Case Reports in Critical Care · Published 2025-01-01 · Journal article · DOI 10.1155/crcc/7521571
Ureaplasma species are urease-producing organisms that can cause fulminant hyperammonemia with rapid neurologic deterioration. Ureaplasma-associated hyperammonemia has been most often described in solid organ transplant recipients, with only rare reports in nontransplant patients receiving chronic immunosuppressive therapy. We present the case of a 45-year-old woman with multiple sclerosis and seronegative arthritis treated with immunomodulatory agents who developed culture-negative septic shock and severe hyperammonemia after gastric surgery. Despite broad-spectrum antimicrobials, measures to limit protein intake and catabolism, renal replacement therapy, and aggressive intracranial pressure-directed management, serum ammonia peaked above 600 μmol·L−1 (reference range: 11–60 μmol·L−1), resulting in refractory cerebral edema and death on postoperative day 14. Ureaplasma parvum was ultimately identified by polymerase chain reaction testing of urine and abdominal fluid. This case highlights the need to consider Ureaplasma infection in nontransplant patients receiving immunosuppressive therapy who develop altered mental status and hyperammonemia, particularly when routine cultures are negative. Early molecular testing, targeted antimicrobial therapy, and aggressive ammonia- and intracranial pressure–lowering interventions may be lifesaving.
Abstract from DOAJ. Public domain (CC0 1.0).
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