within days. Fulop and Hoberman5 argued that a functional abnormality is more likely to be responsible, as even severe AKA usually improves rapidly with treatment.

Deterrence and Patient Education

Alcohol withdrawal, in combination with nausea and vomiting, makes most patients agitated. However, if an AKA patient is lethargic or comatose, an alternative cause should be sought. Lactic acid levels are often elevated because of hypoperfusion and the altered balance of reduction and oxidation reactions in the liver. Limiting the amount of alcohol you drink will help prevent this condition.

• Support groups can be a valuable source of support and can be combined with medication and therapy.
• This is why diagnosis and subsequent treatment can sometimes be challenging, but it’s crucial to receive a proper and timely diagnosis to obtain the correct treatment.
• It is essential to administer thiamine before any glucose administration to avoid Wernicke’s encephalopathy preci