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62 Rectoanal Reflex Parameters in Incontinence and Constipation [2002년 7월 DCR] 2011-11-17 3369
 
Geetinder Kaur, M.S., F.R.C.S., Angela Gardiner, B.Sc., Graeme S. Duthie, M.D.(Hon), F.R.C.S.
 
From the Academic Surgical Unit, Castle Hill Hospital, University of Hull Postgraduate Medical School,
Cottingham, United Kingdom
 
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: Fiftyfive 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.
 
The rectoanal inhibitory reflex (RAIR) was first described by Gowers in 1877 and later confirmed
by Denny-Brown and Robertson in 1935.
The transient relaxation of the internal anal sphincter (IAS)
in response to rectal distention is believed to play an important role in the continence mechanism. Duthie and Bennett proposed the concept of the RAIR reflecting a “sampling mechanism,” allowing the upper anal canal to discriminate between flatus and feces. They considered this sampling response to have a role in continence. The presence of the reflex requires an intact intramural neuronal plexus; it is absent in Hirschsprung’s disease. A false-negative reflex may be obtained if the basal pressure is low or if an insufficient distention volume is used in a patient with megarectum. Nitric oxide (or a related substance) has been implicated as an important mediator of IAS relaxation. However, the exact role played by the extrinsic autonomic innervation is not certain, and varied reports on the effect of rectal excision during sphincter-saving surgery and restorative proctocolectomy have led to a renewed interest in the RAIR and its role in the physiology of continence.
 
Many different methods of eliciting the reflex have been described. Balloon distention of the rectum
is an accepted simple method of measuring rectal compliance, evoking rectal sensation and assessing
the reflex activity of the anal sphincter. Most anorectal physiology laboratories merely report the RAIR as
being either present or absent and state the volume of air required to elicit it. A few recent studies have
attempted to assess the significance of the various parameters of the RAIR, including latency intervals and the duration of the reflex in addition to the amplitude of the pressure changes between the proximal
and distal sphincter both in health and disease. Some investigators have attempted to correlate its
presence with resting anal pressures. All these studies have concentrated on the comparison of various parameters of the RAIR in the proximal, middle, and distal sphincteric zones and have shown greatest relaxation in the proximal IAS. Some have shown a coordinated response to balloon distention of the
rectum with recovery of anal pressure from the distal to the proximal sphincter.
 
Varied results have been reported regarding the differences in the pattern of the RAIR in patients with
anorectal disorders. Some have shown no significant alteration of the components of the reflex in these
patients when compared with healthy control subjects.
 
We considered it important to determine the differences in the nature of the RAIR in response to balloon
inflation of the rectum in incontinent and constipated patients when compared with healthy control subjects. This may help to assist clinical decisions regarding sphincter-saving surgery by predicting postoperative anal function. The aim of this study, therefore, was to assess the different parameters of the RAIR in incontinent and constipated patients and compare them with healthy control subjects.
 
DISCUSSION
Continence is maintained by several factors and as yet is not completely understood. The assessment of the parameters of the RAIR may yield important information regarding the preservation of continence
by the anal sphincter mechanism. This could have significant implications in sphincter-saving surgery-
low anterior resection, restorative proctocolectomy, and repair of anorectal malformations, i.e., operations that compromise the intramural reflex arc.
 
The normal RAIR has been found to be most likely mediated by both the sacral cord and myenteric neurones. Studies on the RAIR in healthy control subjects have suggested that continence is maintained by both sphincters—the anal resting pressure at rest is governed by the IAS, whereas contraction of the external anal sphincter (EAS) occurs on rectal distention.
 
An age-dependent increase has been reported for the pressure threshold required to produce an initial
sensation of rectal filling and the RAIR. The sensory threshold was more pronounced in older females as compared with males. The preinflation and postinflation anal pressures and the residual pressures during rectal distention were higher in males. The mix was the same in all our patient groups.
 
Anal pressures were not found to be significantly different in the two groups except the anal resting
pressure. However, it is universally acknowledged that there is considerable overlap in pressures between healthy control subjects, incontinent patients, and constipated patients, and manometry findings do not always correlate with patient symptomatology.
 
Abnormalities of the rectoanal excitatory and/or inhibitory reflexes in incontinent patients in response
to rectal distention have been described in the literature. Sangwan et al. describe a spectrum of five types of abnormal responses in incontinent patients and suggest that this may be a result of selective absence of the excitatory and inhibitory components of the reflex in neurogenic or traumatic sphincter injuries. Frequent abnormal episodes of IAS relaxation have been postulated to cause occult fecal leakage in patients with pruritus ani.
 
Fewer studies have been performed to assess RAIR in constipated patients. Some have shown lower
values of resting anal tone and amplitude of the RAIR ; others have evaluated patients with obstructed
defecation separately and shown either no difference in RAIR or lower maximal amplitude of the reflex in this subgroup.
 
Studies comparing the RAIR in incontinent and constipated patients are few. Literature on the parameters
of the reflex in these two groups is even more scarce and yields differing results. Martinelli et al. found no alteration of the components of the reflex in patients with anorectal functional disorders as compared with healthy control subjects. On the other hand, Zbar et al. suggest a coordinated response by the IAS to rectal distention from the distal to the proximal sphincter based on their detailed study of the RAIR across the proximal, intermediate, and distal sphincteric zones. This phenomenon of differential recovery is in accordance with the study by Goes et al.who found that anal relaxation induced by small-volume rectal distention involved a pressure and relaxation time gradient between the proximal anal canal and the high-pressure zone. In this study, instead of considering the reflex in different parts of the anal canal, we looked at the progression of the IAS relaxation at one site (proximal anal canal) with increasing volumes of rectal distention and compared the various components of the reflex in healthy control subjects, incontinent patients, and constipated patients.
 
The excitatory component of the RAIR is caused by the brief contraction of the EAS. Our study did not
find any difference in excitation between the groups. This is in accordance with the study by Zbar et al.
 
The clinical importance of the internal sphincter has recently been re-emphasized with the advent of
sphincter-saving surgery and has lead to a renewed interest in the RAIR and its role in continence. We
focused our attention on the inhibitory component of the reflex, i.e., IAS relaxation. Our study showed
greater IAS relaxation in incontinent patients in response to rectal distention at each volume when compared with both healthy control subjects and constipated patients,
in agreement with the report
by Farouk et al.,who found a greater fall in anal pressure and increased duration of IAS relaxation
in patients with pruritus ani with occult fecal leakage.
In addition, our study revealed an increase
in relaxation with increased rectal distention, consistent with some studies and contrary to others. However, this occurred only from the first to the second RAIR in all groups. Further increase in balloon
distention caused a consistent increase in percentage sphincter relaxation only in the incontinent group; a variable response was seen in both the healthy control and the constipated groups. This difference in response in the incontinent patients may have an important implication in understanding the significant role of the IAS in the regulation of continence. As increased filling of the proximal anal canal occurs, progressively increasing IAS relaxation would result in faster delivery of feces to the distal anal canal, where the normal/absent EAS excitatory response may not be able to prevent leakage.
 
We found no significant difference in the latency or duration of the inhibitory reflex between the
groups.
This is in accordance with the report by Martinelli et al., but at variance with the study by
Zbar et al. who found a significant difference in the recovery time (equivalent to our duration of
inhibitory reflex), though no difference in the latency. Differing latency values for proximal and
distal rectoanal excitatory reflexes have been seen in patients with fecal incontinence by Sangwan et
al. It must be remembered that although these investigators studied the RAIR at different sites in the anal canal, it was essentially the first RAIR that was being looked at, whereas this study looked at successive RAIR at the same site.
 
This study re-emphasizes the importance of the IAS in maintaining continence and may explain the leakage that follows hemorrhoidectomy or lateral internal sphincterotomy in some patients with isolated IAS trauma. The excitatory reflex caused by the contraction of the EAS maintains the anorectal pressure gradient and probably prevents the involuntary passage of feces, especially during “reflex sampling.” However, this reflex was absent in many of our constipated patients and present in an equal number of
incontinent patients. Therefore, this is not the main mechanism responsible for maintaining continence,
which suggests that the IAS plays a very significant role, especially in patients in whom the EAS function is impaired, and may explain continence in patients with proven neuropathies.
 
Assessment of the parameters of the RAIR thus significantly contributes to our understanding of various
anorectal disorders and of the variable effects of rectal excision on the RAIR and continence. We propose that altered responses of the IAS to rectal distention in incontinent patients may play a role in the impairment of continence seen in this group, which further emphasizes the importance of the IAS in the maintenance of continence. A significant difference in the components of the RAIR in incontinent patients when compared with healthy control subjects and constipated patients would imply an impaired RAIR in the incontinent group. This finding could have significant implications in the selection of patients for sphincter-saving surgery where a preoperative alteration of RAIR parameters may predict an impaired
postoperative continence.