Abstract: PUB141
A Severe Case of Alcohol-Associated Lactic Acidosis
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Shah, Binoy K., Brown University, Providence, Rhode Island, United States
- Cadore Guzzo, Eduardo, Brown University, Providence, Rhode Island, United States
- Tang, Jie, Brown University, Providence, Rhode Island, United States
Introduction
Alcohol-related severe lactic acidosis is a rare clinical scenario. We present a case report of severe lactic acidosis in a patient with alcoholic hepatitis without significant ketoacidosis.
Case Description
A 64-year-old woman with alcohol use disorder, torsades de pointes with an implantable cardioverter-defibrillator, and macrocytic anemia was admitted with acute alcoholic hepatitis. In the Emergency Department, the patient had a seizure attributed to a glucose level of 41 mg/dL. Labs showed severe metabolic acidosis (pH 7.09, bicarbonate <5 mEq/L) and elevated lactate (10.3 mmol/L), rising to 12.4 mmol/L, prompting urgent Nephrology consultation. Repeat lactates (whole blood 11.6, venous 12.4 mmol/L) with a minimal anion gap made toxic alcohol ingestion unlikely. Urine toxicology screen, acetone, and volatile alcohols were negative. Urinalysis showed trace ketones; ethanol level was 75 mg/dL. The patient was hemodynamically stable without vasopressors and showed no signs of infection. Continuous hemodiafiltration was initiated for refractory acidosis despite bicarbonate infusion. Other causes were excluded, and empiric high-dose thiamine was given. Thiamine level later returned critically low at 59 nmol/L. The patient improved and responded with supplementation.
Discussion
Alcohol-related lactic acidosis involves several metabolic pathways. Thiamine is a critical cofactor for the pyruvate dehydrogenase complex (PDH), which facilitates the conversion of pyruvate to acetyl-CoA for entry into the Krebs cycle. In thiamine deficiency, PDH activity is impaired, resulting in pyruvate accumulation and subsequent conversion to lactate via lactate dehydrogenase. Chronic alcohol use promotes lactic acidosis by increasing hepatic NADH through alcohol and aldehyde dehydrogenase activity, shifting the NADH/NAD+ ratio, and favoring lactate formation over pyruvate regeneration. Compounding this, liver dysfunction impairs lactate clearance, while concurrent factors such as sepsis and tissue hypoperfusion can amplify lactate accumulation. As demonstrated in prior reports, including cases of cardiovascular collapse and refractory acidosis, thiamine deficiency can have severe clinical consequences. Given thiamine supplementation is low risk and has the potential to reverse life-threatening metabolic derangements, empiric thiamine supplementation should be strongly considered in at-risk patients.