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Ammonia encephalopathy secondary to urinary tract infection with Proteus mirabilis
Abstract:
Hyperammonemia with coma, tachypnea, and respiratory alkalosis developed in a 3-year-old boy with prune"-belly syndrome during a urinary tract infection with Proteus mirabilis. Hyperammonemia is thought to have resulted from the production within the massively dilated urinary tract of excessive amounts of ammonia due to bacterial urease, and its subsequent reabsorption into the systemic circulation. The patient rapidly improved following parenteral antibiotic therapy and continuous catheter drainage of the urinary tract.
Insights
A urinary tract infection in a boy with prune-belly syndrome caused severe hyperammonemia. Prompt antibiotic treatment and urinary drainage resolved the condition.
Area of Science:
- Pediatric Nephrology
- Infectious Diseases
- Biochemistry
Background:
- Prune-belly syndrome is a congenital disorder associated with urinary tract abnormalities.
- Hyperammonemia can lead to serious neurological complications.
Observation:
- A 3-year-old boy with prune-belly syndrome developed hyperammonemia, coma, tachypnea, and respiratory alkalosis during a Proteus mirabilis urinary tract infection.
- The massively dilated urinary tract likely facilitated ammonia production and reabsorption.
Findings:
- Bacterial urease from Proteus mirabilis is implicated in excessive ammonia production within the urinary tract.
- Ammonia reabsorption into the systemic circulation led to hyperammonemia.
Implications:
- This case highlights a potential mechanism for hyperammonemia in patients with prune-belly syndrome and urinary infections.
- Effective management involves addressing the infection and improving urinary drainage.