Anal incontinence, the involuntary loss of flatus or stool per anus, afflicts far more women than is often appreciated.^1,2,3 Social embarrassment, fear about the cause, or even a misconception that incontinence is part of the normal aging process may prevent a patient from revealing these symptoms to her gynecologist.^4,5,6 The severity of the condition often mandates continuous protection from soiling. These symptoms may persist for years before a patient vocalizes complaints and obtains relief.

Although variable, the most common cause of anal incontinence is injury to the anal sphincter during parturition.³ Inadequate repair or poor healing of obstetric perineal injuries may present as anal incontinence within days to weeks of delivery. In fact, some authors have reported an incidence of anal incontinence after third- or fourth-degree laceration as high as 40% to 60%.^5,7 In these European studies, between 45% and 68% of women had mediolateral episiotomy, a technique associated with third- or fourth-degree laceration in approximately 25% of women.⁸ In a separate group of 35 women who did not undergo mediolateral episiotomies but experienced obstetric sphincter injury, the incidence of incontinence of flatus was 17% compared to 3% in the intact sphincter group.⁹ Incontinence of liquid or solid stool was not significantly different in the study versus control groups.

Other causes include perineal trauma from straddle injuries or aberrant healing from surgical procedures such as perineoplasty, hemorrhoidectomy, fissurectomy, or radical oncologic procedures. Anal incontinence may even occur as the result of a primary neoplastic process. Less frequently, fecal incontinence may result from congenital anomalies, neurologic disorders affecting the perineum and anal sphincter, or demyelinating diseases that alter multiorgan systems. Fecal incontinence is not common as either an acute or chronic side effect of radiotherapy.^10,11

This chapter addresses the repair of intrinsic anatomic muscular dysfunction. Systemic, malignant, or neurologic disease processes lie outside the scope of the surgical procedures discussed here.

The anatomy and physiology of the anal canal have been well studied. Current literature expands upon Shafik's original work on the triple loop theory.^{12,13,14,15,16} The anal canal measures 2.5 to 4 cm in length and extends from the mucocutaneous junction caudally through the dentate line, above which columnar colonic mucosa is found. Here the anal mucosa is composed of cuboidal cells formed into 8 to 14 folds called the rectal columns of Morgagni, which overlie an internal hemorrhoidal plexus. The arterial blood supply originates from the superior hemorrhoidal artery (the terminal branch of the inferior mesenteric artery) and from the middle and inferior hemorrhoidal arteries, which arise from the anterior division of the internal iliac artery. The venous drainage returns to the portal system by way of the superior hemorrhoidal and inferior mesenteric veins. The middle and inferior hemorrhoidal veins return to the internal iliac system. The boundaries of the anal canal are the coccyx posteriorly, with interposed adipose and muscular tissues; and the ischiorectal fossa, with Alcock's canal laterally.

The anal canal is surrounded by two major muscle groups, the involuntary internal and the voluntary external sphincter systems (Fig. 1) These two systems provide a fine balance between continence and controlled intermittent evacuations of fecal material. The capacity to distinguish between flatus and variable stool consistency is achieved through a complicated integration of pelvic musculature.

The involuntary internal anal sphincter is composed of autonomically innervated circular smooth muscle fibers that lie within the wall of the anal canal. These fibers remain in a steady state of contracture, yielding tone to the anal canal and maintaining it in a collapsed position when nonfunctioning. As the rectal ampulla fills and distends, the sensory stimulus for evacuation begins the process of defecation. The contribution of the internal sphincter to anal continence has been studied with magnetic resonance imaging.⁶ In this study, the internal sphincter was found to contribute 54% of the anterior thickness of the sphincter in nulliparous women. Application of this knowledge has important implications in the repair of third- and fourth-degree perineal lacerations and contrasts with the traditional understanding portrayed in the medical literature.

The voluntary external anal sphincter (Fig. 2,) composed of multiple interrelated skeletal muscle loops (separated by their fascial coverings), lies in close approximation to the levator ani and the muscles of the urogenital diaphragm. This sphincter system contains three muscular loops that surround the anal canal. The top loop is the deepest and fuses with the puborectalis muscle of the levator ani group. It attaches to the pubic symphysis and encircles the colon posteriorly at the anorectal verge. Innervation is provided by the inferior hemorrhoidal branch of the pudendal nerve. This superior loop functions to angulate the anal canal forward in order to maintain continence. The intermediate loop portion of the external sphincter is found anteriorly around the midportion of the anal canal as a fleshy muscle. These fibers terminate posteriorly in an interdigitating fashion and attach to the tip of the coccyx in a fibrous tendon. On voluntary stimulation by the perineal branch of S4, contraction of this intermediate sphincter retracts the anal canal posteriorly to align with the rectum. The third and most superficial muscle of this complex sphincter system is the base loop. The smallest of the three loops, it is composed of skeletal muscle fibers that completely encircle the anal canal distally and attach to the mucocutaneous junction. It is innervated by the inferior hemorrhoidal nerve. These three muscle groups function in concert to provide the capacity for both continence and defecation (Fig. 3.)

Just above the top loop and puborectalis muscles is the pubococcygeus muscle of the levator ani group. Its circular skeletal muscle fibers extend from the pubic bone to the coccyx, where they fuse as decussating tendons called the anococcygeal raphe. The fleshy, muscular portion of the pubococcygeus encircles the hiatal space, through which pass the pelvic viscera. The pubococcygeus muscle adheres to the colonic wall by dense fascial fibers called the hiatal ligament. Muscular traction on the hiatal ligament effects posterior circumferential distention and elevation of the anal canal.

Between the internal sphincter and the three circular muscle loops of the external sphincter lie the longitudinal fibers of the levator plate. These muscle fibers anchor the U-shaped external sphincter loops to the anal wall and perianal skin. Longitudinal bundles of muscle fibers descend from the pubococcygeus muscle between the internal sphincter and the three loops of the external sphincter system. The most medial smooth-muscle group, the medial longitudinal muscle, attaches the levator plate to the anal canal wall, actually fusing with the wall. The intermediate longitudinal muscle group, also called the suspensory ligament, inserts as the central tendon that attaches above the external anal sphincter base loop and the perianal skin. The lateral longitudinal muscle bundle is a condensation from the top loop of the external anal sphincter, which attaches to the medial surface of the intermediate loop, inserting just above the base loop. These three longitudinal muscle bundles provide continuity and attachments between the internal and external sphincter systems.

Interspersed among these muscle fibers are six perirectal spaces. Four intersphincteric spaces lie among the three longitudinal muscle layers and separate their dense fascial coverings. Between the skin and the base loop is the subcutaneous space, which is continuous with the perirectal spaces. The central space is low around the anal canal and communicates with each of the surrounding spaces. It separates the base loop from the intermediate loop and is an insertion site for the longitudinal muscle tendon bundles. These potential spaces play an important role in the development and repair of perirectal abscesses and rectocutaneous fistulae.

Physiology of the Sphincter Systems

Much investigation has centered on the mechanism of defecation.^17,18,19,20 Electromyography, manometric pressure testing, and radiography have been used to explore the function of these muscle systems. When the rectal ampulla fills and distends, the signal for defecation is triggered (see Fig. 3.) Defecation is initiated by Valsalva's maneuver, which increases intra-abdominal pressure. In a reflex manner, the internal anal sphincter must relax to accommodate the bolus. Simultaneous voluntary relaxation of the top loop of the external anal sphincter allows the anal canal to relax posteriorly. Voluntary contraction of the levator plate and the longitudinal muscle bundles acts to widen the anal inlet by means of traction on the hiatal ligament. This action simultaneously shortens the canal length, flares the base loop of the external sphincter outward, and opens the anal orifice. The passage of fecal material distally is completed by intermittent vermicular contractions of the intermediate and base loops, which compress the flow outward. Once emptying is complete, the external loops, anococcygeal raphe, and levator plate all relax, returning to their normal positions, while the puborectalis muscle and the top loop contract, repositioning the canal forward. The process is completed with reflex contraction of the internal sphincter system to recollapse the anal canal, thereby maintaining continence.

Maintenance of a minimal baseline anal pressure is necessary for fecal continence. The internal sphincter contributes approximately 50% of the force necessary to keep the anus closed when empty, and the external sphincter 25% to 30%. Variable filling of the internal hemorrhoidal plexuses provides the remainder of the pressure required to seal the anus by conforming around the sphincters.²¹ As the anus is distended, the contribution of the internal sphincter declines progressively, while stretching of passive canal wall elements other than the sphincters limits capacity and provides the force to maintain continence. The importance of the involuntary internal sphincter and the role of autonomic dysfunction in fecal incontinence can therefore be understood. Manometric evaluation reveals a distinctive pressure profile of the anal canal resulting from the combined effects of the different muscles that constitute the anal sphincters.²² In the upper anal canal, radial pressure measurements indicate a lower pressure anteriorly, corresponding to the posterolateral location of the puborectalis muscle. In the distal anus, the pressure is less posteriorly because of the orientation of the intermediate loop.

MEASUREMENT OF ANORECTAL PRESSURE.

Simple manometric pressure measurements in some incontinent patients do not always distinguish true deficiencies. More sophisticated techniques involving measurement of anorectal pressure gradients or three-dimensional manometry (vector manometry) may prove more accurate, but are not widely available.^23,24

Biofeedback techniques using visual manometry have been successful in the treatment of some patients with fecal incontinence.²⁵ Of motivated patients, 50% to 80% experience improvement in symptoms. An increase in both resting and squeezing pressures can be demonstrated.²⁶ The efficacy persists for at least 5 years in successfully treated patients.²⁷

Of women with idiopathic fecal incontinence, 75% to 80% have evidence of nerve injury to the pelvic floor musculature.²⁸ Such patients have slowing of nerve conduction, which is measured as pudendal nerve terminal motor latency (PNTML) on electromyographic tests.²⁹ Approximately 60% of patients with sphincter injury have concomitant pudendal neuropathy.²⁸ The contributing role of vaginal delivery is underscored by the finding that 42% of women demonstrate slowed conduction in the pudendal nerve (prolonged PNTML) immediately after delivery, of whom 60% recover by 2 months.³⁰

Fiber density, an electromyographic index of the number of muscle fibers innervated by a single nerve axon, is increased in anal incontinence. This effect is believed to result from injury, causing denervation with subsequent reinnervation. Increases in PNTML and fiber density are present in incontinent patients and are associated with aging, multiparity (if delivered vaginally), increased birth weight, and a long duration of the second stage of labor.³⁰ Increases are not found after episiotomy or first- and second-degree perineal lacerations, but do occur after third- or fourth-degree obstetric perineal tears. Patients with anal incontinence have decreased sphincter length, lower maximum resting pressure, and decreased maximum voluntary contraction pressure. Such patients also have decreased sensitivity to electrical stimulation and temperature sensation in the anus.^31,32

In normal, continent patients, sensations of temperature and pressure from stool or flatus in the anal canal are better appreciated and evoke an increase in sphincter tone.³³ Differences in sensation are postulated to contribute to the difficulty that incontinent patients typically experience in differentiating flatus from solid stool. Pudendal neuropathy is most accurately assessed by measurement of PNTML; however this test is not widely available and may be inaccurate unless performed by an experienced clinician. Manometry is not thought to be useful in the determination of pudendal nerve malfunction.³⁴ One preliminary prospective, controlled trial demonstrates that a component of routine manometry, the rectoanal excitatory reflex, may prove useful in this diagnosis.³⁵ The recognition of pudendal nerve injury and the distinction of this disorder from sphincter injury is vital.

Defecography (evacuation proctography), a radiographic technique to evaluate defecation, can demonstrate rectocele, enterocele, or rectal intussusception, but does not aid in the evaluation of anal incontinence.^36,37

Anal endosonography has recently been applied to the evaluation of fecal incontinence. The normal anatomy of the external and internal sphincters as imaged by ultrasound has been described.³⁸ Comparison of anal ultrasonography with anal manometry in normal volunteers demonstrates no correlation of sphincter muscle thickness with squeeze pressure.³⁹

However, defects in the external and/or internal anal sphincters demonstrated ultrasonographically correlate with manometric findings.^40,41 In addition, electromyographic mapping of sphincter abnormalities confirms anal endosonographic results.^41,42,43 A prospective study of 127 women compared anal manometry and anal ultrasonography before and after vaginal delivery.⁴⁴ Sphincter defects can be demonstrated by anal ultrasound in 25% of incontinent women believed to have intact sphincters on the basis of a digital examination. This discrepancy may be related, in part, to difficulty in distinguishing scar tissue during the examination. Ultrasound characteristics of scar tissue differ from those of normal muscle.^40,46 Incontinent patients with normal manometry may also have sphincter abnormalities seen on ultrasound examination.⁴⁶ Finally, a small number of patients with idiopathic incontinence resulting from pudendal neuropathy and confirmed by abnormal PNTML will have coexistent sphincter defects.^41,43,46 Thus, anal endosonography can provide information that may not be obtained by digital examination or traditional testing, and this information is valuable for those making treatment decisions.

All gynecologic patients and certainly parous women should be questioned for a history of anal incontinence. The inability to maintain flatus or solid and liquid stool should be investigated thoroughly. The history should elicit duration, frequency, and severity of symptoms; an inciting event; and the necessity for sanitary protection. External anal sphincter and puborectalis weakness, as measured by maximum squeezing pressure on manometry, is associated with fecal and urinary urge incontinence, fecal incontinence en route to the toilet, and urinary stress incontinence.⁴⁷

Many patients experience loss of flatus or diarrhea, but not solid stool. Patients must be questioned for symptoms of rectocele, such as perineal pressure or protrusion of the rectum into the vaginal introitus. Also, inquiry regarding a prior history of inflammatory bowel disease, vulvar or vaginal infections, venereal diseases, neurologic deficits, or nontraditional sexual practices (e.g., anal intercourse, foreign body manipulation, rape, or sexual abuse) should direct a practitioner toward a diagnostic evaluation before attempted surgical repair.

The physical examination of these patients follows the sequence of a standard gynecologic visit. The perineum is inspected with attention to muscular weakness, asymmetry, or inability to contract the muscles of the urogenital diaphragm or the anal sphincter. Injury to the external sphincter is evidenced by absence of the radial creases anterior to the anus.⁴⁸ With the patient instructed to tighten her anal sphincter, inspection of the perineum should reveal both anal constriction and an inward motion of the anal orifice.⁴⁸

Sensory stimuli should be tested, and an intact bulbocavernosus reflex should be evoked bilaterally by stroking the labia majora and observing tightening of the anal orifice. Perception of sharp pain stimulation over the perineum may be altered. Palpation of the labia majora and the perineal body may reveal laxity or a mass effect. Most commonly, a thinned rectovaginal septum or perineal body indicates functional loss. In a patient with separation of the sphincter, neural dysfunction may be demonstrated by the absence of perianal skin dimpling with anal constriction.⁴⁸ This sign is important because simple repair of the sphincter will not correct the incontinence.⁴⁸ Manometric measurements of maximum squeezing pressure correlate with digital assessment of sphincter strength.⁴⁹

On digital examination, squeezing of the urogenital diaphragmatic musculature, with tightening of the bulbocavernosus and the levator ani muscles, gives an indication of neuromotor stability. To determine the integrity of the septum and the external anal sphincter loops, rectovaginal palpation is performed. The patient is instructed to tighten her anal sphincter around the examining finger; assessment of the levator ani muscles is performed by palpation of the muscular sling located posterior and cephalad to the external sphincter.⁴⁸ The anal canal is elevated toward the symphysis pubis when the patient contracts these muscles.

Finally, the length and thickness of the rectovaginal septum at the vaginal introitus versus the mid and upper third of the vagina should be assessed. The desire to retain sexual capacity should be discussed before attempting surgical correction. Following this thorough history and physical examination, additional testing may be necessary to confirm or clarify the clinical impression. Manometry, electromyographic studies, electrophysiologic studies, and anal ultrasonography may all be useful. To achieve accurate results, experience in test performance and interpretation is necessary. Also, these studies are not readily available at all institutions. When the history and physical examination are suggestive, close attention should be directed to the possibility of a rectovaginal fistula, and dye or barium studies should be performed. For the woman with demonstrable sphincter disruption and no evidence of pudendal neuropathy on examination, surgical repair of the sphincter without extensive evaluation is appropriate. Idiopathic anal incontinence attributed to pudendal neuropathy is diagnosed when a sphincter defect is not apparent on examination. In this instance, pudendal neuropathy may be confirmed by prolonged PNTML on electrophysiologic studies. Pure neuropathic anal incontinence is beyond the scope of surgery. Patients with pudendal neuropathy may also have sphincter abnormalities that are not appreciated on clinical examination, but may be discerned on ultrasound. These women with sphincter defects and concomitant neuropathy will have lower success rates with simple sphincter repair unless postanal repair is included.²⁸

More extensive testing may be especially helpful in patients who have had prior anal surgery, who have not improved with therapeutic interventions, or in whom the clinical picture is unclear.

Before entering into a surgical procedure, the patient must be screened for complicating problems, medications, allergies, and prior surgeries. The basic laboratory evaluation includes a complete blood count and urinalysis, with chest radiography, electrocardiography, or other testing as indicated. The preoperative bowel preparation should empty all solid fecal material by clear liquids for 48 hours in conjunction with citrate of magnesia or an isosmotic bowel preparation such as Golytely the afternoon before surgery. Finally, on the evening before surgery a vaginal cleansing douche should guarantee a clean operative field. Preoperative intravenous prophylaxis is the only antibiotic therapy required.

The preoperative counseling should outline the operative preparations and the general procedure in detail. A summary of the postoperative course, including catheters, intravenous fluids, diet, analgesics, ambulation, and anticipated discharge, will prepare the patient for hospitalization. Finally, a thorough review of all complications, including hemorrhage requiring transfusion, infection, injury to the anus or rectum, failure of repair, or stenosis of the vaginal introitus should be discussed with the patient, including the possibility of dyspareunia or introital and perineal body pain.

Postoperatively, urinary catheterization should continue overnight or until the patient becomes fully ambulatory. The patient should remain on ice chips until the first postoperative day, and then progress no further than clear liquid intake until postoperative day 3, at which time a low-residue diet may be instituted. Preferably, no solid fecal evacuation should challenge the repair until late in the postoperative period. Postoperative sitz baths and perineal heat lamps aid in healing. Spontaneous passage of flatus should not be resisted, nor should the sphincter musculature be voluntarily contracted for 2 weeks. At that time, slow regular exercising of the external sphincter by Kegel exercises or perineal squeezing may begin. These are increased to 10 voluntary contractions four times daily. Gradual restoration of anal control may be attempted. Daily stool softeners and cathartics will ease the passage of fecal bulk and minimize resistance against the sphincter suture line. Normal anal continence should be appreciated by the 6-week postoperative visit.

In obstetrics and gynecology practice, the majority of patients require surgical repair after a postpartum presentation in which the rectovaginal septum has been weakened, or the intermediate or base loops of the external sphincter have been severed. Less commonly, surgical manipulations, such as posterior colporrhaphy, rectovaginal fistulectomy, or incision and drainage of a perirectal abscess, may precede the symptoms. Generally, repair requires dissection of the rectovaginal septum with definition of the rectal wall, external anal sphincter, levator musculature, and vaginal mucosa. After excision of cicatrix, a multilayered repair of healthy, mobile, well-vascularized tissue may be performed with minimal tension, using additional support from the muscles of the urogenital diaphragm. The following repair techniques are the more common approaches available to gynecologists in treating anal incontinence secondary to obstetric or gynecologic trauma.

The layered repair is a common procedure that closes an anovaginal defect by individually dissecting and then reapproximating each tissue plane. A transverse incision (Fig. 4 A) is extended from both edges of the retracted external sphincter and carried along the inferior margin of the rectovaginal septum. Using a scalpel and Metzenbaum's scissors, the vaginal mucosa is separated from the rectal mucosa in the midline, and this plane is extended laterally. The external sphincter muscle fibers are identified and dissected free of cicatrix (Fig. 4 B.) After reapproximation of the rectal mucosa with an interrupted 4-0 delayed-absorbable submucosal suture, the base and intermediate-loop layers of the external sphincter are united by interrupted 0 delayed-absorbable sutures. Plication of the superior puborectalis muscle loop with an interrupted 0 delayed-absorbable suture adds additional support to the repair (Fig. 4 C.) Care must be taken to avoid compromising the vaginal lumen at this step. Plication of the transverse perineal muscles of the urogenital diaphragm reinforces the perineal body as needed. This is followed by closure of the repair with interrupted 2-0 delayed-absorbable subcutaneous sutures and a continuous 2-0 chromic mucosal stitch (Fig. 4 D.)

The Warren flap is a relatively simple dissection of the thinned rectovaginal septum to provide additional length and depth while minimizing the risk of infectious sequelae.⁵⁰ An inverted-U incision is extended laterally beyond the margins of the retracted external sphincter muscle. The rectovaginal septum is dissected, separating off the vaginal mucosa and creating a flap (Fig. 5 A.) The tissue planes are defined laterally, cicatrix is removed, and the edges of the external sphincter are identified. The rectovaginal septum is thickened by plication of the puborectalis musculature with interrupted 0 delayed-absorbable sutures. This step is followed by reapproximation of the base loop with interrupted 0 delayed-absorbable figure-of-eight sutures (Fig. 5 B.) The subcutaneous tissues are approximated with interrupted 2-0 delayed-absorbable sutures after reinforcement of the perineal body by interrupted delayed-absorbable simple stitches through the transverse perineal muscles. The vaginal mucosa is then closed with a continuous 2-0 chromic stitch (Fig. 5 C.) Excessive flap tissue is removed either during surgery or via resorption during healing.

The Noble-Mengert repair (or anal pull-through repair) provides increased rectovaginal septal length while avoiding contamination of the incision site.^51,52 A transverse incision is made along the edge of the rectovaginal septum. The vagina is separated from the anterior rectal mucosa to mobilize the anal canal (Fig. 6 A.) With the anal wall advanced, the dissection is continued laterally, identifying and freeing the ends of the external sphincter muscle. The ends of the external sphincter muscle are united with interrupted 0 delayed-absorbable sutures. The puborectalis muscle can also be approximated with interrupted 0 delayed-absorbable sutures (Fig. 6 B.) Interrupted 2-0 delayed-absorbable stitches plicate the pararectal fascia and subvaginal tissues to thicken the septum. Finally, the vaginal mucosa is closed with a continuous 2-0 chromic suture and the anal mucosa sutured to the perianal skin with interrupted 2-0 chromic stitches (Fig. 6 C.)

The surgical literature is replete with alternative approaches to correct anal incontinence.^1,3 Although often successful in alleviating symptoms resulting from obstetric or gynecologic complications, these procedures were designed to correct defects after anal surgery for infectious, inflammatory, congenital, or neoplastic disorders. Most commonly, the approach is postanal, with dissection into the presacral space. Identification, dissection, and mobilization of the anal canal and its musculature allow successful correction of the conditions just described. In 1971, Sir Allan Parks described an approach in which the base loop of the external sphincter is identified and mobilized with excision of all damaged tissue or scar, using an overlapping technique of repair to reapproximate the sphincter.^53,54 Complications of this procedure are difficulty in voiding, hemorrhage, abscess, and fecal impaction. Success in repair may be as high as 80% to 90%.^1,53 Many of the studies reporting alternative procedures discuss the use of a diverting loop colostomy before attempting the repair of anal incontinence. Generally, the North American surgical literature reflects a trend away from this procedure.⁵⁴ Most recent series suggest a thorough preparatory bowel cleansing with postoperative dietary manipulation to minimize perioperative fecal soiling.

Several techniques for muscle transposition exist.^55,56 The pelvic floor musculature including the puborectalis muscle is dissected and then transected. Using an overlapping suture technique, the muscles are wrapped around the anal canal to provide a spiraling sphincter.⁵⁷ This same technique may be used with the gluteus maximus or gracilis muscle, exercising caution to preserve the vascular supply and innervation.^57,58,59,60 Generally, these series report success rates of 70% to 80%. Some authors have described reconstruction of the puborectalis sling⁶¹ using anterior abdominal wall fascia or a Dacron (Dow Corning Medical Products, Midland MI) or Marlex (Meadox, Oakland, NJ) graft.^62,63,64 The thrust of these techniques is to reposition the angle of the anal canal anteriorly and reinforce the effect of the puborectalis muscle.

Finally, artificial sphincter devices of silicone rubber are under development.^65,66,67 The artificial sphincter consists of a pressure-regulating balloon, a cuff, and a pump through which isotonic radiopaque solution flows to inflate and deflate the cuff. Recent reports on use in animals describe excellent achievement of continence.

Fecal continence is maintained through a delicate yet complex interaction among several neuromuscular systems. These may become impaired in postobstetric or gynecologic patients. Gynecologists should be attuned to the symptoms of this defect, as well as its evaluation and intraoperative management. With minimal intervention, the correction of anal incontinence can significantly improve these patients' quality of life.

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