Anal incontinence can be defined as the involuntary loss of flatus, liquid, or solid stool. Even when it occurs only episodically, anal incontinence has catastrophic consequences on self‐confidence, personal image, and the ability to integrate socially and in employment. It is more frequent in women than men, obstetric trauma being widely recognized as a major predisposing factor.1,2 Because the stigma of this condition is considerable, many patients hide their symptoms, and therefore the true incidence of anal incontinence remains unknown. It has been estimated to affect between 1% and 16% of women,3,4 the prevalence increasing with age.
Urinary and anal incontinence share the same pathophysiologic mechanisms, and so an association would be expected. The most common mechanism is obstetric injury, particularly pelvic floor denervation occurring during childbirth.5–7 Although pudendal neuropathy is considered the most important common causative factor, other factors such as connective tissue disorders may be important and may act selectively.
Few studies have evaluated the prevalence of anal incontinence in women with urinary incontinence and/or genital prolapse, and reported rates go from 30% to 50%.8–11 The aims of this study were to investigate the prevalence of anal incontinence among women presenting for investigation of urinary incontinence or genital prolapse, to identify any variables important in the cause of anal incontinence, with particular focus on obstetric, medical, and surgical factors, and to establish whether there is an association between anal incontinence and urinary incontinence or genital prolapse.
MATERIALS AND METHODS
Between June 1999 and December 2000, 881 women with symptoms of urinary incontinence and/or pelvic organ prolapse were evaluated at the urogynecology unit of our department. A multichoice screening questionnaire covering the presence or absence of bowel dysfunction was provided to all women, and each one underwent a standardized evaluation including a detailed medical, surgical, obstetric, and gynecologic history, and pelvic examination. The questionnaire covered the following items: current and past bowel habits, anal incontinence, stool consistency, need to strain at stool, and symptoms of abdominal discomfort or pain. Anal incontinence was defined as the involuntary loss of gas or feces, occurring once a month or more frequently. Affected women were asked to specify whether the incontinence involved flatus and/or liquid and/or solid stools, and to report the frequency of the events. Constipation was defined as fewer than three bowel movements per week; irritable bowel syndrome was defined on the basis of the recently modified Rome criteria as the presence for at least 12 weeks (not necessarily consecutive) in the preceding 12 months of abdominal discomfort or pain associated with at least two of the following three features: pain relieved by defecation, change in the frequency of bowel movements (diarrhea or constipation), change in the form of the stool (loose, watery, or pellet‐like).12
Pelvic support defects were assessed using the halfway system classification described by Baden and Walker,13 with the patient recumbent and straining down, allowing the clinician to grade the defect of each vaginal site under stress. Pelvic organ prolapse greater than grade 2 in at least one vaginal site was considered clinically significant. Additional testing, as indicated clinically for genital prolapse and/or urinary symptoms such as incontinence, urgency, frequency, and dysuria, included office cystometry or multichannel urodynamic evaluation. Patients were considered incontinent if urine leakage occurred during provocative cystometry or multichannel urodynamics. Urodynamic techniques and measurements, terms, and diagnostic criteria conform to the recommendations of the International Continence Society.14
The Statistical Package for Social Sciences (SPSS Inc., Chicago, IL) was used for data analysis. For univariate analysis, continuous data were reported as means ± standard deviation and tested for statistical significance using two‐tailed t tests. Categoric variables were reported as ratios and analyzed using the χ2 test or Fisher exact test. P < 0.05 was considered statistically significant. Multivariable analysis using logistic regression was done to test the overall significance of all variables that were significantly associated with anal incontinence using univariate analysis. Data are reported as odds ratios and 95% confidence intervals.
Approval for this study was granted by the local human institutional investigation committee. All patients were informed about the aims of the study and gave written consent.
The mean age ± standard deviation of the women considered was 58.6 ± 10 years; 696 were postmenopausal (79%). One hundred and seventy‐eight had anal incontinence, for an overall prevalence of 20%; 74 (8%) reported loss of liquid or solid stool, and 104 complained of incontinence to flatus only. Ninety‐two (52%) reported weekly episodes of incontinence, and 37 (21%) complained of daily events. The basic demographic details and history of women with and without anal incontinence are compared in Table 1. Patients with anal incontinence were on average older, had greater body mass index, and had larger birth weight infants than their continent counterparts. In univariate analysis, anal incontinence was associated with a history of hemorrhoidectomy, collagen diseases, and symptoms of bowel motility disorders. When flatus and fecal incontinence were analyzed separately, no real differences were found in terms of risk factors. Five hundred and eleven women were diagnosed as having urinary incontinence; 122 (24%) also had anal incontinence, and 339 had a genital prolapse greater than grade 2 (beyond the hymenal ring) in at least one vaginal site, of whom 72 (21%) had anal incontinence. Out of the 511 patients with urinary incontinence, 161 also had a genital prolapse. Therefore, after clinical and urodynamic evaluation, 192 patients were considered disease free as they had neither urinary incontinence nor genital prolapse. Women with urinary incontinence were more likely to report anal incontinence events than women continent of urine, with or without prolapse (24% versus 15%, P = .002).
Urinary diagnoses included 358 with genuine stress incontinence, 66 with detrusor instability, and 87 with mixed incontinence. Table 2 compares the prevalence of anal incontinence between women with different urodynamic diagnoses. There was a strong significant association between detrusor overactivity and anal incontinence (P = .004), with 44 of 178 (25%) women with anal incontinence also having detrusor instability on urodynamics, compared with 109 of 703 (14%) patients continent to feces or flatus.
The relationship between the severity of genital prolapse by vaginal segment and anal incontinence is shown in Table 3. Anal incontinence was significantly associated in univariate analysis with severe anatomical defects in the posterior vaginal compartment (Douglas and rectum) and with damage to perineal body. The findings shown in Tables 2 and 3 tended to be even more striking when the control group was limited to the 192 women without either greater than grade 2 prolapse or urinary incontinence (data not shown).
After multivariable analysis of all risk factors by logistic regression analysis, the following were associated with anal incontinence: infant with birth weight 3800 g or greater, rectocele greater than grade 2, urinary incontinence, hemorrhoidectomy, and irritable bowel syndrome (Table 4).
Numerous studies point to a common cause for the development of anal incontinence, urinary incontinence, and pelvic organ prolapse. Damage to the pelvic support mechanism is thought to be the result of a combination of factors including vaginal delivery, connective tissue disorders, pelvic neuropathies, congenital deficiencies, pelvic surgery, and other factors.15,16 Childbirth remains the major contributory factor for the development of either anal or urinary incontinence and genital prolapse, being associated with functional and anatomical alterations in the muscles, nerves, and connective tissue of the pelvic floor.
Denervation injuries of the pubococcygeus muscle and external anal sphincter and damage to the endopelvic fascia and anal sphincter muscles have been reported after vaginal deliveries.17–19 Identified risk factors for weakening or laceration of the levator ani or anal sphincter include midline episiotomy, forceps delivery, nulliparity, birth weight, and perineal lacerations, and for neurologic injury, they include forceps delivery, prolonged second stage, birth weight, and multiparity.
Among the obstetric factors regarded as associated with anal incontinence, only a large birth weight infant was significant in our study. Unlike others,8,20 we did not find any association between anal incontinence and episiotomy, instrumental delivery and parity. However, our results must be viewed with caution. Data based on patients' memories are often inaccurate because of the difficulty of recalling events that happened a long time before. Moreover, our population was composed mainly of women with a diagnosis of pelvic floor dysfunction in which other factors, such as connective tissue disorders, might limit the weight of any individual obstetric variable; it, therefore, may not represent the general population as a whole. Univariate analysis indicated an association between anal incontinence and age, body mass index, hemorrhoidectomy, collagen diseases, and irritable bowel syndrome. On logistic regression analysis, the association with age and body mass index was lost. The association between anal incontinence and irritable bowel syndrome has been reported by other investigators and is probably a consequence of a weak anal sphincter mechanism during episodes of profuse diarrheal stool.8,21 Collagen diseases were significantly associated with anal incontinence in univariate analysis, but the numbers—six—are too small to permit any firm conclusion.
Women with urinary incontinence are more likely to report symptoms of anal incontinence than subjects continent of urine. In this series, urodynamics showed that genuine stress incontinence and detrusor overactivity were both significantly associated with anal incontinence. This is consistent with the theory of a common pathogen mechanism for anal and genuine stress incontinence, pudendal nerve injury, or direct muscle damage being the main cause of both conditions. The relationship between anal incontinence and detrusor overactivity, on the other hand, suggests that a common central or peripheral disorder of smooth muscle function might also be a factor in both conditions. Damage to the muscles and nerves of the pelvic floor is believed to be the main predisposing factor for the development of pelvic organ prolapse. Therefore, it is not surprising when genital prolapse, urinary incontinence, and anal incontinence occur in the same patient. We found a significant association between anal incontinence and severe rectocele. This could be the result of continuous stretching and damage to the pudendal nerve with repeated, prolonged straining at stool, leading to progressive descent of the pelvic diaphragm, weakening of the posterior vagina, and anal incontinence.22
In conclusion, the prevalence of anal incontinence in a relatively large number of women with symptoms of urinary incontinence and pelvic organ prolapse was 20%. The results suggest that women with a diagnosis of urinary incontinence are more likely to report anal incontinence events than subjects continent of urine. Therefore, all women undergoing urogynecologic assessment for urinary incontinence or genital prolapse should be routinely questioned about anal incontinence and other anorectal symptoms.
1. Mac Arthur C, Bick D, Keighley M. Faecal incontinence after childbirth. Br J Obstet Gynaecol 1997;104:46–50.
2. Sultan AH, Kamn MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905–11.
3. Johanson JF, Lafferty J. Epidemiology of fecal incontinence: The silent affliction. Am J Gastroenterol 1996;91:33–6.
4. Faltin DL, Sangalli MR, Curtin F, Morabia A, Weil A. Prevalence of anal incontinence and other anorectal symptoms in women. Int Urogynecol J 2001;12:117–21.
5. Ryhammer AM, Beck KM, Laurberg A. Multiple vaginal deliveries increase the risk of permanent incontinence of flatus and urine in normal premenopausal women. Dis Colon Rectum 1995;38:1206–9.
6. Smith AR, Hosker GL, Warrel DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence in women. Br J Obstet Gynaecol 1989;96:29–32.
7. Sultan AH, Kamn MA, Hudson CN. Pudendal nerve damage during labour: Prospective study before and after childbirth. Br J Obstet Gynaecol 1994;101:22–8.
8. 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.
9. Khullar V, Damiano R, Toozs-Hobson P, Cardozo L. Prevalence of faecal incontinence among women with urinary incontinence. Br J Obstet Gynaecol 1998;105:1211–3.
10. 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.
11. Caputo RM, Benson JT. Idiopathic fecal incontinence. Curr Opin Obstet Ginecol 1992;4:565–70.
12. Horwitz BJ, Fisher RS. The irritable bowel syndrome. N Engl J Med 2001;344:1846–50.
13. Baden WF, Walker TA. Genesis of the vaginal profile: A correlate classification of vaginal relaxation. Clin Obstet Gynecol 1972;15:1048–54.
14. Abrams P, Blaivas JG, Stanton S, Andersen JT. The standardization of terminology of lower urinary tract function. Neurourol Urodyn 1988;7:403–26.
15. Womack NR, Morrison JFB, Williams NS. The role of pelvic floor denervation in the aetiology of idiopathic fecal incontinence. Br J Surg 1984;73:404–7.
16. Kiff ES, Swash M. Slowed conduction in the pudendal nerves in idiopathic (neurogenic) faecal incontinence. Br J Surg 1984;71:614–6.
17. Snooks SJ, Swash M, Setchell M, Henry MM. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984;ii:546–50.
18. Norton PA. Pelvic floor disorders: The role of fascia and ligaments. Clin Obstet Gynecol 1993;36:926–38.
19. Chaliha C, Sultan AH, Bland JM, Monga AK, Stanton SL. Anal function: Effect of pregnancy and delivery. Am J Obstet Gynecol 2001;185:427–32.
20. Meyer S, Schreyer A, De Grandi P, Hohlfeld P. The effects of birth on urinary incontinence mechanism and other pelvic-floor characteristics. Obstet Gynecol 1998;92:613–8.
21. Donnelly VS, O'Herlihy C, Campbell DM, O'Connel PR. Postpartum fecal incontinence is more common in women with irritable bowel syndrome. Dis Colon Rectum 1998; 41:586–9.
22. Kiff ES, Barnes PRH, Swash M. Evidence of pudendal neuropathy in patients with perineal descent and chronic straining at stool. Gut 1984;25:1279–81.