From the Research
Alcohol can cause anion gap lactic acidosis, as evidenced by the most recent and highest quality study available. The study from 2022 1 highlights a case where a patient presented with severe metabolic acidosis, elevated anion gap, and high serum lactate concentration, which was attributed to both alcoholic ketoacidosis and propylene glycol toxicity. This suggests that alcohol consumption can lead to lactic acidosis through various mechanisms, including the increase in NADH levels, impairment of hepatic lactate clearance, and tissue hypoxia.
Key Mechanisms and Considerations
- Alcohol metabolism increases NADH levels, favoring the conversion of pyruvate to lactate.
- Alcoholic ketoacidosis can develop, especially in malnourished individuals with chronic alcohol use.
- Alcohol impairs hepatic lactate clearance, contributing to lactate accumulation.
- Tissue hypoxia from respiratory depression or circulatory compromise can further contribute to lactic acid production.
Diagnosis and Treatment
- Presentation typically includes an elevated anion gap (greater than 12 mEq/L) and high serum lactate concentration.
- Treatment involves discontinuing alcohol, providing IV fluids, correcting electrolyte imbalances, and addressing nutritional deficiencies, as supported by studies such as 2, 3, and 4.
Clinical Approach
- Consider alcoholic ketoacidosis and lactic acidosis in patients with a history of alcohol abuse presenting with high anion gap metabolic acidosis.
- Evaluate for other causes of high anion gap metabolic acidosis, including toxic alcohol ingestion and diabetic ketoacidosis, as discussed in 5.
- Prompt recognition and treatment are crucial to improve outcomes in patients with alcohol-induced anion gap lactic acidosis.