Abstract
A 67-year-old man with advanced alcoholic-associated liver disease developed nondiabetic ketoacidosis shortly after starting empagliflozin for congestive heart failure. He presented with high anion-gap metabolic acidosis, elevated beta-hydroxybutyrate levels, and hypoglycemia. The condition resolved promptly after empagliflozin discontinuation and initiation of intravenous fluids, thiamine, and dextrose therapy. This case highlights the risk of early-onset ketoacidosis in patients with cirrhosis and alcohol use treated with sodium-glucose cotransporter-2 inhibitors, emphasizing careful patient selection and vigilant early monitoring of electrolytes and renal function. As the application of sodium-glucose cotransporter-2 inhibitors expands into managing refractory ascites in cirrhotic patients, further studies are required to confirm their safety.