Treatment of Stress Urinary Incontinence in Women

A Medical and Surgical Review

Kristin Sanders, BSN, RN


Urol Nurs. 2019;39(1):29-35. 

In This Article

Pathogenesis of Stress Urinary Incontinence

The female pelvic floor consists of muscles and connective tissue that span the underneath of the pelvis, leaving openings for the anus, urethra, and vagina (Min et al., 2017). The ability of the urethra to remain closed during periods of rest and increased intra-abdominal pressure depend on the proper support of these structures, as well as a functioning urethral sphincter mechanism (Koelbl et al., 2013). The proximal portion of the urethra is supported by the external urethral sphincter, which is a sleeve of striated muscle located posterior to the pubic bone. A tendinous connection attaches the external urethral sphincter to the levator ani muscle. This allows for closure of the urethral lumen upon increased pressure and maintains urinary continence (Koelbl et al., 2013). Also aiding in continence is the levator ani, coccygeus muscles, and endopelvic fascia, which resemble a sling at the base of the pelvis (Donovan & Terrell, 2018; Koelbl et al., 2013).

SUI is categorized as either urethral hypermobility or intrinsic sphincter deficiency (ISD). A stressful maneuver, such as coughing or sneezing, is associated with an increase in intra-abdominal pressure of 150 cm H2O and a displacement of the proximal urethra by approximately 10 mm downwards. Upon increased pressure, the stretch resistance (or stiffness of the pelvic floor structures) compresses the proximal urethra against the supportive structure, aiding in its closure (Ashton-Miller, Howard, & DeLancey, 2001). Damage to the endopelvic fascia, or levator ani muscle or its nerves would cause the supportive structures and bladder neck to become less stiff, resulting in urethral hypermobility. According to the ICS, ISD is the result of a weakened urethra, resulting in low urethral closure pressure and low valsalva leak point pressures (Koelbl et al., 2013).