Enterocele and Massive Vaginal Eversion
A systematic 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.
- 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.
Recent histologic and MRI studies of enteroceles, however, have challenged this concept. Studies by Tulikangas et al6 and Hsu et al7 show that a distinct break in the fibromuscular layer denoted as the rectovaginal fascia may not necessarily be present. These studies, however, are small in number and further investigation is warranted. Nevertheless, a careful preoperative and intraoperative search for these defects is often helpful for proper diagnosis.
In a population-based Dutch study, the prevalence of pelvic organ prolapse by POP-Q staging was as follows: Stage 0 = 25.0%, stage I = 36.5%, stage II = 33%, stage III = 5.0%, and stage IV = 0.5%.10
Racial differences have been reported for pelvic organ prolapse, although it 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 4-5 times higher risk of symptomatic prolapse, and white women had 1.4-fold higher risk of objective prolapse at or beyond the hymen.1
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.14,15
The precise etiology regarding 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 striated muscles, support and suspensory ligaments, fascial layers, and an intricate neural network. When this system is damaged, pelvic floor failure occurs and pelvic organ prolapse ensues.16
DeLancey describes the anatomy of vaginal vault prolapse in terms of 3 levels of support.17
- 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.
- 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.
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.
Anterior enteroceles are rare and may occur following sacrospinous ligament fixation, when the proximal vaginal tube is pulled somewhat posteriorly, creating a potential space in the anterior compartment. Because they present as a protrusion of the anterior vaginal wall, they may be the major cause of some apparent 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.
A cross-sectional study indicates that urge urinary incontinence is associated with anterior wall prolapse, while stress urinary incontinence is strongly linked to posterior wall prolapse.4 Severe pelvic prolapse may result in ureteral kinking, with the potential for hydroureter, hydronephrosis, and subsequent renal damage. Hydronephrosis occurred with an overall prevalence of 7.7%, with severe hydronephrosis occurring in 0.9%. Hydronephrosis severity was proportional to prolapse severity with a higher likelihood of uterovaginal versus posthysterectomy vaginal prolapse.19