UROLOGICAL SURVEY   ( Download pdf )

 

PEDIATRIC UROLOGY

Myogenic bladder decompensation in boys with a history of posterior urethral valves
Androulakakis PA, Karamanolakis DK, Tsahouridis G, Stefanidis AA, Palaeodimos I Department of Paediatric Urology, Aghia Sophia Children’s Hospital, Athens, Greece
BJU Int. 2005; 96: 140-3.

  • Objective: To investigate whether myogenic bladder decompensation in patients treated for congenital posterior urethral valves (PUV, the most serious cause of infravesical obstruction in male neonates and infants) may be secondary to bladder neck obstruction, as despite prompt ablation of PUV these patients can have dysfunctional voiding during later childhood or adolescence, the so-called ‘valve bladder syndrome’.
  • Patients and Methods: The study comprised 18 boys (mean age 14 years, range 6.2-18.5) who had had successful transurethral ablation of PUV between 1982 and 1996, and had completed a follow-up which included serial assessment of serum creatinine, completion of a standard voiding diary, ultrasonography with measurement of urine before and after voiding, a urodynamic examination with simultaneous multichannel recording of pressure, volume and flow relationships during the filling and voiding phases, coupled with video-cystoscopy at least twice. The mean (range) follow-up was 9.3 (6-17) years.
  • Results: Urodynamic investigation showed myogenic failure with inadequate bladder emptying in 10 patients; five with myogenic failure also had unstable bladder contractions. On video-cystoscopy the posterior bladder neck lip appeared elevated in all patients but in those with myogenic failure it was strongly suggestive of hypertrophy, with evidence of obstruction. At the last follow-up one patient with myogenic failure who had had bladder neck incision and four others who were being treated with alpha-adrenergic antagonists had a significant reduction of their postvoid residual urine.
  • Conclusion: Despite early valve ablation, a large proportion of boys treated for PUV have gradual detrusor decompensation, which may be caused by secondary bladder neck obstruction leading to obstructive voiding and finally detrusor failure. Surgical or pharmacological intervention to improve bladder neck obstruction may possibly avert this course, but further studies are needed to validate this hypothesis.

  • Editorial Comment
    The authors review their experience treating 18 boys with posterior urethral valves, diagnosed from 1982-1996. Many of the children eventually developed myogenic failure. The authors propose that this is due to secondary bladder neck obstruction.
    The observation of progressive myogenic failure in these patients is not new and is increasingly observed as valve patients get older. Clearly this is something that all clinicians should be aware of. The etiology of this is, no doubt, multifactorial, but among the causes is high urine flow and infrequent voiding. The proposal that bladder neck obstruction contributes is intriguing and suggests a potential treatment. However, the data presented are quite limited. Fluro-urodynamic studies are key to the diagnosis and unfortunately no urodynamic data are presented in the paper! The authors present cystoscopic findings, but this condition can not be diagnosed during cystoscopy under anesthesia (or even local anesthesia for that matter). Moreover, the bladder neck musculature is connected to the bladder muscle and it is during bladder contraction that the bladder neck opens. In the case of myogenic bladder decompensation, the bladder neck would not be expected to open. Hence this condition is even more difficult to diagnose once myogenic failure has developed.
    Nonetheless, the proposal to consider alpha-adrenergic antagonist therapy in these patients has some merit. Careful documentation of urodynamic function in patients before and after pharmacological intervention would be very interesting. However, this study should be done early on, before myogenic failure. The ultimate would be to demonstrate that years of alpha-adrenergic antagonist therapy prevents myogenic failure, but this will require a large multi-center, long-term study and probably is not realistic.

Dr. Barry A. Kogan
Chief and Professor of Urology and Pediatrics
Albany Medical College
Albany, New York, USA