Anal incontinence, as defined by the International Consultation on Incontinence,1 is the involuntary loss of gas, liquid, or solid stool that causes a social or hygienic problem. The reported prevalence of anal incontinence in women with pelvic organ prolapse and/or urinary incontinence ranges from 20%2,3 to 54%,4 which is significantly higher than the published rate of approximately 6% in community-dwelling adults.5,6 A recent study of women presenting for routine gynecologic care in the United States, however, found that up to 28% reported experiencing accidental loss of bowel contents in the preceding year.7
The etiology of anal incontinence in women with pelvic organ prolapse and urinary incontinence is likely multifactorial8 but has been strongly associated with anatomic anal sphincter disruption.4 In a previous cross-sectional study of 100 women with pelvic floor disorders, we found that women with anal incontinence were 36 times more likely to have a visible anal sphincter defect on endoanal ultrasonography than women with anal continence.4 Similarly, a study of women with late-onset fecal incontinence after vaginal delivery found that 71% had anatomical anal sphincter defects.9
The aims of this study were to compare the prevalence of anal incontinence and anal sphincter injury in women with pelvic floor disorders with those in a control group of normal, parous women without urinary incontinence or genital prolapse. We wished to determine whether a significant correlation existed between anal incontinence and anatomic sphincter injury in each group. The results may advance our understanding of the pathogenesis of anal incontinence in women with other pelvic floor disorders.
MATERIALS AND METHODS
This study was approved by the Virginia Commonwealth University Medical Center Institutional Review Board, and all study subjects gave written, informed consent. It is an expansion of our previous study of 100 women with pelvic floor disorders (cases) to include a normal control group. The complete methods pertaining to the case group were published in a previous report.4 In summary, for inclusion as a case, subjects had to report urinary incontinence (stress, urge, and overflow incontinence) that was confirmed by formal urodynamic testing and/or stage II or higher pelvic organ prolapse, as measured using the Pelvic Organ Prolapse Quantification System. Control subjects were recruited between June 1, 2003, and February 2005 from the author’s (C.M.N.) benign gynecology clinic in the Department of Obstetrics and Gynecology at Virginia Commonwealth University Medical Center. For inclusion, control subjects had to report full continence of urine (no symptoms of urge or stress incontinence in the preceding year) and have stage 0 or I pelvic organ prolapse, as measured using the Pelvic Organ Prolapse Quantification System.10 Exclusion criteria included age less than 35 years, no prior vaginal delivery, inability to give informed consent, presenting complaint of fecal incontinence, irritable bowel disease as defined by Rome II Criteria,11 inflammatory bowel disease, multiple sclerosis or other degenerative neurological disease, vaginal delivery or surgery within the last 3 months, previous anal surgery, and refusal to undergo endoanal ultrasonography.
Each subject underwent a standardized evaluation including a detailed medical, surgical, obstetric, and gynecologic history. Demographic data were collected. All subjects completed a written questionnaire that asked: “Do you suffer from anal incontinence? This is the involuntary loss of gas, liquid, or solid stool sufficient to be considered a problem by you.” If the response was “yes,” subjects completed the Rockwood Thompson Fecal Incontinence Severity Index (FISI) to assess the degree and frequency of any accidental bowel leakage over the preceding month. The FISI score was then calculated based on the Patient Ratings of Fecal Incontinence, which ranges from 0 to 61, with higher scores indicating more severe incontinence.12
A screening neurologic examination was performed on all patients to assess general mental status as well as sensory and motor function of the pelvis and lower extremities. The patient’s level of consciousness, orientation, memory, speech, and comprehension were assessed to determine overall mental status. Sensory function was tested using light touch and pinprick on the perineum and around the thigh and foot. Sacral reflex activity (S2–S4) was evaluated by stroking the skin adjacent to the anus and observing for the reflex contraction of the anal sphincter (anal wink).
Pelvic support defects were assessed using the Pelvic Organ Prolapse Quantification System, with the patient exhibiting maximal straining effort in the lithotomy position. Urodynamic testing, which had been performed on all cases to confirm leakage, was not performed on the control group. Anal incontinence was defined as the involuntary loss of flatus, liquid, or solid stool, sufficient to be considered a problem by the subject based on history and questionnaire results.
Endoanal ultrasonography was performed as previously described for the case group. All images were recorded on printed paper, and one investigator (C.M.N.), who was blinded to the anal incontinence questionnaire results, interpreted and recorded the ultrasound results. The internal and external anal sphincters were evaluated separately and reported as intact or disrupted.
Statistical analysis was performed with SAS 9.3 (SAS Language and Procedures, SAS Institute, Cary, NC). For univariate analysis, continuous data were reported as mean ± standard deviation (SD) and tested for statistical significance using 2-tailed t tests. Categorical data were reported as ratios or proportions and were compared using the χ2 statistic. Ordinal data were reported as medians, and the Mann-Whitney U test was used for statistical significance. When appropriate, odds ratios (ORs) with 95% confidence intervals (CIs) are reported. Multivariable logistic regression models were used to assess the independent association of demographic and obstetric variables with anal incontinence. P ≪ .05 was considered statistically significant.
One hundred women with pelvic organ prolapse and/or urinary incontinence (cases) and 90 control subjects were studied. A detailed description of the cases was presented in a previous report.4 A comparison of demographic and historic characteristics between cases and controls is presented in Table 1. Women with pelvic floor disorders were significantly older (mean age 57 versus 53), were more likely to be white women, had higher rates of operative vaginal delivery, and had larger infant birth weights than the control group. All cases and controls demonstrated normal cognition and gross motor function. No differences existed in the number of subjects with intact sensation in the distribution of the pudendal nerve, but cases were significantly less likely to demonstrate an anal wink than were the controls (Table 1).
Overall, 54/100 (54%) cases and 16/90 (17.8%) controls reported bothersome anal incontinence (OR 5.4, 95% CI 2.8–10.6, P ≪ .001). The mean FISI scores were significantly higher in cases (22.3 ± 13) than in controls (12.7 ± 6.3), P = .006. Women with pelvic floor disorders were significantly more likely to demonstrate anatomic anal sphincter defects on endoanal ultrasonography than those in the control group (52% versus 30%, P = .007). Table 2 presents a detailed comparison of the integrity of the internal and external anal sphincters in each group. The control group was significantly more likely to have a completely intact anal sphincter complex (P = .002), whereas cases had higher rates of isolated external anal sphincter defects (P = .01) and combined defects of the internal and external sphincters (P = .04).
In the univariate analysis, anal incontinence was strongly associated with an anal sphincter defect on ultrasonography in women with pelvic floor disorders (OR 36.4, 95% CI 12–114, P < .001) and in control women (OR 5.9, 95% CI 3–11, P = .002). Table 3 presents the stratification of anal incontinence by anal sphincter defects in both cases and controls. Also in the univariate analysis, operative vaginal delivery was associated with anal incontinence in cases (OR 3.6, 95% CI 1.6–8.8, P = .002) but not controls (OR 1.8, 95% CI 0.6–6.5, P = .3).
A multivariable logistic regression model was fitted that used anal incontinence as the outcome and age, race, body mass index, parity, highest infant birth weight, and history of operative vaginal delivery as covariates to control for the effect of anal sphincter injury on anal incontinence. The study group (cases or controls) was also included in this model. From this analysis, anal incontinence was found to be significantly associated only with the presence of an anal sphincter defect (OR 16.1, 95% CI 6.8–38.2, P < .001) and the study group designation (OR 4.9, 95% CI 2.1–11.8, P < .001). To determine the risk factors present within each study group, a similar multivariable logistic regression model was fitted separately for cases and controls. This analysis revealed that age (OR 1.1, 95% CI 1.01–1.12, P = .01) and anal sphincter injury (OR 7.2, 95% CI 1.8–28.1, P < .005) were significant for the control group, while operative delivery (OR 4.5, 95% CI, 1.2–17.1, P < .03) and anal sphincter injury (OR 55, 95% CI, 13–230, P < .001) were significant for the cases.
Female pelvic floor disorders, including urinary incontinence, anal incontinence, and pelvic organ prolapse are often found to coexist in the same women.2–4,13–15 In this study, we found that women with genital prolapse and/or urinary incontinence were more than 5 times as likely to report bothersome anal incontinence as a group of healthy controls with normal pelvic supports and no urinary incontinence. In addition to higher overall prevalence rates, women with pelvic floor disorders reported more severe anal incontinence, as reflected by significantly higher FISI scores.
Anal sphincter disruption is a known risk factor for the development of anal incontinence.9,16–18 An increased prevalence of anal incontinence in the case group correlated with significantly higher rates of anatomic anal sphincter defects (52%) than was observed in the control group (30%). It is noticeable that the rate of anal sphincter defects in the control group was very similar to previous reports of “occult” anal sphincter trauma in approximately one third of primiparous women.19,20 Although both cases and controls demonstrated a significant association between the presence of anal incontinence and anatomic anal sphincter injury, the strength of this association was much higher in the group of women with pelvic floor disorders: In the case group, women with anal incontinence were 36 times more likely to have visible anal sphincter defects than those without anal incontinence, whereas in the control group they were only 6 times as likely. The strength of these associations remained after controlling for potentially confounding variables in the logistic regression analyses. We believe that the differential results between the case and control groups support our hypothesis that “occult” anal sphincter trauma is much more likely to become symptomatic in the face of other pelvic floor dysfunction. This, however, can only be confirmed with a prospective longitudinal study.
Operative vaginal delivery20–23 and fetal macrosomia24,25 are known risk factors for anal sphincter injury and were both more commonly reported by cases than controls. From the multivariable regression analysis, however, only operative vaginal delivery remained a significant risk factor for anal incontinence in cases, but not controls. It is possible that “occult” anal sphincter injury occurs more commonly with operative delivery that eventually becomes symptomatic once other pelvic floor dysfunction develops.
Several limitations of this study do exist. Demographic differences in the 2 groups were present despite every attempt to match cases and controls, and this could confound the results. Advancing age is a known risk factor for the development of anal incontinence,8,26 and in this study, cases were significantly older than controls. Is a mean age of 57 versus 53 clinically significant? This is difficult to assess, but because the majority of women in both groups were postmenopausal, we feel that the mean difference in age of 4 years was unlikely to significantly affect the results. Within the case group itself, age was identified as a risk factor for anal incontinence, although the odds ratio was only 1.1 (95% CI 1.01–1.12). Another difference between cases and controls was the racial distribution in each group, which may have introduced a more significant bias. Seventy-eight percent of cases versus only 58% of controls were white. White race is a known risk factor for urinary incontinence and prolapse,27 but no clear association exists between ethnicity and anal incontinence. It is certainly plausible, however, that because white race has been linked with genital prolapse and urinary incontinence, a similar association would be seen with anal incontinence. Over the 2-year study period, approximately 750 white and 300 black women were screened for enrollment in the control group, but the majority of vaginally parous white women failed to meet inclusion criteria, most commonly because of stage I or higher pelvic organ prolapse. It is important to note that in the logistic regression analysis that adjusted for these differences, the magnitude of the association between anal incontinence and anal sphincter injury remained the same.
Anal continence is a complex function that requires not only anatomic integrity of the internal and external anal sphincter, but also intact sensory and motor innervation.16,28 In this study, we did not formally evaluate for differences in pudendal nerve function with electrophysiologic testing but did note differences in sacral nerve activity on physical examination. The control group was significantly more likely to exhibit an intact anal wink than the cases, suggesting that differences in nerve function did exist. The impact of neuropathic versus anatomic injury needs to be investigated further but was beyond the scope of this study.
Is it urinary incontinence, genital prolapse, or the presence of both that is more likely to be associated with anal incontinence? This study was not powered to ascertain the individual risk of anal incontinence in women with prolapse versus urinary incontinence so we cannot answer that question. Because women with urinary incontinence and/or prolapse were collectively analyzed as “cases,” it is possible that one subgroup had a significantly higher risk of anal incontinence. This is a notable limitation and is the subject of a future study.
In conclusion, anal incontinence was significantly more prevalent in women with pelvic floor disorders than in normal control subjects and may be caused by higher rates of anatomic anal sphincter disruption. Women who present with genital prolapse or urinary incontinence should routinely be queried about symptoms of anal incontinence, and imaging of the anal sphincter should be incorporated into the comprehensive evaluation of these patients.
1. Norton C, Christiansen I, Butler U, Harari D, Nelson RL, Pemberton J, et al. Anal incontinence. In: Abrams P, Cardozo L, Khoury S, Wein A, editors. Incontinence. 2nd ed. International Consultation on Incontinence, 2001. Plymouth (UK): Health Publications; 2002. p. 987–1043.
2. Meschia M, Buonaguidi A, Pifarotti P, Somigliana E, Spennacchio M, Amicarelli F. Prevalence of anal incontinence in women with symptoms of urinary incontinence and genital prolapse. Obstet Gynecol 2002;100:719–23.
3. Soligo M, Salvatore S, Milani R, Lalia M, Malberti S, Digesu GA, Mariani S. Double incontinence in urogynecologic practice: a new insight. Am J Obstet Gynecol 2003;189:438–43.
4. Nichols CM, Gill EJ, Nguyen T, Barber MD, Hurt WG. Anal sphincter injury in women with pelvic floor disorders. Obstet Gynecol 2004;104:690–6.
5. Chen GD, Hu SW, Chen YC, Lin TL, Lin LY. Prevalence and correlations of anal incontinence and constipation in Taiwanese women. Neurourol Urodyn 2003;22:664–9.
6. Faltin DL, Sangalli MR, Curtin F, Morabia A, Weil A. Prevalence of anal incontinence and other anorectal symptoms in women. Int Urogynecol J Pelvic Floor Dysfunct 2001;12:117–21.
7. Boreham MK, Richter HE, Kenton KS, Nager CW, Gregory WT, Aronson MP, et al. Anal incontinence in women presenting for gynecologic care: prevalence, risk factors, and impact upon quality of life. Am J Obstet Gynecol 2005;192:1637–42.
8. Bharucha AE, Fletcher JG, Harper CM, Hough D, Daube JR, Stevens C, et al. Relationship between symptoms and disordered continence mechanisms in women with idiopathic faecal incontinence. Gut 2005;54:546–55.
9. Oberwalder M, Dinnewitzer A, Baig MK, Thaler K, Cotman K, Nogueras JJ, et al. The association between late-onset fecal incontinence and obstetric anal sphincter defects. Arch Surg 2004;139:429–32.
10. Bump RC, Mattiasson A, Bo K, Brubaker LP, DeLancey JO, Klarskov P, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7.
11. Boyce PM, Koloski NA, Talley NJ. Irritable bowel syndrome according to varying diagnostic criteria: are the new Rome II criteria unnecessarily restrictive for research and practice? [published erratum in Am J Gastroenterol 2001;96:1319]. Am J Gastroenterol 2000;95:3176–83.
12. Rockwood TH, Church JM, Fleshman JW, Kane RL, Mavrantonis C, Thorson AG, et al. Patient and surgeon ranking of the severity of symptoms associated with fecal incontinence: the fecal incontinence severity index. Dis Colon Rectum 1999;42:1525–32.
13. Jackson SL, Weber AM, Hull TL, Mitchinson AR, Walters MD. Fecal incontinence in women with urinary incontinence and pelvic organ prolapse. Obstet Gynecol 1997;89:423–7.
14. Gonzalez-Argente FX, Jain A, Nogueras JJ, Davila GW, Weiss EG, Wexner SD. Prevalence and severity of urinary incontinence and pelvic genital prolapse in females with anal incontinence or rectal prolapse. Dis Colon Rectum 2001;44:920–6.
15. Uustal Fornell E, Wingren G, Kjolhede P. Factors associated with pelvic floor dysfunction with emphasis on urinary and fecal incontinence and genital prolapse: an epidemiological study. Acta Obstet Gynecol Scand 2004;83:383–9.
16. Madoff RD, Williams JG, Caushaj PF. Fecal incontinence. N Engl J Med 1992;326:1002–7.
17. Kamm MA. Obstetric damage and faecal incontinence. Lancet 1994;344:730–3.
18. Nichols C, Lamb, E, Ramakrishnan R. Differences in outcomes after third- versus fourth-degree perineal laceration repair: a prospective study. Am J Obstet Gynecol 2005;193:530–6.
19. Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905–11.
20. Donnelly V, Fynes M, Campbell D, Johnson H, O’Connell PR, O’Herlihy C. Obstetric events leading to anal sphincter damage. Obstet Gynecol 1998;92:955–61.
21. Casey BM, Schaffer JI, Bloom SL, Heartwell SF, McIntire DD, Leveno KJ. Obstetric antecedents for postpartum pelvic floor dysfunction. Am J Obstet Gynecol 2005;192:1655–62.
22. Christianson LM, Bovbjerg VE, McDavitt EC, Hullfish KL. Risk factors for perineal injury during delivery. Am J Obstet Gynecol 2003;189:255–60.
23. Fitzpatrick M, Behan M, O’Connell PR, O’Herlihy C. Randomised clinical trial to assess anal sphincter function following forceps or vacuum assisted vaginal delivery. BJOG 2003;110:424–9.
24. Handa VL, Danielsen BH, Gilbert WM. Obstetric anal sphincter lacerations. Obstet Gynecol 2001;98:225–30.
25. Dandolu V, Chatwani A, Harmanli O, Floro C, Gaughan JP, Hernandez E. Risk factors for obstetrical anal sphincter lacerations. Int Urogynecol J Pelvic Floor Dysfunct 2005;Apr 5 [Epub ahead of print].
26. Nelson R, Norton N, Cautley E, Furner S. Community-based prevalence of anal incontinence. JAMA 1995;274:559–61.
27. Nygaard I, Bradley C, Brandt D. Pelvic organ prolapse in older women: prevalence and risk factors. Obstet Gynecol 2004;104:489–97.
28. Toglia MR, DeLancey JO. Anal incontinence and the obstetrician-gynecologist. Obstet Gynecol 1994;84:731–40.
Figure. No caption available.