2002 teorías de la incontinencia

Urol Clin N Am 29 (2002) 527–535

Genuine stress incontinence Theories of etiology and surgical correction Louis Plzak III, MD, David Staskin, MD* Division of Urology, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215, USA

This article examines the anatomy of the female continence mechanism and the traditional and newer theories relevant to the etiology and surgical correction of genuine stress incontinence. We review the classical theories of incontinence and unify them with more recent ones, stressing that central to all explanations is the concept that urinary loss secondary to an underactive outlet results from a relative lack of continence mechanism resistance with respect to intravesical pressure. We propose an explanation for the success of newer techniques that involve mid-urethral suspensions. Surgical stabilization of the continence mechanism, at the bladder neck or mid-urethra, compensates for the existing loss of urethral support or function by creating a new zone that provides compression, absorbs transmitted pressure, and preserves sphincteric configuration.

This article reviews the anatomy of the female continence mechanism and the classical and newer theories relevant to the etiology and surgical correction of genuine stress incontinence. We attempt to unify classical and more recent theories, stressing that central to all explanations is the concept that urinary loss ( flow) secondary to an underactive outlet results from a relative lack of continence mechanism resistance, with respect to the intravesical pressure. We propose a developing explanation for the success of newer surgical techniques that support the mid-urethral complex.

Continence mechanism (CM) resistance is a result of intrinsic CM function and CM support.

The CM consists of the bladder neck, urethra, external sphincter, and the surrounding muscular

* Corresponding author.

E-mail address: staskin@att.net (D. Staskin).

and fascial supports. Intrinsic urethral function is the product of coaptation and compression along the length of the bladder neck and proximal and mid-urethra. Anatomic support insures efficient bladder neck and urethral mechanics and facilitates compression and pressure transmission from the surrounding structures.

Suspension procedures do not ‘‘correct’’ stress incontinence. Surgical stabilization of the CM, at the level of the bladder neck or mid-urethra, compensates for the existing loss of urethral support or function by creating a new zone that provides compression, absorbs transmitted pressure, and preserves sphincteric configuration.

The underactive outlet Lower urinary tract function can be divided into storage and emptying, with the functional areas being the bladder and bladder outlet. During urinary storage, the bladder outlet functions as the CM. Failure to store may result from an overactive bladder (urge incontinence [UI]) or underactive CM (genuine stress incontinence [GSI]). Decreased urethral resistance may result from defects in anatomic support (GSI-A) of the CM or intrinsic sphincter deficiency (GSI-ISD), which is a loss urethral coaptation and compression along the urethral length (Fig. 1).

The clinical condition of GSI represents a multifactorial impairment of urethral resistance that encompasses a spectrum of deficits involving urethral coaptation, compression, configuration, and support. The majority of female patients who demonstrate inadequate CM resistance to maintain continence during activity have a mixture of GSI-A and GSI- ISD. The typical patient is has some degree of anatomic motion, which effects

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Fig. 1. Classification of incontinence. (From Staskin DR, Zimmern PE, Hadley HR, et al. The pathophysiology of stress incontinence. Urol Clin North Am 1985;12:271–8; with permission).

transmission pressure and configuration, and some degree of decreased CM tonus, which is manifest by impaired resting function, paradoxical relaxation, or the absence of active contraction during activity.

Pure GSI-A with normal urethral function requires significant pressure transmission and hypermobility of the CM (physical defects or pelvic floor relaxation), for example, a young nulliparous athlete who loses urine at the time of a tennis serve (high transmitted pressure þ levator relaxation). Pure GSI-ISD may present as a complete loss of urethral tone with fixed anatomic support and is observed in patients with surgical or catheter trauma. More typically, GSI-ISD is multifactorial, resulting from a loss of function at the bladder neck and proximal urethra (GSI-ISD-P) or at the level of the external sphincter or midurethra (GSI-ISD-M). GSI-ISD-P is commonly diagnosed and treated with peri-urethral injection.

A clinical example of pure GSI-ISD-M would be the patient who is otherwise ‘‘normal’’ but who has total loss of pudendal nerve function and denervation of the mid-urethral complex (external sphincter). More commonly, we encounter a mixed proximal and mid-urethral deficiency, for instance, the patient who is þ/ estrogen deficient, þ/ previous incontinence surgery (local structural, vascular, and neural changes), þ/ diabetic (autonomic denervation of smooth and nonstriated skeletal muscle), þ/ post partum pudendal neuropathy (somatic denervation), and þ/ ability to identify and contract her pelvic floor musculature.

Anatomic basis of urethral resistance Urethral coaptation and compression are a product of three separate regions: the inner mucosa, a middle spongy vascular tissue, and an outer fibromuscular envelope composed of smooth and striated muscle and elastic tissues [1] (Fig. 2).

The glandular secretions of the mucosa increase the surface tension, which promotes its plasticity and aids its ability to coapt. The pliable mucosal tissue enables the supporting structures and musculature to effectively seal the outlet. Because of the supple nature of the urethral mucosa, even passage of a grooved sound does not cause urinary leakage in normally continent women [2]. Four sources exert constrictive pressure on the urethral mucosa: the rich submucosal vasculature, smooth muscle in the bladder neck and urethra, the internal or proximal sphincter, and the striated muscle that comprises the external sphincter. The abundant vasculature of the submucosa, consisting of thinwalled venous sinuses and arteriovenous connections, accounts for up to 30% of the total closure pressure [3–5]. The vascular cushion assists in efficient transmission of external forces to the mucosa and exerts it own pressure on the urethral lumen.

This tissue, like the other tissues of the urethra, is strongly under the influence of estrogens [6–8].

Postmenopausal estrogen deficiency results in atrophy of this layer and may be one contributor in the multifactorial etiology of stress incontinence.

In most normally continent women, it seems that smooth muscle tone at the bladder neck and

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Fig. 2. Cross-sectional analysis of the urethra demonstrating the inner mucosal layer, the middle vascular region, and the outer fibromuscular zone. (From Delancey JOL. Anatomy. In: Cardozo L, Staskin D, editors. Textbook of female urology and urogynaecology. London: Isis Medical Media, the Livery House. 2001; with permission).

proximal urethra helps maintain continence independently of the external sphincter. It has been proposed that the arrangement of the smooth muscle fibers of the detrusor as they funnel into the bladder neck and their ability to exert constant tonus creates a physiologic sphincter mechanism.

These obliquely aligned fibers actively constrict the bladder outlet during filling and actively open the outlet during detrusor contractions to facilitate storage and emptying, respectively. Other researchers have challenged the concept of a physiologic smooth sphincter in women. They note that unlike the male bladder neck, there is no collar of smooth muscle surrounding the proximal female urethra [9]. Instead, detrusor fibers at the bladder neck are arranged in a longitudinally and extend from the bladder neck to the subcutaneous adipose tissue that surrounds the urethral meatus. These authors contend that the smooth muscle has a passive role in the maintenance of continence during filling and propose that it acts to shorten and open the urethra during micturition. In support of this theory, it has been noted that 21% of normally continent nulliparous women have open bladder necks on transvaginal ultrasound [10] and that 50% of continent women have bladder neck funneling on stress cystograms [11]. The role of smooth muscle in the maintenance of female continence is still uncertain.

The role of the striated muscle of the urethra is less controversial. The striated urogenital sphinc-

ter consists of two components, the rhabdosphincter and the distal urethral sphincter, which includes the compressor urethra and the urethrovaginal sphincter [12] (Fig. 3). The fibers of the rhabdosphincter are circumferentially arranged but are thin at the most posterior point between the urethra and the vagina. Striated muscle is most thickly concentrated in the middle third of the urethra and fans out to span approximately 80% of the overall urethral length. It is deficient posteriorly in the proximal and distal extremes. The muscle bundles are comprised of small-diameter (15 to 20 lm) slow twitch cells capable of tonic contractions of the urethral lumen [13]. The compressor urethra and the urethrovaginal sphincter create a pair of muscular slings that support the mid- and distal urethra. Their fast-twitch fibers contribute to the urethral closure pressure as part of the guarding reflex [14,15].

Anatomic supports Fascial supports An understanding of the anatomic support of the urethra and bladder is paramount to any discussion of GSI. Three-dimensional MRI studies suggest that anatomic support in general is derived from the levator fascia and not from the musculature itself [16]. The ligaments and fascia that support the pelvic organs are comprised of blood

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Fig. 3. Schematic representation of the striated sphincter muscle in women demonstrating the sphincter urethrae, urethrovaginal sphincter, and the compressor urethra. (From Delancey JOL. Anatomy. In: Cardozo L, Staskin D, editors.

Textbook of female urology and urogynaecology. London: Isis Medical Media, the Livery House; 2001; with permission).

vessels, nerves, and fibrous tissue that act as bilateral mesenteries to the genital tract [17]. The pertinent fascia is named according to the structures to which it attaches and is diagrammatically represented in Fig. 4.

The pubourethral ligament is analogous to the puboprostatic fascia in the male and attaches the mid-urethra to the inferior aspect of the pubic symphysis. The supporting structure consists of collagen, smooth muscle, and cholinergic nerve fibers and prevents downward rotational descent of the mid-urethra [18]. It works in conjunction with the pubourethralis muscle, a division of the levator ani muscle (LAM) that forms a sling around the proximal urethra and prevents its rotational descent. Together, the pubourethral ligament and pubourethralis muscle form the mid-urethral complex. However, the main support of the urethra is the urethropelvic ligament, which has two lamellae: the periurethral fascia on the vaginal side and endopelvic fascia on the abdominal side [19] (Fig. 5). These tether the urethra to the tendinous arc and are likely the most important of the fascial supports with regard to continence [20].

The fascia of the bladder fuses with the fascia of the anterior vaginal wall and forms the vesicopelvic fascia laterally as it inserts onto the pelvic wall. This fascia has two surfaces, the perivesical fascia on the vaginal side and the endopelvic fascia on the abdominal side. This provides the posterior support to the bladder and bladder neck.

In the gynecologic literature, the vesico-pelvic fascia, as it extends between the bladder and the

vagina, is referred to as the pubocervical fascia because it suspends and attaches the vagina and cervix to the pelvic sidewall. This fascia has been divided into three zones: the upper (cephalad) zone supports the area of the bladder above the cervix, the middle zone supports the trigone, and the lower zone supports the bladder neck [17]. Laxity or deficiency of fascia in each of the zones results in uterine prolapse, cystoceles, and urethroceles, respectively [17]. Weakness of the medial pubocervical fascia has been termed a ‘‘central defect,’’ whereas deficiency of the lateral vesicopelvic fascia

Fig. 4. The ligamentous supports of the uterus bladder and urethra. (From Raz S, Stothers L, Chopra A. Vaginal reconstructive surgery for incontinence and prolapse. In: Walsh P, Retik A, Vaughan ED, Wein A, editors. Campbell’s urology. Philadelphia: WB Saunders; 1998; with permission).

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ments. Uterine prolapse alone is not a direct cause of incontinence.

Pelvic diaphragm

Fig. 5. Schematic representation of the support of the urethra. (From Raz S, Stothers L, Chopra A. Vaginal reconstructive surgery for incontinence and prolapse. In: Walsh P, Retik A, Vaughan ED, Wein A, editors.

Campbell’s urology. Philadelphia: WB Saunders; 1998; with permission).

creates a ‘‘lateral defect’’ [20]. When both structures are insufficient, a combined central and lateral defect occurs.

Finally, the cardinal ligaments and the more medially located uterosacral ligaments support the uterus and cervix. Uterine prolapse occurs with relaxation of the cardinal and sacrouterine liga-

The pelvic floor musculature, by closing off the pelvic outlet, carries the weight of the pelvic contents and prevents the abdominal pressure from stretching the ligamentous support structures [21]. The pelvic diaphragm consists of the LAMs and their superior and inferior fascial coverings (Fig. 6). The levators can be further divided into two portions, the pubovisceral muscle and the iliococcygeus muscle. The pubovisceral portion contains the puborectalis muscle, which sweeps behind the rectum connecting the pubic bones anteriorly in a U-shaped configuration. It also includes the pubococcygeus muscle, which spans from the pubis to the coccyx. The iliococcygeus runs a straighter course from one side of the arcus tendinous to the other and provides the bulk of the support for the pelvic organs [17]. The urethra and vagina pass through an opening in the levator

Fig. 6. The musculature of the female pelvic diaphragm. (From Anson B. Atlas of human anatomy, Philadelphia: Saunders; 1950; with permission).

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musculature called the urogenital hiatus. The LAMs have constant tone, which keeps the hiatus closed by compressing the vagina and urethra anteriorly toward the pubic bone and lifting the pelvic contents in a cephalad direction. This takes the strain off of the ligamentous supports of the pelvic contents and eliminates any potential spaces through which herniation might occur [17]. When the levator muscles are damaged or weakened and the fascial coverings are stretched, the burden of the pelvic structures is shifted to the ligamentous supports. Over time, these stretch and weaken, and pelvic prolapse develops [17].

Surgery for stress incontinence Early theories concerning the procedures for the correction of stress incontinence focused around two sets of observations that proposed that providing structural support or creating physical compression [22] improved urinary leakage.

The initial approaches were to inject a bulking agent (paraffin) into the sphincteric mechanism of the urethra [23] or to increase the resistance of the urethra by advancing the external meatus [24]. In 1913 Kelly published his experience with ‘‘suturing together the torn or relaxed tissues of the vesical neck’’ [25]. In 1923, Victor Bonney asserted that, ‘‘incontinence depends in some way upon a sudden and abnormal displacement of the urethra and urethrovesical junction immediately behind the symphysis’’ [26]. In 1949, Marshall et al published their experience with ‘‘the correction of stress incontinence by simple vesicourethral suspension’’ [27]. These surgical developments lead to the classic functional hypothesis as popularized by Enhorning in 1961. He postulated that to be competent, the urethra needed to be located above a theoretical pelvic floor plane so that pressure transmitted to the bladder would be equally transmitted to the urethra, resulting in a compensatory increase in closure pressure [14].

Further studies refined the correlation between the intra-abdominal positioning of the urethra and stress incontinence [23]. In 1981, Constantinou proposed that a rise in intra-urethral pressure preceded the rise in intravesical pressure generated by a cough, inferring active contraction of the midurethral complex and the existence of a reflex muscular mechanism [28]. He found that surgical correction brought the mid-urethral pressure transmission ratio to normal and increased the proximal urethral pressure transmission to levels that exceeded those in normal continent control

subjects. Anatomic and functional studies that examined mid-urethral and bladder neck function and support challenged the early theories and inspired new explanations and fostered new surgical techniques.

The Integral theory In 1990, Petros and Ulmsten published the ‘‘Integral’’ theory of stress and urge incontinence [22]. According to the theory, female stress and urge incontinence have a common etiology. Laxity of the anterior vaginal wall allows the activation of stretch receptors in the bladder neck and proximal urethra, which triggers an inappropriate micturition reflex. This may result in detrusor instability and urgency, frequency, and nocturia. Furthermore, the deficient anterior vaginal wall does not efficiently transmit the closure pressure that would otherwise be generated by three separate closure mechanisms [22]. The anterior pubococcygeus muscle lifts the anterior vaginal wall to compress the urethra; the bladder neck is closed by the traction of the underlying vagina wall in a backward and downward fashion; and the pelvic floor musculature, under voluntary control, draws the hammock upward in a cephalad direction, closing the bladder neck. This upward motion is the mechanism that is addressed by pelvic floor exercises [29]. Overall, the laxity of the anterior vaginal wall causes a dissipation of all of these forces, and stress incontinence develops.

The Hammock theory In 1994, DeLancey proposed an explanation coined the ‘‘Hammock’’ theory of pressure transmission [30]. He asserted that urethral closure pressure depended upon the efficient transmission of pressure to the bladder neck and proximal urethra against the rigid support of the pubocervical fascia and anterior vaginal wall (Fig. 7) [30]. This explanation of stress incontinence advocates the use of techniques that restore normal anatomy and urethral support over those that fix the urethra in an unnaturally high position. DeLancey’s theory acknowledges the role of the LAMs in stabilizing the pubocervical fascia.

The essential features of the Hammock and Integral theories are similar, but the Integral theory suggests a more active role for the pelvic musculature in the maintenance of continence and draws a connection between detrusor instability and urge incontinence (‘‘stress-induced urge incontinence’’).

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Fig. 7. The Hammock hypothesis. Intra-abdominal pressure is transmitted to the urethra and bladder neck, closing the outlet as it gets compressed against the supports of the pubocervical fascia and anterior vaginal wall. (From Delancey JOL. Anatomy. In: Cardozo L, Staskin D, editors. Textbook of female urology and urogynaecology. London: Isis Medical Media, the Livery House; 2001; with permission).

The mid-urethral focal point The success of new surgical techniques has prompted a re-evaluation of the stress incontinence paradigm. Continence (ie, satisfactory urethral resistance) is dependent upon multiple factors: resting tone, active contraction, external compression, pressure transmission, and integrity of configuration. The mid-urethra is a focal point for these factors.

The importance of urethral configuration suggests that CM support prevents the separation of the posterior urethral wall from the anterior urethral wall during rotational motion around the inferior portion of the pubic ramus, a concept we refer to as ‘‘shear force.’’ In patients with urethral hypermobility, the floor of the bladder neck and proximal urethra rotates inferiorly and around the pubis. The pubourethral ligaments tether the anterior portion of the urethra. The kinetic energy of the transmitted force on the anterior vaginal wall continues to ‘‘drive’’ or ‘‘pull’’ the posterior urethra when the anterior urethra stops. The result is that the bladder neck, the walls of the proximal urethra, and the circumferential fibers of the striated sphincter mechanically separate, decreasing urethral resistance. Anatomically, during this motion, the anterior urethra (endopelvic fascia) and the posterior urethra (periurethral fascia) separate within this envelope. In contrast to the explanation that proposes a pure transmitted pressure effect, ‘‘shear force’’ suggests that the trans-

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mitted energy mechanically opens the proximal urethra and mid-urethra, independent of, but in conjunction with, the rise in intravesical pressure.

Suspension procedures at the bladder neck or the mid-urethra may prevent this exaggerated posterior urethral motion. Periurethral injection procedures, which depend upon urethral coaptation, should have a higher success rate in patients in whom shear force associated with anatomic motion is limited.

In 1981, Constantinou published his findings of the changes in urethral pressure transmission in patients undergoing endoscopic bladder suspension (Fig. 8) [31]. He noted that in patients with stress incontinence, the changes in urethral pressure never exceeded the changes in bladder pressure as measured during dynamic urethral pressure profiles. Furthermore, the point of maximum urethral closure pressure was displaced to a more distal location. Bladder neck suspension surgery increased the maximum urethral closure pressure throughout the length of the urethra. What is striking about this observation is that the pressure change ratios are highest at the mid-urethra in continent control subjects and in postsurgical patients and that the mid-urethral ‘‘hump’’ is lost in patients with stress incontinence.

It is likely that the new suspension procedures, such as Tension-Free Vaginal Tape (Ethicon, Inc., Somerville, New Jersey) and Suprapubic Arc Sling System (American Medical Systems, Minneapolis,

Fig. 8. Urethral pressure profilometry, demonstrating the maximal pressure transmission at the level of the midurethra in normally continent women.

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mechanism, at the level of the bladder neck or mid-urethra, compensates for the existing loss of urethral support and function by creating new zones for compression, absorption of transmitted pressure, and the preservation of sphincteric configuration. Our understanding of the pathophysiology of stress incontinence and the basis for surgical compensation continues to evolve. Midurethral complex support procedures have stimulated further investigation into the mechanics of continence.

References

Fig. 9. Predicted (hypothetical) urethral pressure profiles for patients following mid-urethral suspension surgery. The pressure transmission ratio would be expected to be highest at the mid-urethra while having less of an effect on the proximal urethra and bladder neck than that found with bladder neck suspensions.

MN) focus the transmission of closure forces at the mid-urethra and block the shear force. We postulate that the postoperative urethral pressure transmission profiles in these patients would likely reveal that the maximum transmitted closure pressures are more centrally located with a narrower distribution than one sees in Stamey bladder neck suspensions (Fig. 9). The transmission of pressure to the proximal urethra would not be as high as after a bladder neck surgery because the proximal urethra is not directly supported. However, because of an increase in support at the midurethra, we would expect a higher transmission of pressure at this point. In this fashion, mid-urethral suspension surgery compensates at a different location. Using dynamic perineal ultrasound, Petros has demonstrated that mid-urethral suspension surgery prohibits the hyperobile bladder neck from opening the mid-urethra [32]. Preoperative and postoperative urethral pressure transmission profilometry studies and dynamic MRI may provide further insights into these mechanisms.

Summary Urinary loss (flow) results from a relative lack of CM resistance with respect to the intravesical pressure. Surgical stabilization of the continence

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