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184
A.A. Hai and N. Roy
and not associated with chills and rigor, and it seldom crosses 101°F. Passage of fresh blood in
stools, anal pain or discharge, and multiple or
recurrent fi stula in ano and perineal ulcerations are
not characteristically distinct from other anal
lesions especially Crohn’s. In developing countries
of the world, tuberculosis is common. The incidence of tuberculosis in Western European countries has decreased in the past few decades. There
are four types of anal and perianal tuberculosis,
ulcerative, verrucous, lupoid, and military, but the
most common is the ulcerative type. It may be due
to focus in the lung or intestine, or it may be primary. Positive diagnosis of anal TB relies on both
histological and bacteriological assessments.
Culture confi rms the diagnosis of TB.
Examination of stool (also perhaps sputum, stomach aspirate, and urine) for M. tuberculosis and
blood and endoscopy with biopsies for histological evaluation are done. Microscopic examination
reveals multiple caseating granulomas consisting
of epithelioid cells and numerous Langhans type
of giant cells with infi ltration of chronic infl ammatory cells and histiocytes around a central
caseating area. The sections stained with Ziehl–
Neelsen method and acid-fast bacilli are identifi ed. A clean-cut ulcer, with an indurated base
and showing a mucopurulent discharge, develops
in the center of the nodule. Modern cultures with
radiometric evaluation and polymerase chain reaction (PCR) are being increasingly used. Miliary
lesions of the anus occur as part of disseminated
tuberculosis. The treatment of the anal tuberculosis is medical. Surgical procedures are needed if
there is a fi stula or abscess. The ulcerative lesions
of the anus associated with tuberculosis regress
in a few weeks following the treatment. All
patients should receive conventional antitubercular therapy for at least 6 months including initial
2 months of rifampicin, isoniazid, pyrazinamide,
and ethambutol.
13.5.5 Syphilitic Ulcers
Venereal ulcers of the rectum are common in
societies where sodomy is practiced. The congenital cases with a rectal ulceration are rarely
encountered. In the acquired group, syphilitic
ulcers may occur in the primary stage or as a
result of breakdown of a gummatous rectal lesion.
It may also be seen in the perianal region and
mucocutaneous area. Mucous patches are infective and are relatively painless. When involving
the anus, the inguinal lymph node may show the
typical fi rm, discrete, and shotty appearance.
The incidence has increased, particularly due
to unprotected anal intercourse. Rectal syphilis is
often missed because it is usually asymptomatic
or causes only mild symptoms. Rectal syphilis is
one of the great masqueraders due to its variable
symptoms including itching, bleeding, tenesmus,
urgency of defecation, and anal discharge, which
may be purulent, mucoid, or blood stained.
However, instances of rectal syphilis extending
between the anal verge and dentate line have
been reported. The rectal chancre shows diffuse
chronic infl ammatory cell infi ltration predominantly composed of plasma cells in the lamina
propria and some blood vessels (hematoxylin and
eosin stain, ×200). Large numbers of spirochetes
are present on a special staining of the rectal
biopsy specimen (Warthin-Starry stain). The
patient is treated with one dose of intramuscular
benzathine penicillin G of 2.4 million units, and a
single dose of penicillin therapy induces rapid
regression of the rectal ulcer.
13.5.6 Dysenteric Ulceration
Dysentery, while it may, and often does, involve
the whole of the large intestine, has its seat most
frequently in the sigmoid fl exure and rectum. It is
in the lower portions of the alimentary canal that
its chronic results occur. This is logistically suggested by the fact that all of the detritus and
infectious bacteria are discharged, carried down
by the peristaltic action of the gut into these lower
segments, as a result of acute, sporadic, or epidemic dysentery. Chronic circumscribed ulcers
of the rectum or sigmoid with the typical symptoms of diarrhea, pus, blood, and mucus in the
stools occur. These symptoms accompany all
forms of rectal ulceration from whatever cause
they arise and render it diffi cult to distinguish a
13 Benign Ulcers of the Anorectum
185
true dysenteric ulceration from other varieties.
Indeed, ulcerations of the rectum and sigmoid are
often mistaken for chronic dysentery. The presence of the amebic dysentery or the bacillus of
Shigella will positively establish the dysenteric
nature of any given ulcer. It begins as infi ltration
of the mucous membrane with a fi brous exudation. This infi ltration increases until it interferes
with the blood supply of the mucous membrane,
the latter sloughs and is cast off, and an ulceration results. If this slough is superfi cial, the
membrane may be soon restored to its normal
condition, but if the infi ltration is deep and
involves the submucous tissues, the loss of substance is more extensive and cicatrization and
stricture of varying degrees may result. The
ulcers may be small and localized, or they may
extend over large areas and sometimes entirely
surround the canal; they may be trough-like, stellate, or irregular in shape; they may be single or
multiple. Perforation has been known to occur,
but it is not a frequent accident to fi nd rectal stricture having followed dysenteric ulceration. A
large number of pharmacological agents starting
with emetine, chloroquine, metronidazole, tinidazole, diloxanide furoate, secnidazole, etc., are
available to manage these cases.
13.5.7 AIDS-Associated Anorectal Ulcers
HIV/AIDS patients frequently present with proctological diseases which present in three forms:
1. Proctological complaints common to the pop-
ulation (hemorrhoids, fi ssure, pruritis)
2. Diseases associated with high-risk behaviors
such as anoreceptive intercourse causing
sphincter damage from intercourse leading to
proctitis and anogenital ulceration
3. Illness associated with HIV infection, such as
anal ulceration and unusual opportunistic
infections
Anorectal ulcers may present in up to onethird of the anorectal pathologies associated with
HIV infections (Gonzalez-Ruiz et al. 2004 ).
Ulcerative disease of the anorectal region in
AIDS patients manifests itself as severe incapacitating pain associated with uncontrollable drainage of feculent material. Like anal fi ssures, they
are associated with pain during defecation, but
AIDS ulcers are more likely to result in disabling
pain unrelated to bowel movements.
The majority of the idiopathic ulcers have a
characteristic appearance. Approximately 80 %
are located in the posterior midline, being somewhat more proximal in the anus, closer to the
dentate line. Unlike fi ssures, they lack a sentinel
tag, and resting anal sphincter tone is usually
diminished. AIDS-related ulcers are broad based
and extremely erosive, dissecting along submucosal and intersphincteric planes with invasion
onto the internal sphincter with more advanced
disease. The edges of the ulcer are usually rolled
over, and a small cavity (cul-de-sac) can be seen
between the mucosa of the anal canal and the
external sphincter. This cavity serves as a reservoir for stool and pus to accumulate, which in
turn causes pelvic pressure and pain radiating
down the legs. In advanced cases, this process
can progress into the postanal space and eventually perforate through the skin. These ulcers
cause severe incapacitating pain with defecation
(Modesto and Gottesman
1997 ).
Long-term cultures from anal ulcer base may
reveal Mycobacterium avium-intracellulare . Viral
cultures can detect cytomegalovirus (CMV) or
acyclovir-resistant strains of HSV which can both
cause extensive anal ulceration. CMV can also
be detected on rectal biopsy. Isolated CMV proctitis is uncommon and presents with nonspecifi c
symptoms like tenesmus, diarrhea, and hematochezia (Weledji
2013 ). Diarrhea encourages
anal ulceration, and stool cultures of Salmonella,
Shigella, campylobacter, and cryptosporidium
with microscopy for cysts and ova of giardia and
amebae are mandatory. Biopsy identifi es treatable
etiologies of these ulcers, including HSV, CMV,
Treponema pallidum , mycobacterium, crypto-
coccus, Haemophilus ducreyi , and Chlamydia
trachomatis (Beck and Wexner 1990 ).
The rare idiopathic anal ulcers constitute a
diagnosis of ruling out the above pathology
(El-Attar and Evans 1999 )
186
Fig. 13.1 SRUS with infl amed anal canal (Courtesy of M. Shahid Siddique)
A.A. Hai and N. Roy
In addition to standard treatment of AIDS,
medical treatment of CMV requires either intravenous ganciclovir or intravenous foscarnet, lasting 3–6 weeks depending on clinical response
(Whitley et al. 1998 ). Relief of pain is achieved
with the use of intralesional steroid injections. Surgical debridement is done to eliminate
“pocketing” of stool and pus. If the sphincter
is involved, internal sphincterotomy may be
required. Marsupialization is performed and the
base of the ulcer is then injected with intralesional
steroid preparation (Modesto and Gottesman
1997 ). Perianal suppurative diseases are common
conditions in AIDS patients. Abscesses should be
drained using small incisions, and judicious use
of draining setons will help lessen recurrent sepsis. The pus should also be cultured and broadspectrum antibiotics given. With the increasing
use of HAART therapy, the incidence of AIDSrelated anorectal ulcers has decreased markedly.
13.5.8 Solitary Rectal Ulcer
Syndrome (SRUS)
13.5.8.1 Introduction
Although described way back in 1813 by
Cruveilhier in Paris and given the present nomenclature of solitary rectal ulcer syndrome (SRUS)
by Lloyd-Devis in 1930, SRUS still remains a
relatively underdiagnosed and ill-understood
entity. This is particularly true in our tropical
setup where a large number of rectal conditions
(e. g. amebiasis, giardiasis, tuberculosis) with
somewhat similar symptomatology further confuse the picture. The fact that rectal cancer in its
early stage can at times mimic SRUS and the rare
instances when the two can coexist are also to be
noted with caution. The prefi x solitary associated
with this condition is also a misnomer as only
20 % of these cases present with a single ulcer
(Madigan and Morson
1969 ).
13.5.8.2 Clinical Features
SRUS presents as a disorder of defecation with the
following typical features (Vaizey et al. 1997 ):
• Passage of blood and mucus from the rectum
associated with straining and a feeling of
incomplete emptying
• Evidence of rectal prolapse, either internal or
external with or without abnormal perineal
descent on evacuation proctography
Sigmoidoscopic appearance varies from
erythema to ulceration or polypoid lesions. These
are commonly solitary but may be multiple.
Although most commonly on the anterior rectal
wall, they may be more extensive and even circumferential (Fig. 13.1 ).
13 Benign Ulcers of the Anorectum
187
There is histological evidence of fi brous obliteration of the lamina propria with disorientation
of the muscularis mucosa and extension of
smooth muscle fi bers into the lamina propria.
Histological fi ndings in cases of solitary rectal
ulcer (SRU) or mucosal prolapse syndrome are as
follows:
1. Nonulcerative phase: intact surface and fos-
sula epithelium
2. Ulcerative phase (manifest SRU syndrome): fl at
erosions with a fi lm consisting of mucus, fi brin,
granulocytes, and desquamated epithelium
3. Obliteration of lamina propria by fi broblasts
and nonstriated muscle fi bers
4. Lamina muscularis mucosae often thickened;
lamina propria not or only slightly infl amed or
infi ltrated
5. Fossula often hyperplastic; goblet cells
reduced in number
The thickening of the lamina propria with the
immigration of fi broblasts (above all into the
muscularis) is of particular importance (Geile
and Stahl 1993 ).
13.5.8.3 Pathogenesis of Solitary
Rectal Ulcer Syndrome
The underlying etiology and pathogenesis are not
fully understood, but multiple factors may be
involved. The most accepted theories are related
to direct trauma, local ischemia, and internal and
external mucosal prolapse. It has been suggested
that descent of the perineum and abnormal contraction of the puborectalis muscle during straining on defecation result in trauma and
compression of the anterior rectal wall against
the upper anal canal. Ulceration is thought to
occur during forceful straining against an immobile or a nonrelaxing pelvic fl oor or anismus.
Mucosal prolapse, overt or occult, is the most
common underlying pathogenetic mechanism in
SRUS. Although this hypothesis seems plausible,
it remains unproven because rectal mucosal
intussusception is common even in healthy subjects, but rectal prolapse and SRUS are rare. In
addition, not all patients with rectal prolapse have
SRUS and vice versa.
This may lead to venous congestion, poor
blood fl ow, and edema in the mucosal lining of
the rectum and ischemic changes with resultant
ulceration. The cause of ischemia may also be
related to fi broblasts replacing blood vessels and
pressure by the anal sphincter. Moreover, rectal
mucosal blood fl ow has been found to be reduced
in SRUS to a level similar to that seen in normal
transit constipation, suggesting similar impaired
autonomic cholinergic gut-nerve activity. Selfdigitation maneuver to reduce rectal prolapse or
to evacuate an impacted stool may also cause
direct trauma of the mucosa and ulceration.
Furthermore, ulcers usually occur in the mid
rectum, which cannot be reached by digital
examinations. Hence, it has been suggested that
rectal prolapse and SRUS are two separate conditions. In children, secondary to chronic mechanical and ischemic trauma, infl ammation by hard
stools, and intussusceptions of the rectal mucosa,
some histological features of SRUS can be seen,
such as fi bromuscular obliteration of the lamina
propria and disorientation of muscle fi bers (Zhu
et al. 2014 ).
13.5.8.4 Investigations
13.5.8.4.1 Sigmoidoscopy
Sigmoidoscopy with rectal biopsy is diagnostic. Ulceration is present in more than half of
the cases. Polypoid lesions are found in about
25 %. Multiple patches of hyperemic mucosa
are found in about one-third. The lesions most
often are found on the anterior or anterolateral
wall of the rectum, centered on a rectal fold.
The distance from the anal verge is about
5–10 cm.
The histologic appearance of SRUS has been
well established. The mucosa is elongated with
distorted glands, especially at the base. When the
glands are displaced to the submucosa, superfi cial bleeding can occur. The lamina propria is
edematous and contains proliferation of fi broblasts. It also is thickened, particularly the inner
circular muscular layer, with less prominent
thickening (edema) of the submucosa. Sometimes
there are unique features, such as decussation of
the two muscular layers, nodular induration of
inner layer, and grouping of the outer longitudinal
188
A.A. Hai and N. Roy
layer. Degeneration of the upper epithelium of
the crypts, surface erosion, engorgement of the
superfi cial capillaries, and a lack of infl ammatory
cells can be found. Histologic proof is necessary
to differentiate SRUS from malignant conditions
or possibly from malignant transformation.
13.5.8.4.2 Defecography
Although defecography can provide insights
regarding pathophysiology, it has a limited role in
establishing diagnosis of SRUS. Abnormalities
like external or internal prolapses are found in
about 75 % of patients with SRUS. Intussusception
and delayed evacuation are also seen frequently
(Felt-Bersma and Cuesta 2001 ).
13.5.8.4.3 Barium Enema
Nodularity of the rectal mucosa, thickening of
the rectal folds, stricture formation, polypoid
lesions, and ulceration may be seen with barium
enema. This is an unreliable method of diagnosis,
however, because these features cannot be differentiated from more sinister conditions.
13.5.8.4.4 Transrectal Ultrasonography (TRUS)
On ultrasonography, marked thickening of the
internal anal sphincter and a thickened muscularis propria is the most striking feature,
although thickening of the submucosa and
external anal sphincter may be present. The
rectal wall may be thickened, especially the
muscularis propria. Fading of the borders
between mucosa and muscularis propria can be
seen. All of these features probably are secondary to chronic straining.
13.5.8.4.5 Anorectal Manometry
Anorectal function tests have been performed,
but the results are variable, and the tests do not
help in establishing the diagnosis or predicting
therapeutic response. No differences in anal
pressure are found surprisingly, or in patients
with a history of long-standing straining and
descending perineum, lower pressures are seen.
The maximum tolerable rectal volume is reduced
and features of anismus can be found. The balloon expulsion time may also be prolonged.
13.5.8.5 Differential Diagnosis
Although the differentiation between SRUS and
early invasive anorectal cancer is of critical
importance, the presence of a large number of
tropical conditions further confuses the picture.
Rectal amebiasis which is so common in
Southeast Asia can mimic SRUS, and the occasional ameboma (amebic granuloma) of the rectum can at times be differentiated form a
malignant ulcer only by a biopsy. Other infective
conditions like giardiases, helminthiasis (particularly pinworm), and STD (like syphilis and gonorrhea) can produce very similar lesion. The
rising incidence of AIDS particularly among the
gay population at times presents with bizarre
anorectal lesions. Infl ammatory bowel diseases
like Crohn’s and ulcerative colitis and vascular
lesions like ischemic necrotizing colitis also have
anorectal lesions as a part of their spectrum.
Stercoral ulcers are due to impacted scabola in
the rectum associated with obstinate constipation
also present with rectal mucosal lesions. Perhaps
because of lifestyle changes, the incidence of
endometriosis is increasing as a whole, and rectal
endometriosis can present with rectal ulceration
and bleed although limited to some South
American countries. Habitual ergometrine suppositories also cause rectal ulceration. Anorectal
trauma, iatrogenic or otherwise particularly when
presenting late (especially when the history is not
forthcoming), can also be a cause. In all such
cases, a proper HPE alone can clinch the diagnosis of SRUS.
13.5.8.6 Management of SRUS
13.5.8.6.1 Conservative Treatment
Therapy should be aimed at restoring a normal
pattern of defecation. The patient should be
instructed to avoid excessive straining and to
regulate his or her defecation habits, in collaboration with a therapist for pelvic fl oor exercises
or behavioral retraining. The diet should contain
enough fi ber and suffi cient fl uid intake.
Modest use of laxatives should be considered.
Psychologic factors should be addressed when
appropriate. If these measures do not solve the
problem, surgery may be considered as a last
choice.
13 Benign Ulcers of the Anorectum
189
A high-fi ber diet can help but by itself is insuffi cient to obtain healing. Avoiding excessive
straining can improve symptoms in about twothirds of patients, and sigmoidoscopic improvement of the ulcer may occur in about 30 %.
Local treatment in the form of topical steroids
and sulfasalazine enemas is not effective.
Sucralfate enemas and 5-aminosalicylate show
some improvement. Local application of human
fi brin sealant has been tried with some response
in few patients.
13.5.8.6.2 Surgery
Surgery should be considered only in those patients
who fail to respond to conservative treatment
including biofeedback and having signifi cant mucosal and full-thickness rectal wall prolapse. The
strong association between chronic straining and
SRUS suggests that surgery should be reserved for
selected cases, especially because surgery can cause
constipation, which is an underlying mechanism for
the problem. Generally, a rectopexy is performed,
although anterior resection with rectopexy and
Delorme’s procedure has been used. Those with
external prolapse are best treated with mucosal
resection or some modifi ed Delorme’s procedure.
When the prolapse is mainly internal, resection or
some form of rectopexy should be tried.
In one study, overall results were disappointing. While 50 % had improved on conservative
line of 66 patients, 14 (30 %) required a stoma,
generally for constipation, and eight (12 %)
patients had additional surgery. Patients with
fecal incontinence and incomplete evacuation
have poor outcome.
In these, nonsurgical interventions are the
basis of treatment. In the absence of any major
rectal prolapse, the cornerstone of treatment lies
in patient counseling, high-fi ber diet, bulk laxatives, and minimizing commode time. They
should avoid straining and anal digitation.
13.5.8.6.3 Physiotherapy and Biofeedback
Training
Biofeedback is a process that enables an individual to learn how to change physiological
activity for the purposes of improving health
and performance. Precise instruments measure
physiological activity such as brainwaves, heart
function, breathing, muscle activity, and skin
temperature. These instruments rapidly and
accurately give feedback information to the user.
The presentation of this information often in conjunction with changes in thinking, emotions, and
behavior supports desired physiological changes.
Over time, these changes can endure without continued use of an instrument. This is the most useful approach. Only a few studies of biofeedback
have emerged so far. In one study, biofeedback
therapy before and after surgery showed a lower
recurrence rate (Binnie et al. 1992 ). In another
study, 13 patients were treated with biofeedback
including fi ve patients, with previous surgery.
Eight patients were cured or were asymptomatic,
although the ulcer did not heal completely in nine
patients (Vaizey et al. 1997 ). In another study,
patients without previous surgery responded well
to biofeedback.
Algorithm to the diagnosis and management
of SRUS is shown in Fig. 13.2 .
13.5.9 Suppository-Related Ulcers
Suppositories are solid drug forms for insertion in
the orifi ces of the body. The anorectal region is an
effective region of drug absorption, due to its neutral
pH, the lack of enzymatic activity, and the fact that
the hemorrhoidal veins bypass the liver and thus the
drugs do not undergo fi rst-pass metabolism.
The toxic action of certain drugs or chemicals,
used in suppositories, has been known to cause
ulceration of the anorectum. Two groups of drugs,
ergotamine and the morphomimetics, have been
shown to cause anorectal ulcers after prolonged use
(Roche et al.
tropropoxyphene and paracetamol suppositories,
taken for the relief of migraine, headache, or other
painful conditions, often results in widespread anorectal ulceration (Fenzy and Bogomoletz 1987 ).
Suppositories containing NSAID are also known to
have induced anorectal ulcers (Gizzi et al. 1990 ).
Anorectal ulcers due to the topical and possibly
additional systemic effects of ergotamine have
been reported. The majority of patients have been
females for unknown reasons (Eigler et al. 1986 ).
2010 ). Prolonged use or abuse of dex-
190
A.A. Hai and N. Roy
Fig. 13.2 Algorithm for the diagnosis and management of SRUS
The pathogenesis of suppository-induced
ulcers is unknown. However, dose-dependent
vasoconstriction is a possible explanation (Roche
et al.
2010 ; Wagner et al. 2014 ). In addition, local
trauma due to suppository introduction could
contribute to the development of ulcers.
wall, with infl ammatory changes in perirectal fat
and nonspecifi c adenopathies (Casas et al.
The endoscopic aspect of the sharply demarcated
distal rectal lesions with squamous and transitional epithelium (anoderm) ascending from the
anal canal is typical (D’Haens et al.
Symptoms are false urge to defecate, rectal
tenesmus, anal pain, rectal bleeding, mucus discharge, and constipation, with intestinal obstruction secondary to stenosis in severe cases (Casas
et al. 2011 ). Perianal skin lesions may be present
in up to half of the patients (D’Haens et al. 1993 ).
the use for strictures of the suppositories. Other
treatment options are topical steroids and endoscopic dilatation as these ulcers are often associated with anorectal stenosis. In severe cases, even
colostomy has to be done (Katsinelos et al. 2007 ).
Large and deep ulcerations are found on the
anorectal mucosa. They are indolent and can
reach the level of the sphincter ani. Colonoscopy
13.5.10 Nicorandil-Induced Ulcers
fi ndings show diffuse mucosal infl ammation, with
ulcerations and pseudopolypoid lesions. In severe
cases, rectal fi brotic stenosis or intramural fi stula
can develop. CT shows thickening of the rectal
Nicorandil is a potassium channel activator with
an adjunctive nitrate effect used as a vasodilator
to control angina. Anal ulceration appears to
2011 ).
1993 ).
In most cases, the ulcers heal after stopping
13 Benign Ulcers of the Anorectum
191
occur in approximately four in every 1000
patients prescribed nicorandil (Colvin et al.
2012 ). It is believed the condition is still widely
underdiagnosed and the pathogenesis remains
unclear. Authors have suspected a dose- dependent
mechanism, a vascular steal phenomenon
(although the pharynx, ileum, and anus are areas
of vascular watershed), and a direct local effect
of either nicorandil itself or a metabolite (Toquero
et al. 2006 ).
The ulcers have similar appearance with a distinctive “punched” out cavity deep enough to
reveal internal sphincter muscle fi bers. The ulcer
margins are well circumscribed and have clean,
undermined edges. Histology reveals granulation
tissue associated with acute infl ammation but no
evidence of granuloma or malignancy. In particular, there is no evidence of vasculitis (Watson
et al. 2004 ). Biopsy should be done to rule out
other causes. The development of ulceration in
association with the use of nicorandil is an indicator of the severity of IHD (Katory et al. 2004 ).
The ulcers heal after drug is withdrawn. Drug
withdrawal should be supervised by the
physician.
13.5.11 Acute Hemorrhagic Rectal
Ulcer (AHRU)
In 1974, Delancy and Hitch fi rst described cases
of acute, asymptomatic, and life-threatening
hemorrhage from solitary ulcers of the rectum
associated with comorbidity (e.g., respiratory
failure, renal failure, diabetes mellitus, atherosclerosis). In 1981, Soeno et al. used the term
“acute hemorrhagic rectal ulcer” (AHRU) to
describe such cases. It is particularly seen in ICU
settings. Clinically, such lesions were characterized by sudden-onset, painless, massive hemorrhage from solitary or multiple rectal ulcer(s) in
patients with serious underlying illnesses. The
lesions usually lie 3–10 cm above the dentate
line, and their pathogenesis is largely unknown
(Tseng et al.
reports on AHRU from Japan and East Asian
countries, but in Western countries, there have
been very few. The reason may be underreporting
2004 ). There have been several
of such cases due to diffi culties in the localization
of causes of lower gastrointestinal bleeding
(Hendrickson et al.
2003 ).
The etiological factors of these ulcers are rectal prolapse, self-digitization, iatrogenic, or idiopathic. A contributory mechanism may be
pressure necrosis-induced mucosal ulceration
from inspissated feces, further complicated by
impaired rectal mucous secretion. Alternatively,
it is proposed that the rectum, like the stomach, is
prone to stress-induced ischemia, leading to the
development of rectal ulcers that resemble ischemic gastric ulcers (Hendrickson et al. 2003 ).
Histopathologic examination may reveal
necrosis with denudation of the covering epithelium, hemorrhage, and multiple thrombi in the
vessels of the epithelium and underlying stroma
which is identical to those of hemorrhagic necrosis of the GI tract as seen in patients with cardiovascular dysfunction, shock or sepsis, and
stress-induced disturbance of the circulation in
the small intramural vessels (Oku et al. 2006 )
The most common endoscopic features are
multiple ulcers in the lower rectum. Most of the
ulcerations are circular. These cases do not show
longitudinal ulceration or thumbprinting appearance, which are often observed in ischemic colitis. Proximal colon ulcerations are also not seen
(Nakamura et al. 1997 ). The irregular type is the
most frequent, followed by nearly round and
Dieulafoy-type ulcers. Solitary ulcers were the
most frequent (Oku et al. 2006 ).
The prognosis of AHRU is primarily dependent on accurate diagnosis and management of
the underlying disorders. Endoscopic hemostasis, using various modalities like injection of epinephrine, heater probe thermocoagulation,
injection sclerotherapy, and clipping can be tried
out (Matsushita et al.
1998 ). However, the risk of
rebleeding is high and angiographic embolization
is an alternative before surgery for the treatment
of life-threatening hemorrhage (Lin et al. 2011 ).
Surgical treatment by per anal suturing of a
bleeder provides a quick, safe, and successful
management of acute hemorrhagic rectal ulcer
(Hung et al. 2006 ). Local excision, transanal liga-
tion, and repeated banding have also appeared to
be highly effective (Hendrickson et al. 2003 ).
192
A.A. Hai and N. Roy
13.6 Radiation-Induced Anorectal Ulcers
Despite tremendous improvements in targeting
ionizing radiation directly to tumors and sparing
adjacent tissue, radiation used in the treatment of
cancer can lead to anorectal damage. Radiationinduced ulcers in the anorectal region are seen
mainly as a result of prostatic brachytherapy
(Phan et al. 2009 ) or due to external beam ther-
apy in the pelvic region (Shadad et al. 2013 ).
According to the recommendations of the
American Radiation Therapy Oncology Group
(RTOG) and the European Organisation for
Research and Treatment of Cancer (EORTC),
acute side effects are those that appear during
days 1–90 following the initiation of treatment,
while chronic changes are those that appear later
or develop from acute changes. Anorectal ulcerations mostly present late. In two RTOG prospective studies, 3.3 % of the patients developed late
intestinal sequelae of grade 3 or greater intensity.
Of these, 1.6 % were regarded as proctitis, 0.4 %
as rectal stricture, and 1.7 % as rectal bleeding or
ulceration (O’Brien 2001 ). A series from
Memorial Sloan Kettering Cancer Center cited
the development of rectal ulcers in fi ve of 92
patients treated with prostatic brachytherapy with
three developing fi stulae (Wallner et al. 1996 ).
Rectal ulcers and fi stula are the most feared complications of chronic radiation proctitis.
Often the symptoms are similar to those of a
malignancy or infl ammatory bowel disease.
Patients present with pain, tenesmus, diarrhea,
malabsorption, and stenotic symptoms, as well as
blood and mucus in the stools. The exact pathology is not understood, but animal studies suggest
a relationship between submucosal changes and
mucosal ulceration (O’Brien 2001). The reason
may be that radiation is more effective against
cells that are actively dividing, are undifferentiated, and have a large dividing cell load. The
mucosa thus becomes the target of choice for
radiation damage.
It is most important to rule out active malignancy and infl ammatory bowel disease. The diagnosis of radiation proctitis is primarily made with
endoscopy and biopsy.
The chronic form features as a damaged
mucosa with reduced to absent vascular markings
and erosions and often deep ulcerations and dirty
gray-green base having smooth borders. Fibrosis
and scarring are present often leading to stenosis.
In addition to ulcerative and atrophic mucosal
changes, the submucosa shows a fi broblastic proliferation with sclerosis of the vessels and connective tissue. Radiological studies identify the
presence and extent of fi stulas, stenoses, strictures, ulcers, and more subtle mucosal changes. If
the endoscopic view is impaired by bleeding or
stenoses, arteriography with special attention to
the inferior mesenteric artery may provide information regarding persistent bleeding as well as
the extent of bowel with impaired circulation
(Stein 2003 ).
Treatment modalities of radiation-induced
ulcers of the anorectal region include enemas/
suppositories of sucralfate, misoprostol, amifostine, and hyperbaric oxygen chamber therapy
(HBOT). Endoscopic therapy preferably with
argon plasma coagulation is safer, less expensive,
and more widely available than heater and bipolar cautery. Nd:YAG laser and topical formalin
may also be tried while surgery is reserved for
cases of rectal strictures and fi stula (Silva et al.
2013 ). Intraluminal ulceration, and likewise fi s-
tulas, may require diversion to allow healing.
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