Abstract: FR-PO1019
Unexplained Encephalopathy in Septic Shock: Noncirrhotic Hyperammonemia Requiring CRRT
Session Information
- Hemodialysis: Clinical Challenges, Patient-Centered Outcomes, and Quality of Life
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Dialysis
- 801 Dialysis: Hemodialysis and Frequent Dialysis
Authors
- Alperstein, Adam S., Southwest Medical Education Consortium, Temecula, California, United States
- Embry, Edsel, Southwest Medical Education Consortium, Temecula, California, United States
- Wang, Jeannine C., Southwest Medical Education Consortium, Temecula, California, United States
Group or Team Name
- Southwest Medical Education Consortium Pulmonary & Critical Care Fellowship Program & Internal Medicine Residency Program
Introduction
Hyperammonemia is classically associated with hepatic failure, but nonhepatic hyperammonemia is an underrecognized cause of severe encephalopathy in critically ill patients. Urease-producing organisms, including Klebsiella species, may generate significant ammonia loads leading to neurologic deterioration. Prompt recognition is critical because hyperammonemia may mimic toxic-metabolic or septic encephalopathy, delaying potentially life-saving therapy. Although renal replacement therapy is established for ammonia clearance in neonates and liver failure, guidance in noncirrhotic hyperammonemia remains limited.
Case Description
A 70-year-old woman with rheumatoid arthritis on chronic immunosuppressive therapy presented with encephalopathy and septic shock secondary to Klebsiella bacteremia. Initial presentation was attributed to toxic-metabolic encephalopathy from severe sepsis; however, persistent neurologic dysfunction prompted further evaluation demonstrating severe hyperammonemia with ammonia levels >200 µmol/L despite absence of cirrhosis or acute liver failure. Given concern for ongoing neurologic injury, continuous renal replacement therapy (CRRT) was initiated for ammonia clearance. CRRT was favored over intermittent hemodialysis due to septic shock, hemodynamic instability, and concern for rebound hyperammonemia. Following CRRT initiation, ammonia levels declined substantially with improvement in metabolic parameters, although neurologic recovery remained limited in the setting of progressive refractory septic shock and multiorgan failure.
Discussion
Nonhepatic hyperammonemia is an underrecognized cause of severe encephalopathy and an important diagnostic mimic in critically ill patients. Urease-producing organisms such as Klebsiella may generate significant ammonia burden, particularly in immunocompromised hosts. This case highlights the importance of considering hyperammonemia in unexplained encephalopathy disproportionate to expected septic physiology. While renal replacement therapy is established for ammonia clearance in hepatic failure, optimal timing and modality in noncirrhotic hyperammonemia remain incompletely defined. This case further highlights the potential role of CRRT as a hemodynamically tolerated strategy for continuous ammonia clearance in septic shock.