S3659 Elevated Bilirubin Levels in Decompensated Liver Failure Causing a Confounding Effect on Acetaminophen Level

Abstract

Introduction: Decompensated liver cirrhosis is a common reason for admission to the hospital that is associated with a high risk for mortality. Common causes of decompensated liver disease are hepatic infections, toxin-induced hepatotoxicity (ie, acetaminophen), or alcohol-related hepatitis. Here, we describe a young patient with acute decompensated liver failure secondary to alcohol abuse that presented with ascites, elevated bilirubin levels, ammonia levels, and hepatic coagulopathy. Case Description/Methods: A 32-year-old female with an extensive history of alcohol abuse and alcoholic liver cirrhosis presented to the emergency department with a three-week history of intermittent fevers, abdominal pain and abdominal distension. The patient stated that she drank nips of vodka 1-2/week. The patient had been diagnosed with liver cirrhosis by biopsy in January 2020. Upon admission, the patient was alert and oriented with stable vitals and significantly jaundiced. Labs were sent which were consistent with decompensated liver failure. The patient was found to have a bilirubin of 41. Alkaline phosphate of 285, and alcoholic transaminitis. Coagulation studies showed increased bleeding risk. Ammonia levels during admission were elevated and trended up. Hepatitis panel was sent which was negative. Acetaminophen levels were sent for which showed elevation to 16.7. Patient was started on NAC protocol for acetaminophen toxicity. Poison control was consulted and stated that elevated bilirubin levels may confound acetaminophen levels, creating a false positive. During her hospital course, the patient was started on lactulose for elevated ammonia levels, which down trended. She was placed on ceftriaxone for spontaneous bacterial peritonitis prophylaxis and was transferred to a larger center for further evaluation. Discussion: In patients who present with liver failure, a cause must be determined. Some potential etiologies of liver failure include alcohol, drug-toxicity including acetaminophen, toxins, or viral hepatitis. Panels and toxin levels are sent to direct the type of care. Due to acetaminophen toxicity being one of the most common cause of acute liver failure, empiric therapy with NAC is often started with elevated levels which has been shown to improve outcomes. In this case, the patient had known liver cirrhosis secondary to alcohol abuse, but NAC therapy was initiated due to elevated acetaminophen levels. It is important to keep in mind that levels can be erroneously elevated due to confounding factors.