A Case of Rapid Decline in Alcohol-Associated Liver Disease.

Abstract

This case demonstrates a rapid clinical decline in a patient with acute‐on‐chronic liver failure affecting the liver, kidneys, and brain. 1 Our patient presented with decompensated alcohol‐associated cirrhosis with accumulation of ascitic fluid and had a variceal bleed on presentation to the emergency department with superimposed ischemic hepatopathy in the setting of hypotension and rapid development of grade IV hepatic encephalopathy, which was unable to be reversed, with eventual development of multiorgan failure. This case highlights the importance of rapid recognition and response to complications of decompensated liver disease, including hepatic encephalopathy. Role of Ammonia According to the most recent American Association for the Study of Liver Diseases practice guidelines, a diagnosis of hepatic encephalopathy requires an evaluation for precipitating factors, which are listed in Table ​Table22. 2 High blood ammonia alone does not add any diagnostic value; however, a normal ammonia level may suggest alternative causes of encephalopathy. 2 Extremely high ammonia level may be associated with cerebral edema even in patients with cirrhosis. 3 Brain imaging is typically indicated for first‐time hepatic encephalopathy given the high risk for intracerebral hemorrhage, estimated at nearly a 5‐fold increased risk for those diagnosed with alcohol‐associated liver disease and cirrhosis. 4 However, brain imaging may not always consistently detect early cerebral edema. New evidence also indicates a prognostic role in ammonia levels, with lack of improvement of ammonia levels within 5 days being associated with higher mortality and multiorgan failure. 5 TABLE 2 Precipitating Factors for Hepatic Encephalopathy