Abstract
Hyperammonemia is a leading cause of encephalopathy in patients presenting with altered mental status. Hyperammonemia is mostly a result of liver cirrhosis, with treatment requiring lactulose and, in some cases, rifaximin to break down ammonia production and decrease ammonia absorption in the gastrointestinal tract. This is a case of acute metabolic encephalopathy secondary to mildly elevated ammonia levels of 39 μmol/L (<35 μmol/L) that resolved with fluid bolus and maintenance fluid for 30 hours without requiring lactulose or rifaximin.