Pelvic organ prolapse (POP) is the downward descent of the female pelvic organs that results in a protrusion of the vagina and/or uterus. It usually involves descent of the bladder, uterus, or posthysterectomy vaginal cuff, and the small and/or large bowel. Vaginal delivery, hysterectomy, chronic straining, normal aging, and abnormalities of connective tissue or connective tissue repair predispose some women to disruption, stretching, or dysfunction of the levator ani complex and/or the connective tissue attachments of the vagina, resulting in prolapse. Women often present with multiple complaints including bladder, bowel, and pelvic symptoms. However, with the exception of vaginal bulging symptoms, none of these symptoms are specific to prolapse. Patients presenting with symptoms suggesting prolapse should undergo a history and pelvic examination. Radiographic evaluation is usually unnecessary. Many women with POP are asymptomatic and do not require treatment. When prolapse is symptomatic, options include observation, pessary use, and surgery. Surgical therapy for prolapse can be broadly categorized into reconstructive and obliterative techniques. Reconstructive techniques may be performed using an abdominal or vaginal approach. Although no effective strategy to prevent prolapse recurrence has been identified, weight loss, minimizing heavy lifting, treating constipation, modifying or reducing obstetrical risk factors, and maintaining or improving pelvic floor muscle strength through pelvic floor physical therapy can be considered.

Apical prolapse is the descent of uterus, cervix, or vaginal vault caused by a weakness of the top of the vagina; the vagina begins to invert, just as a sock can be turned inside-out (Figure 14-1). Prolapse development is multifactorial, with vaginal childbirth and increasing body mass index as the most consistent risk factors (Table 14-1). Patients at a young age are at higher risk for prolapse recurrence following surgery and a lower overall risk from surgery compared with older women (Table 14-2).^1-4

Apical prolapse includes either the uterus or posthysterectomy vaginal cuff, and may involve the small intestine (enterocele), bladder, or colon (sigmoidocele) (Figure 14-2). Enterocele is a hernia in which the peritoneum is in contact with vaginal mucosa. The normal intervening endopelvic fascia is absent, and small bowel fills the hernia sac. Normally, posthysterectomy enterocele is precluded by the apposition of pubocervical and rectovaginal fascia (collectively termed endopelvic fascia) at the apex. The anterior vaginal wall is the most common segment of the vagina to prolapse.⁵ Anterior vaginal prolapse usually involves descent of the bladder and, when it does, it is called a cystocele. Posterior vaginal wall prolapse usually involves the rectum (rectocele) but may also include the small or large bowel. Uterovaginal support can be measured using the Pelvic Organ Prolapse Quantification (POP-Q) system.⁶ In addition to describing precisely the degree of anterior, posterior, and apical vaginal wall descent, POP-Q broadly classifies uterovaginal support using a staging system that ranges from Stage 0 (perfect support) to Stage IV (procidentia or complete vaginal eversion) (Table 14-3).

Generally, enteroceles have been divided into four types: congenital, traction, pulsion, and iatrogenic. Congenital enterocele is rare. Factors that may predispose to the development of congenital enterocele include neurologic disorders, such as spina bifida, and connective tissue disorders. Traction enterocele occurs secondary to uterovaginal descent, and pulsion enterocele results from prolonged increases in intra-abdominal pressure. These two latter types of enterocele may coexist with apical vaginal prolapse. Iatrogenic enterocele occurs after surgical procedures that elevate the normally horizontal vaginal axis toward a vertical direction; examples include colposuspension and needle urethropexy operations for stress incontinence, or hysterectomy, with or without repair, when the vaginal cuff and cul-de-sac are not managed effectively. Clinically, enteroceles are best classified based on their anatomic location. Apical enteroceles herniate through the apex of the vagina, posterior enteroceles herniate posterior to the vaginal apex, and anterior enteroceles herniate anterior to the vaginal apex.

Anatomic support of the pelvic viscera is primarily provided by the levator ani muscle complex and the connective tissue attachments of the pelvic viscera (endopelvic fascia). Disruption or dysfunction of one or both of these components can lead to loss of anatomic support and eventually apical prolapse. The levator ani muscle complex consists of the pubococcygeus, the puborectalis, and iliococcygeus muscles. This muscle complex is tonically contracted at rest and acts to close the genital hiatus and provide a stable platform to support the pelvic viscera. Loss of normal levator ani tone, through denervation or direct muscle trauma, results in a more open urogenital hiatus, loss of the horizontal orientation of the levator plate, and a more bowl-like configuration. Such configurations are seen more often in women with prolapse than in those with normal support.⁷ Visible defects in the pubovisceral and iliococcygeal portion of the levator ani muscle after a vaginal delivery have been found on magnetic resonance imaging (MRI) in 20% of primiparous women and are not seen in nulliparous women, suggesting that vaginal delivery contributes to the development of prolapse through levator ani muscle injury.^8,9 In addition to direct muscle trauma, neuropathic injury of the levator ani muscles can also result from vaginal delivery. Weidner et al. performed concentric needle electromyography of the levator ani muscles on 58 primiparous women in the third trimester, six weeks postpartum, and six months postpartum and found that 24% had evidence of neuromuscular dysfunction at six weeks postpartum and 29% had evidence of dysfunction at six months postpartum. Women having vaginal delivery had a slightly greater proportion of injury at six months, whereas women with elective cesarean had virtually no injury. Spontaneous delivery or cesarean section after labor was associated with greater injury in the lateral levator ani, whereas operative vaginal delivery was associated with greater injury to the medial levator ani.¹⁰ Chronic straining to achieve defecation has also been associated with pelvic muscle denervation.¹¹ The excess straining and associated perineal descent is thought to cause stretch injury to the pudendal nerve and result in neuropathy.¹¹

The endopelvic fascia is the connective tissue network that envelops all of the organs of the pelvis and connects them loosely to the supportive musculature and bones of the pelvis. This loose connective tissue network holds the vagina and uterus in their normal anatomic location, yet allows for the mobility of the viscera to permit storage of urine and stool, coitus, parturition, and defecation. Disruption or stretching of these connective tissue attachments occurs during vaginal delivery or hysterectomy, with chronic straining, or with normal aging.¹² Furthermore, evidence suggests that abnormalities of connective tissue and connective tissue repair may predispose some women to prolapse. Women with prolapse may have altered collagen metabolism including a decrease in type I collagen and an increase in type III collagen.^13-15 It is unclear, however, if this altered metabolism is a cause or effect of prolapse. Women with joint hypermobility have a higher prevalence of prolapse than do women with normal joint mobility.¹⁶ Similarly, women with connective tissue disorders such as Ehlers-Danlos or Marfan syndrome are at increased risk for prolapse.¹⁷ Emerging data using genetic knockout mice show that abnormal elastin homeostasis may also contribute to the development of prolapse through an abnormal tissue response to injury.^18,19

Disruption of the cardinal-uterosacral complex may result in uterine prolapse or apical prolapse. Three levels of support have been described by DeLancey for the vaginal vault (Figure 14-3).

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  Level I involves the support of the upper vagina and cervix or the vaginal cuff (in a woman who has undergone total hysterectomy) by the cardinal-uterosacral ligament complex.

  
  
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  Level II denotes the lateral support of the mid vagina to the arcus tendineus fascia pelvis (white line).

  
  
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  Level III is represented by the fusion of tissue along the base of the urethra and the distal rectovaginal septum to the perineal body.

The conditions of enterocele and vaginal eversion represent failures of level I support, although other compartments may be affected. Uterovaginal prolapse does not denote intrinsic uterine disease and, therefore, may not necessarily require a hysterectomy in all cases. It should be noted, however, that no evidence proves or disproves the benefit of hysterectomy at the time of apical suspension. Apical prolapse occurs because of tearing or attenuation of the cardinal-uterosacral ligament complex. This results in failure to support the upper vagina and/or uterus over the pelvic diaphragm, which should be in a near-horizontal plane in a woman in the erect position. Level I support is considered most important in maintaining adequate overall pelvic support.

The smooth muscle of the vaginal wall is also altered in women with prolapse. The morphology of the vaginal wall in women with prolapse consists of disorganized smooth muscle bundles with a decreased fractional area (26% vs 48%; P < 0.05) of smooth muscle of the muscularis layer compared with normal support controls.²⁰ Histologically, nerve bundles and ganglia are also decreased in the muscularis layer.²⁰ It is not currently known if these alterations in the vaginal wall smooth muscle play a role in the development of prolapse or are the consequence of the mechanical forces associated with prolapse.

Variations in the orientation and shape of the bony pelvis have been associated with the development of prolapse. Specifically, a loss of lumbar lordosis and a pelvic inlet that is less vertically oriented is more common in women who develop genital prolapse than in those who do not.²¹ A less vertical orientation of the pelvic inlet is thought to result in an alteration of the intra-abdominal vector forces that are normally directed anteriorly to the pubic symphysis. As a consequence, a greater proportion of these forces is directed toward the pelvic viscera and their connective tissue and muscular supports. Similarly, women with a wide transverse pelvic inlet appear to be at increased risk for developing prolapse. Some have theorized that a wider pelvic inlet provides a larger hiatus for abdominal pressure transmission to the pelvic floor, which over time leads to loss of pelvic visceral support.²² Variations in the shape and orientation of the bony pelvis are also important factors that influence maternal soft tissue damage and nerve injury during parturition.

Clinical Presentation

Women who develop symptoms may present with a single symptom such as vaginal bulging or pelvic pressure or they may present with multiple complaints including bladder, bowel, and pelvic symptoms. Ellerkmann et al. found that in 237 women evaluated for POP, 63% reported bulge symptoms, 73% urinary incontinence, 86% urinary urgency and/or frequency, 62% voiding dysfunction, and 31% fecal incontinence.²³ Some prolapse-related symptoms are the result of the prolapsing vagina itself and some are caused by coexisting or associated dysfunction of the bladder, lower gastrointestinal tract, or pelvic floor. Common symptoms in women with advanced POP are listed in Table 14-4. With the exception of vaginal bulging symptoms, none are specific to prolapse. There is considerable overlap with other pelvic floor disorders, and clinicians should be cognizant of other potential sources for the patient’s complaints.

In general, only weak-to-moderate correlations exist between the severity or stage of prolapse and the presence of specific symptoms such as bulging, heaviness, and voiding dysfunction.^23,24 A number of symptoms often attributed to prolapse may, in fact, not be related. This seems particularly true for many bowel symptoms.^25,26 The hymen appears to be an important “cut-off point” for symptom development. Swift et al. evaluated symptoms and pelvic organ support in 477 women presenting for annual gynecologic examinations and found that the number of pelvic floor symptoms increased from an average of 0.5 symptoms for patients with Stage I prolapse to 2.1 symptoms for women when the leading edge of the prolapse extended beyond the hymen.²⁷ In contrast, the prevalence of some symptoms, particularly stress urinary incontinence, appears to decline as prolapse extends beyond the hymen, likely from urethral obstruction.²⁴ The relationship between the extent of maximal prolapse and the development of three commonly related symptoms is linear with regard to stage of the maximum POP-Q measurement.

Bulge or herniation symptoms that have been attributed to worsening POP include a sensation of bulging or protrusion in the vagina, a sensation of “something falling out” of the vagina, seeing or feeling a vaginal or perineal bulge, pelvic pressure, fullness, and heaviness. Although many of these symptoms demonstrate some correlation with the presence and severity of prolapse, the only symptom that is consistently acknowledged by patients with severe prolapse is the presence of a vaginal bulge that can be seen or felt.^26,28 Less specific symptoms such as pressure and heaviness appear to have a much weaker relationship to loss of vaginal support.^26,28

Lower urinary tract complaints are common among women with prolapse. In some circumstances, the loss of vaginal support directly influences bladder or urethral function, resulting in symptoms. In other cases, the relationship between prolapse and lower urinary tract dysfunction is less clear. The anterior vaginal wall supports the bladder and urethra. Loss of this support results in urethral hypermobility and cystocele formation, which is thought to contribute to the development of stress urinary incontinence.²⁹ Therefore, it is not surprising that prolapse and stress urinary incontinence often coexist, particularly when the prolapse is mild. In contrast, women with POP that extends beyond the hymen are less likely to complain of stress incontinence and more likely to have obstructed voiding symptoms such as urinary hesitancy, intermittent flow, weak or prolonged stream, feeling of incomplete emptying, the need to manually reduce (splint) the prolapse to initiate or complete urination and, in rare cases, urinary retention.^26,28 The mechanism for these symptoms appears to be mechanical obstruction resulting from urethral kinking that occurs with progressively worsening anterior vaginal prolapse. Up to 30% of women with Stage III or IV prolapse have elevated postvoid residual volume (PVR >100 mL).³⁰ Large posterior vaginal prolapse can also cause mechanical obstruction by direct urethral compression.³¹

Women with prolapse frequently complain of symptoms related to bowel dysfunction including the feeling of incomplete emptying, straining, the need to apply digital pressure to the vagina or perineum (splint) to start or complete defecation, urgency, and incontinence. Interestingly, studies that have investigated the relationship between bowel dysfunction and the presence and severity of prolapse have found either weak correlation between posterior vaginal wall support and specific anorectal symptoms or no correlation at all.^25,26 The defecatory symptom that appears most consistently related to posterior vaginal prolapse is the need to splint the vagina or perineum to defecate.^23,26 However, most women with rectoceles do not have this symptom, and some women without rectoceles also use manual pressure to accomplish defecation.³² Seven to 31% of women with POP report fecal incontinence.^33,34 Although rectal prolapse is a recognized cause of fecal incontinence, it is unlikely that vaginal prolapse contributes to the development of fecal incontinence. Rather, fecal incontinence and prolapse often coexist because they share common risk factors, such as the effects of aging and neuropathic and muscular injury to the pelvic floor after vaginal delivery.

Women with prolapse have similar rates of sexual activity as similarly aged women without prolapse.³⁵ One-third of sexually active women with prolapse complain that their prolapse interferes with their sexual function.³⁶ A study that compared sexual function in women with and without prolapse using a validated sexual function questionnaire found no difference in frequency of intercourse, libido, vaginal dryness, dyspareunia, orgasmic function, or overall sexual function between the two groups.³⁵ Furthermore, women with prolapse report a high rate of sexual satisfaction (81%–84%) who are in an intimate relationship.³⁵

Although it is common for patients with prolapse to attribute back and pelvic pain to their prolapse, there is very little evidence that prolapse causes pain.^27,37 The complaint of pain in a patient with prolapse should prompt clinicians to search for other sources of the pain before attributing it to prolapse.

Physical Examination

Patients presenting with prolapse symptoms should undergo a pelvic examination. The pelvic examination should be performed with the patient resting and straining while supine and standing in order to define the extent of the prolapse and determine the segments of the vagina involved (anterior, posterior, or apical).⁶ It is important that a clinician reproduce the maximum extent of prolapse that the patient exhibits in her daily life. The extent of prolapse of the anterior vaginal wall can be evaluated by placing a Sims speculum or the posterior blade of a bivalve speculum in the vagina to retract the posterior vaginal wall. The patient is asked to strain and the extent of anterior vaginal prolapse is noted. The blade is then placed to retract the anterior vaginal wall and the patient strains to reveal any posterior prolapse. A rectovaginal examination can be useful to identify the presence of a rectocele and determine the integrity of the perineal body. A bivalve speculum is inserted and the cervix or, in women who have had a hysterectomy, the vaginal cuff is identified to evaluate apical vaginal support. Although the patient strains, the speculum is slowly withdrawn and the descent of the vaginal apex is noted. In women with prolapse that protrudes beyond the hymen for a long duration, the vagina and/or cervix can become hypertrophied and develop erosions (Figure 14-4). A bimanual and rectal examination is performed to rule out coexistent gynecologic or rectal pathology.

Although several prolapse grading systems exist, the only system with international acceptance is the POP-Q system.²⁸ The POP-Q examination systematically defines the degree of prolapse during a pelvic examination by measuring anterior, posterior, and apical segments of the vaginal wall in centimeters relative to a fixed anatomical structure, the vaginal hymen (Figure 14-5). This examination provides a highly reliable and reproducible staging system. Apical points are measured with a whole speculum in place, which is slowly withdrawn until maximal descensus is reached.

The need for ancillary testing beyond a comprehensive history and physical examination depends largely on the patient’s presenting symptoms. The majority of women will require minimal additional testing. Women who complain of lower urinary tract symptoms should undergo urinalysis and PVR testing using a urethral catheter or bladder ultrasound. A urodynamic evaluation should be considered in women with significant urinary incontinence, irritative voiding symptoms, or voiding dysfunction. Although urodynamics are currently being used to predict postoperative urinary incontinence, a recent randomized trial has disputed the usefulness of this test as a predictor of altering surgical management.³⁸ Similarly, anal manometry and/or defecography should be considered in women with significant defecatory symptoms, and endoanal ultrasound evaluation should be considered in women with fecal incontinence when an anal sphincter defect is suspected. Generally, radiographic evaluation to determine the extent or characteristics of a patient’s prolapse is unnecessary. Some authors have advocated the use of imaging procedures such as contrast radiography or dynamic MRI to describe the location of the pelvic support defects before attempting surgical repair.³⁹ However, a lack of standardized radiologic criteria currently exists for diagnosing prolapse, and the clinical benefit of such radiographic imaging has yet to be defined. Currently, such imaging studies are primarily used for research purposes.

Loss of normal vaginal support can be seen to some degree or another in as many as 43% to 76% of women.²⁴ Whether this loss of support becomes a condition that causes patients to seek care and/or physicians to offer treatment depends in large part upon the development and severity of associated symptoms. Current management options for women with symptomatic apical prolapse include observation, pessary use, and surgery.

Observation

Women with advanced prolapse may have minimal symptoms and report little or no bother as a result. This is particularly true for women with prolapse that is mild and does not extend beyond the hymen. In these cases, observation or “watchful waiting” is perfectly appropriate. Although several studies have investigated associations between prolapse and lifestyle factors, no studies have investigated the role of lifestyle modifications in the prevention or treatment of prolapse. Pelvic floor muscle training is an effective treatment for urinary and fecal incontinence; however, its role in managing prolapse has yet to be established. One study does suggest that daily pelvic floor muscle strengthening may slow the progression of anterior prolapse in elderly women.⁴⁰ Women with advanced prolapse who choose observation should be examined periodically to identify the development of new symptoms or conditions that might prompt treatment. The development of obstructed urination or defecation, vaginal erosions that do not resolve with conservative management, or hydronephrosis from chronic ureteral kinking are all indications for treatment even in the minimally symptomatic patient.