A51-16 Lactatic Alkalemia in a Patient With Alcohol Use Disorder: A Case Report

Introduction Chronic alcohol use predisposes individuals to a wide spectrum of acid-base disturbances, often presenting as mixed disorders. While metabolic acidosis from ketoacid or lactate accumulation is common, paradoxical alkalemia can occur, particularly when metabolic alkalosis from vomiting or respiratory alkalosis from withdrawal coexists. We report a case of lactatic alkalemia in a patient with chronic alcohol use. Case History A 38-year-old male with a history of alcohol use disorder presented with a three-day history of abdominal pain and coffee-ground emesis. He reported daily alcohol consumption and denied other substance use. On presentation, he was tachycardic (HR 130/min), normotensive, and mildly tachypneic (RR 24/min) on room air. Physical examination revealed an alert, oriented male in mild respiratory distress. Initial labs were notable for severe hyponatremia (Na 114 mEq/L), hypochloremia (Cl < 60 mEq/L), hypokalemia (K 2.3 mEq/L), hypomagnesemia (Mg 2.4 mg/dL), hypocalcemia (Ca 6.6 mg/dL), elevated phosphate (3.9 mg/dL), hypoalbuminemia (3.4 g/dL), and an anion gap >20. Arterial blood gas revealed alkalemia (pH 7.68) with elevated bicarbonate (34 mEq/L), PCO2 42 mmHg, and elevated lactate (14 mmol/L). Other workup, including CBC, liver function tests, coagulation profile, drug screen, serum ketones, and abdominal ultrasound, was unremarkable. The patient was diagnosed with acute-on-chronic hyponatremia due to hypovolemia and beer potomania, with lactate elevation attributed to alkalosis and mildly elevated alcohol level. Management included cautious intravenous fluid and electrolyte repletion, gradual correction of hyponatremia (<8-10 mEq/day), and monitoring of acid-base disturbances. The patient was discharged with close outpatient follow-up. Discussion Lactatic alkalemia refers to elevated blood lactate despite an alkalemic pH. Its pathophysiology is multifactorial. Alcohol metabolism increases the NADH: NAD+ ratio, promoting conversion of pyruvate to lactate. Hypovolemia and vomiting cause metabolic alkalosis via gastric acid loss and volume contraction, while alcohol withdrawal and pain can induce respiratory alkalosis. These alkalinizing processes can offset lactate’s acidifying effect, producing an elevated pH. Alkalemia further stimulates glycolysis, worsening hyperlactatemia. In this case, severe hyponatremia and markedly elevated lactate (14 mmol/L) with a high anion gap were accompanied by severe alkalemia (pH 7.68) and elevated bicarbonate. The predominant driver of hyperlactatemia was likely profound alkalosis, which enhances glycolytic flux. Alcohol may have contributed mildly through its effect on the NADH: NAD+ ratio, but the patient’s stable blood pressure makes hypovolemia less significant. Recognition of this phenomenon is important, as elevated lactate may be misinterpreted as classic lactic acidosis, potentially confusing clinical assessment or prompting unnecessary interventions. This abstract is funded by: None