(506) Oh My Lactate: A Case Highlighting the Relevance of the Warburg Effect and Thiamine Supplementation

Introduction: Lactic acidosis seen in the critical care setting is commonly due to tissue hypoperfusion or hypoxia. The Warburg effect (aerobic glycolysis) is a phenomenon seen in hematologic malignancies where neoplastic cells undergo glycolysis to preferentially produce lactate in the absence of hypoxia. Additionally, thiamine deficiency can also lead to type B lactic acidosis.

Description: A 22-year-old female with a history of stage IV undifferentiated small round cell carcinoma of the uterus on chemotherapy presented to the hospital for vomiting. On arrival, vital signs were significant for sinus tachycardia (heart rate 120-130 bpm). On examination, the abdomen was distended and mildly tender. Labs showed hyponatremia, hypokalemia, anion-gap metabolic acidosis, and lactatemia. Imaging revealed right-sided hydronephrosis and increased peritoneal carcinomatosis. While in the ICU, she underwent cystoscopy with stent placement due to external ureteral compression. The fluid was switched from intravenous Ringer’s lactate to Dextrose 5% with Ringer’s lactate due to poor oral intake in the setting of nausea and vomiting. Infectious workup was negative and there was no evidence of organ hypoperfusion or end-organ damage. However, the lactate continued to trend up from the initial 4.4 to 13.9. A bicarbonate drip was initiated with minimal improvement in acidosis. Subsequently, on the day the lactate peaked, IV thiamine was started, which resulted in same-day resolution of the lactic acidosis.

Discussion: The Warburg effect has been documented in hematologic malignancies as a way for cancer cells to proliferate faster. We suspect aerobic glycolysis by neoplastic cells contributed to the initial lactatemia. Additionally, thiamine deficiency is commonly attributed to malnutrition, alcoholism, and gastroenteric losses. In our case, the patient had a solid organ tumor and was not overtly malnourished. Nonetheless, due to the significant tumor burden, she developed thiamine deficiency in the setting of demand-supply mismatch. Supplementation resulted in quick resolution of the lactatemia and acidosis. Therefore, further investigation into the role of thiamine supplementation in patients with malignancy-related lactic acidosis is needed to initiate prompt recognition and limit unnecessary interventions.