Fecal Incontinence

Surg Clin N Am 82 (2002) 1273–1290

Fecal incontinence Susan Congilosi Parker, MD*, Amy Thorsen, MD Division of Colon and Rectal Surgery, School of Medicine, University of Minnesota, 393 Dunlap Street N, Suite 500, St. Paul, MN 55104, USA

Fecal incontinence is a common problem not frequently discussed between patients and their physicians. More appropriately termed anal incontinence, it encompasses the inability to control the passage of flatus, liquid, or solid stool. What may seem like a minor inconvenience to the physician may be extremely distressing to the patient; the incontinent patient may experience social isolation, feelings of inadequacy and low self-esteem, and sexual dysfunction in addition to the physical symptoms of recurrent genitourinary infections and perianal skin breakdown [1]. Community-based studies reveal a 2.2% prevalence of anal incontinence; 30% of these patients are over the age of 65, and 63% are female [2]. By understanding the anatomic and physiologic mechanisms of fecal incontinence, the surgeon can appropriately evaluate and treat her patient with medical or surgical therapy. Anatomy and physiology of anal continence Fecal continence depends on the interplay of normal anal sphincter and pelvic floor function; rectal compliance, capacity, and sensation; colonic transit and stool consistency; and central nervous system function. An alteration in one or more of these factors can have a positive or negative effect on continence. Etiologies of fecal incontinence are listed in Box 1. The pelvic floor musculature and sphincter complex consists of the levator ani, the puborectalis, and the internal and external anal sphincters. The levators, also known as the iliococcygeus and pubococcygeus muscles, arise from the obturator fascia, pubic bone and ischial spine. Their fibers travel posteriorly, inferiorly, and medially until they decussate with fibers from the

* Division of Colon and Rectal Surgery, University of Minnesota, 393 Dunlap Street N, Suite 500, St. Paul, MN 55104. E-mail address: [email protected] (S. Congilosi). 0039-6109/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 0 0 3 9 - 6 1 0 9 ( 0 2 ) 0 0 0 6 1 - 0

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Box 1 Causes of fecal incontinence Aging Congenital anorectal anomalies Diarrheal states Infectious diarrhea Inflammatory bowel disease Short-gut syndrome Laxative abuse Radiation enteritis Neurologic conditions Congenital anomalies Dementia, stroke Diabetes Multiple sclerosis Neoplasms of brain, spinal cord Pelvic floor denervation Chronic straining at stool Descending perineum syndrome, Multiple pelvic organ prolapse Rectal prolapse Vaginal delivery Overflow incontinence Impaction Encopresis Rectal neoplasms Trauma Accidental injury Anorectal surgery (eg, fistulotomy) Obstetrical injury Adapted from Mado RD, Williams JG, Caushaj PF. Fecal incontinence. Current concepts. N Engl J Med 1992;326(15):1002–1007; with permission.

opposite side to form the anococcygeal raphe and attachments to the coccyx and lower sacrum. Medial to the levators and anterior to the anococcygeal raphe is the levator hiatus. The lower rectum, vagina, and urethra pass through this hiatus and are bound together by a dense fascia. During defecation, the levator ani contract and cause a dilating effect on the pelvic viscera [3]. Inferior to the levators, the puborectalis muscle originates from the back of the pubis and runs posteriorly to form a second U-shaped sling behind the rectum. Through tonic contraction, the puborectalis angulates

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the anorectal junction to approximately 90 degrees at rest, and allows straightening by relaxing during defecation [4]. The levator ani and puborectalis muscles receive innervation superiorly from branches of sacral nerves S2-4 [5]. Along its inferior surface, the puborectalis may also receive branches from the pudendal nerve [6]. Changes in normal pelvic floor function can result from central or peripheral nerve insults, and common causes are spinal injuries, perineal descent, vaginal delivery, rectal prolapse, and chronic straining. The internal anal sphincter (IAS) consists of a thickening of the circular smooth muscle of the rectum as it joins the anal canal. Shorter in length than the external sphincter, it ends approximately 8 mm to 12 mm inferior to the dentate line [7]. At rest, the internal sphincter provides 80% of sphincter tone [8]. A normal IAS will relax in response to rectal distention, but subsequently regain tone during rectal accommodation [9]. The internal sphincter receives both sympathetic innervation from the hypogastric plexus and parasympathetic innervation from S1-3 [10–12]. The external anal sphincter (EAS) is a striated circular muscle which surrounds the entire anal canal. The EAS also contributes to resting sphincter tone [13]. Through normal involuntary reflex pathways, the external sphincter will contract in response to rectal distension, increased intra-abdominal pressure, and change from a supine to upright position [10,14,15]. Voluntary contraction can be performed for 40 to 60 seconds until the EAS fatigues [16]. The external sphincter receives innervation primarily via the inferior rectal branch of the pudendal nerve, and up to a third of patients may receive additional innervation from a separate branch of S4 [6]. The pudendal nerve arises from sacral plexus nerve fibers (S2–4), exits the pelvis through the greater sciatic foramen, crosses the ischial spine, and travels in Alcock’s canal toward the ischial tuberosity. Direct internal and external sphincter injury leading to incontinence can result from obstetric, operative, penetrating, or pelvic trauma. Poor sphincter function may result from interruption of spinal and central pathways from congenital, acquired, or traumatic CNS defects, or from peripheral nerve injury or neuropathy. Changes in rectal capacity and sensation can also affect continence. The compliant rectum can maintain low intraluminal pressures as fecal volume increases [17]. This normal elasticity can be lost in patients with ulcerative colitis, radiation proctitis, and neorectums secondary to sphincter-saving procedures, resulting in high intraluminal pressures, urgency, and incontinence [18–20]. The sensation of rectal distension is most likely mediated by stretch receptors in the puborectalis and levator ani muscles [21]. In contrast, the anal canal epithelium hosts multiple pain, touch, cold, pressure, and friction receptors that detect the nature of rectal contents [22]. Neuropathies, spinal cord malformations, perineal descent, fecal impaction, and encopresis may alter normal sensory thresholds [23]. CNS disturbances, such as dementia, stroke, and encephalopathies, may prevent the patient’s appreciation of rectal distention [24].

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Finally, conditions leading to increased stool volume may overcome the normal storage capacity of the sigmoid and rectum and lead to incontinence. Liquid stool may result from malabsorption, infectious and inflammatory colitis, and irritable bowel syndrome. In fact, stool consistency may be the most important factor influencing fecal incontinence [25].

Evaluation A detailed history and physical exam will often reveal the etiology and severity of incontinence. The addition of anorectal physiology testing may confirm clinical judgment or expose unsuspected deficits. Laboratory evaluation can also quantify the severity of the physiologic defect and is often used to prognosticate the rate of success of a proposed treatment plan. History A history of fecal incontinence may be difficult to obtain from an embarrassed patient. The onset of symptoms and any relationship to a change in bowel habits should be assessed. The degree of incontinence (flatus, liquid, or solid stool), frequency of episodes, and their effects on the patient’s quality of life will document present function and determine whether more aggressive therapies are indicated. As previously discussed, gastrointestinal diseases such as infectious colitis, inflammatory bowel disease, and irritable bowel syndrome may cause or exacerbate fecal incontinence, and previous pelvic radiation resulting in proctitis may cause rectal bleeding, tenesmus, and leakage. Neurologic diseases associated with loss of control include congenital spinal cord abnormalities, spinal trauma, and multiple sclerosis. A history of diabetes may indicate pelvic floor neuropathy as a possible etiology of incontinence [26]. Injuries to the anal sphincters may go unnoticed until other factors exacerbate the physiologic defect; thus a history of prior anorectal surgery or perineal trauma is extremely relevant. Anorectal procedures treating hemorrhoidal disease, fistulas, and fissures may cause occult sphincter injury. Some degree of incontinence may be noted in up to 45% of patients undergoing fistula surgery [27]. Nielson et al [28] demonstrated a 65% incidence of sphincter defects on anal ultrasound after sphincter stretch for fissure-inano. Varying rates of impaired control have been reported after lateral internal sphincterotomy, possibly related to technique [29] or sphincterotomy length [30]. A detailed obstetric history may be extremely revealing in the female patient. In addition to the number of vaginal deliveries, a history of increased birth weight, episiotomy use, instrumented delivery, and prolonged labor should be noted. Clinically recognized sphincter disruption is noted in up to a quarter of all childbirths, and ultrasound studies reveal an additional 11% incidence of unsuspected sphincter injuries [31].

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Independent risk factors for sphincter disruption include midline episiotomy [32], clinicians with higher episiotomy usage [33], and forceps delivery [34]. An active second stage of labor that exceeds one hour may increase the risk of pelvic floor denervation in primiparas [35]. Physical examination A focused physical exam is performed not only to identify obvious defects, but also to differentiate incontinence from fecal soiling due to poor hygiene, prolapse, or fistulous disease. Inspection of the perianal skin may reveal excoriation, scars from previous surgeries or episiotomies, a patulous anus, or an obvious cloacae. A ‘‘keyhole deformity,’’ resulting from a posterior midline sphincterotomy or fistulotomy, may cause fecal leakage as opposed to true incontinence. Prolapsing hemorrhoids, mucosa, or full thickness prolapse may be elicited by valsalva. The presence of an anal wink should be assessed on each side to determine whether normal anocutaneous reflexes are intact. On digital exam, any masses or palpable defects are noted. The presence of impacted stool suggests fecal overflow as the mechanism of incontinence. Resting and squeezing sphincter tone should be assessed subjectively. Puborectalis contraction can be felt posteriorly just above the external sphincter. A bidigital exam can be performed to appreciate perineal body width or detect a rectovaginal fistula. Anoscopy will reveal hemorrhoids or fistulas, and flexible sigmoidoscopy can exclude the presence of masses or inflammatory conditions which may lead to incontinence. A complete colonoscopy should be considered in the patient who reports a change in bowel habits. If the diagnosis of incontinence is in doubt, the ability of the patient to retain a 100 cc water enema can be easily assessed in the office. Anorectal physiology testing Not all patients require laboratory assessment; patients with altered bowel function or minor degrees of incontinence may respond well to medical management. Physiology testing will define anatomic defects, quantify anal sphincter function, and identify neurologic deficits. Laboratory studies include endoanal ultrasound, anal manometry, pudendal nerve latency testing, and occasionally defecography. When performed by an experienced clinician, endoanal ultrasound approaches 100% sensitivity and specificity in identifying internal and external sphincter defects [36,37]. A 15 mm diameter probe with a 360 degree rotating 10 mHz transducer is used to image the sphincters at several levels in the anal canal. The internal anal sphincter is imaged as the hypoechoic ring closest to the transducer, surrounded by a hyperechoic ring representing the external anal sphincter. Lateral breaks in the internal sphincter may be seen after sphincterotomy or hemorrhoidectomy. Obstetrical trauma resulting in sphincter injury may appear as anterior disruptions of both the

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external anal sphincter muscle and internal anal sphincter muscle on ultrasound. The degree of muscle separation can be measured, and perineal body length can be assessed by applying pressure on the posterior vaginal wall. This maneuver may also aid in identifying the presence and location of a rectovaginal fistula. Endosonographic sphincter abnormalities are seen in up to 90% of women whose sole risk factor for fecal incontinence is obstetric trauma [38,39]. Anal manometry quantifies functional deficits in the internal and external sphincters and tests for the presence of normal anorectal reflexes. Using either a microballoon, or a water-perfused or solid-state transducer, resting and squeeze pressures are measured throughout the length of the anal canal. In the relaxed patient, resting pressures mainly reflect internal sphincter function, whereas squeeze pressures represent voluntary external sphincter contraction. Normal values of both resting and squeeze pressures vary among patient populations; lower pressures are found in women and with advancing age [40–42]. Given the wide range of normal pressures and the variety of factors involved with anal continence, absolute values predicting incontinence are difficult to define. Although manometry cannot differentiate a sphincter injury from a neurogenic deficit [43], it can confirm neurogenic dysfunction in patients with intact sphincters and normal pudendal nerve terminal motor latencies [44]. Rectal sensory testing includes volumetric measurements of first detectable sensation, sensation of fullness, and maximal tolerated volume by balloon distention. Hypersensitivity can be seen with inflammatory conditions and poor rectal compliance. Blunted rectal sensation—found in patients with diabetes [45], multiple sclerosis [46], and megarectum [47]—may lead to overflow incontinence. Several studies indicate that successful biofeedback therapy for fecal incontinence may be attributed to improvements in rectal sensation [48–51]. The pudendal nerve, containing fibers from sacral nerves S2–4, provides motor innervation to the external sphincter and receives sensory information from the perineum. Pudendal nerve terminal motor latency (PNTML) measures the conduction time to external sphincter contraction after nerve stimulation at the level of the ischial spine. The nerve may be difficult to identify in obese patients and with technician inexperience. Prolonged latencies may be associated with obstetric injury, perineal descent, prolapse, and medical neuropathies. Pudendal neuropathy is observed in up to 70% of patients with fecal incontinence, and in over 50% of patients with sphincter injury [52]. Controversy exists as to whether prolonged PNTML predicts poor outcome following sphincteroplasty [53–57]. Defecography evaluates rectal emptying of contrast material under fluoroscopy. Incontinent patients are often observed to have a more obtuse anorectal angle on defecography [58]. This study may reveal internal or external prolapse not appreciated on exam, or a poorly emptying rectocele contributing to incontinence associated with sphincter dysfunction.

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The necessity and value of anorectal physiology testing has been debated in the literature. In a prospective study, Liberman et al demonstrated a 10% change in management when physiologic evaluation (endosonography, manometry, and PNTML) was performed after clinical assessment. Transanal ultrasound was found to be the study most likely to alter the clinical treatment plan. Endosonography may reveal unsuspected sphincter injuries in patients thought to have neurogenic incontinence, or a lack of a significant anatomic pathology in patients with suspected sphincter disruption [59]. Although pudendal neuropathy may not affect the decision to correct a sphincter defect, the knowledge of its presence will assist in counseling patients on functional expectations. Anorectal physiology testing has also been demonstrated to be useful in evaluating patients with severe perineal trauma prior to colostomy takedown [60].

Medical management Most patients with fecal incontinence will benefit from an initial attempt at medical management of their problem. Regardless of the etiology of the incontinence, patients with mild to moderate symptoms may improve enough to delay or preclude surgical options, and patients with severe symptoms may obtain a degree of improvement while undergoing further testing or awaiting surgery. Medical management consists of dietary manipulation, use of antidiarrheals, bowel management regimens, and biofeedback. Dietary measures Dietary manipulation refers to the initial common-sense counseling of the patient regarding diarrhea-inducing foods, possible sources of food intolerance, and the addition of bulk-producing agents to the diet. Foods associated with diarrhea include alcohol, caffeine, fruit juices, prunes, licorice, and some vegetables such as beans, broccoli, cauliflower and cabbage. Common sources of food intolerance are lactose and gluten. A daily food diary is the most useful method to pinpoint offending foods, as personal recollection is often faulty. Although this aspect of treating fecal incontinence is more trial and error and less science, the use of increased dietary fiber to increase stool bulk is well accepted [61]. The patient should slowly increase the daily fiber intake, seeking a goal of at least 20 to 25 grams a day and ideally 30 grams a day. The varieties of methycellulose and psyllium products now available over the counter in powder, granule, and pill form make this an achievable goal. Antidiarrheals The most commonly used antidiarrheals are adsorbents and opium derivatives. Adsorbents, such as Kaopectate (Pharmacia & Upjohn, Peapack,

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NJ) are most useful for mild degrees of incontinence and act, as the name suggests, by absorbing excess fluid in stool. Opium derivatives range from the over-the-counter loperamide (Imodium, McNeil Consumer Healthcare, Fort Washington, PA) to the more potent prescription alternatives of diphenoxylate hydrochloride (Lomotil, Searle, Chicago, IL), codeine, and tincture of opium. Low-dose amitriptyline (20 mg daily), a tricyclic antidepressant with anticholinergic and serotoninergic properties, also improves fecal incontinence symptoms, but it is unclear if it acts mainly by decreasing colonic transit or by altering rectal motor contractions [62]. In our practice, loperamide is the most commonly used drug for moderate to severe incontinence. Loperamide combines multiple actions—slowing colonic transit, increasing fluid absorption, and inhibiting mucous secretion—with a lower abuse potential than other opium derivatives. Loperamide is also the only antidiarrheal that acts as a sphincter agonist, increasing anal sphincter pressure [63]. The best use of these medications is prophylactically with a regularly scheduled dose to avoid or decrease episodes of incontinence. Inherent in any discussion of diarrhea and fecal incontinence is consideration of the patient with irritable bowel syndrome (IBS). Irritable bowel syndrome is unlikely to be the sole source of incontinence, but the combination of the diarrheal form of IBS with a mildly compromised anal sphincter can result in a debilitating problem. Medical management, particularly the use of bulking agents, as already outlined, is appropriate for these patients. The variable nature of IBS can make prophylactic use of antidiarrheals problematic. Alosetron (Lotronex, Glaxo Smithkline, Uxbridge, Middlesex, UK), a serotonin type 3 receptor antagonist, is effective for women with diarrhea-predominant irritable bowel syndrome but was withdrawn from the market in 2001 due to episodes of ischemic colitis [64,65]. Reintroduction of this or similar serotonin modulating drugs may offer therapeutic benefits in the future. A final category of medications that are not strictly antidiarrheals but may have the desired effect are the bile salt binders cholestyramine and colestipol. These resins treat bile acid diarrhea by binding with bile salts in the small intestine, but also alter the absorption of fat-soluble vitamins and certain medications (digoxin, warfarin, thiazides). Appropriate patients are those who relate a change in bowel consistency to the timing of a cholecystectomy or those suspected of having altered small bowel reabsorption of bile salts, which occurs by passive diffusion throughout the gut but by active transport in the terminal ileum. A recent area of interest is the use of topical agents such as phenylephrine to increase internal anal sphincter contraction and increase resting tone [66]. Although 10% topical phenylephrine was not successful in an initial randomized, controlled trial, the use of a topical agent remains an intriguing option that may eventually prove useful for the treatment of minor perineal soiling associated with decreased resting tone.

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Bowel management The goal of an effective bowel management program is to allow the patient to produce a complete bowel movement at a scheduled time by using an individualized combination of dietary measures, laxatives, suppositories, enemas, or digitization. This approach to bowel dysfunction, commonly used by spinal-cord injury patients, is also applicable to patients with less complete neurologic disorders (multiple sclerosis, diabetes), congenital disorders (imperforate anus, spina bifida), decreased rectal sensation, or incomplete evacuation. Patient compliance is essential for success and daily care is typical [67]. In a telephone survey of 171 adults with spinal-cord injuries for a mean of 8.9 years, the most common bowel regimen was a chemical rectal stimulant (in 39% of subjects) [68]. If bowel management becomes arduous, particularly for the spinal cord injury patient, a stoma can greatly decrease the time spent on bowel care and provide greater independence [69]. Adult patients with overflow incontinence and pediatric patients with encopresis present with complaints of fecal incontinence due to the constant seepage of stool from a full rectum. Treatment of both patients begins with a complete colonic cleansing. The first step is rectal disimpaction, either manually or with enemas, followed by use of a cathartic such as a polyethylene glycol colonic prep (Nulytely, Braintree Laboratories, Inc, Braintree, MA). Once the colon is empty, the patient uses a regimen of laxatives and daily attempts at defecation after meals, often aided by suppositories or enemas, to avoid recurrent constipation. Use of a polyethylene glycol laxative developed for daily use (Miralax, Braintree Laboratories Inc., Braintree, MA) can simplify a laborious regimen [70]. Other options to consider in patients with evacuation difficulties who fail bowel regimens include retrograde enemas and the antegrade colonic enema (ACE) procedure [71,72]. Biofeedback Biofeedback therapy is best applied to motivated patients with some ability to voluntarily contract the external anal sphincter, even if the muscle is partially disrupted, and intact rectal sensation. Over the course of three to five weekly sessions, a trained biofeedback therapist works with the patient, teaching basic concepts of anatomy and physiology and instructing the patient in appropriate exercises to improve external anal sphincter strength, improve rectal sensory thresholds, and enhance coordination of external anal sphincter function in response to rectal distention. Overall success rates of 64% to 89% are reported, and biofeedback can enhance function after sphincteroplasty [73,74]. Despite its use since 1974, the mechanism of success is unclear, therapists apply varying treatment protocols and instrumentation, and long-term results are infrequently reported [73,75]. Nevertheless, the advantages of biofeedback—that it is safe, effective, and does not preclude other treatments—seem to outweigh its limitations.

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Surgical treatments Surgical therapy for fecal incontinence is considered in patients with anatomic abnormalities and with severe incontinence refractory to medical management. Hemorrhoids or anal fistula leading to fecal soiling should be treated appropriately. Rectal prolapse may be corrected with a perineal or abdominal approach. Sphincter injuries are usually first repaired with overlapping sphincteroplasty. Innovative techniques, such as stimulated graciloplasty, artificial bowel sphincter, and sacral nerve stimulation, are usually reserved for patients with complex anatomic defects, neurogenic incontinence, or failure from other therapies. Fecal diversion may be appropriate and acceptable in selected patients. Sphincteroplasty Originally described by Parks [76], overlapping sphincteroplasty is the most common delayed procedure used to treat traumatic sphincter disruption. With the patient in the prone jackknife position, a curvilinear incision is made in the perineal body over the anterior injury. Anterior vaginal and posterior anodermal flaps are created, and the sphincter muscle is dissected laterally on each side of the defect. Sphincter mobilization is not carried posterior to the midlateral line to avoid pudendal nerve injury. The anterior scar is divided in the middle, but not excised, to aid in suture fixation. The muscle flaps are then overlapped to form a snug anal opening; the repair is then secured with 2-0 absorbable mattress sutures. An anterior levatoroplasty is sometimes added to lengthen the anal canal. The skin is loosely reapproximated in a manner to increase perineal body length and allow adequate drainage of the repair. The success of overlapping sphincteroplasty is reported to be between 70% and 90% [77–80]. Almost two thirds of these patients will have good to excellent results; a small minority of patients will have worse function. Poor preoperative continence (incontinence of solid stool) [81] and previous repairs [82] may be predictive of poorer postoperative continence levels. Advanced age [79,80,83], fecal diversion [80,84,85], or bowel confinement [86] do not appear to affect results. It is controversial whether the presence of unilateral or bilateral pudendal neuropathy affects the outcome of sphincteroplasty [53,54,77,81,87–89]. In the acute setting, a recognized sphincter injury may be primarily repaired. Obstetric injuries are traditionally repaired in an end-to-end manner at the time of disruption. Up to three quarters of these repairs will continue to have external sphincter disruption on postoperative endoanal ultrasound, however [31]. Sultan et al used overlapping sphincteroplasty to repair acute obstetric injuries; only 15% of patients had a persistent external sphincter defect on follow-up ultrasound at three months [90]. It is unclear whether this change in repair technique prevents patients from having symptomatic incontinence in the future.

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The management of nonoperative traumatic injuries, such as open pelvic fractures and perineal impalement injuries, depends on the overall stability of the patient. Commonly associated with motorcycle accidents, mortality rates as high as 32% to 58% have been observed with pelviperineal trauma [91]. Up to 80% of survivors suffer the complication of pelvic sepsis [92]. Hence the standard approach consists of achieving hemodynamic stability, followed by diverting colostomy, distal stump washout, and presacral drainage. Sphincter repair may be performed electively when other acute issues are resolved. Repair at the time of injury may be considered in the stable patient with isolated perineal trauma [93]. Most patients will experience good to excellent continence after delayed repair. Preoperative anorectal physiology testing may detect occult defects and improve the likelihood of successful repair [77]. Innovative treatments for fecal incontinence Innovative treatments for fecal incontinence are typically applied to the patient whose only other option is a stoma because traditional methods have failed or are inadequate to handle an extensive traumatic or neurogenic injury. Additionally, only about half of the patients having an initial successful result from biofeedback or anterior sphincteroplasty retain that functional result for three or more years [75,88,94]. Options include the artificial anal sphincter, dynamic graciloplasty, and sacral stimulation, although other treatments are on the horizon. Dynamic graciloplasty The dynamic graciloplasty and the artificial anal sphincter are both advanced variations of anal encirclement for fecal incontinence. The earliest and simplest version of anal encirclement was the use of silver wire, described by Thiersch. Dynamic graciloplasty combines transposition of the gracilis muscle with electrical stimulation via an implantable pulse generator. The gracilis muscle is preferred because it has a proximal neurovascular bundle and it can be tunneled under the skin in the proximal thigh and wrapped around the anal canal. Applying electrical stimulation to the gracilis muscle allows conversion of the fast-twitch, fatigable leg muscle to a slow-twitch, fatigue resistant muscle that more closely resembles an anal sphincter. Baeten first reported the use of electrical stimulation with a gracilis muscle wrap for fecal incontinence in 1988 and subsequently reported a 72% continence rate [95,96]. The latest report from a multicenter trial found a 63% success rate, with success defined as a 50% improvement in incontinent events, and operative morbidity was high [97]. Use of dynamic graciloplasty is limited to Canada and Europe because FDA approval is not being sought in this country. Total anorectal reconstruction with dynamic graciloplasty is reported but with a high morbidity [98,99].

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Artificial bowel sphincter In our practice, the artificial anal sphincter (Acticon bowel sphincter, American Medical Systems, Minnetonka, MN) has supplanted use of the dynamic graciloplasty, because the two procedures are applicable to many of the same patients. Several features of the artificial bowel sphincter make it a more attractive option than the complex dynamic graciloplasty procedure: it is placed in a single operation, the device is operational six weeks after placement without the need for muscle conditioning, and a painful muscle transposition is avoided. The artificial anal sphincter currently in use is a modification of an artificial urinary sphincter (AMS 800, American Medical Systems). It is an implantable device composed of a silicone elastomer that maintains continence via a fluid-filled cuff that surrounds and compresses the anal canal. The patient controls the device via a pump placed in the scrotum or labia. Squeezing the pump 9 to 12 times forces the fluid from the cuff into a reservoir balloon, which is implanted in the space of Retzius. This deflates the cuff and opens the anal canal, allowing the passage of stool. The cuff then automatically slowly reinflates and occludes the anal canal providing continence until defecation is again desired. Christiansen and Lorentzen first reported implantation of an artificial anal sphincter for fecal incontinence in 1987 [100]. Since then, several groups have reported their experience with the AMS 800 and later modifications of the device [101–106]. Infections occurred in 15% to 25% of patients, 20% of patients were explanted, and final success rates were often over 70%. Complications could be successfully treated without major morbidity. A multicenter clinical trial of the artificial anal sphincter at 19 sites in the United States, Canada, and Europe ended in 2000 [107]: 112 patients were implanted (86 females) and followed a common protocol consisting of quality-of-life questionnaire, incontinence scoring, and physiology testing at six months and one year. At one year after implantation 75 patients (67%) had a functioning device and 3 were lost to follow-up. The infection rate was 25%, and 46% of implanted patients (51 of 112) had revisional surgery: 41 (37%) had devices explanted and 7 were successfully reimplanted. In this study a successful clinical result was defined as a decrease in the fecal incontinence score (FISS) of at least 24 points (score range 0–120), indicating a drop of at least two levels. For example, a patient incontinent of liquid and solid stool daily before surgery could report several incontinent events a month, but not weekly incontinence, to be judged a clinical success. To qualify for the study patients had a FISS of at least 88 or a stoma. At one-year follow-up, the mean FISS score had dropped from 105 (incontinent to liquids and solids daily) to 48 (incontinent to seepage). A valid criticism of this study is the use of a scoring system instead of diary data that may have more accurately reflected a change in continence, but successful patients nonetheless saw a dramatic drop in their scores.

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The artificial bowel sphincter (Acticon, American Medical Systems) received approval from the Food and Drug Administration (FDA) in December of 2001 for use on adults with intractable fecal incontinence. Surgeons who participated in the FDA trial and others who have undergone subsequent training perform the surgery at a limited number of sites in this country. Sacral stimulation Sacral nerve stimulation, like the artificial anal sphincter, was initially devised for urinary incontinence. Matzel, in 1995, introduced the use of sacral stimulation to treat patients with functional but not anatomic deficits of the anal sphincter muscle [108]. The procedure entails placing an electrode in a sacral foramen (S2, 3, or 4), to stimulate the nerve roots. The desired effect is maximum contraction of pelvic muscles with minimal stimulation of the fibers to the lower extremity. Once the optimal site is selected, the lead is connected to a temporary external pulse generator for a test period of stimulation, currently three weeks. If function improves adequately at the end of the test period, implantation of a permanent pulse generator is performed. Both the initial operation for placement of the lead and the subsequent placement of the pulse generator are well tolerated procedures done under light sedation. The indications for sacral stimulation are quickly being expanded due to the low morbidity of the procedure, promising results obtained on a wide variety of urology patients, and findings indicating that the stimulation effect is not confined to the striated muscle [109]. Although stimulation of the efferent motor nerves does seem to result in an increase in anal canal pressure due to contraction of the anal sphincter muscles, conversion of muscle fibers similar to that obtained with dynamic graciloplasty may also occur [108]. Sacral stimulation may modulate sacral reflexes and sacral parasympathetic nerves, thereby altering rectal compliance, anal canal resting tone, and rectal sensitivity [109]. The initial assumption that a patient needs an intact sphincter and pudendal nerve is already being challenged. An international multicenter trial evaluating the use of sacral stimulation for fecal incontinence will help define the patient population for this novel treatment.

Summary The treatment of fecal incontinence is particularly gratifying because the loss of fecal control has a devastating effect on a patient’s lifestyle. One must consider the myriad factors that influence bowel control to properly diagnose and treat each patient. Physiology testing, particularly the use of ultrasound, is essential when treatment extends beyond dietary and medical management. Recent reports suggest that the success of typical treatments

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may diminish with time. This may indicate a greater need in the future for innovative options such as the artificial bowel sphincter or sacral stimulation.

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