Solitary Rectal Ulcer

AJ Shorthouse

Solitary Rectal Ulcer Syndrome (SRUS) is an uncommon condition, affecting females more than males (3:1), with a peak incidence in the third decade. Two forms are recognised: ulcerated and non-ulcerated.

Pathophysiology is poorly understood, but characterized by disordered defaecation due to a spectrum of underlying phenomena; failure of evacuation (50%), rectal intussusception (50-80%), pelvic floor incoordination (50%), rectal hypersensitivity and hypermotility (100%), and overt rectal prolapse (6-39%). Any of these factors, alone or in combination, may precipitate tenesmus and the need for repetetive straining. Evacuation failure, however, is inconsistent and may occur with or without ulceration, and also in non-SRUS patients as anismus. Prolapse is found to a variable degree, but may be absent in some cases. Inappropriate contraction of puborectalis and/or the external sphincter (EAS) is found in a proportion of cases, demonstrated by EMG, endoscopic ultrasound (EUS) and proctography. Rectal hypersensitivity and hypermotility occur in SRUS, anterior mucosal prolapse (AMP) and full thickness rectal prolapse (FTRP), suggesting a common aetiological pathway. FTRP may be the end result of SRUS, at least in some cases.
Ulceration may be due to repetitive trauma from high intra-rectal pressures and shearing forces applied to the leading edge of the intussusception during straining. Ischaemia may result from inappropriate (EAS) contraction, although the histological changes of SRUS are inconsistent with ischaemia. Digitation is a probably a consequence rather than a cause of ulceration from direct trauma.

Clinical presentation is well defined, with rectal bleeding, mucus, tenesmus, disordered defaecation (excessive prolonged straining and multiple visits to the lavatory), a sense of incomplete evacuation, rectal pain (20%), digitation (50-70%), faecal incontinence (50%), and IBS symptoms. Psychological disturbance is common. Weak sphincters, perineal descent and overt rectal prolapse (34%) may be present, best demonstrated by straining down upright on a commode.

Investigation. Sigmoidoproctoscopy typically reveals mucus, mucosal reddening and an anterior, and occasionally circumferential, shallow irregular area of ulceration on the apex of a mid rectal valve, and often seen to intussuscept when insufflation is released. Biopsy differentiates from inflammatory bowel disease, radiation change, infections (e.g. amoebiasis, schistosomiasis), neoplasms, endometriosis, and stercoral ulceration. EUS can be used to differentiate SRUS from tumour in difficult cases: five discrete intact layers with a diffusely thickened muscularis propria are seen in SRUS. Defaecating proctography will demonstrate internal intussusception and inappropriate puborectalis contraction. Anorectal physiology should be performed if surgery is being considered – sphincter weakness (due to pudendal neuropathy from straining) and rectal hypersensitivity/hypermotility are typical. Colonoscopy confirms an otherwise normal colon.

Histopathology shows a thickened lamina propria expanded by collagen deposition from fibroblasts and smooth muscle derived from the muscularis mucosae, which orientate at right angles between the glands. Goblet cell depletion and epithelial hyperplasia are present. Colitis cystica profunda is a variant of SRUS caused by mucus gland entrapment in the submucosa resulting in a polypoid intraluminal mass, which can be mistaken for malignancy.

Treatment is difficult and usually conservative, with bulking agents, glycerine suppositories and advice to avoid straining. The aim is to minimize symptoms, as cure is often impossible.. Time should be allowed for detailed explanation of the condition to the patient, emphasizing the progressive damage caused by straining. Specialist nurse support is helpful, and biofeedback should be used especially if inappropriate puborectalis or EAS activity has been demonstrated on proctography or EUS, and simple conservative measures have failed. Other simple approaches such as sucralfate enemas, argon plasma coagulation or Nd-YAG laser treatment may succeed, but further evidence for their efficacy is required.
Recent results of long-term follow up after biofeedback for SRUS (Malouf et al 2001) have shown that 31% patients were asymptomatic, 30% improved, and 39% failed at 9 months, but at 36 months only 7% were asymptomatic, 39% maintained some improvement, and 54% failed.
Consensus is emerging in favour of surgery for failed conservative treatment, but only when internal intussusception or overt prolapse is clearly evident, in the presence of severe intractable symptoms, and after a failed trial of biofeedback. Rectopexy is the favoured approach. The risks, benefits and success rates must be clearly explained, as surgery may also fail, ultimately leading to a stoma in a proportion of patients.
Rectopexy successfully corrects prolapse and alters rectal configuration, but both factors appear unrelated to functional outcome. The St Marks’ group has shown that prolonged preoperative evacuation on proctography predicts a poor result.
Sitzler et al (1996) reviewed St Marks’ long-term follow up of surgical treatment for SRUS. Most were treated by rectopexy (49/66), of which 22 (43%) failed. Nineteen (86%) of these had further surgery. Four (21%) had low anterior resection and 3 failed. Eleven (58%) had a stoma, and 4 (21%) had other procedures. Ultimately, 14/19 (74%) of rectopexy failures were given a stoma. Delorme’s procedure was performed in 9 patients with success in 5 (56%). Delorme’s procedure should not be attempted for mid rectal SRUS, but should be reserved for low lesions with accessible prolapsing distal mucosa. Low anterior resection and colopouch appears a logical approach, especially in the event of rectopexy failure, but experience suggests that outcomes are generally unsatisfactory. Four of seven patients in the St Mark’s series failed and eventually had a stoma. Antero-posterior rectopexy gave better results than standard posterior rectopexy (66% vs. 47% symptom relief), which was maintained at longer follow up. There was a significant reduction in the median number of visits to the lavatory (8 vs.3) and median time spent there (146 vs.15 minutes). Only two had severe constipation despite total division of lateral ligaments. There was also significant reduction in bleeding, tenesmus, mucus, and incomplete evacuation.
Other procedures such as postanal repair or local ulcer excision have no place in SRUS management
Abdomino-perineal resection is effective in relieving symptoms, and may be the only option in severe refractory cases. However, more data on low anterior resection in carefully selected SRUS patients without prolonged evacuation would be helpful.

REFERENCES
Lubowski DZ. Solitary rectal ulcer syndrome: pathophysiology and treatment. In: Coloproctology and the Pelvic Floor. Ed. MM Henry and M Swash. 2nd ed. 1992 Butterworth-Heinemann Oxford pp 305-15
Nicholls RJ and Banerjee AK. Rectal prolapse and solitary rectal ulcer syndrome. In: Surgery of the Colon and Rectum. Ed: RJ Nicholls and RR Dozois. 1997. Churchill Livingstone. New York. Pp 709-37
Sitzler P, Kamm MA, Nicholls RJ (1996) Surgery for solitary ulcer syndrome. Int J Colorectal Dis.11:136
Malouf AJ, Vaizey CJ, Kamm MA (2001) Results of behavioural treatment (biofeedback) for solitary rectal ulcer syndrome. Dis Colon Rectum. 44:72-6.