Urethral Sphincteric Mechanisms

The glandular secretions of the inner mucosa increase the surface tension, promoting its plasticity and increasing its ability to coapt.² The abundant middle spongy vascular tissue of the submucosa forms a watertight seal and provides up to 30% of the total closure pressure^3–5; this vascular cushion, like the other tissues of the urethra, is under the influence of estrogens.^6–8 Estrogenic deficiency in postmenopausal women results in atrophy of this layer, reduces the hermetic seal of the urethra mucosal, and may contribute to the multifactorial cause of stress incontinence. Although there is some consensus among clinicians about the value of estrogen therapy for treating the symptoms of atrophic vaginitis in postmenopausal stress urinary incontinence, there is no evidence to support the use of exogenous estrogen replacement therapy in treating stress incontinence.⁹

The role of smooth muscle in the maintenance of female continence is still uncertain. The U-shaped loop of the detrusor smooth muscle surrounds the proximal urethra and favors its closure by creating a constant tone. Detrusor fibers at the bladder neck are longitudinally oriented, and they extend from the bladder neck to the subcutaneous adipose tissue that surrounds the urethral meatus. The inner longitudinal smooth muscle layer is surrounded by a circular layer that lies inside the outer layer of striated muscle. The smooth muscle layers are present throughout the upper four fifths of the urethra, and their circular disposition suggests that contraction has a role in constricting the lumen. The longitudinal smooth muscle does not seem to have a passive role during the filling; rather, it has been proposed that it acts by shortening and opening the lumen to initiate micturition.¹⁰

The striated urogenital sphincter consists of two parts, the rhabdosphincter and the compressor urethra and the urethrovaginal sphincter distally.¹¹ The proximal one third of the urethra is surrounded by a sleeve of circular striated muscle that is continuous with a longer ascending cone, which extends to the vaginal introitus. The rhabdosphincter is composed mainly of type 1 fibers, composed of slow-twitch tissue capable of maintaining constant tonic contractions of the urethral lumen.¹² From manometric and electrophysiologic evaluations, this produces the greatest level of resting pressure and electromyography activity.

This part of the urethra is intrapelvic, immediately posterior to the pubic bone. In the past, it was suggested that when the urethra descended and lost this intra-abdominal position, intra-abdominal forces could no longer constrict it during straining, resulting in stress incontinence. This concept, the pressure transmission theory, which was introduced by Enhorning in 1961,¹³ evolved into the hammock theory of DeLancey¹⁴ (1994), which proposes that the vagina posteriorly offers a back plate against which the urethra is compressed during increases in intra-abdominal pressure. During a sudden increase in intra-abdominal pressure, such as during coughing, a reflex contraction of the pubococcygeus muscle occurs. The vaginal hammock is stretched and stiffened, making it easier for the urethral sphincter to close in a slitwise fashion against this firm back plate. The result and increase in intraurethral pressure, which is thought to be lost in patients suffering from stress incontinence, can be recreated by surgical procedures that stabilize or elevate the suburethral vaginal wall.^15–18

If these postulates are correct, an appropriate contributory factor to female continence is provided by the bladder neck’s passive elastic tension, which is important in maintaining urethral closure.^19,20 In the mid-urethra at rest, closure is mostly maintained by the intrinsic striated muscle of the rhabdosphincter; however, the extrinsic striated muscles of pubococcygeus and compressor urethrae may play a significant role in ensuring urethral closure during increases in intra-abdominal pressure. The plasticity of the urethra or its ability to work as a watertight seal is also important in maintaining continence. Approximately one third of the resting urethral pressure is offered by smooth muscle effects, one third by striated muscle effects, and one third by the vascular contribution.²¹

Urethral Support Systems

The urethral support mechanism comprises all the structures extrinsic to the urethra that offer a supportive back plate on which the proximal urethra and mid-urethra lie (Fig. 27-2). The anatomic support is derived more from the fascial structures than from the musculature itself. The pubourethral ligament attaches the mid-urethra to the inferior side of the pubic symphysis and prevents downward movement during its rotational descent.²² It works in conjunction with the pubourethralis muscle, a subdivision of the levator ani muscle that forms a sling around the proximal urethra. Together they form the mid-urethral complex. It has been postulated that elongation of the posterior pubourethral ligaments may be a significant contributory factor to the loss of urethral support seen in stress incontinence. Major fascial support to the urethra also is provided by the urethropelvic ligament, which attaches the urethra to the tendinous arc.²³

Figure 27-2 Principles of maintenance of continence. During a sudden increase in intra-abdominal pressure, such as during coughing, a reflex contraction of the pubococcygeus muscle occurs. This stretches and stiffens the vaginal hammock, which makes it easier for the urethral sphincter to close in a slitwise fashion. A role for the pubourethral ligamentous support also has been advocated.

The vesicopelvic fascia or pubocervical fascia, extending between the bladder and the vagina, suspends and attaches the vagina and cervix to the pelvic side wall, to each arcus tendineus fascia pelvis, thereby offering posterior support to the bladder and bladder neck. It has two surfaces: the perivesical fascia on the vaginal side and the endopelvic fascia on the abdominal side. Its upper zone supports the bladder above the cervix, the middle zone supports the trigone, and the lower zone supports the bladder neck. Laxity of the fascia in each of the zones results in uterine prolapse, cystocele, and urethrocele, respectively.²⁴

The two arcus tendineus fasciae pelvis are tensile structures located bilaterally on either side of the urethra and vagina. They act like the ropes of a suspension bridge and provide the necessary support needed to hang the urethra on the anterior vaginal wall. They originate as fibrous bands from the pubic bone and broaden out as aponeurotic structures moving dorsally to insert into the ischial spine. The cardinal ligaments and the more medially placed uterosacral ligaments support the uterus and cervix; their relaxation results in uterine prolapse.

The pelvic floor musculature, represented by the levator ani muscles, carries the weight of the pelvic contents and prevents the abdominal pressure from stretching the ligamentous support structures. The levator ani includes the puborectalis muscle, which surrounds the rectum, connecting the pubic bones anteriorly in a U-shaped configuration; the pubococcygeus muscle, which crosses from the pubis to the coccyx; and the iliococcygeus muscle. The iliococcygeus arises laterally from the arcus tendineus levator ani and forms a horizontal sheet that spans the posterior opening of the pelvis, providing a shelf on which the pelvic organs lie. The urethra and vagina pass through an aperture in the levator musculature, the urogenital hiatus. The constant muscle tone,²⁵ maintained by predominantly type I (slow-twitch) striated muscle fibers, compresses the vagina and urethra anteriorly toward the pubic bone and keeps the hiatus closed.²⁶

The pudendal nerve provides somatic innervation to the striated muscle of levator ani and to the striated muscle within the external anal and urethral sphincters. The intrapelvic somatic fibers travel along the anterior vaginal wall from the sacral segments S2 through S4 to provide a somatic nerve supply to the pelvic floor.²⁷ Neuromuscular injuries have been proposed as an important factor in predisposing to pelvic floor dysfunction. Childbirth and age are considered the two major factors predisposing to pelvic floor denervation.²⁸ Other factors include pelvic surgery (i.e., rectal and vaginal surgery with extensive pelvic dissection), radiotherapy, and congenital neurologic conditions such as spina bifida and muscular dystrophy.

Support and suspension of the pelvic organs depends on a healthy innervated pelvic floor striated muscle, intact robust connective tissue, and their attachments to the bony frame of the pelvis. A useful analogy is that described by Peggy Norton, who suggested visualizing the relationships of these factors by considering a ship lying moored in dry dock. The ligaments are represented by the mooring ropes and the pelvic floor musculature by the water on which the ship sits. If the dry dock is emptied, then the influence of the supporting water disappears, leaving all of the tension applied to the mooring robes, which will inevitably weaken and fracture (Fig. 27-3).

Figure 27-3 In this representation of the pelvic floor support mechanism, water represents the pelvic floor musculature, the guy ropes are the ligaments, and the ship is the pelvic organs (A). If the pelvic muscles are weakened, undue force is applied to the ligaments (B), which weaken and may be damaged (C).

The levator ani contains type I fibers that provide resting tone and type II (fast-twitch) fibers that maintain the urethral closure under stress and prevent stretching of the pelvic ligaments. Berglas and Rubin showed that in the nulliparous patients, the lower one third of the vagina is oriented more vertically and the upper two thirds deviate horizontally, thereby maintaining the vaginal axis in an almost horizontal position.²⁹ This configuration is maintained by the posterior attachments of the cervix with the cardinal and uterosacral ligaments and by the anterior position of the urogenital hiatus. During stressful maneuvers, such as coughing or straining, the levator hiatus shortens anteriorly by the contraction of the pubococcygeus muscles. In the case if genital prolapse, when the levator ani support is lost, the vaginal axis becomes more vertical, the urogenital hiatus broadens, and fascial supports are strained.