Kate H. Moore1
Department Obstetrics & Gynaecology, St George Hospital, Kogarah, New South Wales, Australia
Before moving on to surgical treatment of stress incontinence, or management of prolapse, we must briefly consider the disorders of defecation.
Before moving on to surgical treatment of stress incontinence, or management of prolapse, we must briefly consider the disorders of defecation.
Many patients with urinary incontinence or prolapse have anal incontinence, recurrent straining with constipation, or other aspects of obstructive defecation. Because surgery may be considered for the defecation disorder, and in some pelvic floor units, these surgeries are performed simultaneously with bladder/prolapse procedures; such conditions are dealt with here.
Basic Physiology of Anal Continence and Defecation for the Gynecologist
Because the anal continence mechanism and the physiology of defecation are not part of normal registrar training in gynecology, the doctor who works in a urogynecology unit needs a basic outline before the treatment of defecation disorders can be understood.
Anal continence depends upon the following:
The first problem is unique to the bowel (although infected urine can cause bladder incontinence). The second and third problems are rather like those seen in an overactive bladder, where the bladder wall may be noncompliant and the subepithelial nerves are dysfunctional. The fourth problem is rather like that of stress incontinence (weak sphincters), except that the anal sphincters are more complex.
Several theories exist as to the mechanism of anal continence. In the 1970s, the main theory was that the normal puborectalis muscle caused an acute anorectal angle so that during rises in intra-abdominal pressure, the rectum was forced down upon the anal canal, with a “kink” at the puborectalis muscle so that feces were denied access to the anal canal. Arising from this concept, the operation of postanal repair was developed, to restore the anorectal angle and improve continence. This operation is still performed today, although success rates are very variable (see below).
Later studies showed that continence was really dependent upon the sphincters and the puborectalis muscle acting together. When the pressure in the rectum rises, the contractility of the anal sphincters increases, by neurological mechanisms. Thus, operations to repair the anal sphincter, which do not increase the anorectal angle, also improve continence.
Even later, it was realized that continence also depends on awareness of rectal filling. This gives one the ability to distinguish whether the rectal contents are gas (when they could be passed in a private location, not necessarily a toilet) or feces, in which case the external sphincter can be contracted voluntarily while looking for a toilet. The anal canal is highly able to discriminate light touch, pain, and temperature. In contrast, the rectum is not very sensitive to these impulses. Instead, rectal sensation is conveyed by stretch receptors within the pelvic floor muscles that respond to the bulk phenomenon of rectal distension.
Distension of the rectum (by feces or flatus) causes relaxation of the internal anal sphincter, along with contraction of the external anal sphincter. This allows the contents of the rectum to enter the sensitive anal canal (but prevents escape of the contents from the anus). Once the contents enter the anal canal, the nerves sense whether gas or feces are present. This is called the anal sampling reflex.
The sensitivity of the anal mucosa declines with age and menopause, partly explaining the increasing prevalence of anal incontinence in older women. Obviously, there is no surgical cure for denervation/declining sensitivity of the anal mucosa.
Filling of the rectum is normally first sensed at volumes of 10–70 ml. Maximum capacity is about 300 ml. Rectal distension initiates contractions of smooth muscle in the rectal wall, which cause the desire to defecate at “fullness.” This normal compliance of the rectal wall is reduced after pelvic irradiation, with inflammatory bowel disease, and sometimes after denervation following radical pelvic surgery.
Finally, strength and innervation of the sphincters are a vital component of continence. The internal anal sphincter (IAS) is continuous with the circular muscle in the wall of the rectum (see Fig. 8.1). It is in a constant state of tonic contraction, to promote continence. This provides the so-called high-pressure zone in the resting state, about 2 cm from the anal verge.
Anterior–posterior view of anorectal musculature
The high-pressure zone also receives a 15% contribution from the three “anal cushions” that have a rich arterial supply and behave like erectile tissue. They are engorged with blood when the IAS is relaxed and form a seal. Their pressure is higher in those with hemorrhoids and can be damaged by vigorous hemorrhoidectomy. Inadvertent division, or marked thinning, of the IAS (i.e., after some vaginal deliveries) is associated with fecal soiling in up to 40% of cases.
The external anal sphincter (EAS) is continuous with the puborectalis muscle (see Fig. 8.2). Although the EAS is striated muscle and is under voluntary control, it is also in a constant state of contraction to promote continence. During cough, the EAS tightens reflexively. Ultrasound studies of the EAS have shown that about 35% of women who delivered by forceps have a partial or complete laceration of the EAS, which generally does not recover and also contributes to anal incontinence.
Lateral view of anorectal muscles. PR puborectalis, UL upper loop, DC decussating fibers of puborectalis that blend with the longitudinal muscle of the rectum, DD decussating fibers that join the perineal body, ML middle loop, ACR anococcygeal raphe, BS bulbospongiosus, TP deep transverse perinei, BL basal loop, perforated by fibers of the conjoint longitudinal layer (Reprinted with permission from Bogduk , Blackwell Publishing)
The motor innervation to the EAS is via the pudendal nerve. Prolonged bearing down in the second stage of labor is associated with a traction neurapraxia of the pudendal nerve, which may not recover. This partly explains the association between prolonged second stage and anal incontinence.
If rectal sensation is poor, and rectal compliance is reduced, and if the sphincters are also weak, then patients can experience anal incontinence before they even get the desire to defecate.
The Act of Defecation
The defecation mechanism is still not completely understood, despite extensive research:
· Stool comes down from the sigmoid colon to the rectum, by peristalsis.
· Stretch receptors in the pelvic floor detect the stool in the rectum, giving the urge to defecate.
· The anal sampling reflex (internal sphincter relaxes, external sphincter stays closed) occurs; the anal mucosa senses whether stool or gas is present and conveys this to the brain.
· If defecation is not socially convenient, the pelvic floor muscles and the puborectalis contract. This propels feces back up into the sigmoid colon, and the internal sphincter contracts again.
· Once the toilet is reached, the pelvic floor muscles are relaxed while sitting on the toilet, allowing the perineum to descend.
· Both sphincters are relaxed. Puborectalis opens.
· The patient gives a Valsalva maneuver to raise intra-abdominal pressure.
· The bolus of feces is expelled. Upon completion, a closing reflex tightens the external sphincter.
Overview of Anal Incontinence
Anal incontinence is really “the last taboo.” Patients are deeply ashamed if they soil themselves and usually consider it far worse than urinary incontinence. Questions must be phrased very tactfully; for example, do you ever lose bowel material on your underwear?
Anal incontinence is actually not uncommon. Large prevalence studies of community-dwelling women indicate that about 2–14% of women have anal incontinence, with up to 47% of those in nursing homes . The most recent study indicates that 8.9% of noninstitutionalized women suffer from accidental loss of solid, liquid, or mucus incontinence in the month before questioning . As can be seen from the discussion of the physiology of defecation, the pathophysiology of anal incontinence is often multifactorial. Full details about assessment of such patients are available in the text by Pemberton et al. . The history assessment has been described in Chap. 1. The Wexner score should be used to measure severity of anal incontinence (shown in Chap. 5). Considerable detail about previous colorectal surgery, previous radiation, inflammatory bowel disease, etc., is needed. Physical examination requires attention to anal sphincter tone, perineal descent, pelvic innervation, etc.
We encourage any patient with regular fecal incontinence to be fully assessed by a dedicated colorectal surgeon. Such a surgeon is part of our unit so that case notes and nursing staff are shared. On the other hand, patients with minor incontinence to flatus or rare incontinence to liquid stool may benefit from conservative pelvic floor muscle training .
The common tests of anorectal function for patients with anal incontinence comprise the following:
Anorectal manometry tests the magnitude of the resting anal pressure at the high-pressure zone (85% comes from IAS rhythmic slow wave contractions, 15% from tonic contraction of EAS). The most common method is a water-perfused catheter containing four recording channels, to detect pressure at various points along the rectum/anal canal, with a balloon at the end. After testing baseline resting pressures, the patient is asked to cough (pressures should rise briefly, to prevent incontinence) and then to squeeze the EAS, which gives the voluntary “squeeze pressure.” The rectal balloon is then distended with fluid to elicit a brief drop in anal pressure, showing competency of the “sampling reflex.”
Pudendal nerve conduction studies test the innervation of the sphincters, by measuring whether the time taken to conduct a stimulus is delayed (the conduction latency). A stimulating electrode, mounted on a gloved finger, is inserted into the rectum; the fingertip is placed on the ischial spine (near the pudendal nerve), with a recording electrode at the external anal sphincter. The latency is the time taken for the electrical stimulus to reach the recording electrode. The test requires an experienced person to produce reliable measurements, and thus some units have discarded it, although it was a standard test for many years. Allen et al. . used this test to provide the first evidence of intrapartum damage to the pudendal nerve, although long-term follow-up showed that most patients’ nerve conduction recovered over time. Prolonged straining at stool is also associated with prolonged pudendal nerve conduction times.
Single-fiber electromyography is another way of detecting nerve damage. Because denervation of a skeletal muscle is accompanied by reinnervation from neighboring axons, a single-fiber EMG electrode can detect multiple axons firing within a small area of the muscle, to indicate that it has been damaged and then reinnervation has occurred.
Anal mucosal sensitivity testing tests the adequacy of anal sensation (that is needed for the anorectal sampling reflex). A ring electrode mounted on a Foley catheter is placed in the anal canal. A tiny current (up to 0.1 mA) is delivered: the patient states when she can feel a tingling sensation. Standard normal values have been derived.
Endo-anal ultrasound is now the best way to measure whether the sphincters are intact, using a rotating probe or a linear probe. Defects of the EAS are detected very accurately. This technique was used by Sultan et al. in a classic paper  to show that about 35% of parous women have defects of the EAS. This does not necessarily mean that they will respond to surgery.
Treatment of Anal Incontinence
Management involves a large range of conservative and surgical treatments. A short summary is provided; for details, see Norton et al. .
Pelvic floor muscle training is done to teach the patient to contract the external anal sphincter, similar to that in urinary incontinence . Biofeedback is often used, by a rectal EMG sensing device, to enhance patients’ awareness of their ability to contract . Electrical stimulation of the muscle has also been used (as for stress incontinence). Success ranges from 12 to 90 % cure/major benefit for anal incontinence .
Regulation of diet to avoid watery stool is often successful for patients who only leak when they have liquid feces. Also, 2–3 dessert spoons of Metamucil or psyllium husks are dissolved in a small amount of water (100–150 ml) to thicken the stool.
The drug Imodium (loperamide) is also used to thicken the stool; it also increases the resting tone of the anal sphincters to promote continence.
Anal sphincter repair (sphincteroplasty) involves dissecting the damaged ends of the external sphincter, freeing them up enough to be laid across each other and sutured, in an “overlap repair,” although recent evidence indicates that the overlapping repair is not significantly better than the end-to-end repair . When performed for obstetric lacerations of the sphincter, continence is achieved in about 80%. Success is best when the pudendal nerve to the sphincter is intact and the internal sphincter is not damaged.
Postanal repair involves plication of the puborectalis muscle posterior to the anorectal junction. The posterior aspect of the external sphincter is usually reinforced with sutures as well. The operation is designed to increase the anorectal angle (originally thought to be very important to the continence mechanism). Audit in the mid-1990s showed that less than 50% of patients have improved continence at 2 years, so the procedure is less commonly performed now.
The dynamic graciloplasty procedure involves taking a segment of gracilis muscle from the inner aspect of the thigh and then tunneling it under the pubic bone to wrap it around the anal sphincter. Because the gracilis is mainly a “fast-twitch” type II muscle that cannot maintain a contraction over time, an implanted electrical stimulator is applied to the muscle, to convert it to a slow-twitch postural-type muscle over 6 months. The patient uses a control device to turn off the stimulus in order to defecate. Initial data from 1999 indicated a 66% success rate .
Unfortunately, the “long-term” data at 2 years showed that only 15 % were continent 100% of the time and 42% had a >50% improvement. In the first large series of 121 patients, there were 211 adverse events, half of which required rehospitalization or repeat surgery . The device has been withdrawn in the USA.
In the last decade, sacral nerve stimulation has become widely used for fecal incontinence. The procedure is as described for patients with detrusor overactivity in Chap. 7, except that after inserting the temporary stimulator (see Fig. 8.3), patients should keep a diary for at least 2–4 weeks because fecal incontinence is often erratic; thus, more time is needed to judge whether >50% benefit is occurring. Implantation of the permanent device is identical . Few long-term studies with objective data have been published, but in patients with a good response to the temporary stimulator who have the permanent implant, the Wexner score improves markedly, down from baseline 14–16 to a median of 1–3 .
Sacral nerve stimulation
Overview of the Disorders of Obstructive Defecation
In the urogynecology patient, the main problems comprise constipation, incomplete evacuation with a need to digitate the vagina, and post-defecation soiling. These symptoms often coexist with rectocele, but such patients are often referred to the colorectal surgeon rather than the urogynecologist.
Debate exists about who should manage rectocele. In our unit, such patients are often assessed jointly by the urogynecology team and the colorectal team, and then a decision is made as to who should manage the patient. The colorectal perspective is given here, derived from experience in our unit.
When patients complain of constipation, only about a third of them are actually concerned about infrequent defecation; the rest are worried about straining at stool or passing hard stools.
The definition of constipation has recently been standardized, now called the “Rome definition,” as a patient who has two or more of the following, for at least 12 months, when not taking laxatives :
· Straining during >25% of bowel movements (BM)
· Sensation of incomplete evacuation in >25 % of BM
· Hard or pellety stools on >25% of BM
· Less than three stools passed per week
It is useful to employ the Bristol Stool Chart to define what type of stool the patient passes (Fig. 8.4).
The Bristol Stool Chart (Reprinted by kind permission of Dr. K. W. Heaton, Reader in Medicine at the University of Bristol, Copyright 2000 Norgine Ltd.)
Other symptoms such as need to digitate to defecate, abdominal cramps, bloating, and so on do not feature in the Rome definition but help one to assess the severity of the constipation. Depending upon the definition used, constipation affects about 4% of the population but about 17% of those aged 30–64 and 40% of those over age 65. It is common in urogynecological patients.
Assessing the Causes of Constipation
Before one treats constipation, one must seek nonbowel (secondary) causes. Some can be reversed. Others indicate that management may be difficult. These include:
· Endocrine causes: hypothyroidism, hypercalcemia, diabetic autonomic neuropathy
· Neurological disorders: Parkinson’s disease, multiple sclerosis, autonomic neuropathy
· Psychiatric causes: depression, anorexia, sexual abuse
· Narcotic analgesic drugs
· Cardiac drugs (nifedipine, verapamil, disopyramide, amiodarone, flecainide)
· Antidepressants (clomipramine, fluoxetine, venlafaxine, sertraline, paroxetine)
· Tranquilizers (alprazolam, olanzapine, risperidone)
· Lipid-lowering drugs (lovastatin, pravachol, cholestyramine)
· Miscellaneous drugs: bromocriptine, valproic acid, ondansetron
Once secondary causes are excluded, other bowel disorders that can manifest as constipation should be considered, such as diverticulosis, polyps, stricture, ischemia/bowel obstruction, and malignancy. One is left with four main types of constipation:
Simple constipation describes patients who have a mild to moderate degree of difficult or infrequent passage of stool, which responds quickly to increased fluid/fiber intake.
Constipation–predominant irritable bowel syndrome includes such patients mainly complaining of abdominal pain, who are commonly young women, and is not considered further here.
Idiopathic slow-transit constipation is a rare disorder, generally affecting young to middle-aged women who seldom feel the urge to defecate and have a very poor response to laxatives or bulking agents.
Outlet obstruction/evacuation disorders comprise the following: Rectal mucosal prolapse is a surgical problem and not considered further here. Intussusception is a prolapse of the anorectal mucosa down into the anal canal; the functional significance of this radiological finding is controversial. Anismus is a condition in which patients have trouble emptying the rectum because they experience involuntary spasm of the striated pelvic floor muscles or of the puborectalis muscle (see below, under biofeedback therapy). Rectocele is a prolapse of the anterior wall of the rectum into the vagina.
The basic investigations that are used to distinguish these four types of primary constipation are as follows:
Anorectal manometry studies (as per fecal incontinence) but with the addition of a balloon expulsion test to elicit spasm of the striated muscles seen in anismus.
A colonic transit study involves the ingestion of radiopaque markers over 3 days; then, an abdominal X-ray is taken on day 4 (or later if markers still present). In normal patients, the gut transit time is 36 h, so all markers should be expelled by day 4; a prolonged test suggests idiopathic slow-transit constipation.
A defecating proctogram (Fig. 8.5) is an X-ray test of the act of defecating a radiopaque porridge-like mixture. It identifies the site and size of rectocele (as well as other defects). If contrast material is trapped in the rectocele after defecation, this can also lead to post-defecation soiling (as the feces slowly seep out from the pocket).
Defecating proctogram. (a) The bulging of the rectocele anteriorly into the vagina. (b) Defecation, with “holdup” in the rectocele. (c) Post-defecation film, with contrast trapped in the anterior rectocele
Colorectal surgeons classify rectocele as low, middle, and high. Middle and high defects are more likely to be associated with enterocele and thus referred for gynecological repair. A low rectocele is more likely to be associated with scarring and shortening of the perineal body and anal sphincter; thus, colorectal surgeons commonly repair these defects.
Overview of Treatment of Disorders of Defecation
Simple constipation is treated as discussed in Chapter 2. A dedicated nurse continence advisor or continence physiotherapist can also help such patients to learn the correct position for defecation (feet elevated to accentuate relaxation of the anorectal angle) and modify their lifestyle so they have enough time to relax and defecate properly as soon as they have the call to stool. Postponement of the defecation impulse because of a busy schedule is a major factor in constipated individuals. See .
Constipation–predominant IBS is difficult to treat (not within the remit of this chapter).
Idiopathic slow-transit constipation, once suspected on the basic tests, requires a more complex study of colonic motility to elicit a reduction in myoelectrical activity as well as serious effort with laxative therapy. If this fails, surgical removal of the colon with ileorectal anastomosis may be indicated, although diarrhea may result. Sacral nerve stimulation is also showing promising results for this type of constipation .
Anismus is treated by biofeedback. Similar intrarectal EMG devices are used to help patients to relax their anal sphincters and puborectalis during the act of defecation.
Rectocele may be treated by transrectal repair; see Fig. 8.6. The advantage of the colorectal approach is that any associated anal sphincter defect can be repaired at the same time as the transanal repair. However, if the anal sphincter is intact, controversy exists about transanal repair because this approach requires the use of anal retractors, which may stretch the sphincters. Anal incontinence after transanal repair of rectocele can occur in up to 30% of patients, although 92–97% of patients will have complete resolution of the hernia defect, with resolution of the need to digitate in order to evacuate.
Transanal repair of rectocele. (a) A mucosal flap is raised around the anterior half of the anal canal. (b) The anterior rectal wall muscle is folded down to the distal anal canal and imbricated so as to abolish the rectocele sac. (c) The now redundant mucosa is excised; the new mucocutaneous function is restored across the anterior lumen of the anal canal (Reprinted with permission from Lawler and Fleshman . Copyright 2002, Elsevier.)
Anal incontinence and disorders of defecation are more common than is generally appreciated. Such problems need to be elicited carefully in urogynecology patients. If minor and rare, conservative therapy may help, but if the problem gives rise to major symptoms, full investigation is needed. Treatment may be carried out in conjunction with the urogynecological condition in certain cases.
A Note Regarding Obstetric Trauma as a Cause of Anal Incontinence
In the last 15 years, colorectal surgeons and obstetricians have become increasingly aware that the management of the second stage of labor has tremendous impact upon the likelihood of anal incontinence developing during a woman’s life.
This subject is vast and controversial. It cannot be adequately dealt with in a short practical text. This does not mean it is not important. Registrars are strongly advised to read the classic text on this subject: Sultan AH, Thakar R Fenner DE, editors. Perineal and anal sphincter trauma. London: Springer; 2009.
The following is a list of some landmark papers that give an overview of the subject:
Engel AF, Kamm MA, Sultan AH, Bartram CI, Nicholls RJ. Anterior anal sphincter repair in patients with obstetric trauma. Br J Surg. 1994;81:1231–4.
Fitzpatrick M, Behan M, O’Connell R, O’Herlihy C. A randomized clinical trial comparing primary overlap with approximation repair of third-degree obstetric tears. Am J Obstet Gynecol. 2000;183:1220–4.
Kamm MA. Faecal incontinence: clinical review. BMJ. 1998;316:528–32.
Kammerer-Doak DN, Wesol AB, Rogers RG, Dominguez CE, Dorin MH. A prospective cohort study of women after primary repair of obstetric anal sphincter laceration. Am J Obstet Gynecol. 1999;181:1317–23.
MacArthur C, Bick DE, Keighley MRB. Faecal incontinence after childbirth. Br J Obstet Gynaecol. 1997;104:46–50.
MacArthur C, Glazener CM, Wilson PD, Herbison GP, Gee H, Lang GD, et al. Obstetric practice and faecal incontinence 3 months after delivery. BJOG. 2001;108:678–83.
Malouf A, Norton C, Engel AF, Nicholls RJ, Kamm MA. Long-term results of anterior overlapping anal-sphincter repair for obstetric trauma. Lancet. 2000;355:260–5.
Reiger NA, Wattchow DA, Sarre RG, Cooper SJ, Rich CA, Saccone GT, et al. Prospective trial of pelvic floor retraining in patients with faecal incontinence. Dis Colon Rectum. 1997;40:821–6.
Royal College of Obstetricians and Gynaecologists. Management of third and fourth degree perineal tears following vaginal delivery. RCOG guideline no. 29. London: RCOG Press. 2001. Available from RCOG Web site.
Spence-Jones C, Kamm MA, Henry MM, Hudson CN. Bowel dysfunction: a pathogenic factor in uterovaginal prolapse and urinary stress incontinence. Br J Obstet Gynaecol. 1997;104:311–5.
Sultan AH, Kamm MA. Faecal incontinence after childbirth. Br J Obstet Gynaecol. 1997;104:979–82.
Sultan AH, Kamm MA, Hudson CN. Obstetric perineal tears: an audit of training. J Obstet Gynaecol. 1995;15:19–23.
Sultan AH, Kamm MA, Hudson CN, Bartram CI. Third degree obstetric anal sphincter tears: risk factors and outcome of primary repair. BMJ. 1994;308:887–91.
Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal sphincter disruption during vaginal delivery. N Engl J Med. 1993;329:1905–11.
Swash M. Faecal incontinence: childbirth is responsible for most cases. BMJ. 1993;307:636–7.
Wood J, Amos L, Reiger N. Third degree anal sphincter tears: risk factors and outcome. Aust N Z J Obstet Gynaecol. 1998;38:414–7.
Allen RE, Hosker GL, Smith AR, Warrell DW. Pelvic floor damage and childbirth, a neurophysiological study. Br J Obstet Gynaecol. 1990;97:770–9.PubMedCrossRef
Bogduk N. Issues in anatomy: the external anal sphincter revised. Aust N Z J Surg. 1996;66(9):626–9.PubMedCrossRef
Drossman DA, Thompson WG, Talley NJ, et al. Identification of sub-groups of functional gastrointestinal disorders. Gastroenterol Int. 1990;3:159–72.
Eccersley AJ, William NS. Fecal incontinence – pathophysiology and management. In: Pemberton JH, Swash M, Henry MM, editors. The pelvic floor, its function and disorders. London: WB Saunders; 2002. p. 341–57. Chapter 24.
Enck P, Frauke M. Biofeedback in pelvic floor disorders. In: Pemberton JH, Swash M, Henry MM, editors. The pelvic floor, its function and disorders. London: WB Saunders; 2002. p. 393–404. Chapter 27.
Fernando R, Sultan AH, Kettle C, Thakar R, Tadley S. Methods of repair for obstetric anal sphincter injury. Cochrane Database Syst Rev. 2006;(3):CD002866.
Fynes M, Marshall K, 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. 1999;42:753–61.PubMedCrossRef
Laurberg S, Matzel KE, Mellgren AF, Minura T, Connell O, Varma MG. Surgery for faecal incontinence, Chapter 17, in Incontinence. In: Abrams P, Cardozo L, Khoury S, Wein A, editors. Incontinence, 4th international consultation on incontinence. Plymouth, UK: Health Publications Ltd.; 2009. p. 1389–417.
Lawler LP, Fleshman JW. Solitary rectal ulcer, rectocele, hemorrhoids and pelvic pain. In: Pemberton JH, Swash M, Henry MM, editors. The pelvic floor: its function and disorders. London: WB Saunders; 2002. p. 368.
Leung L, Riutta T, Kotecha J, Rosser W. Chronic constipation: an evidence-based review. J Am Board Fam Med. 2011;24(4):436–51.PubMedCrossRef
Margolin DA. New options for the treatment of fecal incontinence. Oschner J. 2008;8:18–24.
Norton C. Conservative management of anal incontinence, chapter 11. In: Sultan AH, Thakar R, Fenner DE, editors. Perineal and anal sphincter trauma. London: Springer; 2007. p. 133–43.CrossRef
Norton C, Whitehead W, Bliss DZ, Harari D, Lang J. Conservative and pharmacological management of faecal incontinence in adults, chapter 16 in Incontinence. In: Abrams P, Cardozo L, Khoury S Wein A, editors. Incontinence, 4th international consultation on incontinence. Plymouth, UK: Health Publications Ltd.; 2009.
Pemberton JH, Swash M, Henry MM, editors. The pelvic floor, its function and disorders. London: WB Saunders; 2002. p. 172–213.
Reiger N, Wattchow D, et al. Prospective trial of pelvic floor retraining in patients with fecal incontinence. Dis Colon Rectum. 1997;40:821–6.CrossRef
Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery. N Engl J Med. 1993;329:1905–11.PubMedCrossRef
Wexner SD, Cera SM. Surgical management of anal incontinence, chapter 12b. In: Sultan AH, Thakar R, Fenner DE, editors. Perineal and anal sphincter trauma. London: Springer; 2007. p. 154–65.CrossRef