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Lap Ventral Mesh Rectopexy: the treatment of choice for Solitary rectal Ulcer

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07/05/2012

Laparoscopic ventral mesh rectopexy (LVMR): the treatment of choice for the resolution of solitary rectal ulcer syndrome (SRUS).

 

AH Badrek-Amoudi, T Roe, K Mabey*, H Carter§, A Mills* AR Dixon

 

Departments of Colorectal Surgery and Radiology§ Frenchay Hospital, Bristol & Anorectal Physiology, Bristol Royal Infirmary*, UK

 

Correspondence to Mr AR Dixon

 Anthony.Dixon@nbt.nhs.uk 

 

 

 

 

Key words

Solitary rectal ulcer syndrome, rectal prolapse, obstructed defecation, quality of life, laparoscopic ventral mesh rectopexy

 

 

Abstract 

Aim

The treatment of solitary rectal ulcer syndrome (SRUS) is notoriously difficult. Laparoscopic ventral mesh rectopexy (LVMR) is a non-resectional technique for patients with full thickness external rectal prolapse and obstructed defecation syndrome (ODS), features associated in the pathogenesis of SRUS. Our aim was to assess the short and long-term efficacy of LVMR in the treatment of SRUS and reflect on its demographics and disease characteristics.

Methods 

37 consecutive patients with SRUS who underwent LVMR over a 14-yr period (January 1997 to March 2011) were identified from a prospectively maintained electronic database.  Variables included demographics, peri-operative details and post-operative course.  Primary outcome was ulcer healing and secondary outcomes were patient symptom improvement, Quality of Life (QOL) and satisfaction at their latest outpatient follow-up.

Results

37 patients, 33 females (89%), median age 46-yrs (range 23-80), median BMI 26 kg/m2 (21-40) underwent LVMR as treatment of SRUS.  The median follow-up was 28 months (CI  25-48, range 1-168 months).   All had failed biofeedback therapy and 5 (13%) had relapsed 6-62 months post Stapled Trans Anal Rectal Resection (STARR); two patients had shown no response to STARR.  All 37 patients had high-grade rectal intussusception in association with ODS.  The morbidity was 10 (27%). Ulcer healing at 3 months was complete in all patients.  Improvements in ODS, Wexner faecal incontinence (FI) and QOL Birmingham Bowel and Urinary Symptoms Questionnaire-22 (BBUSQ-22) scores were 68%, 100% and 45%, respectively (p < 0.0001). There were four symptomatic ODS recurrences (11%); posterior rectal wall prolapse successfully treated by STARR (3) and a patient remaining symptom free 18-months following a 3-month period of having a temporary loop ileostomy.  There was one long-term SRU recurrence (3%) in association with a continued intermittent external prolapse.

Conclusion

LVMR provides superior surgical outcomes and sustained improvements in QOL and patient satisfaction in patients with SRUS. Morbidity, recurrence and safety profiles are consistent with LVMR published figures

What is new in this paper?

This is the largest series showing the efficacy of LVMR in treating patients with SRUS and its effect upon patient satisfaction and QOL.

 

 

 

 

 

Introduction

Solitary rectal ulcer syndrome (SRUS) is a benign condition found in association with obstructive defecation (ODS), peaking in young adults with a female predominance1-5.  Symptoms include rectal bleeding, mucus discharge, pain and evacuatory difficulties to include digitation.  Invariably, what is a miss-nominally termed as an ulcer, is in-fact a highly pleomorphic rectal lesion. The diagnosis is made on the basis of symptoms, endoscopic appearance and histology 1, 3, 6, 7.

 

Since Madigan and Morson’s original description1 there has been appreciation of its demographics and clinical manifestations8,9. Its etiology and pathogenesis on the other hand continues to cause debate9, 10, 11-13 with inevitable impact on its treatment and standardization of care.  Occult rectal prolapse is a feature in 28 - 100%1,3,6,11,14-18.  Surgical strategies aim to treat SRUS by treating this prolapse with mixed results.  Dietary and behavioral therapies have been equally disappointing.

 

Nicholls19 first described the potential efficacy of using a ventral surgical approach, a remarkable 86% improvement following the addition of a ventral mesh to the standard posterior open mesh rectopexy.  Laparoscopic ventral mesh rectopexy (LVMR), for full thickness external rectal prolapse, has been shown to be safe, feasible and reproducible in treating internal rectal prolapse and complex symptomatic rectocoele5,20-22.  This autonomic nerve sparing approach offers a functional improvement in ODS and faecal incontinence, without initiating new onset constipation3,22.  In addition to the advantages of minimally invasive surgery20,23, concomitant pelvic compartment abnormalities can also be treated5,20.  Furthermore, this approach reduces the risks of dyspareunia and faecal incontinence associated with perineal and trans-vaginal procedures5,20.  Recent data on 14 SRUS patients treated by the Oxford Group showed symptom resolution in 87%24.

 

In this study, we aimed to provide further evidence on the short and long-term safety and efficacy of LVMR in a larger cohort of 37 patients affected by SRUS, whilst reflecting on the demographics and disease characteristics.

 

 

 

 

 

 

 

 

 

 

Patients and Methods

37 consecutive patients with SRUS treated by LVMR were identified from a prospective, electronic, password-protected, pelvic floor database over a 14-yr period (January 1997 to March 2011). All operations were performed or directly supervised by a single surgeon.

 

Preoperatively, all patients underwent a complete history and physical examination, defecatory rigid proctosigmoidoscopy20, histological assessment, anorectal physiology studies (including manometry and rectal compliance) and defecating proctogram.  Colonoscopy and colonic transit studies were performed selectively when indicated. 

 

Data collected included patient demographics, pre-operative details, ODS (obstructive defecation) score25 and Wexner faecal incontinence26 scores, operative information and post-operative course to last follow-up.  A validated Quality of Life score (Birmingham Bowel and Urinary Symptoms Questionnaire-22, BBUSQ-22)27 was obtained pre-operatively and at regular post-operative intervals (3, 12, 18, 24 months).  Primary outcome measured was endoscopic evidence of ulcer healing.  Secondary outcomes were effect on symptoms, QOL and patient satisfaction as assessed at the time of the latest follow-up.

 

Of the 37 patients, 34 underwent LVMR in the manner described15. Modifications were made in three: laparoscopic resection of the hindgut and primary anastomosis (segmental slow transit constipation) above the LVMR [2] and LVMR in combination with a posterior STARR [1] (excise a significant posterior prolaspe component.

 

Data Analysis

Data pertaining demographics variables and disease characteristics together with changes in pre and postoperative ODS, Wexner and QOL scores were analysed using the paired t-test (2 tailed), Prism 5 for Mac OS X software (version 5.0, © 1994- 2010 Graphpad Software).  A p value < 0.05 was considered significant.

 

 

 

 

 

 

 

 

 

 

 

Results 

Patient Demographics

Thirty-seven patients, 33 females (89%) with SRUS treated by LVMR were identified; median age 46-yrs (range 23-80), median BMI 26 kg/m2 (21-40). The median follow-up was 28 months (CI  25-48, range 1-168). QOL data was available on 35 (94%) patients at 3 months, 26 (70%) at 1 year, 20 (54%) at 18 months and 19 (51%) patients at last follow-up.  ODS and Wexner faecal incontinence scores were available in 21 and 31 patients respectively.

 

Multiparty was noted in 27 (81%), mid cavity Kielands forceps extraction in 13 (39%) and a hysterectomy in 15 (45%).  One male had a major affective disorder; three women adolescent anorexia nervosa including an additional obsessive-compulsive disorder (OCD) in one individual to strain/laxative abuse.  One had a chronic cauda-acquina syndrome.  Preoperative biofeedback and laxative therapy had been employed in all 37 patients.   Four (11%) had undergone a chronic pain management programme and four had used rectal irrigation without benefit. Thirteen (35%) had undergone previous pelvic floor surgery; Milligan Morgan haemorrhoidectomy (3), SRUS relapse 6-60 months post STARR in 5 (13%), failure of response to STARR (2) and failures post sutured trans anal mucosectomy and plication [STAMP procedure] and a trial of sacral nerve stimulation. 

 

Their symptom-profile is shown in Table 1. Eight (22%) patients had an intermittent full thickness rectal prolapse on straining and 29 high-grade rectal intussusception (76%); Oxford grade 3 (50%), grade 4 (13%), grade 5 (13%)  Dynamic proctography demonstrated major pelvic floor disruption in the majority: 37 (100%) had rectoceles >3cm, 35 (95%) >3cm of perineal descent and 30 (81%) an enterocele.  11 anorectal physiology studies (30%) were normal, two showed high resting pressures (5%), two demonstrated rectal hyposensitivity; the remaining 60% (22 patients) had paradoxical contraction of their pelvic floors with additional rectal hypo-sensitivity (27%). ODS, Wexner FI and QOL scores are summarised (Tables 2 – 4) and illustrated (Figures 1-3).

 

The mean operative time was 102 minutes (range 36-250). Operative difficulties occurred in 11 (30%); difficult pelvic access in 10 (27%) and one intra-operative bleed (3%). There were no conversions. The mean time to diet was 19 hours and the mean of length of stay was 2 days (range 1-9 days, CI   1.5-3).  There were ten complications (27%): urinary retention (5), angina, port-site infection, small bowel obstruction at 6/12 and dyspareunia/mesh erosion at four years (repaired trans vaginally).

 

 

 

Surgical Outcomes

Endoscopic evidence of ulcer healing occurred in all patients within three months of surgery.  Thirty-two patients were asked about impact of surgery on their lifestyle; 30 [94%]) responded with moderate to complete improvement, one no change [3%) and one faecal urgency [3%]. Improvement in median ODS and Wexner FI scores were significant with 68% and 100% reductions, respectively (Tables 3 - 4). The overall reduction in QOL median score (improvement) was 45% at last follow-up  (Table 5).  Four patients (11%) developed recurrent ODS symptoms secondary to posterior rectal wall prolapse (n = 3) at a median interval of 22 months.  Revisional surgery in the form of posterior STARR was successful in each case. The 4th patient (previously relapsed her SRUS 60 months post STARR) remains symptom free 18-months following a temporary loop ileostomy for 3 months.  The latter had been performed at 15 months.  There has been only one SRU recurrence (3%), found in association with a recurrent intermittent external prolapse in a patient with OCD and anorexia nervosa.  The latter was treated by re-attachment of the mesh to the sacral promontory.  The patient remains symptomatic after three months and is now awaiting a proctectomy.

 

 

 

 

Discussion

STUS is uncommon affecting 1/100,000 of the population8 with up to a quarter of cases misdiagnosed at presentation28, often preceded by long symptomatic periods 3,8,29 with considerable impact on QOL30.  ODS and anorectal symptoms cause the greatest impact31.  This study, the largest series on the subject in recent years, reaffirms current understanding of its demographics and close association with ODS.

 

The cause is not known. The inherent existence of a rectal prolapse be it internal or external is a core feature in its pathogenesis2,11,15,28,29.  Whether repetitive shearing forces of the prolapse during prolonged straining are sufficient alone to cause rectal mucosal ulceration or whether synchronous puborectalis dyssynergy is needed remains unanswered9,11.  However, it is difficult to see how true anismus can commonly co-exist with prolapse. One is an uncommon disorder of skeletal musculature, with a urological external urethral sphincter correlate (Fowler’s syndrome), the other has a completely different pathophysiology. It seems more likely that the upward force opposing the downward force of the prolapse is generated by the internal anal sphincter (IAS)32.  Endo-anal ultrasound reveals characteristic thickening of IAS in SRUS. This thickening is also seen in ODS from internal rectal prolapse without SRUS.  Patients with SRUS are known to have higher maximum resting pressures than those with prolapse without SRUS.  It is possible that the response of the IAS to the prolapse leads to the development of the SRUS.  If prolapse and anismus co-existed in SRUS one would expect to see poor results in nerve-sparing ventral rectopexy, which treats only the prolapse, and a continued requirement for biofeedback or Botulinum toxin A postoperatively.

 

Although the suggestion that SRUS results from direct trauma through self-inflicted injury33 has we hope been successfully disbanded, not least because most lesions are located beyond the reach of a finger but by its absence in the majority of patients with ODS who do digitate9,34.  It therefore stands to reason that a strategy to eradicate the pressure effects exerted by the intussusceptum at the zone of injury in the rectum is the one that will ensure the most success11,14,35.  In essence, the management of SRUS and ODS is one and the same.  In this study 78% of patients exhibited proctographic evidence of advanced grades of rectal intussusception, where as 22% presented with spontaneous reducible intermittent external prolapse. Anorectal physiology was indeterminate as a diagnostic tool and did not influence the course of management or outcome.

 

The traditional approach over the last two decades has been to avoid surgery and ignore the anatomical abnormalities and treat the condition along functional lines using high fiber diets and biofeedback; success rates range 19%-70%35-37.  Success for biofeedback alone is lower 30-54%38,39.  These figures however, are probably a reflection of small case series and short follow-up as only half of those who initially respond maintain any long-term benefit, the overall success rate falling below 30%40.   Against the backdrop of the surgically biased nature of this study, It would appear that these approaches are less useful in SRUS associated with advanced grade of rectal intussusception or reducible intermittent external prolapse; anatomical correction will not treat any  puborectalis dysynergy other than a pseudo contraction developed in response to the prolapse.

 

Numerous surgical options (table 5) have been used to treat SRUS.  Most reports are retrospective with no uniform primary end points and all examine only small numbers of patients with limited follow-up.  Out of all the failed surgeries we employed for SRUS prior to LVMR, STARR was the prevalent intervention in 7 (19%) patients with only short-term benefit seen in five (one relapsed at five years following a first pregnancy and vaginal delivery). This is contrary to Bocasanta’s report, which claimed 80% symptomatic improvement and complete ulcer healing in 100%18.  Our experience calls for a more circumspect approach to using STARR as the primary treatment. These results are not surprising since STARR merely excises the internal prolapse and does not correct the loss of fascial support to the anterior rectum and pelvic floor.

 

LVMR is an emerging technique that has been shown to be beneficial in full thickness rectal prolapse, faecal incontinence and ODS. The evidence for its role in SRUS is yet to be substantiated.  Preliminary data from Oxford  showed LVMR to be successful in 86% of 14 patients with SRUS. Like our series they included 3 patients who underwent an additional STARR for posterior prolapse24. The bulk of evidence, nonetheless, lies within existing studies on the on the role of LVMR in the treatment of ODS and faecal incontinence.  Individual studies by specialist centers in Leuven5,43, Bristol20 and Oxford21, 22 have all demonstrated similar rates of success (75-88%) and low rates of recurrence (2-4%).   On the other hand, a systematic review of 12 studies44 to assess the efficacy of VMR in 726 patients with ODS, showed only a modest 24% decrease in constipation rate.  The review however, underscored the value of LVMR by including seven studies, which employed the Orr-Loygue procedure and furthermore, included laparoscopic as well as open procedures.

 

This study supports LVMR in the treatment of SRUS demonstrating complete ulcer healing at 3 months, a 100% improvement in FI scores, 68% in ODS scores; culminating in a 45% improvement in QOL scores. The statistically significant margins of improvement in QOL questionnaires were uniformly greatest within the first 18 months of surgery.  Assessment of our patient’s perception of the success of treatment showed complete satisfaction in 92% of patient reported questionnaires (28 patients).  The three modified surgical approaches, laparoscopic hindgut resection with LVMR (n=2) and LVMR with posterior STARR (n=1) do not appear to confer an advantage nor cause additional morbidity, and are in keeping with the overall results.  These findings are in-line with short-term QOL figures examining the impact of laparoscopic-sutured posterior rectopexy in SRUS31, as well as figures from the Oxford24 examining LVMR.

 

There were four symptomatic ODS recurrences (11%); posterior rectal wall prolapse treated by STARR (n=3) and a further patient who remains symptom free 18-months following a 3-month period of having a loop ileostomy formed and then closed.  There was only one long-term SRU recurrence (3%), which developed in association with OCD/anorexia nervosa and recurrent intermittent external prolapse. This again, parallels the Oxford experience24. These findings suggest a need for a closer examination of the morphology of rectal intussusception and its posterior component.  In our cases, STARR in addition to LVMR was sufficient in treating their symptoms. An alternative strategy would be to consider a modified LVMR/Orr-Loygue approach45.

 

 

 

 

 

 

 

References

1.    Madigan MR, Morson BC. Solitary ulcer of the rectum. Gut, 1969; 10: 871-881.

2.    Rutter KRP. Solitary Rectal Ulcer Syndrome. Proc.R.Soc.Med 1975; 68: 22-27.

3.    Tjandra JJ, Fazio VW, Church JM, Lavery IC, Oakley JR, Milsom JW. Clinical Conundrum of Solitary Rectal Ulcer. Dis. Col. Rect. 1992; 35: 227-234.

4.    Sitzler PJ, Kamm MA, Nicholls RJ, McKee RF. Long-term clinical outcome of surgery for solitary rectal ulcer syndrome. Brit. J Surgery 1998; 85: 1246–1250.

5.    Hoore AD, Penninckx F. Laparoscopic ventral recto(colpo)pexy for rectal prolapse: surgical technique and outcome for 109 patients. Surg.Endosc. 2006; 20: 1919–1923.

6.    Stuart M. Proctitis Cystica Profunda, Incidence, Etiology and Treatment. Dis. Col. & Rect. 1984; 27: 153-156.

7.     Chiang JM, Changchien CR, Chen JR. Solitary rectal ulcer syndrome An endoscopic and histological presentation and literature review. Int.J. Colorectal Dis 2006; 21: 348–356.

8.    Martin CJ, Parks TG, Biggart JD. Solitary rectal ulcer syndrome in Northern Ireland, 1971–1980. Br.J.Surg 1981; 68: 744–7.

9.    Vaizey CJ, Van Den Bogaerde JB, Emmanuel AV, Talbot IC, Nicholls RJ, Kamm MA.  Solitary rectal ulcer syndrome. Br.J.Surg, 1998; 85: 1617–1623.

10.Keighley MRB, Shouler P. Clinical and manometric features of the solitary rectal ulcer syndrome. Dis.Colon Rect. 1984; 27: 507-512.

11.Williams NR, Williams NS, Holmfeild JHM, Morrison JFB. Pressure and prolapse the cause of solitary rectal ulceration. Gut 1987; 28: 122 l1233.

12.Sun WM, Read NW, Carmel T, Shourthouse AJ. A common pathophysiology for full thickness mucosal prolapse and solitary rectal ulcer. Br.J.Surg.1989; 76: 290-296.

13.Morio O, Meurette G, Desfourneaux V, D’Halluin PN, Bretagne JF, Siproudhis L. Physiology in Solitary Ulcer Syndrome: A Case-Matched Series. Dis.Colon Rect. 2005; 48: 1917–1922.

14.Schweiger M, Williams JA. Solitary-Ulcer Syndrome of the Rectum, Its Association With Occult Rectal Prolapse. Lancet 1977; 309: 170 -171.

15.Halligan S, Nicholls RJ, Bartram CI. Evacuation Proctography in Patients with Solitary Rectal Ulcer Syndrome: Anatomic Abnormalities and Frequency of Impaired Emptying and Prolapse. Am J Roentgology 1995; 164:91-95.

16.Marchal F, Bresler L, Brunaud L, Adler SC, Sebbag H, Tortuyaux J, Boissel P. Solitary rectal ulcer syndrome: a series of 13 patients operated with a mean follow-up of 4.5 years. Int.J Colorectal Dis. 2001, 16, N 4: 228-233.

17.Torres C, Khaikin M, Bracho J, Luo CH, Weiss EG, Sands DR, Cera S, Nogueras JJ, Wexner SD. Solitary rectal ulcer syndrome: clinical findings, surgical treatment, and outcomes. Int J Colorectal Dis 2007; 22:1389–1393.

18.Boccasanta P, Venturi M, Calabro G, Maciocco M, Roviaro GC, Stapled Transanal Rectal Resection in Solitary Rectal Ulcer Associated with Prolapse of the Rectum: A Prospective Study. Dis Col. Rect. 2008; 51: 348-354.

19.Nicholls RJ, Simson JNL. Anteroposterior rectopexy in the treatment of solitary rectal ulcer syndrome without overt rectal prolapse. Br.J.Surg 1986; 73:  222–224.

20.Slawik S, Soulsby R, Carter H, Payne H, Dixon AR. Laparoscopic ventral rectopexy, posterior colporrhaphy and vaginal sacrocolpopexy for the treatment of recto-genital prolapse and mechanical outlet obstruction. Colorectal Disease 2007; 10: 138–143.

21.Collinson R, Wijffels N, Cunningham C, Lindsey I. Laparoscopic ventral rectopexy for internal rectal prolapse: short-term functional results. Colorectal Disease 2010; 12: 97–104.

22.Boons P, Collinson R, Cunningham C, Lindsey I.  Laparoscopic ventral rectopexy for external rectal prolapse improves constipation and avoids de novo constipation. Colorectal Dis. 2009; 12: 526–532.

23.Sajid MS, Siddiqui MRS, Baig MK. Open vs laparoscopic repair of full-thickness rectal prolapse: a re-meta-analysis. Colorectal Dis. 2009; 12: 515–525.

24.Hompes R, Evans C, Jones O, Cunningham C, Lindsey I. Managing Solitary rectal ulcer syndrome: Ignore the ulcer, treat the underlying advanced rectal prolapse. Colorectal Dis, 2010; conference abstract, vol./is. 12/(29), 1462-8910

25.Renzi A, Izzo D, Di Sarno G, Izzo G, Di Martino N. Stapled transanal rectal resection to treat obstructed defecation caused by rectal intussusception and rectocele. Int.J Colorectal Dis. 2006; 21:661–7.

26.Agachan F, Chen T, Pfeifer J, Petachia R, Wexner S. A constipation scoring system to simplify evaluation and management of constipated patients. Dis.Colon Rectum 1996; 39:681–5.

27.Hiller L, Bradshaw HD, Radley SC, Radley S. Criterion validity of the BBUSQ-22: a questionnaire assessing bowel and urinary tract symptoms in women. Int Urogynecol J Pelvic Floor Dysfunct. 2007; 18:1133-7

28.Kuijpers HC, HStC Hoedmakers RH. Diagnosis of functional disorders of defecation causing the solitary rectal ulcer syndrome. Dis Colon Rectum 1986; 29:126–9.

29.Ford MJ, Anderson JR, Gilmour HM, Holt S, Sircus W, Heading RC. Clinical spectrum of ‘solitary ulcer’ of the rectum. Gastroenterology 1983; 84:1533–40.

30.Meurette G, Siproudhis L, Regenet N, Frampa E, Proux M, Lehur PA. Poor symptomatic relief and quality of life in patients treated for “solitary rectal ulcer syndrome without external rectal prolapse”. Int.J.Colorectal Dis. 2008; 23:521–526.

31.Tweedie Dj, Varma JS. Long-term outcome of laparoscopic mesh rectopexy for solitary rectal ulcer syndrome. Colorectal Dis. 2005; 7: 151–155.

32.Halligan S, Sultan A, Rottenberg G, Bartram CI. Endoscopy of the anal sphincters in solitary rectal ulcer syndrome. Int J Colorectal Dis. 1995; 10: 79-82

33.Thomson H, Hill D. Solitary rectal ulcer: always a self-induced condition? Br.J. Surg 1980; 67: 784–5.

34.Goede AC, D Glancy D, Carter H, Mills A, Mabey K, Dixon AR. Medium-term results of stapled transanal rectal resection (STARR) for obstructed defecation and symptomatic rectal-anal intussusception. Colorectal Disease 2011; 13:1052–1057.

35.Ortega AE, Klipfel N, Kelso R, Petrone P, Román I,  Díaz A,  Ávalos B, Kaufman HS. Changing Concept in the Pathogenesis, Evaluation and management of Solitary Rectal Ulcer Syndrome. The American Surgeon 2008; 74: 10, 967-972.

36.Brandt-Grädel V, Huibregtse K, Tytgat GNJ. Treatment of solitary rectal ulcer syndrome with high-fiber diet and abstention of straining at defecation. Digestive Dis.& Sci. 1984; 29: 1005-1008.

37.Britto E, Borges AM, Swaroop VS, Jagannath P, DeSouzs LJ. Solitary rectal ulcer syndrome: twenty cases seen at oncology centre. Dis.Colon Rectum 1987; 30:381-385.

38.Vaizey CJ, Roy AJ, Kamm MA. Prospective evaluation of the treatment of solitary rectal ulcer syndrome with biofeedback. Gut 1997; 41:817-20.

39.Rao SSC, Ozturk R, De Ocampo S, Stessman M. Pathophysiology and Role of Biofeedback Therapy in Solitary Rectal Ulcer Syndrome. Am.J. Gastroenterology 2006; 101: 613–618

40.Malouf Aj, Vaizey CJ, Kamm MA. Results of behavioral treatment (biofeedback) for solitary rectal ulcer syndrome. Dis Col & Rectum. 2001; 44: 72-76.

41.Binnie NR, Papachrysostomou M, Clare N, Smith AN. Solitary Rectal Ulcer: The Place of Biofeedback in the Treatment of the Syndrome. World.J.Surg. 1992; 16: 836-840.

42.Kargar S, Salmanroughani H, Binesh F, Taghipoor S, Kargar S. Laparoscopic Rectopexy in Solitary Rectal Ulcer.  Acta Medica Iranica, 2011; 49: 810-813.

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44.Samaranayake CB, Luo C, Plank AW, Merrie AEH, Plank LD, Bissett IP. Systematic review on ventral rectopexy for rectal prolapse and intussusception. Colorectal Dis 2009; 12: 504–514.

45.Loygue J, Nordlinger B, Cunci O, Malafosse M, Huguet C, Parc R. Rectopexy to the promontory for the treatment of rectal prolapse. Report of 257 cases. Dis Colon Rectum 1984; 27: 356–9.

 

 

 

 

 

 

 

 

 

Symptoms

N

%

Incomplete evacuation

37

100

Anorectal pain

35

95

Sensation of obstruction

34

92

Rectal bleeding

31

84

Fecal urgency

29

78

Sensation of rectal prolapse

27

73

Digitation

24

65

 

 

Table 1.    Symptoms profiles of the 37 patients with SRUS.

 

 

 

 

 

 

 

 

ODS score

Preoperative

(n=21)

ODS score

Postoperative

(n=21)

Low (0-5)

0

3

Moderate (6-10)

0

16

High >11

21

2

Median

25 ± 3 (CI 22-25)

8 ± 3 (CI 7-10)

 

Statistical test: P<0.0001 t-test

Table 2.  The effect of LVMR on ODS median score

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Wexner score

Preoperative

(n=37)

Wexner score

Postoperative

(n=37)

Low (0)

11

35

Moderate (1-5)

13

0

High >5

13

1

Median

3.5 ± 3 (CI 3-6)

0 ± 1 (CI 0-1)

 

 

 

 

 

 

 

 

Statistical test: P<0.0001, t-test

  

Table 3.  The effect of LVMR on Wexner FI median scores.

 

 

 

 

 

 

 

 

 

 

Preop

3 M

12M

18M

L F/U*

QoL

56

9±(CI 55-60)

34

6±(CI 34-38)

32

5±(CI 31-34)

29

5±(CI 29-33)

30

(CI 28-31)

                                      

Statistical test;t-test: Preop vs 3 months P<0.0001, 3 months vs 12 months P<0.006, 12 months vs 18 months P<0.02, 18 months vs last Follow-Up P<0.29 (not statistically significant)

                                 

 

Table 4.  The effect of LVMR on QOL median score

 

 

 

Reference

 

Year

Country

Patient N (Surgical)

Length

of Study

- Years

Length of Follow

-up / Months

Type of Surgery

Success

Schweiger [14]

1977

UK

12; (10)

5

13

Abd.Rectopexy

100

Martin et al [8]

1981

Ireland

51; (6)

10

n/r

Abd.Rectopexy

50

Stuart [6]

1984

Australia

28; (15)

11

n/r

Abd.Rectopexy

73

Keighley  &

Shouler [10]

1984

UK

33; (14)

7

12m

Abd.Rectopexy

50

Tjandra et al [3]

1992

USA

80; (20)

10

25

Abd.Rectopexy  (10)

70

 

 

 

 

 

 

Resection (10)

50

Binnie et al [41]

1992

UK

31

10

n/r

Transanal excision (12)

42

 

 

 

 

 

 

Abd.Rectopexy (19)

74

Sitzler et al [4]

1998

UK

66

10

21-177

Abd.Rectopexy  (49)

59

 

 

 

 

 

19-107

Delorme's (9)

55

Marchal et al [16]

2001

France

13

10

15-177

Abd.Rectopexy  (3)

66

 

 

 

 

 

 

Delorme's (8)

62

 

 

 

 

 

 

Resection (1)

0

 

 

 

 

 

 

Stoma (1)

Improved

Tweedie and

Varma [31]

2005

UK

11

3

71-106

Lap. Mesh Rectopexy

90

Ortega et al [35]

2008

USA

30; (3)

14

12-120

Resection Rectopexy

50

 

 

 

 

 

 

STARR

Improved

Boccasanta et al [18]

2008

Itlay

14; (10)

n / r

24-34

STARR

80%

Hompes et al [24]

2010

UK

23; (15)

19

n/r

Lap. Ventral Mesh Rectopexy (14)

87%

 

 

 

 

 

 

STARR (1)

Failed

Kargar et al [42]

2011

Iran

62

14

31

Lap. Mesh Rectopexy

64-85

 

 

Table 5.      Surgical series on SRUS

 

 

 

Figure 1     Box & whiskers graph showing changes in QOL scores (mean, CI and range) at set follow-ups

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 2    Box & whiskers graph showing changes in ODS scores (mean, CI and range)  pre & post operatively

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 2    Box & whiskers graph showing changes in pre & post operatively

                 Wexner FI scores (mean, CI and range)

 

 



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