Massive vaginal vault prolapse (uterovaginal prolapse) is a devastating condition with discomfort and genitourinary and defecatory abnormalities as the primary consequences. Vaginal vault prolapse refers to significant descent of the vaginal apex following a hysterectomy.

Enterocele and massive vaginal eversion. Posthysterectomy vaginal vault prolapse.

Apical prolapse is used to denote prolapse of the vaginal apex with or without the presence of a uterus. Prolapse of the vaginal apex may or may not be accompanied by an enterocele. 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 anterior, posterior, and apical compartment defects. The International Urogynecological Association and International Continence Society define pelvic organ prolapse as the descent of 1 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 Yet, a clear demarcation between normal descent and abnormal prolapse has not been determined. 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

The pelvic organ prolapse quantification (POP-Q) has been instituted to address this by defining the extent of prolapse. Stage 0 denotes no prolapse (the apex can descend as far as 2 cm relative to the total vaginal length).
Enterocele and massive vaginal eversion. Swift reported on the frequency of different stages of pelvic organ prolapse based upon the POP-Q staging system.8 In a routine gynecologic clinic population, 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 no women had stage 4 pelvic organ prolapse. 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

Recent epidemiological studies by Dietz et al10 and Slieker-ten Hove et al11 contradict the opinion that female pelvic organ prolapse worsens with age. Current basic science research suggests a molecular etiology of pelvic organ prolapse. The precise etiology regarding pelvic organ prolapse remains elusive. DeLancey describes the anatomy of vaginal vault prolapse in terms of 3 levels of support.17

Enterocele and massive vaginal eversion. Apical prolapse occurs because of tearing or attenuation of the cardinal-uterosacral ligament complex. Level I support is considered most important in maintaining adequate overall pelvic support.

Enterocele and massive vaginal eversion. Normal posthysterectomy vaginal vault. Apical enterocele may present with or without vaginal vault prolapse.

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. Progressive enterocele now demonstrating true vaginal vault prolapse.

Enterocele and massive vaginal eversion. Massive enterocele with total vaginal vault prolapse.

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.

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 severity was proportional to prolapse severity with a higher likelihood of uterovaginal versus posthysterectomy vaginal prolapse.19

Treatment of pelvic organ prolapse is indicated if it is symptomatic or is causing associated morbidity. 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 Denonvillier fascia. The integrity of the vaginal apex following hysterectomy depends on the fusion of the pubocervical fascia with the rectovaginal fascia.

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