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A patient who underwent a nerve-sparing radical retropubic prostatectomy, who was post-operatively continent, developed urinary incontinence associated with erectile recovery. The bladder was stable and minimal distortion of the bladder neck was observable on videourodynamics. We suggest that the mechanism of incontinence is urethral traction, induced by an erect penis causing an anatomically minor, but functionally significant opening of the bladder neck/sphincter mechanism. This case highlights the importance of a stable sphincter mechanism in maintaining continence. It also emphasizes the fine line between success and failure in post radical retropubic prostatectomy continence; and is a reminder of the importance of surgical technique in achieving the goal of a cancer free, potent, continent patient.
We report on a case of urinary incontinence associated with erectile recovery in an otherwise continent man post radical retropubic prostatectomy.
The patient (aged 76) underwent a nerve-sparing radical retropubic prostatectomy for clinically localized prostate cancer. He made an excellent post-operative recovery and regained full continence within 3 months. He suffered from impotence post-operatively, which was only partially responsive to PDE5 inhibitor treatment. Subsequently, he was treated with intracavernosal alprostadil, with good effect. However, he experienced urinary leakage with erections, which occurred despite emptying his bladder pre-injection.
The patient underwent video-urodynamic examination prior to, and subsequently with, an induced erection. This confirmed that the bladder was stable, completely emptied, and that the patient was continent prior to having an induced erection (see Figure 1a). Alprostadil induced a moderate erection at which point significant urinary leakage was observed (see Figure 1b). Slight lengthening of the membranous urethra was observed at the time of erection, however the bladder neck distortion induced by the erection was minimal with no observable descent. It was not felt that the incontinence could be corrected surgically and the patient is contemplating stopping erectile dyfunction treatment.
In our, single surgeon, series of 186 cases our pad-free continence rate is 96%. It is our preferred technique to leave a long intra-pelvic urethral stump prior to urethral division and the dorsal venous complex is divided over a wire and subsequently oversewn to avoid bunching of the complex and distortion of the sphincter. The bladder neck is carefully reconstituted with eversion of the bladder mucosa. We suggest that erectile incontinence occurs when the penis is erect due to traction being exerted on the urethra, which transmits to the vesico-urethral anastomosis, causing an anatomically minor, but functionally significant opening of the external sphincter. This is sufficient to cause urinary incontinence. This report supports the advocation of stabilizing the sphincter by suturing it to the rear of the pubis symphysis.
A previous study1 demonstrated that stretched penile length was reduced in 68% of patients following retropubic prostatectomy; and in 19%, this amounted to a shortening of at least 15%. Post-operative cavernosal fibrosis was suggested as a possible cause, as there was no correlation with prostate size, operative technique or potency. One possibility not suggested was that the shortening was due to urethral traction. Other factors, which have been shown to be associated with increased incontinence post radical retropubic prostatectomy are large prostates, and a membranous urethral length less than an arbitrary 12 mm, measured from pre-operative endo-rectal magnetic resonance imaging scans.2 A large prostate would imply a greater distance for the bladder to be mobilized for the bladder-urethra anastomosis and possibly greater posterior traction. Similarly, a short membranous urethra implies that the posterior traction from the bladder is transmitted more directly to the sphincter and consequently may impair continence.
These studies demonstrate the fine line between success and failure in maintaining urinary continence post radical retropubic prostatectomy. Incontinence post radical retro-pubic prostatectomy occurs in up to 20% patients, and persists after a year in up to 10%. Impotence is reported in up to 80%. Groutz3 found the predominant cause of post radical retropubic prostatectomy incontinence was intrinsic sphincter deficiency. This was present in 88% of patients with persistent incontinence post radical retropubic prostatectomy, but occurred in isolation in only one-third. Detrusor instability, detrusor failure and reduced urethral compliance, consistent with urethral scarring, were all identified as concomitant pathologies although rarely in isolation. Three operative strategies have been suggested to maintain continence post radical retropubic prostatectomy. The first is bladder neck preservation, whereby the circular bladder neck fibres are preserved4. The second is preservation of the puboprostatic ligaments to maintain anterior urethra support and minimize trauma to the striated sphincter5. The third is neurovascular nerve preservation. All of theses have been shown to improve the time to continence, but no statistical difference has been identified in long-term continence, either individually or in combination.6
We believe that this case is the first reported case of incontinence being induced by erectile recovery post radical prostatectomy.
Acknowledgments Appreciation is given to J Garden for her technical assistance.