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Association of urinary tract infection and reflux with uninhibited bladder contractions and voluntary sphincteric
Insights
Recurrent urinary tract infections in children can stem from bladder-sphincter incoordination. Treating involuntary bladder contractions helps maintain sterile urine, reducing infection recurrence without antibiotics.
Area of Science:
- Pediatric Urology
- Nephrology
- Continence Disorders
Background:
- Recurrent urinary tract infections (UTIs) are common in children.
- Bladder-sphincter incoordination is a potential underlying cause.
- Understanding the pathophysiology is crucial for effective management.
Purpose of the Study:
- To investigate the link between bladder-sphincter incoordination and UTIs in children.
- To explore the role of increased intravesical pressure in UTI development and vesicoureteral reflux (VUR).
- To evaluate the efficacy of treating detrusor overactivity in managing recurrent UTIs.
Main Methods:
- Studied 53 neurologically normal children with recurrent UTIs.
- Assessed bladder-sphincter dynamics, measuring intravesical pressure during involuntary bladder contractions.
- Evaluated associated vesicoureteral reflux and ureteral orifice abnormalities.
- Conducted a prospective uncontrolled study on treating detrusor overactivity.
Main Results:
- Bladder-sphincter incoordination with increased intravesical pressure was observed in children with recurrent UTIs.
- Vesicoureteral reflux was present in nearly 50% of children; ureteral orifice abnormalities in 30% of those without reflux.
- Treatment of involuntary bladder contractions led to sterile urine in 58% of patients post-initial infection cure.
Conclusions:
- Increased intravesical pressure due to bladder-sphincter incoordination may cause UTIs and predispose to VUR.
- Addressing detrusor overactivity is a viable strategy for managing recurrent UTIs in children.
- This approach can reduce the need for long-term antimicrobial therapy.
Abstract:
We studied 53 neurologically normal children with recurrent urinary tract infection who were found to have bladder-sphincter incoordination characterized by voluntary sphincteric constriction during involuntary uninhibited bladder contraction. Increased intravesical pressure was documented during these events and was associated with vesicoureteral reflux in nearly 50 per cent of the children and with abnormalities of the ureteral orifice in 30 per cent of those without reflux. We hypothesize that increased intravesical pressure causes urinary infection in these children and produces a spectrum of intravesical anatomic distortion that predisposes to vesicoureteral reflux. In a prospective uncontrolled study treatment of the uninhibited bladder contractions allowed 58 per cent of the patients to maintain sterile urine without subsequent antimicrobial therapy after cure of the initial infection.