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Abstract: PO1488

Profound Lactic Acidosis due to Dextrose Infusion and the Role of Thiamine

Session Information

Category: Trainee Case Report

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Lile, Kristen R., University of Colorado, Denver, Colorado, United States
  • Faubel, Sarah, University of Colorado, Denver, Colorado, United States

Severe metabolic acidosis due to dextrose infusion is a rare but life-threatening complication for which treatment options are poorly described. Normally dextrose is metabolized to pyruvate during glycolysis. Pyruvate is converted to acetyl-CoA via pyruvate dehydrogenase (PDH); this requires abundant oxygen. Thiamine is an essential cofactor for PDH. During anerobic conditions, pyruvate is converted to lactate during a process known as anerobic glycolysis, producing a type A lactate. Pyruvate may also be converted to lactate when oxygen levels are normal via aerobic glycolysis. Aerobic glycolysis produces type B lactate and occurs due to a number of conditions, including thiamine deficiency.

Case Description

A 54-year-old woman with malignant insulinoma was admitted for severe hypoglycemia. The patient was given continuous 20% dextrose infusion; she developed severe lactic acidosis on day seven. Serum bicarbonate was undetectable on blood gas at the time of renal consult; serum lactate was >20. The patient decompensated due to the acidosis, became obtunded, was intubated, and was placed on continuous renal replacement therapy (CRRT). The acidosis failed to improve for 36 hours. Thiamine therapy was begun in an attempt to restore function of the PDH complex and restart the metabolism of pyruvate through the citric acid cycle, halting further type B lactate production. Within hours, lactate levels fell with parallel rise in serum pH. The patient was extubated, alert, and taken off CRRT within 24 hours of beginning thiamine therapy.


This patient developed a profound metabolic acidosis secondary to type B lactic acidosis via accelerated glycolysis from dextrose infusion. This case highlights the intricate regulation of dextrose metabolism as well as thiamine as a vital therapy in type B lactic acidosis. Thiamine therapy was key, presumably reinstituting aerobic respiration through the PDH complex and ultimately leading to cessation of lactate production. Given the critical role of thiamine in this case, it is plausible that thiamine could be crucial for other cases of metabolic acidosis, particularly those secondary to type B lactic acidosis.