A51-51 Intoxicated and Starving: A Presentation of Alcohol-Associated Ketoacidosis

Abstract Introduction Alcohol-associated ketoacidosis (AKA) is a metabolic disorder characterized by high anion gap metabolic acidosis and ketosis in patients with alcohol use. Despite AKA being well-recognized, it is under-diagnosed due to its rapid improvement with volume resuscitation, anti-emetic therapy, and nutritional support. We present a case of a 55-year-old-male with alcohol use disorder and cirrhosis who developed alcohol-associated ketoacidosis. This case highlights the importance of timely recognition and management, as AKA often reflects underlying risk factors of chronic alcohol use and malnutrition, which predispose patients to hepatic complications, including decompensated cirrhosis and acute-on-chronic liver failure. Case Presentation A 55-year-old male with a history of severe alcohol use disorder and alcohol associated cirrhosis presented with abdominal pain, emesis, and encephalopathy. He has previous hospitalizations for alcohol intoxication and complicated withdrawals. He reports drinking 1 to 1.5 pints of vodka daily. Initially, he was hypothermic (92.1 F) and tachycardic (120 bpm). His labs were significant for an elevated anion gap metabolic acidosis (anion gap 40, pH 7.19, bicarbonate 7 mmol/L), elevated b-hydroxybutyrate (38.1 mmol/L), elevated lactate (16.3 mmol/L), and ethanol (310 mg/dL). Nephrology was consulted for oliguria. He started N-acetylcysteine for alcohol-associated hepatitis. There was concern for upper GI bleed; he was started on pantoprazole and empiric ceftriaxone. His liver enzymes continued to rise, with AST and ALT peaking at 17,585 and 2,913, respectively. He then developed severe thrombocytopenia, requiring transfusion of 2 units of platelets. There was concern for acute liver failure as INR and bilirubin continued to rise although LFTs were improving. He developed ascites, underwent paracentesis, and transfusion of 3 units of fresh frozen plasma. The hospital course was complicated by sequelae of decompensated cirrhosis, and the patient ultimately elected to transition to comfort care. Discussion This case illustrates the diagnostic challenge of distinguishing AKA from other causes of metabolic acidosis and hepatic decompensation. AKA develops because of a starvation state and a decreased insulin-to-glucagon ratio, producing elevated β-hydroxybutyrate and lactic acid. Diagnostic criteria include a history of alcohol use disorder or alcohol dependence, elevated anion gap metabolic acidosis, euglycemia or hypoglycemia, and elevated B-hydroxybutyrate. Management involves replenishing volume loss from emesis and diuresis to slow the rate of ketogenesis, allowing ketone body clearance. Additional supportive management involves, correcting electrolyte abnormalities, vitamin supplementation, including thiamine, and correcting glucose. Clinicians should consider alcohol associated ketoacidosis, as recognition mitigates risk for progression to severe hepatic complications, such as acute-on-chronic liver failure. This abstract is funded by: None