Anal incontinence is defined as the involuntary loss of feces or flatus. It is a socially isolating, physically and psychologically disabling condition that often has profound consequences on all aspects of quality of life. The prevalence of fecal incontinence (FI) in the community-based adult UK population is between 2% and 3%,¹ rising with age to approximately 6% to 7% in the elderly people in the community, and 10% of patients in elderly care homes.^2,3 Because anal incontinence is a source of embarrassment, many patients do not volunteer these symptoms or seek medical advice, hence, it is thought that the condition is even more common than these figures suggest. Epidemiologic data suggest that men and women are equally affected,^2,4,5 which is surprising given that most research is focused on anal incontinence in the female population. Simple, low-cost interventions can often improve symptoms in a large number of patients. For refractory patients, more sophisticated second-line investigations and treatments have become available in recent years. This chapter will review the etiology, pathophysiology, and management of anal incontinence, with particular attention focused on the evolving areas of our increased understanding in terms of investigation and management.

FI is rarely attributable to a single factor but usually results from the interplay of multiple pathogenic mechanisms (Table 9-1). Obstetric anal sphincter trauma is the most well-recognized risk factor, and sphincter defects are associated with both abnormal physiology and symptoms of FI.⁶ Due to the stigma of incontinence, it remains grossly underreported with many women suffering in silence,⁷ and many women often present years after the initial obstetric injury. Other risk factors include the effect of aging, declining estrogen support of the pelvic floor connective tissue after menopause, or progression of neuropathy and anal sphincter atrophy.⁶

Most patients with sphincter defects alone do not develop incontinence,^6,8 and equally, abnormal anal canal manometry correlates poorly with symptoms.^9,10 The rectum plays an important role in the continence mechanism—this is most clearly demonstrated by poor functional outcome after surgical rectal excision where symptoms of incontinence correlate with the length of rectal tissue excised.^11,12 It is therefore clear that the anal sphincter complex functions alongside the rectum to maintain FI. The next section of this chapter will review the growing evidence that aberrant anorectal reflexes, as well as rectal sensorimotor dysfunction, are key contributors in the pathophysiology of FI.^13,14

Anal continence is maintained by a complex integration and coordination of the function of the pelvic floor, rectum, and anal sphincters. Understanding of the physiologic roles of each of these organs is essential in order to understand the mechanisms of defecation and maintaining continence.

Mechanism of Defecation

Defecation commences when stool is propelled into the rectum after peristaltic colonic contractions. Rectal distension with stool induces relaxation of the internal anal sphincter (IAS), allowing the sensory epithelium of the anal canal to “sample” the rectal contents (Figure 9-1). If this phenomenon occurs in a socially appropriate setting, the puborectalis and external anal sphincter muscles relax, thereby straightening the anorectal angle. In order for evacuation to occur, the intra-abdominal and rectal pressure must exceed that within the anal canal. This is achieved by performing the Valsalva maneuver or holding the breath and forcibly trying to exhale against a closed glottis, creating a “bearing down” effect. As stool enters the lower rectum, spontaneous giant rectosigmoid contractions are initiated, pushing stool through the relaxed anal canal.¹⁵ Further, large propulsive rectal contractions occur until the rectum is empty. As the stool passes through the anal canal, it stretches the external anal sphincter creating a traction force upon it. After the last bolus of stool is passed, the ‘closing reflex’ of the external sphincter is stimulated by the release of traction,¹⁶ thereby maintaining continence after the act of defecation.

Central Control of Continence

Defecation commences with rectal sensory awareness at a critical level of filling, which is relayed to the cerebral cortex as the perception of the need to evacuate the rectum. The upper motor neurons responsible for innervating the voluntary sphincter muscles lie in the parasagittal motor cortex, which communicate with Onuf’s nucleus (in the sacral spinal cord) by a fast conducting oligosynaptic pathway. Fecal urgency and urge incontinence occur in diseases affecting the upper motor neuron pathway; however, reflex defecation will still remain possible provided the lower motor pathway is still intact. FI can accompany neurologic diseases such as multiple sclerosis and traumatic spinal cord injury due to involvement of central pathways containing the corticospinal tracts that control sphincter function. Systemic disease such as diabetes mellitus can result in autonomic neuropathy, which in turn can also lead to FI.¹⁷

The striated pelvic floor muscle, urethral, and anal sphincters are innervated by the lower motor neurons whose cell bodies are in Onuf’s nucleus. Traction injury of the pudendal nerve secondary to chronic straining at stool or childbirth is the most common cause of lower motor neuron damage. Pudendal nerve injury results in progressive denervation of the pelvic floor-anal sphincter complex resulting in weakness and atrophy of these muscles.¹⁷

The Rectum

The rectum comprises the terminal portion of the colon and acts as a reservoir for stool. The rectum is innervated by the extrinsic autonomic nerves, which act upon the enteric nerves at submucosal plexuses, integrating together to allow rectal accommodation of fecal content, which is measurable as rectal compliance.

The rectal filling sensation coincides with a rise in rectal pressure but only after the rectoanal inhibitory reflex (RAIR) is initiated. After rectal filling sensation reaches consciousness, the parasympathetic driven defecation reflex is initiated unless voluntarily inhibited. Normal rectal function consists of sensory perception co-ordinating fine motor control that can either store or expel luminal contents allowing for timely defecation.

Rectal Compliance

A fundamental property of the rectum is to be capable of accommodating increases in volume with only minor alterations in pressure. This phenomenon of compliance is the volume response to a pressure distension of the rectum and is most pronounced at lower volumes of rectal filling representing active rectal relaxation to accommodate fecal material.¹⁸ As the maximum tolerable volume is approached, even small changes in volume are accompanied by changes in rectal pressure.

Alterations in rectal compliance may result in a variety of clinical and physiologic consequences including altered rectal capacity, impaired ability to perceive rectal distension, and altered threshold for reflexive IAS inhibition by rectal distension. Reduced rectal compliance has been shown in patients with fecal urgency and incontinence, inflammatory conditions such as colitis, pouchitis, or proctitis, fibrosing conditions such as scleroderma and as a long-term consequence of pelvic radiotherapy.^8,19-22 Increased rectal compliance may be seen in constipation.²³

Rectal compliance is a measure of the combined sensorimotor function of the rectum and alterations in compliance may identify factors contributing to bowel dysfunction, which in turn influences management.

The Internal Anal Sphincter

The IAS is a thickened continuation of the circular smooth muscle of the rectum. It measures approximately 3 cm in length and 3 mm in thickness, being slightly longer in men and increased thickness with age.^24,25 It terminates at about 10 mm above the skin of the anal verge.

The IAS is tonically active and under autonomic control. It contributes about 85% of the resting anal sphincter pressure, which measures between 50 and 120 mm Hg in health.²⁶ Weakness or disruption of the IAS may lead to a poor seal and an impaired sampling reflex resulting in passive leakage of fecal contents and incontinence to flatus.

Anorectal Sampling (Rectoanal Inhibitory Reflex)

The RAIR is a response to rectal filling, resulting in reflex relaxation of the upper internal sphincter. The reflex is independent of central control, being mediated by the myenteric plexus, which is itself modulated by the autonomic nervous system. The RAIR reflex is thought to be activated every 8 to 10 minutes as rectal contents are presented to the densely innervated anal mucosa. Discriminatory sensory perception allows the opportunity to distinguish solids from liquids from gas.^27,28 The extent of sphincter relaxation is dependent on the degree of rectal distension, with large volume rectal distension resulting in prolonged IAS relaxation; the opposite is also true, low volume rectal distension results in shorter IAS relaxation.²⁹ The distal portion of the IAS exhibits higher resting pressure than the more proximal portion, therefore, incontinence does not occur. This resting pressure coupled with contraction of the external anal sphincter and puborectalis results in the bowel contents being returned to the rectum and sigmoid following the sampling process.³⁰

The Pelvic Floor, Puborectalis, and Anorectal Angle

The pelvic floor consists of the pelvic diaphragm, urogenital diaphragm, and the perineal body. The pelvic diaphragm is a striated muscular layer, with a central ligamentous structure surrounding the rectum, vagina, and urethra. It is composed of a number of muscles all of which work synergistically with each other. The puborectalis muscle component of the diaphragm plays a significant role in maintenance of the anorectal angle or the acute angle between the rectum and the upper anal canal, and is important in preserving continence. This muscle forms an 80° to 90° sling around the anorectal junction and inserts into the pubic bone. Voluntary contraction of the puborectalis causes closure of the anal canal or decreases in the anorectal angle.

Sir Allan Parks proposed the flap valve theory of FI to explain how the anatomical angulation at the anorectal junction contributes to maintain continence.¹⁷ He believed that a rise in intra-abdominal pressure drives the anterior rectal wall into the upper canal, which causes occlusion.³¹ This concept was disputed by Bartolo et al.³² who radiologically demonstrated separation of the anterior rectal wall from the upper anal canal during the Valsalva maneuver and demonstrated that the anal canal was not occluded by the anterior rectal wall. In addition he showed that after successful anal sphincter repair the anorectal angle may increase, and that there is no difference in the anorectal angle between incontinent patients and controls.^32-34 These findings suggest that an obtuse anorectal angle may represent an epiphenomenon in patients with incontinence, or, in other words, is associated with incontinence but is not causative.³⁵ Both the external anal sphincter and puborectalis derive their innervation from the lower sacral roots; however, the motor supply of the external anal sphincter is via the pudendal nerve (S2, S3, S4) and that of the puborectalis is via direct branches of the sacral nerve (S3, S4). Therefore, the puborectalis can maintain continence even in the absence of both internal and external anal sphincter function.^36,37

Although consequences of obstetric external anal sphincter have been extensively described, puborectalis trauma has received less attention. Levator ani avulsion defects occur in 15% to 35% of parous women delivering vaginally.³⁸ Although levator avulsions are associated with pelvic organ prolapse, a clear correlation with FI remains to be established. It is possible that patients sustaining puborectalis trauma can still maintain continence through preserved distal anal sphincter function, compensating for the loss of the proximal component.

An additional difficulty in understanding the role of puborectalis function is due to the absence of a standardized measurement technique. MRI has been proposed for accurate imaging,³⁹ whereas the perineal dynamometer has also been described as a method for physiologic assessment.⁴⁰ Due to the close proximity of the puborectalis and external anal sphincter, it remains to be seen how current physiologic measures can accurately discriminate between the 2 structures.

The External Anal Sphincter

Proximally, the striated external anal sphincter lies in contiguity with the posterior half of the puborectalis, distally it surrounds the IAS and extends down to the skin at the anal verge.

The external sphincter contributes a small part toward resting anal tone. However, the external anal sphincter is primarily responsible for the voluntary sphincter contraction, which results in the generation of pressures of between 50 and 200 mm Hg being generated. Obstetric external anal sphincter injury is associated with a significant reduction in maximum voluntary squeeze pressure.⁶ The conscious deferment of defecation is achieved by opposing the rise in rectal pressure for a period long enough to allow rectal adaptation to occur, after which rectal pressure declines and the feeling of urgency reduces. This is achieved primarily by external anal sphincter contraction and explains the strong association of external sphincter injury or dysfunction in patients with urgency or urge incontinence.^41-43

Following a thorough history and examination, further investigations may be required to determine the causation of symptoms and to devise a tailored management plan. Endoanal ultrasound and anorectal physiology testing allow assessment of anal anatomical integrity and neuromuscular function of the sphincters, respectively. More recently, external phased MRI and endoanal MRI have been proven to be excellent techniques in the accurate detection of anal sphincter atrophy. Please see Chapter 11 for a full presentation of Anorectal Investigations. Below we present an overview of anorectal testing relevant in the evaluation of anal incontinence.

Endoanal Ultrasound

The introduction of endoanal ultrasonography (EAUS) since the early 1990s has revolutionized our understanding of the pathogenesis of FI, as well as its management.^44,45 Abnormalities of structural integrity of either muscle can be identified, as can more subtle abnormalities of internal sphincter smooth muscle texture and composition.⁴⁵ The procedure is simple, rapid, widely available, inexpensive, does not expose the patient to radiation, and carries a low patient burden. Although interpretation is operator dependent, in the hands of experienced operators sensitivity and specificity approaches 100%.^8,46-49 In the elective setting, close correlation between endosonographic images and anatomical structures have been demonstrated by in vitro, in vivo, and physiologic studies.^49-51

Two-dimensional (2D) EAUS is the conventional imaging modality used to define the anatomy of the anal sphincter complex. This technique is optimal for evaluation of IAS anatomy but visualization of the external anal sphincter can be difficult due to inherent low soft tissue contrast resolution^47,52 (Figure 9-2 EAUS image intact sphincters). Visualization of the condition of the sphincter muscle is crucial in the selection of patients with a sphincter defect for surgery. Sphincter atrophy has been shown to be associated with poor outcome following sphincter repair.⁵² Three-dimensional (3D) EAUS has recently overtaken the role of conventional 2D EAUS due to the ability to provide multiplanar imaging of the anal canal. Unlike conventional EAUS, 3D EAUS produces a digital volume that may be used to perform measurements in any plane, and therefore provides more reliable measurements of the anal sphincter complex.⁵³

EAUS has a complementary role to anorectal manometry. In the treatment of anal incontinence, it is important to link symptoms with muscle pathologies. Passive FI is typically associated with primary degeneration of the IAS occurring with degenerative diseases such as systemic sclerosis, incisional surgery such as lateral sphincterotomy, or fistulotomy and dilatation procedures. Fecal urgency or urge incontinence is typically associated with external sphincter dysfunction most commonly resulting from obstetric trauma (Figure 9-3 EAUS sphincter defect). Idiopathic FI secondary to external sphincter denervation is reported to lead to thinning of the external sphincter muscle and thickening of the internal sphincter muscle.^54,55

The use of EAUS has improved our understanding of the role of obstetrical anal sphincter injury in anal incontinence. The etiology was previously believed to be primarily due to pudendal neuropathy but EAUS has shown that mechanical sphincter trauma is the likely mechanism. The incidence of overt obstetric anal sphincter injury was initially reported to be between 0.6% and 9%⁵⁶; however, since the use of EAUS, the incidence of injury has been identified in up to 36% of women after vaginal delivery in prospective studies.^57-59 The incidence of missed or occult external sphincter tears postdelivery ranges between 12% and 35%.^6,60-64 Even in women who have an identified sphincter injury immediately following delivery, outcomes after primary sphincter repair are still suboptimal, with one study reporting up to 50% (n = 34) of women will still experience impaired continence.⁵⁸ Persistent sonographic defects were identified in 85% of these women, highlighting the need for improved training in anatomy and repair techniques.⁷

Anorectal Physiology

Anorectal manometry is a widely available technique, which provides information about anorectal function in patients with anal incontinence. Resting anal pressure results from continuous rhythmical slow wave activity of the IAS and the tonic activity of the external anal sphincter. Squeeze pressure is caused by contraction of the external anal sphincter. Defects of the external sphincter are associated with significantly lower squeeze pressure increments and defects of the internal sphincter are associated with lower resting pressures.⁶ Studies have demonstrated external anal sphincter bulk to correlate strongly with squeeze increment.⁶⁵

Rectal compliance, or the volume response to a pressure distension of the rectum, can be assessed by balloon inflation with pressure measurement. Rectal compliance is increased in a subset of patients with constipation and decreased in patients with FI.^8,19,23 The lack of standardized protocols and understanding of the contribution of abnormal rectal sensation limits the diagnostic value of compliance measurement. Rectal hypersensitivity defined as a reduced sensory threshold to volumetric rectal distension is common among individuals with fecal urgency with either a normally functioning or dysfunctional external anal sphincter.^22,41,66. Anorectal sensory testing using an electrical stimulus is the simplest way to obtain a quantitative data regarding anorectal innervation. At present, anorectal sensory testing is not proved to aid in the diagnosis and treatment of patients with incontinence, except when it is necessary to distinguish an idiopathic or functional disorder from a primary disorder or from a secondary disorder affecting extrinsic or intrinsic nerves such as diabetes mellitus.⁶⁷

Magnetic Resonance Imaging

Endoanal magnetic resonance imaging (MRI) has recently been proven to be an excellent technique for the detection of fatty sphincter atrophy as the low signal from striated muscle contrasts sharply with the surrounding bright fat. West et al.⁶⁸ carried out a study to compare 3D endoanal ultrasound measurements with endoanal MRI measurements in the detection of external anal sphincter (EAS) atrophy. They found 3D endoanal ultrasound and endoanal MRI were comparable for detecting EAS defects; however, there was poor correlation between the two methods for EAS thickness, length, and area. They concluded that 3D endoanal ultrasound could be used for the detection of EAS defects, but that 3D endoanal ultrasound measurements are not suitable parameters for assessing EAS atrophy. Another conflicting study carried out by Williams et al.⁶⁹ showed excellent correlation and interobserver agreement between 3D endoanal ultrasound and endoanal MRI in the measurement of EAS thickness using a graphics-overlay technique. Further studies have suggested potential endoanal ultrasound markers for assessing EAS atrophy and include a thin IAS and/or poorly defined EAS.⁷⁰ Currently, the role of endoanal MRI in routine assessment of anal incontinence remains unclear.

The main disadvantages with endoanal MRI are the need for an endoanal coil that can lead to patient discomfort, the time required for the study, and the cost of the study which are greater compared to EAUS and external phased-array MRI. Ideally, the use of external phased-array MRI is preferable to endoanal MRI in assessing patients preoperatively because this technique is more widely available and less invasive. A recent study by Terra et al.⁷¹ prospectively compared external phased-array MRI to endoanal MRI for depicting atrophy of the EAS in patients with FI and to evaluate interobserver reproducibility in detecting EAS atrophy with these techniques. Based on their findings, they concluded that both techniques were suitable for depicting EAS atrophy.

The following algorithm addresses some of the common causes of FI providers are likely to encounter and how these patients can be managed (Figure 9-4). Depending on symptom severity and the presence of anatomical and functional abnormalities, certain steps of the algorithm may be bypassed.

First line of therapy for symptomatic FI is primarily nonsurgical and consists of conservative measures, including low-residue diet and containment aspects such as absorbent pads, plugs, and odor control, as well as titrated loperamide. Other conservative options include pelvic floor exercises, behavioral biofeedback therapy, and transanal irrigation. Although these measures are effective in many individuals, up to half of the patients with more severe FI will fail to achieve long-term improvement.^72-74 Surgical options include injection of sphincter bulking agents, anterior external sphincter repair, neosphincter insertion, stomas, and more recently sacral nerve stimulation.¹⁷ The following section will describe in more detail each of these components of the nonsurgical and surgical treatment options for FI.

Nonsurgical Management

Diet

Dietary and fluid intervention may be used to alleviate FI, and thus promote a regimen that helps maintain an appropriate stool consistency and timing of defecation.⁷⁵ Many patients report that timing of food intake is important and triggers the gastrocolic response, thus leading to the restriction or alteration to their diet in an attempt to limit fecal incontinent episodes.⁷⁵ Currently, there are limited data on the effectiveness of dietary modifications for FI symptoms; however, a list of foods perceived by patients to improve or worsen FI has been described.^76,77 Foods reported to worsen FI include caffeinated beverages, which result in stimulation of gastrointestinal motility, chocolate, nuts, fatty foods, dairy products, gluten-containing foods, gas-producing vegetables such as broccoli and cabbage, which result in expulsion of feces by flatus and foods containing naturally occurring laxative compounds including prunes, figs, and rhubarb or laxative properties such as those included in artificial sweeteners like sorbitol.^75-77 Foodstuffs reported to improve FI include high-fiber products such as wholemeal bread, and foods such as yogurt that promote recolonization of the large bowel and promote normal function.⁷⁶

Supplementary soluble dietary fiber affects stool composition and consistency and is useful in the management of FI.^78-80 Soluble fiber is believed to firm stool consistency by reducing free stool water. Whether certain types of soluble fiber are more effective in managing FI than others along with the effect on the use of supplementary fiber versus eating high-fiber foods is unclear.⁸¹

Pharmacologic

Antidiarrheal medications are often used in treating FI, but not always optimally. Low doses of titrated liquid loperamide may help to keep the stools firm, hence, making urge to defecate easier to control. Loperamide is an opioid receptor agonist in the gut, with no dependence or antianalgesic effect. Doses between 1 and 16 mg may be safely used⁷⁵—the drug is well tolerated without evidence of tachyphylaxis or crossing of the blood-brain barrier. The syrup formulation allows easier titration for patients who experience constipation with tablet forms. The drug is often used by patients to minimize FI episodes in specific social situations such as before traveling when away from a lavatory.

Second-line drug therapies include Lomotil and codeine phosphate. Lomotil (diphenoxylate or co-phenotrope) is an opioid derivative that acts by decreasing the speed and amplitude of intestinal peristalsis, thereby increasing water absorption from the intestinal contents and consolidating waste product into a dense solid form. Atropine is added in subtherapeutic dosages to reduce the potential of overdose and abuse due to the ability of lomotil to cross the blood-brain barrier and cause mild euphoria. Lomotil has been shown to reduce stool frequency and stool volume compared with other antidiarrheal agents and placebo and has since been recommended for temporary or intermittent therapy.⁸² Codeine phosphate is divided into daily doses of 30 to 120 mg; it is not first-line therapy because of its higher central side effect profile. Bulking agents should be added cautiously as some patients may experience increased flatus and worsening of symptoms.

Evidence supporting the benefit of pharmacologic therapy in the management of FI is limited. In 2003, a Cochrane review⁸³ compared the only four randomized trials on antidiarrheal treatment versus placebo for FI and reported that active treatment was associated with fewer episodes of fecal urgency and incontinence compared to placebo. However, active treatment was associated with an increase in the number of side effects such as constipation, headache, and abdominal pain.¹⁷

One small study reported on the beneficial effect of hormone replacement therapy (HRT) in postmenopausal women with FI.⁸⁴ They found that after six months of HRT, five of 20 (25%) women were asymptomatic and an additional 13 of 20 (65%) women were symptomatically improved in terms of flatus control, fecal urgency, and passive soiling. The role of HRT in treatment of FI remains unclear.

Behavioral Biofeedback Therapy

Biofeedback therapy has been studied both as a first-line treatment for FI as well as a treatment for those who fail surgery. It is a poorly standardized technique comprising a variety of modalities. In 2001, Norton and colleagues⁸⁵ carried out a systematic review on the use of biofeedback for adults with FI. Of the 46 studies published in English, 1,364 patients underwent biofeedback and of these 275 of 566 patients (48.6%) reported being continent and 617 of 861 patients (71.7%) reported improvement in symptoms. A recent Cochrane review⁸⁶ assessing biofeedback for FI concluded that “there is not enough evidence from trials to judge whether these treatments are beneficial or who will benefit the most.”

Norton et al.⁸⁷ attempted to address this issue in a randomized trial including 171 patients randomized to one of four groups: (1) standard advice, (2) advice plus sphincter exercises, (3) hospital-based computer-assisted sphincter pressure biofeedback, and (4) hospital biofeedback plus home electromyogram biofeedback device. They found that neither pelvic floor exercises nor biofeedback was superior to standard care supplemented by advice and education. Interestingly, group 4, who had the most intensive input, was found to have the smallest degree of improvement. More recently, Heyman et al.⁸⁸ randomized 108 patients to pelvic floor exercises or manometric biofeedback plus pelvic floor exercises. At 12-month follow-up, 24 of 25 biofeedback patients (53%) reported improved continence compared with 22 of 63 (35%) of patients in the pelvic floor muscle exercise group, showing that improved abdominopelvic coordination was central to improvement along with providing definite support for the efficacy of biofeedback.

Transanal Irrigation

Transanal irrigation has recently become an established treatment for patients with spinal cord injuries and neurogenic bowel dysfunction, and also for selected patients with chronic constipation and FI.^89-93 Transanal irrigation is designed to assist the evacuation of feces from the bowel by introducing water into the rectum and colon through the anus. The water is introduced using a specialized single-use catheter and subsequently evacuated, when the catheter is removed, together with the contents of the rectum, sigmoid, and possibly the descending colon. By regularly emptying the bowel in this manner, transanal irrigation is intended to help reestablish controlled bowel function and enable the user to choose the time and place of evacuation. In patients with FI, efficient emptying of the colon and rectum means that new feces do not reach the rectum for approximately two days,⁹⁴ thereby preventing leakage between irrigations.

Evidence for the efficacy of transanal irrigation for FI is limited. Christensen et al.⁹⁵ reported a successful outcome at 21-month follow-up with transanal irrigation in 51% (n = 49) of patients with idiopathic FI and 52% (n = 21) of patients with FI secondary to sphincter disruption. Further larger randomized controlled trials of transanal irrigation in patients with specific pathologies of FI are required.

Sphincter Bulking Agents

FI secondary to IAS weakness or disruption continues to present a difficult therapeutic challenge in clinical practice.⁹⁶ IAS defects are not amenable to direct surgical repair and are associated with poor long-term outcomes.^97,98 The use of injectable bulking agents for the treatment of FI has become an option due to its simplicity and low-risk nature. However, their use has been limited due to lack of sufficient knowledge about long-term efficacy and safety. Materials such as autologous fat,⁹⁹ glutaraldehyde cross-linked collagen,¹⁰⁰ and polytetrafluroethylene¹⁰¹ have been evaluated in small numbers of patients with FI with disappointing long-term results. A larger bulking molecule (Durasphere) has recently been shown in 18 patients to produce a significant improvement in continence, patient satisfaction, and quality-of-life parameters at two-year follow-up.⁹⁶ Kenefick et al.¹⁰² also recently reported the use of silicone biomaterial in six patients showing a significant improvement in incontinence and quality-of-life scores at a median follow-up of 18 months. However, at longer term follow-up (61 months), only two patients still reported slight improvement from baseline.¹⁰³ Larger randomized trials with longer term follow-up are necessary to confirm the efficacy and safety of injectable bulking agents in IAS pathology.

Surgical Management

Sacral Neuromodulation

History and Development

Sacral nerve stimulation (SNS) is an option in those with FI, secondary to a range of etiologies, who have failed to respond to nonsurgical treatment. SNS was first performed in 1982 for the treatment of urinary incontinence.¹⁰⁴ Evidence of simultaneous improvement in bowel symptoms in those patients treated for urinary dysfunction prompted the investigation of SNS for the treatment of functional bowel disorders.¹⁰⁵ In 1995, Matzel et al.¹⁰⁶ published the first results for the use of SNS in the treatment of FI.