(421) The Painless Path to Fatal Hepatic Encephalopathy

Introduction: Acute severe hepatic encephalopathy (HE) is associated with significant mortality of more than 50%. It is rarely seen in patients with compensated liver cirrhosis (CLS). We describe the case of a patient with CLC who developed fatal HE with severe cerebral edema after opioid use.

Description: A 69-year-old female who was recovering after a shoulder arthroplasty for left humeral fracture was brought to the hospital for increased lethargy and reduced responsiveness for 2 days. She had a history of alcoholic liver cirrhosis with esophageal varices (Child-Pugh Class B) which was seen to have resolved on an esophagogastroduodenoscopy done 5 years ago. On presentation, she was disoriented and drowsy. Vitals were unremarkable. Labs were notable for ammonia of 117 mcmol/l with normal cell count, renal and hepatic panel. Computed tomography (CT) scan of the head showed mild cerebral edema. She was started on oral lactulose but soon developed generalized tonic clonic seizures and had to be intubated for airway protection. Repeat ammonia levels were now higher at 250mcmol/l and CT head showed significant cerebral edema without herniation. She was started on lactulose and rifaximin, as well as hypertonic saline for cerebral edema. CT abdomen pelvis showed dilated loops of bowel suggestive of small bowel obstruction vs ileus. As clinical exam findings of hypoactive bowel sounds and soft abdomen suggested ileus, conservative management with bowel decompression was begun. While ammonia levels gradually improved to 70mcmol/l, there was no improvement in mental status and cerebral function. Continuous electroencephalography showed evidence of severe encephalopathy with baseline burst suppression pattern. The patient was taken off life support and transitioned to comfort care.

Discussion: Severe acute HE occurs mostly in patients with acute liver failure or acute-on-chronic liver disease. Medications such as opioids may precipitate HE via constipation and increased ammonia levels. A study of over 6000 patients with CLC showed increased risk of HE with both short term (HR 1.44 95% CI 1.07-1.94) and chronic opioid prescriptions (adjusted HR 1.83, 95% CI 1.07-3.12). Our case illustrates the need for increased caution with analgesic use in patients with liver cirrhosis.