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Perineal body defects and rectovaginal fistulas (RVFs) are part of a spectrum of conditions that impact the posterior pelvic floor. The surgical interventions used to address these defects must be based on a clear understanding of the anatomic structures involved. A postobstetric pinhole fistula may occur in isolation (i.e., the perineal body and anal sphincters [ASs] are completely intact) ( Fig. 29.1 ); or maybe only the tip of an iceberg in which there is a significant defect of the entire perineal body and ASs ( Fig. 29.2 ). Surgical management of these various defects requires a clear understanding of the anatomy of the distal portion of the posterior vaginal wall, the perineal body, the ASs, the rectum, and the anal canal.
The surgical anatomy of the posterior pelvic floor remains an area of controversy among surgeons and anatomists. In recent years, there has been a clearer understanding of the anatomy of the posterior vaginal wall and perineum; however, surgical studies in this area continue to use terms that are not anatomically based. Historically, the tissue that lies between the posterior vaginal wall and anterior wall of the rectum has been termed rectovaginal or Denonvilliers’ fascia. Histologic studies have noted that what has previously been termed fascia is actually vaginal muscularis ( ). At the level of the midvagina, histological assessment of the posterior vaginal wall from the lumen of the vagina to the lumen of the rectum notes the following layers: the vaginal epithelium, the lamina propria of the vagina, the fibromuscular wall of the vagina (smooth muscle cells, elastin, and type II collagen), D the adventitia, the outer muscular wall of the rectum, the inner muscular wall of the rectum, the lamina propria of the rectum, and the rectal mucosa. discussed posterior vaginal wall anatomy in a review article and likened it to an open container. The front wall of the container is formed of the posterior vaginal wall, whereas the bottom of the container is made up of the perineal body and ASs. The levator ani muscles form the lateral sides of the container and the levator plate, where the muscles decussate behind the rectum to create the iliococcygeal raphe, which forms the back wall of the container. The uppermost portion of the container would then be created by the attachment of the posterior vaginal wall to the uterosacral ligaments, which extend below the peritoneum. All of these boundaries are subject to defects that can give rise to different structural failures.
The perineal body has been described as the central tendon between the urogenital and anal triangles ( Fig. 29.3 ). It contains interlacing muscle fibers from the bulbospongiosus and superficial transverse perineal muscles, as well as the anterior portion of the external AS. There is also contribution from the longitudinal rectal muscle and medial portions of the puborectalis muscles.
Normally, the anus appears externally as a closed anterior/posterior lip, with its lateral walls closely opposed. Damage to the surrounding sphincter mechanism may result in what has been termed a patulous anus ( Fig. 29.2 ). The anus is anchored anteriorly by the perineal body and posteriorly by the anococcygeal ligament to the coccyx. The anal canal typifies the meeting of structures, with an endodermal and ectodermal derivation. The dentate line demarcates the boundary between the structures of the inferior hindgut and those of the proctodeum. The columns of Morgagni denote longitudinal folds of rectal mucosa that end as anal valves at the level of the dentate line. There are anal crypts present between the valves, most notably clustered in the posterior anus. Obstruction of these crypts can give rise to infection that may result in abscess or a fistula.
The AS apparatus involves the internal and external sphincters, as well as the conjoint longitudinal muscle that encircles the anus. These structures play a crucial role in fecal continence. The internal AS is a smooth muscle that is a dense continuation of the inner circular layer of the rectum and extends approximately 2.5 to 4 cm ( ). The internal AS arises at the junction of the anus and the rectum (anorectal ring) and ends approximately 1 to 1.5 cm distal to the dentate line. In contrast, the larger external AS is an elliptical band of skeletal muscle circumscribing the entire length of the anal canal. This structure makes up the majority of the perineal body from its anterior portion. Superiorly, the external AS continues as the puborectalis muscle. Many anatomists and surgeons believe it should be considered a component of the puborectalis muscle, even though the two muscles have separate embryologic derivations, and their muscle fibers do not intermingle ( Fig. 29.3 ).
Obstetrical perineal tears are most commonly classified in the following fashion: first-degree is a laceration of the vaginal-epithelium or perineal skin only; second-degree is first-degree with involvement of the perineal muscles and fascia, but not the ASs; third-degree is disruption of the skin, mucous membrane, perineal body, and AS muscles; and fourth-degree is a third-degree tear with disruption of the anal mucosa. More recently, third-degree lacerations have been subdivided into three subcategories, with 3a lacerations involving less than 50% of the external AS, 3b involving more than 50% of external AS thickness, and 3c having both external and internal AS involvement ( ). Appropriate classification of lacerations is necessary, as incorrectly classified lacerations could result in inappropriate repair and suboptimal outcomes.
RVF is a congenital or acquired epithelialized tract between the rectum and the vagina. The communication may occur at any point along the vagina. Most fistulas actually arise in the anal canal distal to the pectinate line. RVFs are classified according to their location and size; careful attention to both features allows determination of the approach for surgical repair. In a low RVF, the rectal opening is located close to the dentate line, with the vaginal opening just inside the hymen. In a high RVF, the vaginal opening is near the cervix (or apex of the vagina in a posthysterectomy patient); the communication into the intestinal tract may be located in either the sigmoid colon or rectum. These fistulas usually require a laparotomy for repair. Such fistulas may not be readily apparent on physical examination or endoscopy and may require contrast studies for diagnosis. A mid-RVF is found somewhere between the hymen and the cervix. RVFs range in size from tiny (<1 mm in diameter) to large, where the rectovaginal defect encompasses the entire posterior vaginal wall. In using size as a criterion, fistulas less than 2.5 cm in diameter are considered small, and those greater than 2.5 cm are described as large. Simple RVFs consist of small, low fistulas secondary to infection or trauma. These fistulas generally have healthy, well-vascularized surrounding tissue that can be repaired with local techniques. RVFs are considered complex if they are large (>2.5 cm), high, or caused by inflammatory bowel disease (IBD). Recurrent fistulas are also considered complex because of their association with tissue scarring and decreased blood supply. Because healthy, well-vascularized tissue needs to be introduced after resection of diseased tissue, complex fistulas require more complicated surgical procedures for repair. A fistula-in-ano is an abnormal tract or cavity that is lined with granulation tissue and that connects a primary opening inside the anal canal to a secondary opening in the perianal skin or vulva; secondary tracts may be multiple and can extend from the same primary opening. Fistula-in-ano are only superficially discussed in this chapter; more detailed discussion of their diagnosis, evaluation, and treatment can be sought elsewhere.
Another method of classification is based on the underlying cause of the fistula, which will be a better predictor of the ultimate success of the repair, as it takes into consideration the integrity of the local tissue and the health of the patient. In 2017, a retrospective cohort study was conducted including 107 women who underwent surgical repair of RVF for various etiologies (cancer, IBD, infection, and other), and concluded that the rate of recurrence at 1 year was significantly different depending on surgical approach ( P < .001), but not etiology ( P = .71), and did not differ based on the surgical subspecialty performing the surgery (e.g., colorectal vs. female pelvic medicine and reconstructive surgery vs. combined/dual surgeon) ( ).
A patient with a perineal breakdown may be asymptomatic or may present with an array of symptoms, including pain and dyspareunia, an enlarged introitus, and a variety of defecatory symptoms, including fecal incontinence if the sphincter mechanism is involved. A patient with an RVF is usually symptomatic. She most often complains of passage of flatus or stool through the vagina. Occasionally, the presenting complaint is a recurrent vaginal or bladder infection, which is the result of fecal soilage. A small fistula may be symptomatic only when gas or loose or liquid stool is passed. Determining the status of the AS mechanism is important when the patient’s complaints are consistent with fecal seepage.
Although the majority of cases of perineal breakdown are postobstetrical events, many different causes of RVFs have been identified ( Box 29.1 ); the cause varies with the location of the fistula. Congenital RVFs are rare and are not discussed here.
Congenital
Obstetric
Previous anorectal surgery
Inflammatory bowel disease
Infection
Carcinoma
Radiation
Lymphoproliferative malignancy
Endometriosis
Obstetric injuries are the most common cause of RVFs and perineal breakdown, causing up to 88% of fistulas in published series ( ). The incidence of perineal wound breakdown has been reported to be anywhere from 1% to nearly 25% of all lacerations ( ; ). American College of Obstetricians and Gynecologists and World Health Organization guidelines recommend only one dose of antibiotics at the time of AS injury repair; however, a growing body of evidence (including a recent multicenter randomized controlled trial with 3400 women) suggests that a more liberal administration of antibiotic prophylaxis, especially in obese women, after operative vaginal delivery may improve outcomes ( ). A recent prospective cohort study with 24 months’ follow-up of primiparous women after third- and fourth-degree laceration found that 9% and 24% of women suffered from fecal incontinence, respectively ( ). Risk factors for development of an obstetric fistula (vesicovaginal or rectovaginal) include teenage status at delivery, primiparity, prolonged labor, home delivery, and short maternal height ( ).
Historically, episiotomy was commonly performed during vaginal deliveries; however, this practice has decreased substantially with increasing evidence that episiotomies promote third- and fourth-degree perineal tears. Approximately 5% of vaginal deliveries or 20% of episiotomies result in a rectal tear or AS disruption. For women undergoing nonoperative vaginal deliveries, a policy of selective rather than routine episiotomy results in 30% fewer women experiencing severe (third- or fourth-degree) perineal tears or vaginal trauma ( ). Although the majority of perineal injuries are successfully repaired at the time of the delivery, dehiscence of an episiotomy repair can occur and is associated with infection, abscess, fistula, or sphincter disruption. Up to 1.5% of women who undergo an episioproctotomy develop an RVF. Such fistulas present either immediately postpartum from failed recognition of a fourth-degree injury or 7 to 10 days after an apparently normal repair. Midline episiotomy with resulting third-degree or fourth-degree laceration produces the greatest risk for development of an RVF. Mediolateral episiotomy, more common in British obstetric practice, causes fewer tears into the AS and rectum compared with midline incision. RVF after infection and dehiscence of an episiotomy most commonly occur low in the rectovaginal septum, but may extend much higher, especially in the case of a traumatic cloaca. Of paramount importance in these patients is an assessment of their degree of incontinence. noted that 27% of women with low RVFs had coexistent fecal incontinence, recommending a careful continence evaluation before embarking on a repair (see Chapter 27 ). A retrospective cohort spanning a 10-year period of women undergoing RVF repair compared the risk of failure of the repair in women with obstetric versus nonobstetric (IBD, iatrogenic, or traumatic) fistulas. The study concluded that women with nonobstetric fistula have a nearly four-fold increased risk of repair failure compared with obstetric fistula. This information is important in directing surgical outcome counseling and setting postoperative expectations ( ).
IBD, specifically Crohn disease, is the second most common cause of RVFs and should be suspected in any instance when attempted repair has failed or in cases of spontaneous nonobstetric RVF. Because ulcerative colitis is not a transmural disease, it usually does not cause such problems. RVFs will occur in up to 10% of female patients with Crohn disease. These types of fistulas originate either from an inflamed anal gland (which is associated with a better prognosis) or from a rectal ulcer (which is associated with poorer prognosis). Low RVFs will usually follow a less aggressive disease course, especially in the absence of rectal inflammation. Symptoms tend to be worse in higher fistulas. Active small bowel Crohn disease and proctitis are usually associated with factors that result in a high risk of failure of fistula repair. Most commonly, RVFs from Crohn disease will occur in the mid portion of the rectovaginal septum; however, in patients with anorectal Crohn disease, a fistula can extend into the most distal aspect of the vagina or perineum. An anovaginal or RVF in Crohn disease is more likely to result in proctectomy or a dysfunctioning stoma than anal Crohn disease without a fistula.
The most common nonobstetric infectious cause of an RVF is formation of a cryptoglandular abscess in the anterior aspect of the anal canal. Extension of such an abscess into the vaginal wall can result in fistula formation. Other infectious processes that may fistulize into the vagina include lymphogranuloma venereum, tuberculosis, and formation of a Bartholin abscess. Acquired RVF may be an early manifestation of human immunodeficiency virus infection in women. Colovaginal fistula can result from diverticulitis, is usually located near the vaginal apex or cuff, and usually occurs in women who are postmenopausal and have previously undergone hysterectomy.
RVF can occur after surgeries that involve the posterior vaginal wall or the anterior rectal wall. These include procedures such as vaginal hysterectomy, rectocele repair, hemorrhoidectomy, local excision of rectal tumors, and low anterior resection.
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