Feb 2010 – by C. Matthews, MD
Fecal incontinence (FI) is defined as the involuntary loss of liquid or solid stool whereas anal incontinence includes the loss of gas. The best estimate of the prevalence of FI in the non-institutionalized adult population in the U.S, provided by the National Health and Nutrition Examination Survey of over 5000 Americans, was 8.9% of women and 7.7% of men. The biggest identified risk factor was age, with 15% of those older than 70 affected.1
The normal storage and evacuation of stool relies on complex neurologic and anatomic factors including normal intestinal tract motility (how fast the stream is flowing downhill), stool consistency (what is in the stream), rectal compliance (how good is the dam), anorectal sensation (do you know what is in the dam and when it's full) and anal sphincter function (how good is the dam wall). With this analogy, one recognizes the myriad of important factors that affect fecal continence besides the function of the anal sphincter. Therefore, comprehensive assessment of each component is essential.
The anorectum comprises the distal 12-15 cm of the gastrointestinal tract, the termination of which are the anal mucosal folds that provide a tight seal to the outside and facilitate wiping clean after a bowel movement. Women with hemorrhoids often complain of anal seepage and inability to wipe clean because this seal is broken. 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 (RAIR), which occurs after a bolus of fecal material is delivered to the rectum, allowing one to discriminate the contents and determine when evacuation is appropriate.
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 (slow twitch, fatigue-resistant) that provides 70-75% of the resting tone but only 40% after sudden rectal distension and 65% during constant rectal distension. Therefore, the IAS is responsible for maintaining the primary barrier against stool leakage. This barrier is reinforced during voluntary squeeze of the EAS where an additional 25% of pressure can be generated. The EAS is made up of striated muscle (fast twitch, fatigable) and has three distinct components: subcutaneous, deep, and a lateral portion. The pudendal nerve, arising from S2-S4, innervates the EAS. A pudendal nerve block creates a loss of sensation in the genital and perianal skin and weakness of the anal sphincter muscle, but does not affect rectal sensation that is most likely transmitted along the S2-S4 parasympathetic nerves that traverse along the pelvic splanchnic nerves.
Obstetric anal sphincter injury (OASIS) is a clearly identified risk factor for fecal incontinence, particularly in younger women. The greatest risk factor for anal sphincter trauma is operative vaginal delivery (forceps > vacuum), followed by primiparity, midline episiotomy, occiput posterior head position, macrosomia, and prolonged second stage. Hispanic and Asian females have a significantly higher prevalence of OASIS than Caucasians or African Americans. Fecal incontinence and/or fecal urgency are reported by 20-50% of women who sustained anal sphincter trauma, with the highest prevalence in those with combined persistent defects of the IAS and EAS. Fourth-degree tears have been shown to have an increased risk of persistent bowel symptoms than third-degree tears, most likely as a result of more persistent IAS defects. 2,3 Current evidence suggests that if a primiparous woman presents with FI, there is a 76.8% chance of an anal sphincter defect being identifiable on endoanal ultrasonography.
When evaluating women with FI, it is helpful to divide etiologies between those that start outside the pelvis (affecting the contents and speed of the stream) such as chronic diarrhea (infectious, malabsorption, irritable-bowel, tumors), overflow incontinence from rectal impaction, and colorectal neoplasms. New FI, in a previously healthy woman with normal bowel habits, should prompt an investigation for neoplasms. FI secondary to pathology within the pelvis can be divided into two broad categories: 1) direct anatomic injury to the anus or anal sphincter complex or 2) neuropathic dysfunction of the pelvic floor and anal sphincter that is likely cumulative and presents later in life.4 In trying to elucidate the potential etiology of FI, targeted questions to distinguish between these disorders is imperative. A comprehensive medical, surgical, and obstetric history should be obtained. An exact understanding of the onset and duration of symptoms, the precise quality and consistency of the stool that is successfully stored versus that which is leaked, and the patient's bowel habit history should be reviewed. Physical examination should include evaluation of the perianal skin for soiling, the presence of a "dovetail" sign, presence of tissue that may preclude anal coaptation, length of the perineal body, and evaluation for pelvic organ prolapse. A gross neurologic exam includes testing the perianal skin for pinprick and light tough discrimination and stroking the perinanal skin to elicit the bulbocavernosus reflex. A digital rectal exam includes evaluating for any masses and measuring resting and squeeze anal tone.
Potentially helpful diagnostic tests include colonoscopy, endoanal ultrasonography, and anal manometry. Ultrasound effectively evaluates anal sphincter anatomy whereas anal manometry provides information about rectal sensation and compliance. Management of FI includes medications to decrease colonic motility (Loperamide, Immodium, Cholestyramine), stool bulking agents (Citrucel or Metamucil), biofeedback, and surgery. In every patient, regardless of the integrity of the anal sphincter complex, maintaining normal stool consistency and frequency is imperative. Sphincteroplasty is reserved for women with large EAS defects but long-term results are less than promising with cure rates ranging from 0-28% after an overlapping repair. Sacral neuromodulation, approved for refractory overactive bladder, is currently under investigation for FI.
- Whitehead WE, Borrud L, Goode PS, Meikle S, Mueller ER, Tuteja A, Weidner A, Weinstein M and Ye W: Fecal incontinence in US adults: epidemiology and risk factors. Gastroenterology. 137: 512-7, 517 e1-2, 2009.
- Nichols CM, Lamb EH and Ramakrishnan V: Differences in outcomes after third- versus fourth-degree perineal laceration repair: a prospective study. Am J Obstet Gynecol. 193: 530-4; discussion 534-6, 2005.
- Fenner DE, Genberg B, Brahma P, Marek L and DeLancey JO: Fecal and urinary incontinence after vaginal delivery with anal sphincter disruption in an obstetrics unit in the United States. Am J Obstet Gynecol. 189: 1543-9; discussion 1549-50, 2003.
- Jorge JM and Wexner SD: Etiology and management of fecal incontinence. Dis Colon Rectum. 36: 77-97, 1993.