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. 2003 Nov;14(5):310-5; discussion 315.
doi: 10.1007/s00192-003-1087-7. Epub 2003 Oct 2.

On the pathogenesis of rectocele: the concept of the rectovaginal pressure gradient

Affiliations

On the pathogenesis of rectocele: the concept of the rectovaginal pressure gradient

Ahmed Shafik et al. Int Urogynecol J Pelvic Floor Dysfunct. 2003 Nov.

Abstract

Coughing or straining evokes reflex bulbocavernosus (BCM) and puborectalis (PRM) muscle contraction, which apparently transforms the vagina into a closed high-pressure cavity. This elevated vaginal pressure counteracts the increased intra-abdominal pressure and the tendency of the uterus to prolapse, and also supports the rectovaginal septum against the high straining-induced intrarectal pressure and possible consequent rectocele (posterior vaginal prolapse) formation. We investigated the hypothesis that a weak BCM and PRM share in the genesis of rectocele by changing the rectovaginal pressure gradient. Twenty-three women with rectocele (mean age 43.2+/-6.6 years) and 12 healthy women volunteers (mean age 41.6+/-6.2 years) were studied. The response of the intrarectal (intra-abdominal) and intravaginal pressure, as well as the EMG activity of the BCM and PRM to straining or coughing, was recorded. In the healthy volunteers the rectal and vaginal pressures showed a significant increase on coughing or straining, with no significant difference between the rectal or vaginal pressures. Also, the BCM and PRM EMG activity exhibited a significant increase. Rectocele patients showed a significantly low resting vaginal pressure. The increase in rectal and vaginal pressure, as well as of the EMG activity of the BCM and PRM on straining or coughing, was significantly lower and the latency of the EMG response was significantly longer than those of the healthy volunteers. A difference in the rectovaginal pressure gradient showing a significant increase in the rectal against the vaginal pressure, particularly on coughing or straining, is suggested to be the basic factor in the genesis of rectocele. This pressure difference appears to be caused by diminished BCM and PRM contractile activity. A disrupted rectovaginal septum is not a prerequisite for rectocele formation, as the septum appears normal in obstructed defecation despite the common occurrence of rectocele. A histopathologic study of the septum in rectocele seems necessary.

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