Chronic Fecal Incontinence Final Submission

7/28/2019 Chronic Fecal Incontinence Final Submission

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Chronic Fecal Incontinence: Review of the Disease State, Therapeutic

Alternatives and Algorithmic Approach to Treatment

Abstract:

Fecal incontinence (FI) is defined as the loss of anal sphincter control leading to unwanted

release of stool or gas. It remains a physical and psychological handicap that has significant

negative impact on the quality of life. In patients affected by chronic fecal incontinence, due to

an uncorrectable etiology, traditional medical management has been the first mainstay of

therapy. When medical therapy failed, standard surgical treatment was available, represented by

direct sphincter repair, or overlapping sphincteroplasty, which in selected cases was successful

but not durable over time. In the past decade, there have been several newer technologic and

therapeutic advancements, both invasive and non-invasive which have held out the promise of

improved continence. These techniques include: biofeedback, implantation or injection ofsynthetic or organic materials, transanal radio frequency energy (Secca procedure), sacral nerve

stimulation, stimulated graciloplasty, and artificial sphincter implantation. Each of these

technologies has associated rates of success and complications. While there remains an objective

need for controlled and comparative long-term studies, using objective data collection methods

and standardized outcome measures, there is an immediate need for a reasoned stepwise

treatment for FI. The treatment algorithm must balance the underlying cause for the disease and

allow for the selection of therapies in a manner that takes into account the rates of success,

contraindications, morbidity, cost, and ability to allow secondary or additive therapies.


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Introduction

Fecal incontinence may be defined as the recurrent uncontrolled passage of fecal material,normally of 1 month or greater duration, in an individual with a developmental age of at least 4years.1 While many patients also have the involuntary passage of flatus, this symptom alone

does not constitute classical fecal incontinence. Despite the fact that the physical consequencesof incontinence are minor, it is the psychosocial stigmata that are overwhelming with diminishedself-esteem, social isolation and stigmatization, and anxiety of anticipated accidents. There mayalso be significant economic ramifications such as loss of employment and the need forinstitutionalization. Unbeknownst to many, incontinence is the second leading cause ofinstitutionalization in the US.234With regard to the associated costs of fecal incontinence, Borrie and Davidson noted that in along-term care facility, the annual cost of nursing time and supplies was over $9,500 per patientfor dealing solely with incontinence.5 It has been estimated by some that the cost of adult diapersand protective clothing in the US exceeds $400,000,000 per year.6Attempts to accurately determine the true prevalence of fecal incontinence is difficult, because

patients are reluctant to mention fecal incontinence to their physicians, and physicians normallydo not inquire about the control of bowel function. In a random telephone survey of 2,570households in Wisconsin, during which time 7,000 people were interviewed, the prevalence ofsignificant incontinence was noted to be 2.2%, and 63% of incontinent individuals were female.In the subsequent multivariate analysis, independent risk factors for fecal incontinence weregender (female), advancing age, poor overall health, and significant physical limitations.7 Similarresults were noted in 2002, in a survey of over 15,000 individuals, during which a prevalence of1.4% of respondents had major fecal incontinence. Advancing age was an independent riskfactor, however there was no sex related differences, suggesting that men may represent an underrecognized served demographic with a significant problem.8 Other studies have found thatprevalence increases with age with a 0.5% to 1% occurrence in people younger than 65 years and3% to 8% in people older than 65 years.9 While the general population based prevalencenumbers appear relatively modest, there is a striking difference in post-partum demographics. Ina survey of 21,824 eligible postpartum women, 8,774 (40%) responded to the survey, and 2,569(29%) reported fecal incontinence since delivery. Forty-six percent of this subset, reportedincontinence of stool, the onset beginning after delivery of their first child.10 In another cohort of457 women, more than one in four women reported developing persistent fecal incontinencewithin 6 months of childbirth.11


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Table 1: Causative Factors of Fecal Incontinence

1. Anal sphincter weakness2. Anatomical disorders of the pelvic floor3.

Disorders of the central nervous systema. Dementia

b. Stroke, brain tumors, spinal cord lesions,c. Multiple system atrophy, multiple sclerosis

4. Fistula, rectal prolapse, perineal dislocation5. Diarrhea related

a. Irritable bowel syndrome, postcholecystectomy diarrheab. Ischemic colitis, metabolic diarrheac. Endocrinediabetesd. Malignancyneuroendocrine tumors

6. IBD: Crohns disease, ulcerative colitis, radiation proctitis7.

Injury relateda. Obstetric or surgical trauma

b. Hemorrhoidectomy, internal sphincterotomy, fistulotomyc. Anorectal infection

8. Miscellaneous non-traumatic injurya. Sclerodermab. Internal sphincter thinning or aging

9. Neuropathy


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Etiology of Incontinence

Multiple factors may contribute to the development of fecal incontinence, and most are listed inTable 1. A number of these conditions include: neurological, obstetric, or traumatic damage,mental disorders, spinal injuries, or conditions that cause a liquid consistency of the stool.

Overall, the most common cause is largely obstetrical which may manifest immediately post-partum or many years later.Fecal incontinence is ultimately due to multiple components which lead to impaired pelvic floorcontinence mechanisms, anal sphincter dysfunction, and disordered bowel habits. Since thegeneral availability of endoscopic anal ultrasound, it has been possible to further delineate theetiology of FI. This technology has made it possible to identify a wide range of priorunrecognized obstetrical trauma. It is now known that clinically overt anal tears and analsphincter defects occur in 35% of women after their first vaginal delivery. These internal andexternal sphincter defects resulted in significantly lower resting and squeeze pressure,respectively.12 Other studies have demonstrated internal sphincter thinning in fecalincontinence.13 Interestingly, there is not a direct correlation between the degree of symptoms of

FI and the magnitude of anal sphincter defects in the immediate post-partum period. In fact, theincidence of postpartum fecal incontinence is much lower; ranging from 0%-10% in separatestudies.1415 It is curious to note that other factors, including aging, menopause, chronicstraining, and disordered bowel habits also likely predispose to FI. Given the fact that themedian age of FI symptom development in women is 61 years old, it is difficult to correlateclinically occult anal sphincter defects to the fecal incontinence that occurs 20-30 years after theobstetrical injury.16With regard to the etiology of FI in males, incontinence is frequently associated with local injuryor disease such as hemorrhoids, fistula, poorly healed surgical scars, proctitis after radiotherapyfor prostate cancer, and a longer anal sphincter of high pressure that causes perianal soiling anddiscomfort.17 Fecal incontinence develops in up to 5% of patients following pelvic irradiation.Postoperative fecal incontinence is noted in up to 45% of patients following lateral internalsphincterotomy, with 1% reported incontinence to solid stool 5 years after surgery.18 The risk offecal incontinence after a fistulotomy has been reported to be in the range of 18% to 52%.19When considering the patient with predisposing neurological disease, injury to the associatednerves plays an important role. As an example, it has been demonstrated that up to 50% ofpatients with multiple sclerosis may have unreported fecal incontinence.20 In the diabetic patientthere are several problems that develop, which include anal sphincter weakness and diminishedsensation that usually parallels the duration of the disease.21

Clinical Evaluation and Diagnostic Testing of the Incontinent Patient

The etiology of fecal incontinence is often multifactorial and proper identification of the cause ofdisease is essential in order to select the most beneficial treatment regimen. Some of the mostimportant factors include: 1) bowel motility, 2) ability to efficiently evacuate the bowel, 3)emotional and psychological issues, 4) integrity of the sphincter, 5) stability of the pelvic floor,6) stool consistency, 7) systemic disease, and 8) neural integrity. A failure of any single factorcan easily lead to a loss of control of either stool or flatus.At a minimum, it is essential that a detailed history and physical exam be performed by thephysician. This examination should include a complete anorectal examination conducted in both


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the left lateral decubitus and seated positions. Assessment of the normal upward and anteriormovement of the puborectalis, as the patient squeezes, perianal sensation, and the anal winkreflex is needed. Examining the patient in the seated position can help to better detect excessivepelvic descent, rectal prolapse and herniation.Diagnostic testing is invaluable to help to determine etiological factors such as concomitant

sphincter and pelvic floor defects that will ultimately affect results of future therapy and offersthe possibility of quantified measurements compared to the often inaccurate subjective findingsof a physical exam. This requires an organized approach to evaluation for optimal managementand to avoid misdiagnosis that may lead to failed outcomes. Testing that should be consideredincludes: endoscopy, endoanal ultrasound, manometry, MRI, and defecography.

Endoscopic assessment of the rectosigmoid mucosa is desirable to evaluate for possiblemucosal disease such as inflammatory bowel disease or colon cancer.

Anorectal manometry and anorectal electrophysiology testing provides anal canalpressures and information about nerve function, respectively. Maximum squeeze pressure lessthan 60 mm Hg in females has been noted to have 60% sensitivity and 78% specificity indiscriminating between asymptomatic controls and fecal incontinence.22 While in another study

of 302 incontinent patients, maximum squeeze pressure was found to have had more than 90%sensitivity and specificity for discriminating between controls and fecal incontinence.23 Notablyalthough these procedures may provide valuable information there is some debate about thecorrelation of finding with disease and outcomes, as there are known wide variations in normalpressures that differ with age and gender, and there may be variable efficacy in correlating withpostoperative symptomatic improvement.

Of all the diagnostic testing available, endoanal ultrasound or similar techniques such astransperineal ultrasound (US) offer some of the most important crucial information, especially indesignation of treatment choices. In particular, endoanal US has supplanted anal sphincterelectromyography (EMG) for identifying sphincter defects.24 Although there can beinterobserver variation, endoanal US identifies sphincter thinning and defects, which are oftenclinically unrecognized and/or amenable to surgical repair.25 In one study, endoanal USidentified all 9 surgically verified external sphincter defects.26 As mentioned prior, it should benoted however that interpretation of external sphincter images may be subjective and operator-dependent due to normal anatomical variations in the external sphincter27 with reports ofsubstantial interobserver variability.2829

Pelvic MRI is another important modality which offers imaging of the sphincter complexas well as the pelvic floor. Using rapid MRI sequences, this modality demonstrates both analsphincter anatomy and global pelvic floor motion in real-time, without radiation exposure.30 Thelocation and extent of anal sphincter defects visualized by this technique was confirmed atsurgery in all 6 patients with postpartum fecal incontinence.31 MRI was felt to be the same orbetter than US for the assessment of the external sphincter.3233 This technique is even betterwhen it comes to identifying external sphincter atrophy with a sensitivity of 89% and specificityof 94% compared with histology.34 This is especially important, as external sphincter atrophy isa valuable prognostic sign of poor continence after repair of external sphincter defects.35 Finally,additional value of the MRI is found in preliminary studies which indicate that dynamic MRIwas useful for accurately characterizing perineal descent, puborectalis dyssynergia, and pelvicorgan prolapse, such as rectocoele, cystocoele, enterocoele, and uterine or vaginal prolapse.36

Pudendal nerve terminal motor latency measurement is another technique which is, intheory, supposed to be a surrogate marker of pudendal nerve injury, as it relates to potential anal


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sphincter weakness attributable to pudendal nerve injury and/or sphincter defect.37 Initial studiessuggested that patients with pudendal neuropathy would not fare as well after surgical repair ofsphincter defects compared to patients without a neuropathy. However, recent studies found thatthe test does not predict improvement, or lack thereof, after surgical repair of anal sphincterdefects, thereby limiting its usefulness.38

One final diagnostic test that should be carefully considered is defecography, sometimesreferred to as evacuation proctography. Prior to the availability of dynamic pelvic MRI,defecography was the only modality available for identifying significant perineal descent,internal rectal intussusception, rectocoeles, sigmoidocoeles or enterocoeles. During theexamination, the patient is observed during evacuation of thickened barium paste from therectum. Although felt to be limited by a lack of standardization, the technique is still felt to beuseful in the incontinent patient prior to surgery, in identifying excessive pelvic floor descent orlarge rectocoeles. As a lower resource requiring procedure it may be useful if the moreexpensive equipment or expertise for dynamic MRI is not readily available.

As an overall view of the varied diagnostic testing, although it is inviting to consider onesingle modality as thesine qua non, limiting evaluation to one test has the risk of missing other

significant factors that could influence treatment outcome. The availability of local resourcesmay be a determining factor as to which studies can be performed. As a minimum, if availabilityto a broader range of testing options is limited, endoanal ultrasonography, with the goal ofidentifying sphincter injury or atrophy is the most likely examination to affect the treatmentrecommendation. However, whenever possible multiple modalities should be employed to assistin the proper selection of which corrective procedure is best indicated or should be avoided dueto expected poor outcomes.

Therapeutic Modalities for Fecal Incontinence

Fecal incontinence is an often complex illness, which strongly compels physicians to findmeasures that will help those who suffer from one of the most socially debilitating disorders.There are several different treatment options for fecal incontinence. In considering how to treatthe disease, it is important to recall the section of the Hippocratic Oath I will use those regimenswhich will benefit my patients according to my greatest ability and judgment, and I will do noharm or injustice to them.

Given the oath, it is imperative that the treatment options are viewed based upon thepublished rates of success and even more importantly with an eye on the morbidity and mortalityassociated with each procedure, as well as cost factors. The fact that the exact mechanism ofaction for many of the technologies is not yet fully known or confirmed, that some of the moreadvanced procedures have associated complication rates of 50% or higher, and that the end pointfor the patient if the final treatment option ends in failure is an ostomy, makes it especiallyimportant to develop a treatment algorithm that allows a stepped manner of treatment that doesthe least amount of harm, yet offers a reasonable opportunity for improvement, without limitingfurther options along the way.

In reviewing the different treatments there are two common elements for all modalities.The first is that there is no randomized, controlled double-blinded, sham crossover studyavailable for any therapy, nor is there likely to ever be one performed. There are no comparativetrials of different procedures. There is however good prospective data on each procedure. The


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second commonality is that the measure of success established for the treatment of fecalincontinence or bowel control disorder, is defined as a 50% or greater improvement in fecalincontinence scores, and not an absolute measure of 0% incontinence. For the patient whosuffers from fecal incontinence even a 50% improvement is a significant event.

Biofeedback

The first line of treatment for patients with significant idiopathic fecal incontinenceis often Biofeedback with or without pelvic floor strengthening exercises. The technique isespecially attractive as it is minimally invasive, painless, and safe. Initially reported in 1974,Engel, Nikoomanesh, and Schuster described biofeedback for fecal incontinence.39 Biofeedbackmay be performed in various ways,either manometric or electromyographic (EMG) based.Normally there is placement of a pressure-sensitive probe transanally to monitor the strength andcoordination of the sphincter and levator ani muscles. The data is transmitted from the probe toa monitor where patients are able to see a representation of the pelvic floor activity in response to

their efforts, and with a series of exercises and visual feedback, improvements can be made inmuscle control, overall defecation and rectal sensation. The goal of this therapy is to increaseexternal sphincter strength, although an increase in anal resting pressure may be seen.Manometric sensory training involves placement of an intra-anal balloon. Patients increase thestrength of contraction in response to smaller and smaller rectal volumes. Regardless of thetreatment modality, therapy involves a significant patient commitment and the interpersonalresponse and dedication of the technician is also a key element of success. Biofeedback sessionslast from 3060 minutes and occur at 3-4 week intervals.

The success of biofeedback in patients with incontinence has been contested over theyears with up to 70% success reported in uncontrolled trials.40 More recent randomized controltrials have demonstrated more promise. In one study, 171 incontinent patients were randomizedinto 4 groups: standard medical/nursing care (i.e., advice only), advice plus verbal instruction onsphincter exercises, hospital-based computer-assisted sphincter pressure biofeedback, or hospitalbiofeedback plus use of a home EMG biofeedback device. Overall, 75% reported improvedsymptoms and 5% were cured, with improvement of symptoms, resting and squeeze pressuressustained at 1 year after therapy.41 In another trial of 72 patients who underwent biofeedbacktraining, the severity of fecal incontinence decreased significantly (11.5/20 to 5.0/20, P < .001),with 86% reporting improved continence, 100% increase in quality of life, and results sustainedfor 2 years.42 Long term improvement in incontinence was also demonstrated in 39 incontinencepatients, after completion of biofeedback therapy, defined as major in 6 patients (15.4%), fair in14 (35.9%), and minor in 14 (35.9%). All responder patients maintained the symptomimprovements through the long-term follow-up period up to 64 months.43

Despite the fact that some earlier studies have shown somewhat contradictory results astobiofeedbacks effectiveness, this was likely due to patient selection, motivation, andcompliance with the therapy. The more recent better controlled studies demonstrate that at aminimum, biofeedback is risk-free, safe and provides drastic improvements for those sufferingfrom fecal incontinence. Since patients exhibiting mild anorectal pathophysiology show goodresponse to biofeedback, it must be considered as the first line of therapeutic modalities beforeconsideration of more invasive and serious alternatives.


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Anal Sphincteroplasty

One of the mainstays of treatment even to this day has been anal sphincter repair orsphincteroplasty. The procedure is usually reserved only for those patients that have failed

medical therapy and biofeedback training, have significant symptoms and a required well-defined sphincter defect. Surgical repair of the chronic thinned or atrophic sphincter is associatedwith uniformly poor outcomes and should be avoided.

Anal sphincteroplasty is usually performed in the prone jack-knife position. Thetechnique may be either direct repair or overlapping technique, which is usually preferred. Ifnecessary both the internal and external anal sphincters can be repaired en bloc or separately.Dissection anteriorly above the level of scar tissue with proper mobilization of the sphincterslaterally provides excellent apposition of scar and muscle for ideal results.44 In a randomizedtrial comparing an overlapping repair with a direct repair, there was no difference or benefitproviding that both ends of the external sphincter were adequately mobilized and the anorectalring was plicated.45

With regard to improvement of fecal incontinence, several studies have demonstratedgood to excellent short-term results in up to two-thirds of patients.4647484950 However, theresults tend to dramatically worsen over time with fewer than 50% of patients retainingacceptable levels of continence. After five years, no patient was fully continent to flatus and lessthan 10 percent were fully continent to solid and liquid stool. After five to ten years, only 40 to45 percent of patients are satisfied with the functional outcome, and after a median of 69 months,only 14 percent of patients at the Cleveland Clinic were completely continent.5152 It is for thesereasons that patients need to be carefully informed of the long term expectations of this invasivemodality.

Transanal Radiofrequency Therapy (Secca)

A relatively new method of treating fecal incontinence is known as the Secca procedure.The device received FDA clearance in March 2002. The Secca procedure entails delivery oftemperature and impedance controlled radiofrequency (RF) energy to the sphincteric complex ofthe anal canal extending up to 2.5 cm above the dentate line. This modality represents a type ofless-invasive treatment of fecal incontinence, as compared to surgery. The procedure isperformed on an outpatient basis using conscious sedation.

The mechanism of action is felt to be multifactorial. Controlled RF energy delivery actson the diverse anorectal structures as well as on anorectal function. Remodeling and shrinkageimproves the mechanical properties of connective tissue by causing the contraction of collagenand lengthening of the anal canal. Activation of fibroblasts leads to increased collagen-1synthesis, fibroblast proliferation and its contraction. Internal anal sphincter (IAS) function isthought to be affected in at least two ways, including a direct effect on smooth muscle cellsmediated by HSP, in which synthesis is activated by tissue warming. This facilitates actinpolymerization improving the efficiency of the muscle contraction and recruitment of inactivefibers. This effect reflects in elongation of high pressure zone length. It is believed that the otherpathway involves interstitial cells of Cajal (ICC). ICCs are very sensitive to any kind of insult.Modulation of the ICCs function affects IAS function, leading to increase in basal pressure. RF


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also affects structure of MMP-1 of striated muscles that result in improved function of theexternal anal sphincter. Changes in anorectal reflexes are also detectable after RF treatment. Themost profound effect is observed in RAIR and rectal sensation. This effect was observed in twoindependent studies, but its exact pathophysiological mechanism remains unexplained. Thereexists some evidence that Vanilloid 1 receptors (V1R) could be responsible for this phenomenon

as the V1R is also sensitive to heat. Alteration of rectal sensation significantly contributes to aneffective continence mechanism.53There have been multiple studies that have demonstrated significant improvement in

fecal incontinence and quality of life following treatment both in the short and long term. In anearly non-randomized study, Takahashi examined the durability and long-term safety of theSecca procedure for the treatment of fecal incontinence and found that significant improvementsin symptoms of fecal incontinence and quality of life persisted 24 months after RF delivery to theanal canal.54 Subsequently, Takahashi reported an extension of the follow-up from their originalstudy, presenting the 5 year data. The Cleveland Clinic Florida Fecal Incontinence Scale (CCF-FI) (0 to 20), fecal incontinence-related quality of life (QOL) score, and Medical OutcomesStudy Short-Form 36 were administered up to 5 years. Differences between baseline and follow-

up were analyzed by using paired t-test. A total of 19 patients were treated and followed for 5years, including 18 females (aged 57.1 years; range of 44 to 77). The mean duration for fecalincontinence was 7.1 years (range of 1 to 21). At 5-year follow-up, the mean fecal incontinencescore had improved from 14.37 to 8.26 (p < 0.00025) with 16 patients (84.2 %) demonstratinggreater than 50 % improvement. All fecal incontinence-related QOL scores improved, includinglifestyle (2.43 to 3.15; p < 0.00075), coping (1.73 to 2.6; p < 0.00083), depression (2.24 to 3.15;p < 0.0002), and embarrassment (1.56 to 2.51; p < 0.0003). The social function component ofthe Short-Form 36 (SF-36) improved from 38.3 to 60 (p < 0.05). There was a trend towardimprovement in the mental component summary of the SF-36 from 38.1 to 48.14. There were nolong-term complications. The authors concluded that significant and sustained improvements infecal incontinence symptoms and QOL are seen at 5 years after treatment with the Seccaprocedure.55 A multi-center open-label, single arm, non-randomized trial followed a total of 43women and 7 men (average age 61 years, range of 29 to 80) for 6 months with a mean durationof fecal incontinence prior to treatment of 15.6 years. At 6 months, the mean CCF-FI scoreimproved significantly from 14.5 to 11.1 (p < 0.0001). Parameters in the fecal incontinencequality of life were improved, including lifestyle (from 2.5 to 3.1; p = 0.0001), coping (from 1.9to 2.3; p = 0.005), depression (from 2.8 to 3.1; p = 0.0008), and embarrassment (from 1.9 to 2.5;p < 0.0001)]. The mean SF-36 mental composite score improved from 45.3 to 48.3 (p = 0.06),and the mean SF-36 social function sub-score improved from 64.0 to 77.3 (p = 0.003). Patientdiaries showed that there was a significant reduction in days with any fecal incontinence (p 50% improvement incontinence) that was durable to year 3, and remarkably 40% of patients achieved 100%continence at 12 months. Most of these patients had implants in the S3 foramen. There was a 10-15% complication rate owing largely to infection or device explantation.81 The results of thisstudy were confirmatory of other earlier smaller studies and suggest that the direct progressionfrom conservative therapies to irreversible invasive surgeries such as dynamic graciloplasty or


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artificial bowl sphincter, or colostomy may not be necessary. At this point, this technology mayhold out real hope for those patients with incontinence that have failed all other less invasivemodalities.

Dynamic Graciloplasty

In 1952, Pickrell et al first described the use of the gracilis muscle transposition fortreating neurogenic incontinence in children.82 Despite the advantages of the gracilis muscleproximity to the anal canal, easy mobilization, proximal blood supply, and innervation,improvement in continence was only marginal due to rapid fatigability of the muscle.Because the gracilis is a fatigue prone Type II (fast twitch) muscle, it was not possible tomaintain sustained contraction. This changed when Salmons and Henriksson found that

electrical stimulation causes the skeletal muscle to undergo changes in morphological,physiological, and biochemical character,83 and changes the gracilis muscle to slow twitch (TypeI) muscle allowing it to function as a sphincter.

The technique involves mobilization of the gracilis muscle from the medial leg bydetaching it distally at the knee. The muscle is then tunneled around the existing sphinctercomplex and sutured to the contralateral tibial tuberosity. Six to eight weeks later electrodes areimplanted through a subcutaneous tunnel into the muscle and a neuro-stimulator is implanted in apocket in the abdominal wall. Stimulation of the gracilis muscle involves progressive increase inactivation of the generator. Normally after 8 weeks of conditioning, the nerve stimulator is lefton continuously, and the patient uses a magnet to turn off the nerve stimulator to defecate.

The success rates after stimulated graciloplasty have been reported in severalstudies, and unfortunately complication rates have been substantial. No randomized controlledtrials have been performed. The largest and most complete series describes the safety, efficacy,and long-term results of 129 patients who had undergone the procedure at 20 institutions.848586The short-term result showed success for 63% and minor improvement in 11%. At 18 monthssuccess decreased to 57% and minor improvement increased to 13%. Anal resting pressures andsqueeze pressures after stimulation increased significantly from 38 mmHg to 58 mmHg andsqueeze pressures from 50 mmHg to 93 mmHg. The long-term results at 24 months revealedthat 15% of patients were continent 100% of the time, 42% had a 50% improvement incontinence from baseline. There was a long term decrease in both liquid and solid stoolincontinent bowel movement as well as decreased pad use at 24 months. In another multicenterstudy from 12 centers, Madoff reported similar success rates in 139 patients.87 Complicationrates however were high, including pain, stimulator problems, and wound complications. Theassociation with substantial morbidity is not restricted to any particular center. There were 123patients enrolled in the Dynamic Graciloplasty Therapy Study Group protocol, and 91(74%) hada total of 189 complications. Infection was the most frequent cause of serious complications andthe most frequent cause of failure of the procedure.88 Presently, very few specialized centersperform this procedure, and it is not approved in the United States.


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Artificial Bowel Sphincter Implant

For individuals with severe fecal incontinence who have failed medical interventions,other less invasive modalities liked the Secca procedure, and sphincter repair, the choices are

limited. In these cases, the artificial bowel sphincter has a role, especially in patients withsignificant sphincter disruption. The artificial bowel sphincter appears to provide goodrestoration of continence for solid and liquid stool, especially if the patient can retain the device.

Artificial sphincters were initially developed for the treatment of urinary incontinence.89The artificial bowel sphincter is a modification of the highly successful artificial urinarysphincter for urinary incontinence. The currently used device is the ActiconTM Neosphincter(American Medical Systems, Inc., Minnetonka, Minn.). Following perineal dissection, the deviceis placed around the existing sphincter complex. The device consists of three interconnectedcomponents: an occlusive cuff, a pressure-regulating balloon and a control pump. The occlusivecuff is implanted around a segment of the anal canal. The device maintains continence in thepatient by using the pressure of the fluid-filled cuff to occlude the anal canal. To evacuate the

bowel, the patient squeezes and releases the pump mechanism, located in the labium or scrotum,several times to move fluid from the cuff to the pressure-regulating balloon implanted in theabdomen. This movement of fluid empties and collapses the cuff, resulting in the release of thecompressive force around the anal canal. Residual pressure within the balloon allows fluid toflow back into the cuff, automatically refilling the cuff within a few minutes.90 Because ofimplantation of a silicone device in the perianal area, the perioperative infection rate is high, anddevice removal due to infection may be necessary. Additionally, the sphincter may needreplacement as often as every 5 years because of device wear.

Reported experience with the artificial bowel sphincter began to surface in 1987.Hundreds of devices have been implanted in the US, Europe and Australia. The largest and mostcomprehensive trial was reported by Wong in 2002.91 In this multicenter cohort study 112artificial sphincters were implanted. The etiology of fecal incontinence was: 29.6% obstetrictrauma, 20% neurologic, 20%, congenital abnormality, 18% trauma, and 12% miscellaneous.12%. In the implanted patients, continence improved significantly with mean improvement inthe continence score of 51 points, with only minor seepage, compared to being completelyincontinent to liquid and solid stool prior. Quality of life measurements increased significantly.Patients with properly functioning implants reported 100% continence at 2 years. Despite theimprovements in continence, however, there were very significant complications. Thirty-eightpatients experienced device-related infections, 28 of whom required surgical revisions. Othercomplications included erosion of the cuff and/or the pump, pain with activation, constipation,and fecal impaction. 36% of patients had complete device explantations, with only 7 of thepatients that could be re-implanted, resulting in an overall failure rate of 30%. The overallcomplication rate was high at 87%, including patients who needed surgery (46%) or deviceexplantation. Others have also reported favorable results, with 63% of patients achievingcomplete continence and 79% of patients continent to both solid and liquid stool. However, theexplantation rate still remained high at 20-37%.929394The artificial bowel sphincter seems mostapplicable to patients with substantial disruption of the anal sphincters, and as the experiencewith artificial bowel sphincter has increased, explantation and infection rates seem to havedecreased.9596

The artificial sphincter is an approved treatment in the United States. This treatment


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option is used for end-stage fecal incontinence in selected patients who do not haveother treatment alternatives, except for colostomy. The artificial anal sphincter is primarily usedat specialist centers or those with dedicated interest and experience, because complication ratesare substantial, especially in inexperienced hands. This is especially important as overall, amajority of the patients implanted experienced at least one device-related adverse event. Besides

pain, the two most common adverse events were infection (31% of implanted patients) anddevice erosion (21%). Surgical intervention was required to address 36% of these adverseevents. Half (50%) of the implanted patients required at least one additional surgical devicerevision after the original implantation procedure and 30 % required total device explantationdue to adverse events.

Treatment Algorithm and OverviewBowel Control Disorder

The approach to the patient with fecal incontinence or bowel control disorder requires, ata minimum, a clear understanding of the contributing cause for the disease, in order to develop

an appropriate stepped treatment plan for the patient. Additional important factors that shouldalways be considered are related not only to the expected success of therapy, but also the costsand morbidity associated with each contemplated action. Table 2 contains a summary of thedifferent therapeutic modalities, with the accompanying rates of success, complications, andassociated costs of performing a given procedure.

Once correctable underlying medical conditions have been excluded, the first line oftherapy is always the simplest and least harmful and begins with the use of bulking agents andmedications to help slow bowel motility and encourage controlled timed evacuation. If thesesimple measures are not successful, then the next level of treatment falls to biofeedback andpelvic floor muscle training. Although the least predictable in terms of permanent treatmentoutcomes, a significant number of patients will require little more to achieve control of theirdisease, and it represents the lowest cost and is the least resource intensive.

Should this level of therapy be insufficient, the next most important decision pointdepends on the condition of the sphincteric complex. The degree of disruption of either theinternal or external anal sphincter represents a critical decision point in the selection of therapy.

Figure 1 is an algorithm that accounts for the different treatments in relation not only toimportant anatomical factors, but also takes into account the selection of modalities that may beemployed in a logical stepped manner, so as to not exclude or contraindicate a subsequentpotentially beneficial option.

The initial anatomic line in the sand is the integrity of the external sphincter. Sphincter

defects >30% are a direct indication for initial surgical correction of the sphincter defect, with itsattendant rate of success being up to 68% in the short term. The only exception is the case of anaccompanying significant internal sphincter disruption and/or external sphincter atrophy, inwhich case the outcome of surgery is known to be poor and contraindicated. Especially in thecase of internal sphincter disruption, it appears that injection of a biological gel may beconsidered the initial treatment of choice. In the event of either failure or non-availability ofproduct, sacral nerve stimulation becomes the next alternative. Another caveat to consider is thatif sphincteroplasty is able to restore the sphincter defect to


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it is possible that these two different therapies used together may provide a positive additiveeffect.

If the initial external sphincter defect is determined to be


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procedures in the event of failure. The next level of therapy may then fall to injection therapy.

If the injection therapy is contraindicated due to the level of the sphincter defect or unsuccessful,

then sacral nerve stimulation would be the next most appropriate intervention based upon its rate

of success and low complication status. Ultimately, in the event of failure of the prior

techniques, artificial sphincter implantation and dynamic graciloplasty, which are associated with

much higher morbidity, may be employed, especially as both procedures are associated with

reasonable improvement in FI.

There are some additional issues that bear careful consideration and study. One such item is the

continued accumulation of long-term data of larger patient groups of current single treatments, as

well as data concerning the potential additive benefit of multiple different interventions, the sum

of which may lead to even higher rates of improvement. In addition, considering that the ultimate

endpoint of failure of newer interventional therapies is permanent bowel diversion or colostomy,

physicians must become strong patient advocates by balancing the desire for the ultimate

research-based evidence that is either not yet or unlikely to ever be available, with already

available prospective clinical patient-based data on therapies that offer significant improvements

in fecal incontinence and an overall sense of wellbeing to patients. Finally, a component of

patient advocacy, given the devastating nature of FI, requires physicians to assist third party

payers to understand the value of each technology, even in the absence of the ultimate in

evidence-based data, and to give careful consideration on a case-by-case basis for

reimbursement.

1

Whitehead WE, Wald A, Norton NJ. Treatment options for fecal incontinence. Dis Colon Rectum 2001;44:131142.2

Crowell M, Schettler-Duncan V, Brookhart K, Barofsky I. Fecal incontinence: impact on psychosocial function and

health-related quality of life. Gastroenterology 1998;114:A738 (abstr).3OKeefe EA, Talley NJ, Zinsmeister AR, Jacobsen SJ. Bowel disorders impair functional status and quality of life in

the elderly: a population-based study. Journals of Gerontology Series A, Biological Sciences and Medical Sciences

1995;50: M184M189.4

Rockwood TH, Church JM, Fleshman JW. Fecal incontinence quality of life scale: quality of life instrument for

patients with fecal incontinence. Dis Colon Rectum 2000;43:916.5

Borrie MJ, Davidson HA. Incontinence in institutions: costs and contributing factors. CMAJ. 1992;147(3):322328.6

Johanson JF, Lafferty J. Epidemiology of fecal incontinence: the silent affliction. Am J Gastroenterol. 1996;91(1):

3336.7

Nelson R, Norton N, Cautley E, et al. Community-based prevalence of anal incontinence. JAMA. 1995;274(7):559

561.8

Perry S, Shaw C, McGrother C, et al. MRC Incontinence Study Team. Prevalence of faecal incontinence in adults

aged 40 years or more living in the community. Gut. 2002;50(4):480484.9

Enck P, Bielefeldt K, Rathmann W, et al. Epidemiology of faecal incontinence in selected patient groups. Int J

Colorectal Dis 1991;6:1436.10

Guise J-M, Morris C, Osterweil, P, Li H, Rosenberg D, Greenlick, M. Incidence of Fecal Incontinence After

Childbirth. Obstetrics and Gynecology 2007; 109,(2) 1,:281-288.


18/21

11

Boreham M, Richter H, Kenton K, Nager C, Gregory T, Aronson M, Vogt V, McIntire D, Schaffer J. Anal

incontinence in women presenting for gynecologic care: Prevalence, risk factors, and impact upon quality of life.

American Journal of Obstetrics and Gynecology (2005) 192, 163742.12

Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery.

N Engl J Med 1993;329:19051911.13

Law PJ, Kamm MA, Bartram CI. Anal endosonography in the investigation of faecal incontinence. Br J Surg1991;78:312314.14

Abramowitz L, Sobhani I, Ganansia R. Are sphincter defects the cause of anal incontinence after vaginal delivery?

Results of a prospective study. Dis Colon Rectum 2000;43:590596.15

Reilly W, Talley N, Pemberton J. Fecal incontinence: prevalence and risk factors in the community.

Gastroenterology 1995;108:A32.16

Chaliha C, Sultan AH, Bland JM, Monga AK, Stanton SL. Anal function: effect of pregnancy and delivery. Am J

Obstet Gynecol 2001;185:427432.17

Parellada CM, Miller AS, Williamson ME, Johnston D. Paradoxical high anal resting pressures in men with

idiopathic fecal seepage. Dis Colon Rectum 1998;41:593597.18

Nyam DC, Pemberton JH. Long-term results of lateral internal sphincterotomy for chronic anal fissure with

particular reference to incidence of fecal incontinence. Dis Colon Rectum 1999;42:13061310.19

Del Pino A, Nelson RL, Pearl RK, Abcarian H. Island flap anoplasty for treatment of transsphincteric fistula-in-ano.

Dis Colon Rectum 1996;39:224226.20

Wiesel PH, Norton C, Glickman S, Kamm MA. Pathophysiology and management of bowel dysfunction in multiple

sclerosis. Eur J Gastroenterol Hepatol 2001;13:441448.21

Epanomeritakis E, Koutsoumbi P, Tsiaoussis I. Impairment of anorectal function in diabetes mellitus parallels

duration of disease. Dis Colon Rectum 1999;42:13941400.22

Felt-Bersma RJ, Klinkenberg-Knol EC, Meuwissen SG. Anorectal function investigations in incontinent and

continent patients. Differences and discriminatory value. Dis Colon Rectum 1990;33:479485.23

Sun WM, Donnelly TC, Read NW. Utility of a combined test of anorectal manometry, electromyography, and

sensation in determining the mechanism of idiopathic faecal incontinence. Gut 1992;33:807813.24

Bartram CI, Sultan AH. Anal endosonography in faecal incontinence. Gut 1995;37:46.25

Nielsen MB, Hauge C, Pedersen JF, Christiansen J. Endosonographic evaluation of patients with anal

incontinence: findings and influence on surgical management. Am J Roentgenol 1993;160:771775.26

Sultan AH, Kamm MA, Talbot IC, Nicholls RJ, Bartram CI. Anal endosonography for identifying external sphincterdefects confirmed histologically. Br J Surg 1994;81:463465.27

Heyer T, Enck P, Gantke B, Schmitt A, Frieling T, Haussinger D. Anal endosonography: are morphometric

measurements of the anal sphincter reproducible. Gastroenterology 1995;108:A613.28

Gold DM, Halligan S, Kmiot WA, Bartram CI. Intraobserver and interobserver agreement in anal endosonography.

Br J Surg 1999;86:371375.29

Enck P, Heyer T, Gantke B. How reproducible are measures of the anal sphincter muscle diameter by endoanal

ultrasound? Am J Gastroenterol 1997;92:293296.30

Fletcher JG, Busse RF, Riederer SJ, et al. Imaging of anatomic and dynamic defects of the pelvic floor in

defecatory disorders. Am J Gastroenterol 2003;98:399411.31

deSouza NM, Puni R, Zbar A, Gilderdale DJ, Coutts GA, Krausz T. MR imaging of the anal sphincter in multiparous

women using an endoanal coil: correlation with in vitro anatomy and appearances in fecal incontinence. Am J

Roentgenol 1996;167:14651471.32 Malouf AJ, Halligan S, Williams AB, Bartram CI, Dhillon S, Kamm MA. Prospective assessment of interobserver

agreement for endoanal MRI in fecal incontinence. Abdom Imaging 2001;26:7678.33

Rociu E, Stoker J, Eijkemans MJ, Schouten WR, Lameris JS. Fecal incontinence: endoanal US vs. endoanal MR

imaging. Radiology 1999;212:453458.34

Briel JW, Zimmerman DD, Stoker J. Relationship between sphincter morphology on endoanal MRI and

histopathological aspects of the external anal sphincter. Int J Colorectal Dis 2000;15:8790.35

Briel JW, Stoker J, Rociu E, Lameris JS, Hop WC, Schouten WR. External anal sphincter atrophy on endoanal

magnetic resonance imaging adversely affects continence after sphincteroplasty. Br J Surg 1999;86:13221327.


19/21

36

Rentsch M, Paetzel C, Lenhart M, Feuerbach S, Jauch KW, Furst A. Dynamic magnetic resonance imaging

defecography: a diagnostic alternative in the assessment of pelvic floor disorders in proctology. Dis Colon Rectum

2001;44:9991007.37

Diamant NE, Kamm MA, Wald A, Whitehead WE. American Gastroenterological Association medical position

statement on anorectal testing techniques. Gastroenterology 1999;116: 732760.38

Malouf AJ, Norton CS, Engel AF, Nicholls RJ, Kamm MA. Longterm results of overlapping anterior anal-sphincterrepair for obstetric trauma. Lancet 2000;355:260265.39

Engel BT, Nikoomanesh P, Schuster MM. Operant conditioning of rectosphincteric responses in the treatment of

fecal incontinence. N Engl J Med. 1974;290(12):646649.40

Heymen S, Jones KR, Ringel Y, Scarlett Y, Whitehead WE. Biofeedback treatment of fecal incontinence: a critical

review. Dis Colon Rectum 2001;44:728736.41

Norton C, Chelvanayagam S, Kamm MA. Randomized controlled trial of biofeedback for fecal incontinence.

Gastroenterology 2002;122:A607.42

Bartlett L, Sloots K, Nowak M, Ho YH. Biofeedback for fecal incontinence: a randomized study comparing

exercise regimens. Dis Colon Rectum. 2011 Jul;54(7):846-56.43

Lee B, Kin N, Kang S, Kim S, Lee K, Im Y, Lee J, Oh J, Park Y, Lee D. The Long-term Clinical Efficacy of Biofeedback

Therapy for Patients With Constipation or Fecal Incontinence. J Neurogastroenterol Motil, Vol. 16 No. 2 April,

2010;177-185.44

Mellgren A, Fecal Incontinence. Surg Clin N Am 2010; 90:185194.45

Tjandra JJ, Han WR, Goh J, Carey M, Dwyer P. Direct repair vs. overlapping sphincter repair: A randomized

controlled trial. Dis Colon Rectum 2003;46:93743.46

Malouf AJ, Norton CS, Engel AF, et al. Long-term results of overlapping anterior anal-sphincter repair for

obstetric trauma. Lancet 2000;355:2605.47

Oliveira L, Pfeifer J, Wexner SD. Physiological and clinical outcome of anterior sphincteroplasty. Br J Surg

1996;83:5025.48

Halverson AL, Hull TL. Long-term outcome of overlapping anal sphincter repair. Dis Colon Rectum 2002;45:345

8.49

Bravo Gutierrez A, Madoff RD, Lowry AC, et al. Long-term results of anterior sphincteroplasty. Dis Colon Rectum

2004;47:72731.50

Trowbridge ER, Morgan D, Trowbridge MJ, et al. Sexual function, quality of life, and severity of anal incontinence

after anal sphincteroplasty. Am J Obstet Gynecol 2006;195:17537.51Engel AF, Kamm MA, Sultan AH, Bartram CI, Nicholls RJ. Anterior anal sphincter repair in patients with obstetric

trauma. Br J Surg 1994;81:12314.52

Zorcolo L, Covotta L, Bartolo DC. Outcome of anterior sphincter repair for obstetric injury: comparison of

early and late results. Dis Colon Rectum 2005;48:52431.53

Herman R, Sococki J. Radio-frequency Anal RemodelingA New Technique for Fecal Incontinence

Treatment. US Gastro Review. 2006; 34-35.54

Takahashi T, Garcia-Osogobio S, Valdovinos MA, et al. Extended two-year results of radio-frequency energy

delivery for the treatment of fecal incontinence (the Secca procedure). Dis Colon Rectum. 2003;46(6):711-715.55

Takahashi T, Morales M, et al. SECCA procedure for the treatment of fecal incontinence: Results of five-year

follow-up. Dis Colon Rectum. 2008;51(3):355-359.56

Efron JE, Corman ML, Fleshman J, et al. Safety and effectiveness of temperature-controlled radio-frequency

energy delivery to the anal canal (Secca procedure) for the treatment of fecal incontinence. Dis Colon Rectum.

2003;46(12):1606-1616; discussion 1616-1618.57

Felt-Bersma RJ, Szojda MM, Mulder CJ. Temperature-controlled radiofrequency energy (SECCA) to the anal canal

for the treatment of faecal incontinence offers moderate improvement. Eur J Gastroenterol Hepatol.

2007;19(7):575-580.58

Kim DW, Yoon HM, Park JS, et al. Radiofrequency energy delivery to the anal canal: Is it a promising new

approach to the treatment of fecal incontinence? Am J Surg. 2009;197(1):14-1859

Ruiz D, Pinto R, Hull T, Efron J, Wexner S. Does the Radiofrequency Procedure for Fecal Incontinence Improve

Quality of Life and Incontinence at 1-Year Follow-Up? Dis Colon Rectum 2010; 53:7 10411046.


20/21

60

Lefebure B, Tuech J, Bridoux V, Gallas S, Leroi AM, Denis P, Michot F. Temperature-controlled radio frequency

energy delivery (Secca procedure) for the treatment of fecal incontinence: results of a prospective study. Int J

Colorectal Dis (2008) 23:993997.61

Parisien C, Corman M. The Secca Procedure for the Treatment of Fecal Incontinence: Definitive Therapy or

Short-Term Solution. Clinics in Colon and Rectal Surgery, volume 18, number 1, 2005.62

Walega P, Jasko K, Kenig J, Herman R, Wojciech M. Radiofrequency waves in the treatment of faecalincontinence. Preliminary report. Nowak Proktologia 2009, 10 (2), p. 134-143.63

Malouf AJ, Vaizey CJ, Norton CS, Kamm MA. Internal anal sphincter augmentation for fecal incontinence using

injectable silicone biomaterial. Dis Colon Rectum. 2001;44(4):595-600.64

Maeda Y, Vaizey CJ, Kamm MA. Long-term results of perianal silicone injection for faecal incontinence. Colorectal

Dis. 2007;9(4):357-361.65

Dehli T, Lindsetmo RO, Mevik K, Vonen B. Anal incontinence--assessment of a new treatment. Tidsskr Nor

Laegeforen. 2007;127(22):2934-2936.66

Altomare DF, La Torre F, Rinaldi M, et al. Carbon-coated microbeads anal injection in outpatient treatment of

minor fecal incontinence. Dis Colon Rectum. 2008;51(4):432-435.67

Ganio E, Marino F, Giani I, et al. Injectable synthetic calcium hydroxylapatite ceramic microspheres (Coaptite) for

passive fecal incontinence. Tech Coloproctol. 2008;12(2):99-102.68

Maeda Y, Laurberg S, Norton C. Perianal injectable bulking agents as treatment for faecal incontinence in adults.

Cochrane Database Syst Rev. 2010;5:CD007959.69

Dodi G, Jongen J, de la Portilla F, Raval M, Altomare D, Lehur PA. An Open-Label, Noncomparative,Multicenter

Study to Evaluate Efficacy and Safety of NASHA/Dx Gel as a Bulking Agent for the Treatment of Fecal Incontinence.

Gastroenterology Research and Practice. 2010, 1-10.70

Frudinger A, Klle D, Schwaiger W, et al. Muscle-derived cell injection to treat anal incontinence due to obstetric

trauma: Pilot study with 1 year follow-up. Gut. 2010;59(1):55-61.71

Jarrett MED, Mowatt G, Glazener CMA, et al. Systematic review of sacral nerve stimulation for faecal

incontinence and constipation. Br J Surg 2004;91:155969.72

Tanagho EA. Concepts of neuromodulation. Neurourol Urodyn 1993;12:4878.73

Kenefick NJ, Emmanuel A, Nicholls RJ, et al. Effect of sacral nerve stimulation on

autonomic nerve function. Br J Surg 2003;90:125660.74

Tan JJ, Chan M, Tjandra JJ. Evolving therapy for fecal incontinence. Dis Colon Rectum 2007;50:195067.75

Tjandra JJ, Lim JF, Matzel K. Sacral nerve stimulation: an emerging treatment forfaecal incontinence. ANZ J Surg 2004;74:1098106.76

Leroi AM, Michot F, Grise P, et al. Effect of sacral nerve stimulation in patients with fecal and urinary

incontinence. Dis Colon Rectum 2001;44:77989.77

Ganio E, Luc AR, Clerico G, et al. Sacral nerve stimulation for treatment of fecal incontinence: a novel approach

for intractable fecal incontinence. Dis Colon Rectum 2001;44:61929.78

Jarrett MED, Varma JS, Duthie GS, et al. Sacral nerve stimulation for faecal incontinence in the UK. Br J Surg

2004;91:75561.79

Rosen HR, Urbarz C, Holzer B, et al. Sacral nerve stimulation as a treatment for fecal incontinence.

Gastroenterology 2001;121:53641.80

Tjandra JJ, Chan MK, Yeh CH, et al. Sacral nerve stimulation is more effective than optimal medical therapy for

severe fecal incontinence: a randomized, controlled study. Dis Colon Rectum 2008;51:494502.81

Steven D. Wexner, MD, John A. Coller, MD, Ghislain Devroede, MD, Tracy Hull, MD, Richard McCallum, MD,

Miranda Chan, MD, Jennifer M. Ayscue, MD, Abbas S. Shobeiri, MD, David Margolin, MD, Michael England, MD,

Howard Kaufman, MD, William J. Snape, MD, Ece Mutlu, MD, Heidi Chua, MD, Paul Pettit, MD, Deborah Nagle, MD,

Robert D. Madoff, MD, Darin R. Lerew, PhD, and Anders Mellgren, MD, PhD. Sacral Nerve Stimulation for Fecal

Incontinence, Results of a 120-Patient Prospective Multicenter Study. Annals of Surgery Volume 251, Number 3,

March 201082

Pickrell KL, Broadbent TR, Masters FW, et al. Construction of a rectal sphincter and restoration of anal

continence by transplanting the gracilis muscle; a report of four cases in children. Ann Surg.1952;135(6):853862.


21/21

83

Salmons S, Henriksson J. The adaptive response of skeletal muscle to increased use. Muscle Nerve. 1981;4(2):94

105.84

Wexner SD, Baeten C, Bailey R, et al. Long-term efficacy of dynamic graciloplasty for fecal incontinence. Dis

Colon Rectum.2002;45(6):809818.85

Matzel KE, Madoff RD, LaFontaine LJ, et al. Complications of dynamic graciloplasty: incidence, management, and

impact on outcome. Dis Colon Rectum. 2001;44(10):14271435.86

Geerdes BP, Heineman E, Konsten J, Soeters PB, Baeten CG. Dynamic graciloplasty. Complications and

management. Dis Colon Rectum 1996;39:912917.87

Madoff RD, Rosen HR, Baeten CG, LaFontaine LJ, Cavina E, Devesa M, Rouanet P, Christiansen J, Faucheron JL,

Isbister W, Kohler L, Guelinckx PJ, Pahlman L. Safety and efficacy of dynamic muscle plasty for anal incontinence:

lessons from a prospective, multicenter trial. Gastroenterology 1999;116:549556.88

Baeten CG, Bailey HR, Bakka A, 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. 2000;43(6):743

751.89

Scott FB, Bradley WE, Timm GW. Treatment of urinary incontinence by an implantable prosthetic urinary

sphincter. J Urol 1974;112:7580.90

O'Brien PE. Restoring control: The Acticon Neosphincter artificial bowel sphincter in the treatment of anal

incontinence. Dis Colon Rectum. 2000; 43(9):1213-1216.91

Wong WD, Congliosi SM, Spencer MP, et al. The safety and efficacy of the artificial bowel sphincter for fecal

incontinence: results from a multicenter cohort study. Dis Colon Rectum. 2002;45(9):11391153.92

Casal E, San Ildefonso A, Carracedo R, Facal C, Sanchez JA. Artificial bowel sphincter in severe anal

incontinence. Colorectal Dis 2004;6:1804.93

Michot F, Costaglioli B, Leroi AM, Denis P. Artificial anal sphincter in severe faecal incontinence: outcome

of prospective experience with 37 patients in one institution. Ann Surg 2003;237:526.94

Christiansen J, Rasmussen O, Lindorff-Larsen K. Longterm results of artificial anal sphincter implantation

for severe anal incontinence. Ann Surg 1999;230:458.95

Mundy L, Merlin TL, Maddern GJ, Hiller JE. Systematic review of safety and effectiveness of an artificial

bowel sphincter for faecal incontinence. Br J Surg 2004;91:66572.96

OBrien PE, Dixon JB, Skinner S, Laurie C, Khera A, Fonda D. A prospective, randomized, controlled clinical

trial of placement of the artifical bowel sphincter (Acticon Neosphincter) for the control of fecal incontinence.

Dis Colon Rectum 2004;47:185260.

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Chronic Fecal Incontinence Final Submission