Bladder and Urethral Sphincter Function after Radical Retropubic Prostatectomy: A Prospective Long-Term Study

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1 european urology 54 (2008) available at journal homepage: Voiding Dysfunction Bladder and Urethral Sphincter Function after Radical Retropubic Prostatectomy: A Prospective Long-Term Study Antonella Giannantoni *, Ettore Mearini, Alessandro Zucchi, Elisabetta Costantini, Luigi Mearini, Vittorio Bini, Massimo Porena Department of Urology and Andrology, University of Perugia, Perugia, Italy Article info Article history: Accepted October 25, 2007 Published online ahead of print on November 5, 2007 Keywords: Radical retropubic prostatectomy Urodynamics Voiding dysfunction Abstract Objective: In a prospective study we analysed the 3-yr results of the effects of radical retropubic prostatectomy (RRP) on detrusor and sphincter function by comparing urodynamic status preoperatively with that during longitudinal follow-up. Methods: Fifty-four consecutive patients underwent urodynamics with pressure flow studies and Valsalva leak point pressure measurements 3 7 d before RRP (baseline), and then 8 mo after surgery. Thirty-two patients were studied again 3 yr later. We analysed bladder compliance, detrusor overactivity (DO), detrusor contractility, and intrinsic sphincter deficiency (ISD). Results: There was a significant increase in the number of patients with reduced bladder compliance at the 8-mo follow-up. De novo reduced bladder compliance was detected in 32.3% of patients and persisted in 28.1% at the 36-mo follow-up. De novo detrusor hypocontractility was observed in 51% of patients at 8 mo ( p < 0.05) and persisted in 25% of cases 3 yr later. No patients showed any postvoid residual volume. The associations between detrusor hypocontractility with DO and between detrusor hypocontractility with ISD were detected in 76.2% and 44% of patients, respectively, at 8 mo, and in 25% and in 34% of cases, respectively, at 36 mo of follow-up ( p < 0.05 and p < 0.001). Conclusions: Following RRP detrusor hypocontractility, decreased bladder compliance, and ISD represent de novo dysfunction probably due to bladder denervation during surgery. They become established conditions over time in about 30% of patients. Nevertheless, they do not produce voiding symptoms because patients develop new voiding behaviours. # 2007 European Association of Urology. Published by Elsevier B.V. All rights reserved. * Corresponding author. Department of Urology and Andrology, University of Perugia, Policlinico Monteluce, Via Brunamonti 51, 06122, Perugia, Italy. Tel ; Fax: address: agianton@tin.it (A. Giannantoni) /$ see back matter # 2007 European Association of Urology. Published by Elsevier B.V. All rights reserved. doi: /j.eururo

2 658 european urology 54 (2008) Introduction Many urologists consider radical retropubic prostatectomy (RRP) the treatment of choice for patients with localised prostate cancer [1,2]. Despite increasing understanding of pelvic anatomy and recent developments in surgical techniques, urinary incontinence continues to be one of the most devastating complications. Predicting the time to recovery of urinary incontinence after RRP remains an impossible task, and the causes for the challenge are the multifactorial nature of incontinence, which involves preoperative, intraoperative, and postoperative factors [3]. Because urinary incontinence is a source of anxiety for both patients and physicians, new solutions and interventions are needed [4,5]. Urinary incontinence does not represent the only bladder dysfunction due to the operation. Bladder dysfunction after RRP may be represented by involuntary detrusor contractions, impaired bladder filling sensation, low bladder compliance (BC), and impaired detrusor contractility [6,7]. It has been suggested that these dysfunctions occur de novo following bladder denervation during surgery. However, they may also be induced by preexisting long-term bladder outlet obstruction (BOO) or may represent a consequence of bladder aging [8]. Although most previous studies on lower urinary tract dysfunction following RRP focussed on the prevalence and causes of urinary incontinence, only a few studies investigated, with only a shortterm follow-up, the presence of other urodynamic abnormalities and their clinical relevance. In a previous study we investigated clinical and urodynamic parameters in patients who underwent RRP by studying detrusor and urethral function before and after the operation over an 8-mo followup [6]. This present, prospective study analyses the influence of RRP on detrusor and sphincter function over a long-term follow-up. 2. Patients and methods 2.1. Demographics We included 54 consecutive patients with clinically localised prostate cancer (ct1c ct2c) undergoing RRP. All patients were informed about the scientific nature of the investigation and provided written informed consent Surgical technique The surgical technique adhered to that described by Walsh and was performed by two surgeons (M.P. and E.M.), with nerve-sparing and bladder-neck preserving techniques based on clinical stage, cancer location, patient age, and preoperative sexual function [1]. Briefly, with regard to the handling of the dorsal vein complex, after opening the endopelvic fascia bilaterally, a right-angle clamp was passed between the urethra and the dorsal vein complex, close to the prostate apex. A non-reabsorbable suture was passed through this tunnel and the dorsal vein complex was tied proximally. The dorsal vein complex was then tied distally, close to the bladder neck, using three interrupted sutures. The dorsal vein complex was then sectioned Clinical and urodynamic evaluation After we obtained the patient s history and conducted a physical examination, we performed urodynamic evaluation with Valsalva leak point pressure (VLPP) measurement 3 7 d before surgery (baseline evaluation), and 1 and 8 mo after surgery. An early time point (1 mo postoperatively) was established to study any early vesicourethral dysfunction. To obtain a more comprehensive picture of the dysfunction over time, we established the second time point at 8 mo because it has not been reported previously. Urodynamic evaluation was performed in the absence of any urinary tract infection, as detected with urinalyses and cultures. Thirty-two patients were able to be studied again 3 yr later because they were completely free from cancer and did not present with any previous therapy performed to control any recurrence of the disease (pharmacotherapy, radiotherapy). For incontinent patients we recorded the number of daily pads (0 1 vs. >1) and daily episodes of urgency or urge incontinence. Urodynamic assessment was performed according to the International Continence Society Standards [10] and involved water cystometry with 37 8C normal saline solution at a filling rate of 50 ml/min. A 6F double-lumen Nelaton transurethral catheter was used for infusion and for recording intravesical pressure, and a 16-channel intrarectal balloon catheter was used to record abdominal pressure. We assessed detrusor overactivity (DO) and BC, defined as normal (>20 ml/cm water), impaired (10 20 ml/cm), and poor (<10 ml/cm water) [10]. At capacity, patients were asked to void, and the maximum flow rate (Q max ), detrusor pressure at maximum flow rate (Pdet max ), and postvoid residual volume were recorded. BOO and detrusor contractility were assessed on pressure flow studies using the Schafer nomogram [11]. Grades 0 2 bladder outlet conditions were considered unobstructed, whereas grades 3 6 were considered obstructed. The nomogram was also used to classify detrusor strength as normal, weak, or very weak. During the pressure flow study, voiding by straining or by detrusor contraction was recorded [12]. VLPP was evaluated with the patient in an upright position, at a filling volume of 200 ml, after the urethral catheter was removed. Defined as the lowest abdominal pressure induced by cough or Valsalva manoeuvre causing visible stress incontinence, it provided an assessment of intrinsic sphincter deficiency (ISD) [13]. DO, BC, impaired detrusor contractility, and ISD have been stratified by nervesparing status (bilateral, monolateral, non nerve-sparing technique).

3 european urology 54 (2008) Data analysis Statistical analysis was performed using tests for repeated nonparametric data, namely, the Friedman and Cochran Q tests. The Bonferroni correction was applied to the Wilcoxon and McNamara tests for post-hoc multiple comparisons. The x 2 test was applied for trend. The level of statistical significance was set at p < All data analyses were performed using SPSS, release for Windows (SPSS, Chicago, IL, USA). and nomogram results, respectively. DO was detected in 33 patients (61.2%), impaired detrusor contractility in 21 patients (38.8%), and reduced BC in 20 (37.1%). BOO was found in 32 patients (59.3%). We observed the following associations: BOO with reduced BC in 12 patients (22.2%), impaired detrusor contractility associated with DO in 9 patients (16.6%), and BOO with DO in 19 cases (35.2%). On VLPP examination no patients showed ISD. Table 2 lists results on BC and on pressure flow studies. 3. Results 3.1. Demographics Mean patient age standard deviation was 67 5 yr. RRP involved bilateral, unilateral, and non nervesparing techniques in 29, 15, and 10 patients, respectively. Bladder-neck preservation was performed in all cases. Overall, no severe complications or lymphoceles were detected. A surgical evacuation of haematomas in the Retzius space was performed in two patients soon after surgery Baseline evaluation (54 patients) Three patients complained of urgency with urge incontinence, but none used pads or collecting devices. Table 1 and Fig. 1 present the urodynamic 3.3. Follow-up at 8 mo (54 patients) Table 1 shows urodynamic results. DO was detected in 38 (70.3%) patients, and in 8 (14.8%) it appeared as a new-onset dysfunction; DO disappeared in 3 cases. Twenty-one patients (55.5%) with DO complained of overactive bladder symptoms. There was a significant increase in the number of patients with reduced BC (29 vs. 20, p < 0.05). As a de novo dysfunction, reduced BC was detected in 11 (20.4%) patients and it was a pre-existing abnormality in 18. Reduced BC resolved in 2 patients. BOO disappeared in 30 patients, and 4 presented with de novo BOO because of the presence of an anastomotic stricture. These strictures were promptly treated with a surgical incision, and the patients were followed up again. Fig. 2 presents the results using the Schafer nomogram. Table 1 Urodynamic dysfunction in 54 patients observed preoperatively and 8 mo following radical retropubic prostatectomy Urodynamics Baseline 8 mo p value No. of patients % No. of patients % Bladder outlet Normal Obstructed Detrusor Normal Hyperactive n.s. Bladder compliance Normal Impaired or poor Detrusor contractility Normal Weak Voiding Without straining With straining ISD DO and hypocontractility DO and BOO Hypocontractility and ISD ISD = intrinsic sphincter deficiency; DO = detrusor overactivity; BOO = bladder outlet obstruction.

4 660 european urology 54 (2008) Fig. 1 Detrusor pressure at maximum detrusor pressure (Pdet max ) and maximum flow rate (Q max ), as assessed by the Schafer nomogram in 54 patients observed before radical retropubic prostatectomy. With regard to detrusor contractility, the strength of the detrusor muscle significantly worsened as compared to baseline ( p < 0.01). Twenty-two (40.7%) patients showed normal detrusor function, and 32 (59.3%) had impaired detrusor contractility. Sixteen (29.6%) patients with a normal detrusor function at baseline presented with de novo detrusor hypocontractility after surgery. Impaired detrusor contractility persisted in 16 (76.2%) patients. Five (9%) patients recovered to a normal detrusor strength. No patient showed any postvoid residual volume. Overall, 6 of 32 patients with impaired detrusor contractility complained of reduced and interrupted urinary stream. ISD with stress urinary incontinence was observed in 40 patients (74%), 9 patients presented with mixed incontinence, 2 patients with urge incontinence, and 3 free from incontinence. All but one patient needed one or no pads daily. Overall, there was a significant increase in the number of patients who presented with DO associated with impaired detrusor contractility (21 vs. 9, Fig. 2 Detrusor pressure at maximum detrusor pressor (Pdet max ) and maximum flow rate (Q max ), as assessed by the Schafer nomogram in 54 patients observed 8 mo following radical retropubic prostatectomy. The dark circles refer to 32 patients followed up at 1, 8, and 36 mo. p < 0.05). This association was detected as a de novo condition in 16 (29.6%) patients. Finally, we could detect the association between impaired detrusor contractility and urethral sphincter weakness in 24 patients (44.4%, p < ). At this follow-up we found a significant difference in the number of strain voiders as compared to baseline (26 vs. 11, p < 0.05). When stratifying DO, BC, impaired detrusor contractility, and ISD by nerve-sparing status, no significant linear-by-linear association was detected at 1-, 8-, and 36-mo follow-up Follow-up at 36 mo (32 patients) Table 3 presents the results in the 32 patients available at 36 mo. Fig. 3 shows the nomogram results. DO was detected in 18 (56.3%) patients. In 5 (15.6%) patients it was a de novo dysfunction and in 13 (43.7%) a pre-existing abnormality. Table 2 Mean bladder compliance, Pdet max, and Q max in 54 patients preoperatively and at 8 and 36 mo (32 patients) following radical retropubic prostatectomy Mean SD, baseline Mean SD, 8 mo Mean SD, 36 mo (13 patients) Bladder compliance, ml/cm H 2 O Pdet max,cmh 2 O Q max, ml Baseline versus 8 and 36 mo, p < Pdet max = maximum detrusor pressure; Q max = maximum flow rate; SD = standard deviation.

5 european urology 54 (2008) Table 3 Urodynamic dysfunction in 32 patients observed preoperatively and 8 and 36 mo following radical retropubic prostatectomy Urodynamics 36 mo Total no. of patients % Preoperative condition, no. of patients De novo condition, no. of patients Bladder outlet Normal Obstructed 0 0 Detrusor Normal Hyperactive Bladder compliance Normal Impaired or poor Detrusor contractility Normal Weak Voiding Without straining With straining ISD DO and hypocontractility DO and BOO Hypocontractility and ISD ISD = intrinsic sphincter deficiency; DO = detrusor overactivity; BOO = bladder outlet obstruction. Eight patients recovered normal detrusor function. Overall, 8 patients (44.4%) presenting with DO complained of overactive bladder symptoms. Reduced bladder compliance persisted in 9 (28.1%) patients and was resolved in 8. Five (15.6) patients showed de novo reduced compliance. With regard to the status of detrusor contractility, 8 (25%) patients presented with detrusor hypocontractility and 5 recovered normal detrusor function. A low degree of stress urinary incontinence (few drops/wk) persisted in 19 (59.3%) patients, whereas no patient complained of urge urinary incontinence. DO associated with impaired detrusor contractility was detected in 7 (21.8%) patients; it was a de novo condition in 4 of these. No patients showed any postvoid residual volume. Impaired detrusor contractility associated with urethral sphincter weakness was detected in 11 (34.4%) patients. It was a persisting condition in 8 cases and a de novo dysfunction in 3. Eight patients with impaired detrusor contractility at 8 mo recovered normal detrusor function. No patients showed any postvoid residual volume. At this follow-up there was a significant difference between the number of patients presenting with impaired detrusor contractility and urethral sphincter weakness as compared to that at baseline ( p < ). Fig. 3 Detrusor pressure at maximum detrusor pressure (Pdet max ) and maximum flow rate (Q max ), as assessed by the Schafer nomogram in 32 patients observed 36 mo following radical retropubic prostatectomy. The dark circles refer to 32 patients followed up at 1, 8, and 36 mo. 4. Discussion After RRP a wide spectrum of clinical and urodynamic abnormalities can be detected, and urethral sphincter weakness, which is usually the only

6 662 european urology 54 (2008) described dysfunction, is frequently associated with DO, reduced BC, impaired detrusor contractility, and voiding by straining [6,7,9,12,14,15]. The wide anatomic dissection around the prostate during surgery damages the afferent and efferent innervation of the trigone, striated sphincter, bladder neck, and posterior urethra, with resulting incompetence of the continence mechanisms and partial denervation of the detrusor muscle. Until now, few prospective studies have been published to investigate the role of RRP as a cause of detrusor or sphincter damage, by comparing preoperative and postoperative urodynamic conditions [6,9,16 23]. Moreover, in these previous studies, the maximum reported follow-up is 23 mo. To our knowledge, the present study is the first one reporting the results on bladder and urethral sphincter function after RRP in a long-term followup. The investigation of urinary symptoms in these patients allowed us to quantify the clinical impact of the dysfunction, even if the use of standardised questionnaires would have helped to better study these symptoms and quality of life after RRP. This study shows that after RRP a high proportion of patients (70.3%) were affected by DO and about the half of these patients complained of overactive bladder symptoms. It is worth noting that DO was also observed in 61.2% of patients before surgery, which indicates that the abnormality can be attributed to the surgical damage in a small percentage of patients. At the 36-mo follow-up, the dysfunction persisted in 56.3% of 32 men, and about 40% of these presented with overactive bladder symptoms. Also in this case, DO was found as a newonset dysfunction in about half of this limited number of patients. Thus, it appear to be more significant that, although the relief of obstruction with the operation should have reversed DO, sustained neuroplasticity due to BOO could maintain the abnormality over time [21]. Another explanation may be due to the loss of the guarding reflex as a result of the operation. Indeed, surgical damage to the pelvic innervation, with a loss of afferent innervation, may have impaired the guarding reflex of the striated urethral sphincter, thus leading to leakage with bladder filling [24,25]. The presence of urine in the proximal urethra activates neuronal circuits from the sphincter to the bladder, thus inducing involuntary detrusor contractions [26]. In a small number of patients some urodynamic dysfunction documented before the intervention disappeared soon after. This is the case for DO and reduced BC, which disappeared in three and two patients, respectively, at the 8-mo follow-up. Because these patients showed severe BOO preoperatively, as documented in the Schafer nomogram (both in class 5), it is possible to argue that a dramatic resolution of the obstruction together with mild surgical damage could have determined the resolution of the dysfunction. This study confirms our previously reported data concerning the reduction of BC in a great proportion of patients who have undergone RRP [9]. In the present study, the dysfunction persisted in about 28% of patients over the 36-mo follow-up. Only Hellstrom et al reported impairment of BC in 82 patients but in a short-term follow-up of 8 wk [15].In the present study, recovery of normal BC was observed in about the half the patients at 36 mo. Given that impaired BC may be related to partial surgical decentralisation of the bladder [1], the recovery of normal compliance could be due to reinnervation of the bladder or to a resolution of postoperative tissue changes [8]. With regard to impaired detrusor contractility, the results of this study confirm that the dysfunction can be detected early, after the operation, in more than half the patients. At the 3-yr follow-up, the dysfunction persisted in 25% of cases. It is worth noting that impaired detrusor contractility was frequently associated with ISD. One possibility is partial decentralisation of the bladder as a result of its mobilisation during prostatectomy [12], combined with somatic denervation, because the branches of the pudendal nerves innervating the pelvic floor muscles and the striated urethral sphincter split before reaching the urogenital diaphragm [27]. The stage of prostate cancer does not seem to influence this neurologic damage [27]. The association between detrusor hypocontractility and ISD persisted in about 34% of cases at the second follow-up. This suggests that after RRP, dysfunction of both the detrusor muscle and the urethral sphincter are persisting conditions with time in a substantial proportion of patients. The association between impaired detrusor contractility and ISD may also indicate the acquisition of a new voiding behaviour, because patients find it easier and faster to void by straining through a sphincter mechanism with decreased resistance [12]. Furthermore, the new voiding pattern can explain why patients with a worsened detrusor strength did not show any postvoid residual volume. Indeed, in the present study voiding by straining was also present in 20% of cases before the operation. Because the majority of these patients had BOO, it is more reasonable to suppose that straining during voiding was a learned habit to empty the bladder completely.

7 european urology 54 (2008) Conclusions Bladder and urethral sphincter function can be adequately assessed by comparing urodynamic status before RRP and during longitudinal followup. Impaired detrusor contractility, decreased BC, and ISD occur as de novo dysfunctions in a substantial proportion of patients as a consequence of bladder denervation. They become established conditions over time in about 30% of cases. Nevertheless, these dysfunction do not produce voiding symptoms because patients develop new voiding behaviours to completely empty the bladder. Conflicts of interest The authors have nothing to disclose. References [1] Walsh PC. Anatomic radical retropubic prostatectomy ed 7. In: Walsh PC, Retik AB, Vaughan Jr ED, Wein AJ, editors. Campbell s urology, vol 3. Philadelphia: WB Saunders; p [2] Aus G, Abbou CC, Bolla M, et al. EAU guidelines on prostate cancer. Eur Urol 2005;48: [3] Touijer K. Urinary incontinence after radical prostatectomy: beauty is in the eye of the beholder. Eur Urol 2007;51: [4] Reheder P, Gozzi C. Trans-obturator sling suspension for male urinary incontinence including post-radical prostatectomy. Eur Urol 2007;52: [5] Onur R. Editorial comment on: Trans-obturator sling suspension for male urinary incontinence including post-radical prostatectomy. Eur Urol 2007;52: [6] Majoros A, Bach D, Keszthelyi A, et al. I. Urinary incontinence and voiding dysfunction after radical retropubic prostatectomy (prospective urodynamic study). Neurourol Urodyn 2006;25:2 7. [7] Porena M, Mearini E, Mearini L, Vianello A, Giannantoni A. Voiding dysfunction after radical retropubic prostatectomy: more than external urethral sphincter deficiency. Eur Urol 2007;52: [8] Chao R, Mayo ME. Incontinence after radical retropubic prostatectomy: detrusor or sphincteric causes. J Urol 1995;154:16 8. [9] Giannantoni A, Mearini E, Di Stasi SM, et al. Assessment of bladder and urethral sphincter function before and after radical retropubic prostatectomy. J Urol 2004;171: [10] Abrams P, Blaivas JG, Stanton SL, et al. The standardisation of terminology of lower urinary tract function. The International Continence Society Committee on Standardisation of Terminology. Scand J Urol Nephrol 1988;114: [11] Schafer W. Principles and clinical application of advanced urodynamic analysis of voiding function. Urol Clin North Am 1990;17: [12] Groutz A, Blaivas JC, Chaikin DC, et al. The pathophysiology of post-radical prostatectomy incontinence: a clinical and video-urodynamic study. J Urol 2000;163: [13] McGuire EJ, Fitzpatrick CC, Wan J, et al. Clinical assessment of urethral sphincter function. J Urol 1993;150: [14] Gohma MA, Boone TB. Voiding patterns in patients with post-prostatectomy incontinence: urodynamic and demographic analysis. J Urol 2003;169: [15] Hellstrom P, Lukkarinen O, Kontturi M. Urodynamics in radical retropubic prostatectomy. Scand J Urol Nephrol 1989;23:21 4. [16] Hammerer P, Huland H. Urodynamic evaluation of changes of urinary control after radical retropubic prostatectomy. J Urol 1997;175: [17] Kleinhans B, Gerharz E, Melekos M, Weingärtner K, Kälble T, Riedmiller H. Changes of urodynamic findings after radical retropubic prostatectomy. Eur Urol 1999;35: [18] Foote J, Yun S, Leach GE. Postprostatectomy incontinence: pathophysiology, evaluation and management. Urol Clin North Am 1991;18: [19] Constantinou CE, Frehia FS. Impact of radical prostatectomy on the characteristics of bladder and urethra. J Urol 1992;148: [20] Leach GE, Yun SK. Post-prostatectomy incontinence: part 1. The urodynamic findings in 107 men. Neurourol Urodynam 1992;11:91 7. [21] Leach GE, Trockman B, Wong A, et al. Post-prostatectomy incontinence: urodynamic findings and treatment outcomes. J Urol 1996;155: [22] Kielb SJ, Clemens JQ. Comprehensive urodynamic evaluation of 146 men with incontinence after radical prostatectomy. Urology 2005;66: [23] Huckabay C, Twiss C, Berger A, et al. A urodynamics protocol to optimally assess men with post-prostatectomy incontinence. Neurourol Urodynam 2005;24: [24] Steers WD, Ciambotti J, Erdman S, et al. Morphological plasticity in efferent pathways to the urinary bladder of the rat following urethral obstruction. J Neurosci 1990;10: [25] Presti Jr JC, Schmidt RA, Narayan PA, et al. Pathophysiology of urinary incontinence after radical prostatectomy. J Urol 1990;143: [26] Jung SY, Fraser MO, Ozawa H, et al. Urethral afferent nerve activity affects the micturition reflex; implication for the relationship between stress incontinence and detrusor instability. J Urol 1998;162: [27] Steiner MS, Morton RA, Walsh PC. Impact of anatomical radical prostatectomy on urinary incontinence. J Urol 1991;145:512 4.

8 664 european urology 54 (2008) Editorial Comment on: Bladder and Urethral Sphincter Function after Radical Retropubic Prostatectomy: A Prospective Long-Term Study Dragan Golijanin, Ganesh S. Palapattu University of Rochester School of Medicine, Rochester, NY, USA Ganesh_Palapattu@URMC.Rochester.edu Urinary incontinence is one of the most devastating complications after open retropubic radical prostatectomy and its incidence ranges widely, from 1% [1] to 31% [2]. Published literature varies in reported incontinence rates largely due to variances in both patient and physician factors. If patients are personally interviewed by investigators, reported urinary incontinence rates after 1 yr are 5 23% [3,4], but this rate is significantly higher, reaching up to 31%, when patients are assessed by self-administered questionnaires or population surveys [2]. In a multivariate analysis the age of the patient, surgical technique, preservation of the neurovascular bundles, and development of bladder-neck contracture are known independent predictors of urinary incontinence after radical prostatectomy [3]. Urodynamic changes resulting from radical prostatectomy have been well documented. Fortunately, many of these abnormalities do not translate into bothersome lower urinary tract symptoms [5,6]. In the present study from Italy [7], the authors sought to study bladder and urethral sphincter function longitudinally with urodynamics, beginning before radical prostatectomy. Fifty-four consecutive patients were assessed preoperatively and then postoperatively (8 mo). Thirty-two patients were studied out to 36 mo. The main findings of the study are that detrusor hypocontractility, decreased bladder compliance (BC), and intrinsic sphincter deficiency (ISD) occur in a significant proportion of men postoperatively de novo and that these findings may persist in a significant proportion of men. At baseline, evidence of bladder outlet obstruction was seen in 59.3% of patients, detrusor overactivity in 61.2%, and reduced BC in 37.1%. Validated questionnaires were not used. At 8 mo of follow-up 70.3% of patients were affected by detrusor overactivity (DO) and about the half of these patients complained of symptoms of overactive bladder. New-onset decrease in bladder capacity was seen in 11 patients (20.4%). One third of patients developed detrusor hypocontractility postoperatively. Interestingly, only 10% patients with decreased detrusor contractility complained of reduced urinary stream. At the 3-yr follow-up, detrusor contractility dysfunction persisted in 25% evaluable cases. It is worth noting that impaired detrusor contractility was frequently associated with ISD and persisted in about 34% of cases at the second follow-up. The present report [7] makes important observations regarding the urodynamic changes that occur after prostatectomy. What should not be lost is the value of adhering to good surgical technique and the imperative to treat the patient, not numbers. References [1] Kielb S, Dunn RL, Rashid MG, et al. Assessment of early continence recovery after radical prostatectomy: patient reported symptoms and impairment. J Urol 2001;166: [2] Fowler Jr FJ, Barry MG, Lu-Yao G, et al. Patient-reported complications and follow-up treatment after radical prostatectomy. The National Medicare Experience: (updated June 1993). Urology 1993;42: [3] Eastham JA, Kattan MW, Rogers E, et al. Risk factors for urinary incontinence after radical prostatectomy. J Urol 1996;156: [4] Noh C, Kshirsagar A, Mohler JL. Outcomes after radical retropubic prostatectomy. Urology 2003;61: [5] Porena M, Mearini E, Mearini L, Vianello A, Giannantoni A. Voiding dysfunction after radical retropubic prostatectomy: more than external urethral sphincter deficiency. Eur Urol 2007;52: [6] Majoros A, Bach D, Keszthelyi A, et al. Urinary incontinence and voiding dysfunction after radical retropubic prostatectomy (prospective urodynamic study). Neurourol Urodyn 2006;25:2 7. [7] Giannantoni A, Mearini E, Zucchi A, et al. Bladder and urethral sphincter function after radical retropubic prostatectomy: a prospective long-term study. Eur Urol 2008;54: DOI: /j.eururo DOI of original article: /j.eururo