Case Presentation: An 82-year-old woman with a history of bladder diverticulum, neurogenic bladder, and atrial fibrillation was admitted to the intensive care unit because of an altered mental status. For 10 years, she had experienced recurrent urinary tract infections (UTIs) following total hysterectomy. She had no history of alcohol abuse or liver disease. On examination, her body temperature was 36.3°C, pulse was 105 beats/min, blood pressure was 130/90 mmHg, respiratory rate was 18 breaths/min with an O2 saturation of 99% in room air, and her Glasgow coma scale (GCS) score was E3V4M5. A venous blood sample showed normal electrolytes, liver function, and blood count, but her level of ammonia was elevated to 230 μg/dL (normal range: 12.0–66.0). Urinanalysis showed a pH of 8.5 and more than 100 white blood cells per high-power field. Her cerebral computed tomography (CT) results were normal. Abdominal CT showed a huge bladder diverticulum and distended bladder. Therefore, we suspected hyperammonemia due to obstructive urinary tract infection. On the first day of admission, antibiotics were administered, and we catheterized the bladder and drained pyuria and hematuria. On the second day, her venous ammonia level had decreased to 122 μg/dL, and her GCS score improved to E4V4M6. On the same day, bladder perfusion was initiated using a triple-lumen bladder catheter. On the third day of admission, her level of consciousness returned to the baseline level (GCS:E4V5M6), along with normalized serum ammonia. Klebsiella pneumoniae with urease production was detected in her urine culture. As dementia progressed during hospitalization, she was unable to perform intermittent self-catheterization. We inserted a permanent bladder catheter, and subsequently, there was no recurrence of cystitis.
Discussion: UTIs are caused by urinary tract abnormalities such as urinary obstruction; urinary retention sometimes leads to the complication of hyperammonemia. Urease-producing bacteria catalyze the hydrolysis of urea into ammonia and carbon dioxide. Ammonia induces an alkaline pH of urine; ammonium is then transformed into ammonia (NH3), a liposoluble base that easily crosses cell membranes. In addition to an increase in ammonia production, an overextended bladder increases the surface area of the venous plexus of the bladder, which enhances the shift of ammonia into the bloodstream. As a result, hyperammonemia correlates with an altered consciousness level. Based on previous case reports, a urine pH of 8.0 or higher and the presence of urinary tract abnormalities, especially urinary outflow abnormalities, confer a high risk of hyperammonemia. In this case, there was a huge bladder diverticulum, and intermittent self-catheterization could not effectively drain the urine in the diverticulum. Therefore, urease-producing bacteria flourished in the bladder diverticulum.
Conclusions: In patients with hyperammonemia due to obstructive urinary tract infection, which causes disturbance of consciousness, it is important to immediately drain urine from the bladder.