**1. Introduction**

Prostate cancer is the most common tumor among men. It has a strong genetic component and is the second most diagnosed tumor worldwide after lung cancer [1, 2]. Radical prostatectomy (RP) and radiation beam therapy represent comparable treatment options for localized disease [3].

One of the major complications of RP is urinary incontinence (UI), with a notoriously negative impact on the patient's quality of life (QoL) and daily activities [4]. UI is the complaint of any involuntary loss of urine [5], with a prevalence of 11–34% in older men [6, 7]. The occurrence of post-prostatectomy urinary incontinence (PPUI) rate varies from 5 to 40% [8] up to 69% [9], depending on the series of patients examined. These differences in PPUI incidence have been attributed to the surgeon's experience, surgical technique, length of follow-up, data acquisition methods, and differing continence definitions [10]. Current definitions of continence vary from no leakage at all, no pads use but loss of few drops of urine [11], or the use of no more than 1 pad per day, defined as social continence [12].

The etiology of PPUI is often multifactorial and may depend on the patient's characteristics, sphincteric competence, anatomic support, pelvic innervation, and technical surgical factors such as extensive dissection, neurovascular bundle damage, and the development of postoperative fibrosis [13]. Several risk factors have been reported, including greater age at surgery, obesity, shorter membranous urethral length (MUL), prostate volume, prior transurethral resection of the prostate (TURP), bladder dysfunction, tumor stage and no nerve-sparing surgery [8, 14].

The most common type of PPUI is stress urinary incontinence (SUI), which consists of involuntary leakage during exertion, sneezing, or coughing [5].

Overactive bladder syndrome (OAB) with urge urinary incontinence can also occur after RP. The underlying mechanisms are still under debate, with an outlined hypothesis of detrusor overactivity due to partial bladder denervation during prostate surgery [13].

Continence status continues to evolve from more than 1 year after RP and about 80% of incontinent patients regain continence status without direct treatment [15]. Conservative strategies for the management of PPUI should be trialed as a first option before proceeding to more invasive options. The most common conservative treatments include behavioral therapy, pelvic floor muscle training (PFMT) with or without biofeedback, electronic stimulation, and pharmacotherapy [16]. When these options fail, surgical management is the treatment of choice with artificial urinary sphincter and male sling implantation.

### **2. Pathophysiology and anatomic components**

The pathophysiology of PPUI has yet to be entirely understood. However, numerous theories have been proposed. Pelvic support and neuromuscular anatomic components have been recognized as significant contributing factors to PPUI [17]. Biological and preoperative factors such as age, high BMI, preexisting lower urinary tract symptoms (LUTS), prostate size, short MUL, and functional bladder alterations have a negative impact on continence status after RP [14].

#### **2.1 Direct damage to the urethral sphincter complex**

The urethral sphincter's complex, which extends from the vesical orifice to the perineal membrane, comprises an internal sphincter (lissosphincter) made of smooth muscle and an external sphincter (rhabdosphincter) made of skeletal muscle [18]. During everyday activities, when there is minimal strain on the bladder outflow, the internal sphincter is responsible for maintaining continence (passive continence). It sustains tone for an extended time with little effort [14, 18]. On the other hand, the external sphincter is responsible for continence under stress (active continence). It comprises slow and fast twitch fibers that allow a tonic contraction for baseline continence and temporary recruitment in response to rapid pressure rise and/or voluntary blockage of the urine flow [18, 19].

Preservation of the internal sphincter is believed to be achievable through bladder neck-sparing surgery. The preservation of the internal sphincter complex has been observed to lead to a quicker return to continence and a reduced incidence of postoperative incontinence [20, 21]. However, Marien and Lepor [22] showed that sparing the bladder neck does not significantly impact continence rates. Furthermore, bladder neck preservation may increase the risk of positive surgical margins in case of a tumor located at the prostatic base.

*Post-Prostatectomy Urinary Incontinence DOI: http://dx.doi.org/10.5772/intechopen.114136*

External urethral sphincter deficiency is considered the most important determinant of PPUI [23]. Transurethral ultrasound examination has revealed thinning or atrophy, and compromised contractility [24]. Sphincteric incontinence is the urodynamic measurement's most common finding [25].

The contribution of neurovascular bundles (NVBs) in the innervation of the external urethral rhabdosphincter is a topic of ongoing debate. At the same time, the effect of NVB preservation during RP on erectile function is evident [26]. Some authors believe that NVB damage affects the continence mechanism and that preservation leads to at least an earlier continence recovery after surgery [20, 27–29]. However, other authors found no difference in continence rates between nerve-sparing and nonnerve-sparing techniques [22]. Recent results from a randomized clinical trial (IMPROVE trial, NCT02367404) [30] of 240 men with organ-confined prostate cancer who underwent RP, demonstrated that NVB preservation was the only factor associated with continence recovery.

#### **2.2 Damage to the supporting structures of the membranous urethra**

The male urethra's supporting structures can be divided into the anterior and posterior supporting structures and the pelvic floor (levator ani muscle). The pubovesical, puboprostatic ligaments and the tendinous arch of the pelvic fascia form the anterior urethral support structures. The ligaments stabilize the location of the bladder neck and the membranous urethra to the pubic bone [31]. The posterior support comprises the central perineal tendon, the Denonvilliers' fascia, and the rectourethralis muscle [32]. The third support structure includes the levator ani muscle and surrounding fascia [33]. The pelvic floor is not directly connected to the urethra, but it contributes to continence by exerting an occlusive force on the urethra via increased intra-abdominal pressure [33, 34].

PPUI can be improved by maintaining the integrity of the puboprostatic and pubovesical ligaments, allowing proper sphincter functioning [35, 36]. Several studies have demonstrated that the reconstruction of the posterior musculofascial plate of Denonvilliers (also known as the *Rocco stitch*) appears to improve PPUI [36–38]. However, some surgeons did not observe a similar improvement in continence after RP [22]. Total pelvic reconstruction with anterior and posterior fixation and anchoring of the bladder urethra anastomosis and the sphincteric complex appear to improve biomechanics and continence [36]. Like the Rocco stitch, this technique prevents urethral stump recession [37] and reduces anastomosis tension, improving mucosal coaptation. However, definitive evidence of their efficacy in the prevention of long-term PPUI still needs to be identified.

Due to the anatomical complexities of the structures surrounding the prostate gland, the surgeon's experience level is one of the most significant determinants of successful outcomes. The primary intraoperative and postoperative mechanisms of injuries are summarized in **Table 1** [24].

#### **2.3 Detrusor dysfunctions**

Detrusor dysfunctions have been attributed to postoperative bladder decentralization, inflammation and/or infection, and geometric bladder wall alteration linked to preexisting hypoxemia with/without neuroplasticity [39]. Detrusor dysfunction was infrequently a single diagnosis and was typically accompanied by intrinsic sphincteric dysfunction. Surgical damage to the pudendal nerve fibers that innervate the


#### **Table 1.**

*Intraoperative and postoperative injuries directly or indirectly affecting external urethral sphincter function.*

rhabdosphincter has functional consequences. In 2–77% of patients, detrusor overactivity was a *de novo* dysfunction. Patients with impaired bladder compliance ranged from 8 to 39%, with approximately 50% of cases being *de novo*. Detrusor hypocontractility was observed in 29–61% of patients, was *de novo* in 47%, and recovered in about 50% of patients [39].

Detrusor contractility may be impaired during surgery. Postoperative detrusor underactivity following RP seems to be an irreversible phenomenon persisting even over the long term [40].
