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are critical to the safe practice of this technique: a recent study confirmed the low rate of
colonic perforation associated with the regular use of TACI.
33
Anterograde enemas can be performed through a surgical caecostomy or append ectomy (Malone procedure), or through a catheter implanted in the caecum endoscopically.
34
The results seem to be interesting at least on the short term, chronic wound
pain being the most frequent cause of removal of the system. Percutaneous endoscopic
caecostomy should still be considered in the context of clinical trials and with experienced
endoscopists.
35
Sacral nerve stimulation (SNS) has been proposed as a possible mini-invasive
approach for the treatment of chronic constipation.
36
This therapy is used worldwide
for the treatment of fecal incontinence resistant to medical treatment. Preliminary reports
suggested SNS to be efficient in the treatment of chronic constipation, although no clear
phenotype could be defined as the responder to therapy. Recent publications have shown
that SNS does not produce better results than sham stimulation, thus limiting at this stage
the use of SNS to treat chronic constipation.
37,38
In the context of STC, surgery with colonic resection should only be considered when
all nonsurgical possibilities have failed, and when the severity of symptoms impacts
severely on the quality of life. An intensive workup is recommended; including global evaluation of digestive motility, as well as a psychologic and psychiatric evaluation (eating disorders should always be excluded). Results are extremely variable in the literature,
although laparoscopi c colectomy with ileorectal anastomosis remains the most recommended surgical approach. A recent review concluded that colectomy may benefit some
patients, at the cost of substantial short- and long-term morbidity. Current evidence is
insufficient to guide patient or procedural selection.
39
In conclusion, chronic constipation management should rely on a thorough interrogation and clini cal examination including perineum. Functional investigations may help to
characterize the mechanisms involved in the generation of symptoms, and to orient the
therapy. Surgery may be helpful for defecatory disorders associated with welldocumented pelvic-floor disorders. Surgical caution should be the rule when dealing with
chronic constipation resistant to medical therapy.
References
1.
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2. Sanchez MI, Bercik P. Epidemiology and burden of chronic constipation. Can J Gastroenterol. 2011;25
(Suppl B):11B–15B.
3. Bharucha AE, Dorn SD, Lembo A, Pressman A. American gastroenterological association medical posi-
tion statement on constipation. Gastroenterology. 2013;144:211–217.
4. Bellini M, Gambaccini D, Salvadori S, et al. Different perception of chronic constipation between
patients and gastroenterologists. Neurogastroenterol Motil. 2018;8, e13336.
5. Moore-Gillon V. Constipation: what does the patient mean? J R Soc Med. 1984;77:108–110.
6. Probert CS, Emmett PM, Cripps HA, Heaton KW. Evidence for the ambiguity of the term constipation:
the role of irritable bowel syndrome. Gut. 1994;35:1455–1458.
224 ANORECTAL DISORDERS
7. Bharucha AE, Pemberton JH, Locke 3rd GR. American gastroenterological association technical review
on constipation. Gastroenterology. 2013;144:218–238.
8. Remes-Troche JM, Coss-Adame E, Lopez-Colombo A, et al. The Mexican consensus on chronic con-
stipation. Rev Gastroenterol Mex. 2018;83:168–189.
9. Palit S, Thin N, Knowles CH, Lunniss PJ, Bharucha AE, Scott SM. Diagnostic disagreement between
tests of evacuatory function: a prospective study of 100 constipated patients. Neurogastroenterol
Motil. 2016;28:1589–1598.
10. O’Donnell LJ, Virjee J, Heaton KW. Detection of pseudodiarrhoea by simple clinical assessment of
intestinal transit rate. BMJ. 1990;300:439–440.
11. Vitton V, Damon H, Benezech A, et al. Clinical practice guidelines from the French National Society of
coloproctology in treating chronic constipation. Eur J Gastroenterol Hepatol. 2018;30:357–363.
12. Carrington EV, Scott SM, Bharucha A, et al. Expert consensus document: advances in the evaluation of
anorectal function. Nat Rev Gastroenterol Hepatol. 2018;15:309–323.
13. Heinrich H, Sauter M, Fox M, et al. Assessment of obstructive defecation by high -resolution anor-
ectal manometry compared with magnetic resonance defecography. Clin Gastroenterol Hepatol.
2015;13(7). 1 310-1317.e1.
14. Benezech A, Cappiello M, Baumstarck K, Grimaud JC, Bouvier M, Vitton V. Rectal intussusception: can
high resolution three-dimensional ano-rectal manometry compete with conventional defecography?
Neurogastroenterol Motil. 2017;29(4), e12978.
15. Mion F, Garros A, Brochard C, et al. 3D high-definition anorectal manometry: values obtained in
asymptomatic volunteers, fecal incontinence and chronic constipation. Results of a prospective
multicenter study (NOMAD). Neurogastroenterol Motil. 2017;29. e13049.
16. Diaz Tartera HO, Webb DL, Al-Saffar AK, et al. Validation of smart pill((R)) wireless motility capsule for
gastrointestinal transit time: intra-subject variability, software accuracy and comparison with video
capsule endoscopy. Neurogastroenterol Motil. 2017;29:1–9.
17. Dinning PG, Carrington EV, Scott SM. The use of colonic and anorectal high-resolution manometry
and its place in clinical work and in research. Neurogastroenterol Motil. 2015;27:1693–1708.
18. Lazzaroni M, Casini V, Bianchi Porro G. Role or carbon dioxide-releasing suppositories in the treat-
ment of chronic functional constipation: a double-blind, randomised, placebo-controlled trial. Clin
Drug Investig. 2005;25:499–505.
19. Chiarioni G, Whitehead WE, Pezza V, Morelli A, Bassotti G. Biofeedback is superior to laxatives for nor-
mal transit constipation due to pelvic floor dyssynergia. Gastroenterolog y. 2006;130:657–664.
20. Cotelle O, Cargill G, Marty MM, et al. A concomitant treatment by CO
2
-releasing suppositories
improves the results of anorectal biofeedback training in patients with dyschezia: results of a randomized, double-blind, placebo-controlled trial. Dis Colon Rectum. 2014;57:781–789.
21. Shim LS, Jones M, Prott GM, Morris LI, Kellow JE, Malcolm A. Predictors of outcome of anorectal bio-
feedback therapy in patients with constipation. Aliment Pharmacol Ther. 2011;33:1245–1251.
22. Emile SH, Elfeki HA, Elbanna HG, et al. Efficacy and safety of botulinum toxin in treatment of anismus:
a systematic review. World J Gastrointest Pharmacol Ther. 2016;7:453–462.
23. Halmos EP, Power VA, Shepherd SJ, Gibson PR, Muir JG. A diet low in FODMAPs reduces symptoms of
irritable bowel syndrome. Gastroenterology. 2014;146:67–75 [e5].
24. Lee-Robichaud H, Thomas K, Morgan J, Nelson RL. Lactulose versus polyethylene glycol for chronic
constipation. Cochrane Database Syst Rev. 2010;7:CD007570.
25. Urganci N, Akyildiz B, Polat TB. A comparative study: the efficacy of liquid paraffin and lactulose in
management of chronic functional constipation. Pediatr Int. 2005;47:15–19.
26. Gordon M, MacDonald JK, Parker CE, Akobeng AK, Thomas AG. Osmotic and stimulant laxatives for
the management of childhood constipation. Cochrane Database Syst Rev. 2016;8:CD009118.
Chapter 17 • Constipation and Dyssynergic Defecation 225
27. Mueller-Lissner S, Kamm MA, Wald A, et al. Multicenter, 4-week, double-blind, randomized, placebo-
controlled trial of sodium picosulfate in patients with chronic constipation. Am J Gastroenterol.
2010;105:897–903.
28. Ahuja NK, Mische L, Clarke JO, Wigley FM, McMahan ZH. Pyridostigmine for the treatment of gastro-
intestinal symptoms in systemic sclerosis. Semin Arthritis Rheum. 2018;48(1):111–116.
29. Bharucha AE, Low P, Camilleri M, et al. A randomised controlled study of the effect of cholinesterase
inhibition on colon function in patients with diabetes mellitus and constipation. Gut.
2013;62:708–715.
30. Camilleri M, Kerstens R, Rykx A, Vandeplassche L. A placebo-controlled trial of prucalopride for severe
chronic constipation. N Engl J Med. 2008;358:2344–2354.
31. Nee J, Zakari M, Sugarman MA, et al. Efficacy of treatments for opioid-induced constipation: a system-
atic review and meta-analysis. Clin Gastroenterol Hepatol. 2018;16(10). 1569-1584.e2.
32. Emmett C, Close H, Mason J, et al. Low-volume versus high-volume initiated trans-anal irrigation
therapy in adults with chronic constipation: study protocol for a randomised controlled trial.
Trials. 2017;18:151.
33. Christensen P, Krogh K, Perrouin-Verbe B, et al. Global audit on bowel perforations related to transanal
irrigation. Tech Coloproctol. 2016;20:109–115.
34. Duchalais E, Meurette G, Mantoo SK, et al. Percutaneous endoscopic caecostomy for severe consti-
pation in adults: feasibility, durability, functional and quality of life results at 1 year follow-up. Surg
Endosc. 2015;29:620–626.
35. Wilkinson-Smith V, Bharucha AE, Emmanuel A, Knowles C, Yiannakou Y, Corsetti M. When all seems
lost: management of refractory constipation-surgery, rectal irrigation, percutaneous endoscopic
colostomy, and more. Neurogastroenterol Motil. 2018;30. e13352.
36. Dinning PG, Hunt L, Patton V, et al. Treatment efficacy of sacral nerve stimulation in slow transit con-
stipation: a two-phase, double-blind randomized controlled crossover study. Am J Gastroenterol.
2015;110:733–740.
37. Pilkington SA, Emmett C, Knowles CH, et al. Surgery for constipation: systematic review and practice
recommendations: results V: sacral nerve stimulation. Colorectal Dis. 2017;19(Suppl 3):92–100.
38. Zerbib F, Siproudhis L, Lehur PA, et al. Randomized clinical trial of sacral nerve stimulation for refrac-
tory constipation. Br J Surg. 2017;104:205–213.
39. Knowles CH, Grossi U, Chapman M, Mason J, NIHR CapaCiTY working group, Pelvic floor Society.
Surgery for constipation: systematic review and practice recommendations: results I: colonic resection. Colorectal Dis. 2017;19(Suppl 3):17–36.
226 ANORECTAL DISORDERS
18
Solitary Rectal Ulcer Syndrome
Alejandra Altamirano-Barrera
*, Jos!e Marı´a Remes-Troche†,
Enrique Coss Adame
*
* D E P A R T ME N T O F G A S T RO E N T E RO L O G Y AND G I MO TI L I T Y LAB O R A T OR Y , N AT I O N A L
IN S T I T UT E O F MED I C A L SCI E N C E S A N D N UT R I T I ON S A L V A D O R ZU B I R A´N, M E X IC O C I TY ,
ME X I C O
†
DI G E S T I V E P H Y S I O L O G Y A N D G A ST R O I N TE S T I N AL M O T IL I T Y LA BO R A T O R Y ,
IN S T I T UT E O F ME D I C A L A N D BI OL O G I C AL R E S E A R C H , UN IV E R S I T Y O F VE RA C R U Z AN A ,
VE R A C R U Z, M E X IC O
18.1 Introduction
Solitary rectal ulcer syndrome (SRUS) is an unusual rectal disorder associated with an
ulcer formation, it can affect different parts of the rectum and other sites of the gastrointestinal tract.
1–3
The cause of this syndrome is unclear and may involve several factors,
including rectal prolapse, mucosal ischemia, and chronic severe constipation. SRUS
was first described in 1830 by Cruveilhier but was only recognized as a clinical entity in
1969 by Madigan and Morson.
4,5
SRUS is one of a number of pelvic-floor disorders, like
rectal prolapse, intussusception, and rectocele, which have similar pathogenesis. SRUS
is often caused by or associated with chronic constipation, which may produce changes
in the habitual characteristics of the evacuations, such as straining, rectal bleeding, tenesmus, mucoid secretion from the rectum, rectal pain, and a sense of incomplete evacuation.
6–8
The etiology, pathophysiology, and clinical manifestations of SRUS are not fully
understood. Given the different clinical symptoms and endoscopic findings, it may be
confused with other etiologies, such as inflammatory bowel disease (IBD) and rectal
neoplasms.
9
18.2 Epidemiology
The prevalence of this syndrome is not exactly known, which is s econdary to the difficulties in diagnosis and an underestimation of cases. There are reports from different parts of
the world that estimate a prevalence of one in 100,000 people per year
10,11
and an annual
incidence estimated at 1–3.6 per 100,000.
12
It have been demonstrated that it is more often
presented in men in the third decade and in women in the fourth decade of life
13
and it has
been estimated that about 80% of patients are less than 50 years of age. The mean age of
presentation is 49 years and only 25% present after 60 years,
14
although there are some
cases that have been reported in younger patients, meaning that it can occur at any
age.
15–18
Gender distribution is either equal or slightly higher in females.
Anorectal Disorders.
https://doi.org/10.1016/B978-0-12-815346-8.00018-7
© 2019 Elsevier Inc. All rights reserved.
227
18.3 Pathophysiology
The pathogenesis of SRUS is not well identified, various factors may be involved in its
development. Nevertheless the most important theories are that it is associated with direct
trauma and causes of local ischemia.
16
Some of the factors associated are: (a) the presence
of excessive straining , (b) lengthening of the rectal mucosa during straining, and (c) direct
trauma to the mucosa during bowel movements in the patient who suffers from constipation.
18
Self-induced trauma by self-instrumentation can occurred when individuals
attempt to remove impacted stool by rectal digitation.
19
There may be the presence of
a paradoxical contraction of puborectalis muscle produced by an uncoordinated muscle
contraction in the puborectalis muscle that increases the intrarectal and the anal canal
pressures, resulting in ischemic production and ulceration.
11
Rectal prolapse and intus-
susception lead to localized vascular trauma and consequently the onset of solitary local
ulceration.
20
18.4 Clinical Features
The classical symptoms of SRUS are rectal pain, rectal prolapse, bleeding, tenesmus, passage of mucus, chronic and severe constipation, lengthened straining on defecation, pelvic discomfort, and a sense of incomplete evacuation. It is important to note that up to
26% of patients may be asymptomatic.
14
The most common clinical symptom reported
is rectal bleeding. The amount of hemorrhage varies in this condition, severe rectal hemorrhage, which requires emergency endoscopy to diagnose the underlying cause, is rarely
reported.
21
Constipation is present in about 55% of patients, but diarrhea is seen in
20%–40% of patients.
14
The median time between presentation and diagnosis varies
between 3 months and 30 years.
5
A history of the repeated use of laxatives has been reported in many patients.17Also
self-induced trauma has been reported through rectal digitation.
22,23
In a retrospective
analysis it was demonstrated that 26% of patients with SRUS were misdiagnosed initially
and treated for other causes such as IBD. There are some patients in whom an underlying
psychological disorder, such as obsessive-compulsive disorder, may be present.
14
18.5 Diagnosis
The correct identification and diagnosis of this syndrome is challenging and its low prevalence partially explains that it is not properly diagnosed. Another factor is the lack of
knowledge of SRUS, and finally, a lack of physician experience leading to misdiagnosis.
The diagnosis of SRUS is made through the combination of several findings: s ymptomatology, endoscopy, sigmoidoscopy, and histology.
Sigmoidoscopy with rectal biopsy is key for the diagnosis. The macroscopic appearance of the typical SRUS it is characterized be a small shallow ulcer with a white secretion
or a hyperemic mucosal wall, usually on the anterior wall of the rectum (
Fig. 18.1A).
5
228 ANORECTAL DISORDERS
FIG. 18.1 Representative images of SRUS lesions. (A) An anterior rectal wall ulcer covered with fibrin is seen on the left, lesion is slightly elevated due to edema
and margins are active with erythema. (B) Besides the ulcer there is a polypoid lesion, elevated and irregular at margins, covered with friable mucosa. (C)
Histopathological findings with crypt hyperplasia, chronic inflammatory cell infiltration. Below on the right, Masson’s staining shows fibrosis predominately
at lamina propria.
Chapter 18 • Solitary Rectal Ulcer Syndrome 229
Ulceration is present in about 57% of patients. Polypoid lesions are found in about 25%, as
shown in Fig. 18.1B.
24
Patches of hyperemic mucosa are found in 18% of cases. The distance from the anorectal mucosal transition is about 5–10 cm. Lesions can be multiple in
up to 30% of cases.
25
SRUS is usually found on the anterior or anterolateral wall of the
rectum, centered on a rectal fold.
18.5.1 Histology
The histological features that characterize this syndrome are depicted in Fig. 18.1C and
include: (a) crypt hyperplasia and distortion, (b) thickening of the mucosal and muscular
layers, (c) lamina propria fibrosis (landmark for SRUS), (d) chronic inflammatory cell infiltration, and (e) segmental surface ulceration.
26–28
Biopsies of the ulcers are necessary to make the correct diagnosis, by which we
can differentiate other etiologies as nonsteroidal antiinflammatory drugs, malignant
conditions, or malignant transformation.
29
18.5.2 Radiology
As has been pointed out, SRUS usually is accompanied by prolapse or other pelvic-floor
disorders and that is why it is very important to take the correct approach. There are
other studies that help to establish SRUS diagnosis or to rule it out by differential diagnosis. Medical imaging techniques such as conventional defecography or magnetic resonance defecography (MRD), endoanal ultrasound, and barium enema have been
reported to be the most important diagnostic methods for imaging evaluation in these
patients.
30,31
Endoanal ultrasonography is a very useful tool and there are several papers highlighting the key elements often present in patients with SRUS, for example, an absence of distinction between the mucosa and the muscularis propria, thickened muscularis propria,
thickening of both the internal anal sphincter and external sphincter, and a thickened
submucosal layer.
30–33
Gopal et al. in 2001 published a very interesting work in which they emphasized the
utility of the ultrasound in the evaluation of the thickness of the anal sphincter in patients
suffering from SRUS.
34
Other findings, such as the thickening of the internal anal sphinc-
ter, previously have been described to be associated with rectoanal intussusception.
32
In
other paper it was been reported that the thickening of the submucosal layer may be
linked to rectal mucosa prolapsing into the anus, with secondary edema in the rectum
wall.
32–34
Defecography is another radiological study in which the different stages of defecation
are capt ured by fluoroscopy and by which conditions, including anorectal prolapse, external prolapse of rectum, intussusception, and nonrelaxing puborectalis muscle, are diagnosed, which are often found to be associated with defecation disorders.
35
MRD can
demonstrate the integrity of pelvic muscles, the anal sphincter included, and rectal
function. This method can show the anatomic abnormalities frequently associated with
230 ANORECTAL DISORDERS
constipation and other pelvic-floor anatomic disorders (cystoceles, enteroceles).36One of
the principal uses of the MRD is to properly assess patients with suspected malignancy
based on endoscopic findings. MRD is not routinely used for the diag nosis and management of patients with SRUS.
37
Barium enema as a type of X-ray imaging method can be used for the examination of
muscle function and its coordination, as well as prolapse. It can be used to show the thickening of the rectal folds, polypoid lesions and ulcers, and stricture formation, but these
observations can result in a misdiagnosis where the results are markedly similar to
malignant lesions.
38
18.5.3 Anorectal Function Tests
Anorectal function tests do not help in establishing the diagnosis or predicting therapeutic
response. Tjandra et al.
14
and Keighley39did not find any differences on anorectal
manometry parameters. The rectum is hypersensitive, the maximum tolerable rectal volume is reduced
40
and a high incidence of dyssynergic defecation can be found and balloon
expulsion time may be prolonged.
22,39
Differential diagnoses for SRUS are: IBD, infection (amebiasis, lymphogranuloma
venereum, syphilis), malignancy, chronic vascular insufficiency (chronic ischemic colitis),
endometriosis, colitis cystica profunda, drug induced, pressure ulcers, trauma, and
idiopathic.
19
18.6 Treatment
The management of SRUS is based on the severity of the disease and correlates with the
presence of symptoms and presence of rectal prolapse. The spectrum of management is
from conservative therapy to surgery. Asymp tomatic patients usually only require behavioral changes and other types of treatment may not be required. The first treatment strategy is conservative: patient education and behavioral modification.
39,41,42
Patients who
are asymptomatic or mildly symptomatic may be treated with stool softener and bulking
agents, bowel retraining, and reassurance to avoid any kind of rectal manipulation
(digitalization, enemas, suppositories).
18.6.1 Conservative/Biofeedback
The toilet habits (time spent in the toilet) should be adjusted and defecation training
should be noted. It is noteworthy that dietary and behavioral changes, especially in
patients with mild-to-moderate symptoms, can produce a favorable response in the
absence of mucosal prolapse, which can help in the improvement and prevention of disease progression.
40,43
A high-fiber diet can help, but by itself is insufficient, response rates vary between 19%
and 70%. Avoiding excessive straining can improve symptoms in up to 67% of patients and
sigmoidoscopic improvement of the ulcer may occur in about 30%.
44
Chapter 18 • Solitary Rectal Ulcer Syndrome 231
In more advanced cases, conservative management may not be the primary treatment
of choice, especially if there are more complications, such as fibrosis, external prolapse or
a high-de gree intussusception. In these more complicated scenarios, biofeedback helps to
improve symptoms. Biofeedback comprises a series of exercises that create a behavioral
change in the process of defecation and produce an effective pushing mechanism leading
to a reduction in excessive straining.
45
The effects are seen more rapidly in children than in
adults. In adults the process usually takes more sessions to understand and improve the
process of defecation. The different outcomes can be explained by two reasons: first, children have had a shorter time with SURS and, second, the adults’ altered defecation
maneuvers have become habitual.
Several studies have shown that biofeedback is an appropriate and useful treatment for
patients with SRUS. Jarret et al. in 2004, after several sessions, noted in 16 patients with
SRUS and 26 healthy controls an increased rectal mucosal blood flow assessed with laser
Doppler mucosal flowmetry performed before and after biofeedback therapy. Symptomatic improvement was reported by 75% of SRUS patients after treatment and five (31%)
had sigmoidoscopic ulcer resolution.
46
Rao studied 11 patients with refractory SRUS that
were sent for biofeedback therapy; 82% had dyssynergic defecation. After biofeedback,
stool frequency and straining effort decreased. In 56% bleeding ceased and five discontinued digital maneuvers, and in four there was complete healing (36%).
47
Like in any other treatments, there are some patients that do not respond to biofeedback. The factors that are associated with refractoriness to biofeedback therapy includes:
(a) a lack of understanding on how to perform pelvic floor retraining, (b) not performing
the exercises periodically as instructed, and (c) patients continuing to carry out rectal
manipulation.
48
The durability and efficacy of biofeedback therapy is uncertain for SRUS.
18.6.2 Local Therapy
Topical therapy has been reported to be effective in some patients. Sucralfate of sulfasalazine enemas and corticosteroids have been reported to be effective in improving
symptoms in refractory cases. However, their long-term effectiveness needs further evaluation.
49,50
Moreover, topical glucocorticoids, salicylates, and botulinum toxin have also
been used, but these show different outcomes.
49,51
The durability of each of the treatment
modalities varies over time; for example, botulinum toxin injection seems to last about
3months
52
and depends on many factors (doses, location of the application, doctor’s
experience).
18.6.3 Surgery
The indications for surgical treatment are patients who suffer from full-thickness or rectal
mucosal prolapse or those who are resistant to conservative management and biofeedback treatment.
53
There are several techniques options, which include: rectopexy, perineal
proctectomy (Altemeier procedure), excision, diversion, and the Delorme procedure for
mucosal resection.
54
Removing lesions by endoscopy or local excision has been
232 ANORECTAL DISORDERS
successful, but their long-term effects remain unclear. Rectopexy is helpful and intended
to correct anal prolapse.
55
Antiprolapse surgery has been reported to substantially
improve symptoms in patients with resistant SRUS to medical treatment long term.
56
In general, antiprolapsal surgery has led to promising long-term outcomes for about
60% of patients undergoing surgery.
57
Previous studies have shown that rectopexy has
been very effective in improving the rectal configuration and successful in the treatment
of rectal prolapse in SRUS. Mucosal resection or perineal proctectomy has been previously
utilized for a full thick prolapse.
58
The fecal diversion approach has also been effective in
improving the symptoms of patients and can be performed in patients for whom other
surgical methods have failed. Surgeries, including rectopexy, excision of ulcer, and, rarely,
colostomy, have been used in children with continuous hemorrhage per rectum that was
not curable.
55,59
Fig. 18.2 shows an algorithm for SRUS treatment.
18.7 Summary
SRUS is a chronic, benign disorder, related to straining or abnormal defecation. The pathogenesis of SRUS is not well understood, but many factors contribute. The correct diagnosis begins with clinical suspicion: clinical manifestations, endoscopical, and
histological findings are essential. A variety of therapies have been tried, patient education
and biofeedback are the first steps. Therapy should be aimed at restoring a normal pattern
of defecation. More severe disease may require surgery. Psychological factors should be
addressed whenever appropriate.
FIG. 18.2 Proposed treatment algorithm for SRUS.
Chapter 18 • Solitary Rectal Ulcer Syndrome 233
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