Pathophysiology of pelvic floor disorders

Connective tissue.

Studies have shown that both collagen and elastin play a role in urinary continence in women. found that nulliparous women with SUI have significantly less collagen than controls and have a decreased ratio of type I to type III collagen. A study by found a mutated type I collagen gene more frequently in women with SUI. Genes involved in elastin metabolism are differently expressed in periurethral vaginal tissue from women with SUI than controls. Elastin remodeling may be important in the molecular etiology of SUI ( ). There may also be a hormonal component to these changes in elastin metabolism.

Another study by showed that, during the secretory phase, elastolytic activity is increased in pelvic tissues from women with SUI compared with controls, and that this is mediated through an increase in neutrophil elastase and a concurrent decrease in alpha-1 antitrypsin expression. showed that expression of estrogen-β, elastin, decorin, fibromodulin, and vasoactive intestinal peptide are all significantly lower in women with SUI versus controls. They theorized that estrogen receptor β–dependent remodeling of the extracellular matrix of vaginal tissue is a cause of SUI. These studies show that further research is needed in this area to elucidate causes of urinary incontinence.

Bladder.

The bladder wall is composed of smooth muscle and connective tissue. During bladder filling, the bladder accommodates to the increasing urine volume with little to no increase in intravesical pressure. This is mediated by activation of a spinal sympathetic reflex pathway that inhibits parasympathetic ganglionic transmission and stimulation of β-adrenergic receptors in the bladder body, thus relaxing detrusor contraction.

Urethra.

The urethra is supported inferiorly by the anterior vaginal wall and laterally by the pubourethral ligaments that attach to the levator ani. These ligaments have been described on magnetic resonance imaging, but their existence is still controversial ( ; ; ). The support provided by the anterior vagina has been likened to a hammock ( Fig. 5.2 ) ( ). The anterior vagina is laterally attached to the arcus tendineous fasciae pelvis (ATFP), which is a condensation of fascia arising from the levator ani muscles. The ATFP is also the attachment point between the levator ani and obturator internus muscles. The importance of the vaginal “hammock” is discussed in the sections that follow.

The female urethra is 3.5 to 4.5 cm in length. At least two-thirds of this is above the levator ani. Additional contributions to continence are made by the urethral smooth muscle and vascular coaptation. Smooth muscles at the intramural portion of the urethra aid in continence. Longitudinal and circular smooth muscle runs the length of the urethra and surrounds a vascular plexus, which aids in urethral coaptation. The role of the longitudinal smooth muscle is less clear.

The urethra is a pliable structure that must be sealed or coapted completely to maintain continence. showed using mechanical models that there is higher resistance to water flow with a softer lumen and lubricating filler in the outflow tube. Studies rarely address urethral softness or mucosal seal when investigating incontinence. When surgery or radiation cause a stiff urethra, urethral closure is poor. The effects of surgery or radiation may be related to changes in the vascular plexus affecting coaptation, or to changes in the muscles or nerves. More study in this area is needed to delineate the role of urethral softness.

There are three muscles that compose the female urethral sphincter: the rhabdosphincter, the compressor urethrae, and the urethrovaginal sphincter. The rhabdosphincter is the most analogous to the anal sphincter, a circular striated muscle that encompasses the urethral lumen. The compressor urethrae and urethrovaginal sphincter are striated muscles that arch over the urethral lumen and exert downward pressure on the urethra against the anterior vaginal wall with contraction. All three muscles are innervated by branches of the pudendal nerve (S2–S4).

Levator ani.

The iliococcygeus, pubococcygeus, and puborectalis muscles together make up the levator ani. The pubococcygeus has three components: the puboperineus, pubovaginalis, and puboanalis. The pubococcygeus and puborectalis muscles close the urogenital hiatus with contraction to compress the urethra, vagina, and rectum. This augments the support of the pubourethral ligament and anterior vaginal wall in creating a firm support for the urethra to maintain continence. Although the urethral sphincter muscles are innervated by the pudendal nerve, these muscles are all innervated from a nerve that arises from S2 to S4 and travels along the medial aspect of the levator muscles. Because of their separate innervation, it is possible for a woman to have functional levator ani and a dysfunctional urethral sphincter.

The levator ani provide support to all pelvic organs including the urethra. As they pass through the urogenital hiatus, the urethra, vagina, and anus are supported by the tonic contractions of the levator ani muscles. The levator ani provide urethral support that is distinct from and in addition to the vaginal “hammock.” Both anterior vaginal wall support and levator ani support of the urethra are important in maintaining continence. Many authors have concluded that continence during increased intraabdominal pressure depends on maintaining the proximal urethra in a retropubic position ( ; ; ). A stable anterior vaginal wall attached to the ATFP with tonic contraction of the levator ani prevents urethral and bladder neck descent and contributes to urethral compression with straining. This theory of the importance of the retropubic urethra is supported by the success of retropubic operations for the correction of SUI (i.e., Burch and Marshall–Marchetti–Krantz urethropexies). This theory, however, is challenged by the fact that midurethral slings are successful and yet do not modify the position of the proximal urethra. They work by providing a stable suburethral support for effective urethral closure.

The pubourethral ligaments are the lateral fascial and muscular attachments of the urethra to the levator ani. These ligaments likely also contribute to continence. They are distinct from the pubovesical muscles, which arise from the ATFP and insert on the urethra.

The levator ani, together with the striated periurethral muscles (rhabdosphincter, compressor urethrae, and urethrovaginal sphincter) have two roles in maintaining continence. Slow-twitch fibers provide resting urethral tone, and fast-twitch fibers provide rapid contraction in response to increased intraabdominal pressure. With rapid increases in intraabdominal pressure there are reflex as well as voluntary increases in periurethral striated muscle contraction to augment urethral pressure. This occurs predominantly in the mid- and distal urethra. In fact, urethral pressure spikes have been shown to precede intravesical pressure spikes during cough in continent women ( ). used cinefluorography to study what happens when a woman is asked to interrupt her urine stream. The voluntary musculature immediately interrupts the urine stream in the midurethra owing to the periurethral striated muscle contraction against a stable suburethral base (anterior vaginal wall) and levator plate. The urine distal to the contracted area is voided, and the urine proximal flows back into the bladder. The bladder is then seen to rise cephalad owing to the effect of levator contraction on the position of the anterior vaginal wall and bladder. This is representative of fast-twitch muscle contraction. This demonstrates that normal urinary continence in women involves multiple interconnected mechanisms.

Coordinating reflexes.

There is evidence that female urinary incontinence is not just a structural abnormality, but also results from neuromuscular dysfunction. An example of this coordination is the guarding reflex, which maintains continence with progressive bladder distension. With bladder filling, stretch receptors in the detrusor send afferent signals to the spinal cord, activating pudendal somatic efferent stimulation. The afferent stimulation increases with increasing bladder volume. At the same time, the efferent stimulation to the external urethral sphincter increases to maintain continence via augmented sphincter and urethral smooth muscle tone. Another sacral reflex is the activation of the pelvic floor muscles immediately before increased abdominal pressure, leading to a measurable rise in urethral pressure.