- Email: [email protected]
Obstructive defecation: a failure of rectoanal coordination
THE AMERICAN JOURNAL OF GASTROENTEROLOGY Copyright © 1998 by Am. Coll. of Gastroenterology Published by Elsevier Science Inc.
Vol. 93, No. 7, 1998 ISSN 0002-9270/98/$19.00 PII S0002-9270(98)00207-X
Original contributions Obstructive Defecation: A Failure of Rectoanal Coordination Satish S. C. Rao, M.D., Ph.D., Kimberly D. Welcher, B.S., and Jennifer S. Leistikow, B.S. Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
Objective: The pathophysiology of obstructive defecation is unclear. We investigated whether impaired rectoanal coordination causes obstructive defecation and if this dysfunction can be corrected by biofeedback therapy. Methods: We prospectively studied 25 healthy subjects and 35 consecutive patients with constipation (>1 year) with anorectal manometry and balloon expulsion test. Symptoms were assessed from diary cards. Patients found to have obstructive defecation were offered biofeedback therapy. After treatment, their defecation dynamics and symptoms were reassessed. Results: Eighteen patients had obstructive defecation and 17 had normal defecation dynamics (nonobstructive). Five normals (20%) exhibited obstructive pattern but only one failed to expel balloon. In the obstructive group, during straining, the intrarectal pressure and defecation index were lower (p < 0.05), and anal residual pressure was higher (p < 0.01) when compared with the nonobstructive group or normals. After biofeedback therapy, the intrarectal pressure and defecation index increased (p < 0.02) and anal residual pressure decreased (p < 0.001); stool frequency, degree of straining, and bowel satisfaction scores improved (p < 0.05); 67% stopped laxatives and 11 patients discontinued stooling with digitation. Conclusion: Patients with obstructive defecation showed impaired rectal contraction, paradoxical anal contraction, or inadequate anal relaxation. These features suggest that rectoanal coordination was impaired. Biofeedback therapy rectified these pathophysiological disturbances and improved constipation. (Am J Gastroenterol 1998;93:1042–1050. © 1998 by Am. Coll. of Gastroenterology)
INTRODUCTION It has been estimated that 50% of patients referred to tertiary care centers with chronic constipation have obstructive defecation (1, 2), a condition also referred to as anismus or pelvic floor dyssenergia (3–5). Its pathophysiology is, however, incompletely understood. It has been proposed that the inability to relax the external anal sphincter may be the chief underlying mechanism (3). However, 20 –30% of healthy subjects also exhibit this phenomenon (4, 5). Furthermore, based on the notion that obstructive defecation is a spasmodic dysfunction of the anal sphincter, surgical myotomy has been performed (6). Although preliminary studies were encouraging, a more critical assessment has shown that surgery may help only 10 –30% of patients (7). Hence, the inability to relax the external anal sphincter is unlikely to be the sole mechanism that leads to obstructive defecation. Defecation is a complex process that involves involuntary propulsion of stool through the colon, perception of stool when it arrives in the anorectal segment, and a coordinated movement that consists of rectal contraction, reflex relaxation of internal anal sphincter and voluntary relaxation of external anal sphincter. In this study, we tested the hypothesis that the inability to perform a coordinated movement of the pelvic floor may cause obstructive defecation. Our objectives were: 1) to identify the pathophysiological mechanism(s) that may cause obstructive defecation, and 2) to assess whether biofeedback therapy can correct the underlying dysfunction(s). The study was performed in two phases. In the first phase, healthy subjects and consecutive patients referred with chronic constipation were investigated with tests of anorectal function. At the end of this phase, we identified two groups of patients: those with normal defecation dynamics (nonobstructive group), and those with obstructive defecation. In the second phase, patients with obstructive defecation were offered a treatment program consisting of neuromuscular conditioning using biofeedback techniques. After biofeedback therapy, tests of anorectal
Received Oct. 15, 1997; accepted Jan. 30, 1998. 1042
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
1043
function and symptom patterns were reassessed to identify pathophysiological changes. MATERIALS AND METHODS Subjects We studied 35 consecutive patients referred to a tertiary care center with chronic constipation, male/female ratio 5 5/30, mean age 44 yr. (range 21– 81 yr). During the previous year all patients reported at least three of the following symptoms with 25% of bowel movements (when not taking laxatives): 1) stool frequency of less than two/wk, 2) passage of hard stools, 3) excessive straining, or 4) a feeling of incomplete evacuation (8). All patients underwent standard investigations that included barium enema or colonoscopy to exclude other pathology and secondary causes of constipation. Studies were also performed in 25 healthy control subjects who reported normal bowel function, had no previous gastrointestinal surgery, and were not taking any medication. These subjects were recruited through hospital advertisement. The studies were approved by the Human Ethics Committee of the University of Iowa. In the first phase, the following protocol was used to assess anorectal and colonic function and to identify patients with obstructive defecation. Phase 1 Anorectal manometry. Patients were asked to empty their bowels before the study and a bowel preparation was not routinely used. With the subject lying in the left lateral position and hips flexed to 90°, a flexible probe, 8 mm in diameter, with 5 strain gauge transducers (Gaeltec Ltd., Isle of Skye, UK) was placed in the rectum. One sensor was located 1 cm from the tip of the probe, and four sensors, arrayed 90° to each other, were located 9 cm from the tip. A 5-cm long latex balloon (Trojan-enz, Carter-Wallace, New York, NY) was fastened to the tip of the probe enclosing the terminal sensor. The probe was connected to a recorder (Gaeltec 7 MPR) with a sampling frequency of 8 MHz. Pressure activity was displayed on a computer/monitor (Gateway 2000, Sioux Falls, SD). After allowing the pressures to stabilize for 10 min, the resting and squeeze sphincter pressures were determined by station pull through techniques. The probe was then positioned so that the anal sensors were located 1.5 cm from the anal verge. Each subject was then asked to bear down as if to defecate, on three separate occasions, with a 2-min rest between each maneuver. Next, the rectal balloon was inflated with 60 cc of air, and the subjects were asked to bear down once more. Thereafter, intermittent graded balloon inflations were performed by distending the rectum with volumes up to 320 cc of air (9). The probe was then removed. Balloon expulsion test. A 3-mm diameter flexible tube with a 4-cm long balloon attached to its tip was placed in the rectum. The balloon was filled with 50 ml of water at 37°C. The patient was asked to sit on a commode and expel the
FIG. 1. Typical manometric changes in the rectum and anal canal during straining. In a normal subject the rectal pressure rises and the anal pressure decreases, whereas in a patient with obstructive defecation, there is insignificant rise in rectal pressure and paradoxical contraction of the anus (external sphincter). This abnormality improves after biofeedback therapy.
simulated stool, in privacy. After 5 min of straining, if the subject failed to expel the balloon, it was deflated and removed. The time taken for expelling the balloon was recorded. Colonic transit assessment. Patients ingested a capsule containing 24 radiopaque markers (Sitzmarks, Konsyl Pharmaceuticals, Irving, TX). After 5 days (120 h later) a plain x-ray film of the abdomen was obtained (10). Starting two days before and during the test, patients refrained from taking laxatives, enemas, or suppositories and were encouraged to eat their normal diet. Defecography. This test was performed only in patients with manometric evidence of obstructive defecation. Barium paste, 150 ml, was placed in the rectum. Thereafter, lateral videofluoroscopic images of the anorectal segment were obtained at rest, during cough, and during attempts to bear down as if to defecate (11). A diagnosis of obstructive defecation was made if the patients exhibited an obstructive pattern of defecation, defined as a paradoxical increase of anal sphincter pressure (Fig. 1) or ,20% relaxation of the resting anal sphincter pressure during straining as if to have a bowel movement (Fig. 1), in particular, after inflating a balloon in the rectum with 60 cc of air. Additionally, patients had to fulfill at least two of the following criteria: 1) inability to expel a 50-ml
1044
RAO et al.
water-filled balloon within 5 min; 2) inability to expel, or .50% retention, of barium during defecography; and 3) prolonged colonic transit .5 markers at 120 h. Owing to ethical constraints regarding radiation exposure, defecography and colon transit study were not performed in healthy control subjects and defecography was not performed in the nonobstructive group. All subjects also answered a questionnaire in which they described their stool frequency, degree of straining, and stool consistency. Phase 2 Patients with obstructive defecation were offered a twostage outpatient treatment program of neuromuscular conditioning using biofeedback techniques. To improve the abdominal effort during defecation, in the first stage (4 – 6 wk) patients were taught diaphragmatic breathing exercises (12). This consisted of distending the abdomen by inhaling slowly and then holding the breath for $10 –15 sec. The patients were asked to practice this maneuver for $20 min, three times a day. In the second stage (2– 4 wk), patients were asked to attend the motility laboratory twice a week. Biofeedback therapy was performed by using the manometric equipment described earlier, and by employing visual and verbal feedback techniques. The aim of this treatment was to improve rectal sensation and to establish a normal pattern of straining. The visual feedback was provided by observing the changes in pressure activity on the monitor screen. The verbal feedback was provided by the physician/ nurse therapist. This consisted of either complimenting the patient for performing a correct maneuver or rectifying any errors. Each 60 –90-min treatment session comprised the following three maneuvers. The goal of sensory conditioning was to improve perception of rectal distention by intermittently inflating a balloon in the rectum, using varying volumes of air (13–15). After establishing sensory thresholds, the balloon was inflated up to the volume that induced the urge to defecate. The patient was instructed to observe the monitor and to use the visual cue that was provided by the rise in intrarectal pressure (which occurs with each inflation) and to associate this cue with any possible rectal sensation. Thereafter, with each successive inflation, the distending volume was decreased by 10 –15%. By trial and error, the patient was gradually trained to recognize smaller volumes of inflation. Thereby, lower sensory thresholds were established. The goal of rectoanal coordination was to educate the patient to perform a coordinated maneuver (during simulated defecation) that consisted of a rise in rectal pressure synchronized with anal relaxation (Fig. 1). With the manometry catheter in situ and seated on a commode in front of the monitor, the patients were asked to bear down as if to defecate. During the maneuver, their posture and breathing techniques were corrected. Next, the rectal balloon was distended, using the newly established volume for urge to defecate, and again the patients were asked to bear down.
AJG – Vol. 93, No. 7, 1998 After the maneuver, the balloon was deflated. These maneuvers were repeated 20 times, and with each attempt the patient was instructed to titrate the degree of abdominal and anal effort required to achieve a normal pattern of defecation. Appropriate verbal reinforcement was provided by the therapist throughout the procedure. The balloon expulsion test was performed as described previously. But here, patients were advised regarding appropriate techniques for relaxing the pelvic floor. If they were unable to expel the device, gentle traction was applied to the balloon while reinforcing their straining technique (12, 13, 16). The maneuver was repeated a few times. Assessment of symptoms and follow-up Patients were asked to maintain a daily log of bowel symptoms. In this diary, they recorded stool frequency, degree of straining (1 5 normal, 2 5 moderately excessive, 3 5 severe), stool consistency (hard, normal, loose), and how often they practiced diaphragmatic exercises, and the type and amount of laxative consumed. During this phase, patients were also asked to score their satisfaction or dissatisfaction with bowel habit on a visual analogue scale. During this phase, patients were advised to take laxatives ad libitum. The number of training sessions was customized for each patient. Biofeedback training was discontinued when patients reported a) at least 33% improvement in their difficulty with defecation or in their stool frequency, and b) that without feedback, they were able to demonstrate consistently or at least 50% of attempts in two consecutive training sessions, a normal pattern of defecation. After completion of biofeedback therapy, anorectal manometry and balloon expulsion tests were repeated. Patients were asked to return at 6 months. Before this visit they were asked to complete a 1-wk diary of bowel symptoms and to score their satisfaction with bowel habit on a visual analog scale (0 –10). Measurements and analysis Anorectal manometry. The mean of the three highest values for the anal sphincter pressures at any level in the anal canal during rest and during squeeze was taken as the maximum resting and the maximum squeeze pressure (9). The pressure values obtained when the balloon was distended inside the rectum were subtracted from the pressure values that were obtained during balloon distention with similar volumes outside the rectum (9). The thresholds for first sensation, desire to defecate, and urgency to defecate were also measured (9). Of the three trials of simulated defecation, the effort that closely resembled a normal pattern of defecation (Fig. 1) was used to measure the pressure changes in the rectum and anus and to calculate the following values: Defecation Index (D.I.). This index was used as an overall measure of the coordinated effort (pressure gradient) between the rectum and anus and was calculated from the following equation:
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
Defecation Index (D.I.) 5 Rectal pressure when straining 4 Anal residual pressure when straining The anal residual pressure was defined as the minimal pressure in the anal canal (at any channel) during attempts to strain as if to defecate. Assessment of subjective parameters. All patients were asked to grade their satisfaction or dissatisfaction with bowel habits, both before and after biofeedback therapy, using a visual analog scale of 1–10, where 10 was normal. Additionally, their stool diaries were analyzed to calculate the mean stool frequency/wk, the mean strain score per bowel movement, and the laxative consumption score/wk (0 5 no laxatives, 1 5 high fiber diet 6 bran, 2 5 oral laxatives 6 suppositories, 3 5 enemas, magnesium citrate, solution polyethylene glycol electrolyte solution (GoLYTELY, Braintree Labs, Braintree, MA). Statistics. During Phase 1, the manometric parameters between the two groups and between patients and healthy control subjects were compared using multifactorial analysis of variance with Bonferroni’s correction. During phase 2, the manometric changes within the obstructive group were compared using the paired Student’s t test. Statistical differences between healthy control subjects and the obstructive group after biofeedback therapy were also compared using the Student’s t test. The differences in subjective parameters of bowel function were compared among the three groups by using Wilcoxon’s rank sum tests. The differences in the number of subjects from each group who could expel a 50-ml water filled-balloon were compared by the Fisher’s exact test. Results are expressed as mean 6 95% confidence interval. RESULTS Demographics We found that 18 of 35 (51%) patients with constipation had obstructive defecation (m/f 5 3/15, mean age 48 yr) and 17 of 35 (49%) patients had normal defecation dynamics. The latter group of patients were classified as the nonobstructive group (m/f 5 2/15, mean age 42 yr). The mean duration (range) of constipation for the obstructive versus nonobstructive group was 20 yr (3–54 yr) versus 11 yr (1–20 yr) and the mean stool frequency/wk was 3.8 (0.5–24) versus 1.6 (0.5–3). A need for digital disimpaction of stool was reported by eleven patients with obstructive defecation and by one patient with slow transit constipation (p , 0.01). All 18 patients with obstructive defecation completed biofeedback therapy. The mean number (range) of sessions was 6 (3–11). The healthy control group consisted of 25 subjects, (m/f 5 10/15, mean age 50 yr, range 33–71 yr). Their mean stool frequence/wk was 6.5 (3–15).
1045
Baseline investigations In the obstructive group, 13 (72%) patients had slow colon transit and five (28%) patients had normal colon transit (10). In the nonobstructive group, 11 (65%) patients had slow colon transit and six (35%) patients had normal transit. There was no difference between the two groups. Defecography showed an inability to expel or .50% retention of barium in eight of 18 patients with obstructive defecation. The anorectal angle either became more acute or failed to change in nine of 18 (50%) patients. Six patients showed rectal mucosal intussusception. Anal sphincter pressures The rectoanal inhibitory reflex was present in all of our subjects, both patients and normals, excluding Hirschsprung’s disease. The maximum anal resting and the maximum anal squeeze pressure were not significantly different between the three groups of subjects and in the obstructive group after biofeedback therapy (Table 1). Changes in anal pressure during simulated defecation When straining, the anal residual pressure was higher (p , 0.001) in the obstructive group when compared with the nonobstructive group or healthy control subjects (Fig. 2 and Table 1). After biofeedback treatment, the anal residual pressure decreased (p , 0.0001) (Fig. 2), and the new values were similar to those observed in healthy controls and in the nonobstructive group (Table 1). Patients with nonobstructive constipation also showed a lower (p , 0.05) anal residual pressure compared to normals (Table 1). Five healthy subjects (20%) also exhibited an obstructive pattern of defecation. Changes in intrarectal pressure during simulated defecation The intrarectal pressure was lower (p , 0.05) in the obstructive group compared with the nonobstructive group, when straining either with an empty rectum (Fig. 3) or after rectal distension with a 60 cc balloon (Table 1). The intrarectal pressure was also lower (p , 0.005) in the obstructive group compared with normals. No differences were seen between normals and nonobstructive group. After biofeedback therapy, the intrarectal pressure increased (p 5 0.009) during straining in the obstructive group. Before biofeedback therapy, five of 18 (28%) patients with obstructive defecation showed high rectal pressure (.70 mm Hg); in these subjects, after treatment, the rectal pressure decreased (Fig. 3). Defecation index The mean defecation index was lower (p , 0.001) in obstructive group compared with either the nonobstructive group or healthy controls (Fig. 4). After biofeedback therapy, the defecation index increased (p , 0.001) in the obstructive group and was similar to that observed in the nonobstructive group or healthy controls (Fig. 4).
1046
RAO et al.
AJG – Vol. 93, No. 7, 1998
TABLE 1 Objective and Subjective Parameters of Anorectal Function in the Three Groups of Subjects and in the Obstructive Group After Biofeedback Therapy
Anal and rectal pressures Max. anal resting pressure (mm Hg) Max. anal squeeze pressure (mm Hg) Anal residual pressure (mm Hg) Rectal pressure during straining (after inflation of 60-cc balloon) (mm Hg) Rectal sensation Threshold volume for first perception (cc) Threshold volume for desire to defecate (cc) Threshold volume for urge to defecate (cc) Subjective parameters Strain score Laxative consumption score Bowel satisfaction score
Obstructive (n 5 18)
Normal (n 5 25)
Nonobstructive (n 5 17)
71 (57–85) 148 (121–175) 48 (39–57) 78 (65–91)
66 (58–75) 132 (109–156) 25 (21–29)# 51 (43–59)
59 (52–67) 110 (90–129)‡ 78 (66–90)*‡ 44 (33–55)‡
22 (14–30) 98 (71–125) 142 (104–180)
27 (19–34) 85 (62–108) 120 (89–151)
47 (20–74) 100 (64–136) 141 (102–180)
12 (6–19)‡§ 41 (33–49)†§ 63 (50–76)†§
1.2 (0.8–1.6) –
2.0 (1.6–2.4) 1.9 (1.5–2.3)
2.6 (2.3–2.9)*‡ 2.7 (2.5–2.9)* 1.1 (0.9–1.4)
1.6 (1.4–1.8)† 1.3 (1.0–1.6)† 7.8 (7.0–8.6)†
Before
After 64 (55–73) 122 (96–146) 37 (31–44)† 60 (51–69)‡
Mean (95% confidence interval). * p , 0.001, nonobstructive versus obstructive. † p , 0.001, ‡ p , 0.05, obstructive group, before and after biofeedback. ‡ p , 0.05, normal group versus obstructive group before biofeedback. § p , 0.05, normal group versus obstructive group after biofeedback. # p , 0.05, normal group versus nonobstructive group.
Rectal sensation The threshold volumes required for evoking a first sensation, desire to defecate, and urgency to defecate were not significantly different between the two patient groups (Table 1). When compared with normals, the threshold for first sensation was higher (p , 0.05) in the obstructive group, before biofeedback therapy. After biofeedback therapy, the thresholds for all three parameters of rectal sensation decreased (p , 0.001) (Table 1) in the obstructive group. The thresholds for a desire to defecate and urge to defecate were similar between patients with obstructive defecation and normals before biofeedback therapy, but were lower (p , 0.05) after treatment (Table 1). Balloon expulsion test Sixteen (89%) patients with obstructive defecation were unable to expel a 50 ml water filled balloon, compared with four (23%) patients with nonobstructive constipation (p , 0.01) and four (16%) normal subjects (p , 0.01) (Fig. 5). Patients with obstructive defecation also took more time (p , 0.001) to expel the balloon compared with other groups (Fig. 5). After biofeedback therapy, all 18 patients were able to expel the artificial stool within 3 min (p , 0.001) (Fig. 5). Of the four normal subjects who could not expel a balloon, only one showed an obstructive pattern of defecation, but all four had a low defecation index (0.8 – 1.2). Subjective parameters When compared with healthy normals, the mean stool frequency was significantly lower (p , 0.05) in both groups of patients but there was no difference between the patient groups. After biofeedback therapy, the stool frequency in-
creased (p , 0.05) in the obstructive group (Fig. 6). Interestingly, three of 18 (17%) patients had $13 stools/wk. After biofeedback therapy, their stool frequency decreased (Fig. 6). The mean strain score (degree of straining) was higher (p , 0.05) in the obstructive group compared with the nonobstructive group. After biofeedback therapy, both the mean strain score and the mean laxative consumption score decreased (p , 0.01) in the obstructive group, and the bowel satisfaction score increased (p , 0.01) (Table 1). Also, after therapy, all eleven patients who could not defecate without digital disimpaction of stools were able to discontinue this habit. Follow-up Six months after biofeedback therapy, 13 of 18 (72%) patients with obstructive defecation returned for a follow-up assessment. Their mean stool frequency/wk was 10.7 (range 4 –22); this was significantly higher (p , 0.05) than baseline but was similar to that observed at the end of biofeedback therapy (Fig. 6). The mean strain score and the amount of laxatives consumed were lower and the bowel satisfaction scores (8.0 [range 7.1– 8.9]) were significantly higher (p , 0.01) at 6 months than at baseline but not after biofeedback therapy. Five patients did not return. Of these, three patients answered a telephone inquiry and reported that their bowel function was much improved. Two patients moved out of state and could not be contacted. DISCUSSION Obstructive defecation is generally regarded as a failure of anal relaxation (3–7). However, therapeutic attempts at reducing anal sphincter pressure either by surgical myotomy
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
1047
FIG. 2. This shows the individual values and the mean 6 95% CI for the anal residual pressure during straining in normals, in patients with nonobstructive constipation, and in patients with obstructive defecation before and after biofeedback therapy.
FIG. 3. This shows the individual values and the mean 6 95% CI for the intrarectal pressure during straining as if to defecate, in normals and in the two groups of patients, and the changes in the obstructive group after therapy.
FIG. 4. This shows the changes in the defecation index for the three groups of subjects (mean 6 95% CI).
1048
RAO et al.
FIG. 5. This shows the individual values for the time taken to expel a 50-ml water-filled balloon (mean 6 95% CI).
(6, 7) or by injection of botulinum toxin (17, 18) were only partially effective. Our objective was to investigate the pathophysiological mechanism(s) that may account for this problem. Based on anorectal function, we identified two groups of patients with refractory constipation: those with obstructive defecation and those with normal pelvic floor function (nonobstructive). However, the demographics, duration of symptoms, and colon transit measurements were similar between the two groups. Approximately two-thirds of patients in each group had slow colon transit. Thus, there was an overlap and many patients with obstructive defecation also had slow colon transit. This confirms recent observations (19, 20) and questions the validity of classifying patients into those with slow transit constipation or obstructive defecation, based on transit measurements only. It is our impression that one should make a diagnosis of slow transit constipation only after excluding obstructive defecation. During attempts to strain as if to defecate, we found that the intrarectal pressure was significantly lower in nearly two-thirds of patients with obstructive defecation compared with other groups. After biofeedback therapy, the intrarectal pressure increased significantly and was similar to that of the nonobstructive group or normals. Because the intrarectal pressure is governed by the contraction of rectal muscles together with raised intraabdominal pressure, our findings suggest that many patients with obstructive defecation have impaired pushing force during defecation. However, this was not seen in all of our patients. About one-third of patients with obstructive defecation produced either normal or higher intrarectal pressures during straining. Because this finding was associated with high anal residual pressure and with paradoxical anal contraction, it is likely that, in some
AJG – Vol. 93, No. 7, 1998
FIG. 6. This shows the stool frequency in each patient with obstructive defection before, at the end of biofeedback therapy, and after 6 months (mean 6 95% CI).
patients, excessive straining may also be counterproductive. Thus, either the inability to generate adequate pushing force or excessive straining may lead to obstructive defecation. By educating patients to titrate their abdominal pushing force, biofeedback therapy proved effective in both groups of patients. We found that patients with obstructive defecation exhibit paradoxical anal contraction when they strain with an empty rectum (3, 4, 12–15) but also when they strain with a 60 ml balloon inflated in the rectum, i.e., after a sensation of rectal fullness. Furthermore, we have documented that obstructive defecation is associated with high anal residual pressure. In five of 18 (28%) patients, during straining, either there was no change in anal resting pressure or there was an insignificant (,10%) decrease. This shows that patients with obstructive defecation not only exhibit paradoxical anal contraction but also absent or impaired anal relaxation. After biofeedback therapy, all of these patients were able to relax the anal sphincter. Five normal subjects also exhibited an obstructive pattern of defecation but only one of them was unable to expel a balloon. This confirms that up to 20% of normals may exhibit an obstructive pattern of defecation (4). It also reaffirms that in some subjects there is a poor correlation between the obstructive pattern, bowel habit, and ability to expel a simulated stool. Because normals may exhibit this manometric finding, a diagnosis of obstructive defecation should not be made solely on the basis of this manometric finding. Other evidence such as dyschezia, digital disimpaction of stool, inability to expel a simulated stool or barium, and retention of markers on colon transit study should be
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
required to establish this diagnosis. Because these studies were not performed in our healthy group, we are unable to describe how many of our normals would have fulfilled the criteria for obstructive defecation. We have proposed a new index for quantifying the rectoanal pressure gradient during simulated defecation—the defecation index. The mean defecation index in the nonobstructive group was 2.2 and in healthy controls was 1.8. In contrast, the obstructive group had a low index of 0.7. This low index could be caused by either high anal residual pressure (high resistance) or low intrarectal pressure (poor pushing force) or both. After biofeedback therapy, the mean index rose to 2.0, suggesting that the pressure gradient had improved. Four normal subjects who failed to expel a balloon also had a low defecation index (,1.2). Hence, it is our impression that a pressure gradient between the rectum and anus which is (at least) greater than a factor of 1.5 is required to facilitate expulsion of stool, and that a low defecation index may serve as a better test for diagnosing obstructive defecation than merely the pattern of paradoxical anal contraction. Rectal sensory perception was impaired in the obstructive group compared with healthy subjects and confirms previous observations (14, 15). After biofeedback therapy, sensory perception improved, and the values were lower than for normals. The heightened visceral sensation may be a consequence of sensory conditioning. Repeated reinforcement has been reported to alter sensory thresholds even in normals (21). Thus, impaired rectal perception may play a role in the pathogenesis of obstructive defecation, but it is unclear whether this is primary or secondary to rectal distention from fecal stasis. In our patients with obstructive defecation, the subjective parameters such as bowel satisfaction score, mean stool frequency, and degree of straining improved significantly after treatment, confirming previous findings (12–16, 20). However, at the outset, not all patients with obstructive defecation had decreased stool frequency. In fact, 40% of patients had one or more bowel movement per day and often these patients expelled small, pellet-like stools several times a day. In this group, after biofeedback treatment, stool frequency decreased, suggesting more complete evacuation of stools. Furthermore, most patients reduced their dependence on laxatives and twelve (67%) stopped using laxatives. Six months later, 15 of 18 (83%) patients reported persistent improvement in their bowel function. Biofeedback therapy has been advocated for the treatment of obstructive defecation (12–16, 20) and in a metaanalysis was shown to be useful in $70% of patients (22). But there is little evidence for objective improvement. In two studies (14, 20), the pattern of paradoxical anal contraction improved, but changes in rectal and anal pressures and rectal sensation were either not measured or did not change appreciably. Additionally, no previous study has systematically compared the manometric parameters in patients with
1049
obstructive defecation and healthy control subjects. Our study shows that biofeedback therapy can improve subjective and objective parameters of anorectal function and can restore normal bowel function in .80% of patients with obstructive defecation. After treatment, we did not repeat a colon transit study or defecography because the defecation dynamics, balloon expulsion time, and symptoms had all improved substantially. Moreover, there is poor correlation between the results of these test and clinical outcome (20). Whether the beneficial outcome of biofeedback therapy is due to excessive attention or improvement in bowel function is unclear, but it merits further study. The objective improvement, however, suggests a real change in the underlying pathophysiology. Our study reveals that patients with obstructive defecation exhibit either impaired rectal contraction (61%), paradoxical anal contraction (78%), or impaired anal relaxation (22%), or a combination of these mechanisms. These findings suggest that these patients have dyssynergic defecation with impaired coordination between the rectum and anal sphincter muscles. This dysfunction was corrected by biofeedback therapy, reaffirming its pathogenic role. ACKNOWLEDGMENTS The authors wish to thank Dr. K. Hubel for his critique, Ms. Susie McConnell for her superb secretarial assistance, and Ms. Janel Happel, R.N., for her help with biofeedback therapy. Portions of this manuscript were presented at the annual meeting of the American Gastroenterological Association and published as an abstract (Gastroenterology 1994;106(4):A557). Reprint requests and correspondence: Dr. Satish S. C. Rao, M.D., Ph.D., F.R.C.P. (Lon), 4612 JCP/Division of Gastroenterology/Hepatology, The University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242.
REFERENCES 1. Rao SSC, Patel RS. How useful are tests of anorectal function in the management of defecation disorders. Am J Gastroenterol 1997;92: 469 –75. 2. Surrenti E, Rath DM, Pemberton JH, et al. Audit of constipation in a tertiary referral gastroenterology practice. Am J Gastroenterol 1995; 90:1471–5. 3. Preston DM, Lennard-Jones JE. Anismus in chronic constipation. Dig Dis Sci 1985;30:413– 8. 4. Jones PN, Lubowski DZ, Swash M, et al. Is paradoxical contraction of puborectalis muscle of functional importance? Dis Colon Rectum 1987;30:667–70. 5. Duthie GS, Bartolo DCC. Anismus. The cause of constipation? Results of investigation and treatment. World J Surg 1992;16:831–5. 6. Martelli H, Devroede G, Arhan P, et al. Mechanisms of idiopathic constipation: Outlet obstruction. Gastroenterology 1978;75:623–31. 7. Pinho M, Yoshioka K, Keighley MRB. Long term results of anorectal myectomy for chronic constipation. Br J Surg. 1989;76:1163– 4. 8. Whitehead WE, Chaussade S, Corazziari E, et al. Report of an international workshop on management of constipation. Gastroenterol Intl 1991;4:99 –113. 9. Rao SSC, Read NW, Davison PA, et al. Anorectal sensitivity and responses to rectal distension in patients with ulcerative colitis. Gastroenterology 1987;93:1270 –5.
1050
RAO et al.
10. Evans RC, Kamm MA, Hinton JM, et al. The normal range and a simple diagram for recording whole gut transit time. Int J Colorectal Dis 1992;7:15–7. 11. Mahieu P, Pringot J, Bodart P. Defecography. Description of a new procedure and results in normal patients. Gastrointest Radiol 1984;9: 247–51. 12. Koutsomanis D, Lennard-Jones JE, Roy AJ, et al. Controlled randomized trial of visual biofeedback versus training without a visual display for intractable constipation. Gut 1995;37:95–9. 13. Bleijenberg G, Kuijpers HC. Treatment of spastic pelvic floor syndrome with biofeedback. Dis Colon Rectum 1987;30:101–11. 14. Papachrysostomou M, Smith AN. Effects of biofeedback on obstructive defecation—reconditioning of the defecation reflex? Gut 1994;35: 242–5. 15. Loening-Baucke V. Modulation of abnormal defecation dynamics by biofeedback treatment in chronically constipated children with encopresis. J Pediatr 1990;116:214 –22. 16. Wexner SD, Cheape JD, Jorge JMN, et al. Prospective assessment of
AJG – Vol. 93, No. 7, 1998
17. 18. 19. 20. 21. 22.
biofeedback for the treatment of paradoxical puborectalis syndrome. Dis Colon Rectum 1992;35:769 –76. Hallan RI, Williams NS, Melling J, et al. Treatment of anismus in intractable constipation with Botulinum A toxin. Lancet 1988;ii: 714 –7. Joo JS, Agachan F, Wolff B, et al. Initial North American experience with botulinum toxin type A for treatment of anismus. Dis Colon Rectum 1996;39:1107–11. Karlbom U, Pahlman L, Nilsson S, et al. Relationship between defecographic findings, rectal emptying and colonic transit time in constipated patients. Gut 1995;36:907–12. Koutsomanis D, Lennard-Jones JE, Kamm MA. Prospective study of biofeedback treatment for patients with slow and normal transit constipation. Eur J Gastroenterol Hepatol 1994;6:131–7. Ness TJ, Metcalf AM, Gebhart GF. A psychophysiological study in humans using phasic colonic distension as noxious visceral stimulus. Pain 1990;43:377– 88. Enck P. Biofeedback training in disordered defecation: A critical review. Dig Dis Sci 1993;38:1953– 60.
Vol. 93, No. 7, 1998 ISSN 0002-9270/98/$19.00 PII S0002-9270(98)00207-X
Original contributions Obstructive Defecation: A Failure of Rectoanal Coordination Satish S. C. Rao, M.D., Ph.D., Kimberly D. Welcher, B.S., and Jennifer S. Leistikow, B.S. Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
Objective: The pathophysiology of obstructive defecation is unclear. We investigated whether impaired rectoanal coordination causes obstructive defecation and if this dysfunction can be corrected by biofeedback therapy. Methods: We prospectively studied 25 healthy subjects and 35 consecutive patients with constipation (>1 year) with anorectal manometry and balloon expulsion test. Symptoms were assessed from diary cards. Patients found to have obstructive defecation were offered biofeedback therapy. After treatment, their defecation dynamics and symptoms were reassessed. Results: Eighteen patients had obstructive defecation and 17 had normal defecation dynamics (nonobstructive). Five normals (20%) exhibited obstructive pattern but only one failed to expel balloon. In the obstructive group, during straining, the intrarectal pressure and defecation index were lower (p < 0.05), and anal residual pressure was higher (p < 0.01) when compared with the nonobstructive group or normals. After biofeedback therapy, the intrarectal pressure and defecation index increased (p < 0.02) and anal residual pressure decreased (p < 0.001); stool frequency, degree of straining, and bowel satisfaction scores improved (p < 0.05); 67% stopped laxatives and 11 patients discontinued stooling with digitation. Conclusion: Patients with obstructive defecation showed impaired rectal contraction, paradoxical anal contraction, or inadequate anal relaxation. These features suggest that rectoanal coordination was impaired. Biofeedback therapy rectified these pathophysiological disturbances and improved constipation. (Am J Gastroenterol 1998;93:1042–1050. © 1998 by Am. Coll. of Gastroenterology)
INTRODUCTION It has been estimated that 50% of patients referred to tertiary care centers with chronic constipation have obstructive defecation (1, 2), a condition also referred to as anismus or pelvic floor dyssenergia (3–5). Its pathophysiology is, however, incompletely understood. It has been proposed that the inability to relax the external anal sphincter may be the chief underlying mechanism (3). However, 20 –30% of healthy subjects also exhibit this phenomenon (4, 5). Furthermore, based on the notion that obstructive defecation is a spasmodic dysfunction of the anal sphincter, surgical myotomy has been performed (6). Although preliminary studies were encouraging, a more critical assessment has shown that surgery may help only 10 –30% of patients (7). Hence, the inability to relax the external anal sphincter is unlikely to be the sole mechanism that leads to obstructive defecation. Defecation is a complex process that involves involuntary propulsion of stool through the colon, perception of stool when it arrives in the anorectal segment, and a coordinated movement that consists of rectal contraction, reflex relaxation of internal anal sphincter and voluntary relaxation of external anal sphincter. In this study, we tested the hypothesis that the inability to perform a coordinated movement of the pelvic floor may cause obstructive defecation. Our objectives were: 1) to identify the pathophysiological mechanism(s) that may cause obstructive defecation, and 2) to assess whether biofeedback therapy can correct the underlying dysfunction(s). The study was performed in two phases. In the first phase, healthy subjects and consecutive patients referred with chronic constipation were investigated with tests of anorectal function. At the end of this phase, we identified two groups of patients: those with normal defecation dynamics (nonobstructive group), and those with obstructive defecation. In the second phase, patients with obstructive defecation were offered a treatment program consisting of neuromuscular conditioning using biofeedback techniques. After biofeedback therapy, tests of anorectal
Received Oct. 15, 1997; accepted Jan. 30, 1998. 1042
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
1043
function and symptom patterns were reassessed to identify pathophysiological changes. MATERIALS AND METHODS Subjects We studied 35 consecutive patients referred to a tertiary care center with chronic constipation, male/female ratio 5 5/30, mean age 44 yr. (range 21– 81 yr). During the previous year all patients reported at least three of the following symptoms with 25% of bowel movements (when not taking laxatives): 1) stool frequency of less than two/wk, 2) passage of hard stools, 3) excessive straining, or 4) a feeling of incomplete evacuation (8). All patients underwent standard investigations that included barium enema or colonoscopy to exclude other pathology and secondary causes of constipation. Studies were also performed in 25 healthy control subjects who reported normal bowel function, had no previous gastrointestinal surgery, and were not taking any medication. These subjects were recruited through hospital advertisement. The studies were approved by the Human Ethics Committee of the University of Iowa. In the first phase, the following protocol was used to assess anorectal and colonic function and to identify patients with obstructive defecation. Phase 1 Anorectal manometry. Patients were asked to empty their bowels before the study and a bowel preparation was not routinely used. With the subject lying in the left lateral position and hips flexed to 90°, a flexible probe, 8 mm in diameter, with 5 strain gauge transducers (Gaeltec Ltd., Isle of Skye, UK) was placed in the rectum. One sensor was located 1 cm from the tip of the probe, and four sensors, arrayed 90° to each other, were located 9 cm from the tip. A 5-cm long latex balloon (Trojan-enz, Carter-Wallace, New York, NY) was fastened to the tip of the probe enclosing the terminal sensor. The probe was connected to a recorder (Gaeltec 7 MPR) with a sampling frequency of 8 MHz. Pressure activity was displayed on a computer/monitor (Gateway 2000, Sioux Falls, SD). After allowing the pressures to stabilize for 10 min, the resting and squeeze sphincter pressures were determined by station pull through techniques. The probe was then positioned so that the anal sensors were located 1.5 cm from the anal verge. Each subject was then asked to bear down as if to defecate, on three separate occasions, with a 2-min rest between each maneuver. Next, the rectal balloon was inflated with 60 cc of air, and the subjects were asked to bear down once more. Thereafter, intermittent graded balloon inflations were performed by distending the rectum with volumes up to 320 cc of air (9). The probe was then removed. Balloon expulsion test. A 3-mm diameter flexible tube with a 4-cm long balloon attached to its tip was placed in the rectum. The balloon was filled with 50 ml of water at 37°C. The patient was asked to sit on a commode and expel the
FIG. 1. Typical manometric changes in the rectum and anal canal during straining. In a normal subject the rectal pressure rises and the anal pressure decreases, whereas in a patient with obstructive defecation, there is insignificant rise in rectal pressure and paradoxical contraction of the anus (external sphincter). This abnormality improves after biofeedback therapy.
simulated stool, in privacy. After 5 min of straining, if the subject failed to expel the balloon, it was deflated and removed. The time taken for expelling the balloon was recorded. Colonic transit assessment. Patients ingested a capsule containing 24 radiopaque markers (Sitzmarks, Konsyl Pharmaceuticals, Irving, TX). After 5 days (120 h later) a plain x-ray film of the abdomen was obtained (10). Starting two days before and during the test, patients refrained from taking laxatives, enemas, or suppositories and were encouraged to eat their normal diet. Defecography. This test was performed only in patients with manometric evidence of obstructive defecation. Barium paste, 150 ml, was placed in the rectum. Thereafter, lateral videofluoroscopic images of the anorectal segment were obtained at rest, during cough, and during attempts to bear down as if to defecate (11). A diagnosis of obstructive defecation was made if the patients exhibited an obstructive pattern of defecation, defined as a paradoxical increase of anal sphincter pressure (Fig. 1) or ,20% relaxation of the resting anal sphincter pressure during straining as if to have a bowel movement (Fig. 1), in particular, after inflating a balloon in the rectum with 60 cc of air. Additionally, patients had to fulfill at least two of the following criteria: 1) inability to expel a 50-ml
1044
RAO et al.
water-filled balloon within 5 min; 2) inability to expel, or .50% retention, of barium during defecography; and 3) prolonged colonic transit .5 markers at 120 h. Owing to ethical constraints regarding radiation exposure, defecography and colon transit study were not performed in healthy control subjects and defecography was not performed in the nonobstructive group. All subjects also answered a questionnaire in which they described their stool frequency, degree of straining, and stool consistency. Phase 2 Patients with obstructive defecation were offered a twostage outpatient treatment program of neuromuscular conditioning using biofeedback techniques. To improve the abdominal effort during defecation, in the first stage (4 – 6 wk) patients were taught diaphragmatic breathing exercises (12). This consisted of distending the abdomen by inhaling slowly and then holding the breath for $10 –15 sec. The patients were asked to practice this maneuver for $20 min, three times a day. In the second stage (2– 4 wk), patients were asked to attend the motility laboratory twice a week. Biofeedback therapy was performed by using the manometric equipment described earlier, and by employing visual and verbal feedback techniques. The aim of this treatment was to improve rectal sensation and to establish a normal pattern of straining. The visual feedback was provided by observing the changes in pressure activity on the monitor screen. The verbal feedback was provided by the physician/ nurse therapist. This consisted of either complimenting the patient for performing a correct maneuver or rectifying any errors. Each 60 –90-min treatment session comprised the following three maneuvers. The goal of sensory conditioning was to improve perception of rectal distention by intermittently inflating a balloon in the rectum, using varying volumes of air (13–15). After establishing sensory thresholds, the balloon was inflated up to the volume that induced the urge to defecate. The patient was instructed to observe the monitor and to use the visual cue that was provided by the rise in intrarectal pressure (which occurs with each inflation) and to associate this cue with any possible rectal sensation. Thereafter, with each successive inflation, the distending volume was decreased by 10 –15%. By trial and error, the patient was gradually trained to recognize smaller volumes of inflation. Thereby, lower sensory thresholds were established. The goal of rectoanal coordination was to educate the patient to perform a coordinated maneuver (during simulated defecation) that consisted of a rise in rectal pressure synchronized with anal relaxation (Fig. 1). With the manometry catheter in situ and seated on a commode in front of the monitor, the patients were asked to bear down as if to defecate. During the maneuver, their posture and breathing techniques were corrected. Next, the rectal balloon was distended, using the newly established volume for urge to defecate, and again the patients were asked to bear down.
AJG – Vol. 93, No. 7, 1998 After the maneuver, the balloon was deflated. These maneuvers were repeated 20 times, and with each attempt the patient was instructed to titrate the degree of abdominal and anal effort required to achieve a normal pattern of defecation. Appropriate verbal reinforcement was provided by the therapist throughout the procedure. The balloon expulsion test was performed as described previously. But here, patients were advised regarding appropriate techniques for relaxing the pelvic floor. If they were unable to expel the device, gentle traction was applied to the balloon while reinforcing their straining technique (12, 13, 16). The maneuver was repeated a few times. Assessment of symptoms and follow-up Patients were asked to maintain a daily log of bowel symptoms. In this diary, they recorded stool frequency, degree of straining (1 5 normal, 2 5 moderately excessive, 3 5 severe), stool consistency (hard, normal, loose), and how often they practiced diaphragmatic exercises, and the type and amount of laxative consumed. During this phase, patients were also asked to score their satisfaction or dissatisfaction with bowel habit on a visual analogue scale. During this phase, patients were advised to take laxatives ad libitum. The number of training sessions was customized for each patient. Biofeedback training was discontinued when patients reported a) at least 33% improvement in their difficulty with defecation or in their stool frequency, and b) that without feedback, they were able to demonstrate consistently or at least 50% of attempts in two consecutive training sessions, a normal pattern of defecation. After completion of biofeedback therapy, anorectal manometry and balloon expulsion tests were repeated. Patients were asked to return at 6 months. Before this visit they were asked to complete a 1-wk diary of bowel symptoms and to score their satisfaction with bowel habit on a visual analog scale (0 –10). Measurements and analysis Anorectal manometry. The mean of the three highest values for the anal sphincter pressures at any level in the anal canal during rest and during squeeze was taken as the maximum resting and the maximum squeeze pressure (9). The pressure values obtained when the balloon was distended inside the rectum were subtracted from the pressure values that were obtained during balloon distention with similar volumes outside the rectum (9). The thresholds for first sensation, desire to defecate, and urgency to defecate were also measured (9). Of the three trials of simulated defecation, the effort that closely resembled a normal pattern of defecation (Fig. 1) was used to measure the pressure changes in the rectum and anus and to calculate the following values: Defecation Index (D.I.). This index was used as an overall measure of the coordinated effort (pressure gradient) between the rectum and anus and was calculated from the following equation:
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
Defecation Index (D.I.) 5 Rectal pressure when straining 4 Anal residual pressure when straining The anal residual pressure was defined as the minimal pressure in the anal canal (at any channel) during attempts to strain as if to defecate. Assessment of subjective parameters. All patients were asked to grade their satisfaction or dissatisfaction with bowel habits, both before and after biofeedback therapy, using a visual analog scale of 1–10, where 10 was normal. Additionally, their stool diaries were analyzed to calculate the mean stool frequency/wk, the mean strain score per bowel movement, and the laxative consumption score/wk (0 5 no laxatives, 1 5 high fiber diet 6 bran, 2 5 oral laxatives 6 suppositories, 3 5 enemas, magnesium citrate, solution polyethylene glycol electrolyte solution (GoLYTELY, Braintree Labs, Braintree, MA). Statistics. During Phase 1, the manometric parameters between the two groups and between patients and healthy control subjects were compared using multifactorial analysis of variance with Bonferroni’s correction. During phase 2, the manometric changes within the obstructive group were compared using the paired Student’s t test. Statistical differences between healthy control subjects and the obstructive group after biofeedback therapy were also compared using the Student’s t test. The differences in subjective parameters of bowel function were compared among the three groups by using Wilcoxon’s rank sum tests. The differences in the number of subjects from each group who could expel a 50-ml water filled-balloon were compared by the Fisher’s exact test. Results are expressed as mean 6 95% confidence interval. RESULTS Demographics We found that 18 of 35 (51%) patients with constipation had obstructive defecation (m/f 5 3/15, mean age 48 yr) and 17 of 35 (49%) patients had normal defecation dynamics. The latter group of patients were classified as the nonobstructive group (m/f 5 2/15, mean age 42 yr). The mean duration (range) of constipation for the obstructive versus nonobstructive group was 20 yr (3–54 yr) versus 11 yr (1–20 yr) and the mean stool frequency/wk was 3.8 (0.5–24) versus 1.6 (0.5–3). A need for digital disimpaction of stool was reported by eleven patients with obstructive defecation and by one patient with slow transit constipation (p , 0.01). All 18 patients with obstructive defecation completed biofeedback therapy. The mean number (range) of sessions was 6 (3–11). The healthy control group consisted of 25 subjects, (m/f 5 10/15, mean age 50 yr, range 33–71 yr). Their mean stool frequence/wk was 6.5 (3–15).
1045
Baseline investigations In the obstructive group, 13 (72%) patients had slow colon transit and five (28%) patients had normal colon transit (10). In the nonobstructive group, 11 (65%) patients had slow colon transit and six (35%) patients had normal transit. There was no difference between the two groups. Defecography showed an inability to expel or .50% retention of barium in eight of 18 patients with obstructive defecation. The anorectal angle either became more acute or failed to change in nine of 18 (50%) patients. Six patients showed rectal mucosal intussusception. Anal sphincter pressures The rectoanal inhibitory reflex was present in all of our subjects, both patients and normals, excluding Hirschsprung’s disease. The maximum anal resting and the maximum anal squeeze pressure were not significantly different between the three groups of subjects and in the obstructive group after biofeedback therapy (Table 1). Changes in anal pressure during simulated defecation When straining, the anal residual pressure was higher (p , 0.001) in the obstructive group when compared with the nonobstructive group or healthy control subjects (Fig. 2 and Table 1). After biofeedback treatment, the anal residual pressure decreased (p , 0.0001) (Fig. 2), and the new values were similar to those observed in healthy controls and in the nonobstructive group (Table 1). Patients with nonobstructive constipation also showed a lower (p , 0.05) anal residual pressure compared to normals (Table 1). Five healthy subjects (20%) also exhibited an obstructive pattern of defecation. Changes in intrarectal pressure during simulated defecation The intrarectal pressure was lower (p , 0.05) in the obstructive group compared with the nonobstructive group, when straining either with an empty rectum (Fig. 3) or after rectal distension with a 60 cc balloon (Table 1). The intrarectal pressure was also lower (p , 0.005) in the obstructive group compared with normals. No differences were seen between normals and nonobstructive group. After biofeedback therapy, the intrarectal pressure increased (p 5 0.009) during straining in the obstructive group. Before biofeedback therapy, five of 18 (28%) patients with obstructive defecation showed high rectal pressure (.70 mm Hg); in these subjects, after treatment, the rectal pressure decreased (Fig. 3). Defecation index The mean defecation index was lower (p , 0.001) in obstructive group compared with either the nonobstructive group or healthy controls (Fig. 4). After biofeedback therapy, the defecation index increased (p , 0.001) in the obstructive group and was similar to that observed in the nonobstructive group or healthy controls (Fig. 4).
1046
RAO et al.
AJG – Vol. 93, No. 7, 1998
TABLE 1 Objective and Subjective Parameters of Anorectal Function in the Three Groups of Subjects and in the Obstructive Group After Biofeedback Therapy
Anal and rectal pressures Max. anal resting pressure (mm Hg) Max. anal squeeze pressure (mm Hg) Anal residual pressure (mm Hg) Rectal pressure during straining (after inflation of 60-cc balloon) (mm Hg) Rectal sensation Threshold volume for first perception (cc) Threshold volume for desire to defecate (cc) Threshold volume for urge to defecate (cc) Subjective parameters Strain score Laxative consumption score Bowel satisfaction score
Obstructive (n 5 18)
Normal (n 5 25)
Nonobstructive (n 5 17)
71 (57–85) 148 (121–175) 48 (39–57) 78 (65–91)
66 (58–75) 132 (109–156) 25 (21–29)# 51 (43–59)
59 (52–67) 110 (90–129)‡ 78 (66–90)*‡ 44 (33–55)‡
22 (14–30) 98 (71–125) 142 (104–180)
27 (19–34) 85 (62–108) 120 (89–151)
47 (20–74) 100 (64–136) 141 (102–180)
12 (6–19)‡§ 41 (33–49)†§ 63 (50–76)†§
1.2 (0.8–1.6) –
2.0 (1.6–2.4) 1.9 (1.5–2.3)
2.6 (2.3–2.9)*‡ 2.7 (2.5–2.9)* 1.1 (0.9–1.4)
1.6 (1.4–1.8)† 1.3 (1.0–1.6)† 7.8 (7.0–8.6)†
Before
After 64 (55–73) 122 (96–146) 37 (31–44)† 60 (51–69)‡
Mean (95% confidence interval). * p , 0.001, nonobstructive versus obstructive. † p , 0.001, ‡ p , 0.05, obstructive group, before and after biofeedback. ‡ p , 0.05, normal group versus obstructive group before biofeedback. § p , 0.05, normal group versus obstructive group after biofeedback. # p , 0.05, normal group versus nonobstructive group.
Rectal sensation The threshold volumes required for evoking a first sensation, desire to defecate, and urgency to defecate were not significantly different between the two patient groups (Table 1). When compared with normals, the threshold for first sensation was higher (p , 0.05) in the obstructive group, before biofeedback therapy. After biofeedback therapy, the thresholds for all three parameters of rectal sensation decreased (p , 0.001) (Table 1) in the obstructive group. The thresholds for a desire to defecate and urge to defecate were similar between patients with obstructive defecation and normals before biofeedback therapy, but were lower (p , 0.05) after treatment (Table 1). Balloon expulsion test Sixteen (89%) patients with obstructive defecation were unable to expel a 50 ml water filled balloon, compared with four (23%) patients with nonobstructive constipation (p , 0.01) and four (16%) normal subjects (p , 0.01) (Fig. 5). Patients with obstructive defecation also took more time (p , 0.001) to expel the balloon compared with other groups (Fig. 5). After biofeedback therapy, all 18 patients were able to expel the artificial stool within 3 min (p , 0.001) (Fig. 5). Of the four normal subjects who could not expel a balloon, only one showed an obstructive pattern of defecation, but all four had a low defecation index (0.8 – 1.2). Subjective parameters When compared with healthy normals, the mean stool frequency was significantly lower (p , 0.05) in both groups of patients but there was no difference between the patient groups. After biofeedback therapy, the stool frequency in-
creased (p , 0.05) in the obstructive group (Fig. 6). Interestingly, three of 18 (17%) patients had $13 stools/wk. After biofeedback therapy, their stool frequency decreased (Fig. 6). The mean strain score (degree of straining) was higher (p , 0.05) in the obstructive group compared with the nonobstructive group. After biofeedback therapy, both the mean strain score and the mean laxative consumption score decreased (p , 0.01) in the obstructive group, and the bowel satisfaction score increased (p , 0.01) (Table 1). Also, after therapy, all eleven patients who could not defecate without digital disimpaction of stools were able to discontinue this habit. Follow-up Six months after biofeedback therapy, 13 of 18 (72%) patients with obstructive defecation returned for a follow-up assessment. Their mean stool frequency/wk was 10.7 (range 4 –22); this was significantly higher (p , 0.05) than baseline but was similar to that observed at the end of biofeedback therapy (Fig. 6). The mean strain score and the amount of laxatives consumed were lower and the bowel satisfaction scores (8.0 [range 7.1– 8.9]) were significantly higher (p , 0.01) at 6 months than at baseline but not after biofeedback therapy. Five patients did not return. Of these, three patients answered a telephone inquiry and reported that their bowel function was much improved. Two patients moved out of state and could not be contacted. DISCUSSION Obstructive defecation is generally regarded as a failure of anal relaxation (3–7). However, therapeutic attempts at reducing anal sphincter pressure either by surgical myotomy
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
1047
FIG. 2. This shows the individual values and the mean 6 95% CI for the anal residual pressure during straining in normals, in patients with nonobstructive constipation, and in patients with obstructive defecation before and after biofeedback therapy.
FIG. 3. This shows the individual values and the mean 6 95% CI for the intrarectal pressure during straining as if to defecate, in normals and in the two groups of patients, and the changes in the obstructive group after therapy.
FIG. 4. This shows the changes in the defecation index for the three groups of subjects (mean 6 95% CI).
1048
RAO et al.
FIG. 5. This shows the individual values for the time taken to expel a 50-ml water-filled balloon (mean 6 95% CI).
(6, 7) or by injection of botulinum toxin (17, 18) were only partially effective. Our objective was to investigate the pathophysiological mechanism(s) that may account for this problem. Based on anorectal function, we identified two groups of patients with refractory constipation: those with obstructive defecation and those with normal pelvic floor function (nonobstructive). However, the demographics, duration of symptoms, and colon transit measurements were similar between the two groups. Approximately two-thirds of patients in each group had slow colon transit. Thus, there was an overlap and many patients with obstructive defecation also had slow colon transit. This confirms recent observations (19, 20) and questions the validity of classifying patients into those with slow transit constipation or obstructive defecation, based on transit measurements only. It is our impression that one should make a diagnosis of slow transit constipation only after excluding obstructive defecation. During attempts to strain as if to defecate, we found that the intrarectal pressure was significantly lower in nearly two-thirds of patients with obstructive defecation compared with other groups. After biofeedback therapy, the intrarectal pressure increased significantly and was similar to that of the nonobstructive group or normals. Because the intrarectal pressure is governed by the contraction of rectal muscles together with raised intraabdominal pressure, our findings suggest that many patients with obstructive defecation have impaired pushing force during defecation. However, this was not seen in all of our patients. About one-third of patients with obstructive defecation produced either normal or higher intrarectal pressures during straining. Because this finding was associated with high anal residual pressure and with paradoxical anal contraction, it is likely that, in some
AJG – Vol. 93, No. 7, 1998
FIG. 6. This shows the stool frequency in each patient with obstructive defection before, at the end of biofeedback therapy, and after 6 months (mean 6 95% CI).
patients, excessive straining may also be counterproductive. Thus, either the inability to generate adequate pushing force or excessive straining may lead to obstructive defecation. By educating patients to titrate their abdominal pushing force, biofeedback therapy proved effective in both groups of patients. We found that patients with obstructive defecation exhibit paradoxical anal contraction when they strain with an empty rectum (3, 4, 12–15) but also when they strain with a 60 ml balloon inflated in the rectum, i.e., after a sensation of rectal fullness. Furthermore, we have documented that obstructive defecation is associated with high anal residual pressure. In five of 18 (28%) patients, during straining, either there was no change in anal resting pressure or there was an insignificant (,10%) decrease. This shows that patients with obstructive defecation not only exhibit paradoxical anal contraction but also absent or impaired anal relaxation. After biofeedback therapy, all of these patients were able to relax the anal sphincter. Five normal subjects also exhibited an obstructive pattern of defecation but only one of them was unable to expel a balloon. This confirms that up to 20% of normals may exhibit an obstructive pattern of defecation (4). It also reaffirms that in some subjects there is a poor correlation between the obstructive pattern, bowel habit, and ability to expel a simulated stool. Because normals may exhibit this manometric finding, a diagnosis of obstructive defecation should not be made solely on the basis of this manometric finding. Other evidence such as dyschezia, digital disimpaction of stool, inability to expel a simulated stool or barium, and retention of markers on colon transit study should be
AJG – July 1998
RECTOANAL COORDINATION AND OBSTRUCTIVE DEFECATION
required to establish this diagnosis. Because these studies were not performed in our healthy group, we are unable to describe how many of our normals would have fulfilled the criteria for obstructive defecation. We have proposed a new index for quantifying the rectoanal pressure gradient during simulated defecation—the defecation index. The mean defecation index in the nonobstructive group was 2.2 and in healthy controls was 1.8. In contrast, the obstructive group had a low index of 0.7. This low index could be caused by either high anal residual pressure (high resistance) or low intrarectal pressure (poor pushing force) or both. After biofeedback therapy, the mean index rose to 2.0, suggesting that the pressure gradient had improved. Four normal subjects who failed to expel a balloon also had a low defecation index (,1.2). Hence, it is our impression that a pressure gradient between the rectum and anus which is (at least) greater than a factor of 1.5 is required to facilitate expulsion of stool, and that a low defecation index may serve as a better test for diagnosing obstructive defecation than merely the pattern of paradoxical anal contraction. Rectal sensory perception was impaired in the obstructive group compared with healthy subjects and confirms previous observations (14, 15). After biofeedback therapy, sensory perception improved, and the values were lower than for normals. The heightened visceral sensation may be a consequence of sensory conditioning. Repeated reinforcement has been reported to alter sensory thresholds even in normals (21). Thus, impaired rectal perception may play a role in the pathogenesis of obstructive defecation, but it is unclear whether this is primary or secondary to rectal distention from fecal stasis. In our patients with obstructive defecation, the subjective parameters such as bowel satisfaction score, mean stool frequency, and degree of straining improved significantly after treatment, confirming previous findings (12–16, 20). However, at the outset, not all patients with obstructive defecation had decreased stool frequency. In fact, 40% of patients had one or more bowel movement per day and often these patients expelled small, pellet-like stools several times a day. In this group, after biofeedback treatment, stool frequency decreased, suggesting more complete evacuation of stools. Furthermore, most patients reduced their dependence on laxatives and twelve (67%) stopped using laxatives. Six months later, 15 of 18 (83%) patients reported persistent improvement in their bowel function. Biofeedback therapy has been advocated for the treatment of obstructive defecation (12–16, 20) and in a metaanalysis was shown to be useful in $70% of patients (22). But there is little evidence for objective improvement. In two studies (14, 20), the pattern of paradoxical anal contraction improved, but changes in rectal and anal pressures and rectal sensation were either not measured or did not change appreciably. Additionally, no previous study has systematically compared the manometric parameters in patients with
1049
obstructive defecation and healthy control subjects. Our study shows that biofeedback therapy can improve subjective and objective parameters of anorectal function and can restore normal bowel function in .80% of patients with obstructive defecation. After treatment, we did not repeat a colon transit study or defecography because the defecation dynamics, balloon expulsion time, and symptoms had all improved substantially. Moreover, there is poor correlation between the results of these test and clinical outcome (20). Whether the beneficial outcome of biofeedback therapy is due to excessive attention or improvement in bowel function is unclear, but it merits further study. The objective improvement, however, suggests a real change in the underlying pathophysiology. Our study reveals that patients with obstructive defecation exhibit either impaired rectal contraction (61%), paradoxical anal contraction (78%), or impaired anal relaxation (22%), or a combination of these mechanisms. These findings suggest that these patients have dyssynergic defecation with impaired coordination between the rectum and anal sphincter muscles. This dysfunction was corrected by biofeedback therapy, reaffirming its pathogenic role. ACKNOWLEDGMENTS The authors wish to thank Dr. K. Hubel for his critique, Ms. Susie McConnell for her superb secretarial assistance, and Ms. Janel Happel, R.N., for her help with biofeedback therapy. Portions of this manuscript were presented at the annual meeting of the American Gastroenterological Association and published as an abstract (Gastroenterology 1994;106(4):A557). Reprint requests and correspondence: Dr. Satish S. C. Rao, M.D., Ph.D., F.R.C.P. (Lon), 4612 JCP/Division of Gastroenterology/Hepatology, The University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242.
REFERENCES 1. Rao SSC, Patel RS. How useful are tests of anorectal function in the management of defecation disorders. Am J Gastroenterol 1997;92: 469 –75. 2. Surrenti E, Rath DM, Pemberton JH, et al. Audit of constipation in a tertiary referral gastroenterology practice. Am J Gastroenterol 1995; 90:1471–5. 3. Preston DM, Lennard-Jones JE. Anismus in chronic constipation. Dig Dis Sci 1985;30:413– 8. 4. Jones PN, Lubowski DZ, Swash M, et al. Is paradoxical contraction of puborectalis muscle of functional importance? Dis Colon Rectum 1987;30:667–70. 5. Duthie GS, Bartolo DCC. Anismus. The cause of constipation? Results of investigation and treatment. World J Surg 1992;16:831–5. 6. Martelli H, Devroede G, Arhan P, et al. Mechanisms of idiopathic constipation: Outlet obstruction. Gastroenterology 1978;75:623–31. 7. Pinho M, Yoshioka K, Keighley MRB. Long term results of anorectal myectomy for chronic constipation. Br J Surg. 1989;76:1163– 4. 8. Whitehead WE, Chaussade S, Corazziari E, et al. Report of an international workshop on management of constipation. Gastroenterol Intl 1991;4:99 –113. 9. Rao SSC, Read NW, Davison PA, et al. Anorectal sensitivity and responses to rectal distension in patients with ulcerative colitis. Gastroenterology 1987;93:1270 –5.
1050
RAO et al.
10. Evans RC, Kamm MA, Hinton JM, et al. The normal range and a simple diagram for recording whole gut transit time. Int J Colorectal Dis 1992;7:15–7. 11. Mahieu P, Pringot J, Bodart P. Defecography. Description of a new procedure and results in normal patients. Gastrointest Radiol 1984;9: 247–51. 12. Koutsomanis D, Lennard-Jones JE, Roy AJ, et al. Controlled randomized trial of visual biofeedback versus training without a visual display for intractable constipation. Gut 1995;37:95–9. 13. Bleijenberg G, Kuijpers HC. Treatment of spastic pelvic floor syndrome with biofeedback. Dis Colon Rectum 1987;30:101–11. 14. Papachrysostomou M, Smith AN. Effects of biofeedback on obstructive defecation—reconditioning of the defecation reflex? Gut 1994;35: 242–5. 15. Loening-Baucke V. Modulation of abnormal defecation dynamics by biofeedback treatment in chronically constipated children with encopresis. J Pediatr 1990;116:214 –22. 16. Wexner SD, Cheape JD, Jorge JMN, et al. Prospective assessment of
AJG – Vol. 93, No. 7, 1998
17. 18. 19. 20. 21. 22.
biofeedback for the treatment of paradoxical puborectalis syndrome. Dis Colon Rectum 1992;35:769 –76. Hallan RI, Williams NS, Melling J, et al. Treatment of anismus in intractable constipation with Botulinum A toxin. Lancet 1988;ii: 714 –7. Joo JS, Agachan F, Wolff B, et al. Initial North American experience with botulinum toxin type A for treatment of anismus. Dis Colon Rectum 1996;39:1107–11. Karlbom U, Pahlman L, Nilsson S, et al. Relationship between defecographic findings, rectal emptying and colonic transit time in constipated patients. Gut 1995;36:907–12. Koutsomanis D, Lennard-Jones JE, Kamm MA. Prospective study of biofeedback treatment for patients with slow and normal transit constipation. Eur J Gastroenterol Hepatol 1994;6:131–7. Ness TJ, Metcalf AM, Gebhart GF. A psychophysiological study in humans using phasic colonic distension as noxious visceral stimulus. Pain 1990;43:377– 88. Enck P. Biofeedback training in disordered defecation: A critical review. Dig Dis Sci 1993;38:1953– 60.