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Keywords:

  • Childbirth;
  • 3D ultrasound;
  • prolapse;
  • rectocele;
  • translabial ultrasound;
  • transperineal ultrasound

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References

Objective  Clinically, rectocele is common in parous women and assumed to be due to distension or tearing of the rectovaginal septum in labour. In a prospective study, we examined the prevalence of such defects in primiparae before and after childbearing in order to define the role of childbearing in the aetiology of rectocele.

Design  Prospective observational study.

Setting  Tertiary urogynaecological clinic.

Population  A total of 68 nulliparous women between 35 + 6 and 40 + 1 weeks of gestation.

Methods  Participants underwent a standardised interview and were assessed by translabial ultrasound. Presence and depth of a rectocele was determined on maximal Valsalva, as was descent of the rectal ampulla. Fifty-two women were reassessed 2–6 months postpartum.

Main outcome measures  Presence of a true rectocele, rectal descent.

Results  True rectoceles were identified in 2 of the 68 women before childbirth and in 8 of the 52 women after childbirth (P= 0.02). After childbirth, the ampulla descended >22 mm further than before (P < 0.0001 on paired t test). Symptoms such as digitation (n= 2), straining at stool (n= 10) and incomplete emptying (n= 11) were not uncommon 2–6 months postpartum; but out of eight rectoceles, four were asymptomatic.

Conclusions  True rectoceles occur in young nulliparae. However, childbirth is associated with an increase in prevalence and size of such defects.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References

Rectocele, i.e. the formation of a rectal diverticulum through a defect of the rectovaginal septum1 causing a herniation of rectal muscularis, mucosa and contents into the vagina, is common in women symptomatic for pelvic floor disorders, but it also occurs in asymptomatic volunteers.2–4 Also, while it is clear that symptoms of prolapse and bowel dysfunction are sometimes due to a rectocele, many women who have such symptoms show no defects of the rectovaginal septum.4 Investigation of the aetiology of rectocele has to date been hampered by the fact that posterior compartment prolapse may be due to a number of different anatomical abnormalities such as a true rectocele, perineal hypermobility or excessive distensibility of an intact rectovaginal septum, an isolated enterocele or simply a deficient perineum.5 Some of the above are very likely to be related to childbirth (such as a deficient perineum), others (such as an enterocele) much less so. The authors consider it impossible to distinguish between these different entities without the use of imaging, and the most widely available, convenient and patient-friendly method is translabial or pelvic floor ultrasound.6 This method has opened up new possibilities in the investigation of posterior compartment descent. In a recent observational study in symptomatic women seen at urogynaecological clinics, we were unable to show a significant association between childbirth and rectocele,7 which prompted us to undertake a prospective study to examine the prevalence of defects of the rectovaginal septum or ‘true rectocele’ in primiparous women, 1–4 weeks before and 2–6 months after childbirth.

Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References

In a prospective observational study, the authors saw 68 women between 35 + 6 and 40 + 1 weeks of gestation. These women had been recruited from antenatal clinic at a tertiary institution. Inclusion criteria were an uncomplicated, first continuing singleton pregnancy (no previous pregnancies beyond 20 weeks), with the patient aiming for a vaginal delivery. Approximately half of all women approached by us agreed to take part in the study. Participants completed a standardised interview and were assessed by translabial ultrasound using Philips HDI 4000 and Toshiba SSD 255 systems, with 7–4 or 5 MHz curved array transducers, supine and after voiding. The methodology of pelvic floor ultrasound has been described elsewhere in detail.6 The presence of a rectocele was determined on maximal Valsalva. The best of at least three attempts was used, with no attempt at standardisation for intra-abdominal pressure. A defect of the rectovaginal septum was diagnosed if there was a discontinuity or gap in the anterior anorectal muscularis, measuring ≥10 mm in depth (1Figure 1).5

image

Figure 1. Comparison of posterior compartment imaging (midsagittal plane) in the third trimester (left) and 3 months postpartum (right), on maximal Valsalva manoeuvre. The anorectal junction appears normal on the left. On the right, there is a rectocele, with a depth of about 2 cm, filled with stool.

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A test–retest series conducted by the authors as part of a previously published series5 yielded a Cohen's kappa of 0.72 for the diagnosis of a defect of the rectovaginal septum. The intraclass correlations between measurements of ampullary descent was 0.75, of rectocele depth 0.93 and of rectocele width 0.91, signifying excellent repeatability of these measures.5

The parent study, designed to evaluate potential predictors of normal vaginal delivery, was approved by the local Human Research Ethics Committee (CSAHS X02/0250). A study extension was requested and approved in order to allow us to evaluate perinatal alterations in pelvic floor anatomy and function. Statistical analysis was performed after normality testing (histogram analysis and/or Kolmogorov–Smirnov testing), using Minitab version 13 (Minitab Inc., State College, PA, USA). Analysis of variance statistics were used to compare group means. Student's t test and Fisher's exact test were also used. A P < 0.05 was considered statistically significant.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References

The antenatal visit occurred between 35 + 6 and 40 + 1 weeks of gestation. At that time, the age of the 68 study recruits was 31.3 years (range 20–40 years) on average. They were all nulliparous and carrying a singleton pregnancy, aiming for a normal vaginal delivery. The second visit occurred on average 3.7 months postpartum (range 2.4–6.8 months). 1Table 1 gives obstetric data on the 52 women (76%) who returned for their postpartum follow up.

Table 1.  Obstetric data on 52 women who returned for pelvic floor ultrasound 2–6 months after childbirth
Gestational length in weeks (mean, range)40.2 (36.5–41.9)
Second stage in minutes (median, range)59 (0–385)
Delivery mode 
 Elective caesarean section1
 Emergency caesarean section12
 Vacuum/forceps12
 Normal vaginal delivery27

Symptoms of bowel dysfunction were mentioned by only seven women before childbirth, with four reporting chronic constipation, three incomplete emptying, four chronic straining and one digitation. Defects of the anorectal muscularis, implying a true rectocele, were identified in 2 of the 68 women before childbirth (both asymptomatic) and in 8 of the 52 women after childbirth (P= 0.02 on Fisher's exact test), with 4 of them symptomatic (incomplete emptying, straining at stool and/or digitation). In those two women in whom defects were diagnosed before childbirth, they had deepened from 14 to 23 mm and from 15 to 18 mm. Defects were filled by stool contents in four women; in the remaining four, the rectocele contained only rectal mucosa.

Of the eight women with rectoceles detected postpartum, six had delivered vaginally. In the two women who had delivered by caesarean section, the defects detected postpartum were small (12.6 and 12 mm), and in both women, there had been defects on antenatal imaging, which were not rated as such, being below the cutoff of 10 mm (5 and 8.3 mm).

After childbirth, the ampulla or rectal contents descended over 22 mm further than before (P < 0.0001 on paired t test; see 2Figure 2, for an example of increased ampullary mobility postpartum), but this was not significantly related to delivery mode. Symptoms regarded as typical for a rectocele, i.e. digitation (n= 2), straining at stool (n= 10) and incomplete emptying (n= 11), were not uncommon 2–6 months postpartum; but, as mentioned above, out of eight rectoceles, four were asymptomatic. In only one woman, there was a reduction in symptoms of obstructive defecation postpartum; in 11 women (21%), such symptoms first arose after childbirth.

image

Figure 2. Comparison of posterior compartment imaging (midsagittal plane) in the third trimester (left) and 3 months postpartum (right), on maximal Valsalva. The anorectal junction is normal on the left. The right image shows increased bladder descent and perineal mobility, resulting in displacement of the rectal ampulla below the symphysis pubis. There is no actual rectocele, i.e. no defect of the rectovaginal septum as shown in Figure 1.

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Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References

Rectocele is a condition that has received little attention from clinical research, and our means of assessing and treating rectocele are limited. Generally, a diagnosis is made by observing surface anatomy, i.e. a ventrocaudal displacement of the posterior vaginal wall on Valsalva. The diagnostic accuracy of clinical examination alone is very likely to be poor even in experienced hands8 in view of the fact that such prolapse of the posterior vaginal wall may be due to a rectocele, an enterocele, a deficient perineum or a hypermobile perineum, i.e. an abnormally distensible rectovaginal septum and/or levator ani muscle.5 Defecating proctography is regarded as the ‘gold standard’, but this diagnostic method is anything but standardised and seems to identify rectoceles in a large number of asymptomatic women.9 It is rarely used by gynaecologists. Clearly, there is a need for a simple, cheap and easily accessible method for diagnosing rectoceles, and translabial ultrasound, whether with10 or without6 contrast and actual defecation, may fill this need.

Improved diagnostic methods may also help with elucidating aetiology, as was attempted in this study. At present, there are no data on the natural history of the condition. While expert opinion holds that rectocele is due to obstetric events,8 to date, this has been an unproven hypothesis. Defects of the rectovaginal septum, i.e. true rectoceles, occur in asymptomatic, young nulliparous women,11 and this finding has been confirmed by the study presented here. However, childbirth seems associated with an increase in the prevalence and size of such defects, and parturition seems to cause increased downwards displacement of the rectal ampulla and its contents, i.e. perineal hypermobility.

It appears that the aetiology of rectocele is more complex than previously assumed. Clearly, childbirth does play a role, with some defects enlarged and others newly evident at 2–6 months postpartum. This observation supports the theory that crowning of the fetal head may cause disruption of the rectovaginal septum1: the theoretical basis for the fascial defect repair championed by Richardson.12 Unfortunately, our study is not sufficiently powered to assess the impact of obstetric factors such as delivery mode, length of second stage or birthweight. The same holds true for a more detailed analysis of symptoms and their potential association with anatomical findings and obstetric history. The authors are currently undertaking a larger study to answer related questions.

Vaginal childbirth seems to be a factor in the aetiology of rectocele. However, rectoceles were also observed in late gestation and after childbirth in women who had delivered by caesarean section. It seems likely that pregnancy itself—or just the passage of time—can be responsible for changes in the integrity of the rectovaginal septum. One explanation may be that a number of women are born with pre-existing defects that slowly grow larger with the passage of time until they become evident on imaging or clinically. Pregnancy, with or without vaginal childbirth, may simply speed up a process that would otherwise take much more time. This concept is supported by our observation of two very small defects, which only reached the cutoff of 10 mm in depth after a caesarean delivery, and by the fact that in later life, vaginal parity—as opposed to age—does not seem to be strongly associated with true rectoceles or their depth.5

Finally, as is the case later in life,13 the finding of a rectocele is not necessarily associated with bowel symptoms. The deepest and largest rectocele observed in this study, which was 26 mm deep and reached 22 mm below the symphysis on Valsalva and filled with stool was completely asymptomatic.

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References

True rectoceles, i.e. defects of the rectovaginal septum, occur in young nulliparae. However, vaginal childbirth is associated with an increase in prevalence and size of such defects. Many remain asymptomatic.

Acknowledgement

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References

We would like to thank Dr Philippa Ramsay and her staff, Specialized Ultrasound for Women, Sydney, for access to imaging equipment and Dr Valeria Lanzarone, Sydney, for help with data acquisition.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. Acknowledgement
  9. References
  • 1
    Halban J, Tandler J. Anatomie und Aetiologie der Genitalprolapse beim Weibe. Vienna, Austria: Braumueller, 1907.
  • 2
    Swift S, Theofrastous JP. Aetiology and classification of pelvic organ prolapse. In: CardozoL, StaskinD, editors. Female Urology and Urogynecology. London: Isis Medical Media; 2001. p. 57685.
  • 3
    Kahn MA, Stanton SL. Posterior vaginal wall prolapse and its management. Contemp Rev Obstet Gynecol 1997;9: 30310.
  • 4
    Kenton K, Shott S, Brubaker L. The anatomic and functional variability of rectoceles in women. Int Urogynecol J Pelvic Floor Dysfunct. 1999;10: 969.
  • 5
    Dietz HP, Steensma AB. Posterior compartment prolapse on two-dimensional and three-dimensional pelvic floor ultrasound: the distinction between true rectocele, perineal hypermobility and enterocele. Ultrasound Obstet Gynecol 2005;26: 737.
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    Dietz HP. Ultrasound imaging of the pelvic floor. Part I: two-dimensional aspects. Ultrasound Obstet Gynecol 2004;23: 8092.
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    Steensma AB, Dietz HP. The prevalence of defects of the rectovaginal septum. Ultrasound Obstet Gynecol 2004;24: 259.
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    Brubaker L. Rectocele. Curr Opin Obstet Gynecol 1996;8: 8769.
  • 9
    Shorvon PJ, McHugh S, Diamant NE, Somers S, Stevenson GW. Defecography in normal volunteers: results and implications. Gut 1989;30: 173749.
  • 10
    Beer-Gabel M, Teshler M, Schechtman E, Zbar AP. Dynamic transperineal ultrasound vs. defecography in patients with evacuatory difficulty: a pilot study. Int J Colorectal Dis 2004;19: 607.
  • 11
    Dietz HP, Clarke B. Prevalence of rectocele in young nulliparous women. Aust N Z J Obstet Gynaecol 2005;45: 3914.
  • 12
    Richardson AC. The rectovaginal septum revisited: its relationship to rectocele and its importance in rectocele repair. Clin Obstet Gynecol 1993;36: 97683.
  • 13
    Karram M, Porter R. Pathophysiology, diagnosis and management of rectoceles. In: CardozoL, StaskinD, editors. Female Urology and Urogynaecology. London: Isis Medical Media; 2001. p. 61625.