Filling is believing...?

Sensation is an essential aspect of fecal continence. We aimed to correlate manovolumetric and radiologic changes at successive levels of rectal filling sensation. Combined anorectal manometry and proctography were performed in nine volunteers. Images, volumes, and pressures were analyzed at the start of the test, at 20 s before first sensation, and at first, constant, urge, and maximum tolerable sensation. Consecutive levels of rectal filling sensation were associated with progressive opening and dilation of the upper anal canal (up to 44 mm) and sliding down of the rectal contents (14 mm), which had already started before the first sensation. This coincided initially with a pressure decrease in the proximal anal canal (from 94 to 42 mm Hg). With constant sensation and particularly with urge sensation, rectal pressure increase appeared to be responsible for further proximal anal dilation. This was accompanied by a significant increase of proximal anal pressure (up to 133 mm Hg) and sharpening of the angle between the anal axis and the horizontal reference line. The proximal anal canal or its surrounding structures plays an important role in the desire-to-defecate sensation. They can be activated by a progressive buildup of rectal reservoir pressure in the presence of a competent distal anal sphincter barrier.     

Combined Radiologic and Manometric Study of Rectal Filling Sensation

PURPOSE: Sensation is an essential aspect of fecal continence. We aimed to correlate manovolumetric and radiologic changes at successive levels of rectal filling sensation. METHODS: Combined anorectal manometry and proctography were performed in nine volunteers. Images, volumes, and pressures were analyzed at the start of the test, at 20 seconds before first sensation, and at first, constant, urge, and maximum tolerable sensation. RESULTS: Consecutive levels of rectal filling sensation were associated with progressive opening and dilation of the upper anal canal (up to 44 mm) and sliding down of the rectal contents (14 mm), which had already started before the first sensation. This coincided initially with a pressure decrease in the proximal anal canal (from 94 to 42 mmHg). With constant sensation and particularly with urge sensation, rectal pressure increase appeared to be responsible for further proximal anal dilation. This was accompanied by a significant increase of proximal anal pressure (up to 133 mmHg) and sharpening of the angle between the anal axis and the horizontal reference line. CONCLUSION: The proximal anal canal or its surrounding structures play an important role in the desire-to-defecate sensation. They can be activated by a progressive buildup of rectal reservoir pressure in the presence of a competent distal anal sphincter barrier.     

Sonographic Characteristics of Rectal Sensations in Healthy Females

Purpose This study was designed to characterize rectal sensations by visualizing the internal and external anal sphincter and intra-anal transport of bolus during elicited rectal sensations. Methods The anal canal was visualized with real-time transperineal ultrasonography in 13 healthy female volunteers. Rectal sensations were elicited by injecting water into the rectum. The ultrasound images were recorded on a videotape and analyzed offline. Results The median time between an injection of water and the events studied was calculated in 105 rectal sensations. A relaxation in the internal anal sphincter (4 seconds after the injection of water), an antegrade transport of bolus (4 seconds) into the anal canal, and a contraction in the external anal sphincter (5 seconds) were observed before a sensation (6 seconds) was reported. The antegrade flow continued until the distal internal anal sphincter contracted (18 seconds) and the bolus moved in a retrograde transport direction (17 seconds) thereafter the sensation disappeared (18 seconds) and the external anal sphincter relaxed (22 seconds). A significant correlation in time between the end of the sensation, contraction in the internal anal sphincter, reversed flow of anal contents, and relaxation of the external anal sphincter was found (Pearson, P<0.01). Conclusions The results verified that the internal anal sphincter contributes to the perception of rectal sensations by a relaxation allowing intra-anal bolus to increase the pressure on the anoderm during rectal contraction. A new observation is presented on the time relation between contraction in the distal internal anal sphincter, reversed flow in the anal canal, and the end of rectal sensations. Presented at the meeting of the International Continence Society, Christchurch, New Zealand, November 27 to December 1, 2006. Supported by Hitachi Ultrasound, Supfstrasse 24, 6300 Zug Switzerland provided the sonography system. Reprints are not available.     

The relation of sensation in the anal canal to the functional anal sphincter: a possible factor in anal continence

In normal subjects the length of the functional anal sphincter has been compared with the extent of sensation to light touch in the anal canal. At rest, the sphincteric zone was the longer. On distension of the rectum, a decrease in pressure in the anal canal so shortened the functional sphincter that intrarectal pressure extended down to contact the sensory zone. This mechanism may allow the sensation in the anal canal to play a part in the fine adjustment of anal continence.     

Sensory and motor responses to rectal distention vary according to rate and pattern of balloon inflation

Anorectal motor activity and rectal sensation were recorded in 12 normal male subjects during ramp distention of the rectum with water and air at randomized rates of 10, 20, 50, and 100 mL/min and during intermittent rapid distention with air. There were no significant differences between the results of ramp inflation with water or with air, and the repeated infusion of the same medium yielded reproducible results. Ramp distention induced sigmoid pressure-volume profiles. Different sensations occurred at specific points on the pressure-volume curve and were maintained until succeeded by the next sensation. Initial perception of the distention occurred during the initial steep pressure increase, the sensation of wind occurred during the plateau phase, and the desire to defecate occurred at the onset of the final rapid ascent. Rectal sensations were induced at lower volumes at low infusion rates when the slope of the pressure-volume relationship was shallower than at high infusion rates. This suggests that the receptor triggering rectal sensation is not a simple volume or pressure receptor, but is more likely to be a slowly adapting mechanoreceptor lying parallel to the circular muscle of the rectal wall. During rapid intermittent distention, the rectal volumes required to elicit rectal sensations were lower than during ramp distention, although the pressure-volume curve was steeper. Moreover, sensations often only lasted a short period of time but recurred on deflation. These data suggest activation of an additional population of rapidly adapting or high threshold mechanoreceptors. Anal relaxation was always evoked by intermittent rectal distention and was almost always associated with a rectal sensation and an increase in external anal sphincter activity. In contrast, anal relaxation could be absent or delayed during ramp inflation, especially at lower infusion rates, suggesting that internal sphincter can maintain continence for a long period of time while the rectum is slowly filling. Rectal sensation and concomitant external anal sphincter activity was not associated with anal relaxation during ramp inflation; most subjects felt the sensation long after the pressure reached its lowest level. However, under all circumstances the onset of rectal sensation was associated with an increase of external anal sphincter electrical activity. In conclusion, the rectal sensory and anorectal motor responses to distention depend on the rate and pattern of distention, which may activate a different population of receptors. Results from different laboratories cannot be compared directly unless the pattern and rate of distension are the same.     

Influence of pudendal block on the function of the anal sphincters.

The function of the anal sphincters has been studied by obtaining continuous recordings of the pressure in the anal canal and the electromyographic activity in the striated sphincter muscles during expansion of the ampulla recti by means of an air balloon. Ten healthy subjects were examined before and after the striated muscles had been entirely paralysed by bilateral pudendal block, making it possible to record the activity from the internal sphincter alone. The results show that the internal sphincter contributes about 85% of the pressure in the anal canal at rest but only about 40% after a sudden substantial distension of the rectum. During constant substantial rectal distension, the internal sphincter accounts for about 65% of the anal pressure. It is concluded that the internal sphincter in the adult is chiefly responsible for anal continence at rest. In the event of sudden substantial distension of the rectum, continence is maintained by the striated sphincter muscles, whereas both sphincter systems probably have an important function during constant distension of the rectum.     

Rectoanal reflex parameters in incontinence and constipation

PURPOSE: The transient relaxation of the internal anal sphincter in response to rectal distention is believed to play an important role in the continence mechanism. Most anorectal physiology laboratories merely report the rectoanal inhibitory reflex as being either present or absent. This study aimed to assess the parameters of the rectoanal inhibitory reflex in incontinent and constipated patients and healthy control subjects, in an attempt to analyze differences in internal anal sphincter function in these groups. We analyzed each response of the internal anal sphincter to rectal distention with progressively increasing volumes of air at a single site (proximal anal canal). METHODS: Fifty-five constipated and 99 incontinent patients and healthy control subjects underwent manometry. Various parameters of the rectoanal inhibitory reflex were analyzed, and percentage sphincter relaxation was calculated at each volume at which rectoanal inhibitory reflex occurred. RESULTS: There was no difference in the volume of rectal distention required to elicit sensation (P = 0.626) or the rectoanal inhibitory reflex (P = 0.371) in the three groups. There was a significant correlation between the volume required to elicit the rectoanal inhibitory reflex and that at which sensation was first felt only in the incontinent (P = 0.0001) group. Significantly greater sphincter relaxation was seen at each volume (P = 0.001) in the incontinent as compared with the constipated patients. With progressive rectoanal inhibitory reflex, consistently progressive increases in internal anal sphincter relaxation were found only in the incontinent group. This consistent relationship was not seen in the constipated patients or in healthy control subjects. CONCLUSIONS: Assessment of various parameters of the rectoanal inhibitory reflex yielded important information regarding the continence mechanism. Altered responses of the internal anal sphincter in anorectal disorders plays a role in the associated physiologic impairment. This may have significant clinical implications with regard to sphincter-saving resections.     

Internal anal sphincter

The internal anal sphincter, the smooth muscle component of the anal sphincter complex, has an ambiguous role in maintaining anal continence. Despite its significant contribution to resting anal canal pressures, even total division of the internal anal sphincter in surgery for anal fistulas may fail to compromise continence in otherwise healthy subjects. However, recently reported abnormalities of the innervation and reflex response of the internal anal sphincter in patients with fecal incontinence indicate its significance in maintaining continence. The advent of sphincter-saving surgery and restorative proctocolectomy has re-emphasized the major contribution of the internal anal sphincter to resting pressure and its significance in preventing fecal leakage. The variable effect of rectal excision on rectoanal inhibitory reflex has led to a reappraisal of the significance of this reflex in discrimination of rectal contents and its impact on anal continence. Electromyographic, manometric, and ultrasonographic evaluation of the internal anal sphincter has provided new insights into its pathophysiology. This article reviews advances in our understanding of internal anal sphincter physiology in health and disease.     

Treatment of fecal incontinence

Opinion statement Fecal incontinence is a symptom of many disorders that can affect the nerves and muscles controlling defecation; it is not just due to exceptionally voluminous diarrhea. Underlying problems should be identified and treated, because that may improve incontinence. If treatment of the underlying problem does not correct incontinence, several approaches can be employed successfully. General approaches include stimulation of defecation at intervals to empty the rectum under supervised conditions; treatment of diarrhea, if present; addressing coexisting psychologic problems, such as depression; use of continence aids, such as adult diapers; and perineal skin care to prevent skin breakdown. Drug therapy includes use of constipating drugs, such as loperamide or diphenoxylate, that can impede the gastrocolic reflex, thereby limiting rectal filling and the likelihood of incontinence. Biofeedback training is useful in patients with some ability to sense rectal distention and to contract the external anal sphincter; instrumental learning using manometric or electromyographic biofeedback can be used to reinforce the rectoanal contractile response to rectal distention. Improvement in continence has been noted in up to 70% of suitable candidates with a single biofeedback training session. Patients with external anal sphincter disruption due to childbirth injury or other trauma may benefit from direct external anal sphincter repair (sphincteroplasty). In others, tightening up the anal canal by encirclement with nonabsorbable mesh (Thiersch procedure), perianal injection of fat, collagen, or synthetic gel, or radiofrequency electrical energy (Stretta procedure) may provide some palliation. Creation of a new sphincter mechanism by muscle transposition and encirclement of the anal canal is another approach that has been improved by use of electrical stimulators to keep the neosphincter contracted. Artificial anal sphincters patterned after artificial urinary sphincters have met with some success, but local infection remains problematic. When all else fails, fecal diversion (ileostomy, colostomy) can be effective in rehabilitating patients.     

Abnormal visceral autonomic innervation in neurogenic faecal incontinence.

Changes of denervation in the anal sphincter striated and smooth muscle in patients with neurogenic faecal incontinence are well established. This study aimed to determine if there is also a more proximal visceral autonomic abnormality. Thirty women with purely neurogenic faecal incontinence (prolonged pudendal nerve latencies and an intact sphincter ring) and 12 patients with neuropathic changes together with an anatomical disruption were studied. Two control groups consisted of 18 healthy volunteer women and 17 women with normal innervation but an anatomically disrupted sphincter. Rectal sensation was assessed using balloon distension and electrical mucosal stimulation, and anal sensation by electrical stimulation. Rectal compliance was studied to determine whether sensory changes were primary or caused by altered rectal wall viscoelastic properties. Anal canal pressure changes in response to both rectal distension and rectal electrical stimulation were measured to assess the intrinsic innervation of the internal anal sphincter. Patients with neurogenic incontinence alone had impaired rectal sensation to distension (53.1 v 31.5 ml, p < 0.05, neurogenic v controls) and to electrical stimulation (24.4 v 14.8 mA, p < 0.005). Patients with neurogenic incontinence and sphincter disruption also showed impaired sensation compared with healthy controls (55.8 ml v 31.5 ml, p < 0.05 and 22.9 mA v 14.8 mA, p < 0.05). Patients with only a disrupted sphincter had normal visceral sensation to both types of testing. Both rectal compliance and the response of the internal anal sphincter to rectal distension and electrical stimulation were normal in all patient groups. This study suggests that there is a visceral sensory abnormality in patients with neurogenic incontinence which is not caused by altered rectal compliance. As evaluated in this study the intrinsic innervation of the internal anal sphincter is not affected in this process.     

Recovery of anal sphincter function following transabdominal repair of rectal prolapse: Cause of improved continence?

Twenty-eight patients with complete rectal prolapse underwent anorectal manometry before and 6 months and 1–2 years after abdominal rectopexy and sigmoid resection in a study of the mechanisms responsible for postoperatively improved anal continence. Preoperatively, 22 patients reported defective anal control. Seven patients (all with minor incontinence) regained normal control and eight other patients achieved improved continence after surgery. Anal resting, squeeze, and voluntary contraction pressures were significantly lower for defective than for normal control, with a significant rise in these pressures at 6 months after the operation, except for those incontinent patients in whom continence was not improved. No further pressure rise was seen later. Improvement of continence was not accompanied by changes in rectal sensation or reflexive functions of the internal anal sphincter. These results suggest that recovery of the resting and voluntary contraction functions of the sphincter muscles was the cause of continence improvement observed after surgery. Anal manometry was unable to predict outcome of function. Therefore, supplementary procedures for restoration of continence are not advisable, although patients with only minor incontinence are likely to regain full continence after rectopexy alone.     

Preservation of faecal continence during rises in intra-abdominal pressure: is there a role for the flap valve?

Studies were carried out in 15 normal subjects and 14 patients with idiopathic faecal incontinence to test whether a rectoanal flap valve could be responsible for maintaining faecal continence in man. Intraluminal pressures were recorded from the rectum and from three sites in the anal canal during serial increases in intra-abdominal pressure, produced by forced expiration into a sphygmomanometer keeping the height of the column of mercury at prescribed levels. The anal pressures in the normal volunteers always remained higher than the intrarectal pressures even when these were as high as 230 cm H2O. This pressure gradient was the reverse of that which would be found if an anterior rectal flap valve maintained continence and suggests instead that continence is normally maintained by a reflex contraction of the external anal sphincter. The anal pressures in patients with idiopathic faecal incontinence, however, fell below the rectal pressure as the intra-abdominal pressure increased, creating the conditions for a flap valve. The valve was incompetent, however, because fluid infused into the rectum leaked from the anus whenever the rectal pressure exceeded the anal pressure.     

Balloon topography

Ballon topography was developed to simultaneously measure anal canal pressure, anal canal length, and anorectal angle. It is performed using a cylindrical flexible ballon placed into the anal canal and rectum and filled with liquid radiopaque contrast dye under low pressure. The pressure of the dye inside the balloon is controlled by the investigator, and does not vary with changes in balloon volume. The shape of the balloon within the anal canal is recorded using fluoroscopy and plain radiopaques. The patient receives less radiation than the would receive during a single contrast barium enema. We have performed the test on 27 subjects including a normal control, rectal prolapse patients, and incontinent patients. Early results demonstrate the usefulness of the test in examining anal sphincter and pelvic floor function in maintaining fecal continence in health and disease. The test measures multiple aspects of anopelvic function simultaneously that previously required separate investigations.     

Relation between rectal sensation and anal function in normal subjects and patients with faecal incontinence.

The relation between sensory perception of rapid balloon distension of the rectum and the motor responses of the rectum and external and internal anal sphincters in 27 normal subjects and 16 patients with faecal incontinence who had impaired rectal sensation but normal sphincter pressures was studied. In both patients and normal subjects, the onset and duration of rectal sensation correlated closely with the external anal sphincter electrical activity (r = 0.8, p less than 0.0001) and with rectal contraction (r = 0.51, p less than 0.001), but not with internal sphincter relaxation. All normal subjects perceived a rectal sensation within one second of rapid inflation of a rectal balloon with volumes of 20 ml or less air. Six patients did not perceive any rectal sensation until 60 ml had been introduced, while in the remaining nine patients the sensation was delayed by at least two seconds. Internal sphincter relaxation occurred before the sensation was perceived in three of 27 normal subjects and 11 of 16 patients (p less than 0.001), and could be associated with anal leakage, which stopped as soon as sensation was perceived. The lowest rectal volumes required to induce anal relaxation, to cause sustained relaxation, or to elicit sensations of a desire to defecate or pain were similar in patients and normal subjects. In conclusion, these results show the close association between rectal sensation and external anal sphincter contraction, and show that faecal incontinence may occur as a result of delayed or absent external anal sphincter contraction when the internal anal sphincter is relaxed.     

A new concept of the anatomy of the anal sphincter mechanism and the physiology of defecation

The role of the external and internal anal sphincters in the mechanism of anal continence is presented. The external sphincter induces continence by 1) preventing internal sphincter relaxation, what I have called the “voluntary inhibition action,” and 2) mechanical compression of the rectal neck and anal canal proper. The mechanism of both actions is described. The internal sphincter plays a significant role not only in involuntary, but also in voluntary, continence. The importance of this role in the correction of anal incontinence is clarified. “Stress defecation,” a condition which follows internal sphincter damage, is discussed. A “single loop continence” theory is presented, based on the fact that each of the three loops of the external sphincter has its own innervation, attachment, and direction of muscle bundles; each loop thus acts as a separate sphincter. The clinical application of this theory is presented.     

Manometric tests of anorectal function in healthy adults

OBJECTIVE: Although tests of anorectal function are useful in the assessment of defecation disorders, there is inadequate and inconsistent information regarding normative data. Also, there are discrepancies in manometric techniques and data interpretation. Our aim was to perform a comprehensive evaluation of anorectal function in healthy adults. METHODS: We used a 6-mm diameter probe containing six radially arrayed microtransducers, and a 4-cm-long latex balloon for performing anorectal manometry in 45 healthy subjects who were controlled for gender and age. Sequentially, subjects were asked to squeeze, bear down, or blow up a party balloon. Subsequently, rectal sensation, rectal compliance, and rectoanal reflexes were assessed simultaneously by performing intermittent phasic balloon distentions. Additionally, balloon defecation, pudendal nerve latency, and saline continence tests were performed. RESULTS: In men, the anal sphincter was longer (p < 0.05) and squeeze sphincter pressure and squeeze duration were higher (p < 0.01), but resting sphincter pressure was similar to that in women. When bearing down, although not significant, the defecation index was higher in men. Distinct thresholds for rectal sensation were identified but there was no gender difference. Likewise, rectal compliance and balloon expulsion time were similar. However, during saline infusion, the onset of first leak and total volume retained were higher (p < 0.001) and pudendal nerve latency was shorter (p < 0.05) in men. Overall, parity or age did not influence anorectal function. CONCLUSIONS: This study represents the most comprehensive age- and gender-controlled assessment of anorectal function using solid state technology. Gender influences some parameters of anorectal function. Our results could serve as a valuable resource of normative data.     

A new balloon-retaining test for evaluation of anorectal function in incontinent patients

The balloon-retaining test consists of progressive filling of a compliant intrarectal balloon in a patient in the sitting position. The pressure inside the balloon is monitored and the patient is asked to retain the balloon as long as possible and to report first, constant, and maximal tolerable sensation levels. A balloon is used to simulate semisolid and solid stool. This test is a more realistic approach to the evaluation of fecal continence than the rectal saline infusion test and anal manometry. The test evaluates the rectal reservoir function, sensation, and sphincter competence simultaneously; however, the real rectal distensibility and compliance must be determined by compliance measurement until the maximal tolerable level for patients in a reclining position is reached. This test also permits objective evaluation of the effect of different treatments in incontinent patients.     

Anorectal functioning in fecal incontinence

Manometric testing was performed on three groups of subjects: 14 patients complaining of fecal incontinence, 14 age- and sex-matched continent patients, and 14 sex-matched younger normal controls. The younger group displayed significantly stronger contractions of the external anal sphincter and puborectalis than the two patient groups, which did not differ. No differences were found in the relaxation of the internal anal sphincter. The incontinent group required a significantly larger stimulus in order to detect rectal distension compared to either the continent patients or the younger normals. An additional group of unmatched normals and incontinent patients demonstrated significant differences in their ability to retain rectally infused saline. The patients leaked sooner and retained less;however, the performance of the normals was considerably reduced from that reported in previous studies. The aging process seems to result in weakening of the striated muscles of the anal canal, although fecal incontinence need not occur. The afferent limb of the anorectal sensorimotor mechanism does not necessarily deteriorate with aging. A lower threshold for sensation of rectal distension among continent individuals apparently helps them to avoid incontinent episodes, even though maximum contractile pressures in their anal canal are no different from a comparable group of incontinent individuals.     

Use of anorectal manometry during rectal infusion of saline to investigate sphincter function in incontinent patients

Anal and rectal pressures and external sphincter electromyogram were recorded continuously during rectal infusion of 1.5 L saline in 18 normal subjects and 37 patients who complained of diarrhea and fecal incontinence. All subjects exhibited a pattern of regular fluctuations in anorectal pressure and electromyogram. All except 1 of the normal subjects were able to retain 1500 ml saline without leakage, and their pressure record comprised simultaneous rectal contractions, internal sphincter relaxations, and external sphincter contractions. None of the incontinent patients were able to retain 1500 ml saline without leakages, and leakages always coincided with the peaks of rectal pressure. Two manometric patterns were observed. Fifty-nine percent of incontinent patients exhibited a pattern of contractions of similar profile occurring throughout the anorectum. This finding was associated with low basal sphincter pressures, an easily inhibited anal sphincter tone, an obtuse anorectal angle, and a funnel-shaped configuration to the anal canal. These results suggested that, in this group, the internal sphincter was weak and easily inhibited so that the whole anorectum behaved as one fluid-filled compartment recording contractions of the external sphincter. The remaining 41% of incontinent patients exhibited a normal pattern of anorectal pressure fluctuations and had normal maximum basal pressures, although maximum squeeze pressures, rectoanal inhibitory reflex, and anorectal angles were abnormal. Peak rectal pressures were abnormally high in this group during saline infusion, suggesting that abnormally strong rectal contractions may play a role in the incontinence in this group.     

Effect of continuous rectal distention on anal resting pressure

PURPOSE: Intermittent distention of the rectum induces internal anal sphincter relaxation, but whether continuous rectal distention might affect the resting pressure of the anal canal and the frequency of internal anal sphincter relaxations has not yet been investigated. The aim of this study was to record anal pressure under resting conditions and at two levels of continuous rectal distention. METHODS: Anal pressure was recorded by means of water-perfused catheters under resting conditions and at two levels of rectal distention controlled by an electronic barostat in eight healthy subjects. RESULTS: Continuous rectal distention did not significantly change mean anal resting pressure, but it did significantly decrease the amplitude of ultraslow waves (from 29±9 mmHg under resting conditions to 23±6 and 21±3 mmHg during lesser and greater rectal distention;P=0.017 andP=0.012, respectively) and increase the frequency of internal anal sphincter relaxations (from 1.3±1.3/hour under resting conditions to 8.8±4.3/hour and 11.0±4.8/hour during lesser and greater distention;P=0.012 in both comparisons). CONCLUSIONS: The resting pressure of the anal canal is maintained during continuous rectal distention. The decreased amplitude of ultraslow waves and increased frequency of the internal anal sphincter relaxations induced by rectal distention reveal a complex functional relationship between the rectum and the anal canal.Supported by the Associazione Amici della Gastroenterologia del Padiglione Granelli and the CARIPLO Foundation.