A51-54 Profound Confusion: The Use of CRRT in Hyperammonemia Metabolic Encephalopathy

Introduction Acute metabolic encephalopathy secondary to hyperammonemia in patients with advanced liver disease is a well-documented phenomenon. Admission to the intensive care unit (ICU) is often required due to profound physiological derangements and changes in mental status. This patient’s case highlights the use of continuous renal replacement therapy (CRRT) to treat hyperammonemia in liver failure when gastrointestinal elimination is not an option. Case Presentation A 52-year-old female with past medical history of alcohol and metabolic dysfunction-associated steatohepatitis (MASH) decompensated liver cirrhosis with previously noted portal hypertension, splenomegaly and multiple abdominal varices presented to an outside hospital with profound multiple day constipation. Patient became increasingly altered, was intubated as she was unable to protect airway. On arrival to ICU, the Glasgow Coma Scale was 3 with mildly dilated poorly reactive pupils on minimal sedation. Computer tomography of abdomen and pelvis showed a large fecal impaction with stercoral colitis. Blood work revealed significantly elevated ammonia (>330 umol/L). Decision made to place patient on CRRT to rapidly clear ammonia given the anticipated delay and reduced clinical benefit of lactulose and rifaximin due to severe constipation and ileus. Further investigation with MRI showed symmetrical hyperintense signal diffusely throughout various forebrain/midbrain structures consistent with hyperammonemia toxicity. The patient had a rapid interval correct of ammonia levels back to baseline and improvement of mental and clinical status. Discussion Hyperammonemia is a key factor in hepatic encephalopathy primary through neurotoxicity and cerebral edema. CRRT is recognized for its utilization in rapid ammonia clearance and potential to improve clinical outcomes in patients with acute liver failure. However, its effectiveness in patients with acute-on-chronic liver failure is less well known. In this patient group, cerebral edema and intracranial hypertension are less common due to compensation. This case demonstrates that the significant elevation of ammonia involves a multifactorial neurotoxicity mechanism, and rapid ammonia clearance with CRRT may be an effective treatment for hepatic encephalopathy in acute-on-chronic liver failure, especially in patients who are not candidates for more traditional gastrointestinal elimination. Conclusion CRRT can be employed as a viable intensive care unit treatment technique in severe cases of hyperammonemia in acute-on-chronic decompensated liver failure patients.