EPIDEMIOLOGY

The inability to control feces is a devastating problem. Many people find this problem socially incapacitating and stay home, thus minimizing social contact to avoid an embarrassing situation. To estimate the number of people afflicted with fecal incontinence is difficult because many do not mention the problem to their caregivers. In a study by Johanson and Lafferty (1996), only about a third of patients discussed their incontinence with their physicians. Others incorrectly describe their symptoms and may refer to their incontinence as “diarrhea,” making it difficult for the physician to understand the problem without careful questioning. Thus, estimates probably grossly underreport the prevalence, which ranges from 0.1% to 18%. Studies in the United States found an overall prevalence of 18.4%, with a higher prevalence of 26% in patients who visited a gastroenterologist. Definitions of fecal incontinence also vary from report to report, making comparisons difficult.

Caring for incontinent patients is a tremendous financial responsibility. Over $400 million is spent annually on adult diapers, and fecal and urinary incontinence are primary reasons for nursing home placement (outnumbering senile dementia). Fecal incontinence probably increases progressively with age, although it can affect all ages, even children. It affects men as well as women, and some studies find men affected more commonly than women.

ETIOLOGY

Defecation is a complex process that involves an intricate interaction between anal function and sensation, rectal compliance, stool consistency, stool volume, colonic transit, and mental alertness. An alteration in any of these can lead to incontinence. Box 24-1 lists some common causes of fecal incontinence.

A large component of continence is the function of the anal sphincter complex. It consists of the internal anal sphincter (IAS) muscle, the external anal sphincter (EAS) muscle, and the puborectalis (PR). The smooth muscle of the IAS is innervated by the autonomic nervous system. The IAS is responsible for more than half of the resting tone. The striated muscle of the EAS is innervated by the inferior branch of the pudendal nerve and is responsible for about a third of the resting tone. Defecation is a result of voluntary relaxation of the EAS and PR that are innervated by the S3 to S4 nerves in response to rectal distension that is dictated by receptors in the pelvic floor and the anal transition zone. Anatomical disruption of the sphincter complex or disruption due to neurologic reasons is a common cause of fecal incontinence.

Childbirth is increasingly being recognized as commonly injuring the mother’s sphincter complex. In a study by Sultan et al. (1993), women were evaluated before and after childbirth, with interviews, anal physiology testing, and anal endosonography. They found that 35% of primiparous women and 44% of multiparous women had sphincter defects after delivery. The IAS was injured more often than the external sphincter—sometimes when no breach occurred in the perineal skin. A strong correlation was found between sphincter defects and the development of bowel symptoms, although only about a third of women with sphincter defects developed bowel symptoms. Incontinence may not appear until decades after the obstetric injury, so it remains to be seen how many of these women develop incontinence later in life. In the past, these patients, particularly women with delayed symptoms years after childbirth injury, were labeled with idiopathic incontinence. However, with the advent of more sophisticated evaluation techniques, defects in the sphincter complex have been found.

Fecal incontinence also appears to be associated with urinary incontinence and pelvic organ prolapse. In one study by Jackson et al. (1997), a third of women presenting to a urogynecologist for urinary incontinence also had fecal incontinence, and 7% of women with isolated pelvic organ prolapse had fecal incontinence. In another study by Tetzscher et al. (1996), 18% of women who had a previous obstetric anal sphincter disruption had both urinary and fecal incontinence. Besides obstetric injury, other causes thought to possibly contribute to both conditions include chronic constipation with straining at stool, aging, and relaxation of pelvic support.

EVALUATION

Diagnostic Testing

The use of additional testing depends on the severity of the problem and the amount of distress it causes the patient. Further tests may be helpful in establishing the diagnosis and in planning the most appropriate treatment. These tests are discussed individually.

ENEMA

To determine whether the patient is truly having incontinence, an enema may help clarify the problem. About 100 mL of tap water is given, and it is noted whether the patient can hold this for more than a few minutes. Because liquid is more difficult to control than solid stool, patients who can hold a tap water enema probably do not have significant incontinence. They may need to be questioned more carefully to fully understand their symptoms.

ANORECTAL PHYSIOLOGY TESTING

Many methods are available to assess anorectal physiology. Manometry, electromyography (EMG), rectal compliance, and pudendal nerve studies may all be helpful. Manometry provides quantitative information regarding the resting and squeeze pressures of the sphincter muscles. The resting pressures reflect the constant tone of the internal sphincter muscles. The squeeze pressures reflect the pressure generated by the external sphincter muscle. The length of the anal canal can be determined by the measured distance of these pressures. A shortened anal canal length may reflect injury to the muscle. Positive rectoanal inhibitory reflex rules out Hirschsprung’s disease (see Chapter 25).

Rectal compliance can be determined by inserting a balloon and determining the minimal volume that the rectum can sense, then sequentially inflating the balloon to a volume that cannot be tolerated. Decreased compliance signals a rectal reservoir that does not appropriately store stool and may push the fecal bolus past sphincter muscles, even if the sphincter muscle pressures are adequate. Note that normal manometric findings do not exclude incontinence, and normal people without symptoms of fecal incontinence may have abnormal manometry.

EMG is used to study the innervation of the external sphincter complex and to examine for reinnervation seen in pelvic neuropathy. Traditionally, needle EMG has been used with concentric or single-fiber electrodes, although this is quite painful for the patient. An increase in fiber density implies compensatory reinnervation after denervation of the external sphincter. Surface electrodes (attached to the skin overlying the subcutaneous portion of the external anal sphincter) give a less precise EMG but still provide some information.

Pudendal nerve terminal motor latency can be determined using an electrode attached to a glove inserted into the anal canal. A prolonged conduction in the pudendal nerve may signal damage to the innervation of the external sphincter and puborectalis muscle.

DEFECOGRAPHY

Defecography is indicated if rectal prolapse or internal intussusception (occult prolapse) is suspected. See Chapter 27 for a more thorough discussion.

COLONOSCOPY AND BARIUM ENEMA

Proctoscopy, sigmoidoscopy, colonoscopy, and barium enema are appropriate in some patients, particularly if diarrhea and blood are associated or contributing symptoms. Colitis and neoplasms can be ruled out with these tests.

ENDORECTAL ULTRASONOGRAPHY (ERUS)

Endosonography is recognized as a valuable tool in the assessment of fecal incontinence. A probe is inserted into the rectum and withdrawn through the anal canal allows for a 360-degree visualization of the internal and external anal sphincters. Particularly in patients with surgical or obstetric injury who did not develop incontinence until many years (even decades) after the insult, endosonography allows visualization of defects in the sphincter muscle, which, in turn, can lead to surgical correction. In the past, many of these patients would have been diagnosed with idiopathic incontinence, and surgical repair may have not been considered (Fig. 24-1

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