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Abstract: SA-PO502

A Case of Severe Alcoholic Ketoacidosis and Hyperlactatemia

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical


  • Wooden, Benjamin, Columbia University Irving Medical Center, New York, New York, United States
  • Rosen, Raphael Judah, Columbia University Irving Medical Center, New York, New York, United States
  • Ahn, Wooin, Columbia University Irving Medical Center, New York, New York, United States

Alcoholic ketoacidosis is a cause of metabolic acidosis in patients with heavy alcohol use and poor nutrition. We report a case of alcoholic ketoacidosis notable for severe acidemia and hyperlactatemia, which resolved with dextrose administration.

Case Description

A 37 year-old woman with alcohol use disorder presented with abdominal pain in the setting of 1 week of heavy alcohol use. She was tachycardic but normotensive. Mental status was normal. Labs showed serum bicarbonate <6 mmol/L and an anion gap of >52. Blood gas revealed pH 6.85 and pCO2 18 mm Hg. Venous lactate was 16 mmol/L. She was dosed 25 mEq IV bicarbonate, and subsequent blood gas shoed pH 7.05 and pCO2 16. Ethanol level was 79 mg/dL, beta-hydroxybutyrate 8.47 mmol/L, AST 253, ALT 54, total bilirubin 0.8, INR 1.1, and serum osmolality 336 mOsm/kg. Calculated osmolality was 301, indicating an osmolal gap of 35. The patient denied ingesting any substances apart from store-bought whiskey. She admitted to poor food intake. She was treated with thiamine and a dextrose infusion, without further bicarbonate. Within 3 hours, her serum bicarbonate increased to 9 mmol/L, and rose to 23 mmol/L less than 18 hours after dextrose was initiated. The hyperlactatemia resolved as well, though it took 3 days to fully normalize. She was stable for discharge on hospital day 4.


Alcoholic ketoacidosis is the result of disturbed metabolism that occurs with heavy alcohol use and malnutrition. Notable features include a relatively normal mental status (vs. diabetic ketoacidosis of similar metabolic severity), and typically prominent GI symptoms including nausea and pain. Labs show anion gap metabolic acidosis and elevated serum ketones. Serum osmolality is elevated due to accumulation of ketones and ethanol. Lactate elevation can occur (due to NADH accumulation favoring conversion of pyruvate to lactate), but is typically not severe. In our patient, she had a severe hyperlactatemia for which no alternative cause was found, illustrating that alcoholic ketoacidosis should be kept on the differential in alcohol-using patients with anion gap metabolic acidosis and osmolar gap, even in the setting of marked hyperlactatemia. Preserved mental status and normotension, despite severe acidemia, may be clues to the diagnosis. Dextrose administration (with thiamine to protect against Wernicke encephalopathy) can rapidly reverse the acidosis.