Kidney Week

Abstract: TH-PO0522

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

Session Information

• Dialysis: Novel Therapeutics and Medication Management
  November 06, 2025 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

• 801 Dialysis: Hemodialysis and Frequent Dialysis

Authors

• Rajendran, Jackson, RWJBarnabas Health, Toms River, New Jersey, United States

Jackson Rajendran, MD

• Lorenzo Capps, Maria Jose, RWJBarnabas Health, Toms River, New Jersey, United States

Maria Jose Lorenzo Capps, MD

• Yaziji, Muataz, RWJBarnabas Health, Toms River, New Jersey, United States

Muataz Yaziji, MD

• Chiapaikeo-Poco, Katherine, RWJBarnabas Health, Toms River, New Jersey, United States

Katherine Chiapaikeo-Poco, DO

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

Digital Object Identifier (DOI)

• doi: 10.1681/ASN.2025e3dkdne9