Ammonia Beyond Renal Reach: Fatal Cerebral Edema Despite Renal Replacement Therapy in Decompensated Cirrhosis and Small-Bowel Obstruction

Introduction: Hyperammonemia in decompensated cirrhosis is primarily managed through hepatic metabolism and enteric elimination using agents such as lactulose and rifaximin. When enteral access is lost, renal replacement therapy (RRT) is used as an adjunct to remove ammonia. However, in cases of extremely elevated ammonia, RRT alone cannot match the rate of ammonia production. Case Description: A 56-year-old male with decompensated alcoholic cirrhosis, diabetes, and bipolar disorder was found unresponsive at home with signs of urinary and fecal incontinence and agonal breathing. He was intubated and transported to the emergency department. Initial labs revealed: Ammonia: 420 µmol/L Creatinine: 1.3 mg/dL Blood Urea Nitrogen: 44 mg/dL Total bilirubin: 3.28 mg/dL Non-contrast CT of the head revealed architectural distortion and possible early cerebral edema. The patient received one dose of lactulose and rifaximin. Due to his altered mental status and high ammonia level, intermittent hemodialysis was initiated, followed by transition to CRRT. A subsequent CT abdomen/pelvis revealed an incarcerated ventral hernia causing small bowel obstruction, rendering further enteral therapy impossible. Despite being on CRRT, the patient’s ammonia level continued to rise to a peak of 481 µmol/L, and he developed seizures and worsening cerebral edema. Hypertonic saline and neuroprotective strategies were initiated, but neurologic function deteriorated. Imaging confirmed diffuse cerebral edema, and transcranial Doppler later demonstrated absent cerebral blood flow, confirming brain death within 48 hours of presentation. Discussion: In cases of severe hyperammonemia with impaired hepatic and gastrointestinal function, renal replacement therapy alone is insufficient to prevent ammonia accumulation and neurologic deterioration. This case illustrates the critical need for adjunctive or alternative ammonia-lowering strategies in complex presentations. Clinical Timeline - Timeline Ammonia (µmol/L) Key Event Admission 420 Intubation, lactulose + rifaximin given 10 hours 413 Post-hemodialysis, CRRT initiated 18 hours - SBO confirmed via CT 22 hours 481 Rising ammonia despite CRRT 36 hours 343 On CRRT 54 hours 284 Brain death confirmed

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Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025e3dkdne9
Primary Topic
Organ Donation and Transplantation
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article
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article

Ammonia Beyond Renal Reach: Fatal Cerebral Edema Despite Renal Replacement Therapy in Decompensated Cirrhosis and Small-Bowel Obstruction

Katherine Chiapaikeo-Poco, Maria Jose Lorenzo Capps, Muataz Yaziji, Jackson Rajendran
Journal of the American Society of Nephrology
Organ Donation and Transplantation
article

Ammonia Beyond Renal Reach: Fatal Cerebral Edema Despite Renal Replacement Therapy in Decompensated Cirrhosis and Small-Bowel Obstruction

Katherine Chiapaikeo-Poco, Maria Jose Lorenzo Capps, Muataz Yaziji, Jackson Rajendran
article en

Abstract

Introduction: Hyperammonemia in decompensated cirrhosis is primarily managed through hepatic metabolism and enteric elimination using agents such as lactulose and rifaximin. When enteral access is lost, renal replacement therapy (RRT) is used as an adjunct to remove ammonia. However, in cases of extremely elevated ammonia, RRT alone cannot match the rate of ammonia production. Case Description: A 56-year-old male with decompensated alcoholic cirrhosis, diabetes, and bipolar disorder was found unresponsive at home with signs of urinary and fecal incontinence and agonal breathing. He was intubated and transported to the emergency department. Initial labs revealed: Ammonia: 420 µmol/L Creatinine: 1.3 mg/dL Blood Urea Nitrogen: 44 mg/dL Total bilirubin: 3.28 mg/dL Non-contrast CT of the head revealed architectural distortion and possible early cerebral edema. The patient received one dose of lactulose and rifaximin. Due to his altered mental status and high ammonia level, intermittent hemodialysis was initiated, followed by transition to CRRT. A subsequent CT abdomen/pelvis revealed an incarcerated ventral hernia causing small bowel obstruction, rendering further enteral therapy impossible. Despite being on CRRT, the patient’s ammonia level continued to rise to a peak of 481 µmol/L, and he developed seizures and worsening cerebral edema. Hypertonic saline and neuroprotective strategies were initiated, but neurologic function deteriorated. Imaging confirmed diffuse cerebral edema, and transcranial Doppler later demonstrated absent cerebral blood flow, confirming brain death within 48 hours of presentation. Discussion: In cases of severe hyperammonemia with impaired hepatic and gastrointestinal function, renal replacement therapy alone is insufficient to prevent ammonia accumulation and neurologic deterioration. This case illustrates the critical need for adjunctive or alternative ammonia-lowering strategies in complex presentations. Clinical Timeline - Timeline Ammonia (µmol/L) Key Event Admission 420 Intubation, lactulose + rifaximin given 10 hours 413 Post-hemodialysis, CRRT initiated 18 hours - SBO confirmed via CT 22 hours 481 Rising ammonia despite CRRT 36 hours 343 On CRRT 54 hours 284 Brain death confirmed

Journal of the American Society of NephrologyVol. 36(10S)
Advanced Memory Research Institute of New Jersey (US)
Openalex Percentile: Top 59%
Organ Donation and Transplantation
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