What is the role of urethral hypermobility in the pathophysiology of urinary incontinence?

Updated: Sep 23, 2019
  • Author: Sandip P Vasavada, MD; Chief Editor: Edward David Kim, MD, FACS  more...
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Urethral hypermobility is related to impaired neuromuscular functioning of the pelvic floor coupled with injury, both remote and ongoing, to the connective tissue supports of the urethra and bladder neck. When this occurs, the proximal urethra and the bladder neck descend to rotate away and out of the pelvis at times of increased intra-abdominal pressure.

Because the bladder neck and proximal urethra move out of the pelvis, more pressure is transmitted to the bladder. During this process, the posterior wall of the urethra shears off the anterior urethral wall to open the bladder neck when intrinsic sphincter deficiency is present.

In women without urethral hypermobility, the urethra is stabilized during stress by three interrelated mechanisms. One mechanism is reflex, or voluntary, closure of the pelvic floor. Contraction of the levator ani complex elevates the proximal urethra and bladder neck, tightens intact connective tissue supports, and elevates the perineal body, which may serve as a urethral backstop.

The second mechanism involves intact connective tissue support to the bladder neck and urethra. The pubocervicovesical or anterior endopelvic connective tissue in the area of the bladder neck is attached to the back of the pubic bone, the arcus tendineus fascia pelvis, and the perineal membrane. The pubourethral ligaments also suspend the middle portion of the urethra to the back of the pubic bone.

These connective-tissue components form the passive supports to the urethra and bladder neck. During times of increased intra-abdominal pressure, if these supports are intact, they augment the supportive effect of muscular closure of the pelvic floor.

The third mechanism involves 2 bundles of striated muscle, the urethrovaginal sphincter and the compressor urethrae, found at the distal aspect of the striated urethral sphincter. These muscles may aid in compressing the urethra shut during stress maneuvers. These muscles do not surround the urethra, as the striated sphincter does, but lie along the lateral and ventral aspects.

The exact function and importance of these muscles are controversial. Some authors suggest that the urethrovaginal sphincter and the compressor urethrae may provide compression and increased pressure in the distal urethra during times of stress.

Damage to the nerves, muscle, and connective tissue of the pelvic floor is important in the genesis of stress incontinence. Injury during childbirth probably is the most important mechanism. Aging, hypoestrogenism, chronic connective tissue strain due to primary loss of muscular support, activities or medical conditions resulting in long-term repetitive increases in intra-abdominal pressure, and other factors can contribute.

During childbirth, 3 types of lesions can occur: levator ani muscle tears, connective tissue breaks, and pudendal/pelvic nerve denervation. Any of these injuries can occur in isolation but 2 or more in combination are more likely to occur. The long-term result may be the loss of active and passive urethral support and loss of intrinsic urethral tone.

The loss of urethral and bladder neck support may impair urethral closure mechanisms during times of increased intra-abdominal pressure. This phenomenon can be viewed in several ways.

Some hypothesize that under normal circumstances, any increase in intra-abdominal pressure is transmitted equally to the bladder and proximal urethra. This is likely due to the retropubic location of the proximal and mid urethra within the sphere of intra-abdominal pressure. At rest, the urethra has a higher intrinsic pressure than the bladder. This pressure gradient relationship is preserved if acute increases in intra-abdominal pressure are transmitted equally to both organs.

When the urethra is hypermobile, pressure transmission to the walls of the urethra may be diminished as it descends and rotates under the pubic bone. Intraurethral pressure falls below bladder pressure, resulting in urine loss.

A related way of describing the mechanism of hypermobility-related stress incontinence is the hammock theory posited by DeLancey. [13] Normally, an acute increase in intra-abdominal pressure applies a downward force to the urethra. The urethra is then compressed shut against the firm support provided by the anterior vaginal wall and associated endopelvic connective tissue sheath. If the endopelvic connective tissue is detached from its normal lateral fixation points at the arcus tendineus fascia pelvis, optimal urethral compression does not take place.

A simple analogy is that of a garden hose (urethra) running over a pavement surface (anterior endopelvic connective tissue). A force is applied in a downward direction using the foot (increased intra-abdominal pressure). This force compresses the hose shut, occluding flow. If the same hose is run through a soft area of mud (damaged connective tissue), then the downward force does not occlude the hose but, rather, pushes the hose deeper into the mud.

An alternative theory of the mechanism of stress incontinence stems from research involving ultrasound visualization of the bladder neck and proximal urethra during stress maneuvers. This research found that 93% of patients with stress incontinence displayed funneling of the proximal urethra with straining, and half of those individuals also showed funneling at rest. [14] In addition, during stress maneuvers, the urethra did not rotate and descend as a single unit; rather, the posterior urethral wall moved farther than the anterior wall.

Although mobile, the anterior urethral wall has been observed to stop moving, as if tethered, while the posterior wall continued to rotate and descend. Possibly, the pubourethral ligaments arrest rotational movement of the anterior wall but not the posterior wall. The resulting separation of the anterior and posterior urethral walls might open the proximal urethral lumen, thus allowing or contributing to stress incontinence.

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