Severe Alcohol-Associated Lactic Acidosis Presenting With Extreme Hyperlactataemia: A Case Report.

Alcohol-associated lactic acidosis (AALA) is a rare but potentially life-threatening complication of acute or chronic alcohol exposure. Severe hyperlactataemia attributed primarily to alcohol is uncommon and should prompt careful evaluation for alternative or co-existing causes, including sepsis, hypoperfusion, toxic ingestion, seizures and ischaemia. We report the case of a 42-year-old man who presented to the emergency department with generalised malaise and vomiting following one week of heavy alcohol consumption involving whisky and beer. He had a history of recurrent hospital admissions related to alcohol intoxication but no significant documented medical comorbidities. Initial venous blood gas analysis revealed profound high anion gap metabolic acidosis, with a pH of 6.86, bicarbonate of 5.9 mmol/L, anion gap of 40 mmol/L, and lactate greater than 20 mmol/L. Serum ethanol concentration was elevated at 297 mg/dL, and blood ketones were markedly elevated at 6.5 mmol/L. Initial investigations showed mild leucocytosis, a normal C-reactive protein level, mildly elevated serum creatinine with preserved estimated glomerular filtration rate, and transaminitis with aspartate transaminase predominance. Paracetamol and salicylate levels were negative, methanol was within the laboratory reference range, and contrast-enhanced computed tomography of the chest, abdomen, and pelvis did not identify an infective, ischaemic, or intra-abdominal cause. The patient was admitted to the intensive care unit and managed supportively with intravenous fluids, intravenous thiamine supplementation, and close biochemical monitoring. He showed rapid clinical and metabolic improvement, with lactate decreasing to 4.6 mmol/L by 10 hours and normalising by 16 hours. He remained stable without vasopressor support, ventilatory support, or renal replacement therapy and was discharged home on day four. This case highlights the importance of considering AALA with concomitant ketoacidosis in patients with severe high anion gap metabolic acidosis and significant alcohol exposure. Early recognition, systematic evaluation for life-threatening alternative diagnoses, and supportive treatment with fluid resuscitation and thiamine replacement may be associated with rapid clinical and biochemical recovery.