TY - JOUR
AU - Finlay, I G
AB - Abstract Background Patients with rectal prolapse have abnormal hindgut motility. This study examined the effect of rectal prolapse surgery on colonic motility. Methods Twelve patients undergoing sutured rectopexy were studied before and 6 months after surgery by colonic manometry, colonic transit study and clinical assessment of bowel function. The results were compared with those from seven control subjects. Results Before surgery colonic pressure was greater in patients than controls (P < 0·050). Controls responded to a meal stimulus by increasing colonic pressure; this increase was absent in patients. After rectopexy, colonic pressure reduced towards control values and patients' colonic pressure response to a meal returned. High-amplitude propagated contractions (HAPCs) were seen in all controls but in only three patients before and two patients after surgery. Three patients had prolonged colonic transit before and eight after rectopexy. Conclusion Patients with rectal prolapse have abnormal colonic motility associated with reduced HAPC activity. Rectopexy reduces colonic pressure but fails to restore HAPCs, reduce constipation or improve colonic transit. These observations help explain the pathophysiology of constipation associated with rectal prolapse. Introduction Transabdominal rectal dissection with intra-abdominal fixation (rectopexy) effectively corrects rectal prolapse with recurrence rates of less than 5 per cent1. However, the procedure is associated with poor postoperative function. Approximately half of the patients develop severe constipation that has been attributed variously to postoperative autonomic neuropathy, loss of rectal compliance and/or the presence of a redundant loop of sigmoid colon1–3. Addition of sigmoid colon resection to rectopexy reduces the incidence of postoperative constipation4,5 but it is not known why this is effective. A possible explanation is that resection of sigmoid colon removes a length of bowel rendered neuropathic by rectal dissection and/or division of the lateral ligaments6–9. Using colonic manometry, it has been shown that patients with rectal prolapse have a hindgut motility disorder before surgery10,11. The effect of surgery (rectopexy) on this hindgut motility disorder is unknown. The aim of the present study was to measure colonic function prospectively in patients with rectal prolapse before and after rectopexy by determination of colonic motility and colonic transit, and clinical assessment of bowel function. The results were compared with those obtained from normal controls. Patients and methods Patients presenting for rectal prolapse surgery were managed according to a protocol that allocated those who were unfit for an abdominal operation to a perineal procedure3. All remaining patients were allocated to sutured abdominal rectopexy. A sigmoid resection was added for patients who did not report faecal incontinence and who did not have manometric evidence of reduced anal sphincter pressure. It might be argued that all patients with preoperative constipation could be better served by a resection rectopexy to minimize the risk of postoperative constipation4,5,12. However, it was considered that colonic resection would carry an unacceptable risk of postoperative diarrhoea and faecal incontinence in constipated patients with reduced sphincter pressure. Consecutive patients with full-thickness rectal prolapse undergoing sutured abdominal rectopexy, without colonic resection, were included in the present study. Patients were compared with healthy controls. All subjects gave informed consent. The ethics committee of Glasgow Royal Infirmary University NHS Trust approved the study. Surgical treatment Surgery was undertaken through a lower midline abdominal incision under general anaesthesia. The rectum was mobilized fully both anteriorly and posteriorly to the level of the pelvic floor. Rectopexy was achieved by unilateral suturing of the pararectal tissues to the presacral fascia using monofilament sutures. Colonic manometry Inpatient colonic manometry was undertaken 48 h before and 6 months after surgery as described previously10. Briefly, a multilumen manometry catheter (M3 eight-lumen colonic catheter; Lectromed UK, Letchworth, Herts, UK) was inserted to at least the transverse colon using a colonoscope (Fig. 1). The manometry catheter was then connected to an infusion pump (Hydraulic Capillary Infusion System with float and filter; Arndorfer Medical Specialties, Milwaukee, Wisconsin, USA) and infused with sterile water at a pressure of 51·58 kPa, resulting in a flow of 0·4 ml per channel per min. Pressure was measured via water pressure transducers (Medex, Rossendale, UK) linked to a computerized system that recorded pressures up to a maximum of 220 mmHg (version 3 Release 0.3 920 703; Gaeltec, Isle of Skye, UK). Fig. 1 Open in new tabDownload slide Plain abdominal radiograph illustrating the manometry catheter position and colonic pressure recordings over 1 h at perfusion sites 1 (proximal ascending colon) to 7 (sigmoid colon) during a high-amplitude propagated contraction in one patient (x axis, time; y axis, pressure in mmHg). The magnitude of the high-amplitude propagated contraction increases as it travels distally along the colon from recording point 1 to point 7 Colonic pressure was recorded for 24 h. Abdominal radiography was undertaken before recording colonic pressure to ensure that the manometry catheter had not migrated distally. The number of high-amplitude propagated contractions (HAPCs) was recorded13. A HAPC was defined as a contraction of greater than 100 mmHg that was propagated distally in three separate channels. The number of pressure peaks larger than 5 mmHg, the number of pressure peaks larger than 50 mmHg and the area under the colonic pressure–time curve (AUC) were measured at the descending and sigmoid colon for 1 h before and 1 h after a standardized 1000-kcal meal stimulus. Pressure artefacts secondary to movement, coughing or sneezing were noted. Colonic transit Colonic transit was assessed in patients before operation and 6 months after rectopexy. Twenty radio-opaque markers were ingested. Plain abdominal radiography was undertaken 1, 5 and 10 days later, and reported by a consultant radiologist. No laxatives were consumed during the transit study. Prolonged colonic transit was diagnosed when more than 80 per cent of ingested markers were present after 5 days14. Bowel function Frequency of defaecation and laxative consumption were recorded. Patients were considered to suffer constipation if they required regular laxatives for at least 3 months before surgery or at the time of postoperative review. Statistical analysis Data are reported as median (range). The Mann–Whitney U test was used for comparison of resting colonic pressure in patients and controls. The Wilcoxon signed rank test was used for analysing premeal versus postmeal measurements in controls and patients, and postoperative versus preoperative resting colonic pressure in patients. Results Twelve patients (one man), of median age 57 (range 37–74) years, were included in the study. The median age of the seven control subjects (two men) was 42 (range 19–69) years. None of the patients or controls was suffering from a psychiatric disorder or was being treated with neuroleptic drugs. During rectal mobilization, the lateral ligaments were divided in six patients and preserved in the other six patients. Preoperative, postoperative and control colonic manometric data are shown in Table 1. Before surgery, resting colonic pressure was increased in patients compared with controls. This increased pressure in patients reached statistical significance for 5-mmHg peaks (P = 0·002), 50-mmHg peaks (P = 0·020) and AUC (P < 0·001) in the descending colon, and for 5-mmHg peaks (P = 0·026), 50-mmHg peaks (P = 0·037) and AUC (P = 0·013) in the sigmoid colon. After a meal stimulus, control subjects exhibited a significant increase in 5-mmHg (P = 0·028) and 50-mmHg (P = 0·042) peaks in the descending colon, and 50-mmHg (P = 0·043) peaks in the sigmoid colon. Patients did not have a significant change in 5-mmHg or 50-mmHg pressure peaks in the descending or sigmoid colon after a meal, but AUC was significantly decreased in the descending colon (P = 0·021). Table 1 Colonic manometry data . Controls . Patients . . Preop. . Postop. . Descending colon  5-mmHg peaks before meal (per h) 34 (19–92) 98 (53–195)* 70 (39–145)‡  50-mmHg peaks before meal (per h) 0 (0–2) 1 (0–8)* 0 (0–6)  AUC before meal (mmHg × min for 1 h) 128 (55–194) 566 (204–1049)* 255 (79–555)‡  5-mmHg peaks after meal (per h) 84 (30–324)† 141 (50–156) 135 (73–172)†  50-mmHg peaks after meal (per h) 1 (0–6)† 1 (0–8) 4 (0–20)†  AUC after meal (mmHg × min for 1 h) 123 (32–352) 306 (47–567)† 288 (100–743) Sigmoid colon  5-mmHg peaks before meal (per h) 47 (2–117) 105 (38–187)* 81 (36–109)  50-mmHg peaks before meal (per h) 0 (0–1) 2 (0–8)* 1 (0–12)  AUC before meal (mmHg × min for 1 h) 103 (13–216) 388 (101–1039)* 155 (24–558)‡  5-mmHg peaks after meal (per h) 116 (12–354) 135 (41–176) 108 (75–152)†  50-mmHg peaks after meal (per h) 1 (0–4)† 1 (0–40) 3 (0–28)†  AUC after meal (mmHg × min for 1 h) 125 (53–356) 319 (64–749) 191 (99–606) . Controls . Patients . . Preop. . Postop. . Descending colon  5-mmHg peaks before meal (per h) 34 (19–92) 98 (53–195)* 70 (39–145)‡  50-mmHg peaks before meal (per h) 0 (0–2) 1 (0–8)* 0 (0–6)  AUC before meal (mmHg × min for 1 h) 128 (55–194) 566 (204–1049)* 255 (79–555)‡  5-mmHg peaks after meal (per h) 84 (30–324)† 141 (50–156) 135 (73–172)†  50-mmHg peaks after meal (per h) 1 (0–6)† 1 (0–8) 4 (0–20)†  AUC after meal (mmHg × min for 1 h) 123 (32–352) 306 (47–567)† 288 (100–743) Sigmoid colon  5-mmHg peaks before meal (per h) 47 (2–117) 105 (38–187)* 81 (36–109)  50-mmHg peaks before meal (per h) 0 (0–1) 2 (0–8)* 1 (0–12)  AUC before meal (mmHg × min for 1 h) 103 (13–216) 388 (101–1039)* 155 (24–558)‡  5-mmHg peaks after meal (per h) 116 (12–354) 135 (41–176) 108 (75–152)†  50-mmHg peaks after meal (per h) 1 (0–4)† 1 (0–40) 3 (0–28)†  AUC after meal (mmHg × min for 1 h) 125 (53–356) 319 (64–749) 191 (99–606) Values are median (range). AUC, area under the colonic pressure–time curve. * P < 0·050 versus controls (Mann–Whitney U test); † P < 0·050 versus same group before meal, ‡P < 0·050 versus before operation (Wilcoxon signed rank test) Open in new tab Table 1 Colonic manometry data . Controls . Patients . . Preop. . Postop. . Descending colon  5-mmHg peaks before meal (per h) 34 (19–92) 98 (53–195)* 70 (39–145)‡  50-mmHg peaks before meal (per h) 0 (0–2) 1 (0–8)* 0 (0–6)  AUC before meal (mmHg × min for 1 h) 128 (55–194) 566 (204–1049)* 255 (79–555)‡  5-mmHg peaks after meal (per h) 84 (30–324)† 141 (50–156) 135 (73–172)†  50-mmHg peaks after meal (per h) 1 (0–6)† 1 (0–8) 4 (0–20)†  AUC after meal (mmHg × min for 1 h) 123 (32–352) 306 (47–567)† 288 (100–743) Sigmoid colon  5-mmHg peaks before meal (per h) 47 (2–117) 105 (38–187)* 81 (36–109)  50-mmHg peaks before meal (per h) 0 (0–1) 2 (0–8)* 1 (0–12)  AUC before meal (mmHg × min for 1 h) 103 (13–216) 388 (101–1039)* 155 (24–558)‡  5-mmHg peaks after meal (per h) 116 (12–354) 135 (41–176) 108 (75–152)†  50-mmHg peaks after meal (per h) 1 (0–4)† 1 (0–40) 3 (0–28)†  AUC after meal (mmHg × min for 1 h) 125 (53–356) 319 (64–749) 191 (99–606) . Controls . Patients . . Preop. . Postop. . Descending colon  5-mmHg peaks before meal (per h) 34 (19–92) 98 (53–195)* 70 (39–145)‡  50-mmHg peaks before meal (per h) 0 (0–2) 1 (0–8)* 0 (0–6)  AUC before meal (mmHg × min for 1 h) 128 (55–194) 566 (204–1049)* 255 (79–555)‡  5-mmHg peaks after meal (per h) 84 (30–324)† 141 (50–156) 135 (73–172)†  50-mmHg peaks after meal (per h) 1 (0–6)† 1 (0–8) 4 (0–20)†  AUC after meal (mmHg × min for 1 h) 123 (32–352) 306 (47–567)† 288 (100–743) Sigmoid colon  5-mmHg peaks before meal (per h) 47 (2–117) 105 (38–187)* 81 (36–109)  50-mmHg peaks before meal (per h) 0 (0–1) 2 (0–8)* 1 (0–12)  AUC before meal (mmHg × min for 1 h) 103 (13–216) 388 (101–1039)* 155 (24–558)‡  5-mmHg peaks after meal (per h) 116 (12–354) 135 (41–176) 108 (75–152)†  50-mmHg peaks after meal (per h) 1 (0–4)† 1 (0–40) 3 (0–28)†  AUC after meal (mmHg × min for 1 h) 125 (53–356) 319 (64–749) 191 (99–606) Values are median (range). AUC, area under the colonic pressure–time curve. * P < 0·050 versus controls (Mann–Whitney U test); † P < 0·050 versus same group before meal, ‡P < 0·050 versus before operation (Wilcoxon signed rank test) Open in new tab After rectopexy there was a trend for patients' resting colonic pressure to diminish compared with preoperative measurements (change towards normality). These reductions reached statistical significance for 5-mmHg peaks (P = 0·022) and AUC (P = 0·007) in the descending colon, and for AUC (P = 0·026) in the sigmoid colon. Rectopexy was associated with restoration of a colonic pressure response to a meal stimulus; there was a significant increase in 5-mmHg (P = 0·007) and 50-mmHg (P = 0·021) peaks in the descending colon, and for 5-mmHg (P = 0·002) and 50-mmHg (P = 0·028) peaks in the sigmoid colon. HAPCs were seen in all controls, in three patients before operation and in two patients after surgery. Colonic transit was prolonged in three patients before operation and remained prolonged in two of these patients after rectopexy. Six other patients developed prolonged transit after rectopexy; the radio-opaque markers stayed in the sigmoid colon in five patients and the transverse colon in one patient. Six patients were constipated before surgery, five of whom remained constipated after rectopexy. Three other patients suffered de novo constipation after surgery. There was no evidence from manometric, transit marker or clinical investigations that colonic function in patients in whom the lateral ligaments of the rectum had been preserved was any different from that in patients in whom the ligaments had been divided during rectopexy. Discussion Although rectopexy for rectal prolapse is associated with a low recurrence rate, postoperative gastrointestinal function is poor. Approximately half of the patients develop severe constipation and one-third are incontinent1–3. In many patients constipation predates surgery but is exacerbated by the operation. In the present study three patients had objective evidence of delay in colonic transit before surgery, increasing to eight after operation. In contrast, preoperative incontinence often improves after rectopexy3. The cause of constipation before and after surgery in patients with rectal prolapse is unknown. It has been shown that patients with rectal prolapse have a similar hindgut motility abnormality to that observed following spinal cord injury10. This offers a possible explanation for preoperative constipation. The present study provides a detailed prospective analysis of the effect of rectal prolapse surgery on colonic motility. Surgical intervention was restricted to rectal mobilization (with or without lateral ligament division) with simple suture of one side of the mesorectum at the pelvic brim. Consequently any detrimental effect on motility should be attributable to these specific technical steps. The use of foreign material was avoided as it has been shown to be unnecessary and reduces rectal compliance15,16. The present study confirms, in an expanded cohort, that colonic motility is abnormal in patients with rectal prolapse before surgery compared with that in controls10. Resting hindgut pressure was significantly greater in patients. Patients also failed to exhibit increased hindgut pressure in response to a meal stimulus, possibly reflecting loss of this reflex. Alternatively, patients with rectal prolapse might reach their maximum hindgut pressure while at rest, precluding any further pressure increase in response to a meal. After surgery, resting hindgut pressure fell towards control values and there was restoration of the hindgut pressure response to a meal stimulus. Only one other study has used colonic manometry to assess hindgut motility in rectal prolapse11. It compared patients with rectal prolapse with another group of patients who had undergone rectopexy, and showed no statistically significant difference in colonic manometric data between the two groups. The significance of a 24-h colonic manometric recording in a hospital environment can be debated. It is recognized that the Arndorfer manometry system has substantial limitations that may influence results10. However, the present study compared paired preoperative and postoperative data; consequently the confounding element of the manometry system was restricted to a constant variable. Nevertheless statistical significance was not demonstrated between the groups for all colonic pressure measurements; this probably reflects a Type 2 error related to the small numbers of subjects studied. It is also possible that the differences between the groups might be explained by differences in age (controls were slightly younger than patients). Surgical management was planned according to a protocol that allocated constipated patients with rectal prolapse, who had normal findings on anal manometry and did not report faecal incontinence, to colonic resection in addition to suture rectopexy3; these patients were excluded from the present study. It might therefore be argued that the cohort studied represents a biased subset who were less constipated than the typical patient with rectal prolapse. The results of the present study suggest that the hindgut pressure abnormality observed before surgery is reversible and is presumably secondary to the presence of the rectal prolapse. Because the abnormality is similar to that observed in spinal injury it might simply reflect a reversible traction injury to the autonomic nerve supply to the gut as a consequence of the loss of rectal support. It is of note that patients with rectal prolapse also have reduced anal canal pressures and evidence of pelvic floor neuropathy before surgery17,18, but that these normalize after rectopexy18,19. In contrast, perineal repair of rectal prolapse using the Delorme procedure is not associated with increased anal canal pressure20,21. These observations have implications for understanding the aetiology of rectal prolapse as pelvic floor and hindgut neuropathy appear to be secondary features of rectal prolapse. As it has been postulated that rectal prolapse is an intussusception of the mid-rectum or pouch of Douglas22, the primary abnormality may be loss of the uterosacral and/or rectosacral support rather than neuropathy. Although rectopexy normalized colonic pressure in the present study, postoperative constipation, as measured by both transit marker studies and clinical features, became worse. There are a number of possible explanations for this. First, rectopexy may leave a redundant sigmoid colon that might kink and produce a mechanical obstruction. Removal of this loop of bowel may explain the apparent success of partial hindgut resection4,5. Second, constipation may be related to the absence of HAPC activity as all control subjects exhibited HAPCs compared with only one-quarter of patients. Furthermore HAPCs were not regained after rectopexy and lack of such contractions is considered to be a key element in constipation11,14. This does not entirely explain, however, why constipation worsened after rectopexy. There was poor correlation between HAPC, transit studies and clinical constipation. For example, nine patients had no preoperative HAPCs, of whom four had normal transit and were not constipated before rectopexy. Of these four patients, three developed postoperative constipation and prolonged transit. It would be interesting to explore whether patients with rectal prolapse regain HAPCs after resection rectopexy. Third, other elements of the surgical procedure, for example rectal lateral ligament division, have been proposed as a cause of constipation after rectopexy6,23. The structure, function and very existence of rectal lateral ligaments have been vigorously debated. Four comparative studies have addressed rectal lateral ligament division in patients undergoing rectopexy6–9. Three studies found that division of the lateral ligaments increased the risk of constipation after rectopexy6,8,9, whereas the fourth failed to demonstrate any differences in constipation or colonic transit whether or not the lateral ligaments were divided7. The present study was underpowered to address this issue. However, the effect of lateral ligament division on colonic pressure has not been reported previously. It is conceivable that the rectal lateral ligaments and the nerves that they may contain are already stretched and damaged by the process of rectal prolapse before any operation takes place. This argument is consistent with the observed abnormal preoperative colonic function and absence of postoperative manometric differences between patients whose ligaments were preserved and those whose ligaments were divided. Rectal prolapse is associated with constipation, increased hindgut pressure, slow colonic transit and reduced HAPC activity. Rectopexy reduces hindgut pressure towards control values but fails to restore HAPCs. This suggests that the observed hindgut pressure abnormality is a secondary rather than primary abnormality. These data make a contribution to understanding the pathophysiology and aetiology of rectal prolapse. Acknowledgements The authors are grateful to Dr W. Angerson for assistance with statistical analysis, Mr C. Roger for contributing to collection of control data and Dr F. W. Poon for assessment of colonic transit. References 1 Kuijpers HC . Treatment of complete rectal prolapse: to narrow, to wrap, to suspend, to fix, to encircle, to plicate or to resect? World J Surg 1992 ; 16 : 826 – 830 . Google Scholar OpenURL Placeholder Text WorldCat 2 Mann CV , Hoffman C. Complete rectal prolapse: the anatomical and functional results of treatment by an extended abdominal rectopexy . Br J Surg 1988 ; 75 : 34 – 37 . Google Scholar OpenURL Placeholder Text WorldCat 3 Brown AJ , Anderson JH, McKee RF, Finlay IG. Strategy for selection of type of operation for rectal prolapse based on clinical criteria . Dis Colon Rectum 2004 ; 47 : 103 – 107 . Google Scholar OpenURL Placeholder Text WorldCat 4 McKee RF , Lauder JC, Poon FW, Aitchison MA, Finlay IG. A prospective randomized study of abdominal rectopexy with and without sigmoidectomy in rectal prolapse . Surg Gynecol Obstet 1992 ; 174 : 145 – 148 . Google Scholar OpenURL Placeholder Text WorldCat 5 Luukkonen P , Mikkonen, Järvinen H. Abdominal rectopexy with sigmoidectomy vs. rectopexy alone for rectal prolapse: a prospective, randomized study . Int J Colorectal Dis 1992 ; 7 : 219 – 222 . Google Scholar OpenURL Placeholder Text WorldCat 6 Speakman CTM , Madden MV, Nicholls RJ, Kamm MA. Lateral ligament division during rectopexy causes constipation but prevents recurrence: results of a prospective randomized study . Br J Surg 1991 ; 78 : 1431 – 1433 . Google Scholar OpenURL Placeholder Text WorldCat 7 Mollen RMHG , Kuijpers JHC, van Hoek F. Effects of rectal mobilization and lateral ligaments division on colonic and anorectal function . Dis Colon Rectum 2000 ; 43 : 1283 – 1287 . Google Scholar OpenURL Placeholder Text WorldCat 8 Scaglia M , Fasth S, Hallgren T, Nordgren S, Öresland T, Hultén L. Abdominal rectopexy for rectal prolapse. Influence of surgical technique on functional outcome . Dis Colon Rectum 1994 ; 37 : 805 – 813 . Google Scholar OpenURL Placeholder Text WorldCat 9 Selvaggi F , Scotto di Carlo E, Silvestri A, Festa L, Piegari V. Surgical treatment of rectal prolapse: a randomized study . Br J Surg 1993 ; 80 ( Suppl ): S89 (Abstract). Google Scholar OpenURL Placeholder Text WorldCat 10 Brown AJ , Horgan AF, Anderson JH, McKee RF, Finlay IG. Colonic motility is abnormal before surgery for rectal prolapse . Br J Surg 1999 ; 86 : 263 – 266 . Google Scholar OpenURL Placeholder Text WorldCat 11 Siproudhis L , Ropert A, Gosselin A, Bretagne J-F, Heresbach D, Raoul J-L et al. Constipation after rectopexy for rectal prolapse. Where is the obstruction? Dig Dis Sci 1993 ; 38 : 1801 – 1808 . Google Scholar OpenURL Placeholder Text WorldCat 12 Frykman HM , Goldberg SM. The surgical treatment of rectal procidentia . Surg Gynecol Obstet 1969 ; 129 : 1225 – 1230 . Google Scholar OpenURL Placeholder Text WorldCat 13 Narducci F , Bassotti G, Gaburri M, Morelli A. Twenty four hour manometric recording of colonic motor activity in healthy man . Gut 1987 ; 28 : 17 – 25 . Google Scholar OpenURL Placeholder Text WorldCat 14 Bassotti G , Gaburri M, Imbimbo BP, Rossi L, Farroni F, Pelli MA et al. Colonic mass movements in idiopathic chronic constipation . Gut 1988 ; 29 : 1173 – 1179 . Google Scholar OpenURL Placeholder Text WorldCat 15 Allen-Mersh TG , Turner MJ, Mann CV. Effect of abdominal Ivalon rectopexy on bowel habit and rectal wall . Dis Colon Rectum 1990 ; 33 : 550 – 553 . Google Scholar OpenURL Placeholder Text WorldCat 16 Novell JR , Osborne MJ, Winslet MC, Lewis AAM. Prospective randomized trial of Ivalon sponge versus sutured rectopexy for full-thickness prolapse . Br J Surg 1994 ; 81 : 904 – 906 . Google Scholar OpenURL Placeholder Text WorldCat 17 Parks AG , Swash M, Urich H. Sphincter denervation in anorectal incontinence and rectal prolapse . Gut 1977 ; 18 : 656 – 665 . Google Scholar OpenURL Placeholder Text WorldCat 18 Farouk R , Duthie GS, Bartolo DC, MacGregor AB. Restoration of continence following rectopexy for rectal prolapse and recovery of the internal anal sphincter electromyogram . Br J Surg 1992 ; 79 : 439 – 440 . Google Scholar OpenURL Placeholder Text WorldCat 19 Eu KW , Seow-Choen F. Functional problems in adult rectal prolapse and controversies in surgical treatment . Br J Surg 1997 ; 84 : 904 – 911 . Google Scholar OpenURL Placeholder Text WorldCat 20 Plusa SM , Charig JA, Balaji V, Watts A, Thompson MR. Physiological changes after Delorme's procedure for full-thickness rectal prolapse . Br J Surg 1995 ; 82 : 1475 – 1478 . Google Scholar OpenURL Placeholder Text WorldCat 21 Penninckx F , D'Hoore A, Sohier S, Kerremans R. Abdominal resection rectopexy versus Delorme's procedure for rectal prolapse: a predictable outcome . Int J Colorectal Dis 1997 ; 12 : 49 – 50 . Google Scholar OpenURL Placeholder Text WorldCat 22 Choi JS , Hwang YH, Salum MR, Weiss EG, Pikarsky AJ, Nogueras JJ et al. Outcome and management of patients with large rectoanal intussusception . Am J Gastroenterol 2001 ; 96 : 740 – 744 . Google Scholar OpenURL Placeholder Text WorldCat 23 Douard R , Frileux P, Brunel M, Attal E, Tiret E, Parc R. Functional results after the Orr–Loygue transabdominal rectopexy for complete rectal prolapse . Dis Colon Rectum 2003 ; 46 : 1089 – 1096 . Google Scholar OpenURL Placeholder Text WorldCat Author notes Presented to a meeting of the Association of Coloproctology of Great Britain and Ireland, Edinburgh, July 2003, and published in abstract form as Colorectal Dis 2003; 5(Suppl 1): 14 Copyright © 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Copyright © 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd.
TI - Prospective study of the effect of rectopexy on colonic motility in patients with rectal prolapse
JF - British Journal of Surgery
DO - 10.1002/bjs.4990
DA - 2005-10-19
UR - https://www.deepdyve.com/lp/oxford-university-press/prospective-study-of-the-effect-of-rectopexy-on-colonic-motility-in-uVy0Kwk3Eq
SP - 1417
EP - 1422
VL - 92
IS - 11
DP - DeepDyve
ER -