Stress urinary incontinence is a common condition that occurs most often in women. Stress incontinence is defined by the International Continence Control Association as a sudden increase in abdominal pressure that causes involuntary flow of urine, not caused by the contractile pressure of the detrusor muscle or the tension pressure of the bladder wall on the urine. It is characterized by a sudden increase in abdominal pressure without loss of urine in a normal state and by the automatic flow of urine. Although it is not a life-threatening disease, it seriously affects the quality of life and physical and mental health of patients. Therefore, active prevention and treatment of urinary incontinence is the most urgent task to protect women’s health. The clinical characteristics of SUI and new advances in diagnosis and treatment are reviewed as follows.
The exact pathogenesis of SUI is not well understood, but it is related to reduced urethral resistance, altered urethrocystal pressure relationship, abnormal anatomical relationship of the urethrocystal bladder and damage to the pelvic floor support tissue. In recent years, some new theories have been proposed, which are summarized below.
1. 1 The integral pelvic floor theory, proposed by Petros and Ulmsten in 1990, is that the mechanism of urethral closure occurs in 3 ways: the anterior pubococcygeus muscle holds up the anterior vaginal wall to compress the urethra; the bladder neck is closed by a vaginal-based backward and downward contraction; and the pelvic floor anal raphe plate closes the bladder neck by pulling upward on the “hammock structure under its own control. Defects in the anterior vaginal wall result in dissipation of these forces and ineffective maintenance of closed urethral pressure during increased abdominal pressure, resulting in stress urinary incontinence.
The hammock theory, developed by Delancey in 1994, suggests that the maintenance of urethral closure pressure depends on the effective transmission of pressure along the pubic bladder fascia and the supporting structures (hammock) of the anterior vaginal wall to the bladder neck and proximal urethra, with the levator plate being an important component in stabilizing this structure. If this support structure is disrupted, the vaginal compression of the urethra is reduced and stress incontinence occurs.
1. 3 Urethral hypermobility This theory suggests that a birth injury or aging causes the pelvic floor tissue to weaken, causing the proximal urethra to descend to a lower, more isolated position. When abdominal pressure increases, the pressure is not transmitted equally to the bladder and proximal urethra, but more to the bladder, causing pressure in the bladder to exceed the closed urethral pressure, resulting in stress incontinence.
Injury to the pubic nerve, which innervates the external urethral sphincter, can cause disruption of the innervation and function of the urethra, resulting in a decrease in urethral resistance and stress urinary incontinence. Animal studies have demonstrated a direct causal relationship between pubic nerve injury and stress urinary incontinence symptoms. However, no hypothesis for the pathogenesis of SUI has been widely accepted.
Many studies have reported risk factors such as age, gender, childbirth, gynecologic surgery, obesity, family history, and severe pelvic organ prolapse. The incidence of urinary incontinence tends to increase with age. The relationship between age and stress incontinence is multifactorial, as aging leads to progressive relaxation of the pelvic floor muscles and a gradual decrease in the number of transverse muscles in the urethral wall, especially after menopause, and a decrease in estrogen can also lead to atrophy of the urethral mucosa. Women are more likely to suffer from urinary incontinence than men.
The relationship between childbirth and stress incontinence is characterized by temporary damage to the pelvic floor muscles, urethra, and peripheral nerves, and the incidence of stress incontinence is particularly high in multiple births. Damage to the pelvic floor muscles can lead to stress incontinence or exacerbate existing symptoms. Damage to the pelvic floor nerves not only impairs the ability of the urethra to control urine, but can also lead to difficulty in urination due to weak contraction of the bladder forceps.
The effect of obesity on urinary control is mainly due to the long-term increase in abdominal pressure caused by obesity, which impairs the function of the pelvic floor and its supporting ligaments and eventually leads to significant downward displacement of the urethra behind the bladder neck and stress urinary incontinence.
It is well documented that the incidence of stress urinary incontinence is significantly higher in those with a family history of stress urinary incontinence and that this effect may be polygenic. Pelvic organ prolapse (POP) is an adverse consequence of defective, damaged, and dysfunctional pelvic floor support structures, and it is also strongly associated with stress incontinence. It is also closely related to stress urinary incontinence. 50% of patients with POP have SUI and 80% of patients with SUI have POP. Smooth muscle fiber thinning, disorganization, connective tissue fibrosis and muscle fiber atrophy in the pelvic floor support tissue of patients with SUI and POP may be associated with its development.
3. Classification and typing
3.1 SUI is classified into 3 degrees according to symptoms
Grade I, the leakage occurs when the abdominal pressure is increased by coughing, sneezing and laughing;
Grade II, leakage occurs during sudden movements, rapid walking and jumping;
In degree III, continuous leakage occurs during standing.
3. 2 In order to better understand the pathogenesis and progression of stress incontinence, the following two typologies are briefly described.
The posterior urethra of the bladder neck is closed at rest on imaging urodynamics and is located at or above the inferior border of the pubic symphysis. In the stressed state, the posterior urethra of the bladder neck moves down and opens.
Type I: The bladder neck is closed and located at or above the inferior border of the pubic symphysis during the resting phase of the detrusor. The posterior urethra of the bladder neck is open and inferiorly displaced under stress, but the distance of inferior displacement is less than 2 cm. there is no or only slight bladder bulge.
Type IIa: The bladder neck is closed above the inferior border of the pubic symphysis during the resting phase of the detrusor muscle, and the posterior urethra of the bladder neck opens under stress. Urinary incontinence is evident with increased abdominal pressure.
Type IIb: The bladder neck is closed below the inferior border of the pubic symphysis during the resting phase of the detrusor, and may or may not continue to descend under stress, but the proximal urethra opens and incontinence occurs. Type III: The urethra is open behind the bladder neck during the resting phase of the detrusor, and the proximal urethra loses its ability to control urination. A slight increase in abdominal pressure or gravity alone is sufficient to produce significant urinary incontinence.
The two main mechanisms of SUI pathogenesis have been classified as anatomic stress incontinence and stress incontinence with loss of the urethral sphincter due to excessive subluxation of the posterior bladder neck and failure or absence of the urethral sphincter due to laxity of the pelvic floor and supporting ligaments. This classification has been important in the selection of clinical surgical procedures. For the former, procedures to restore the anatomic level of the posterior bladder neck urethra, such as the Burch suspension, are used; for the latter, procedures such as suburethral suspension, submucosal bladder neck graft injection, or artificial urethral sphincter are used. However, at present, transvaginal suburethral midurethral suspension has the same efficacy for both, which makes the clinical significance of this classification increasingly ambiguous.
SUI usually occurs in the presence of increased abdominal pressure (e.g., coughing, sneezing, laughing, or holding a heavy object) and is not accompanied by symptoms of urinary frequency and urgency (overactive bladder syndrome). The diagnosis is based on history, physical examination (pelvic floor examination, vaginal examination, abdominal examination, neurological examination) and some special tests (24-h urinary card, pad test, SUI provocation test, bladder neck lift test, swab test, cystourethrography, urodynamics, cystoscopy) and urodynamic evaluation (uroflow rate, residual urine measurement, assessment of urethral function, assessment of bladder forcing muscle function). The assessment of urodynamic assessment (urinary flow rate, residual urine measurement, urethral function, bladder muscle function), etc.
In principle, non-surgical treatment for mild to moderate stress urinary incontinence is based on behavioral, physical, pelvic floor exercises, pelvic biofeedback, and medications; surgical treatment for moderate to severe stress urinary incontinence is based on a variety of methods, which can be summarized into three categories: anterior vaginal wall repair, retropubic bladder suspension, and suspensory banding.
5. 1 Non-surgical treatment
5. 1. 1 Physiotherapy includes pelvic floor electrical stimulation, acupuncture, magnetic therapy, etc. Among them, pelvic floor electrical stimulation was introduced in 1963 and was only used in a large number of clinical applications in the 1980s.
5. 1. 2 Pelvic floor exercises, also known as Kegel exercises, were first introduced by Arnold Kegel in 1948 and are the most traditional non-surgical treatment for patients who consciously perform voluntary contractions of the pelvic floor muscles, mainly the anal raphe, to strengthen urinary control and pelvic floor muscle strength. Based on this, biofeedback-assisted pelvic floor muscle training has been developed, i.e., using simulated audio or visual signals to indicate the activity status of normal and abnormal pelvic floor muscles to obtain correct and more effective pelvic floor exercises. The most commonly used devices are vaginal and rectal pressure balloons and vaginal and rectal electromyography detectors.
5. 1. 3 Medication
(1) Estrogen: The mechanism is to stimulate the growth of urethral epithelium; increase the blood supply to the submucosal venous plexus of the urethra; affect the function of the paraurethral connective tissue of the bladder; and most importantly, increase the tension of the supporting pelvic floor structures. It is used in patients who are not surgical candidates or who have mild stress incontinence;
(2) Sympathetic alpha agonist: It is used for α-1 adrenergic receptor of perineal motor nerve to stimulate the contraction of smooth muscle of urethra and bladder neck to improve the urinary outlet resistance, thus improving the urinary control ability, suitable for patients with mild to moderate SUI. Midodrine hydrochloride is commonly used;
(The mechanism of action of Duloxetine is to treat urinary incontinence by selectively stimulating the nerves innervating the urethral sphincter to increase urethral closure pressure;
(4) polyacrylamide hydrogel (PAHG), a new transurethral injection, was used to treat 17 patients (age 3584 years) with stress urinary incontinence and 8 patients (age 3584 years) with mixed urinary incontinence from 2001 to 2003. The long-term efficacy of PAHG for SUI needs further observation and accumulation of more samples.
5. 2 Surgical treatment
5.2.1 Anterior vaginal wall repair was developed from Kelly’s (1913) anterior vaginal wall suture procedure. This procedure is based on the hypothesis that the pelvic floor fascia between the bladder and urethra is damaged or weakened due to a weakened vesicourethral support. By increasing the action of the posterior wall of the vesicourethra, the internal diameter of the urethra is reduced and, in rare cases, the bladder neck is raised slightly to achieve a therapeutic goal. The anatomic and clinical results of this procedure are poor, with a cure rate of approximately 30% at 1 year and decreasing over time. The reason for Kelly’s recurrence is the loss of the urethral fold and the flattening of the urethra after anterior vaginal wall repair, which is an anatomic change that can lead to incontinence. This procedure is currently used only in patients with pelvic organ bulge combined with mild stress urinary incontinence.
There are a number of approaches to this procedure, including the transabdominal and “stitch” approaches. The transabdominal posterior pubic bladder urethral suspensions include the Marshall-Marchetti-Krantz (MMK) and the Burch procedure. The “suture” method includes the Gittes, Stamey, Pereyra, Raz, and Muzsani techniques. All of these procedures follow two basic principles, but differ only in their application.
(1) Suturing of the paravaginal or perivaginal tissue to raise the vesicourethral junction;
(2) The suture is usually attached to a relatively strong and durable structure, most commonly the iliopubic ligament, the Cooper ligament (Burch procedure). The purpose of the procedure is to raise and support the vesicourethral junction, narrow the posterior angle of the urinary bladder, and increase the resistance of the bladder neck to enhance pressure transmission to the urethra when abdominal pressure increases, preventing the bladder neck from opening and improving control of urinary overflow. The surgical cure rate is about 90%. In recent years, with the development of laparoscopic technology and the advancement of minimally invasive surgical techniques, the minimally invasive treatment of SUI has also made great progress. Laparoscopic Burch surgery can be accomplished by both intraperitoneal and extraperitoneal routes.
In 1907, VonGiordano was the first to use a sling to treat stress urinary incontinence, and since then, surgical techniques and sling materials have evolved. The suspension belt can be made of self-fascia (rectus abdominis, lateral fascia, round ligament) or a synthetic silicone band. A tunnel is made through the lower abdominal incision under the bladder neck to insert the suspensory band, and both suspensory bands are sewn to the iliopubic ligament to form a small tension to support the urethra at the junction of the bladder and urethra and partially compress the urethra, with a cure rate of 80%90%.
In recent years, there has been a rapid development of medical synthetic suspensions, with different names for different materials and routes. The medical synthetic suspensions have been developed rapidly in recent years and are known by different names using different materials and different routes, such as tensionfreevaginaltape (TVT), intra-vaginalsling (IVS), trans-obturatortape (TOT) and suprapubicandarc (SPARC). (SPARC), and in the United States, an adjustable elastic device is installed in the sling to facilitate minimally invasive surgical adjustment in case of recurrence of symptoms after surgery, but this device is expensive.
Several prospective randomized reports from the 2004 International Urinary Control Congress[20] showed good outcomes for both TVT and laparoscopic Burch surgery, both of which are gold standard procedures for the treatment of stress urinary incontinence. Suspension banding is more widely used because it is more minimally invasive and simple. SUI is a worldwide health problem, but for a number of reasons, access and treatment rates are low. The study of gynecologic urology and SUI in China is still in its early stages, and the prevalence and distribution of SUI in China, as well as the risk factors for its development, need to be studied. With the improvement of new concepts and technologies, more and more attention and understanding will be given to SUI, which will lead to a faster development of the field.