Anal Incontinence
Frida Carswell
James Oliver Keck
Peter L. Dwyer
Introduction
Anal incontinence (AI) is defined as involuntary loss of flatus and/or feces.1 Although it may affect men, it is generally more common and more severe in women. It is often underdiagnosed and may result in depression, anxiety, and impaired sexual function and has significant impact on women’s quality of life. The most common cause of AI in women is obstetric trauma, including obstetric anal sphincter injury (OASI). The sphincter injury may not be symptomatic or recognized at birth termed occult OASI. Investigation and management of AI should be targeted at finding and treating reversable causes. Many women can be managed conservatively, but a proportion of women will require surgical management. Primary anal sphincter repair following delivery with OASI may fail in up to 30% of cases, and some women will require a second repair.
EPIDEMIOLOGY AND ETIOLOGY
AI has been estimated to occur in 15% of women,2 but the true incidence may be more as only a third of women with incontinence ever mention this to their physician.3 AI may be caused by a complex interplay of numerous pathophysiologic factors including aberrant anorectal sensation or innervation, colorectal motility, consistency and volume of stool, as well as structural changes or damage to the pelvic floor and sphincter complex. Indeed, women who sustain obstetric trauma often do not present with symptoms of AI until many years postpartum with the added atrophy of aging and denervation of the smooth and striated musculature of the anal sphincters and pelvic floor.4
Anatomy and Physiology of Defecation
The internal anal sphincter (IAS) and the external anal sphincter (EAS) encircle the anal canal and maintain continence together with the puborectalis muscle.
The IAS is a continuation of the circular rectal smooth muscle layer and generates most of the anal resting pressure and helps prevent AI at rest.5 The IAS is under reflex control. The EAS muscle is composed of striated muscle cells, is continuous with the levator ani and pelvic floor, and is partially under voluntary control. The EAS contributes to the anal resting pressure, but its main function is to generate anal squeeze pressure (Fig. 56.1).
The puborectalis muscle forms a sling around the upper part of the anal canal. The tone of the puborectalis muscle creates the anorectal angle, which prevents movement of feces from the rectum to the anal canal between defecations (Fig. 56.2).3,4 The puborectalis is a 0.5- to 1.0-cm thick u-shaped muscle that forms a flaplike valve that creates a forward pull and reinforces the anorectal angle (Fig. 56.3). Recent work using transperineal ultrasound has shown that all three muscles contribute to a mechanical barrier to flatus and stool.6
Etiology
A common cause of AI in women is anal sphincter dysfunction from obstetric injury to the pudendal nerve, anal sphincter muscle, or both. Another common cause of fecal incontinence is remnant feces in the rectum from obstructed defection, for example, due to rectocele or simple constipation. Stool left in the rectum may trigger the rectal-anal inhibitory reflex (RAIR) causing the sphincter to relax. If the sphincter is relaxed, soiling and incontinence can occur. Soiling can also result from incomplete closure of the sphincter due to a fullthickness rectal prolapse, rectal mucosal prolapse, or hemorrhoids. Large anal tags may interfere with cleaning (Table 56.1).
Anal sphincter dysfunction
Disruption of the anal sphincter caused by obstetric injury, as well as by anorectal surgery or less commonly external trauma, is the most common cause of AI.7 OASI is a major risk factor for AI. Sultan and Thakar recently reviewed the literature and found 35 studies reporting outcomes of primary sphincter repair after delivery and found a prevalence of AI of 39% (range, 15% to 61%) over the long term.8 The severity of incontinence was related to the degree of the injury with women who had a minor (grade 3a/3b) tear having a
better outcome than those with a major (grade 3c/4) tear (P < .05) in terms of defecatory symptoms, associated quality of life, and anal manometry.8
better outcome than those with a major (grade 3c/4) tear (P < .05) in terms of defecatory symptoms, associated quality of life, and anal manometry.8
 FIGURE 56.1 Anatomy of anal canal. (Reprinted from Rao SS. Advances in diagnostic assessment of fecal incontinence and dyssynergic defecation. Clin Gastroenterol Hepatol 2010;8[11]:910-919. Copyright © 2010, with permission from Elsevier.) |
 FIGURE 56.2 Obstetric anal sphincter injury classification. (Reprinted from Rao SS. Advances in diagnostic assessment of fecal incontinence and dyssynergic defecation. Clin Gastroenterol Hepatol 2010;8[11]:910-919. Copyright © 2010, with permission from Elsevier.) |
 FIGURE 56.3 Obstetric anal sphincter injury bundle at time of delivery. |
The OASI classification described by Sultan and Thakar8 has been adopted by the International Consultation on Incontinence and the Royal College of Obstetricians and Gynaecologists (Table 56.2).
Third-degree tears occur in around 6% (1.8% in 2000 to 5.9% in 2011) of vaginal deliveries with the incidence increasing. This may be due to improved reporting as well as an increase in maternal and fetal birth weight.9 Occult sphincter injury has been reported in one-third of deliveries and may be significant cause of AI in later life.10,11 Another contributing factor to AI is levator ani avulsion and pudendal nerve denervation, which occurs more frequently during prolonged vaginal deliveries or when forceps are used.11
The most common finding is a defect in the anterior EAS, which manifests clinically as urgency of defection and urge AI. Associated disruption of the internal sphincter may cause additional symptoms of passive or stress fecal incontinence.12
However, even after fourth-degree tears, women with complete disruption of the anal sphincter complex fecal control may have reasonable fecal control, emphasizing the importance of the puborectalis and levator muscles in AI (Fig. 56.4).
TABLE 56.1 Causes of Anal Incontinence | |||||||
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TABLE 56.2 Obstetric Anal Sphincter Injury Classification | ||||||||
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Anorectal disease
Anorectal disease as well as anorectal surgery is a significant risk factor for AI. Surgery for anal fistula may involve injury to the internal sphincter, external sphincter, or both. Lateral sphincterotomy for anal fissure is done rarely in modern colorectal practice but involves deliberate partial division of the internal sphincter. Perianal Crohn disease results in fistulas, ulcers, tags, and anal stenosis, which may all cause anal leakage or soiling. Prolapsing hemorrhoids as well as full-thickness and mucosal rectal prolapse may affect closure of the anal canal and cause stretching of the internal sphincter leading to incontinence. Scleroderma is a systemic disease which often involves IAS dysfunction, minor degrees of mucosal prolapse, and fecal leakage.
Fast colorectal transit time
Women with intact continence mechanisms will sometimes leak if bowel movements are loose. Common causes of loose stools include dietary intolerances, celiac disease, irritable bowel syndrome (IBS), inflammatory bowel disease (IBD—such as Crohn and ulcerative colitis), and small intestinal bacterial overgrowth SIBO.
The majority of patients with IBS experience worsening of symptoms related to carbohydrate malabsorption and ingestion of foods high in dietary FODMAPs (fermentable oligo-, di-, and monosaccharides and polyols).13 FODMAPs are naturally occurring sugars such as lactose, fructose, sorbitol, mannitol, and sucrose found in milk and dairy products, fruits and vegetables,
cereals, and processed foods. These dietary sugars are poorly absorbed in the gut, and fermentation of the sugar by colonic flora results in an osmotic effect and gas production. In IBS sufferers, this causes functional gut symptoms such as bloating, pain, and diarrhea. Restricted intake of FODMAPs has been shown in randomized controlled trials (RCTs) to relieve symptoms of IBS in up to 75% of patients.14
cereals, and processed foods. These dietary sugars are poorly absorbed in the gut, and fermentation of the sugar by colonic flora results in an osmotic effect and gas production. In IBS sufferers, this causes functional gut symptoms such as bloating, pain, and diarrhea. Restricted intake of FODMAPs has been shown in randomized controlled trials (RCTs) to relieve symptoms of IBS in up to 75% of patients.14
Small intestinal bacterial overgrowth in certain individuals causes symptoms almost identical to IBS. Patients with SIBO may also have unexplained weight loss and less frequently, nutritional deficiencies (such as vitamin B12 and vitamin D deficiency). This condition can be treated with prolonged courses of antibiotics.13,14
 FIGURE 56.4 Sphincter defect on per rectum (PR) (A and B). Sphincter defect on visual inspection (C). |
Neurologic disorders
A wide variety of neurologic diseases of the central and peripheral nervous system can affect colonic and anorectal function and are associated with AI including cerbrovascular accident, multiple sclerosis, spina bifida, and diabetic neuropathy.
PREVENTION
Obstetric trauma resulting in OASI is one of the most important etiologic factors in the pathogenesis of AI.
Improved Detection of Occult Obstetric Anal Sphincter Injury
A prospective cohort study by Andrews et al.15 of 254 primiparous women showed that the prevalence of OASI increased significantly from 11% to 24.5% when women were more carefully examined. In this study, 98.8% of the missed OASI were subsequently detected on clinical examination by a trained research fellow prior to endoanal ultrasound.15 A Cochrane review from 2015 included a large RCT from a single center that showed a reduction of severe AI postpartum with the use of endoanal ultrasound of all second-degree tears.16 There has been reported a reduction in the rate of third- and fourth-degree tears with a care bundle involving perineal support, perineal massage, warm compresses, and medical and midwife education in in the detection and suturing of OASI17 (Table 56.3).
Forceps versus Vacuum Delivery
Forceps is an established risk factor for both anal sphincter and levator trauma. Although such trauma also occurs after normal vaginal delivery and vacuum extraction, it is much more likely after forceps.18
Forceps have shown to almost double the risk of fecal incontinence compared to vaginal birth and
cesarean section (Table 56.4).19 This may also be related to obstetrics factors that often lead to use of forceps such as macrosomia and OP position with prolonged labor rather than the forceps per se.
cesarean section (Table 56.4).19 This may also be related to obstetrics factors that often lead to use of forceps such as macrosomia and OP position with prolonged labor rather than the forceps per se.
Cesarean Section versus Vaginal Birth
A Cochrane review in 2010 concluded that cesarean section was not protective for AI, although one trial showed a possible benefit in the long term.20 In another meta-analysis in 2008 at 1 year postpartum in 12,237 women, cesarean was protective over vaginal birth with an odds ratio of 1.47.21
Women at high risk for pelvic floor dysfunction postpartum can be identified using the URCHOICE calculator developed by Drs. Bob Freeman and Don Wilson.22 The calculator is based on three large pelvic floor epidemiologic studies (SWEdish Pregnancy, Obesity, and Pelvic floor [SWEPOP] and PROlapse and incontinence LONG-term research [PROLONG] Cleveland Clinic) and gives women an individual score of their risk of urinary incontinence, prolapse, and AI for each particular pregnancy.
TABLE 56.3 Obstetric Anal Sphincter Injury Bundle at Time of Delivery | ||||
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TABLE 56.4 Logistic Regression Subsidiary Models of More Severe Urinary Incontinence and More Severe Fecal Incontinence and Delivery Mode History | ||||||||||||||||||||||||||||||||||||||||||||||||
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Subsequent Delivery following Overt or Occult Obstetric Anal Sphincter Injury
Women who have already sustained a third-degree tear have a 17% risk of developing worsening symptoms after subsequent vaginal delivery.23
There are no systematic reviews or RCTs to suggest the best method of delivery following OASI. Scheer et al. performed a prospective study of pregnant women with a history of OASI. Women who had a sonographic defect of the external sphincter of more than 30° and with a squeeze pressure of less than 20 mm Hg were offered a cesarean section. All other women were advised to have a vaginal delivery. Short-term follow-up of this cohort of 73 women showed that the women who underwent vaginal delivery suffered no significant deterioration in anal sphincter function or quality of life.24
Women with OASI at high risk for AI should ideally be followed up in a dedicated perineal clinic with the availability of endoanal ultrasound and manometry and be managed by a multidisciplinary team with colorectal surgeons, physiotherapists, and urogynecologists.
CLINICAL EVALUATION
Symptoms
AI can be classified as either active or passive. Active incontinence involves severe urgency, often brought on by exercise including walking. Active incontinence is usually due to injury or dysfunction of the EAS. It is worse with loose or liquid stool but may also occur with formed or solid stool. Passive incontinence is loss of small amounts of solid or liquid stool or mucus which is often insensible. It is usually due to injury or
dysfunction of the internal sphincter. Patients may present with mainly active or mainly passive incontinence depending on the cause of their incontinence, although a proportion will have both. Postdefecatory fecal soiling is a form of incontinence that can occur when there is incomplete closure of the anal sphincter or incomplete emptying of the rectum during defecation. This can be due to space occupying lesions such as hemorrhoids or in functional conditions such as obstructed defecation (Table 56.5).
dysfunction of the internal sphincter. Patients may present with mainly active or mainly passive incontinence depending on the cause of their incontinence, although a proportion will have both. Postdefecatory fecal soiling is a form of incontinence that can occur when there is incomplete closure of the anal sphincter or incomplete emptying of the rectum during defecation. This can be due to space occupying lesions such as hemorrhoids or in functional conditions such as obstructed defecation (Table 56.5).
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