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Glassberg, K. I.: Myogenic failure in posterior urethral valve disease: real or imagined? J Urol, 168: 1844, 2002 EDITORIAL COMMENT Clinically there are many similarities between valve and neuro- genic bladders. In each condition the abnormal detrusor behavior creates voiding inefficiencies and frequently compromises the upper urinary tract. Using videourodynamics these authors make a com- pelling case for a second look at children with persistent hydrouret- eronephrosis following urethral valve ablation. Their studies re- vealed a treatable and potentially reversible pathological condition. It is generally believed that bladder neck prominence in PUV is a part of global detrusor hypertrophy and bladder neck surgery is to be avoided. However, these authors unmasked BNO in a third of their patients and successfully treated them with -adrenergic blockers and/or transurethral incision. However, it is unclear whether blad- der neck dyskinesia in these children was due to contraction of the bladder neck during voiding or simply to a failure of relaxation. Another important message is that they successfully treated poor bladder emptying with CIC, something I am unable to achieve in the majority of children with sensate urethra. I have had to resort to the Mitrofanoff procedure to make CIC feasible. Moneer K. Hanna New York Weill-Cornell Medical Center New York, New York REPLY BY AUTHORS The vast majority of PUV studied by voiding cystourethrography will have an abnormal appearing “collar” or relative narrowing at the level of the bladder neck. This abnormal appearance may represent bladder neck hypertrophy that is potentially obstructive or simply reflect a visual anomaly created by the adjacent dilated prostatic urethra. Therefore, the diagnosis of secondary bladder neck obstruc- tion hangs not on the appearance of narrowing/perceived obstruc- tion, but on videourodynamically documented obstruction localized to the bladder neck. We believe that this obstruction is directly related to detrusor/bladder neck hypertrophy secondary to previous chronic outlet obstruction and is a separate entity from the neuro- logically mediated dyskinesia/altered tone associated with primary bladder neck dysfunction. While both can be adequately treated with -adrenergic antago- nists, they are separate distinct entities. The former tends to have high voiding pressures, greater association with upper tract changes and no significant effect on the time to initiation of urine flow, while the latter typically has the opposite characteristics. In addition, we believe that the duration of treatment with -blockers is limited in secondary bladder neck obstruction, while it may be lifelong in pri- mary bladder neck dysfunction. We agree with Hanna that attempts at surgical reconstruction of the bladder neck in patients with valves as was done 3 to 4 decades ago was misguided and should be avoided. As for getting our pa- tients/parents to undertake a program of urethral CIC, our experi- ence has been different than his. While the number of patients requiring CIC in our study was small, all of them were also reluctant to undertake a program of CIC initially. We found that with persua- sive arguments as to its necessity, and an attentive, persistent nurs- ing staff for its implementation, we were successful initiating CIC in every case requiring it in the group we reported on and in all but one other patient to date. In our overall CIC experience we too have encountered other patients in whom initiating urethral CIC has not been successful and a Mitrofanoff procedure was required. However, the problem was not with the sensate urethra per se, but rather with urethras difficult to catheterize because of anatomic distortion/ob- struction (eg epispadias, exstrophy). Ultimately it is our hope that early intervention for residual bladder dysfunction will over time obviate the need for later augmentation and/or CIC programs in patients with PUV altogether. HYDROURETERONEPHROSIS AND POSTERIOR URETHRAL VALVES 711

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Glassberg, K. I.: Myogenic failure in posterior urethral valvedisease: real or imagined? J Urol, 168: 1844, 2002

EDITORIAL COMMENT

Clinically there are many similarities between valve and neuro-genic bladders. In each condition the abnormal detrusor behaviorcreates voiding inefficiencies and frequently compromises the upperurinary tract. Using videourodynamics these authors make a com-pelling case for a second look at children with persistent hydrouret-eronephrosis following urethral valve ablation. Their studies re-vealed a treatable and potentially reversible pathological condition.It is generally believed that bladder neck prominence in PUV is a

part of global detrusor hypertrophy and bladder neck surgery is to beavoided. However, these authors unmasked BNO in a third of theirpatients and successfully treated them with �-adrenergic blockersand/or transurethral incision. However, it is unclear whether blad-der neck dyskinesia in these children was due to contraction of thebladder neck during voiding or simply to a failure of relaxation.Another important message is that they successfully treated poorbladder emptying with CIC, something I am unable to achieve in themajority of children with sensate urethra. I have had to resort to theMitrofanoff procedure to make CIC feasible.

Moneer K. HannaNew York Weill-Cornell Medical CenterNew York, New York

REPLY BY AUTHORS

The vast majority of PUV studied by voiding cystourethrographywill have an abnormal appearing “collar” or relative narrowing at thelevel of the bladder neck. This abnormal appearance may representbladder neck hypertrophy that is potentially obstructive or simplyreflect a visual anomaly created by the adjacent dilated prostaticurethra. Therefore, the diagnosis of secondary bladder neck obstruc-

tion hangs not on the appearance of narrowing/perceived obstruc-tion, but on videourodynamically documented obstruction localizedto the bladder neck. We believe that this obstruction is directlyrelated to detrusor/bladder neck hypertrophy secondary to previouschronic outlet obstruction and is a separate entity from the neuro-logically mediated dyskinesia/altered tone associated with primarybladder neck dysfunction.While both can be adequately treated with �-adrenergic antago-

nists, they are separate distinct entities. The former tends to havehigh voiding pressures, greater association with upper tract changesand no significant effect on the time to initiation of urine flow, whilethe latter typically has the opposite characteristics. In addition, webelieve that the duration of treatment with �-blockers is limited insecondary bladder neck obstruction, while it may be lifelong in pri-mary bladder neck dysfunction.We agree with Hanna that attempts at surgical reconstruction of

the bladder neck in patients with valves as was done 3 to 4 decadesago was misguided and should be avoided. As for getting our pa-tients/parents to undertake a program of urethral CIC, our experi-ence has been different than his. While the number of patientsrequiring CIC in our study was small, all of them were also reluctantto undertake a program of CIC initially. We found that with persua-sive arguments as to its necessity, and an attentive, persistent nurs-ing staff for its implementation, we were successful initiating CIC inevery case requiring it in the group we reported on and in all but oneother patient to date. In our overall CIC experience we too haveencountered other patients in whom initiating urethral CIC has notbeen successful and a Mitrofanoff procedure was required. However,the problem was not with the sensate urethra per se, but rather withurethras difficult to catheterize because of anatomic distortion/ob-struction (eg epispadias, exstrophy). Ultimately it is our hope thatearly intervention for residual bladder dysfunction will over timeobviate the need for later augmentation and/or CIC programs inpatients with PUV altogether.

HYDROURETERONEPHROSIS AND POSTERIOR URETHRAL VALVES 711