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Stress Urinary Incontinence in Women: Epidemiology and Etiology
- Stress urinary incontinence in women: epidemiology and etiology
- Stress urinary incontinence: symptoms and diagnostic workup
- Stress urinary incontinence: medical and surgical treatment
Definition of stress urinary incontinence
The International Continence Society (ICS) defines urinary incontinence as "the complaint of any involuntary loss of urine". Stress urinary incontinence is urine leakage, which is associated with increased abdominal pressure and insufficient urethral sphincter mechanism. The main symptom of stress incontinence is the loss of urine on exertion, sneezing, or coughing.
Epidemiology of stress urinary incontinence
Vaginal deliveries are a risk factor for stress urinary incontinence:
The prevalence of incontinence in nulliparous women is around 10%, after cesarean section 16%, and in women with vaginal deliveries up to 21%. Comparative studies between cesarean sections and vaginal deliveries found a different prevalence of stress incontinence: 7% (cesarean sections) vs. 12% (vaginal deliveries).
Further risk factors:
Age [see the following table], pelvic surgery, adipositas, COPD, and estrogen deficiency.
| Age | Women | Men |
| 15–44 years | 5–7% | 3% |
| 45–64 years | 8–15% | 3% |
| >65 years | 10–20% | 7–10% |
Etiology and Pathogenesis of Stress Urinary Incontinence
Components of the bladder sphincter mechanism:
Components of the bladder sphincter are the urethral closure pressure caused by the sphincter muscles and active and passive pressure transmission during the elevation of abdominal pressure.
Urethral closure pressure:
Urethral closure pressure is mainly created by the external sphincter muscle (striated muscle) and internal sphincter muscle (smooth muscle) [see section bladder anatomy].
Passive pressure transmission:
If the abdominal pressure rises, additional pressure is transmitted on the bladder sphincter without muscle contraction of the pelvic floor. Passive pressure transmission is enabled by the connective tissue suspension of the urethra, bladder, and vagina.
Active pressure transmission:
If the abdominal pressure rises, contraction of the striated muscles of the pelvic floor and bladder sphincter causes an increase in urethral closure pressure.
Causes of Stress Urinary Incontinence:
Any defect causing a reduced urethral closure pressure or impaired pressure transmission with rising abdominal pressure will cause stress urinary incontinence. The most common causes of stress incontinence are a hypermobile urethra and an intrinsic sphincter deficiency (hypotonic urethra).
Hypermobile urethra:
The caudal displacement of the urethra due to rising abdominal pressure into the extra-abdominal compartment leads to a lack of passive pressure transmission, opening of the bladder neck, and, thus, stress urinary incontinence.
The stability of the suburethral connective tissue is a crucial factor for continence under stress. Vaginal deliveries increase the risk of stress urinary incontinence due to damage to the connective tissue, muscle tearing, and the innervation of the pelvic floor and sphincter muscles. The defects also lead to pelvic floor deficiency and prolapse of the pelvic organs.
Pelvic organ prolapse is a clinical sign of stress urinary incontinence but may also mask incontinence. The prolapse may cause kinking and obstruction of the urethra. An excessive kinking of the urethra may lead to residual urine and urinary retention. After correction of prolapse, incontinence may become clinically relevant. The effect of hysterectomy on stress incontinence is controversial.
Intrinsic sphincter deficiency :
Insufficiency of the urethral sphincter, regardless of the cause, is called intrinsic sphincter deficiency.
- Neurogenic causes of intrinsic sphincter deficiency: most common for sacral and peripheral lesions of the sphincter innervation [see also section neurogenic lower urinary tract dysfunction].
- Scarring in the region of the proximal urethra and bladder neck: after incontinence surgery.
- Age and estrogen deficiency lead to atrophy of the urethral mucosa with deterioration of sphincter closure pressure.
Chronic elevated abdominal pressure:
Diseases or circumstances that elevate the abdominal pressure aggravate existing stress urinary incontinence, e.g., COPD, obesity, or carrying heavy loads.
Integral theory of stress urinary incontinence by Petros and Ulmsten:
The integral theory of stress urinary incontinence by Petros and Ulmsten relates symptoms to anatomical defects of the pelvic region. The vagina acts like a hammock under the urethra and bladder and plays a central role in pressure transmission and in preventing urge symptoms. The proximal urethra is the zone of critical elasticity; this elasticity is essential for bladder filling. Scarring of the proximal urethra causes urgency. Depending on the location of the pelvic floor defects, various symptoms and therapeutic consequences may be distinguished, see the following table:
| Level III | Level II | Level I | |
| Location | Lesion between the bladder neck and symphysis | Lesion between the bladder neck and cervix or hysterectomy scar | Lesion between cervix or hysterectomy scar and os sacrum |
| Defective structures | Ligamentum pubourethrale, pubococcygeus muscle | Arcus tendinous fascia pelvis | Cardial ligaments and uterosacrcal ligaments |
| Signs and Symptoms | Stress incontinence | Stress incontinence, cystocele | Residual urine, urge symptoms, rectocele or enterocele |
| Treatment | Pubovaginal slings (TVT, TOT) | Colporrhaphia anterior | Colporrhaphia posterior, sacrocolpopexy |
| Cystitis cystica | Index | SUI Diagnosis |
Index: 1–9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
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Deutsche Version: Belastungsinkontinenz der Frau
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