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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Anal incontinence

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Anal incontinence is the inability to control the evacuation of flatus or stool. It is a distressing social condition, associated with loss of self-esteem and poor personal hygiene (1). A recent population -based survey revealed a prevalence of 2.2% in the study population (2). It is more common in females and elderly patients. However it is believed that the true prevalence may be higher as many patients are reluctant to admit to this problem because of embarrassment (3).

The continence mechanism

Normal anal continence is a complex process involving integration of the rectum, the internal and external anal sphincter complex, the pelvic floor and inter-related motor and sensory neural pathways. Neural pathways can be local nervous plexuses in the wall of the rectum, sensory receptors in the pelvic floor and lining of the anal canal, the regional spinal reflexes and ultimately, higher control centers in the brain for deferring defecation until social conditions permit.

Several theories have been proposed to explain the continence mechanism. Sir Alan Parks in 1975 popularized the flap valve theory and the importance of the acute anorectal angle in which intra-abdominal forces were applied to the anterior rectal wall (4). With a rise in intra-abdominal pressure, the top of the anal canal is occluded by anterior rectal mucosa, which plugs it and prevents rectal contents from reaching the anus. Incontinence was associated with perineal descent and an obtuse anorectal angle which rendered the flap valvular mechanism ineffective. The Parks’ postanal repair was developed to recreate this anorectal angle.

Bartolo and coworkers however did not agree with the above flap valve theory. In 1986, they showed that the rectal pressures are consistently lower than anal canal pressure and that continence is associated with increased external anal sphincter and puborectalis activity. Sphincter repairs with successful outcomes were associated with significant increases in resting and squeeze pressure while the anorectal angle altered little. This was confirmed by Womack et al. in 1988 when they reported that restoration of the anorectal angle was not a pre-requisite for successful postanal repair (5).

The rectoanal inhibitory reflex is the lowering of resting sphincter pressures in response to rectal filling (6). This reflex has a role in both anorectal sampling and in defecation (7). When the anal canal becomes funnel shaped, rectal contents gain access to the specialized sensory epithelium. This anal sampling reflex allows the anorectal content to be sampled after each filling period. Continence is preserved by the external anal sphincter which maintains a high-pressure zone in the distal anal canal (8). With increasing degrees of rectal distention, internal anal sphincter relaxation increases. If defecation is deferred for too long, the external anal sphincter finally fatigues and evacuation becomes inevitable (9, 10). Some accommodation occurs by retro-peristaltic contraction in the rectum propelling stools for storage in the sigmoid, descending and transverse colon.

Another major factor in the maintenance of continence is rectal compliance. Capacitance allows deferral of emptying during continual filling. While rectal filling is appreciated from a volume of 10 ml or more, the rectum can often tolerate more than 300 ml before a feeling of fullness develops, such that there is an urgent desire to defecate. Rectal filling and distention cause regular contractions (11). The rectal pressure is said to increase with each contraction until the pressure rise exceeds tolerance, resulting in an urgent desire to defecate (12). Low compliance results in increased frequency and urgency of defecation as seen in post-irradiated pelvis (13), proctocolitis (14) or presence of extensive neoplasm. Incremental filling of the rectum results in rectoanal inhibition and anal sampling reflex. This enables a continual updating of the perception of rectal contents.

Conscious central nervous system control is essential. The exact mechanism by which continence is maintained is still unclear. In different disease states, sensory and motor impairment exert their effects in differing ways, leading to disordered continence and defecation.

Causes of anal incontinence

Common causes of this disorder include injuries to the sphincter complex, neurogenic deficits and congenital defects (table I). In females, a common cause of fecal incontinence is obstetrical injury (15, 16). In a series of 20,500 consecutive vaginal deliveries, the rate of third and fourth degree perineal tears was 5% and the rate of fecal incontinence was 0.02% (17). A recent study also estimated that 35% of primiparous females having vaginal delivery but not caesarian section sustain occult sphincter and/or pudendal nerve injuries (18).

Table I. Causes of fecal incontinence.

Table I

Causes of fecal incontinence.

Mechanism of Obstetric Anal Sphincter Injury

These result from disruption of the anal sphincter, crush and stretch injury to the pudendal nerve or both.

Anal sphincter disruption

Direct trauma to the anal sphincter can occur during episiotomy (18), application of obstetric forceps and third degree perineal lacerations from poorly controlled vaginal delivery (19). The site of injury is usually anterior, which is amenable to direct sphincter repair with generally excellent results (20, 21). However, the majority of patients undergoing sphincter repair also have some degree of pudendal neuropathy, which may progress with time, resulting in longterm failure of sphincteroplasty (22, 23). Laurberg and Gilliland found that the poor results in patients with failed sphincter repair correlated with a prolongation of pudendal nerve terminal motor latency, which suggests neuropathy (22, 24). However this issue remains controversial as other investigators have not found a similar correlation (25, 26).

Pudendal nerve injury

It is believed that the pudendal nerves which innervate the external anal sphincter are susceptible to traction injury from descent of the perineal floor as in chronic straining, descending perineal syndrome or vaginal delivery (22). The nerve injury can be documented clinically using a glovemounted electrode which measures pudendal nerve conduction time (Pudendal Nerve Terminal Motor Latency [PNTML]). Normal PNTML is less than 2.2 msecs while a latency of > 2.2 msecs but < 2.6 msecs indicates probable nerve damage and a latency measurement of > 2.6 msecs is confirmatory of pudendal nerve injury (22). Nerve injury may be unilateral or bilateral (27). A prospective study on the effect of vaginal deliveries on pelvic floor musculature found 80% of primigravida sustained reversible pudendal nerve damage. Parity, forceps and prolonged second stage were associated with more severe injuries. When the same group of patients were reviewed five years later, the occult pudendal nerve damage persisted or was more marked (2831). Existent pudendal neuropathy may be aggravated by chronic straining in defecation or by onset of menopause. With menopause, the pelvic floor musculature weakens, thereby leading to perineal descent. This further stretching of nerves would worsen any existing symptoms (32).

Consequences of pudendal neuropathy

The external anal sphincter is innervated bilaterally by the pudendal nerves with crossover in the midline (33). Hence unilateral nerve injury may result in weakening of only part of the external anal sphincter muscle and consequently, mild episodes of incontinence. Bilateral pudendal neuropathy will, by contrast, result in more severe symptoms. Large areas of denervation however may not be compensated by re-innervation. This results in progressive muscle fiber atrophy and replacement fibrosis.

Physiological importance of the external anal sphincter

The external anal sphincter (voluntary striated muscle) is responsible for approximately 20% of the resting anal pressure. The remaining 80% of resting anal pressure is contributed by the internal anal sphincter (involuntary smooth muscle) (34). Reduction in the resting anal pressure may lead to episodes of soiling and fecal leakage. The main function of the external sphincter is to ensure reflexive and voluntary recruitment of a high squeeze anal pressure in situations of increased intra-rectal or intra-abdominal pressure, such as with filling of the rectal ampulla (and consequent relaxation of internal sphincter), sneezing or coughing (10). Small reductions in the ability to generate a maximal squeeze pressure may cause incontinence to gas while larger squeeze deficits will result in gross fecal leakage and incontinence to gas, liquid and solid stools.

Current treatment of anal incontinence

Effective treatment for fecal incontinence depends on ascertaining the correct etiology and choosing the appropriate treatment (table II).

Table II. Surgical therapy for fecal incontinence.

Table II

Surgical therapy for fecal incontinence.

Anal sphincter defect alone

Patients with minor incontinence are treated with stool firming medication and/or biofeedback therapy (Grade C) (3539). Patients with major incontinence affecting their daily lives may be treated by anal sphincter repair with good results (Grade C). Surgical repair can be primary (at the time of injury) or secondary (delayed), the former being preferred. In secondary repair, the retracted free ends of muscle are mobilized and an overlapping repair is performed (40). Overlapping sphincteroplasty, has reported success rates of 78 to 90% (Grade C) (41). However it must be borne in mind that the definition of success in the evaluation of results vary between study groups. Common causes of failure are wound infection, fistula formation and pelvic floor neuropathy. Factors such as advanced age, previous repair and long duration of incontinence may also adversely affect the outcome (Grade C) (21, 22).

Anal sphincter defect and pudendal neuropathy

Most surgeons would still attempt an anatomic repair of the sphincter even in the presence of neuropathy. However in the majority of patients where there is an element of permanent neuropathy, the benefits of sphincteroplasty may be shortlived because of progressive pudendal neuropathy and external anal sphincter denervation taking its toll. Pudendal nerve terminal motor latency (PNTML) was found to be a significant predictor of outcome in several studies (Grade C) (2022).

Pudendal Neuropathy

Current management consists of either biofeedback therapy (3537, 42), sphincter and pelvic floor plication procedures or construction of a neosphincter.

Sphincter and pelvic floor plication

Post anal repair was advocated by Parks (4) for patients with intact but poorly functioning sphincter and a wide anorectal angle. This consisted of plication of the puborectalis muscle posteriorly in an attempt to recreate an acute anorectal angle and lengthen the anal canal. Parks and coworkers found restored continence in 83% of their patients. However other investigators have reported long-term continence rate in less than 60% of patients (Grade C) (4, 43). It has also been suggested that the postanal repair worsened the neurogenic damage to the pelvic floor (Grade C) (44). Subsequently, anterior plication of the anal sphincter and levator ani has been described (45) to be beneficial but with the advent of endoanal ultrasound, it became clear that only patients with demonstrable sphincter defects would benefit from this procedure (Grade C) (46). A recent modification, total pelvic floor repair, which combines anterior plication of anal sphincter and levator ani and post anal repair have also been described (47). This procedure, advocated by Keighley for neurogenic incontinence associated with obstetric injuries, creates a circumferential buttress around the anorectum. In a prospective randomized study by Keighley, 89% of patients undergoing total pelvic floor repair were continent to liquid and solid stools two years after surgery (Grade A) (48).

Neoanal sphincters

Several biological and non-biological sphincters have been described.

Artificial anal sphincter

The concept of a totally implantable artificial bowel sphincter was derived from the successful experiences with the artificial urinary sphincter. Patients failing surgical repair or not suited to a skeletal muscle transfer may be suited for this procedure. A modified device was developed for use in the anal region (4951). The artificial bowel sphincter (ABS), like its urological counterpart, has three components. There is a cuff that goes around the anal canal, a pressure regulating balloon and a pump which is located in the scrotum or labium majus. The patient uses the pump to control continence by inflating or deflating the cuff around the anal canal. In a series of twelve patients at the University of Minnesota, Wong reported a success rate of seventyfive percent. There were three infections and three mechanical complications in four patients (33%). Mean follow-up was 58 months. An elevated high pressure zone was reestablished and of the seven patients who completed a functional assessment, all reported continence to solid stools and fully satisfied with the outcome (52). Lehur also reported similar results with a success rate of seventy percent in a series of thirteen patients. Three patients developed complications necessitating explantation and a colostomy and in the remaining ten patients, nine reported continence to stools and five, continent to flatus. Median follow-up was 20 (range, 4–60) months. Infection and mechanical failure of device was again the most common complication (53). These results show that the artificial sphincter holds considerable promise in the management of severe anal incontinence where standard therapy has failed or is not applicable (Grade C).

Muscle transfers

Chetwood in 1902, described the use of the gluteus maximus muscle, transposed to create a neoanal sphincter (54). In 1952, Pickrell created neoanal sphincters in children with spina bifida and meningomyelocele using the gracilis muscle (55). Both the gracilis and the gluteus maximus muscle are still commonly used for muscle transfer but results have been disappointing because the patients are unable to sustain voluntary contraction of the skeletal muscles (56, 57). The observation by Salmons and Henriksson (58) that fast twitch, fatigueable muscle could be converted to slow twitch fatigue resistant muscle by low frequency electrostimulation paved way to successful clinical application in lattissimus dorsi flaps for cardiac assistance (59, 60). An implantable electrical pulse generator is used to convert and then continuously stimulate the muscle. This technique has been applied to the treatment of fecal incontinence by use of an electrically stimulated anal neosphincter (6164).

The construction of an electrically stimulated anal neosphincter requires several stages. In stage 1, the gracilis muscle is mobilized by dividing its distal tendinous attachment. Proximal vascular channels ensure an adequate blood supply to the distal half of the gracilis muscle when transposed to the perineum hence a delay prior to muscle transposition to enable revascularisation is seldom performed nowadays (65). A stoma if not already present is created for fecal diversion. In stage 2, the pulse generator and stimulating electrodes are implanted after an interval of six weeks from the 1st stage. In stage 3, the patient undergoes a period of training whereby a period of chronic electrical stimulation over two months converts the Type 2 fast twitch muscle to Type 1 slow twitch (66). At the completion of the training period, the muscle is continuously stimulated and the pulse generator only turned off when the patient wishes to defecate. The pulse generator is controlled with a hand held magnet that is passed over the skin to turn it on or off. The impulse generator will need to be changed after approximately 7 years.


Baeten reported that in his own personal series of 52 patients who underwent dynamic graciloplasty, 38 (73%) were continent after a median follow-up of 2.1 years (range 12 weeks to 7.4 years). Median frequency of defecation decreased from 5 to 2 times per 24 hours, median time defecation could be deferred increased from 9 seconds to 19 minutes and the median time an enema could be retained increased from 0 to 180 seconds (64). The results from a multicenter clinical experience were similarly encouraging with 71% of patients achieving and maintaining a successful outcome over the four year follow-up period (Grade C) (67).


However the procedure does come with a complication rate that cannot be ignored. Complications can result from technical problems, problems from infection, and problems attributable to an abnormal muscle or an anorectal functional imbalance (68) (table III). Infectious morbidity was high in most series, reflecting the location of surgery in a contaminated perianal area and the addition of foreign material to the operative site. Madoff reported major wound complications i.e. requiring one or more operations to treat, in one third of patients. Another third of patients had minor wound healing problems, including seromas, cellulitis, and small localized abscesses. Infectious complications had a significant effect on outcome. Forty percent of all failures were associated with major wound complications, and 41% of major wound complications led to failure of therapy (67).

Table III. Complications following dynamic graciloplasty.

Table III

Complications following dynamic graciloplasty.


Most technical problems, concerning the transposition and stimulation of the gracilis muscle can be treated. Infective problems however, are more difficult and would usually require explantation of the stimulator and leads (68). Careful attention must be paid to skin preparation, pre-operative antibiotics and surgical technique. We have found it useful to have separate teams, comprising of both surgeons and scrub nurses with separate surgical instruments, one for the perineal procedure (gracilis wrap and intramuscular leads implantation) and one for the abdominal procedure (impulse generator implantation). Soaking the leads and pulse generator in antibiotic solution before implantation and use of a resorbable antibiotic sponge at the stimulator site has been reported to help decrease the infection rate (Grade C) (64, 69). Surprisingly, the presence of a defunctioning stoma did not protect the wound from infection (Grade C) (67, 70). The effect of prior experience is important as the procedure has a steep learning curve. In a multi-center study, the 12month major wound complication rate at the two most experienced centers was 17% compared with 33% at centers new to the technique. Overall success in the experienced centers was also higher (80% vs. 47%) than the new centers. It was proposed from these results that dynamic graciloplasties be reserved for regional specialty centers where an adequate experience may be obtained and clinical expertise maintained (67).

Quality of life

Patients with a successful outcome also have a better quality of life in terms of improved effectiveness in their occupations, ability to perform tasks around the home, personal relationships, sexual function and social life. They become less isolated socially (Grade C) (64).

Cost analysis

Although dynamic gracilloplasty was considerably more expensive when compared with conventional surgery, it was found to be significantly cheaper than the costs of colostomy, including lifelong stoma care. Hence for patients who have failed conventional treatment, dynamic graciloplasty have been found to be a more cost-effective option and recommendations have been made to insurers regarding reimbursement (Grade C) (71).

Colonic irrigation

By keeping the distal colon empty of stools, one can achieve satisfactory continence. Several methods have been described in the literature. One involves the fashioning of a non-refluxing, catheterisable appendico-caecostomy (Malone antegrade continent stoma for enema administration i.e. MACE in short). An alternative is the use of a conventional colostomy irrigation set to irrigate the distal part of the colon. Both techniques are time consuming, requires motivation, dedication and commitment. However the results reported have been encouraging and offers a major improvement to quality of life (Grade C) (72, 73).

Stoma procedure

A colostomy remains an option which offer a more acceptable lifestyle than fecal incontinence when surgical repairs or neosphincters have failed or are unlikely to succeed.


There are many causes of anal incontinence and therapy therefore must be individualized for good results to be obtained. There is no single standard treatment applicable to all. As such, it is difficult to perform prospective controlled trials comparing the different surgical options available. Most of the evidence concerning the effectiveness of a particular procedure or treatment comes from case series, non-randomized historic cohort studies or non-randomized concurrent cohort studies (Grade C). Thus a good understanding of the patho-aetiology and best treatment option in each case is the only way to ensure consistently good results.


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Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6875


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