Nichols, Catherine Matthews MD*; Gill, Edward J. MD*; Nguyen, Tuc*; Barber, Matthew D. MD, MHS†; Hurt, W Glenn MD*
Urinary incontinence, anal incontinence, and pelvic organ prolapse are the 3 major clinical syndromes included in the term female pelvic floor disorder and are often found to coexist in the same woman. Anal incontinence can be defined as the involuntary loss of gas, liquid, or solid stool. Fecal incontinence refers only to the loss of solid stool. Seventeen to thirty percent of women with urinary incontinence and/or pelvic organ prolapse also report fecal incontinence.1,2 The impact of double incontinence can be devastating. Fialkow et al3 determined that patients with a combination of urinary and fecal incontinence had a significantly reduced quality of life and a lower functional status than those with urinary incontinence alone. Despite this negative impact, many patients are reluctant to seek medical attention because of social embarrassment. The etiology of fecal incontinence in women with pelvic floor disorders is unknown but has largely been attributed to neuropathic injury sustained during vaginal childbirth4,5 or chronic straining during defecation.6,7 With the advent of endoanal ultrasonography, however, the perception regarding the pathogenesis of anal incontinence in younger women has been altered. Sultan et al8 reported that 35% of primiparous women sustained an occult anal sphincter defect during vaginal childbirth, and even though pudendal nerve terminal latencies were prolonged at 6 weeks postpartum, most appeared to recover by 6 months. This study suggests that anatomic disruption of the anal sphincter needs to be considered separately from a strictly neuropathic origin for incontinence.
We performed a cross-sectional study of women who presented with pelvic organ prolapse and/or urinary incontinence to test the hypothesis that anal incontinence is associated with anatomic anal sphincter disruption in this population. Risk factors for anal incontinence and sphincter injury were identified. Awareness of anal sphincter injury in this group of women may allow for comprehensive evaluation and treatment.
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. A sample size of 106 was projected to identify approximately 25 women with fecal incontinence and 35 women with anal sphincter defects, based on a reported prevalence of anal incontinence of 20% in women with prolapse or urinary incontinence and 1% in the general population and a 35% rate of occult anal sphincter disruption in women after vaginal childbirth, respectively.1,8 This calculation was based on a 5% significance level and power of 0.8. We anticipated that at least 10 women would be identified as having anal sphincter disruption on ultrasonography without having symptoms of anal incontinence. Study subjects were recruited between August 1, 2002, and May 30, 2003, from the urogynecology practices of 3 authors in the Department of Obstetrics and Gynecology at Virginia Commonwealth University Medical Center (C.M.N., E.J.G., W.G.H.). For inclusion, subjects had to demonstrate urinary incontinence (stress, urge, or mixed incontinence) that was confirmed by multichannel cystometric studies or stage II or greater pelvic organ prolapse, as measured using the Pelvic Organ Prolapse Quantification system.9 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,10 inflammatory bowel disease, multiple sclerosis or other degenerative neurological disease, vaginal delivery or surgery within the last 3 months, and refusal to undergo endoanal ultrasound testing.
Each subject underwent a standardized evaluation, including a detailed medical, surgical, obstetric, and gynecologic history. Demographic data were collected. Subjects completed the Rockwood Thompson Fecal Incontinence Severity Index, which was developed by The American Society of Colon and Rectal Surgeons to assess the degree and frequency of any accidental bowel leakage over the preceding month. The Fecal Incontinence Severity Index Score (FISI) was then calculated based on the Patient Ratings of Fecal Incontinence, which ranges from 0–64, with higher scores indicating more severe incontinence.11
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 was assessed to determine overall mental status. The strength and tone of the pelvic diaphragm and anal sphincter was evaluated using a standardized 5-point rating scale developed by Chiarelli.12 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. Multichannel cystometric studies and stress testing were completed in standard fashion. Subjects were considered continent of urine if no leakage was demonstrated on formal urodynamic testing, whereas those who demonstrated leakage during testing were considered incontinent. Stress, urge, and mixed incontinence were analyzed collectively as urinary incontinence. 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 with a 360° rotating rectal probe, a 7-MHz transducer (focal range 2–4.5 cm), and a hard sonolucent plastic cone with the subject in the left lateral decubitus position (Bruel and Kjaer, Naerum, Denmark). All images were recorded on printed paper. One investigator (C.M.N.), who was blinded to the FISI results, interpreted and recorded the ultrasound findings. The endosonographic interpretation of the appearance of muscle layers has been previously validated: an external sphincter defect appears as a break in the normal texture of this muscle ring and an internal sphincter defect as a gap in the hypoechoic ring.13–15 The internal anal sphincter and the external anal sphincter were evaluated separately and were reported as either intact or disrupted. Examples of an intact anal sphincter complex, an internal sphincter defect, and an external anal sphincter defect are demonstrated in Figures 1A, 1B, and 1C, respectively.
The extent of the anal sphincter tear was then characterized by degrees of a circle. For example, if a defect was visualized from 10 o'clock to 1 o'clock this would be a 90° tear. If the defect extended from 9 o'clock to 3 o'clock, this would correspond to a 180° tear.
Statistical analysis was performed using SPSS 11.5 (SPSS Inc, Chicago, IL). 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. The degree of fecal incontinence was compared to the degree of anal sphincter injury and stage of pelvic organ prolapse using the Pearson correlation coefficient. P ≤ .05 was considered statistically significant.
One hundred women were enrolled between August 1, 2002, and May 30, 2003. Mean age (± SD) and body mass index were 57.1 ± 13.2 years and 29.8 ± 6.8 kg/m2, respectively. Median parity was 3.7 Fifteen percent of subjects had pelvic organ prolapse only, 28% had urinary incontinence only, and 57% had both pelvic organ prolapse and urinary incontinence. The demographic and historic characteristics of these women are presented in Table 1. Women with prolapse or combined prolapse and urinary incontinence were significantly older (P = .005) and had higher maximum infant birth weights (P = .03) than women with isolated urinary incontinence. The number of subjects with stages II, III, and IV prolapse were 31, 30, and 11, respectively. All subjects demonstrated normal cognition and gross motor function. Ninety-one percent of subjects had intact sensation in the distribution of the pudendal nerve, and 74% demonstrated normal sacral reflex activity. Table 2 compares the demographic and historic characteristics of women with and without anal incontinence. Subjects without anal incontinence were significantly more likely to have an intact anal wink reflex than those with anal incontinence (Table 3). The overall prevalence of anal incontinence was 54% (54/100). Twenty-three percent reported incontinence of gas only, whereas 31% reported fecal incontinence. The mean FISI score (± SD) of subjects with anal incontinence was 22.3 ± 13. The prevalence of anal sphincter defects was 52% (52/100). Of these, 58% (30/52) had involvement of the external sphincter only, 2% (1/52) of the internal sphincter only, and 40% (21/52) had evidence of combined defects of both the internal and external anal sphincters. The stratification of anal sphincter defects between women with and without anal incontinence is presented in Table 4. Anal incontinence was significantly associated with the presence of an anal sphincter defect on endoanal ultrasonography (OR 36.4, 95% confidence interval [CI] 12–114, P < .001). Increasing degrees of fecal incontinence were positively correlated with increasing degrees of anal sphincter injury, with a Pearson correlation coefficient of 0.81, (P < .001) (Fig. 2). The FISI did not correlate with increasing degrees of pelvic organ prolapse severity (r = 0.23).
Patients with both pelvic organ prolapse and urinary incontinence were significantly more likely to have anal incontinence (OR 2.72, 95% CI 1.2–6.1, P < .02) and anal sphincter injury (OR 4.0, 95% CI 1.7–9.3, P < .001) than patients with urinary incontinence only or pelvic organ prolapse only. A history of operative vaginal delivery was significantly associated with anal incontinence (OR 3.75, 95% CI 1.6–8.7, P = .002) and anal sphincter injury (OR 2.56, 95% CI 1.2–5.8, P = .025). A statistical trend did exist for an association between increasing vaginal parity (P = .06) and largest infant birth weight of more than 3,500 grams (P = .09) with anal sphincter injury, but there was inadequate power to confirm these findings.
Although data regarding the community prevalence of fecal incontinence exist, there is a paucity of data regarding anal incontinence, a condition that may be equally embarrassing. Published data regarding rates of fecal incontinence range from 1.3–18.4%,16 but are as high as 50% in the physically disabled and in nursing home residents.17 The incidence of fecal incontinence is 8 times higher in women than in men, primarily because of the effects of vaginal childbirth.18
Numerous studies suggest a common etiology between the development of anal incontinence, urinary incontinence, and pelvic organ prolapse, namely pudendal nerve injury19,20 and disruption of the muscles and connective tissue of the pelvic floor.4 Parks et al21 demonstrated histological and neurophysiological evidence of pelvic floor denervation in patients suffering from fecal incontinence. Subsequent studies4,5 revealed that up to 80% of women had pudendal nerve injury after their first vaginal delivery. With the introduction of endoanal ultrasonography, however, emphasis has shifted to the impact of anatomic anal sphincter disruption on anal incontinence. Prospective studies before and after childbirth have shown that up to one third of women sustain an anatomic anal sphincter defect that is not recognized after delivery.8,22 Although pudendal nerve terminal latency measurements were initially prolonged, the majority appeared to recover by 6 months postpartum. The impact of this “occult” anal sphincter disruption is unclear but is likely to affect the development of anal incontinence in later life. Faltin et al23 found that a second vaginal delivery significantly increased the risk of fecal incontinence, and this risk was highest (39%) in patients with external anal sphincter defects on ultrasonography after their first vaginal delivery.
In our cohort of women with pelvic floor disorders, the prevalence of anal incontinence and anal sphincter disruption was 54% and 52%, respectively. Women with anal incontinence were 36 times more likely to have a visible anal sphincter defect on ultrasonography than women without anal continence. Furthermore, the severity of anal incontinence was significantly correlated with the degree of anal sphincter disruption, which provides additional validation to the observed association between sphincter injury and symptomatology. In a selected high-risk group of women with pelvic floor disorders, this rate of visible anal sphincter defects on ultrasonography is not unexpected, given that approximately one third of all primiparous women have a visible defect postpartum.8,22
Women with both urinary incontinence and pelvic organ prolapse were significantly more likely to suffer from anal incontinence and demonstrate an anal sphincter defect than women with isolated urinary incontinence or prolapse. This suggests that women with multiple pelvic floor disorders are likely to have suffered a greater degree of injury to the muscles, connective tissue, and nerves of the pelvic floor than those who have a single pelvic floor disorder. It also supports, at least in part, a common pathogenic mechanism for each of these disorders. The collective grouping of different types of incontinence as a single variable, however, may have confounded this result. An additional possible confounding variable was the younger age of subjects with isolated urinary incontinence. This may have affected the rate of anal incontinence in this subgroup but should not have altered the rate of visible anal sphincter defects.
Numerous studies have demonstrated a strong correlation between operative vaginal delivery, anal sphincter disruption, and anal incontinence.22,24–26 In our population, a history of operative vaginal delivery was again significantly associated with the presence of both anal incontinence and anal sphincter injury. This result may be biased, because information regarding mode of delivery was based solely on patient recall. This study did not have adequate power to detect an association between anal sphincter injury and vaginal parity or increasing birth weight. Previous studies have identified fetal macrosomia as a risk factor for anal sphincter injury.27
If “occult” anal sphincter disruption that was sustained many years prior is identified as the primary cause of anal incontinence in women with pelvic floor disorders, how does one explain the interim lack of symptomatology? We postulate that younger women have stronger pelvic floor muscles that they are able to recruit to compensate for reduced anal squeeze pressure. With aging and the weakening of these adjuvant pelvic supports, however, these defects become clinically evident and present as anal incontinence.
This study has several limitations. First, the interpretation of endoanal ultrasound images is subjective and may be influenced by operator experience, patient position, and possibly, posterior wall prolapse. The appearance of the internal anal sphincter is probably less subject to variations in interpretation than the external anal sphincter, because defects appear as a clear break in a hypoechoic ring. Since 40% of subjects had combined defects of both the internal and external sphincters, there was less likelihood of misinterpretation. We attempted to minimize measurement bias by blinding the operator to the anal incontinence questionnaire results until the ultrasonography had been interpreted and the results recorded. The second limitation was that we did not include a control group and, therefore, cannot fully assess the relationship between pelvic organ prolapse and/or urinary incontinence and anatomic anal sphincter disruption. Finally, we did not evaluate pudendal nerve function with electrophysiologic testing and thus could not directly measure the relationship between neuropathic injury and anal incontinence. It is possible that, even though the anal sphincter was mechanically disrupted, concomitant pudendal neuropathy was responsible for the symptoms of anal incontinence. We did, however, evaluate sacral neurological function by means of a standardized physical examination. Subjects with anal incontinence were significantly less likely to have an intact anal wink than those with anal continence. This absence of sacral reflex activity is suggestive of concomitant pudendal neuropathy, and the impact of neuropathic versus anatomic injury needs to be investigated further.
Anal incontinence is a devastating condition that has a profoundly negative impact on quality of life. Anatomic anal sphincter disruption is common in women with other pelvic floor disorders and likely plays a significant role in the development of anal incontinence in this population. As endoanal ultrasonography has been found to be the most accurate modality in establishing the diagnosis of anal sphincter disruption.14,28 It should routinely be performed as part of a comprehensive evaluation of these patients.
1. 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.
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. Fialkow MF, Melville JL, Lentz GM, Miller EA, Miller J, Fenner DE. The functional and psychosocial impact of fecal incontinence on women with urinary incontinence. Am J Obstet Gynecol 2003;189:127–9.
4. Allen RE, Hosker GL, Smith AR, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770–9.
5. Snooks SJ, Setchell M, Swash M, Henry MM. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984;2:546–50.
6. Snooks SJ, Barnes PR, Swash M, Henry MM. Damage to the innervation of the pelvic floor musculature in chronic constipation. Gastroenterology 1985;89:977–81.
7. Lubowski DZ, Swash M, Nicholls RJ, Henry MM. Increase in pudendal nerve terminal motor latency with defaecation straining. Br J Surg 1988;75:1095–7.
8. Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905–11.
9. Bump RC, Mattiasson A, Bo K, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7.
10. 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? Am J Gastroenterol 2000;95:3176–83.
11. 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.
12. Chiarelli PE. Incontinence: the pelvic floor function. Aust Fam Physician 1989;18:949, 953–4, 956–7.
13. Sultan AH, Kamm MA, Hudson CN, Nicholls JR, Bartram CI. Endosonography of the anal sphincters: normal anatomy and comparison with manometry. Clin Radiol 1994;49:368–74.
14. Sultan AH, Kamm MA, Talbot IC, Nicholls RJ, Bartram CI. Anal endosonography for identifying external sphincter defects confirmed histologically. Br J Surg 1994;81:463–5.
15. Sultan AH, Nicholls RJ, Kamm MA, Hudson CN, Beynon J, Bartram CI. Anal endosonography and correlation with in vitro and in vivo anatomy. Br J Surg 1993;80:508–11.
16. Johanson JF, Lafferty J. Epidemiology of fecal incontinence: the silent affliction. Am J Gastroenterol 1996;91:33–6.
17. Borrie MJ, Davidson HA. Incontinence in institutions: costs and contributing factors. CMAJ 1992;147:322–8.
18. Henry MM. Pathogenesis and management of fecal incontinence in the adult. Gastroenterol Clin North Am 1987;16:35–45.
19. Womack NR, Morrison JF, Williams NS. The role of pelvic floor denervation in the aetiology of idiopathic faecal incontinence. Br J Surg 1986;73:404–7.
20. Kiff ES, Swash M. Slowed conduction in the pudendal nerves in idiopathic (neurogenic) faecal incontinence. Br J Surg 1984;71:614–6.
21. Parks AG, Swash M, Urich H. Sphincter denervation in anorectal incontinence and rectal prolapse. Gut 1977;18:656–65.
22. 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.
23. Faltin DL, Sangalli MR, Roche B, Floris L, Boulvain M, Weil A. Does a second delivery increase the risk of anal incontinence? BJOG 2001;108:684–8.
24. Fenner DE, Genberg B, Brahma P, Marek L, DeLancey JO. Fecal and urinary incontinence after vaginal delivery with anal sphincter disruption in an obstetrics unit in the United States. Am J Obstet Gynecol 2003;189:1543–9; discussion 1549–50.
25. Farrell SA. Cesarean section versus forceps-assisted vaginal birth: it's time to include pelvic injury in the risk-benefit equation. CMAJ 2002;166:337–8.
26. 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.
27. Handa VL, Danielsen BH, Gilbert WM. Obstetric anal sphincter lacerations. Obstet Gynecol 2001;98:225–30.
28. Law PJ, Bartram CI. Anal endosonography: technique and normal anatomy. Gastrointest Radiol 1989;14:349–53.
© 2004 by The American College of Obstetricians and Gynecologists.