The Valve Bladder Syndrome: 35D Years Later IN the late 1970s and early 1980s a number of reports appeared regarding boys with a history of a posterior urethral valve (PUV), persistent hydroureteronephrosis (HUN) and incontinence. 1e3 In most cases HUN was thought to be secondary to a noncompliant bladder, especially when associated with a large urine output secondary to renal loss of ability to respond to antidiuretic hormone. We pro- posed that the incontinence and HUN resulted from increased detrusor pressures (Pdets) during filling, detrusor overactivity and nephrogenic diabetes insipidus. 1,2 The term “valve bladder syndrome,” first introduced by Mitchell, 3 has endured as a useful moniker to characterize this constellation of findings. Warshaw et al in 1985 suggested that the trig- gering factor of early onset renal failure was renal dysplasia. 4 However, in those who demonstrated renal failure later in childhood the authors believed that the triggering factor was chronic bladder dysfunction. Three years later Parkhouse et al iden- tified daytime urinary incontinence at age 5 years to be a poor prognostic sign and the most significant prognostic indicator. 5 They found that 46% of boys who were incontinent at age 5 years ended up with chronic renal failure, while only 4% of those continent at age 5 ended up with renal failure. It was not until 1997 that we began reporting on the effectiveness of pharmacotherapy in improving hydronephrosis, correcting vesicoureteral reflux, decreasing post-void residuals and rendering these children continent. 6,7 Holmdahl et al in 1996 suggested that many boys with PUV end up with large hypercompliant blad- ders at puberty, often without the ability to sustain an effective emptying detrusor contraction, or what is now referred to as myogenic failure. 8 De Gennaro et al made similar observations while hypothesizing that myogenic failure results as a consequence of the bladder response to chronically increased detrusor pressures when younger. 9 However, few articles at that time suggested early urodynamic investigations to identify increased detrusor pres- sures, or advocated an aggressive proactive phar- macological approach to prevent progression to myogenic failure. Instead most authors seemed to accept that myogenic failure was inevitable in some boys with PUV. Like De Gennaro, we believe that myogenic failure is less an inevitability and more a consequence of untreated bladder dysfunc- tion, and we treat these boys with anticholinergics early on, often beginning in early infancy. As a result, we have successfully prevented development of myogenic failure, a condition reported by Lopez Pereira 10 and Misseri 11 et al, in nearly all of our valve patients in addition to poor compliance, which is associated with increased renal failure. More controversial is the existence of secondary bladder neck obstruction (BNO), a condition charac- terized by increased voiding Pdet and depressed uroflow in the absence of residual valve tissue and urethral stricture. Before 1970 secondary BNO was considered to be common in patients with PUV, and many boys, especially in Finland, underwent trans- urethral bladder neck incision (BNI). However, once it was reported that boys could end up incontinent following bladder neck widening procedures, these fell out of favor. McGuire and Weiss in 1975 reported successful use of the alpha blocker phenoxybenz- amine for secondary BNO in 2 boys with PUV who had difficulty voiding. 12 In 2004 we reported on 7 boys with persistent HUN who did not have improvement on anticholinergics and were diagnosed with sec- ondary BNO on urodynamics. 7 All 7 patients were treated, 2 with BNI and 5 with alpha blocker therapy. Five of the 7 patients subsequently had resolution or significant reduction of their HUN. Kajbafzadeh et al in 2007 reported on 22 boys who underwent BNI at valve ablation, with no patient demonstrating any bladder dysfunction at a mean followup of 4.5 years. 13 Interestingly none of 10 boys who are now older than 21 ended up with retrograde ejaculation or inconti- nence (personal communication). More recently Androulakakis et al suggested that myogenic failure is a consequence of persistent BNO, and that either alpha blocker therapy or BNI should be used to treat or prevent myogenic failure. 14 It is important to recognize that secondary BNO is a urodynamic diagnosis and not a diagnosis that can be made endoscopically or radiographically. A bladder neck that is obstructive can occasionally have a normal maximum flow rate (Qmax) because of a 0022-5347/16/1961-0016/0 THE JOURNAL OF UROLOGY ® Ó 2016 by AMERICAN UROLOGICAL ASSOCIATION EDUCATION AND RESEARCH,INC. http://dx.doi.org/10.1016/j.juro.2016.04.049 Vol. 196, 16-17, July 2016 Printed in U.S.A. 16 j www.jurology.com