Enterocele and Massive Vaginal Eversion

Updated: May 11, 2016
  • Author: Rony A Adam, MD; Chief Editor: Kris Strohbehn, MD  more...
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Massive vaginal vault prolapse is a devastating condition with discomfort, genitourinary and defecatory abnormalities as the primary consequences. Pelvic organ prolapse is prevalent and associated with significant health–related quality of life and economic impact. [1] References to prolapse of the womb were first made in ancient Egypt, dating back to 1550 BC. Vaginal vault prolapse refers to significant descent of the vaginal apex following a hysterectomy (see the image below) while uterovaginal prolapse denotes apical prolapse of the cervix, uterus and proximal vagina.

Enterocele and massive vaginal eversion. Posthyste Enterocele and massive vaginal eversion. Posthysterectomy vaginal vault prolapse.

These apical failures are often accompanied by anterior and or posterior vaginal compartment prolapse with or without enterocele. Although this obviously is not a new condition, apical prolapse is thought to be increasingly common as life expectancy increases. According to population projections from the U.S. Census Bureau from 2010 to 2050 and published age-specific prevalence estimates for bothersome, symptomatic pelvic floor disorders and pelvic organ prolapse, the number of women with uterovaginal prolapse is expected gradually to increase from 3.3 to 4.9 million from 2010 to 2050. [2]

Whereas complete vaginal eversion is obvious, lesser degrees of prolapse and the presence of enterocele are more difficult to discern and require careful evaluation of all anterior, posterior, and apical compartment defects. Also, associated functional abnormalities, whether concurrent or potential, must be properly explored, evaluated, and discussed with the patient.



A uniform definition of what constitutes apical prolapse or any pelvic organ prolapse does not exist. The International Urogynecological Association and International Continence Society define pelvic organ prolapse as the descent of one or more of the anterior vaginal wall, posterior vaginal wall, the uterus (cervix), or the apex of vagina (vaginal vault or cuff scar after hysterectomy). [3] Indeed, a degree of uterine/vaginal descensus is present in many, if not most, women who are multiparous. Not all patients with prolapse are symptomatic, and the degree of prolapse often does not correlate with the degree of symptoms reported by the patient. Furthermore, pelvic floor- related symptoms do not predict the anatomic location of the prolapse especially in women with mild to moderate prolapse. [4] A systematic and comprehensive description of pelvic organ prolapse is useful to help document and communicate the severity of the problem, to establish treatment guidelines, and to improve the quality of research to standardizing definitions.

The pelvic organ prolapse quantification (POP-Q) system was developed to address deficiencies in measuring and reporting the extent of prolapse. Specific sites are defined separately on the anterior, posterior, and apical vaginal compartments and are measured with respect to a fixed reference point, the hymen. These measurements can then be categorized into an ordinal staging system ranging from 0-4.

  • Stage 0 denotes no prolapse (the apex can descend as far as 2 cm relative to the total vaginal length).
  • Stage 1 means that the most distal portion of the prolapse descends to a point more than 1 cm above the hymen.
  • Stage 2 denotes that the maximal extent of the prolapse is within 1 cm of the hymen (outside or inside the vagina).
  • Stage 3 means that the prolapse extends more than 1 cm beyond the hymen but no more than within 2 cm of the total vaginal length.
  • Stage 4 denotes complete eversion, which is defined as extending to within 2 cm of the total vaginal length. The POP-Q staging system has been validated and demonstrates good interobserver and intraobserver reliability. Although POP-Q staging adequately addresses the extent of prolapse, assumptions about which organ is behind the visualized bulge should be made with caution and should be made only after a complete evaluation. Regarding enterocele, the definition is somewhat more difficult. Previous texts have defined enterocele as a hernia in which peritoneum and abdominal contents displace the vagina and is palpable within the cul-de-sac, as evaluated during a rectovaginal examination in the erect position.  Patients with such findings may have a deep cul-de-sac and thus represent a normal variant.  A more anatomic definition was proposed by Richardson, who suggested that enterocele occurs when endopelvic fascia does not intervene between the peritoneum and vagina (see image below). [5]  The differences in these approaches have not been completely resolved as data does not support the endopelvic fascial defects proposed.
Enterocele and massive vaginal eversion. Large api Enterocele and massive vaginal eversion. Large apical endopelvic fascial defect representing an enterocele demonstrated by the transabdominal route. Note the proximal cervicovaginal and rectovaginal fascia separate from the peritoneum.





Frequency and Prevalence

Pelvic organ prolapse (POP) when defined by symptoms has prevalence of 3-6% and up to 50% when based upon vaginal examination. Moreover, the prevalence of surgical correction of the prolapse varies widely from 6 to 18% with incidence of POP surgery from 1.5 to 1.8 per 1,000 women years and peaks in women aged 60-69. [6] Swift reported on the frequency of different stages of pelvic organ prolapse in a routine gynecologic clinic population based upon the POP-Q staging system. Most women had stage 1 or stage 2 prolapse (43.3% and 47.7%, respectively), few women had stage 0 or stage 3 prolapse (6.4% and 2.6%, respectively), and none had stage 4 pelvic organ prolapse. [7] Samuelsson et al report a prevalence of 30.8% for any prolapse, using the Baden-Walker halfway system, in a study of the general population in Sweden. Vaginal vault prolapse is thought to occur postoperatively in 0.5% of hysterectomy cases, whether they are performed vaginally or abdominally. [8] In a population-based Dutch study the prevalence of pelvic organ prolapse based on POP-Q staging were: stage 0 = 25.0%; stage I = 36.5%; stage II = 33%, stage III = 5.0%; stage IV = 0.5%. [9]



Current evidence support a multifactorial etiology of POP. Swift reported that significant trends for increasing prolapse were found with advancing age, parity, postmenopausal status, previous hysterectomy, and prior corrective surgery for prolapse. [7]  Multivariate analysis in a study performed by Samuelsson et al revealed independent statistical associations with age, parity, maximal birth weight, and pelvic floor muscle strength. [8]  Such associations were not found regarding weight or hysterectomy status. Some epidemiologic evidence contradicts the opinion that female pelvic organ prolapse worsens with age. [8] Furthermore, Sze et al demonstrated that vaginal birth is not associated with POPQ stages III and IV prolapse, but it is associated with an increase in POPQ stage II defect. [10]

It is well recognized that POP runs in the families, giving credence to a hereditary contribution to the phenotype with some evidence that loci on chromosomes 10q and 17q may contribute to the etiology of prolapse. [11, 12, 13, 14] Racial differences have been reported for pelvic organ prolapse, although is not yet clear whether the differences are biological or sociocultural. Whitcomb et al showed that compared with African-American women, Latina and white women had four to five times higher risk of symptomatic prolapse, and white women had 1.4-fold higher risk of objective prolapse  at or beyond the hymen. [1] More recently, data obtained from African American and Hispanic women who were enrolled in the Women’s Health Initiative Hormone Therapy with available genotyping data from Women’s Health Initiative-SHARe, suggests that common germ-line variations may contribute to increased risk of POP among African Americans and Hispanics; however, further research with larger minority sample sizes is necessary to confirm this finding. [15]



As discussed, genetic factors may play a significant role in development of uterovaginal prolapse. Current basic science research suggests a molecular etiology of pelvic organ prolapse. Some studies demonstrate an increased rate of apoptosis and significant depletion of mitochondrial DNA in uterosacral ligaments in women with uterovaginal eversion. [16, 17]

The precise etiology of pelvic organ prolapse remains elusive. Additional theories include diminished sacral nerve function and/or defects in collagen. The pelvic floor is a unique and complex system constructed of skeletal and striated muscles, support and suspensory ligaments, fascial layers and an intricate neural network. When this system is damaged, pelvic floor failure may occur and pelvic organ prolapse ensues. [18]

DeLancey describes the anatomy of vaginal vault prolapse in terms of 3 levels of support (see image below). [19]

Enterocele and massive vaginal eversion. Levels of Enterocele and massive vaginal eversion. Levels of support as described by DeLancey (1992). Note that level I refers to apical (or uterovaginal) support.

See the list below:

  • Level I refers to 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.
  • Level II denotes the lateral support of the mid vagina to the arcus tendineus fascia pelvis (white line).
  • 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 primary in maintaining adequate overall pelvic support.

Richardson describes an enterocele in anatomic terms, as a break in the integrity of endopelvic fascia at the vaginal apex (see image below). [20]

Enterocele and massive vaginal eversion. Normal po Enterocele and massive vaginal eversion. Normal posthysterectomy vaginal vault. Note the presence of continuity of the endopelvic fascia at the vaginal apex, resulting from the fusion of cervicovaginal and rectovaginal fascia, and their fusion with the uterosacral ligament portion of endopelvic fascia.

Normally, posthysterectomy enterocele is precluded by the apposition of pubocervical and rectovaginal fascia (collectively termed endopelvic fascia) at the apex. Anterior, apical, and posterior enteroceles have been described based upon the location of the fascial defect and the location of the ensuing herniation of bowel.

Apical enterocele is the most common enterocele and is primarily associated with post-hysterectomy vaginal vault prolapse. Apical enterocele may present with or without vaginal vault prolapse (see images below).

Enterocele and massive vaginal eversion. Early ent Enterocele and massive vaginal eversion. Early enterocele with no vault prolapse. Note contact of peritoneal contents with vaginal mucosa, with no intervening endopelvic fascia.
Enterocele and massive vaginal eversion. Progressi Enterocele and massive vaginal eversion. Progressive enterocele now demonstrating true vaginal vault prolapse.
Enterocele and massive vaginal eversion. Massive e Enterocele and massive vaginal eversion. Massive enterocele with total vaginal vault prolapse.

Anterior enteroceles are rare and may occur following sacrospinous ligament fixation, when the proximal vagina is displaced posteriorly, creating a potential space in the anterior compartment. Because they present as a protrusion of the anterior vaginal wall, they may be the true etiology of some cystoceles. In women with an intact uterus, posterior enteroceles have been described. These are due to tearing of the proximal rectovaginal fascia from its attachment to the cardinal-uterosacral ligament complex, which results in descent of the peritoneal contents down the posterior aspect of the vagina (see image below). 

Enterocele and massive vaginal eversion. Posterior Enterocele and massive vaginal eversion. Posterior enterocele in a patient with a uterus. Note that peritoneal contents have dissected between the vaginal mucosa and rectovaginal fascia through a proximal defect.

Posterior enterocele is usually accompanied by significant uterovaginal prolapse and prolapse of other compartments as well. [20]

Histologic studies by Tulikangas et al failed to find breaks in the fibromuscular layer in women who underwent surgical correction for enterocele compared with controls (women who did not have pelvic organ prolapse). [21] Admittedly, the authors' findings did not correlate with their subjective clinical findings of thinning of the vaginal wall in enteroceles. Hsu et al similarly found a lack of difference in vaginal wall thickness on MRI studies of patients with prolapse and their normal controls. [22] The numbers in these studies, however, were small and further investigation is needed before this controversy is fully resolved.  Nonetheless the authors believe that considering this theory in the context of surgical correction has merit and aids in properly managing these conditions.



Patients may present with an obvious vaginal bulge that is visualized or felt by the patient. Conversely, the patient may report a vague sense of pelvic heaviness or a sensation that something is about to fall out. The bulging is often noted to be worse toward the end of the day, as compared with when the patient first wakes up, or when the patient is straining at defecation or urination. When vaginal epithelium remains exteriorized, it undergoes cornification and, often, ulceration, which can result in significant pain, vaginal bleeding, discharge and infection.

Functional difficulties may be encountered during coitus. Defecation may be difficult; associated constipation is very common. Incomplete bladder emptying also is common, and, in severe cases, complete obstruction may occur. Voiding dysfunction may result in frequent urinary tract infections and, occasionally, overflow incontinence. Due to kinking of the urethra, occult (potential) stress incontinence and even intrinsic sphincter deficiency may be present. A history of stress incontinence that spontaneously improved and/or resolved as the prolapse progressively worsened is especially concerning for the presence of occult stress incontinence. In a cross-sectional study urinary urge incontinence was associated with anterior wall prolapse, while stress urinary incontinence was strongly linked to posterior wall prolapse. [4] Advanced pelvic prolapse may result in ureteral kinking with the potential for hydroureter, hydronephrosis in 30% of cases. [23]

A detailed history is required to evaluate the patient. Information regarding any functional problems that may be caused by the prolapse should be ascertained. Essential to the preoperative evaluation and surgical decision-making is the review of any prior pelvic surgery, including obtaining operative reports, especially if surgery was performed for prior pelvic floor dysfunction. It is imperative to evaluate and stabilize the patient’s general health to assess for and mitigate against any increased surgical risks

A commitment to surgically treat all associated and relevant pelvic floor defects requires a careful and comprehensive urogynecologic examination. A diligent search for all pelvic support defects and repair of these defects increases the likelihood of overall surgical success and patient satisfaction. The apical, anterior, and posterior compartments are evaluated separately, with and without straining and/or coughing in the supine position and again in the erect position if needed, preferably with an empty bladder. A standardized examination should be performed and documented. The POP-Q exam is helpful for quantifying the extent of prolapse and accurate follow-up. Carefully evaluate the rectovaginal septum for integrity, strength, and thickness along its entire length. Look for any signs of enterocele, such as bowel peristalsis, along the posterior vagina or near the apex. Look for any obvious pubocervical/rectovaginal detachments at the periphery of an apical bulge. Evaluate the cul-de-sac in the supine and standing positions, with and without Valsalva maneuvers.



Treatment of pelvic organ prolapse is indicated if it is symptomatic or is causing associated morbidity. Asymptomatic prolapse, with minor degrees of protrusion that cause no other problems, must be discussed with the patient but does not necessarily require treatment.  In the older population, even extensive prolapse may be asymptomatic from the patient's point of view, but questioning her family or caregiver may reveal troublesome symptoms, and further evaluation may reveal significant resultant morbidity.

Offer conservative management to these patients as the initial management option. Conservative management may include observation with mild degrees of asymptomatic prolapse or a pessary fitting. Surgical management may be considered in appropriate candidates if conservative therapies fail or are declined by the patient.


Relevant Anatomy

The cardinal-uterosacral ligaments are localized thickenings of the endopelvic fascia that invest the pelvic organs. The same endopelvic fascia that is anterior to the vagina is called pubocervical; posteriorly, it is termed rectovaginal fascia or Denonvilliers fascia. Laterally, the endopelvic fascia attaches the vagina to the arcus tendineus fascia pelvis to provide lateral support to the mid-vaginal compartment, whereas the distal rectovaginal fascia attaches laterally to the aponeurosis of levator ani. [24]

The integrity of the vaginal apex following hysterectomy depends on the fusion of the pubocervical fascia with the rectovaginal fascia. Surgically, the uterosacral ligaments lie medial to the ureters in the pelvis. The proximal uterosacral ligament fans out and attaches to the lateral aspect of the sacrum. MRI studies show slight variations in the attachment of the uterosacral ligament, although most overlay the sacrospinous ligament/coccygeus muscle. The proximal vagina usually points into the hollow of the sacrum towards S3 and S4 and maintains a near-horizontal plane when the woman stands erect.

Although the term fascia is frequently used to denote the surgically significant layer used for pelvic reconstruction, histologically, it is a fibromuscular layer with varying amounts of smooth muscle, collagen, and elastin that is located deep to the epithelium.



Pessary use is contraindicated in the presence of vaginal ulceration and breakdown or in the presence of an active vaginal infection. Severe vaginal atrophy is best treated prior to starting pessary use, in the absence of contraindications for estrogen use.

The medical evaluation of a patient for surgical repair is a topic that is too broad for this article. However, one should tailor the proposed operation to the specific defects noted preoperatively, taking into consideration the patient's overall health and prior surgical history. The chosen approach, whether vaginal, abdominal, laparoscopic, or robotically-assisted should be selected with careful consideration of these patient-related points, in addition to the surgeon's level of skill and available local resources. Appropriate consultations and referrals during the preoperative evaluation can ensure the highest degree of success and safety.