Context
The incidence and awareness of postprostatectomy incontinence (PPI) has increased during the past few years, probably because of an increase in prostate cancer surgery. Many theories have been postulated to explain the pathophysiology of PPI.
Objective
The current review scrutinizes various pathophysiologic mechanisms underlying the occurrence of PPI.
Evidence acquisition
A search was conducted on PubMed and EMBASE for publications on PPI. The primary search returned 2518 publications. Animal and basic research studies, letters, publications on prostatectomy for benign reasons, pathology of prostatic carcinoma, radiotherapy and hormone therapy of prostatic carcinoma, and review articles were all used as criteria for exclusion from the study. A total of 128 publications were selected for final analysis.
Evidence synthesis
Neuromuscular anatomic elements and pelvic support are known to influence PPI as evidenced by multiple publications. A number of non-anatomic and surgical elements have been postulated as contributing factors to PPI. Biological factors and preoperative parameters include: functional bladder changes, age, body mass index (BMI), pre-existing lower urinary tract symptoms (LUTS), prostate size, and oncologic factors. Multiple studies reported the impact of specific anatomic/surgical factors, including fibrosis, shorter membranous urethral length (MUL), anastomotic stricture, damage to the neurovascular bundle, and extensive dissection, all of which have a negative impact on the continence status of patients following radical prostatectomy (RP). Investigation of the impact of techniques to spare the bladder neck and additional procedures to reconstruct the posterior or anterior support structures (eg, the Rocco stitch) on continence status is ongoing.
Conclusions
Anatomic support and pelvic innervation appear to be important factors in the etiology of PPI. Biological/preoperative factors including greater age at time of surgery, pre-existing LUTS, high BMI, shorter MUL, and functional bladder changes have a negative impact on continence after RP. Extensive dissection during surgery, damage to the neurovascular bundle, and postoperative fibrosis also have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior fixation of the bladder-urethra anastomosis are associated with better continence rates. There is still debate about whether posterior pelvic reconstruction leads to better postoperative continence rates.
Patient summary
Radical prostatectomy is an oncologic procedure and thus requires removal of the entire prostate gland and seminal vesicles, ideally with negative surgical margins. This sometimes results in urinary incontinence. The factors contributing to urinary incontinence are explained in this article.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
Persistent urinary incontinence (UI) after radical prostatectomy (RP), commonly referred to as postprostatectomy incontinence (PPI), is an adverse event that leads to significant distress. Rates of PPI vary and depend on the definition of incontinence, severity, bother, and the methodology to assess its magnitude. While multiple factors are associated with the development of PPI, surgical modifications also play a role. The influence of advanced surgical techniques such as laparoscopic robot-assisted RP (RARP) on continence remains a point of debate. With the increase in surgery for prostate cancer, there has been a concomitant increase in the prevalence of PPI and thus greater awareness of the problem. The etiology of PPI is multifactorial and has been the subject of much study.
In a systematic review of more than 8000 men who underwent RARP, laparoscopic prostatectomy, or retropubic prostatectomy, Ficarra et al [1]
The natural history of urinary function recovery after RP is such that most patients regain urinary continence within the first year; however, modest improvement in urinary continence can still be observed through the second year [2]
Knowledge about the anatomy of the urethral sphincter complex and its surrounding structures and innervation in relation to urinary continence is well described in the literature. We provide a brief description of the latest understanding of the anatomy in Section 3. The function of these anatomic structures and their specific role in maintaining urinary continence is much less well understood. The role of these structures in urinary continence is mostly inferred from the effect of applying correcting measures to improve urinary continence. More review manuscripts have been published that elucidate the mechanisms underlying PPI. For example, Loughlin and Prasad [3]
Pub Med and EMBASE were searched for publications on PPI from January 1, 1990 to May 20, 2015. We chose 1990 because this year was approximately when RP was first performed. The search terms were: urinary incontinence, urinary stress incontinence, urinary urge incontinence, and RP. Details of search methods are shown in the Supplementary material. The search was limited to publications written in English. The inclusion criteria were source publications (clinical studies) describing risk factors and potential pathologic mechanisms underlying urinary incontinence following RP and their impact on current surgical correction practice. The exclusion criteria were: animal studies; case reports; letters; publications on simple prostatectomy, transurethral resection of the prostate, cryotherapy, laser vaporization, and other less invasive approaches; articles on the pathophysiology of benign prostatic hyperplasia, the pathology of prostatic carcinoma, and radiotherapy and hormonal therapy for prostatic carcinoma; and review articles. The primary search returned 2518 publications, from which 128 articles were selected for final analysis after applying the inclusion and exclusion criteria. A flow diagram of the selection process is shown in Figure 1. The level of evidence (LE) and sample size for studies included in the final analysis are shown in the evidence synthesis to indicate the strength of evidence for each potential PPI contributory factor.
The urethral sphincter complex consists of two functionally independent components, an internal or lissosphincter of smooth muscle and an outer or external rhabdosphincter of skeletal muscle, that are thought to be responsible for passive and active continence, respectively [4]
The supporting structures of the male urethra can be divided into the anterior and posterior support structures and the pelvic floor. The anterior urethral support structures contain the pubourethral ligaments, comprising the pubovesical ligament (PVL), the puboprostatic ligament (PLL), and the tendinous arch of the pelvic fascia. These ligaments stabilize the position of the bladder neck as well as the external sphincter complex, and help to secure the membranous urethra to the pubic bone [8]
The posterior support consists of the perineal body (central perineal tendon), Denonvillier's fascia, the rectourethralis muscle, and the levator ani complex [9]
The third support structure is the pelvic floor, composed of the levator ani muscle and the surrounding fascia [11]
It is postulated that the overall role of the support structures is to provide all-round stability and suspensory support for the urethral sphincter complex [13]
Normally the omega-shaped urethral rhabdosphincter has its anchoring points dorsally at the so-called conjoined fibrous tissue [14]
It has been shown that preservation of the PPL and PVL to allow proper sphincter functioning improves PPI (LE 1b–3, sample size range 34–691) [6]
There has been much recent debate about the so-called hypermobility of the bulbous urethra that causes PPI and the restoration of continence by correction of this hypermobility and repositioning of the bulbous urethra in males. This is analogous to the hammock theory for women as reported by DeLancey [22]
Burnett and Mostwin [23]
A well-performed RP will probably not injure any of the pelvic floor musculature. However, it will change the support for the bladder and may result in varying degrees of incontinence. Direct damage to the puboperinealis muscle and the puboprostatic ligaments can occur after extensive dissection of the prostatic apex or while trying to create a more defined urethral stump. Placing sutures for urethrovesical anastomosis into lateral tissue may also damage the puboperinealis muscle and probably should be avoided; conversely, reconstruction of periprostatic tissue probably leads to better urinary continence outcomes.
Evidence was retrieved from studies with LE 3 and a sample size ranging from 36 to 985 patients. Tuygun et al [28]
The pudendal nerve supplies innervation to the urethral sphincter complex [30]
Newly elucidated anatomic dissections point to the cavernous nerves providing at least a small portion of the innervation to the membranous urethra [42]
The urothelium is surrounded by elastic tissue and fibers of smooth and striated muscle. At the junction of the inferior bladder and the proximal urethra, the urothelium becomes a key component of sphincter function. The elastic components of the proximal urethral wall are responsible for coaptation of the urothelium (zone of coaptation). This proper adhesion of the urethral wall provides primary resistance to the urine to maintain continence (LE 3, sample size 985) [29]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 66 to 268 patients. The development of de novo post-RP detrusor overactivity (DO) is another biological risk factor that has been suggested to be associated with PPI. Functional changes including DO and reduced compliance may develop after RP due to denervation or devascularization of the urinary bladder [47]
Evidence was retrieved from studies with LE 3 and a sample size ranging from 111 to 2849 patients. Older patients are expected to have pre-existing LUTS before RP because of an enlarging prostate and/or age-related functional changes in the urinary bladder and urethra. In a study that included 268 patients with LUTS after RP. In a study that included 308 patients who underwent RARP, Novara et al [50]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 111 to 2849 patients. Wolin et al [55]
Evidence was retrieved from studies with LE 3 for sample sizes ranging from 30 to 124 patients. In a group of 30 patients who underwent TURP before RP, Elder et al [58]
In a study using American Urological Association symptom scores (LE 3, sample size 106), 74 of 106 patients reported occasional leakage after RP; these patients had significantly more noticeable LUTS compared to the 32 patients who were completely dry [60]
Evidence was retrieved from studies with LE 2b–3 for sample sizes ranging from 64 to 2849 patients. Urethral length preservation during RP improves continence outcomes [62]
Nguyen et al [67]
On the contrary, Borin et al [69]
In a systematic review of evidence regarding urinary incontinence after salvage RP, Chade [70]
In an attempt to clarify preoperative predictors of urinary continence after prostatectomy, Matsushita [52]
Table 1 and Table 2 summarize the factors presumed to cause PPI. Publications both in favor of and contesting these factors are listed to give a clear picture of the current state of the art. Quantitative data are provided in Supplementary Tables 1 and 2.
Table 1
Biological factors contributing to postprostatectomy incontinence
LE = level of evidence; RP = radical prostatectomy; TURP = transurethral resection of prostate; RT = radiation therapy; LUTS = lower urinary tract symptoms.
Table 2
Surgical factors contributing to postprostatectomy incontinence
LE = level of evidence.
There is evidence in the literature that anatomic support and pelvic innervation are important factors in the etiology of PPI. Damage to the urethral sphincter complex, the surrounding structures, or their innervation leads to higher rates of PPI. Certain biological factors and parameters known preoperatively, including greater age, higher BMI, pre-existing LUTS, lower MUL, and functional bladder changes, have a negative impact on continence rates after RP. Among the many surgical and technical factors proposed in the literature as contributing to the development of UI following RP, extensive dissection during surgery, damage to the NVB, and the development of postoperative fibrosis have a substantial negative impact on the continence status of men undergoing RP. Sparing of the bladder neck and anterior, and possibly posterior, fixation of the bladder-urethra anastomosis are associated with better continence rates.
Author contributions: John Heesakkers had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Heesakkers, Stenzl, Farag.
Acquisition of data: Farag, Heesakkers, Bauer, Sandhu, De Ridder.
Analysis and interpretation of data: Heesakkers.
Drafting of the manuscript: Heesakkers, Farag, Bauer, Sandhu, De Ridder.
Critical revision of the manuscript for important intellectual content: Farag.Statistical analysis: None.
Obtaining funding: Heesakkers.
Administrative, technical, or material support: Heesakkers, Farag.
Supervision: Heesakkers, Stenzl.
Other: None.
Financial disclosures: John Heesakkers certifies that all conflicts of interest, including specific financial interests and relationships and affiliations relevant to the subject matter or materials discussed in the manuscript (eg, employment/affiliation, grants or funding, consultancies, honoraria, stock ownership or options, expert testimony, royalties, or patents filed, received, or pending), are the following: Jaspreet Sandhu has received consultancy fees from American Medical Systems (now Boston Scientific). The remaining authors have nothing to disclose.
Funding/Support and role of the sponsor: This manuscript is part of COST Action BM1209 ReST funded by the EU. The sponsor played no direct role in the study.
