The role of childbirth in the aetiology of rectocele
Article first published online: 22 JUN 2006
BJOG: An International Journal of Obstetrics & Gynaecology
Volume 113, Issue 7, page 849, July 2006
How to Cite
Spencer, C. and Pakarian, F. (2006), The role of childbirth in the aetiology of rectocele. BJOG: An International Journal of Obstetrics & Gynaecology, 113: 849. doi: 10.1111/j.1471-0528.2006.00979.x
- Issue published online: 22 JUN 2006
- Article first published online: 22 JUN 2006
- Accepted 19 April 2006.
We read with interest Dr Dietz’s article on the role of labour and subsequent development of rectocele.1
Throughout the manuscript, reference is made to the aetiology of this condition being related to rectovaginal septum disruption and this notion dates from around the turn of the century. Nevertheless, we would like to emphasise that the anatomical demonstration of this structure has often been a matter of debate and surgical clarity of this structure is also problematic. Pathological research on female cadavers has failed to show histological evidence of a rectovaginal septum per se but instead an adventitious, or natural, line of cleavage.2 While it is generally agreed that both nulliparous and multiparous women can suffer from rectocele formation, it is not clear what role, exactly, childbirth has to play. In an earlier study, the same authors reported a 12% incidence in rectocele existence in nulliparous women, with constipation and high body mass index (BMI) being the risk factors.3 Could it be that weight gain and/or constipation in pregnancy play a major part in subsequent rectocele formation and that parturition has a small role? Abdominal surgery performed in women with a high BMI is frequently hampered by bulging of the lateral extraperitoneal space due to excess adipose tissue. It is possible that the same accumulation of fat occurs within the rectovaginal space and presents as a rectocele to attending clinicians. With regard to the authors’ cohort of women, we would be interested to know whether a relationship exists between weight gain and subsequent rectocele formation, or the opposite situation regarding resolution of rectocele symptoms with weight loss.
We would agree that this important piece of work should have implications on the eligibility of surgical repair of rectoceles in women. Combining posterior colporrhaphy with other pelvic floor procedures in asymptomatic women would seem to be unnecessary and risks an increase in surgical morbidity. These risks include increased postoperative pain, dyspareunia due to vaginal narrowing and visceral perforation.