Normal bowel continence and evacuation are complex ­processes that involve the coordinated interaction between multiple different neuronal pathways and the pelvic and perineal musculature.1 The importance of the anatomic relationships of the pelvic floor in maintaining normal continence has been suggested since the 1950s.2 However, the complex series of neural and behavioral-mediated interactions, combined with a lack of an ideal study to take all elements into account, makes complete understanding of anorectal anatomy and physiology’s role in preserving continence difficult.3 Complicating this are multiple other factors that play a role in normal regulation such as systemic disease, sphincter integrity, bowel motility, stool consistency, evacuation efficiency, pelvic floor stability, cognitive and emotional affects.4

The anus and rectum have been observed, dissected, measured, and recorded in every imaginable condition to try to explain their unique ability to voluntarily withhold and evacuate both solid stool and flatus. Conventional anorectal physiology testing using techniques such as manometry, endoanal ultrasound, electrophysiologic studies, and defecography help to elucidate anorectal structures and function. However, diagnostic dilemmas occur when patients report normal function with grossly abnormal test results or abnormal function with a normal test profile. Physicians with an in-depth knowledge of normal and abnormal anorectal physiology can apply results in a meaningful way to diagnose and direct therapy while searching for other, currently unmeasured, factors. This chapter reviews the current knowledge regarding muscular, neurologic, and mechanical factors.

Muscles of the Pelvic Floor and Sphincter Complex

Control of stool can be thought of as a pressure vector diagram, with continence represented as a balance of propulsive and resistive forces. Contraction of the muscles of the pelvic floor and sphincter complex provides resistance and tone is noted during periods of rest or deep sleep. ­Voluntary ­contraction of the puborectalis and external sphincter increase resistance and defers defecation. The anal sphincter is not a paired muscle structure, like the biceps and triceps in the arm; there is no extensor ani muscle. Evacuation occurs when propulsive forces (increased intra-abdominal pressure and peristalsis of the colon and rectum) overcome the resistance of the pelvic floor and sphincter muscles. Simple skeletal or smooth muscles alone cannot perform these functions.

The pelvic floor consists of a striated muscular sheet through which viscera pass. This striated muscle, the paired levator ani muscles, is actually subdivided into four muscles defined by the area of attachment on the pubic bone. The attachments span from the pubic bone, along the arcus tendineus (a condensation of the obturator fascia), to the ischial spine. The components of the levator ani are therefore named the pubococcygeus, ileococcygeus, and ischiococcygeus. The pubococcygeus is further subdivided to include the puborectalis. Between the urogenital viscera and the anal canal lies the perineal body. The perineal body consists of the superficial and deep transverse perinei muscles and the ventral extension of the external sphincter muscle to a tendinous intersection with the bulbocavernosus muscle.5

The fourth sacral nerve innervates the levator ani muscles. Controversy continues regarding the innervation and origin of the puborectalis muscle. Cadaver studies differ from in vivo stimulation studies as to whether the puborectalis muscle receives innervation only from the sacral nerve or also from the pudendal nerve. Comparative anatomy and histological studies of fiber typing also support the inclusion of the puborectalis muscle with the sphincter complex and not as a pelvic floor muscle. In addition, electromyography (EMG) studies of the external anal sphincter (EAS) and puborectalis muscle indicate that the muscles function together with cough and strain.6

The rectal smooth muscle consists of an outer muscularis mucosa, inner circular muscle, and the outer longitudinal layer. The inner circular muscle forms the valves of Houston proximally and distally extends down into the anal canal becoming the internal anal sphincter (IAS). This is not a ­simple extension of muscle as there are histologic differences between the upper circular muscle and the IAS. For instance, the IAS is thicker than the circular muscle due to an increased number of smaller muscle cells. The outer longitudinal layer surrounds the sigmoid colon coalescing proximally into thicker bands called taenia coli. This same layer continues down to the anorectal junction where it forms the conjoined longitudinal muscle along with fibers from the pubococcygeus muscle. Distally, this muscle lies in the intersphincteric plane and fibers may fan out and cross both the internal and EAS muscles. In an ultrasound view of the anal canal, the longitudinal muscle is seen as a narrow hyperechoic line in the intersphincteric space.

The puborectalis muscle, EAS, and IAS muscles are easily viewed with endoanal ultrasound. In the hands of an experienced ultrasonographer, the technique is highly sensitive and specific in identifying internal and external sphincter defects.

External Anal Sphincter

Anatomical and sonographic studies indicate that the EAS begins development, along with the puborectalis muscle, at 9–10 weeks gestation. At 28–30 weeks it is mature and the anal sphincter then consists of three components, the striated puborectalis muscle, the smooth IAS muscle, and the smooth and striated EAS muscle.7 Further differentiation of the EAS into two or three components is highly debated. In 1715, Cowper described it as a single muscle. Later, Milligan and Morgan promoted the naming of the components as subcutaneous, superficial, and deep. Recently, Dalley makes a convincing point that the three components can only be seen in the exceptionally dissected specimen and, in most cases, the muscle is one continuous mass and should be considered as such.8

The EAS is innervated bilaterally by the pudendal nerve arising from S2 to S4. Motorneurons arise in the dorsomedial and ventromedial divisions of Onuf’s nucleus in the ventral horn of the spinal cord. Cross-over of the pudendal innervation was first suggested in studies by Swash and Henry on rhesus monkeys.9 Hamdy and associates evaluated corticoanal stimulation of humans and found variable cross-over which was symmetric in some and either right- or left-sided dominant in others.10 This has been offered as one possible explanation for the inconsistent relationship between unilateral pudendal neuropathy and fecal incontinence.

The EAS maintains tonic activity at rest due to monosynaptic spinal reflex. The tone can be abolished with spinal anesthesia and in conditions such as tabes dorsalis, where large-diameter afferent sensory fibers are destroyed, and over distension of the rectum, due to the inflation response. Maximum tone, due to phasic activity in the EAS, can be maintained for only about 1 min, before fatigue is encountered. Of interest, the only other striated muscles that maintain ­continuous low-level resting activity are the abductor of the larynx, the cricopharyngeus and the external urinary sphincter.11

Internal Anal Sphincter

The IAS is an involuntary, smooth muscle. It is the major source of anal resting pressure and is relatively hypoganglionic.12 There are nerve fibers expected in an autonomic muscle – cholinergic, adrenergic, and nonadrenergic noncholinergic fibers. It receives sympathetic innervation via the hypogastric and pelvic plexus. Parasympathetic innervation is from S1, S2, and S3 via the pelvic plexus. There is considerable evidence that the sympathetic innervation is excitatory but conflicting information regarding the parasympathetic effect.12 The IAS contributes 55% to the anal resting pressure. The myogenic activity that contributes 10 and 45% is due to the sympathetic innervation. The remainder of the resting tone is from the hemorrhoidal plexus (15%) and the EAS (30%).13 Spinal anesthesia decreases rectal tone by 50% and the decreased resting tone seen in diabetic patients may be due to an autonomic neuropathy.14

The IAS has slow waves occurring 6–20 times each minute increasing in frequency toward the distal anal canal. Ultraslow waves occur less than two times a minute and are not present in all individuals occurring in approximately 5–10% of normal individuals. Ultraslow waves are associated with higher resting pressures, hemorrhoids, and anal fissures.12 The occurrence of anal slow-wave activity with rectal pressure waves exceeding anal resting pressure suggests a role for anal slow waves in preserving continence.15 Ultrasound examination of the anal canal shows the hypoechoic IAS ending approximately 10 mm proximal to the most distal portion of the hyperechoic EAS.

Sensory Factors

Many authors describe the important relationship between anorectal sensation and fecal continence. Conventional concepts of the sensory innervation of the rectum have been challenged by data from continent patients following sphincter saving surgery and ileal pouch-anal anastomosis (IPAA).

Anal canal sensation to touch, pinprick, heat, and cold are present from the anal verge to 2.5–15 mm above the anal valves. This sensitive area is thought to help discriminate between flatus and stool but local anesthesia does not obliterate that ability. The rectum is only sensitive to distention. Rectal sensation may be due to receptors in the rectal wall but also in the pelvic fascia or surrounding muscle. The sensory pathway for rectal distention is the parasympathetic system via the pelvic plexus to S2, S3, and S4. Below 15-cm rectal distention is perceived as flatus, but above 15-cm air distention causes a sensation of abdominal discomfort. Anal canal sensation is via the inferior rectal branch of the pudendal nerve that arises from S2, S3, and S4. This is the first branch of the pudendal nerve and along with the second branch, the perineal nerve, arises from the pudendal nerve in the pudendal canal (Alcock’s canal). The remainder of the pudendal nerve continues as the dorsal nerve of the penis or clitoris.16

Many articles report daytime continence following low rectal resections with coloanal or IPAA. The reports of nighttime soiling following these procedures suggest that the ability to interpret sensory input from the neo-rectum requires conscious thought and not simple reflex contraction and relaxation. It is not clear if the decreased continence rate at night is solely due to impaired sensation (and subsequent defective discrimination of solid stool and gas) or if other factors limit fine control.

Reflexes

There are a great number of reflexes that end with the name “… anal reflex.” The reason for this is, in part, that the EAS is readily accessible and represents a convenient end point for recording during electrophysiological study. Consequently, there are a number of ways that one can assess the integrity of neurological connection through or around the spinal cord.11

Cutaneous-Anal Reflex

The cutaneous-anal reflex was first described by Rossolimo in 1891, as a brief contraction of the anal sphincter in response to pricking or scratching the perianal skin.17 This is a spinal reflex that requires intact S4 sensory and motor nerve roots. Both afferent and efferent pathways travel within the pudendal nerve.17 If a cauda equina lesion is present, this reflex will usually be absent. Henry et al. recorded the latency of the anal reflex in 22 incontinent patients as compared to 33 control subjects. The mean latency was 13.0 ms vs. 8.3 ms, respectively. The mean latency was within normal range in only three (14%) of the incontinent patients.18 However, Bartolo et al. have suggested that latency measurement of the cutaneous-anal reflex may be an inadequate means of demonstrating nerve damage in patients with fecal incontinence.19 From a practical standpoint, this is a sacral reflex that can be interrogated during physical examination by simply scratching of the perianal skin with visualization of contraction of the subcutaneous anal sphincter. The response to perianal scratch fatigues rapidly so it is important to test this as the first part of the sphincter examination.

Cough Reflex

Chan et al., using intercostal, rectus abdominis, and EAS electrodes, studied the latencies in response to voluntary cough and sniff stimulation. When compared to latencies from transcranial magnetic stimulation it appeared that the EAS response was consistent with a polysynaptic reflex pathway.20 Visible contraction of the subcutaneous EAS as a consequence to cough and sniff stimulation is a simple nonintrusive validation of the pathways involved in the anal reflex. This response can also be displayed during anal sphincter manometry. Amarenco et al. demonstrated that the greater the intensity of the cough, the greater was the electromyographic response within the anal sphincter.21 The reflex is preserved in paraplegic patients with lesions above the lumbar spine, but it is lost if the trauma involves the lumbar spine or with cauda equine lesions. The mechanism of the cough-anal reflex contributes to the maintenance of urinary and fecal continence during sudden increases in intra-abdominal pressure as might also be seen with laughing, shouting, or heavy lifting.

Bulbocavernosus Reflex

The bulbocavernosus reflex was first described by Bors and Blinn in 1959.22 The bulbocavernosus reflex is the sensation of pelvic floor contraction elicited by squeezing the glans penis or clitoris.23 The EAS is used as the end point, because it is easily accessed either for visual assessment or by concentric needle EMG recording. The BCR latency will be prolonged by various disorders affecting the S2–S4 segments of the spinal cord.

Rectal Anal Inhibitory Reflex

The rectoanal inhibitory reflex (RAIR) represents the relaxation of the IAS in response to distension of the rectum. This was first described by Gowers in 1877 and documented by Denny-Brown in 1935.24,25 It is felt that this permits fecal material or flatus to come into contact with specialized sensory receptors in the upper anal canal.26 This sampling process, the sampling reflex, creates an awareness of the presence of stool and a sense of the nature of the material present. It is felt that this process of IAS relaxation with content sampling is instrumental in the discrimination of gas from stool and the ability to pass them independently.26 The degree to which IAS relaxation occurs appears to be related to the volume of rectal distension more so in incontinent patients than in constipated or healthy control patients.27 Lower thresholds for the RAIR have been found to be associated with favorable response to biofeedback therapy in patients with fecal incontinence for formed stool.28 The amplitude of sphincter inhibition is roughly proportional to the volume extent of rectal distension.

The RAIR is primarily dependent upon intrinsic nerve innervation in that it is preserved even after the rectum has been isolated from extrinsic influences, following transaction of hypogastric nerves and the presence of spinal cord lesions. The inhibition response is in part controlled by ­nonadrenergic, noncholinergic (NANC) mediators.29 The reflex matures quite early in that it is generally present at birth and has been detected in 81% of premature infants older than 26 weeks postmenstrual age.30 The reflex is destroyed in Hirschsprung’s disease when myenteric ganglia are absent. In addition, the reflex is lost after circumferential myotomy and after generous lateral internal sphincterotomy.31 Saigusa et al. found that at an average of 23 months following closure of ileostomy after IPAA, only 53% of patients maintained a positive RAIR as compared to 96% preoperatively. The incidence of nocturnal soiling was significantly greater, 72% in those who did not have preserved, or recovered RAIR as compared to those 40% who had postoperative preserved RAIR.32

The RAIR appears to be nearly abolished in the early postoperative period following LAR resection for cancer. In a study involving 46 patients, O’Riordain found that the RAIR that had been present in 93% of patients preoperatively was only present in 18% of patients 10 days following low anterior resection. However, at 6–12 months the RAIR was intact in 21% of patients and this increased to 85% after 2 years.33 Similarly, van Duijvendijk et al., in a study of 11 patients, found the RAIR present in only 36% of patients after undergoing total mesorectal excision for carcinoma at 4 months postoperation. However, 81% of patients had a detectable RAIR at 12 months postsurgery.26

Loss of the RAIR is often a consequence of restorative proctocolectomy. Saigusa et al. found that the RAIR was present in only 53% of double-stapled IPAA patients at a mean of 23 months after closure of the ileostomy. Preservation of the RAIR correlated with less nocturnal soiling.32

The RAIR in children can be elicited even when general anesthetic agents or neuromuscular blockers are used. Glycopyrrolate, an anticholinergic appears to inhibit RAIR.34,35

Disturbances in the RAIR appear to be involved in the incontinence that is associated with systemic sclerosis. Heyt et al. found that 25 of 35 (71.4%) patients with systemic sclerosis demonstrated an impaired or absent RAIR compared with none of 45 controls. Impaired RAIR was closely correlated with fecal incontinence in that 11 of 13 (84%) of incontinent systemic sclerosis patients exhibited an impaired RAIR.36

Rectal Anal Excitatory Reflex

The rectal anal excitatory reflex (RAER) or inflation reflex is the contraction of the EAS in response to rectal distension. Rectal distension sensation is most likely transmitted along the S2, S3, and S4 parasympathetic fibers through the pelvic splanchnic nerves.37 However, on the motor side, a pudendal nerve block abolishes the excitatory reflex suggesting that pudendal neuropathy may interfere with the RAIR. Common methodologies for assessing the integrity of the pudendal nerve involve both single fiber density (SFD) of the EAS and pudendal nerve terminal motor latency (PNTML). However, derangement of the distal RAER was shown by Sangwan et al. to compare favorably with these more traditional and discomforting methodologies as an indicator of neuropathic injury to the EAS. It would appear that patients that have both an abnormal PNTML and an abnormal distal RAER do not require further study with SFD.38

Mechanical Factors of Continence and Defecation

Anorectal Angle and Flap-Valve

As a part of the pelvic floor musculature, the puborectalis arises from the pubic bone and passes horizontally and ­posteriorly around the rectum as the most medial portion of the levator ani muscle. This forms a U-shaped sling around the rectum near its anatomic junction with the anus, pulling the rectum anteriorly, and giving rise to the so-called anorectal angle. There are differences of opinion as to whether the puborectalis and anorectal angle are truly important in maintaining continence. Unlike the fine control of the external and internal sphincter muscles, the puborectalis sling is felt to be more involved with gross fecal continence.39 Parks postulated a mechanism by which this takes place.40 As intra-abdominal pressure is increased – such as with sneezing, coughing, or straining – the force is transmitted across the anterior wall of the rectum at the anorectal angle. The underlying mucosa is opposed against the upper anal canal, creating a flap-valve mechanism that prevents stool from passing to the lower anal canal and preserving continence. Yet other authors have disputed this flap-valve mechanism and downplayed the role and reliability of measuring the anorectal angle. Bannister et al., in a study of 29 patients including 14 patients with incontinence, found no evidence of a flap-valve in the normal subjects by using manometric measurements during rising intra-abdominal pressures.1 However, in the incontinent patients, the manometric pressures were consistent with a flap-valve. Yet subjects still had leakage of stool, questioning the contribution to overall continence. Bartolo and colleagues also used manometric and EMG measurements in 13 subjects both at rest and during Valsalva, demonstrating a similar rise in rectal and sphincter pressures and puborectalis EMG recordings.19 Yet, with concomitant barium studies the anterior rectal wall separated from the mucosa, allowing contrast to fill the rectum. The authors proposed that the puborectalis functions more like a sphincter rather than contributing to the flap-valve mechanism.

Furthermore, quantifying the anorectal angle and relating that to patient symptoms has resulted in mixed views. One study noted significant interobserver variation in anorectal angle measurements between three interpreters but good intraobserver consistency, suggesting that variation in anorectal angle measurements may be due to subjective interpretation of the rectal axis along the curved rectal wall. In another study assessing the reproducibility of anorectal angle ­measurement in 43 defecating proctograms, the authors found significant intra- and interobserver variations, and concluded that the anorectal angle is an inaccurate measurement.41 Jorge and associates measured the anorectal angle during rest, squeeze, and push in 104 consecutive patients and also found highly significant differences in each measurement category.42

Reservoir

As an additional part of the continence mechanism, the rectum must be able to function as a temporary storage site for liquid and solid stool. With passage of the fecal stream into the rectum, the pliable rectal walls are able to distend and delay the defecation sequence until an appropriate time. This process relies both on rectal innervation to sense and tolerate the rising volume of stool (capacity), as well as maintain a relatively low and constant pressure with increases in volume (compliance). Extremes of either of these components can lead to fecal incontinence through decreased accommodation or overflow states. Although decreased compliance has been demonstrated more often in patients with fecal incontinence, it has also been shown to occur as a normal consequence of aging.43 In addition, Bharucha and associates in a study of 52 women with fecal incontinence demonstrated that the rectal capacity was reduced in 25% of women, and these lower volume and pressure thresholds were significantly associated with rectal hypersensitivity and urge fecal incontinence.44 Furthermore, following low anterior resection for cancer, those patients with resultant lower rectal compliance and lower rectal volume tolerability (capacity) have been associated with higher rates of fecal incontinence.45

Normal Defecation

The awareness of the need to defecate occurs in the superior frontal gyrus and anterior cingulate gyrus. The process begins with movement of gas, liquid, or solid contents into the rectum. Distention of the rectum leads to stimulation of pressure receptors located on the puborectalis muscle and in the pelvic floor muscles, which in turn stimulate the RAIR. The IAS relaxes allowing sampling of contents. If defecation is to be deferred, voluntary contraction of the EAS and levator ani muscles occurs, and the rectum accommodates with relaxation after an initial increase in pressure. When the anal canal is deemed to have solid contents and a decision to defecate is made, the glottis closes, pelvic floor muscles contract, and diaphragm and abdominal wall muscles contract, all increasing abdominal pressure. The puborectalis muscle relaxes, resulting in straightening of the anorectal angle, and the pelvic floor descends slightly. The EAS relaxes and anal canal contents are evacuated. Upon normal complete evacuation, the pelvic floor rises and sphincters contract once more in a “closing reflex.”

Pathologic Conditions

Incontinence

Incontinence is the inability to defer the passage of gas, liquid, or solid stool until a desired time. Numerous alterations in anorectal physiology can lead to incontinence and many patients have more than one deficit. Structural defects in the internal or EAS muscles occur due to obstetric injury, trauma, or anorectal surgery. The keyhole deformity is a groove in the anal canal allowing the seepage of stool or mucus. Originally described as a complication after the posterior midline fissurectomy or fistulotomy, it can also occur with lateral IAS defects. Intact sphincter muscles with impaired neurologic function, due to pudendal nerve damage or systemic disorders, such as diabetes, can also result in incontinence, especially if the impaired sphincter is further stressed by diarrhea or irritable bowel syndrome.

Abnormal rectal sensation can lead to incontinence in two ways. Conditions such as proctitis due to inflammation or radiation can result in hyperacute sensation. The rectum fails to accommodate and the reservoir function is impaired leading to urgency and frequent stools. Fragmentation of stools is commonly described by patients after low anterior resection, particularly if the pelvis has been radiated as in the case of adjuvant therapy for the treatment of rectal cancer. In the case of blunted sensation, due to a large rectocele, megarectum, or neurogenic disorders, the rectum becomes over distended and overflow incontinence occurs.

The majority of patients with rectal prolapse are incontinent. Chronic stretching of the anal sphincters from full thickness prolapse leads to a patulous anus through which gas and liquid stool easily leak. A reflex relaxation of the IAS may also occur as the rectal wall descends toward the anal canal. Patients with mucosal prolapse may have seepage of mucus or small amounts of liquid stool. Correction of the prolapse can resolve the incontinence if the anal sphincter tone sufficiently returns. Age and duration of prolapse can affect this.

Obstructed Defecation

Suspected Enterocele or Rectocele (Obstructed Defecation)

Patients with symptoms of enterocele or rectocele describe prolonged straining at defecation, with a sensation of partial or complete blockage (frequently a “closed trap door” preventing passage of stool). Defecography can demonstrate the presence of a rectocele or enterocele, suggest the presence of a peritoneocele, and clarify contributing disorders such as a nonrelaxing pelvic floor, rectal intussusception or prolapse, and potentially uterovaginal prolapse.

Rectocele

A rectocele is defined as greater than 2 cm of rectal wall outpouching or bowing while straining, and can precede or accompany rectal intussusception. The rectocele can prevent passage of stool both by obstructing the anal orifice and by acting as a diverticulum to sequester stool. Patients with rectoceles commonly complain of the need for frequent sequential episodes of defecation, and even for manual compression or splinting of the anterior perineum or posterior vagina in order to completely evacuate. Additionally, patients may experience incontinence with relaxation, leading to reduction of the rectocele and return of the sequestered stool to the lower rectum.

Van Dam and associates investigated the utility of defecography in predicting the outcome of rectocele repair.46 Rectocele size, barium trapping, intussusception, evacuation, and perineal descent were measured during defecography exams of 74 consecutive patients with symptomatic rectoceles. The patients then underwent a transanal/transvaginal repair, followed by 6-month postoperative defecography and reassessment of the five most common presenting symptoms (excessive straining, incomplete evacuation, manual assistance required, sense of fullness, bowel movement less than three times per week). No postoperative defecograms demonstrated a persistent or recurrent rectocele; however, one-third of patients had a poor result based on persistent symptoms. There was no association between defecography measurements and outcome of the repair. Still, the authors concluded that defecography serves three major purposes in the evaluation of a rectocele: preoperative evidence of its presence and size, documentation of additional pelvic floor abnormalities, and an objective assessment of postoperative changes.

An abnormal increase in perineal descent (typically greater than 2 cm) has been described among both incontinent patients and continent patients who strain during defecation.32,33 These conflicting data underscore the poorly understood relationship between neuropathic pelvic floor damage and symptomatology. Bartolo and associates evaluated patients with perineal descent using manometric, radiographic, and neurophysiologic studies.47 When comparing 32 patients with incontinence and increased perineal descent with 21 patients with obstructed defecation and increased perineal descent, the authors found no significant difference in the extent of perineal descent or neuropathic damage to the EAS. Patients who were incontinent had lower manometric pressures (both resting and squeeze pressures) while those with obstructed defecation had normal manometric pressures. In a separate study, these authors also found that incontinent patients with increased perineal descent had severe denervation of both the puborectalis and the EAS compared to continent patients with increased perineal descent, who had partial denervation of the EAS only.47 Miller and colleagues evaluated sensation in two similar patient groups.48 Patients who were frankly incontinent actually had less perineal descent than continent patients with descent but had severely impaired anal sensation.

Berkelmans and others tried to determine if women with increased perineal descent and straining at stool were at risk for future development of incontinence.49 The authors identified 46 women with perineal descent who strained during defecation but were continent. Twenty-four of the 46 were followed after 5 years and 13 of these (54%) had developed fecal incontinence, compared with 3 of 20 (15%) control patients. During their initial evaluation, the patients who previously strained and later developed incontinence had significantly greater perineal descent at rest and less elevation of the pelvic floor during maximal sphincter contraction than the women who strained but did not develop incontinence.

Thus, perineal descent may be a predictor of incontinence among patients with denervation of both the EAS and the puborectalis, and in patients with impaired anal sensation. Among patients with constipation, perineal descent and straining at stool may predict future fecal incontinence.

Dyskinetic Puborectalis

Dyskinetic puborectalis, paradoxical puborectalis, nonrelaxing puborectalis, and anismus are terms that describe the absence of normal relaxation of pelvic floor muscles during defecation, resulting in rectal outlet obstruction.50 Once diagnosed, dyskinetic puborectalis is usually treated with biofeedback and bowel management. Patients who fail conservative treatment have been offered botulism toxin injections into the puborectalis muscle with limited success.51

Continence

The interplay of all the aforementioned anatomy and physiology ensures continence. It does not follow that a deficit in any one area ensures incontinence. Continence achieved in the ileoanal pouch patient is proof that the rectum is not essential. An intact and functional puborectalis muscle can provide continence in the pediatric imperforate anus patient, but incontinence can ensue during adulthood. Even profound deficits do not necessarily lead to incontinence if stool consistency is solid, while minor deficits can easily lead to incontinence to gas. To determine and treat abnormal fecal incontinence requires a systematic approach focusing on identifying the specific deficits present, applying appropriate testing to elucidate anal physiology and anatomy, and then directing therapy accordingly.

Summary

The unique physiology of the anus and rectum and the ability to master the complex task of fecal continence has many interesting facets. Understanding the anatomy, innervation, and reflexes of the pelvic floor and anal sphincters is the key to assessing disorders of continence. Further work in this area remains promising.