DISCUSSION

The prevalence of fecal incontinence among this sample of high-risk postpartum women was 6.9%. This includes 2.6% of women who had solid stool incontinence and 4.9% who had liquid stool incontinence. This prevalence is slightly lower than the 9.6% prevalence reported by MacArthur et al for their sample of UK and New Zealand women at 3 months postpartum. This difference is perhaps surprising, given that our sample was restricted to high-risk women, where a higher prevalence might be expected. Alternatively, our later 12-month follow-up could be seen to represent a more accurate assessment of enduring incontinence symptoms.

Unlike earlier studies that have demonstrated marked differences in the prevalence rates for primiparous and multiparous women, the proportion of frank fecal incontinence in the present study was not statistically different for the two groups. This was the case for both solid and liquid stool incontinence, and for precursor flatal incontinence symptoms. Given that Sultan et al included all three symptoms in their definition of anal incontinence, it is unlikely that definitional differences account for this disparity. Instead, the results suggest that the protective effect of primiparity might be reduced among women who have undergone high-risk deliveries.

Not surprisingly, the prevalence of each of the three precursors to fecal incontinence was somewhat higher than for symptoms of frank incontinence. Specifically, the prevalence rates were 24.4% for flatal incontinence, 14.8% for fecal urgency, and 10.9% for soiling on underwear. In the Swedish study of primiparous women, a similar 26% reported symptoms of flatal incontinence at 9 months postpartum. A higher rate of 41% flatal incontinence has been shown for women who sustain a third-degree tear during childbirth, and a lower rate of 6% for those who do not. For fecal urgency, rates of 26% and 7%, respectively, were reported for these two groups. Thus, for both flatal incontinence and fecal urgency, the prevalence rates demonstrated for high-risk women in the present study are between the two extremes reported by Sultan et al. Although MacArthur et al reported relatively low rates of around 4% fecal urgency and 1% soiling at 10 months postpartum for a sample of UK women, their focus on new symptoms makes comparison difficult.

Four factors were significantly associated with fecal incontinence among this sample of high-risk women: having concurrent urinary incontinence, being aged over 35, having joint hypermobility, and having experienced periods of constipation in the postpartum. Two of these same factors-concurrent urinary incontinence and constipation-were also associated with the presence of precursor symptoms.

It is not surprising that both urinary incontinence and constipation were associated with fecal incontinence and its precursors. Like fecal incontinence, urinary incontinence can be the result of nerve damage sustained during childbirth. Likewise, constipation has been shown to result from damage to the pelvic floor muscles and their innervation sustained during childbirth, and it is commonly considered a risk factor for subsequent fecal incontinence. Indeed, urinary incontinence and constipation have been shown to be interrelated. Repeated straining at the stool is thought to exacerbate the perineal damage, resulting in weakness of the pelvic floor, perineal descent during straining, and secondary anatomic changes that result in anorectal dysfunction and further difficulty in defecation. These factors further increase the risk of subsequent fecal incontinence. Encouragement with pelvic floor exercises, which have been shown to improve pelvic floor muscle integrity, might be beneficial for women with these symptoms.

Similarly, the association with age is consistent with previous research. Studies by both Zetterstrom et al and MacArthur et al demonstrated that older maternal age is associated with higher rates of fecal incontinence. Even in the community generally, both US and Australian studies have demonstrated that the prevalence of fecal incontinence increases with age.

Joint hypermobility and flow-stopping inability were associated with fecal incontinence and precursor symptoms, respectively. This provides support for the hypothesis that fecal incontinence is associated with loss of pelvic floor muscles integrity. Indeed, although few previous studies have explored their association with fecal incontinence, the present findings suggest that hypermobility and flow-stopping inability might represent two useful indicators of fecal incontinence risk. In particular, hypermobility represents a trait characteristic that can be assessed during pregnancy, thereby enabling opportunities for monitoring for high-risk women.

Although we found no difference in fecal incontinence rates for primiparous and multiparous women, multiparity was associated with the presence of precursor symptoms. Most notably, rates of soiling and fecal urgency were higher among multiparous women. Sultan et al similarly demonstrated higher rates of precursors (flatal incontinence and fecal urgency) among multiparous women. As discussed earlier, though, the effect of primiparity was less pronounced in the present sample.

Three factors that have been linked to fecal incontinence in previous studies were not significant in the present study. Specifically, forceps delivery, episiotomy and major anal sphincter tearing have all been shown to increase the risk of fecal incontinence. In the present study, neither instrumental delivery (either forceps or ventouse extraction) nor perineal trauma (defined as either episiotomy or sutured tearing) was associated with fecal incontinence or its precursors. This might again be explained by the inclusion of only high-risk women in the present study. Moreover, the combining of forceps and ventouse deliveries might have masked the risks of forceps delivery, because some studies have suggested that the use of ventouse is associated with significantly less tearing sphincter defects and subsequent fecal incontinence than the use of forceps. However, other studies suggest that both interventions increase fecal incontinence risk-hence the approach taken in the present study. Finally, occult anal sphincter damage was not measured in the present study. Instead, because of the practical difficulties associated with clinical examination for a large sample of women, episiotomy and/or suturing were used as indicators of perineal trauma.

There are three other potential limitations to this study, two of which have been noted previously. First, the study response rate indicates that only 54.3% of women eligible for the study participated at baseline. To some extent, this limits the generalizability of the present study findings. Second, because the sample was drawn from only three hospitals, the external validity of the study might have been compromised. Importantly, though, the three hospitals served diverse population groups: urban public, urban private, and rural. Finally, the study relies on retrospective reports of anal incontinence symptoms over 12 months, which might be subject to recall bias. However, this was minimized through the use of validated questionnaire items.

CONCLUSION: The present findings suggest that older and multiparous women, and women with joint hypermobility are at increased risk of postpartum anal incontinence symptoms after a high-risk delivery. Concurrent urinary incontinence, flow-stopping inability, and constipation are also associated with postpartum anal incontinence symptoms after high-risk deliveries.

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Chiarelli, Pauline PhD; Murphy, Barbara PhD; Cockburn, Jill PhD
Obstetrics & Gynecology:
December 2003 - Volume 102 - Issue 6 - p 1299-1305

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School of Health Sciences and the School of Medical Practice and Population Health, University of Newcastle, Newcastle, New South Wales, Australia.

Full article Fecal Incontinence After High-Risk Delivery