eMedicine Specialties > Obstetrics and Gynecology > Prolapse and Incontinence

Fecal Incontinence: Treatment

Author: Sonia Ranganath, MD, Resident Physician, Department of Obstetrics and Gynecology, Tufts Medical Center
Coauthor(s): Tanaz R Ferzandi, MD, Assistant Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Division Director, Urogynecology and Pelvic Reconstructive Surgery, Tufts Medical Center
Contributor Information and Disclosures

Updated: Sep 30, 2009

Treatment

Medical Therapy

Conservative treatment options for fecal incontinence include bulking agents and biofeedback. After history and physical examination findings have helped exclude systemic disease and local anal pathology as the source of the patient's problem, the provider can initiate treatment.

The goal of medical therapy is to reduce stool frequency and improve stool consistency. A regular bowel regimen including daily laxatives should be established. If impacted, manual disimpaction and a daily tap-water enema may help prevent reaccumulation. The etiology of diarrhea should be diagnosed and treatment initiated. Mild incontinence can often be improved by initiating simple conservative measures. For patients with infrequent, low volume stools, bulking agents are helpful, as formed stools are easier to control than liquid stools. Methylcellulose (Citrucel) or psyllium (Metamucil, Fiberall, Hydrocil) can be taken daily. Additional firming of the stool can be obtained by restricting fluid with intake of the bulking agent. This may be helpful therapy in the patient who has incontinence of soft stool or liquid stool.

In patients with diarrhea due to noninfectious etiologies or with reduced rectal compliance due to radiation proctitis or inflammatory bowel disease, agents that slow the motility of the gut may be helpful. Loperamide hydrochloride increases gut transit time, allowing for increased absorption of water from the volume of stool. This results in a firmer, more easily controlled stool. The maximum daily dosage is 16 mg. The usual dose regimen is 2-4 mg twice or three times daily to control symptoms. An additional benefit of the opiate derivative loperamide (Imodium) is that it increases internal anal sphincter tone and may improve rectal compliance.47 Diphenoxylate hydrochloride/atropine (Lomotil) has also been used; however, diphenoxylate hydrochloride can cause dependence and is a schedule V medication under the Controlled Substance Act.

Biofeedback is a safe, minimally invasive behavioral technique that uses auditory or visual feedback to reeducate the pelvic floor musculature. Although many different therapies have been used, several studies that have demonstrated a significant improvement in fecal incontinence by treatment with biofeedback.48,49 Other data, including a recent Cochrane review, does not provide clear evidence of therapeutic benefit.50 The most commonly used techniques are rectal sensitivity training and anal sphincter strength training.

During rectal sensitivity training, a rectal balloon is gradually distended with air or water and the patient is asked to report first sensation of rectal filling. Once this threshold volume is determined, repeated reinflations of the balloon are performed with the objective being to teach the patient to feel the distension at progressively lower volumes. The rationale is that some patients are found to have high threshold volumes and if the patient detects stool arriving sooner, there is more possibility to either find a toilet or use an anal squeeze, or both. Conversely, the same technique has also be used to teach the patient to tolerate progressively larger volumes in those with urgency and a hypersensitive rectum.50

Biofeedback techniques have also been used to demonstrate anal sphincter pressures or activity to the patient, thereby enabling teaching of anal sphincter exercises and giving feedback on performance and progress. This can be achieved by using EMG skin electrodes, manometric pressures, intra-anal EMG, or anal ultrasonography. The patient is encouraged, by seeing or hearing the signal, to enhance squeeze strength and endurance. There is no consensus on an optimum exercise regimen for use at home between sessions, nor on the number of squeezes, frequency of exercises, or treatment duration. Different authors may describe very different programs.50

Biofeedback requires some rectal sensation and the ability to voluntarily contract the sphincter. It appears to be effective for neurogenic and idiopathic anal incontinence and for incontinence related to disruption of anal sphincters49 , but a recent Cochrane review did not demonstrate conclusive therapeutic benefits.50 Biofeedback's success seems to depend on improving rectal sensation, because manometric studies have not shown consistent improved sphincter pressure. Personal units are now available (without prescription) for home use after initial clinical instruction. They use a vaginally placed, air-filled sensor that provides information on force and duration of contractions. Results from biofeedback can diminish over time, but home devices provide the patient the opportunity for a prolonged course of therapy and intermittent reeducation in a private setting.

Surgical Therapy

Once medical therapy has been maximized, minimally invasive and surgical therapies may be considered. In select patients, injectable materials may provide improvement in anal sphincter function.

Several reports have described injection of various materials to augment the function of the internal anal sphincter. Injectable silicone has been shown to be effective. In a study of 82 patients with severe fecal incontinence and a low anal resting pressure caused by internal anal sphincter dysfunction, patients were randomized to silicone injection into the intersphincteric space and internal anal sphincter with (Group A, n = 42) or without (Group B, n = 40) guidance by endoanal ultrasonography. Results show that fecal incontinence improved significantly in both groups with up to 12 months of follow-up but to a greater extent in the group in whom injection was ultrasonographically guided. No serious complications occurred.51

Results with carbon-coated microbeads have been less promising. In a pilot study of 33 patients, the submucosal injection of carbon-coated microbeads improved minor fecal incontinence by increasing anal pressure but did not significantly improve quality of life.52 Experience with collagen injections has been more limited.

Several surgical procedures are performed for the treatment of anal incontinence. The type of procedure used is based on the patient history, physical examination findings, and results of diagnostic evaluation. The current philosophy in pelvic reconstructive surgery is restoration of normal anatomy. Usually, sphincter complex defects are secondary to obstetric injury, fistula repair, or lateral internal sphincterotomy. The standard procedure for anal incontinence due to anal sphincter disruption is the anterior overlapping sphincteroplasty. This procedure was first proposed by Parks et al in 1971 and modified by Slade et al in 1977.

Anterior sphincteroplasty consists of dissecting out the external anal sphincter, dividing the scar tissue in the midline, and then overlapping the scar so that muscle is approximated to muscle as closely as possible. The surgery can be performed with the patient in the prone jackknife position or the dorsal lithotomy position. Controversy exists as to the need to identify and plicate the internal anal sphincter. Its value in the continence mechanism has been discussed. Several postoperative studies have demonstrated improvement in resting and squeeze pressures, which suggest that either the internal sphincter was plicated intentionally or that the internal anal sphincter was also unintentionally plicated in the process of overlapping the scar mass. In an older study, Fang and colleagues suggest not separating the internal from the external anal sphincters; however, they do not discuss the reasoning for this.53

Several other studies have performed ultrasonography of the sphincters postoperatively, yet few specifically mention the condition of the internal sphincter. Briel et al compared 2 groups of patients who underwent surgical repair. One group had surgical repair of only the external sphincter between 1973 and 1989. The second group underwent surgical repair consisting of restoration of the rectovaginal septum, perineal body, and repair of the external and internal sphincters. These patients had surgical repair between 1989 and 1994. They found that the more complex repair conferred no advantage. The measured outcome focused on anal continence, which was restored or improved in 63% and 68%, respectively.54

For the internal anal sphincter repair, the surgical approach requires dissection along the intersphincteric plane and identification of the internal anal sphincter. The sphincter is then dissected free from the rectal mucosa and mobilized. The surgical technique varies depending on the bulk of scar tissue. The scar tissue is either divided or left intact as the sphincter is plicated.

Abou-Zeid performed isolated internal sphincter repair in 8 patients with ultrasonographically proven defects of the internal anal sphincter. All patients had anal incontinence of varying degrees. All had undergone a prior surgical procedure, such as hemorrhoidectomy or sphincterotomy, and had developed symptoms subsequently. All patients underwent preoperative ultrasonography, and 6 patients underwent postoperative endoanal ultrasonography to document internal sphincter anatomy. Continence scores improved in all patients, and 2 patients achieved complete continence.10 The small numbers of this cases series are encouraging, but do not allow for definitive conclusions.

Most reconstructive surgeons perform colporrhaphy and perineorrhaphy as part of the overall repair. Numerous articles describe the physiologic and supportive role of the rectovaginal septum and perineal body. In a study of 143 women, Weber and colleagues found that defects in the posterior compartment often coexist with bowel symptoms; however, they were unable to show a direct correlation between stage of prolapse and severity of bowel symptoms. This study did not proceed with surgical repair and evaluate for symptoms postoperatively.55 Wexner and Olivera support the philosophy of repair of all defects and suggest that failure to recognize and repair concomitant injuries of the anal sphincter mechanism is usually accompanied by continued anal incontinence.56

Pudendal nerve neuropathy is associated with a higher failure rate after sphincteroplasty. As discussed previously, Gilliland found that the only factor predictive of successful outcome of overlapping sphincteroplasty was bilaterally intact PNTML.42 Sangwan et al found that patients with unilaterally intact pudendal nerves had a less favorable outcome than those with bilaterally normal latencies.43 Chen et al evaluated patients who had normal (1), unilateral (7), or bilateral (4) prolongation of PNTML with preoperative and postoperative incontinence scores. They found significant improvement in incontinence scores among all groups. These results were sustained at 20 to 72 month follow-up.

Different studies have demonstrated that anterior overlapping sphincter repair can improve continence scores, resting pressures, and squeeze pressures regardless of pudendal nerve latencies; therefore, if sphincter disruption is present, repair should be offered. Counseling patients regarding surgical outcomes and risks is imperative.

Some researchers perform postanal repair in patients with anal incontinence from a neurogenic or idiopathic cause. This type of anal incontinence is often associated with denervation of the pelvic floor. Patients have a decreased ability to sense impending defecation and may initially become aware of the need for a bowel movement only after they have passed stool and notice the odor or sensation of fecal material around the anus. The internal and external anal sphincters are usually intact. Evaluation often demonstrates an increase in the anorectal angle, which has also been described as a "flattening" of the anorectal angle.

The original theory behind postanal repair was restoration of the anorectal angle and lengthening of the anal canal. The incision is made posterior to the anal canal and carried to the levator plate. The dissection is carried in the intersphincteric plane between the internal and external anal sphincters. Once identified, the ileococcygeus, puborectalis, and pubococcygeus muscles are plicated posterior to the rectum. The internal anal sphincter, external anal sphincter, or both can also be plicated during the procedure. This approach was first described by Sir Alan Parks, whose initial series had an 83% success rate. Many subsequent series by different investigators have been unable to match this original success rate.

In an attempt to better understand the mechanism of postanal repair, several investigators have performed preoperative and postoperative physiologic evaluation of patients. In a review of 30 patients who had undergone postanal repair, Setti Carraro et al found that 19 of the 30 patients had breaks in the internal anal sphincter (6), the external anal sphincter (4), or both (9) on endoanal ultrasonography.57 Matsuoka and colleagues performed preoperative PNTML, EMG, and manometry and found no predictive factor in the outcome of postanal repair.58 Scott et al performed manometry prior to postanal repair and were unable to show any correlation between manometry and successful outcome.

Laurberg et al performed extensive preoperative and postoperative evaluation including manometry, perineal descent, PNTML, and single-fiber EMG. They found minimal correlation with preoperative physiologic testing and successful surgical outcome. Of interest in this study is the finding of increased fiber density and prolonged PNTML in those patients who improved with surgery, suggesting damage as a result of postanal surgical repair.59 Setti Carraro et al also found postoperative prolongation of PNTML, from 2.2 milliseconds to 2.85 milliseconds, in patients with a successful surgical outcome. They found that the only preoperative factor predicting successful outcome was intact PNTML.57 Others also found that intact PNTML is associated with better surgical outcomes. These findings seem to indicate that the patient with idiopathic fecal incontinence and normal PNTML has a better chance of success compared to a patient with a neurogenic cause of incontinence.

Both Laurberg et al and Setti Carraro et al have found that postanal repair may cause trauma to the pudendal nerves that did not exist preoperatively. The potential consequences of this are not known. Jameson et al evaluated patients 2 years following postanal repair and found a decrease in the number of patients who had some benefit (83% to 53%), with only 28% who were markedly better at 2 years.60

The effect of postanal repair on the anorectal angle has also been evaluated. Bartolo and colleagues have shown that restoration of the anorectal angle does not correlate with the success of postanal repair. Failure of postanal repair to restore the anorectal angle has been confirmed by other investigators. Womack et al had improvement in 70% of 16 patients and found no significant change in the anorectal angle when measured radiographically. They recommend that the procedure not be limited to those patients with widening of the anorectal angle.61

In a comparison of anterior sphincteroplasty and postanal repair, Orrom and colleagues found no postoperative advantage for either procedure.62 They found that patients who had undergone postanal repair had no change in anorectal angle, whereas those who had undergone anterior sphincteroplasty with anterior plication of the levators had a more obtuse anorectal angle. They concluded that restoration of the anorectal angle was not important, and their group has abandoned the postanal approach. Matsuoka et al concluded that although the success rate for postanal repair was low (~35%), it is a valid therapeutic approach because of low morbidity and the absence of mortality.58 The alternative for these patients, in whom other modalities have failed, is to live with this very disabling condition, undergo diverting colostomy, or undergo muscle transfer.

Muscle-wrap techniques have been developed in which striated muscles from the gracilis or gluteus muscles are transposed and wrapped around the anal canal to increase tone. The use of the gluteus muscle has largely been replaced by gracilis transfer. These techniques create a neosphincter when there is not enough muscle present to repair. The procedure may be indicated in patients who have congenital absence of the anal sphincter or in those who have lost the anal sphincter as a result of disease, although some have undertaken this procedure after attempts at sphincter repair have failed.

To perform gracilis transfer, the muscle is mobilized while maintaining the proximal attachments and the neurovascular bundle. Care must be taken to prevent devitalization of the muscle. The muscle is tunneled and then wrapped around the anus. The distal end is sutured to the contralateral ischial tuberosity. Implantation of a nerve stimulator to the transposed muscle to aid in long-term contraction is described. Results have been good, with a success rate of 66% in a series of 139 patients.63 However, the procedure has a high complication rate and is usually performed in the research setting.64 In patients with severe anal incontinence or those in whom other procedures have failed, muscle transposition may offer an improvement in quality of life.65

The artificial bowel sphincter (Acticon Neosphincter) was designed to act as a patient's own anal sphincter in cases of severe fecal incontinence. This implantable device is produced by American Medical Systems and is available in the United States. The inflatable cuff is placed around the anus, and an inflation reservoir is placed in the space of Retzius. As the patient feels the need to have a bowel movement, a control pump is squeezed and forces water out of the cuff and into the reservoir. This allows the patient to have a bowel movement. The cuff slowly refills over several minutes. Its use in patients with fecal incontinence has been somewhat limited and recent long-term data has been disappointing. In a study of 25 patients who were followed for a median of 50 months, only 3 had good functional results with the system. Complications included infection, erosion, chronic pain, and obstructed defecation; the device removal rate was approximately 50% in this series.66

When fecal incontinence persists after medical and surgical therapies have failed, a colostomy may be considered. This converts a perineal stoma into a manageable abdominal stoma and removes the constant fear of public humiliation.

Preoperative Details

Once the decision has been made to proceed with surgical repair, mechanical bowel cleansing is performed. This can be performed with a variety of agents. Full mechanical bowel preparation with large volumes of solution is probably unnecessary, although it has some benefits for postoperative management. Smaller volumes of solution are better tolerated by patients, with some surgeons using only Fleet enemas prior to repair. The value of a more thorough preparation, such as GoLYTELY, is in the postoperative period when most surgeons are concerned about delaying mechanical stretch to the newly repaired sphincter.

Antimicrobial prophylaxis for colorectal operations can consist of an oral antimicrobial bowel preparation, preoperative parenteral antimicrobials, or a combination of both. Oral prophylaxis consists of neomycin plus erythromycin, or neomycin plus metronidazole, started no more than 18-24 hours before surgery along with a mechanical bowel preparation. Current recommendations for parenteral antibiotic prophylaxis include a third generation cephalosporin with metronidazole. A single preoperative parenteral dose of antibiotic is sufficient and should be administered within 1 hour prior to incision.67

Intraoperative Details

To minimize the risk of surgical site infections, care should be taken to keep the operative field clean from contamination. Preoperative antibiotics should be administered prior to beginning the procedure.

During overlapping sphincteroplasty, maintaining the scar tissue on the muscle belly and using this to decrease the likelihood of suture pull-through has been one of the most important factors improving surgical outcomes. The adequate mobilization of the existing scar tissue and separation of the scar in the midline to allow for overlap is also important. The judicious use of cautery to prevent devascularization is also wise.

Postoperative Details

Postoperative management after surgical treatment for fecal incontinence varies significantly according to provider. Agreement exists about the use of postoperative stool softeners and dietary fiber, and several products are available (see Medical therapy). Mineral oil may be used for a short period of time postoperatively, but long-term use is associated with absorption problems.

Specific dietary restrictions are commonly used postoperatively. Many surgeons delay feeding and keep patients on clear liquid diets or soft foods for several days. Others allow a more liberal diet and use stool softeners and mineral oil to decrease stool firmness. If a mechanical bowel preparation is used, the time to first bowel movement will be delayed, especially if the patient is kept NPO for the immediate postoperative period. Many encourage patients to use sitz baths as a means of decreasing perianal edema and to assist with cleanliness. However, some believe that osmotic gradients actually allow for more swelling and tissue maceration, and they promote the use of peribottles to wash the perineum and rectum. In these cases, showering is acceptable as the perineum is not submerged in water.

The use of postoperative antibiotics is controversial. Due to the location and nature of the tissues, infection of the surgical site is a risk; however, the blood supply to this area is rich and, unless compromised with extensive electrocautery, the need for postoperative antibiotics is questioned.

Follow-up

Due to the nature and location of the surgical repair, pain control is an important issue. Patients should have adequate access to their surgeon for additional medications as necessary. Because the rate of separation of superficial tissues is as high as 25% and because of the potential for infection, patient concerns and symptoms must be taken seriously. Evaluation by trained providers, if only to reassure the patient, allows the surgeon to detect serious complications early.

Postoperative evaluation should be scheduled for 4-6 weeks after the procedure. At this time, most postoperative swelling and tissue distortion is usually resolved. A history of the patient's bowel habits should be taken and problems addressed. If modification of the stool softener regimen is required, it can be done at this time. Mineral oil regimens should be stopped if the patient has continued these medications postoperatively. Additional follow up can be scheduled depending on the individual needs of the patient and practice of the surgeon.

Complications

The complication rate from surgical repair of the anal sphincter varies based on the series reviewed. The patient population requiring surgical repair may have significant comorbidities that predispose them to postoperative complications. A review of several series for both postanal repair and anterior sphincteroplasty reveals that most patients are in the fifth through seventh decade of life. Underlying medical conditions, such as obesity, diabetes, or heart disease, can increase the postoperative risk of myocardial infarction or deep vein thrombosis.

The most common complication is superficial separation of skin and subcutaneous tissues, and the frequency rate is as high as 25% in some series. Care must be taken to place as little tension as possible on these tissues. Conversion of the curvilinear incision into a Y-shaped incision at the time of closure can place a great deal of tension on the perineal skin and predispose it to separation. Plication of the bulbospongiosus and superficial transverse perineum muscles can remove tension from the overlying skin and serve to restore anatomy. Devascularization of the vaginal or rectal mucosa can result in necrosis of these tissues.

Risk of infection is 3-5%. Opening the wound to allow for drainage and treatment with antibiotics may allow the physician to salvage the surgical repair. Fistula formation occurs in fewer than 1% of the series reviewed, but it is more common in those cases in which infection develops.

Bleeding and hematoma formation are also possible complications. Bleeding can usually be controlled with pressure achieved with packing. Hematoma formation into the perirectal space can go unnoticed and result in the sequestration of large amounts of blood. Treatment requires evacuation of the hematoma and surgical hemostasis.

Other complications include anal stricture, fecal impaction, and pain. Pain may be associated with bowel movements and intercourse, leading to a great deal of frustration for both the provider and patient. Many of these problems improved with time. Most complications that arise do not affect the sphincter repair. Although patients may be distressed, they should be reassured that the risk of failure of the procedure is not increased.

More on Fecal Incontinence

Overview: Fecal Incontinence
Workup: Fecal Incontinence
Treatment: Fecal Incontinence
Follow-up: Fecal Incontinence
Multimedia: Fecal Incontinence
References

References

  1. [Guideline] Landefeld CS, Bowers BJ, Feld AD, Hartmann KE, Hoffman E, Ingber MJ. National Institutes of Health state-of-the-science conference statement: prevention of fecal and urinary incontinence in adults. Ann Intern Med. Mar 18 2008;148(6):449-58. [Medline].

  2. Nelson R, Norton N, Cautley E, Furner S. Community-based prevalence of anal incontinence. JAMA. Aug 16 1995;274(7):559-61. [Medline].

  3. Johanson JF, Lafferty J. Epidemiology of fecal incontinence: the silent affliction. Am J Gastroenterol. Jan 1996;91(1):33-6. [Medline].

  4. Nelson RL, Furner S. Jesudason V. Fecal Incontinence in Wisconsin nursing homes. Dis Colon Rectum. 1998;41:1226-1229.

  5. Guise JM, Morris C, Osterweil P, Li H, Rosenberg D, Greenlick M. Incidence of fecal incontinence after childbirth. Obstet Gynecol. Feb 2007;109(2 Pt 1):281-8. [Medline].

  6. Melville JL, Fan MY, Newton K, Fenner D. Fecal incontinence in US women: a population-based study. Am J Obstet Gynecol. Dec 2005;193(6):2071-6. [Medline].

  7. Nygaard IE, Rao SS, Dawson JD. Anal incontinence after anal sphincter disruption: a 30-year retrospective cohort study. Obstet Gynecol. Jun 1997;89(6):896-901. [Medline].

  8. Mellgren A, Jensen LL, Zetterstrom JP, et al. Long-term cost of fecal incontinence secondary to obstetric injuries. Dis Colon Rectum. Jul 1999;42(7):857-65; discussion 865-7. [Medline].

  9. Sung VW, Rogers ML, Myers DL, Akbari HM, Clark MA. National trends and costs of surgical treatment for female fecal incontinence. Am J Obstet Gynecol. Dec 2007;197(6):652.e1-5. [Medline].

  10. Abou-Zeid AA. Preliminary experience in management of fecal incontinence caused by internal anal sphincter injury. Dis Colon Rectum. Feb 2000;43(2):198-202; discussion 202-4. [Medline].

  11. Pretlove SJ, Thompson PJ, Toozs-Hobson PM, Radley S, Khan KS. Does the mode of delivery predispose women to anal incontinence in the first year postpartum? A comparative systematic review. BJOG. Mar 2008;115(4):421-34. [Medline].

  12. Zetterstrom J, Mellgren A, Jensen LL, et al. Effect of delivery on anal sphincter morphology and function. Dis Colon Rectum. Oct 1999;42(10):1253-60. [Medline].

  13. Abramowitz L, Sobhani I, Ganansia R, et al. Are sphincter defects the cause of anal incontinence after vaginal delivery? Results of a prospective study. Dis Colon Rectum. May 2000;43(5):590-6; discussion 596-8. [Medline].

  14. Sultan AH, Kamm MA, Hudson CN, Bartram CI. Third degree obstetric anal sphincter tears: risk factors and outcome of primary repair. BMJ. Apr 2 1994;308(6933):887-91. [Medline].

  15. Tetzschner T, Sorensen M, Rasmussen OO, et al. Pudendal nerve damage increases the risk of fecal incontinence in women with anal sphincter rupture after childbirth. Acta Obstet Gynecol Scand. Jul 1995;74(6):434-40. [Medline].

  16. Tetzschner T, Sorensen M, Lose G, Christiansen J. Anal and urinary incontinence in women with obstetric anal sphincter rupture. Br J Obstet Gynaecol. Oct 1996;103(10):1034-40. [Medline].

  17. Varma A, Gunn J, Lindow SW, Duthie GS. Do routinely measured delivery variables predict anal sphincter outcome?. Dis Colon Rectum. Oct 1999;42(10):1261-4. [Medline].

  18. Fynes M, Donnelly VS, O'Connell PR, O'Herlihy C. Cesarean delivery and anal sphincter injury. Obstet Gynecol. Oct 1998;92(4 Pt 1):496-500. [Medline].

  19. Gooneratne ML, Scott SM, Lunniss PJ. Unilateral pudendal neuropathy is common in patients with fecal incontinence. Dis Colon Rectum. Apr 2007;50(4):449-58. [Medline].

  20. Allen RE, Hosker GL, Smith AR, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol. Sep 1990;97(9):770-9. [Medline].

  21. Ryhammer AM, Laurberg S, Hermann AP. Long-term effect of vaginal deliveries on anorectal function in normal perimenopausal women. Dis Colon Rectum. Aug 1996;39(8):852-9. [Medline].

  22. Guise JM, Boyles SH, Osterweil P, Li H, Eden KB, Mori M. Does cesarean protect against fecal incontinence in primiparous women?. Int Urogynecol J Pelvic Floor Dysfunct. Jan 2009;20(1):61-7. [Medline].

  23. Haadem K, Dahlstrom JA, Ling L. Anal sphincter competence in healthy women: clinical implications of age and other factors. Obstet Gynecol. Nov 1991;78(5 Pt 1):823-7. [Medline].

  24. Bannister JJ, Abouzekry L, Read NW. Effect of aging on anorectal function. Gut. Mar 1987;28(3):353-7. [Medline].

  25. Laurberg S, Swash M. Effects of aging on the anorectal sphincters and their innervation. Dis Colon Rectum. Sep 1989;32(9):737-42. [Medline].

  26. Jameson JS, Chia YW, Kamm MA, et al. Effect of age, sex and parity on anorectal function. Br J Surg. Nov 1994;81(11):1689-92. [Medline].

  27. Rao SS. Pathophysiology of adult fecal incontinence. Gastroenterology. Jan 2004;126(1 Suppl 1):S14-22. [Medline].

  28. Miller R, Bartolo DC, Cervero F, Mortensen NJ. Anorectal sampling: a comparison of normal and incontinent patients. Br J Surg. Jan 1988;75(1):44-7. [Medline].

  29. Cornes H, Bartolo DC, Stirrat GM. Changes in anal canal sensation after childbirth. Br J Surg. Jan 1991;78(1):74-7. [Medline].

  30. Rockwood TH, Church JM, Fleshman JW, et al. Fecal Incontinence Quality of Life Scale: quality of life instrument for patients with fecal incontinence. Dis Colon Rectum. Jan 2000;43(1):9-16; discussion 16-7. [Medline].

  31. Reilly WT, Talley NJ, Pemberton JH, Zinsmeister AR. Validation of a questionnaire to assess fecal incontinence and associated risk factors: Fecal Incontinence Questionnaire. Dis Colon Rectum. Feb 2000;43(2):146-53; discussion 153-4. [Medline].

  32. Toglia MR, DeLancey JO. Anal incontinence and the obstetrician-gynecologist. Obstet Gynecol. Oct 1994;84(4 Pt 2):731-40. [Medline].

  33. Law PJ, Bartram CI. Anal endosonography: technique and normal anatomy. Gastrointest Radiol. Fall 1989;14(4):349-53. [Medline].

  34. Law PJ, Kamm MA, Bartram CI. Anal endosonography in the investigation of faecal incontinence. Br J Surg. Mar 1991;78(3):312-4. [Medline].

  35. Bartram CI, Sultan AH. Anal endosonography in faecal incontinence. Gut. Jul 1995;37(1):4-6. [Medline].

  36. Sultan AH, Kamm MA, Talbot IC, et al. Anal endosonography for identifying external sphincter defects confirmed histologically. Br J Surg. Mar 1994;81(3):463-5. [Medline].

  37. Burnett SJ, Spence-Jones C, Speakman CT, et al. Unsuspected sphincter damage following childbirth revealed by anal endosonography. Br J Radiol. Mar 1991;64(759):225-7. [Medline].

  38. Solomon MJ, McLeod RS, Cohen EK, Cohen Z. Anal wall thickness under normal and inflammatory conditions of the anorectum as determined by endoluminal ultrasonography. Am J Gastroenterol. Apr 1995;90(4):574-8. [Medline].

  39. Burnett SJ, Speakman CT, Kamm MA, Bartram CI. Confirmation of endosonographic detection of external anal sphincter defects by simultaneous electromyographic mapping. Br J Surg. Apr 1991;78(4):448-50. [Medline].

  40. Tjandra JJ, Milsom JW, Schroeder T, Fazio VW. Endoluminal ultrasound is preferable to electromyography in mapping anal sphincteric defects. Dis Colon Rectum. Jul 1993;36(7):689-92. [Medline].

  41. Felt-Bersma RJ, Cuesta MA, Koorevaar M. Anal sphincter repair improves anorectal function and endosonographic image. A prospective clinical study. Dis Colon Rectum. Aug 1996;39(8):878-85. [Medline].

  42. Gilliland R, Altomare DF, Moreira H Jr, et al. Pudendal neuropathy is predictive of failure following anterior overlapping sphincteroplasty. Dis Colon Rectum. Dec 1998;41(12):1516-22. [Medline].

  43. Sangwan YP, Coller JA, Barrett RC, et al. Unilateral pudendal neuropathy. Impact on outcome of anal sphincter repair. Dis Colon Rectum. Jun 1996;39(6):686-9. [Medline].

  44. Fynes M, Donnelly V, Behan M, et al. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet. Sep 18 1999;354(9183):983-6. [Medline].

  45. Osterberg A, Graf W, Edebol Eeg-Olofsson K, et al. Results of neurophysiologic evaluation in fecal incontinence. Dis Colon Rectum. Sep 2000;43(9):1256-61. [Medline].

  46. Chen AS, Luchtefeld MA, Senagore AJ, et al. Pudendal nerve latency. Does it predict outcome of anal sphincter repair?. Dis Colon Rectum. Aug 1998;41(8):1005-9. [Medline].

  47. Bellicini N, Molloy PJ, Caushaj P, Kozlowski P. Fecal incontinence: a review. Dig Dis Sci. Jan 2008;53(1):41-6. [Medline].

  48. Ryn AK, Morren GL, Hallbook O, Sjodahl R. Long-term results of electromyographic biofeedback training for fecal incontinence. Dis Colon Rectum. Sep 2000;43(9):1262-6. [Medline].

  49. Fynes MM, Marshall K, Cassidy M, et al. A prospective, randomized study comparing the effect of augmented biofeedback with sensory biofeedback alone on fecal incontinence after obstetric trauma. Dis Colon Rectum. Jun 1999;42(6):753-8; discussion 758-61. [Medline].

  50. Norton CC, Cody JD, Hosker G. Biofeedback and/or sphincter exercises for the treatment of faecal incontinence in adults. The Cochrane Collaboration. 2009;2:[Full Text].

  51. Tjandra JJ, Lim JF, Hiscock R, Rajendra P. Injectable silicone biomaterial for fecal incontinence caused by internal anal sphincter dysfunction is effective. Dis Colon Rectum. Dec 2004;47(12):2138-46. [Medline].

  52. Altomare DF, La Torre F, Rinaldi M, Binda GA, Pescatori M. Carbon-coated microbeads anal injection in outpatient treatment of minor fecal incontinence. Dis Colon Rectum. Apr 2008;51(4):432-5. [Medline].

  53. Fang DT, Nivatvongs S, Vermeulen FD, et al. Overlapping sphincteroplasty for acquired anal incontinence. Dis Colon Rectum. Nov 1984;27(11):720-2. [Medline].

  54. Briel JW, de Boer LM, Hop WC, Schouten WR. Clinical outcome of anterior overlapping external anal sphincter repair with internal anal sphincter imbrication. Dis Colon Rectum. Feb 1998;41(2):209-14. [Medline].

  55. Weber AM, Walters MD, Ballard LA, et al. Posterior vaginal prolapse and bowel function. Am J Obstet Gynecol. Dec 1998;179(6 Pt 1):1446-9; discussion 1449-50. [Medline].

  56. Wexner SD, Oliveira L. Anal incontinence. In: Beck DE, Wexner SD, eds. Fundamentals of Anorectal Surgery. 2nd ed. Philadelphia, Pa: WB Saunders; 1998:115-52.

  57. Setti Carraro P, Kamm MA, Nicholls RJ. Long-term results of postanal repair for neurogenic faecal incontinence. Br J Surg. Jan 1994;81(1):140-4. [Medline].

  58. Matsuoka H, Mavrantonis C, Wexner SD, et al. Postanal repair for fecal incontinence--is it worthwhile?. Dis Colon Rectum. Nov 2000;43(11):1561-7. [Medline].

  59. Laurberg S, Swash M, Henry MM. Effect of postanal repair on progress of neurogenic damage to the pelvic floor. Br J Surg. May 1990;77(5):519-22. [Medline].

  60. Jameson JS, Speakman CT, Darzi A, et al. Audit of postanal repair in the treatment of fecal incontinence. Dis Colon Rectum. Apr 1994;37(4):369-72. [Medline].

  61. Womack NR, Morrison JF, Williams NS. Prospective study of the effects of postanal repair in neurogenic faecal incontinence. Br J Surg. Jan 1988;75(1):48-52. [Medline].

  62. Orrom WJ, Miller R, Cornes H, et al. Comparison of anterior sphincteroplasty and postanal repair in the treatment of idiopathic fecal incontinence. Dis Colon Rectum. Apr 1991;34(4):305-10. [Medline].

  63. Madoff RD, Rosen HR, Baeten CG, LaFontaine LJ, Cavina E, Devesa M. Safety and efficacy of dynamic muscle plasty for anal incontinence: lessons from a prospective, multicenter trial. Gastroenterology. Mar 1999;116(3):549-56. [Medline].

  64. Baeten CG, Bailey HR, Bakka A, Belliveau P, Berg E, Buie WD, et al. Safety and efficacy of dynamic graciloplasty for fecal incontinence: report of a prospective, multicenter trial. Dynamic Graciloplasty Therapy Study Group. Dis Colon Rectum. Jun 2000;43(6):743-51. [Medline].

  65. Corman ML. Gracilis muscle transposition for anal incontinence: late results. Br J Surg. Sep 1985;72 Suppl:S21-2. [Medline].

  66. Altomare DF, Binda GA, Dodi G, La Torre F, Romano G, Rinaldi M. Disappointing long-term results of the artificial anal sphincter for faecal incontinence. Br J Surg. Oct 2004;91(10):1352-3. [Medline].

  67. Bratzler DW, Houck PM. Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Am J Surg. Apr 2005;189(4):395-404. [Medline].

  68. Oliveira L, Pfeifer J, Wexner SD. Physiological and clinical outcome of anterior sphincteroplasty. Br J Surg. Apr 1996;83(4):502-5. [Medline].

  69. Barisic GI, Krivokapic ZV, Markovic VA, Popovic MA. Outcome of overlapping anal sphincter repair after 3 months and after a mean of 80 months. Int J Colorectal Dis. Jan 2006;21(1):52-6. [Medline].

  70. Halverson AL, Hull TL. Long-term outcome of overlapping anal sphincter repair. Dis Colon Rectum. Mar 2002;45(3):345-8. [Medline].

  71. Tjandra JJ, Chan MK, Yeh CH, Murray-Green C. Sacral nerve stimulation is more effective than optimal medical therapy for severe fecal incontinence: a randomized, controlled study. Dis Colon Rectum. May 2008;51(5):494-502. [Medline].

  72. Altomare DF, Ratto C, Ganio E, Lolli P, Masin A, Villani RD. Long-term outcome of sacral nerve stimulation for fecal incontinence. Dis Colon Rectum. Jan 2009;52(1):11-7. [Medline].

  73. Boyle DJ, Knowles CH, Lunniss PJ, Scott SM, Williams NS, Gill KA. Efficacy of sacral nerve stimulation for fecal incontinence in patients with anal sphincter defects. Dis Colon Rectum. Jul 2009;52(7):1234-9. [Medline].

  74. Deen KI, Kumar D, Williams JG, et al. Anal sphincter defects. Correlation between endoanal ultrasound and surgery. Ann Surg. Aug 1993;218(2):201-5. [Medline].

  75. Ganio E, Masin A, Ratto C, Altomare DF, Ripetti V, Clerico G. Short-term sacral nerve stimulation for functional anorectal and urinary disturbances: results in 40 patients: evaluation of a new option for anorectal functional disorders. Dis Colon Rectum. Sep 2001;44(9):1261-7. [Medline].

  76. Kafka NJ, Coller JA, Barrett RC, et al. Pudendal neuropathy is the only parameter differentiating leakage from solid stool incontinence. Dis Colon Rectum. Oct 1997;40(10):1220-7. [Medline].

  77. Kaufman HS. Pathophysiology, Etiology, and Treatment of Fecal Incontinence. Postgraduate course on Colorectal Dysfunction presented at: American Urogynecologic Society 21st Annual Scientific Meeting. 2000.

  78. Matzel KE, Stadelmaier U, Hohenfellner M, Hohenberger W. Chronic sacral spinal nerve stimulation for fecal incontinence: long-term results with foramen and cuff electrodes. Dis Colon Rectum. Jan 2001;44(1):59-66. [Medline].

  79. Nielsen MB, Hauge C, Rasmussen OO, et al. Anal endosonographic findings in the follow-up of primarily sutured sphincteric ruptures. Br J Surg. Feb 1992;79(2):104-6. [Medline].

  80. Scheuer M, Kuijpers HC, Jacobs PP. Postanal repair restores anatomy rather than function. Dis Colon Rectum. Nov 1989;32(11):960-3. [Medline].

  81. Scott AD, Henry MM, Phillips RK. Clinical assessment and anorectal manometry before postanal repair: failure to predict outcome. Br J Surg. Jun 1990;77(6):628-9. [Medline].

  82. Snooks SJ, Swash M, Henry M. Electrophysiologic and manometric assessment of failed postanal repair for anorectal incontinence. Dis Colon Rectum. Nov 1984;27(11):733-6. [Medline].

  83. Sultan AH, Kamm MA, Bartram CI, Hudson CN. Anal sphincter trauma during instrumental delivery. Int J Gynaecol Obstet. Dec 1993;43(3):263-70. [Medline].

  84. Sultan AH, Kamm MA, Hudson CN, et al. Anal-sphincter disruption during vaginal delivery. N Engl J Med. Dec 23 1993;329(26):1905-11. [Medline].

  85. Varma MG, Brown JS, Creasman JM, Thom DH, Van Den Eeden SK, Beattie MS. Fecal incontinence in females older than aged 40 years: who is at risk?. Dis Colon Rectum. Jun 2006;49(6):841-51. [Medline].

  86. Wexner SD, Marchetti F, Salanga VD, et al. Neurophysiologic assessment of the anal sphincters. Dis Colon Rectum. Jul 1991;34(7):606-12. [Medline].

  87. Yilmaz E, Nas T, Korucuoglu U, Guler I. Manometric evaluation of anal sphincter function after vaginal and cesarean delivery. Int J Gynaecol Obstet. Nov 2008;103(2):162-5. [Medline].

Further Reading

Keywords

fecal incontinence, anal incontinence, anal sphincter disruption, spina bifida, myelomeningocele, prolonged second stage of labor, forceps delivery, significant tears, episiotomy, pudendal nerve injury, birth trauma, anterior overlapping sphincteroplasty

Contributor Information and Disclosures

Author

Sonia Ranganath, MD, Resident Physician, Department of Obstetrics and Gynecology, Tufts Medical Center
Sonia Ranganath, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Tanaz R Ferzandi, MD, Assistant Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Division Director, Urogynecology and Pelvic Reconstructive Surgery, Tufts Medical Center
Tanaz R Ferzandi, MD is a member of the following medical societies: American Association of Gynecologic Laparoscopists, American College of Obstetricians and Gynecologists, American Urogynecologic Society, International Urogynaecology Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Jose A Perez Jr, MD, MSEd, MBA, Consulting Physician, Department of Internal Medicine, Residency Director, Vice Chair of Education Department of Medicine, The Methodist Hospital, Houston; Associate Professor of Clinical Medicine, Weill Cornell Medical College
Jose A Perez Jr, MD, MSEd, MBA is a member of the following medical societies: American College of Physician Executives, American College of Physicians, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

David Chelmow, MD, Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Program Director, Tufts University Affiliated Hospitals Obstetrics/Gynecology Residency Program; Chair, Tufts University Health Sciences Campus Institutional Review Board; Vice Chair for Research and Education, Department of Obstetrics/Gynecology, Tufts Medical Center
David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical Decision Making
Disclosure: Nothing to disclose.

CME Editor

Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.

Chief Editor

David Chelmow, MD, Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Program Director, Tufts University Affiliated Hospitals Obstetrics/Gynecology Residency Program; Chair, Tufts University Health Sciences Campus Institutional Review Board; Vice Chair for Research and Education, Department of Obstetrics/Gynecology, Tufts Medical Center
David Chelmow, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Phi Beta Kappa, Sigma Xi, Society for Gynecologic Investigation, and Society for Medical Decision Making
Disclosure: Nothing to disclose.

 
 
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