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30 T.L. Hull
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39. Metcalf AM, Phillips SF, Zinsmeister AR, MacCarty RL, Beart RW, Wolff BG. Simplified assessment of segmental colonic tran­sit. Gastroenterology 1987;92:40–47.
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41. Rao SSC, Sadeghi P, Beaty J, Kavlock R, Ackerson K. Ambulatory 24-h colonic manometry in healthy humans. Am J Physiol Gastointest Liver Physiol 2001;280:G629–G639.
42. Bassotti G, Gaburri M. Manometric investigation of high­amplitude propagating contractive activity of human colon. Am J Physiol Gastrointest Liver Physiol 1988;255:G660–G664.
43. Rao SSC, Beaty J, Chamberlain M, Lambert P, Gisolfi C. Effects of acute graded exercise on human colonic motility. Am J Physiol Gastrointest Liver Physiol 1999;276:G1221–G1226.
44. Narducci F, Bassotti G, Gaburri M, Morelli A. Twenty-four hour manometric recordings of colonic motor activity in healthy man. Gut 1987;28:17–25.
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45. Steadman CJ, Phillips SF, Camilleri M, et al. Variation of mus­cle tone in the human colon. Gastroenterology 1991;101: 373–381.
46. Steadman CJ, Phillips SF, Camilleri M, et al. Control of muscle tone in the human colon. Gut 1992;33:541–546.
47. Sarna SK, Otterson MF. Myoelectric and contractile activities. In: Schuster MM, ed. Atlas of Gastrointestinal Motility in Health and Disease. Baltimore: Williams & Wilkins; 1993:3–42.
48. Dapoigny M, Trolese J-F, Bommelaer G, et al. Myoelectric spik­ing activity of right colon, left colon, and rectosigmoid of healthy humans. Dig Dis Sci 1988;33:1007–1012.
49. Bassotti G, Germani U, Morelli A. Human colonic motility: physiological aspects. Int J Colorect Dis 1995;10:173–180.
50. Bassotti G, Iantorno G, Fiorella S, Bustos-Fernandez L, Bilder C. Colonic motility in man: features in normal subjects and in patients with chronic idiopathic constipation. Am J Gastroen­terol 1999;94:1760–1770.
51. Crowell MD, Bassotti G, Cheskin LJ, Schuster MM, Whitehead WE. Method for prolonged ambulatory monitoring of high­amplitude propagated contractions from colon. Am J Physiol 1991;261:G263–G268.
52. Bassotti G, Betti C, Fusaro C, Morelli A. Colonic high-amplitude propagated contractions (mass movements): repeated 24-h studies in healthy volunteers. J Gastrointest Motil 1992;4:187–191.
53. Garcia D, Hita G, Mompean B, et al. Colonic motility: electric and manometric description of mass movement. Dis Colon Rectum 1991;34:577–584.
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55. Rae MG, Fleming N, McGregor DB, Sanders KM, Keef KD. Control of motility patterns. I. The human colonic circular mus­cle layer by pacemaker activity. J Physiol 1998;510.1:309–320.
56. Lyford GL, He Cl, Soffer E, et al. Pan-colonic decrease in inter­stitial cells of Cajal in patients with slow transit constipation. Gut 2002;51:496–501.
57. Camborova P, Hubka P, Sulkova I, Hulin I. The pacemaker activ­ity of interstitial cells of Cajal and gastric electrical activity. Physiol Res 2003;52:275–284.
58. Vanderwinden JM. Role of interstitial cells of Cajal and their relationship with the enteric nervous system. Eur J Morphol 1999;37:250–256.
59. Szurszewski JH. Electrical basis for gastrointestinal motility. In: Johnson LR, ed. Physiology of the Gastrointestinal Tract. New York: Raven Press; 1987:1435–1466.
60. Sanders KM, Stevens R, Burke EP, Ward SM. Slow waves actively propagate at submucosal surface of circular layer in canine colon. Am J Physiol 1990;259:G258–G263.
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62. Rao SSC, Hatfield RA, Suls JM, Chamberlain MJ. Psychological and physical stress induce differential effects on human colonic motility. Am J Gastroenterol 1998;93:985–990.
63. Cheskin LJ, Crowell MD, Kamal D, et al. The effects of acute exercise on colonic motility. J Gastrointest Motil 1992;4: 173–177.
64. O’Brien MD, Phillips SF. Colonic motility in health and disease. Gastroenterol Clin North Am 1996;25:147–162.
65. Duthie H-L. Colonic response to eating. Gastroenterology 1978;75:527–529.
66. Niederau C, Faber S, Karaus M. Cholecystokinin’s role in regu­lation of colonic motility in health and in irritable bowel syn­drome. Gastroenterology 1992;102:1889–1898.
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68. Bampton PA, Kinning PG, Kennedy ML, Lubowski DZ, deCarle D, Cook IJ. Spatial and temporal organization of pressure pat­terns throughout the unprepared colon during spontaneous defe­cation. Am J Gastroenterol 2000;95:1027–1035.
69. Kamm MA, van der Sup JR, Lennard-Jones JE. Colorectal and anal motility during defecation. Lancet 1992;339:820.
70. Karaus M, Sarna SK. Giant migrating contractions during defe­cation in the dog colon. Gastroenterology 1987;92:925–933.
71. Lubowski DZ, Meagher AP, Smart RC, et al. Scintigraphic assessment of colonic function during defecation. Int J Colo­rectal Dis 1995;10:91–93.
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3
Anal Physiology
Susan M. Parker and John A. Coller
Normal bowel continence is a complex process that involves the coordinated interaction between multiple different neu­ronal pathways and the pelvic and perineal musculature. The importance of the anatomic relationships of the pelvic floor in maintaining normal continence has been suggested since the 1950s. ioral-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. ple other factors that have a role in normal regulation such as systemic disease, emotional effects, bowel motility, stool consistency, evacuation efficiency, pelvic floor stability, and sphincter integrity.
Anorectal physiology testing allows evaluation of the patient with pelvic floor complaints using techniques such as manometry, endoanal ultrasound, electrophysiologic studies, and defecography, all of which help to elucidate anorectal structures and function. A physician with an in-depth knowl­edge of normal and abnormal anorectal physiology can apply the results in a meaningful way to diagnose and direct ther­apy. This chapter reviews the current knowledge regarding muscular, neurologic, and mechanical factors.
2
Yet the complex series of neural and behav-
3
Complicating this are multi-
4
Pelvic Floor Muscles
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.
1
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 histologic 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, electromyographic (EMG) studies of the external anal sphincter (EAS) and puborectalis muscle indicate that the muscles function together with cough and strain.
The rectal smooth muscle consists of an outer muscularis mucosa, inner circular muscle, and 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 because there are histologic differences between the upper circular muscle and the IAS. For instance, the IAS is thicker than the circular muscle because of 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 IAS 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 terminal fibers extend to skin as the corrugation cutaneous ani muscles.
6
External Anal Sphincter
Anatomic 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
5
33
34 S.M. Parker and J.A. Coller
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,
8
Dalley
made 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.
The EAS is innervated bilaterally by the pudendal nerve arising from S2-S4. Motor neurons arise in the dorsomedial and ventromedial divisions of Onuf’s nucleus in the ventral horn of the spinal cord. Crossover of the pudendal innervation was first suggested in studies by Wunderlich and Swash rhesus monkeys. Hamdy and associates
10
evaluated corti-
9
on
coanal stimulation of humans and found variable crossover which was symmetric in some and either right- or left-sided dominant in others. This has been offered as one possible explanation for the inconsistent relationship between unilat­eral pudendal neuropathy and fecal incontinence.
Internal Anal Sphincter
The IAS is an involuntary, smooth muscle. It is relatively hypoganglionic. nomic 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. pressure. The myogenic activity contributes 10%, and 45% is attributed to the sympathetic innervation. The remainder of the resting tone is from the hemorrhoidal plexus (15%) and the EAS (30%). 50% and the decreased resting tone seen in diabetic patients may be attributable to an autonomic neuropathy. has slow waves occurring 6–20 times each minute increasing in frequency toward the distal anal canal. Ultraslow waves occur less than 2 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. examination of the anal canal shows the hypoechoic IAS end­ing approximately 10 mm proximal to the most distal portion of the hyperechoic EAS.
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.
11
There are nerve fibers expected in an auto-
11
The IAS contributes 55% to the anal resting
12
Spinal anesthesia decreases rectal tone by
13
The IAS
11
Ultrasound
Sensory
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 attributable 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.
14
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 electrophysiologic study. Consequently, there are several ways that one can assess the integrity of neurologic connection through or around the spinal chord.
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. This is a spinal reflex that requires intact S4 sensory and motor nerve roots. Both afferent and efferent pathways travel within the puden­dal nerve. usually be absent. Henry et al. anal reflex in 22 incontinent patients as compared with 33 control subjects. The mean latency was 13.0 versus 8.3 ms, respectively. The mean latency was within normal range in only 3 (14%) of the incontinent patients.
18
et al. neous-anal reflex may be an inadequate means of demon­strating nerve damage in patients with fecal incontinence. From a practical standpoint, this is a sacral reflex that can be interrogated during physical examination by simply scratch­ing 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.
15
16
If a cauda equina lesion is present, this reflex will
17
recorded the latency of the
17
However, Bartolo
have suggested that latency measurement of the cuta-
16
3. Anal Physiology 35
Cough Reflex
Chan et al.,19using intercostal, rectus abdominis, and EAS electrodes, studied the latencies in response to voluntary cough and sniff stimulation. When compared with latencies from transcranial magnetic stimulation, it appeared that the EAS response was consistent with a polysynaptic reflex path-
19
way.
The 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.
20
demonstrated that the greater the intensity of the cough, the greater was the electromyo­graphic response within the anal sphincter. 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 intraabdominal pressure as might also be seen with laughing, shouting, or heavy lifting.
Bulbocavernosus Reflex
The bulbocavernosus reflex was first described by Bors and
21
Blinn
in 1959. The bulbocavernosus reflex is the sensation of pelvic floor contraction elicited by squeezing the glans penis or clitoris.
22
The EAS is used as the end point because it is easily accessed either for visual assessment or by con­centric needle EMG recording. The bulbocavernosus reflex latency will be prolonged by various disorders affecting the S2-S4 segments of the spinal chord.
Rectoanal 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 Brown and Robertson fecal material or flatus to come into contact with specialized sensory receptors in the upper anal canal. process, the sampling reflex, creates an awareness of the pres­ence of stool and a sense of the nature of the material present. It is believed 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. IAS relaxation occurs seems to be related to the volume of rec­tal distension more so in incontinent patients than in constipated or healthy control patients. have been found to be associated with favorable response to biofeedback therapy in patients with fecal incontinence for formed stool.
27
proportional to the volume extent of rectal distension.
The RAIR is primarily dependent on intrinsic nerve inner­vation in that it is preserved even after the rectum has been iso­lated from extrinsic influences, following transaction of
23
in 1877 and documented by Denny-
24
in 1935. It is believed that this permits
25
This sampling
25
The degree to which
26
Lower thresholds for the RAIR
The amplitude of sphincter inhibition is roughly
hypogastric nerves and the presence of spinal chord lesions. The inhibition response is in part controlled by nonadrenergic, noncholinergic mediators.
28
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
29
age.
The reflex is destroyed in Hirschsprung’s disease when myenteric ganglion are absent. In addition, the reflex is lost after circumferential myotomy and after generous lateral inter­nal sphincterotomy.
30
Saigusa et al.31found that at an average of 23 months following closure of ileostomy after ileal pouch anal anastomosis, only 53% of patients maintained a positive RAIR as compared with 96% preoperatively. The incidence of nocturnal soiling was significantly greater: 72% in those who did not have preserved, or recovered RAIR as compared with 40% who had postoperative preserved RAIR.
31
The RAIR seems to be nearly abolished in the early post­operative period after low anterior resection for cancer. In a study involving 46 patients, O’Riordain et al.
32
found that the RAIR that had been present in 93% of patients preoperatively was only present in 18% 10 days after low anterior resection. However, at 6–12 months, the RAIR was intact in 21% of patients and this increased to 85% after 2 years. van Duijvendijk et al.,
25
in a study of 11 patients, found RAIR
32
Similarly,
present in only 36% of patients after undergoing total mesorectal excision for carcinoma at 4 months after opera­tion. However, 81% of patients had a detectible RAIR at 12 months after surgery. 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.
33
Loss of RAIR is often a consequence of restorative procto-
colectomy. Saigusa et al.
31
found that the RAIR was present in only 53% of double-stapled ileal pouch anal anastomosis patients at a mean of 23 months after closure of the ileostomy. Preservation of the RAIR correlated with less nocturnal soiling.
The RAIR in children can be elicited even when general anesthetic agents or neuromuscular blockers are used. Glycopyrrolate, an anticholinergic, seems to inhibit RAIR.
34
Disturbances in the RAIR seem to be involved in the incon­tinence that is associated with systemic sclerosis. Heyt et al. found that 25 of 35 patients (71.4%) 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.
Rectoanal Excitatory Reflex
The rectoanal excitatory reflex (RAER), or inflation reflex, is the contraction of the EAS in response to rectal distension. Rectal distension sensation is likely transmitted along the S2, S3, and S4 parasympathetic fibers through the pelvic splanchnic
36
nerves. abolishes the excitatory reflex suggesting that pudendal neu­ropathy may interfere with the RAER. Common methodologies
However, on the motor side, a pudendal nerve block
35
36 S.M. Parker and J.A. Coller
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.
37
to compare favorably with these more traditional and discomforting methodologies as an indicator of neuropathic injury to the EAS. It would seem that patients that have both an abnormal PNTML and an abnormal distal RAER do not require further study with SFD.
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 believed to be more involved with gross fecal continence. postulated a mechanism by which this takes place. As intra­abdominal pressure is increased—such as with sneezing, coughing, or straining—and 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.,
1
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 increasing intraabdominal pressures. 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
18
also used manometric and EMG measure­ments in 13 subjects both at rest and during Valsalva, demon­strating a similar increase in rectal and sphincter pressures and puborectalis EMG recordings. 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. Jorgensen and colleagues
40
noted significant interobserver
variation in anorectal angle measurements among three
38
Parks
interpreters but good intraobserver consistency, suggesting that variation in anorectal angle measurements may be attrib­utable to subjective interpretation of the rectal axis along the curved rectal wall. The authors of another study, assessing the reproducibility of anorectal angle measurement in 43 defecat­ing proctograms, found significant intra- and interobserver variations, and concluded that the anorectal angle is an inac-
41
curate measurement. 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.
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 increasing 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 inconti-
39
nence, it has also been shown to occur as a normal conse­quence of aging.
42
In addition, Bharucha and associates,43in 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. Furthermore, after 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.
44
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
3. Anal Physiology 37
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 IAS or EAS muscles occur because of 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, because of 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 caused by inflammation or radiation can result in hyperacute sensation. The rectum fails to accommodate and the reservoir function is impaired lead­ing to urgency and frequency stooling. Fragmentation of stools is often 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, because of a large rectocele, megarectum, or neurogenic disorders, the rectum becomes overdistended and overflow incontinence occurs.
The majority of patients with rectal prolapse are inconti­nent. Chronic stretching of the anal sphincters from full­thickness 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 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 often 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 raphy in predicting the outcome of rectocele repair. Rectocele size, barium trapping, intussusception, evacuation, and perineal descent were measured during defecography examinations 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 defeca-
31,32
tion.
These conflicting data underscore the poorly under­stood relationship between neuropathic pelvic floor damage and symptomatology.
Bartolo and associates descent using manometric, radiographic, and neurophysio­logic studies. 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) whereas 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 external sphincter compared with continent patients with increased perineal descent, who had
45
investigated the utility of defecog-
46
evaluated patients with perineal
38 S.M. Parker and J.A. Coller
partial denervation of the external sphincter only.46Miller and colleagues
47
evaluated sensation in two similar patient groups. Patients who were frankly incontinent actually had less per­ineal descent than continent patients with descent, but had severely impaired anal sensation.
Berkelmans et al.
48
tried to determine whether women with increased perineal descent and straining at stool were at risk for future development of incontinence. 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 external sphinc­ter 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.
49
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.
50
Continence
The dynamic intention 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 patients with an ileoanal pouch is proof the rectum is not essen­tial. An intact and functional puborectalis muscle can provide continence in the patient with pediatric imperforate anus, but incontinence can ensue during adulthood. Even profound deficits do not necessarily lead to incontinence if stool consistency is solid, whereas minor deficits can easily lead to incontinence and 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.
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