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Fecal incontinence in adults: Etiology and evaluation

Fecal incontinence in adults: Etiology and evaluation
Authors:
Kristen M Robson, MD, MBA, FACG
Anthony J Lembo, MD
Section Editor:
Nicholas J Talley, MD, PhD
Deputy Editor:
Shilpa Grover, MD, MPH, AGAF
Literature review current through: Jul 2022. | This topic last updated: Aug 30, 2022.

INTRODUCTION — Fecal incontinence has a significant social and economic impact and significantly impairs quality of life [1-4]. Fecal incontinence can contribute to the loss of the ability to live independently [5-7]. This topic will review the etiology and evaluation of fecal incontinence in adults. Our recommendations are largely consistent with the American College of Gastroenterology and European clinical practice guidelines [8,9]. The management of fecal incontinence in adults is discussed in detail separately. (See "Fecal incontinence in adults: Management".)

TERMINOLOGY AND CLASSIFICATION

Fecal incontinence is defined as the involuntary loss of solid or liquid feces.

Anal incontinence is defined as the involuntary loss of solid or liquid feces or flatus.

Based on the mechanism of incontinence, fecal incontinence is divided into the following:

Urge incontinence is characterized by the desire to defecate, but incontinence occurs despite efforts to retain stool.

Passive incontinence is characterized by the lack of awareness of the need to defecate before the incontinent episode.

EPIDEMIOLOGY

Prevalence — Studies possibly underestimate the prevalence of fecal incontinence as many patients are reluctant to report it [10]. Estimates of the prevalence of fecal incontinence vary depending upon the definition used and the study population [11-15]. In a United States population-based survey of 71,812 individuals, 10,033 respondents (14 percent) had experienced fecal incontinence, among whom 3094 respondents (33 percent) reported stool leakage within the past week [16]. In the Rome Foundation Worldwide Study involving 54,127 individuals in 26 countries, the prevalence of fecal incontinence defined as recurrent uncontrolled passage of fecal material for more than three months was 1.6 percent (1.5 to 1.7) [17]. In a systematic review of 38 studies with sample sizes ranging from approximately 300 to over 20,000 individuals, the median prevalence of fecal incontinence was 7.7 percent (range 2 to 21 percent) [15]. Although the prevalence of fecal incontinence increased with advancing age, the rates were similar in men and women (8.1 versus 8.9 percent) [15]. In an observational study that included 5560 women aged 82 to 87 years, the prevalence of fecal incontinence was higher among non-community dwellers versus community-dwelling women (14 versus 10 percent) [18]. In a cross-sectional survey of over 64,000 women ages 62 to 87 years included in the Nurses' Health Study, the prevalence of dual urinary and fecal incontinence was 7 percent, and of fecal incontinence alone was 4 percent [19].

Risk factors — Risk factors for fecal incontinence include [15,18,20-22]:

Older age

Diarrhea

Fecal urgency

Urinary incontinence

Diabetes mellitus

Hormone therapy

Hormone therapy is associated with an increased risk of fecal incontinence among postmenopausal women. In a study of over 55,000 women participating in the Nurses' Health Study, the risk of developing fecal incontinence was increased in both past and current users of hormone therapy (hazard ratio [HR] 1.3, 95% CI 1.2-1.3 and HR 1.3, 95% CI 1.2-1.5, respectively) [23].

PHYSIOLOGY OF DEFECATION — The processes involved in normal defecation are complex, involving a sequence of events that are initiated by the entry of stool into the rectum (figure 1) [24]. Progressive rectal distension leads to reflex relaxation of the internal anal sphincter. The urge to defecate increases as stool continues to enter the rectum from the sigmoid colon. When defecation is desired, the anorectal angle is voluntarily straightened (which is facilitated by squatting or sitting), and abdominal pressure is increased by straining. This results in descent of the pelvic floor, contraction of the rectum, and inhibition of the external anal sphincter, thereby evacuating the rectal contents.

Continence depends upon a number of factors including cognitive function, stool volume and consistency, colonic transit, rectal distensibility, anal sphincter function, anorectal sensation, and anorectal reflexes. Within the anorectum, anatomic barriers that help preserve continence include the rectum, the internal anal sphincter, external anal sphincter, and puborectalis muscle.

The rectum contains three distinctive semilunar mucosal folds, which help to maintain its capacitance. The rectum can accommodate up to 300 mL without any significant increase in intraluminal pressure. Beyond 300 mL of volume, the intraluminal pressure increases and results in a feeling of urgency [24]. Retrograde colonic cyclic motor patterns have been hypothesized to act as a "rectosigmoid brake" to limit filling of the rectum [25,26].

The internal anal sphincter is a thickened, circular smooth-muscle layer innervated by the enteric nervous system. It is tonically contracted and accounts for 80 to 85 percent of the anal canal resting pressure. The internal anal sphincter relaxes transiently in response to rectal distension, a reflex known as the anorectal inhibitory reflex. The role of the anorectal inhibitory reflex is not entirely clear, although it may permit the sampling of rectal contents by sensory receptors in the anal canal, thereby helping to distinguish solid from liquid stool or gas. It does not appear to be essential for continence since continence is preserved even with an absent anorectal inhibitory reflex, as typically occurs following ileoanal anastomosis [27].

The external anal sphincter and the puborectalis muscle represent the voluntary components of fecal continence, since they are composed of striated muscle with somatic innervation (the external anal sphincter by the pudendal nerve and the puborectalis muscles by pelvic branches of S3 to S4). Despite their independent innervation, the external anal sphincter and puborectalis muscle function as a unit. Contraction of the external anal sphincter normally doubles the pressure in the anal canal, although this pressure cannot be sustained for more than a few minutes. A spinal reflex causes the external anal sphincter to contract during sudden increases in intraabdominal pressure, such as coughing or lifting, thereby helping to maintain continence [28].

The puborectalis muscle is part of the pelvic diaphragm, which consists of the levator ani, pubococcygeus, iliococcygeus, and the puborectalis muscle. The puborectalis muscle originates from the pubic arch, loops posteriorly behind the rectum and then travels back to the pubic arch, thereby forming a sling around the anorectum. This angle (which is typically between 80 and 110 degrees at rest, and less than 80 degrees during voluntary squeeze) helps maintain continence by forming an anatomic barrier against the discharge of stool. Dysfunction of the levator ani muscle appears to have a strong association with the severity of incontinence [29].

ETIOLOGY AND PATHOGENESIS — Loss of continence can result from dysfunction of the anal sphincters, abnormal rectal compliance, decreased rectal sensation, altered stool consistency, or a combination of any of these abnormalities. Incontinence is usually multifactorial, since these abnormalities often coexist. Mild impairment of any one mechanism will usually not cause incontinence, since the other mechanisms for maintaining continence can usually compensate. Patients with urge incontinence often have weakness of the external anal sphincter as well as decreased rectal capacity and rectal hypersensitivity, and patients with passive fecal incontinence often have weakness of the internal anal sphincter. Some of the more common causes of incontinence will be discussed below (table 1).

Anal sphincter weakness — Anal sphincter weakness may be due to traumatic or atraumatic causes. Atraumatic causes of anal sphincter weakness include neurologic disorders such as diabetes or spinal cord injury, or infiltrative disorders (eg, systemic sclerosis). Decreased anal sphincter pressures can result from anal trauma, such as after childbirth or surgery on the anal sphincter or surrounding structures (eg, anal fistulas, hemorrhoids, or uncommonly after injection of botulinum toxin for anal fissures) [30-32].

Anal sphincter laceration or trauma to the pudendal nerve during vaginal delivery may result in fecal incontinence. Fecal incontinence may occur immediately or many years after delivery [33]. Risk factors for fecal incontinence after vaginal delivery include the use of forceps, a high-birthweight infant, a long second stage of labor, and occipitoposterior presentation of the fetus [34]. However, all anal sphincter tears do not result in fecal incontinence. A systematic review that included more than 100 patients who underwent endoanal ultrasonography after vaginal delivery estimated that anal sphincter defects were detectable in 27 percent of primiparous women, but only 29 percent of women with an anal sphincter defect were symptomatic [35]. In a population-based study, rectal urgency, rather than obstetrical sphincter injury, appeared to be the main risk factor for fecal incontinence in women [36]. (See "Fecal and anal incontinence associated with pregnancy and childbirth: Counseling, evaluation, and management".)

Decreased perception of rectal sensation — Rectal hyposensitivity may be detected in patients with fecal incontinence or constipation. A number of conditions are associated with impaired rectal sensation including diabetes mellitus, Parkinson disease, and spinal cord injuries [37]. Patients with diabetes mellitus can have reduced internal anal sphincter resting pressure, which may result in incontinence. Diarrhea secondary to autonomic neuropathy may also contribute to fecal incontinence in these patients. (See "Diabetic autonomic neuropathy of the gastrointestinal tract".)

Decreased rectal compliance — Decreased rectal compliance leads to increased frequency and urgency of bowel movements because the ability of the rectum to store fecal matter is reduced. This can lead to fecal incontinence even if sphincter function is normal. Disorders associated with decreased rectal compliance include ulcerative proctitis, radiation proctitis, and proctectomy [24,38]. (See "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults", section on 'Clinical manifestations' and "Radiation proctitis: Clinical manifestations, diagnosis, and management", section on 'Clinical manifestations'.)

Overflow — Fecal retention and fecal impaction are common causes of fecal incontinence in older adults. Hard stool results in fecal impaction that produces constant inhibition of internal anal sphincter tone, permitting leakage of liquid stool around the impaction. A number of factors may contribute to the development of fecal impaction in older adults including impaired cognitive function, immobility, rectal hyposensitivity, and inadequate intake of fluids. (See "Constipation in the older adult", section on 'Pathophysiology'.)

Idiopathic — Idiopathic fecal incontinence occurs most commonly in middle-aged or older women. Although by definition, the cause cannot be identified, it is probably due to denervation of pelvic floor muscles resulting from stretch injury to pudendal and sacral nerves as might occur following a prolonged vaginal delivery or defecatory straining and is often associated with disorders of the anal sphincters/puborectalis, rectal capacity or sensation [39,40].

EVALUATION — Evaluation of patients with fecal incontinence begins with a history, physical examination, and endoscopic evaluation. In patients who fail to respond to initial management, we perform additional testing to detect functional and structural abnormalities of the anal sphincters, the rectal wall, and the puborectalis muscle and provide a better understanding of the underlying pathophysiology that is needed to guide management. (See "Fecal incontinence in adults: Management", section on 'Initial management'.)

History — Screening for fecal incontinence is important because many individuals do not discuss their symptoms with health care providers [41]. The history should initially focus on determining whether fecal incontinence is truly present, and its severity. True incontinence must be differentiated from frequency and urgency without loss of bowel contents [42]. Questions should focus on the onset, duration, frequency, amount (small stain, moderate amount but not a full bowel movement or a full bowel movement), type of leakage (solid, liquid, or gas), presence of urgency, nocturnal episodes, and precipitating events (occurring in the setting of diarrhea, medication use). The presence of lower back or perineal pain and motor or sensory symptoms in the lower extremities, and urinary incontinence are suggestive of a neurologic cause of incontinence (eg, spinal cord lesion). A history of prior anorectal surgery, pelvic irradiation, diabetes, or neurologic disease should be sought. Obstetric history should include the number of vaginal deliveries, prolonged labor, the use of forceps, and perineal laceration. The patient should also be asked if tissue ever protrudes from the anal canal to suggest the presence of hemorrhoidal disease or a rectal prolapse.

Physical examination — The physical examination should include inspection of the perianal area and a digital rectal examination. Inspection of the perianal area may reveal chemical dermatitis, suggesting chronic incontinence, a fistula, prolapsing hemorrhoids, or rectal prolapse. Perianal sensation should be tested by evoking the anocutaneous reflex (anal wink sign). This is done with a cotton swab by gently stroking the perianal skin towards the anus and observing a reflexive contraction of the external anal sphincter [43]. An anal wink should be elicited bilaterally. The absence of this reflex suggests nerve damage and interruption of the spinal arc.

Digital rectal examination should be performed to detect anal pathology (such as a mass or fecal impaction) and provide a basic assessment of the anal resting tone that is mostly due to tonic contraction of the internal anal sphincter. Patients should be instructed to bear down and then to squeeze against the finger, which permits appreciation of the movement and angle of the puborectalis muscle, pelvic floor descent, and squeeze pressure [44,45]. Weak squeeze pressure and normal contraction of the puborectalis suggests the presence of external anal sphincter weakness.

Laboratory studies — In patients with diarrhea, we perform stool studies to determine the underlying etiology. The evaluation of patients with chronic diarrhea is discussed in detail, separately. (See "Approach to the adult with chronic diarrhea in resource-abundant settings", section on 'Initial evaluation'.)

Endoscopy — In patients who are ≤40 years and are at average risk for colon cancer, we perform a flexible sigmoidoscopy to exclude mucosal inflammation or masses. In patients older than 40 years and in patients with persistent or unexplained chronic diarrhea or risk factors for colorectal cancer or inflammatory bowel disease, we perform a colonoscopy. (See "Screening for colorectal cancer: Strategies in patients at average risk".)

Additional studies — In patients who fail to respond to initial management, we perform anorectal manometry and endorectal ultrasound or magnetic resonance imaging (MRI). We reserve defecography for patients who have refractory symptoms, especially if surgery is being considered. (See "Fecal incontinence in adults: Management", section on 'Subsequent management'.)

Anorectal manometry — Anorectal manometry can diagnose functional sphincter weakness and can detect abnormal rectal sensation, which is an important predictor of response to biofeedback training. Decreased resting pressure suggests isolated internal anal sphincter dysfunction, while decreased squeeze pressure suggests isolated external anal sphincter dysfunction. Patients with severe weakness of the external anal sphincter may have prolapsed rectum [46]. Anorectal manometry can measure parameters such as maximal resting anal pressure, amplitude and duration of squeeze pressure, the rectoanal inhibitory reflex, threshold of conscious rectal sensation, rectal compliance, and rectal and anal pressures during straining [47]. High-resolution anorectal manometry and three-dimensional high-definition anorectal manometry (HDAM) provide greater anatomic detail than water-perfused manometry. Additionally, HDAM assesses for anal sphincter symmetry and defects [48,49].

Rectal sensation can be assessed by inflating a rectal balloon to detect the threshold (smallest volume of rectal distension) for three common sensations: the first detectable sensation (rectal sensory threshold), the sensation of urgency to defecate, and the sensation of pain (maximum tolerable volume). (See "Fecal incontinence in adults: Management", section on 'Biofeedback'.)

Endorectal ultrasound/magnetic resonance imaging — Structural abnormalities of the anal sphincters, the rectal wall, and the puborectalis muscle can be detected with endorectal ultrasound or magnetic resonance imaging (MRI) (image 1A-B) [50]. The internal sphincter is visualized more clearly by endoanal ultrasound, whereas MRI is superior for discriminating between an external anal sphincter tear and a scar and for identifying external sphincter atrophy [8].

A defect in the internal anal sphincter is accompanied by lower resting pressures while external anal sphincter defects are associated with lower anal squeeze pressure [51]. Furthermore, the size of the external anal sphincter defect inversely correlates with the maximum squeeze pressure [52]. (See "Endorectal endoscopic ultrasound (EUS) in the evaluation of fecal incontinence".)

Defecography — Defecography (barium defecography or MRI defecography) should be performed in patients with refractory fecal incontinence, especially if surgery is being considered. Defecography can detect enteroceles, rectoceles and rectal prolapse in addition to evaluating the length of the anal sphincter, anorectal angle, and pelvic descent.

Barium defecography is performed by instilling a barium paste into the rectum while, with the patient seated on a radiolucent commode, films are taken of the anorectal anatomy at rest and during straining and defecation. MRI defecography (also known as dynamic MRI imaging) has the advantage of better resolution of soft tissue surrounding the rectum and anal canal, better visualization of the anal sphincter and levator ani muscles with endoanal MRI, and avoidance of radiation. In contrast to barium defecography, which is performed in the seated position, MRI defecography is performed in the supine position [53,54].

Other

Balloon expulsion test – We perform a balloon expulsion test in patients with fecal impaction and overflow fecal incontinence in order to identify dyssynergic defecation. (See "Etiology and evaluation of chronic constipation in adults", section on 'Balloon expulsion' and "Etiology and evaluation of chronic constipation in adults", section on 'Dyssynergic defecation'.)

Pudendal nerve terminal latency and saline infusion test have no role in the evaluation of fecal incontinence [55].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Fecal incontinence".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Fecal incontinence (The Basics)")

Beyond the Basics topics (see "Patient education: Fecal incontinence (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Fecal incontinence is defined as the involuntary loss of solid or liquid feces. Anal incontinence is defined as the involuntary loss of solid or liquid feces or flatus. Fecal urge incontinence is characterized by the desire to defecate, but incontinence occurs despite efforts to retain stool. Passive fecal incontinence is characterized by the lack of awareness of the need to defecate before the incontinent episode. (See 'Terminology and classification' above.)

Continence depends upon a number of factors including cognitive function, stool volume and consistency, colonic transit, rectal distensibility, anal sphincter function, anorectal sensation, and anorectal reflexes. Within the anorectum, anatomic barriers that help preserve continence include the rectum, the internal anal sphincter, external anal sphincter, and puborectalis muscle. (See 'Physiology of defecation' above.)

Loss of continence can result from dysfunction of the anal sphincters, abnormal rectal compliance, decreased rectal sensation, or a combination of any of these abnormalities. Incontinence is usually multifactorial, since these derangements often coexist. Mild impairment of any one mechanism will usually not cause incontinence, since the other mechanisms for maintaining continence can usually compensate (table 1). (See 'Etiology and pathogenesis' above.)

Initial evaluation in a patient with fecal incontinence consists of a focused history, physical examination, and endoscopic evaluation to rule out colonic inflammation or neoplasia. In patients with diarrhea, we perform laboratory studies to determine the underlying etiology. (See 'History' above and 'Physical examination' above and "Approach to the adult with chronic diarrhea in resource-abundant settings", section on 'Initial evaluation'.)

In patients who fail to respond to conservative measures, we perform anorectal manometry and endorectal ultrasound or magnetic resonance imaging. We reserve defecography for patients who have refractory symptoms, especially if surgery is being considered (table 2). (See 'Additional studies' above and "Fecal incontinence in adults: Management", section on 'Refractory symptoms'.)

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