Posterior wall prolapse, bulging or herniation of the bowel along the dorsal aspect of the vagina, is a component of the constellation of pelvic floor disorders. Pelvic floor dysfunction, primarily involving pelvic organ prolapse, urinary and fecal incontinence, affects nearly one in four (23.7%) community-dwelling women.¹ As women age, prolapse and incontinence become more common. One-half of women aged 80 years and older have at least one pelvic floor disorder.¹

The elderly population is expected to grow significantly over the next 40 years. By 2050, those 65 years of age or older are projected to more than double, from 38.6 million to 88.5 million.² The population of people 85 years or older is expected to grow exponentially from 5.4 to 19 million and the majority of people in this category will be women.² Therefore, the demand for prevention and treatment of pelvic floor dysfunction will also grow dramatically.

Treatment for pelvic floor disorders varies from conservative measures to surgical management. The lifetime risk of undergoing surgery for pelvic organ prolapse or urinary incontinence is approximately 11%.^3,4 Currently, approximately 200,000 women undergo prolapse surgery in the United States each year.⁵ One-third to one-half of all the prolapse surgeries include posterior wall prolapse repair.^3,5 Understanding the anatomy, etiology, and treatment options for posterior wall prolapse is vital and will become increasingly important as our aging population multiplies.

Prolapse of the posterior vaginal wall may be secondary to the presence of a rectocele, sigmoidocele, enterocele, or a combination of these entities (Figure 13-1A, B and C). This loss of support may be defined symptomatically, radiographically, or by physical examination.

To recognize and correct abnormal anatomy such as prolapse, you must understand normal anatomy. Support of the posterior vaginal wall is provided by a complex interaction of the integrity of the vaginal tube, the connective tissue support, and muscular support of the pelvic floor. John DeLancey divided the connective tissue support of the vagina into three levels.⁶ All three levels of support should be evaluated and addressed during the physical examination and in consideration of surgical management of the posterior vaginal wall.

At level I, the apical portion of the posterior vaginal wall is suspended and supported primarily by the cardinal-uterosacral ligaments.^7,8 This mesentery of support originates at the sacrum and the pelvic sidewalls and inserts onto the posterior cervix and upper vagina. With normal support, the apical posterior wall of the vagina is dorsally directed to lie upon the rectum in a horizontal fashion overlying the levator ani muscles. With increases in abdominal pressure, the vaginal tube is closed and primarily supported by the pelvic floor muscles including the levator ani and coccygeus muscles.

Level II includes the support for the midportion of the vagina. This support is provided by the endopelvic fascia attaching the lateral posterior vaginal wall to the aponeurosis of the levator ani, specifically the pubococcygeus muscle, on the pelvic sidewall and by the tonically contracted sling-like component of the puborectalis muscle dorsally.⁸ Most of the fibers of the endopelvic fascia extend from the lateral edge of the vaginal tube to the pelvic sidewall.⁷ Very few of the fibers actually run uninterrupted, like a sheet from sidewall to sidewall. The proximal half of the anterior and posterior vagina is supported by endopelvic attachment to the arcus tendineus fasciae pelvis. The lateral attachment of the posterior wall diverges dorsally from the arcus tendineus fasciae pelvis in the distal vagina (Figure 13-2).

Level III or distal support of the posterior vaginal wall is primarily provided by the perineal body. The perineal body resists caudally directed abdominal pressure and imparts a physical barrier between the vagina and rectum. Distally, this 3-dimensional structure has the bony support of the ischiopubic rami through the interlacing fibers of the bulbospongiosus, superficial transverse perineal muscle, perineal membrane, and external anal sphincter. The perineal body extends cranially approximately 2 to 3 cm proximal to the hymenal ring and is suspended by the puborectalis muscle. On magnetic resonance imaging (MRI), the perineal body descends more caudally in women with posterior wall prolapse or with levator defects than controls.^9,10

The puborectalis provides a sling of support, enclosing the genital hiatus, through which the urethra, vagina, and anorectum pass. In a woman with an intact pelvic floor, the puborectalis is in a chronic state of contraction and the anterior and posterior vaginal walls are in direct apposition. With defecation, the increased pressure placed on the posterior vaginal wall is equilibrated by the opposing pressure on the anterior vaginal wall. There is no stress placed on the endopelvic fascial attachments (Figure 13-3A). In the presence of muscular or neurologic damage to the puborectalis, the levator hiatus widens and the vaginal canal opens. The increased rectal pressure and distension associated with defecation now places strain on the endopelvic fascial attachments and the fibromuscularis of the posterior vaginal wall (Figure 13-3B).

The rectovaginal space exists between the vaginal tube and the rectum. This potential space, occupied by areolar tissue, allows the vagina and rectum to function independent of one another.

Abnormalities in the complex interplay of bony and connective tissue support of the posterior vaginal wall, which is tonically and actively maintained by the pelvic floor muscles, can impact urinary, sexual, and defecatory function. This chapter will review the pathophysiology, evaluation, nonsurgical, and surgical management of posterior compartment disorders as well as factors associated with recurrence of posterior vaginal wall prolapse.

The vagina is a fibromuscular tube that extends from the abdominal cavity to the perineal body. The bony and muscular support and the connective tissue of this tube are dynamic. Disruption of support leading to a herniation of the surrounding organs (pelvic organ prolapse) is most likely due to an accumulation of injuries. Risk factors for the development of prolapse may begin at conception and continue to accrue until death (Table 13-1).

Women may carry a genetic code that predisposes to developing pelvic organ prolapse. Familial predisposition for the development of prolapse has been evaluated through chromosomal linkage analysis in affected families and phenotypical analysis of sisters. Extensive family study has linked the predisposition to the development of prolapse to an area on the long arm of chromosome 9 (9q21).¹¹

Genetic damage to the structure of the pelvic floor affects the attributable risk of and the age of development of pelvic organ prolapse. Disorders dramatically affecting these structures, such as bladder exstrophy, may lead to the emergence of prolapse at an early age.¹²

Collagen is the most common protein in the body and is the primary fiber of the extracellular structure. There are 14 types of collagen. The amount, type, and cross-linking contributes to the property and strength of the tissue. Connective tissue disorders also predispose a woman to early onset pelvic organ prolapse. Ehlers-Danlos syndrome is a result of genetic mutations in the genes coding for collagen synthesis and processing and affects collagen types I, IV, and V. Clinical manifestations of Ehlers-Danlos syndrome include severe skin hyperelasticity, joint hypermobility, hernias, and pelvic organ prolapse.¹³ Women with Marfan’s syndrome are also more commonly afflicted with pelvic organ prolapse. Marfan’s syndrome is primarily due to a mutation in the gene coding for fibrillin-1 (a glycoprotein that is the main component of the microfibrils of the extracellular matrix).¹⁴ Women with less pronounced connective tissue disorders often have hyperextensible skin. Following a vaginal delivery, the vagina will not be able to “spring” back in shape and resultant prolapse commonly occurs.¹⁵ Women with joint hypermobility are more likely to have rectal evacuation disorders and rectocele.¹⁶ Histologic changes in the expression of collagen and the proteins that remodel collagen have been demonstrated in women with prolapse and incontinence.^17,18 Further elucidation of the timing of the shift in balance of the remodeling process toward degradation will serve to establish if degradation contributes to the development of prolapse or merely is a result of previous prolapse development.

Given the genetic link to pelvic organ prolapse, it is not surprising that a high concordance of prolapse was demonstrated between 101 pairs of nulliparous and parous postmenopausal sisters.¹⁹ While genetics predisposed sisters to prolapse, inciting factors were also important. The vast majority (88%–100%) of cases of discordancy between sisters found more advanced prolapse in the parous sister.¹⁹

Trauma to the posterior vaginal wall most commonly occurs at the time of pelvic surgery or vaginal delivery. In addition, hysterectomy has been identified as a risk factor for the subsequent development of pelvic organ prolapse.²⁰ In a large case-control study, Dällenbach et al. found the primary risk factor for development of prolapse after a hysterectomy was the degree of prolapse before the hysterectomy. The risk of subsequent prolapse repair in a woman with prolapse to the hymen at the time of hysterectomy was eight times that of a woman without prolapse, regardless of the route of surgery.²¹

Pelvic surgery may promote the development of posterior wall prolapse through damage to connective tissue support, innervation, or due to a change in the vaginal axis. Ventral deviation of the anterior vaginal wall following a Burch colposuspension may expose the apex and posterior vaginal wall to increased abdominal pressure. A prospective, long-term study of the women who had undergone a colposuspension revealed that 29 of 77 (38%) of these women had developed symptomatic prolapse. Of those who developed prolapse, the majority (76%) had surgical repair.²⁰ Cruikshank et al. described rectoceles or enteroceles in 57% of women 2 to 12 years after a colposuspension.²² Most of these women were asymptomatic at the time of the report. Development of pelvic organ prolapse is significantly lower following a “tension-free” midurethral sling as compared to a colposuspension.²³

Vaginal delivery of a term infant is thought to be the most significant event promoting the development of pelvic organ prolapse. Vaginal delivery, particularly in the occiput-posterior position, may damage the connective tissue support, innervation, and levator ani muscles. Interruption in the support of the perineal body will allow the posterior vaginal wall, perineal body, and the distal portion of the anterior rectal wall to descend with increased rectal pressure (Figure 13-4A and B).

Birth-related injury to the levator ani muscle has been visualized using MRI.²⁵ Defects in the levator ani alter the anatomy of the pelvic floor. The perineal body and external anal sphincter are more caudally placed regardless of prolapse status.¹⁰ The alteration of anatomy due to levator ani damage and dysfunction may be causal in the development of prolapse.¹⁰

The levator hiatus has been shown to be larger in women with prolapse than in women with normal support.^26,9 Women with pelvic organ prolapse more commonly have a major levator ani defect than those without prolapse (odds ratio [OR] 7.3).²⁸

Whether inherited, surgically or obstetrically induced, the damaged posterior vaginal wall support may not be symptomatic for years. Aging or other promoting factors such as repetitive lifting and straining may be necessary for prolapse propagation.

As woman age, muscles weaken, connective tissue loses elasticity and strength, and devascularization and denervation occur throughout the body. Our understanding of how the aging process occurs is growing quickly. Hormonal and cellular changes contribute as well as the cumulative effects of living an active life.

During the lifetime of a woman, there are repetitive straining activities that she may perform that promote the development or recurrence of prolapse. The vector force created by a Valsalva maneuver is partially dissipated through the weakness in the rectovaginal septum. The woman will increase her strain in response to this, which leads to further increase in the size of the rectocele. Chronic illnesses such as chronic pulmonary disease may increase the repetitive abdominal pressure placed on the pelvis. Chronic pulmonary disease was found to be an independent risk factor for the development of prolapse after hysterectomy (OR 14.3, 95% confidence interval [CI] 1.2–178).²⁹ Chronic constipation has been linked to the development of prolapse.³⁰ Posterior vaginal wall prolapse is a common finding in women with constipation.³¹

The magnitude of pressure placed in the pelvis also impacts the support. Obesity is associated with an increased risk of prolapse and recurrent anatomic and symptomatic prolapse.³² Obesity is also an independent risk factor for prolapse progression. In an analysis of the 16,608 postmenopausal women (ages 50–79 years) enrolled in the Women’s Health Initiative, the risk of posterior vaginal wall prolapse progression increased by 37% in overweight and 58% in obese women as compared to women with a healthy body mass index (BMI).³³ Additionally, repetitive heavy lifting may also be a risk factor. Woodman et al. found that women in the lower socioeconomic income who work as laborers or factory workers were more likely to have prolapse.³⁴

The etiology of posterior vaginal wall prolapse is likely multifactorial. On the cellular level, changes are seen in the connective tissue supports, the vaginal wall, and the pelvic floor muscles. Pelvic trauma and aging result in tissue trauma, denervation, devascularization, and enhanced collagen degradation. With time, this weakened connective tissue and pelvic floor musculature can produce posterior wall prolapse.

Understanding the pathophysiology of the pelvic floor and posterior wall prolapse greatly enhances the provider’s ability to delineate and quantify posterior wall prolapse and interpret coexisting pelvic floor dysfunction. Symptoms related to posterior wall prolapse include the physical herniation of bowel contents into the vagina and the functional results of this herniation. A woman will commonly complain of a lump or bulge in the vagina that is more prominent after standing for long periods of time.

A bulging posterior wall of the vagina may provide structural support of the urethra, masking stress urinary incontinence. Cystometry with prolapse reduction can be performed to evaluate for occult incontinence. A distal or advanced posterior wall prolapse may partially obstruct the external urethral meatus resulting in spraying of the urine stream or sense of hesitancy. Multichannel urodynamic evaluation may be helpful in the diagnosis of urinary symptoms in women with stage III or stage IV posterior wall prolapse. With replacement of the posterior wall prolapse that simulates correction of the posterior wall prolapse, a significant decrease of the maximum urethral closure pressure and functional urethral length can occur, “unmasking” urinary incontinence.

Defecatory function may be impacted by a multitude of medical and behavioral factors. Dysfunction may be simply related to insufficient fiber or fluid intake. Systemic illnesses, such as diabetes, thyroid disorders, and neuromuscular disease may significantly impact defecatory function. Hirschsprung disease, malignancy, inflammatory bowel disease, rectal intussusceptions, or prolapse can cause mechanical bowel obstruction. Medications can alter bowel motility and lead to constipation. Common culprits include aluminum antacids, anticholinergics, antidepressants, anti-inflammatory drugs, beta-blockers, calcium channel blockers, iron sulfate, and opiates. Psychiatric conditions such as abuse (psychologic, physical, and sexual), eating disorders, and pelvic pain can also affect bowel function.³⁵

Many women complain of constipation, which may be defined as excessive straining, hard lumpy stools, splinting, feeling of incomplete emptying, and infrequent stools. Women with slow-transit colon respond less favorably to surgical management of rectocele as compared to women with normal transit studies.³⁶ The most common defecatory complaint noted in women with symptomatic posterior wall prolapse is difficulty or incomplete emptying of stool.^37,35 Obstructed defecation is frequently related to issues other than posterior wall prolapse such as anismus or nonrelaxing pelvic floor or pelvic floor dyssynergia. While the symptom of incomplete rectal emptying is common in women with posterior wall prolapse, the defecatory symptom most specific for posterior wall prolapse is vaginal digitation to relieve the incomplete emptying.³⁸

Sexual function is multifaceted. Pelvic organ prolapse can alter a woman’s body image.³⁹ Both partners can be affected by the appearance or sensation of a change in the vaginal anatomy. An enlarged genital hiatus may lead to decreased sensation by both partners. If stool is trapped in the rectocele, intercourse may lead to fecal incontinence or instill a fear of fecal incontinence leading to avoidance of intercourse.

The posterior vaginal wall may be evaluated for evidence of prolapse through physical examination or imaging. Further physiologic testing may be indicated. The physical examination includes a quantification of prolapse. The pelvic organ prolapse quantification (POP-Q) system is a standard, validated tool that permits comparisons of patients and allows individual patients to be followed longitudinally⁴⁰ (Figure 13-5). The patient is generally examined in the dorsal lithotomy position and asked to Valsalva maneuver to maximize descent of the prolapse. If this fails to recreate the degree of prolapse that the patient describes, a standing examination should be performed. It is physically more difficult to make measurements of the prolapse in this position. The perineal body should be evaluated for support and descent. A rectovaginal examination can facilitate evaluation of the support and descent of the perineal body as well as evaluate the protrusion of the anterior rectum into the posterior vaginal wall. Palpation of loops of small bowel or sigmoid colon in the rectovaginal space may confirm an enterocele or sigmoidocele, respectively. Performing this examination in the standing position can allow gravity to bring the bowel into the rectovaginal space and facilitate detection of an enterocele or sigmoidocele (Figure 13-6). Pressure on the posterior wall of the vagina, directed toward the rectum, may facilitate identification of rectal prolapse. Assessment of the anal sphincter may also be performed including evaluation of anal tone, squeeze, and symmetry.

A focused neurologic examination includes evaluation of sensation, motor function, and reflexes of sacral nerves 2–4. The patient is asked to discriminate between sharp and dull on the perineum. Pelvic floor muscle strength may be assessed by asking the patient to contract and relax the pelvic floor muscles around the examiner’s fingers in the vagina. Reflex testing includes the bulbocavernosus reflex and anal wink.

The clinical examination enables documenting the presence or absence of prolapse, but is not accurate in identifying the location of the connective tissue defect or presence of an enterocele or sigmoidocele.⁴² Imaging and functional evaluation of the bowel may be warranted.

A woman with defecatory dysfunction and pelvic organ prolapse may benefit from further testing. Defecography provides a two-dimensional view of the efficiency of anorectal emptying during simulated defecation and quantification of rectal parameters. Prior to the test, a woman ingests diluted barium, the rectum is filled with a barium paste that has the consistency of soft stool and the barium gel is placed in the vagina. Evaluation includes rest, squeeze, strain, and evacuation. Rectocele, enterocele, and rectal intussusception can be graded based on the anatomic evaluation obtained with defecography (Figure 13-1B, C and Table 13-2). Diagnostic categories obtained are internal procidentia, rectocele, enterocele, sigmoidocele, descending perineum, and the functional description of spastic pelvic floor.

Some degree of rectocele is present in most symptomatic women and up to 20% of asymptomatic women.⁴³ Radiographically, a rectocele is considered significant if the anterior rectal wall extension is greater than 2 cm from the midrectal canal (grade 2 or 3). Descent of the perineal body and descent of the bowel into the rectovaginal space can be visualized and graded (Table 13-3). Retention of more than 10% of the barium following defecation is referred to as barium trapping. It should be recognized that this examination provides an artificial environment, which may make the patient more prone to incomplete emptying. Paradoxical contraction of the puborectalis and rectal intussusception may be diagnosed with this functional test. The advantages of defecography over magnetic resonance (MR) defecography or perineal ultrasound are that it is simple to perform, cost-effective, and widely available. The disadvantages include exposure to radiation and inability to image soft tissues.

The performance of MR defecography requires the patient’s rectum to be filled with synthetic stool such as potato starch mixed with 1.5 mL of gadopentetate dimeglumine or ultrasound gel. The vagina may be delineated with insertion of ultrasound gel. Ideally, the patient is able to complete this study in an open configuration MR imaging system in the sitting position, although some studies are done with the patient in the supine position. The pelvis is imaged at rest, maximum squeeze, maximum strain, and evacuation. The technique in the sitting position simulates the functional testing achieved with defecography with the added advantages of superb soft tissue imaging, large field of view, avoidance of ionizing radiation, direct multiplanar capability, and high temporal resolution. If an open configuration MRI is not available, the test may be performed in a closed MRI. However, an accurate picture of the extent of prolapse may not be demonstrated with a Valsalva maneuver in the supine position and the woman’s legs closed to fit in the MRI scanner. Furthermore, this is not a normal position for defecation and may not simulate the woman’s ability to defecate. Disadvantages of MR defecography primarily include cost and availability of open MR imaging.^43,45

Translabial, perineal, and three-dimensional endoanal ultrasound has been described to evaluate the pelvic organs at rest, contraction, and maximum Valsalva maneuver.⁴⁴ Ultrasonography has been found to compare favorably to defecography in the identification of rectocele, enterocele, paroxysmal contraction of the puborectalis, and rectal intussusception.^44,46 The advantages of ultrasound evaluation includes avoidance of ionizing radiation, less expense, physician view in real-time rather than static images, and the avoidance of the embarrassment of defecating in public. However, to date there is no standardization of parameters or techniques. Evaluation of efficiency of evacuation is not performed.

At this time, a standardized method of establishing a radiologic diagnosis of a rectocele is lacking. There is poor correlation between imaging and clinical examination.^47,48 Clinical examination fails to identify women with enteroceles as defined by defecography.⁴⁸ While defecatory dysfunction is common in women with prolapse, the extent of the prolapse generally correlates with the symptom of feeling or seeing a bulge rather than functional complaints.⁴⁹ If a woman’s primary complaint is defecatory dysfunction or fecal incontinence rather than a bulge, correction of a rectocele or perineal body defect may not correct her symptoms. Ancillary testing is then pursued based on the woman’s complaints. Validated functional and quality-of-life questionnaires are now available. These questionnaires may be performed pre- and postoperatively to provide a standardized method of evaluating functional surgical outcomes. The patient’s preoperative symptoms and surgical goals will guide the provider in the selection of additional testing.

A woman who describes life-long infrequent bowel movements defined as less than one bowel movement per week and an absence of a daily urge to defecate is unlikely to be cured of her constipation with a rectocele repair. A colon transit study may be helpful in identifying patients with slow transit colon. Dietary modifications including fiber and laxatives should be encouraged in any woman whose main complaint is constipation. Severely constipated women tend to have multiple findings on defecography.⁴³

Women who have failed conservative management of fecal incontinence should undergo further evaluation prior to rectocele repair. An endoanal ultrasound will provide anatomical detail of the integrity of the external and internal anal sphincter, while electromyography (EMG) study of the external anal sphincter and pudendal nerve can provide neurologic information on the innervation of these muscles.

The pelvic floor muscles are constantly active and contracted. During straining, a coordinated relaxation of the levator ani and external anal sphincter occurs. Failure to relax the pelvic floor muscles is a sign of anismus. The balloon expulsion test (BET) and manometry can indirectly measure the function of the pelvic floor muscles. A woman with a normally functioning pelvic floor should easily be able to expel a 60 mL balloon filled with air or water. Failure to expel the balloon suggests a functional abnormality.⁴³ Women with anismus should be treated with biofeedback.