10/1/2015 - Catherine A. Matthews, MD
Fecal incontinence is defined as the involuntary loss of liquid or solid stool, whereas anal incontinence, commonly termed “accidental bowel leakage” (ABL), also includes the loss of flatus. The prevalence of ABL in large ambulatory populations ranges from 1% to over 20%. The biggest identified risk factors include diarrhea and advancing age.
The normal storage and evacuation of stool relies on complex neurologic and anatomic factors including normal intestinal tract motility, stool consistency, rectal compliance, anorectal sensation and anal sphincter function. The anus is separated from the rectum by the dentate line that demarcates the transition from stratified to columnar epithelium and from somatic to autonomic innervation. The sensitive somatic nerves of the anal canal are able to sample the contents of the rectum during the rectoanal inhibitory reflex, which occurs after a bolus of fecal material is delivered to the rectum.
The anal sphincter complex is made up of the internal (IAS) and external anal sphincters (EAS) that provide both resting and increased voluntary tone of the anal canal. The IAS is a condensation of the circular smooth muscle of the bowel wall that provides 75% of the resting tone and serves as the primary barrier against stool leakage. The EAS is made up of striated muscle and is innervated by the pudendal nerve. The external sphincter and puborectalis muscle provide the voluntary components of fecal continence.
Fecal incontinence may be caused by anatomical abnormalities including effects on the sphincter, puborectalis, or nerve injury, including the pudendal nerve. Functional abnormities such as anorectal sensation, stool characteristics including consistency, and medications may affect continence. Anal sphincter weakness may be atraumatic (such as neurologic disorders) or traumatic, including obstetric injury and pudendal nerve injury. Additionally, rectal urgency is a significant risk factor for fecal incontinence in women. The greatest risk factor for anal sphincter injury is operative vaginal delivery (forceps higher risk than vacuum), followed by primiparity, midline episiotomy, occiput posterior head position, macrosomia, and prolonged second stage.
Evaluation should include a comprehensive medical, surgical, and obstetric history, to include distinguishing true incontinence form urgency, medications, and signs/symptoms of neurologic disease. Questions should include the onset and duration of symptoms, the quality and consistency of the stool that is successfully stored versus leaked, and the patient's bowel habit history. Physical examination includes evaluation of the perianal area and digital rectal examination, as well as assessment of perineal sensation and evaluation of pelvic support. Digital exam may evaluate for sphincter tone and weakness but may not always provide accurate assessment. Potentially helpful diagnostic tests include sigmoidoscopy or colonoscopy, endoanal ultrasonography, and anal manometry. Ultrasound effectively evaluates anal sphincter anatomy, while anal manometry provides information about rectal sensation and compliance.
Management includes medications to decrease colonic motility (Loperamide, Immodium, Cholestyramine), stool bulking agents, biofeedback, a vaginal insert with a balloon that obstructs the rectum, sphincter bulking agents, sacral neuromodulation and surgery. Maintaining normal stool consistency and frequency is imperative, regardless of the integrity of the anal sphincter complex. Sphincteroplasty is reserved for women with evidence of an anatomic defect who do not respond to initial management, Short-term benefit is achieved in over 80% of patients; however, long-term success rates only approximate 50%.
American College of Gastroenterology Clinical Guideline: Management of Benign Anorectal Disorders. Am J Gastroenterol 2014; 109: 1141
Initial Approval: 5/1/2015, Reaffirmed: 11/1/2016
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