2275 Anoxic Brain Injury From Hepatic Encephalopathy in Acute on Chronic Liver Failure: A Case Report

Abstract

INTRODUCTION: Hepatic encephalopathy (HE) is a complication seen in both acute liver failure and acute on chronic liver failure (ACLF). There is a paucity of data regarding IV HE resulting in global anoxic brain injury in those with ACLF. We present a case of anoxic brain injury from severe HE in a patient with ACLF. CASE DESCRIPTION/METHODS: 74-year-old male with a past medical history of hypertension and CAD had recently been diagnosed with NASH cirrhosis when he presented to an outside hospital with ascites. Two months later he presented to our hospital with acute change in mental status. On presentation, the patient had normal vital signs. Physical examination revealed obtundation with response to noxious stimuli. There was no scleral icterus and labs were significant for WBC 5.1, platelet count 82, BUN/Cr 32/1.81, lactate 3.2, NH3 248, LFTs unremarkable, MELD Na 23. CT head and chest X-ray were negative for acute processes. On physical exam, patient was non-jaundiced with a mildly distended abdomen. He was started on lactulose every 6 hours. His mentation continuously deteriorated and he was intubated for airway protection and transferred to ICU 8 hours after admission, where he was started on rifaximin. Nephrology was consulted and CRRT was initiated after NH3 was noted to be >500 in the ICU. Repeat CT head now showed increased intracranial pressure, and subsequent MRI one day later showed global hypoxic ischemic injury. EEG with global slowing pattern signifying anoxic brain injury. Ammonia levels normalized on CRRT (although patient required dialysis for anuria after completion of 6 days of CRRT) and SSEP was done which did show evoked potentials, however no improvement was noted on neurological exam. Family eventually made the decision to transition care to comfort measures and the patient expired soon after. DISCUSSION: Overt cerebral edema leading to coma in HE and ACLF is rare given the chronicity of high ammonia and brain adaptation. The pathophysiologic mechanism for HE in ACLF is thought to be a combination of elevated serum ammonia and systemic inflammatory changes. Our attempts with hemodialysis did not change the clinical course suggesting irreversible tissue damage. Advanced therapies including embolization of portosystemic shunts was not pursued as none were identified on contrast enhanced imaging. Preventing decompensation and early recognition may be the modifiable factor in this high mortality disease.