Beyond the Bottle: Lactic Acidosis as a Consequence of Alcoholic Ketoacidosis

Introduction: Alcoholic ketoacidosis (AKA), a consequence of chronic alcohol use disorder in malnourished individuals. Ketoacidosis is caused by accumulation of ketone bodies when glucose availability is limited for metabolic energy. Lactic acidosis (LA) is classically type A acidosis due localized or systemic hypoperfusion. LA in the absence of evidence of hypoperfusion is type B acidosis. Case Description: A 60-year-old male with a past medical history significant for alcohol abuse presented to the emergency department after a fall. No abdominal pain, fever, dizziness, lightheadedness, or loss of consciousness reported. On admission, vital signs were stable. Physical exam was unremarkable. Investigations revealed leukocytosis and metabolic acidosis. Serum lactic acid was elevated at 21.8 mmol/L on admission. Urinalysis showed presence of 3+ ketones. Liver function tests were unremarkable except for marginally elevated AST peaking at 109 u/l. Blood alcohol level was 179 on presentation. Beta-hydroxybutyrate was checked due to concerns for AKA and was 45.70 on presentation. HIV screen was negative. Patient was started on D5 water to help with ketoacidosis. Urine ketones and serum beta-hydroxybutyrate normalized 48 hours after admission with subsequent resolution of lactic acidosis. Discussion: Type B LA causes include medications such as Metformin, malignancy, HIV infection, thiamine deficiency and mitochondrial dysfunction. Patients with chronic alcohol use disorder and malnutrition are at risk for developing AKA. Ketoacidosis usually presents after alcohol ingestion has ceased and after a binge episode. When ethanol levels start to decrease, catecholamines and cortisol rise, increasing lipolysis, accelerating the production of ketones. During the metabolism of ethanol, high amounts of NADH are generated. The reduction of NAD+ and consequential accumulation and imbalance of NADH in the metabolism of ethanol has several important consequences including an inhibition of the citric acid cycle and hepatic gluconeogenesis. The LA seen in AKA is due to an abnormal redox state. This case highlights the need to assess for unusual causes of LA when there is no evidence of either systemic or local hypoperfusion. This can help identify any underlying problem such as AKA, thiamine deficiency or HIV when there may sometimes be no other clues about these diagnoses.