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James Oliver Keck
Peter L. Dwyer
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
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
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
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;8:910-919. 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;8:910-919. 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
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
Anal sphincter dysfunction (congenital malformation, radiation, OASI, anal surgery, perianal fistulas, sexual abuse)
Rectal disorders (IBS, radiation, rectocele, rectal intussusception, rectal prolapse, fecal impaction)
Neurologic disorders (spinal cord, stroke, MS, spina bifida, diabetic neuropathy, obstetric nerve damage)
Myopathy (systemic scleroderma)
Fast colorectal transit time (chronic diarrhea, IBS)
Psychological (encopresis, dementia)
MS, multiple sclerosis.
From Sultan AH, Monga A, Lee J, et al. An International Urogynecological Association (IUGA)/International Continence Society (ICS) joint report on the terminology for female anorectal dysfunction. Neurourol Urodyn 2017;36(1):10-34.
TABLE 56.2 Obstetric Anal Sphincter Injury Classification
Injury to perineal skin and/or vaginal mucosa
Injury to perineum involving perineal muscles but not involving the anal sphincter
Injury to perineum involving the anal sphincter complex: grade 3a tear: less than 50% of EAS thickness torn; grade 3b tear: more than 50% of EAS thickness torn; grade 3c tear: both EAS and IAS torn
Injury to perineum involving the anal sphincter complex (EAS and IAS) and anorectal mucosa
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
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
FIGURE 56.4 Sphincter defect on per rectum (PR) (A and B). Sphincter defect on visual inspection (C).
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.
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