S5723 Hyperammonemic Encephalopathy Primarily Driven by Klebsiella pneumoniae Pneumonia in a Cirrhotic Patient

Introduction: Hyperammonemic encephalopathy (HAE) is classically caused by liver dysfunction disrupting the urea cycle, leading to toxic ammonia accumulation. Ammonium ions cross the blood-brain barrier, increase astrocyte osmolarity, and result in cerebral edema. Clinically, HAE presents with altered mental status and asterixis. However, non-hepatic triggers, such as urease-positive bacteria, can mimic hepatic encephalopathy (HE). Klebsiella pneumoniae, though often linked to urinary tract infections (UTIs) and abscesses, has not been previously reported as a pulmonary trigger for HAE. Recognizing this rare etiology is critical to guiding appropriate and timely treatment. Case Description/Methods: An 83-year-old woman with cirrhosis and recurrent UTIs presented with unresponsiveness. She had underwent an open reduction and internal fixation of her right femur after a traumatic fall 13 days prior and was discharged on a Xa inhibitor for DVT prophylaxis. She was intubated for airway protection due to a GCS of 7. Initial labs show: WBC 8.6, Hgb 9.7, aspartate aminotransferase 34, alanine aminotransferase 24, alkaline phosphatase 86, Tbili 1.7, ammonia 152, lactate 2.0, international normalized ratio (INR) 3.7, and respiratory culture positive for K.pneumoniae. Brain MRI was consistent with hypoxic brain injury; right upper quadrant ultrasound confirmed cirrhosis. She was started on ceftriaxone, lactulose, and rifaximin with improvement of mentation. Asterixis was noted once she could follow commands. She was eventually extubated and cleared for discharge. Discussion: This case illustrates that not all encephalopathy in cirrhotic patients is hepatic in origin. While elevated INR and ammonia in a cirrhotic patient suggest HE, INR was elevated due to Xa inhibitor use, and other markers of acute liver dysfunction did not match her level of altered mentation (expected Grade I HE). Infections with K.pneumoniae can lead to elevated ammonia levels due to the activity of the urease enzyme, which hydrolyzes urea into ammonia. There are case reports of patients with K.pneumoniae UTI’s and abscesses presenting with HAE. However, no cases based on pneumonia have been discussed. This case highlights the importance of considering urease-positive bacterial infection as an underlying mechanism for HAE even in patients with underlying liver dysfunction. Early identification of infection will prompt early induction of antibiotic therapy in addition to other ammonia-reducing medications such as lactulose and rifaximin.