Idiopathic urinary bladder perforation in early childhood
Published in the journal KI Reports, the authors present
a unique case of spontaneous urinary bladder perforation presenting with urinary ascites and an acute kidney injury picture in early childhood without underlying urogenital anomaly or trauma.

A previously healthy 2.5-year-old boy presented to the emergency department with severe generalized abdominal pain, persistent vomiting, and decreased urine output. His preceding history was relevant for 5 days of dysuria and suprapubic abdominal pain, initially relieved with sitz baths.

The abdomen was distended with demonstrable ascites and generalized tenderness without rebound, which was most severe in the suprapubic area.

Initial laboratory investigations suggested acute kidney injury.
An abdominal X-ray revealed centrally distributed bowel loops compatible with ascites, with no signs of obstruction or perforation, and abdominal ultrasound revealed anechoic ascites extending throughout the peritoneal cavity.

The patient was maintained nil per os, received a bolus of 20 ml/kg of 0.9% saline solution, and was then fluid restricted to insensible fluid losses and urine output replacement. Potassium-lowering therapy was administered in the form of sodium polystyrene sulfonate (1 g/kg), salbutamol (2-mg nebulizer), and sodium bicarbonate (1 mmol/kg). After remaining anuric for 6 hours, the patient was catheterized with a Foley catheter inserted by the urology fellow without difficulty or trauma to the urethra.

Of note, he had been catheterized with a Foley catheter for urine culture collection at the referring hospital without documented difficulty in catheterization. After catheter insertion, the urine was initially clear then became grossly bloody, with intermittent clearing. Urinalysis showed specific gravity 1.025, pH 6.0, protein 1.0 g/l, glucose negative, ketones 1.5 mmol/l, nitrite negative, and microscopic hematuria. A spot protein/creatinine ratio was elevated at 169.8 mg/mmol (normal range is <20 mg/mmol; nephrotic-range proteinuria is >200 mg/mmol). Urine microscopy revealed numerous uniform red cells, with no red cell casts, compatible with a nonglomerular source.

Following catheterization, urine output as well as biochemical abnormalities improved dramatically, which coupled with results of urine microscopy and raised suspicion of a genitourinary anomaly. A voiding cystourethrogram (VCUG) was obtained and was in keeping with a bladder perforation, with extravasation of contrast from a point near the bladder dome. The Foley catheter was left in situ on straight drainage, and following the VCUG confirmation of a urinary leak, a peritoneal drain was inserted by interventional radiology and was also left to straight drainage. Peritoneal fluid and serum creatinine were 164 μmol/l and 65 μmol/l, respectively, in keeping with the diagnosis of urinary ascites.

Although serum biochemistry returned to normal, significant output from the abdominal drain persisted for 1 week, suggesting an ongoing urine leak. The patient therefore underwent cystoscopy, which showed a normal anterior and posterior urethra, with both ureteric orifices in the normal orthotopic position.

A large defect with some adjacent inflammatory reaction was seen along the right posterior wall of the bladder, confirming the diagnosis of bladder rupture. The 3-cm defect was repaired surgically, with cessation of the abdominal drainage. No biopsy of the bladder wall was performed at the time of the repair. After 3 months, a follow-up VCUG was performed and was normal.

Key takeaways:-
-A careful history and physical examination, as well as a high index of suspicion, are required to prevent delayed diagnosis.

- Early surgical repair combined with biopsy of the margin of the defect is suggested in this age group, to prevent unnecessary intervention and complications as well as to diagnose inflammatory lesions as a possible risk factor for the bladder wall perforation.

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