ESSENTIALS OF DIAGNOSIS
• Inability to control elimination of rectal contents.
• Characterization of rectal contents that are uncontrolled.
• Characterization of timing of incontinence.
Continence is dependent upon rectal compliance, anorectal sensation, anorectal reflexes, and anal sphincter function. The stool consistency (liquid versus solid) and quantity of stool also affect continence. The incidence of fecal incontinence is difficult to assess due to underreporting and lack of agreement as to what constitutes incontinence (eg, minor seepage versus complete incontinence). Although it is well accepted that incontinence is more commonly found in parous women, a high prevalence also occurs in men.
In women, the external sphincter is a thin band of muscle anteriorly, and thus especially susceptible to complete transection in this location resulting in incontinence. Obstetrical trauma during delivery may cause mechanical injury to the external sphincter. There is an increased incidence of incontinence after third-degree perineal tears, multiple vaginal deliveries, and infection of an episiotomy repair.
Neurogenic causes of incontinence include pudendal nerve stretch secondary to prolonged labor or to chronic straining during defecation. Vaginal deliveries are associated with reversible pudendal nerve injury in 80% of primagravida births. The injury may be unilateral or bilateral. If the nerve injury is permanent or is repeated multiple times, denervation and weakening of the external sphincter and pelvic floor result. The neuropathy and sphincter dysfunction progress because a weakened pelvic floor is unable to withstand increased intraabdominal pressure leading to further perineal descent and stretch injury. Similarly, descending perineum syndrome leads to cumulative stretch injury. Straining causes descent of the pelvic floor resulting in stretch of the pudendal nerve over the ischial spine.
Incontinence may also result from the treatment of perianal abscesses, fistula-in-ano, or perianal Crohn’s disease due to disruption or division of the external sphincter.
Other causes of incontinence include systemic diseases affecting either the muscular or neurologic systems (eg, scleroderma, multiple sclerosis, dermatomyositis, and diabetes) or local anorectal problems (eg, radiation proctitis with fibrosis and decreased rectal compliance and tumors of the distal colon and rectum). Incontinence may also occur in people with normal anorectal neuromuscular function due to diarrhea or fecal impaction with overflow incontinence.
A. Symptoms and Signs
It is important to distinguish complete incontinence (which has major social consequences and virtually always denotes a significant neurologic or muscular disorder) from partial incontinence. Complete incontinence results in lack of control of gas, liquid, and solid stool. By contrast patients with partial incontinence have the ability to control solid stool but varying inability to control liquid stool and/or gas. Urgency, seepage, and soiling may occur regularly or intermittently, depending on the nature of the stool presenting to the rectum. Seepage of small amounts of fecal-stained mucus is extremely common with aging due to prolapsed hemorrhoidal tissue and inadequate dietary fiber. Soiling with urgency may be seen in patients with normal sphincteric function but a poorly distensible rectum due to proctitis or irritable bowel syndrome. However patients complaining of gross incontinence of solid fecal matter or an inability to sense stool until after incontinence has occurred often have a neurologic or muscular injury. Physical examination should include inspection and digital examination. On inspection, one should look for evidence of seepage or maceration of the perianal skin. The presence of external hemorrhoids or prolapsed internal hemorrhoids should be noted. Patients with gross incontinence may have a patulous anus. The anus should be inspected when the patient is instructed to squeeze: damage to the external sphincter may result in asymmetry or focal loss of corrugation of the anal verge. The patient should be instructed to perform a Valsalva to look for exaggerated descent of the perineum with straining or prolapse of hemorrhoidal tissue. Neurologic function is assessed grossly by looking for an anal wink and by testing for cutaneous pinprick sensation on both sides of the perianal gluteal region. Digital examination may detect a reduction in resting sphincter tone (primarily internal sphincter) or diminished voluntary squeeze pressures (primarily external sphincter).
B. Laboratory and Imaging Studies
Patients with incontinence warrant anoscopy and proctoscopy to exclude fissures, fistula, hemorrhoidal disease, proctitis, and anorectal neoplasms. Further evaluation usually is not required in patients with minor seepage alone. Patients with complete or partial incontinence usually warrant further evaluation. Anorectal manometry, transrectal ultrasound, and pudenal nerve latency studies may all be part of the evaluation of the incontinent patient.
Anorectal manometry defines the presence of sphincteric injury by measuring the resting pressure, maximum squeeze pressure, sphincter length and symmetry, minimum sensory volume, presence or absence of the rectoanal inhibitory reflex, and ability to relax the puborectalis muscle. Normal resting pressures generally range from 40-80 mm Hg and maximal squeeze pressures range from 80-l60 mm Hg. The minimum sensory volume is approximately 10 mL. The rectoanal inhibitory reflex is seen as a decrease in resting anal pressure when an air-filled balloon distends the rectum. The ability of the patient to relax the pelvic floor appropriately during defecation is assessed with the balloon expulsion test, which requires the patient to expel a fully inflated 60-mL latex balloon.
Transrectal ultrasound of the internal and external sphincters can provide imaging of anal sphincter defects. Transrectal ultrasound has largely replaced electromyography (EMG) for documentation of sphincter injury.
Pudendal nerve latency studies define the presence of neurologic injury in incontinent patients. If one or both nerves are injured success in surgical or nonsurgical treatment of incontinence may be diminished. The study is performed by placing a gloved finger with a stimulating electrode at the tip of the finger in the rectum and stimulating the pudendal nerve as it traverses the ischial spine. An electrode at the base of the examining finger records the delay between stimulation and contraction of the external sphincter. A normal “delay” is 2.0 ± 0.2 seconds. This may be prolonged with age, after childbirth, in individuals with a history of excessive straining to defecate and perineal descent, and in certain systemic disease states such as diabetes and multiple sclerosis.
The causes of incontinence are discussed above. In addition, incontinence may result from obstructed defecation secondary to tumor or intussusception. Rare patients with straining to defecate may develop intussusception, causing obstruction and apparent constipation. After straining is stopped, there is uncontrolled release of fluid. This may be detected by defecography. Chronic straining at defecation stretches the pudendal nerve over the ischial spine, leading to “idiopathic fecal incontinence” in the elderly.
Patients with seepage or minor incomplete incontinence may be treated with conservative measures. Patients should be given fiber supplements to reduce stool liquidity and mucus seepage after bowel movements. Symptomatic hemorrhoids should be treated. Patients should be instructed to cleanse the perinal area with Tucks™ or nonperfumed lanolin wipes but should avoid excessive cleansing with water or soaps, which may lead to irritation and dermatitis. Application of a cotton ball adjacent to the anus after bowel movements may absorb small amounts of seepage. Patients with urgency due to irritable bowel syndrome or proctitis may benefit from use of loperamide. Partial incontinence caused by weakness of the external sphincter or decreased rectal sensation secondary to incomplete neurologic injury or aging may respond to retraining with biofeedback and sphinteric muscle exercises.
If a sphincteric defect is limited and there is no neurologic injury, surgical correction with an overlapping sphincter reconstruction restores continence by reestablishing a complete ring of muscle. However, if there is extensive loss of sphincter muscle or severe neurologic injury, simple overlapping repair is not as successful, and consideration must be given either to colostomy or to muscle flap or encirclement procedures. The stimulated gracilis, gracilis, and gluteal muscle flap procedures have been reserved for those patients with complete neurologic injury or extensive muscle loss who wish to avoid a colostomy. Success with these muscle wrap procedures is limited. A new artificial sphincter is under trial and early reports are promising.
Anal encirclement procedures with foreign material have been reserved for the critically ill or patients with a short life expectancy. The anal canal is encircled with either a synthetic mesh or a silver wire. Patients are given daily enemas to evacuate the rectum providing a form of continence with artificial obstruction and stimulated evacuation. The foreign body is prone to infection and erosion into the rectum, which often necessitates removal.
Incontinence associated with rectal prolapse resolves after repair of the prolapse if there has not been significant nerve injury. Prior to repair, the prolapsing segment stimulates the rectoanal inhibitory reflex decreasing internal sphincter pressure, and impairing the external sphincter. The incontinence resolves with surgical repair in roughly 70% of patients.
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Source: Mark Lane Welton, MD
Portions of this article are reprinted from Way LW, Doherty GM (eds): Current Surgical Diagnosis & Treatment, 11th ed. New York: McGraw-Hill, 2003