Pathophysiology of pelvic floor disorders





Introduction


This chapter addresses the pathophysiology of stress urinary incontinence, pelvic organ prolapse, and fecal incontinence (FI). As Fig. 5.1 depicts, overlap of pelvic floor disorders in women suggests that there may be common risk factors or a common pathophysiology to these disorders. Pathophysiologic pathways involved in urgency urinary incontinence and overactive bladder are described in Chapter 31 .




Fig. 5.1


Venn diagram showing the prevalence and concurrence of pelvic floor disorders in 1517 older women in a community setting in Australia.

(From Zeleke BM, Bell RJ, Bilah B, Davis SR. Symptomatic pelvic floor disorders in community-dwelling older Australian women. Maturitas . 2016;85:34. with permission.)


Stress urinary incontinence


Urinary incontinence is defined by the International Continence Society as the unintentional, accidental loss of urine. Stress urinary incontinence (SUI) is the complaint of any involuntary loss of urine on effort or physical exertion or on sneezing or coughing ( ).


Continence is dependent on the integrated function between pelvic floor muscles, fascia, and nerves. Failure of one without compensation from the others leads to incontinence. This section reviews the anatomy and physiology of continence, the pathophysiology of SUI, and the impact of childbirth on SUI.


Elements of urinary continence


To maintain continence, the urethral pressure must be greater than the intravesical pressure at rest and under stress conditions. This sounds simple but involves a complex interplay of neurologic, muscular, and connective tissue supports to function.


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.




Fig. 5.2


Hammock hypothesis for stress continence. Lateral view of pelvic floor with urethra, vagina, and fascial tissues at level of bladder neck, indicating compression of the urethra by downward force ( arrow ) against supportive tissues (levator ani muscles and vaginal hammock suspended by attachments to the arcus tendineous fasciae pelvis), indicating influence of abdominal pressure on urethra.

(From DeLancey JOL. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol. 1994;170:1713. With permission.)


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.


Neurophysiologic considerations


Although stress incontinence is thought of as an anatomic problem, it is clear that there is also a neurologic basis for SUI. This is seen clinically with the treatment of SUI with duloxetine. A study by also showed that SUI may be a neuromuscular defect, as continent women had better motor unit recruitment with larger-amplitude, longer-duration motor unit action potentials on electromyography testing compared with women with SUI, suggesting better urethral innervation. A detailed description of the neurophysiology of the lower urinary tract, including the efferent and afferent pathways related to bladder and urethral function, is included in Chapter 3 .


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.


Mechanisms of female urinary continence and incontinence


Historical insights.


Theories of female urinary incontinence historically were based on two ideas: urethral support defects or a dysfunctional urethral sphincter. Victor Bonney examined female urinary incontinence in 1923 and proposed that incontinence was associated with a loss of distal anterior vaginal wall support. In the 1930s Stevens and Smith developed a new theory about the importance of urethral sphincter function over anterior vaginal wall support in maintaining continence based on their work using bead-chain cystography ( ). Other prominent surgeons of the time echoed this thought with the idea that incontinence could come from an increase in expulsive force, a decrease in urethral resistance, or a combination of both ( ). In the 1980s, Hilton and Stanton determined that deficient pressure transmission ratios were noted in incontinent subjects and not in continent controls and concluded that this is the main cause of SUI. They also found that subjects with SUI had lower total urethral length and lower maximum urethral pressure, and that these factors decreased with increasing severity of incontinence ( ). They did not, however, correlate pressure transmission ratios to urethral mobility or determine if the deficient pressure transmission results from urethral hypermobility, abnormal reflex urethral muscle contraction, or other factors.


In the mid-1900s, research on SUI using bead-chain cystourethrograms contributed to the idea that a posterior urethrovesical (PUV) angle between 90 and 100 degrees is essential to maintaining continence, and it was suggested that abnormal PUV angles were always associated with SUI ( ; ). However, this theory was later rejected when the reliability of bead-chain cystourethrography in the diagnosis of SUI was found to be poor ( ).


Work in the 1960s cast doubt on the theory that the urethra is an abdominal organ and that loss of position causes urinary incontinence ( ). This work placed more support on the argument of urethral sphincter function in the maintenance of continence. Later research focused on pudendal nerve dysfunction as a plausible cause of stress incontinence. Indeed, it was shown that pudendal terminal motor latency is delayed in women with urinary incontinence. confirmed this by demonstrating that partial denervation of pelvic floor muscles with subsequent reinnervation is a normal part of aging and is increased with childbirth. In fact, women with urinary incontinence, FI, and pelvic organ prolapse all have significantly greater denervation of the pelvic floor than asymptomatic women.


Rather than seeing this as evidence that urinary incontinence may arise from multiple mechanisms (e.g., neuromuscular dysfunction and defective support), one or two mechanisms have typically been seen as prevailing theories on the cause of SUI in women. The Agency for Health Care Policy and Research published a monograph in 1992 that popularized the term “intrinsic sphincter deficiency” (ISD). This was described as a subset of SUI defined as loss of sphincter function, possibly as a result of neuromuscular injury. There is not, however, a clear pathophysiologic mechanism to explain ISD, and it remains a clinical diagnosis.


Lastly, in the 1980s work by Blaivas and Olsson defined urinary incontinence by type in an effort to predict treatment outcome. They divided urinary incontinence into five types based on fluoroscopic urodynamic testing ( ). These classifications, however, did not define the cause of support loss or sphincteric loss or the extent to which each of those contributed to dysfunction. Treatments then did not stem from precise correction of the continence anatomy, and this classification system has fallen out of use.


Unifying theories on the causes of urinary incontinence.


As noted, over the past 100 years anatomists, physiologists, and clinicians have struggled to identify the cause of SUI, and no single mechanism appears to explain this condition. More recently, two theories emerged to explain a more comprehensive view of SUI that accounts for many of the varied observations described previously.


Petros and Ulmsten’s Integral Theory arose at the time of the development of the tension-free midurethral sling for the treatment of SUI. It stated that “stress and urge incontinence both arise from the same anatomic defect, a lax vagina” ( ). The Integral Theory, based on the authors’ understanding of pelvic anatomy, described the vagina as having two anatomic regions, with the pubourethral ligament in between them to act as a fulcrum. These regions function together to maintain urinary continence and normal bladder sensation by transmitting voluntary and involuntary muscle contractions involved in bladder neck and urethral closure. The vaginal segments also support hypothesized stretch receptors in the proximal urethra and trigone. The pubourethral ligament, in their theory, is hypothesized to extend from the midurethra to the symphysis pubis. The Integral Theory describes three urethral closure mechanisms. The two normal closure mechanisms are at the urethra and bladder neck. The third is the recruitment of the pelvic floor muscles, should the first two mechanisms fail. The urethral closure mechanism is located in the vaginal segment between the urethral meatus and the pubourethral ligament (the hammock) and is oriented vertically. The second urethral closure mechanism is located in the vaginal segment between the pubourethral ligament and the bladder neck (the supralevator vagina) and is horizontal. In this theory, the pubococcygeus and external urethral sphincter muscles contract at the hammock portion of the vagina to facilitate urethral closure. This pulls the hammock portion of the vagina ventrally. (It should be noted that this “hammock” is not the same structure described in the hammock hypothesis described later.) Part of the supralevator vagina lies in the “zone of critical elasticity,” which is below the proposed stretch receptors at the bladder base. This area of the supralevator vagina is pulled back and downward with levator contraction, thus closing the bladder neck. If the “zone of elasticity” does not adequately support the stretch receptors, this leads to symptomatic detrusor overactivity. The complicated and complex anatomic relationships proposed in the integral theory make this difficult to understand and apply.


The hammock hypothesis was introduced by DeLancey in 1994 ( Fig. 5.2 ). In this hypothesis the anterior vagina provides support to the urethra and bladder through its attachment to the levator ani muscles and the ATFP. This support causes urethral compression during increased intraabdominal pressure. It also provides a base for the striated urethral sphincter muscles to exert compression. This hypothesis does not include the need for an intraabdominal urethral position. However, it also emphasizes the importance of the levator ani in maintenance of continence. The hammock hypothesis does not attempt to explain detrusor overactivity like the Integral Theory. It does attempt to merge the support versus sphincter debate with the statement that urinary continence is “most likely related to a combination of independent factors” ( ).


Impact of childbirth on urinary incontinence


It is clear that increased parity is related to increased prevalence of urinary incontinence. In the 2005 to 2006 National Health and Nutrition Examination Survey, 6.5% of nulliparous women and 24% of women with three or more children reported urinary incontinence. Some 25% to 75% of all pregnant women report symptoms of SUI during pregnancy. Primiparous women have three times higher prevalence of SUI than their nulligravid counterparts ( ).


It is less clear whether pregnancy itself or vaginal delivery is the cause of SUI in most women. Given that occasional urinary incontinence is very common, it may be better to evaluate the impact of delivery on clinically significant incontinence. A large Norwegian study found that women who delivered vaginally had a 2.2-fold increased risk of moderate to severe urinary incontinence compared with those who delivered via cesarean section ( ). In a retrospective cohort study of parous women 5 to 10 years after delivery, the odds of bothersome SUI doubled with at least one vaginal birth compared with women who delivered only via cesarean section ( ). Additionally, operative vaginal birth has been associated with increased rates of SUI ( ). Women who deliver vaginally have three times the odds, and women with operative delivery 20 times the odds, of having surgery for SUI than women who deliver via cesarean section ( ).


The term breech trial assessed the differences in pelvic floor symptoms between women with planned elective cesarean delivery and planned vaginal birth at 3 months postpartum. Women in the planned cesarean delivery group reported less urinary incontinence than those in the planned vaginal delivery group (4.5% vs. 7.3%). These findings were limited because of the number of women in the planned vaginal delivery group who ultimately delivered by cesarean section ( ).


Note that, although these studies show an increase in bothersome urinary incontinence with vaginal over cesarean delivery, the protective effect of cesarean delivery and nulliparity decreases with time. By age 50 to 60 years, the rates of urinary incontinence in women are the same regardless of mode of delivery.


Pelvic organ prolapse


Elements of support


The pelvic viscera are supported by a system of muscles and connective tissue. The anatomy of pelvic organ support is described in Chapter 1 .


Levator ani muscle.


As previously described, a critical component of uterovaginal support is the levator ani muscle complex, comprising the iliococcygeus, pubococcygeus, and puborectalis muscles. The urethra, vagina, and rectum pass through the levator hiatus, a space between these paired muscles. Posterior to the rectum is the levator plate, which extends from the levator hiatus to the coccyx.


The levator muscles are unique skeletal muscles, in that they maintain tone in the absence of voluntary contraction ( ). The resting tone of the pubococcygeus muscle maintains closure of the urogenital hiatus. In addition, levator tone maintains a relatively horizontal position of the levator plate, which then forms a platform that supports the uterus, proximal vagina, and rectum.


Connective tissue.


The uterosacral and cardinal ligaments support the proximal vagina and uterus by pulling the vaginal apex and cervix toward the sacrum, thus positioning these organs over the levator plate and allowing these organs to be supported by the levator ani muscle ( ). Prolapse is hypothesized to occur if the vagina and uterus are instead positioned over the levator hiatus, such as might happen with hiatal widening or disruption of the uterosacral ligaments. In that situation, the pelvic organs are not supported by the levator ani muscle complex. As the organs descend into the levator hiatus, the support provided by attachments of the uterosacral and cardinal ligaments eventually becomes insufficient and fails over time. This hypothesis was advanced by , who likened the support of the pelvic organs to a boat at the dock ( Fig. 5.3 ), in which the ligaments serve as the “lines” tethering the ship to the dock. According to this analogy, the uterosacral and cardinal ligaments hold the “ship” (vagina and uterus) in position, but they are not sufficient to support the ship if the water (analogous to the intact and functional levator ani muscle complex) is withdrawn.


Nov 27, 2021 | Posted by in GYNECOLOGY | Comments Off on Pathophysiology of pelvic floor disorders
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