Overview of Stress Urinary Incontinence



Overview of Stress Urinary Incontinence


Alexandra Dubinskaya

Jennifer T. Anger



Introduction

Approximately 1 in 3 women will experience stress urinary incontinence (SUI) in their lifetime.1 SUI affects a woman’s quality of life on many levels. Often, this condition is considered to be a normal part of aging, and, unfortunately, the general public is not widely aware of curative treatment options. This chapter describes the anatomy and the mechanisms underlying SUI. Conservative methods, considered to be an initial step in therapy, including pelvic floor muscle (PFM) exercises, incontinence devices, and pessaries are reviewed.

Furthermore, this chapter provides an overview of surgical techniques that have evolved rapidly over time, culminating in the synthetic midurethral sling, along with the outcomes of the most notable trials which consist of successes, failures, and complication rates.2,3,4


ANATOMY AND MECHANISM OF ACTION

Urinary continence in women is achieved by a combination of urethral constriction and urethral support. Several components are required to maintain continence: a healthy urethral mucosa and submucosa, functioning intrinsic urethral smooth muscles and striated sphincter, intact pudendal nerve function, and properly functioning PFM.5 The urethral mucosal lining produces secretions that increase surface tension. The submucosal layer contains an abundant amount of spongy vascular tissue that contributes to the closure pressure. The sphincteric mechanism controls the urine flow from the bladder to the urethra and contains two parts: an involuntary internal urethral sphincter and a voluntary external urethral sphincter. The internal sphincter consists of smooth muscle and is continuous with the detrusor muscle of the bladder. The external sphincter is located more distally and contains striated muscle: the compressor urethrae (the rhabdosphincter) that passes anteriorly and connects to the ischial rami and the urethrovaginal sphincter that surrounds both the vagina and urethra. In contrast to the compressor urethrae, which constricts just the urethra, the urethrovaginal sphincter constricts both the urethra and vagina. Innervation of the sphincteric mechanism comes from the S2 to S4 nerve roots. Control of the voluntary sphincter is provided by the pudendal nerve and nicotinic receptors. The involuntary sphincter is controlled by the autonomic nervous system via hypogastric nerves and alpha-1 receptors.6,7,8

The anatomic support of the urethra comes from the endopelvic fascia. Because the anterior vaginal wall is fused with the urethra and this connective tissue in turn attaches to the arcus tendinous fascia pelvis (ATFP) this forms the backstop by which the urethra is compressed during increases in intra-abdominal pressure.9 These attachments prevent the downward movement of the urethra. Damage to these structures is a significant predisposing factor for SUI (Fig. 23.1).10,11,12

According to the integral theory by Petros and Woodman,13 connective tissue laxity of the vagina and its supporting ligaments are the main cause of pelvic organ prolapse and SUI symptoms. This theory describes intimately dependable relationships between the pelvic organs and suspensory ligaments. According to this theory, the organs are storage containers (bladder stores urine, the bowel holds feces, and the uterus holds the fetus), each of them connected to the outside by a tubelike urethra, anus, or vagina. Muscles pull against the ligaments to close these tubes by compressing them and open them by stretching them. The bladder, vagina, and rectum are connected to the pelvic brim via ligaments, including the bulbourethral, cardinal/uterosacral, and ATFP. Weakening and damage to the suspensory system cause dysfunction that manifests as incontinence, retention, and/or organ prolapse.13,14 In addition, weakening of the pelvic floor causes the upper part of the urethra to relax and funnel into the bladder, which interferes with equal pressure transmission. This creates a situation in which bladder pressure is higher than urethral pressure, resulting in incontinence.15,16 This is the theoretical mechanism by which the Burch procedure (retropubic colposuspension) works. The main goal is to bring the urethra back into the pelvis and restore equal distribution of pressure. This is the same way that the traditional bladder neck sling works—by keeping the urethra closed with increased intra-abdominal pressures (Fig. 23.2).








De Novo Stress Urinary Incontinence

With worsening of vaginal prolapse, SUI tends to “improve” as the urethra becomes progressively “kinked” as the anterior vaginal wall prolapse (cystocele) worsens. Manual reduction of the prolapse or placement of a pessary will trigger the return of incontinence symptoms. This phenomenon is classically present in association with anterior prolapse; however, it can present in cases of severe apical or posterior compartment prolapse causing external compression of urethra.17 This phenomenon has been called latent, masked, or occult SUI. In the Colpopexy and Urinary Reduction Efforts (CARE) trial, women without SUI but with pelvic organ prolapse were randomly assigned to undergo abdominal sacrocolpopexy (ASC) alone or ASC with the addition of a Burch procedure in order to prevent possible de novo SUI postoperatively. They demonstrated a significant reduction in postoperative SUI with Burch (32% vs. 57.4%).18 A 7-year follow-up of this study, reported as eCARE, demonstrated that even
though efficacy decreased over time, urethropexy prevented SUI longer than no urethropexy.19






Another multicenter randomized controlled trial (RCT), the Outcomes Following Vaginal Prolapse Repair and Mid Urethral Sling (OPUS) trial, randomized women with apical and/or anterior vaginal prolapse to vaginal repair (anterior colporrhaphy, paravaginal repair, colpocleisis, use of allograft, xenograft, or synthetic graft material) with or without a prophylactic midurethral sling placed at the time of surgery. The sling group had significantly lower rates of de novo postoperative SUI at 12 month follow-up (27.6% vs. 43%) but higher rates of adverse events.20,21

Performing prophylactic continence procedures, such as a midurethral sling, on preoperatively continent patients remains controversial. It is important to evaluate patients for the presence of occult stress incontinence before surgery, in order to best predict the need for concomitant correction with a midurethral sling. To best assess this, prolapse reduction can be performed using a variety of methods with different rates of success in detection of de novo incontinence: manually 16% (19 of 122), pessary 6% (5 of 88), swab 20% (32 of 158), and speculum 30% (35 of 118).22 The goal of the prolapse reduction is to simulate the prolapse repair and assess the risk for developing SUI postoperatively. Patients can wear a pessary at home and assess for SUI, or urodynamics can be performed in the office with the prolapse reduced. Of note, it is important to not obstruct the urethra because this would give an inaccurate result.


May 1, 2023 | Posted by in GYNECOLOGY | Comments Off on Overview of Stress Urinary Incontinence

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