Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1199_Библиотеки_им_академика_М_И_Перельмана.pdf
Benign Tumors of the Anorectum
Rajshekar Mohan
1 5
15.1 Introduction
The anorectal region is a common site for
tumors and tumor-like conditions, some of
which are extremely rare. Although the tumors
described in this chapter are benign, some have
potential to turn malignant. Because of their
clinical appearance and location, sometimes
they may be mistaken for malignant lesions.
These tumors frequently pose diagnostic challenges and dilemmas in planning treatment. A
thorough knowledge of the diverse clinical presentations and variations in pathology is essential for planning treatment and surgery.
Macroscopically visible mass or lesion is
called a polyp which may be neoplastic or nonneoplastic (hamartomas, hyperplastic, infl ammatory). Neoplastic polyps may be of epithelial
(adenomas) or nonepithelial (lipoma, leiomyoma, lymphomatous) in origin.
R. Mohan
Department of Surgery ,
Sri Dharmasthala Manjunatheshwara
College of Medical Sciences and Hospital ,
Dharwad 580009 , Karnataka , India
rajshekarm@rediffmail.com
e-mail:
15.2 Benign Tumors of Epithelial Origin
15.2.1 Infl ammatory
Cloacogenic Polyp
It is a rare, nonneoplastic tumor occurring in the
anal canal, fi rst described in 1981 (Lobert and
Appelman 1981 ). Patients usually present with
bleeding per rectum. In most patients, the tumor is
located anteriorly in the proximal anal canal and
arises from the epithelial transition zone at the
anorectal junction (Mathialagan et al. 2000 ). The
incidence is more in men than in women. The etiology of this tumor is uncertain, but it is thought
to occur due to ischemia or due to trauma caused
either by passage of hard stools or due to straining
at passing stools or due to a congenital cause.
Because of clinical and structural similarities with
solitary rectal ulcer syndrome, it is also thought
that prolapse of the transitional zone mucosa may
be responsible in the development of this condition (Lobert and Appelman
Macroscopically it is a raised polypoidal
lesion with reddish overlying mucosa (Fig. 15.1 ).
Microscopic evaluation reveals a characteristic
tubulovillous growth pattern, shallow superfi cial
ulcers, displaced crypts, and chronically infl amed
fi bromuscular stoma which may extend into the
lamina propria (Fig. 15.2 ) (Parfi tt and Shepherd
2008 ). The tumor is treated by a local surgical
1981 ).
© Springer India 2016
N.A. Chowdri, F.Q. Parray (eds.), Benign Anorectal Disorders:
A Guide to Diagnosis and Management, DOI 10.1007/978-81-322-2589-8_15
205
206
R. Mohan
Fig. 15.1 Infl ammatory cloacogenic polyp
resembles squamous cell carcinoma. The tumor
is treated by local excision or by electrocoagulation, after histological confi rmation of the diagnosis (Jensen and Sjølin
1985 ).
15.2.3 Adenoma or
Adenomatous Polyp
Adenoma or adenomatous polyp is a benign neoplasm of epithelial origin. They are the most common type of colorectal polyps found in adults with
an increasing incidence with age. Adenomas can
grow in size, demonstrate increasing dysplastic
changes and turn malignant, and are considered
premalignant. About 3 % of colorectal adenomas
are located in the rectum (Gillespie et al. 1979 ).
They can occur sporadically or as part of a hereditary syndrome (familial adenomatous polyposis).
15.2.3.1 Etiopathogenesis
The various etiological factors associated with
the development of these adenomas are:
Fig. 15.2 Microphotograph of infl ammatory cloacogenic polyp
resection. Anal intraepithelial neoplasia has been
noted to occur in these polyps, and hence, careful
histological examination is very important
(Hanson and Armstrong 1999 ).
15.2.2 Keratoacanthoma
This is a benign skin lesion, associated with
excessive exposure to sunlight, which can occur
rarely in the perianal skin and within the anal
canal. It occurs as an exophytic, nodular lesion,
usually with a central crater, measuring half centimeter to 2 cm in size (Jensen and Sjølin 1985 ).
On histological examination, the lesion closely
1. Genetic/molecular basis. There is accumula-
tion of lesions in a variety of genes. Genetic
mutation leads to disordered local DNA repli-
cation. Oncogenes get activated and tumor
suppressor genes are deactivated. KRAS
Oncogene is found in 9 % of small adenomas
and 58 % of adenomas (1 cm in size). APC
gene mutation is seen in 30–60 % of sporadic
adenomas and is important for adenoma
formation; mutation of TP53 gene on 17p is
seen in 50 % of adenomas and 75 % of
adenocarcinoma.
2. Lifestyle and dietary factors:
• Protective foods:
• Dietary fi bers
• Plant food
• Folates
• Risk factors:
• Excessive fat
• Alcohol
• Cigarette smoking
3. Acromegaly: These patients have 14–35 % risk.
4. Ureterosigmoidostomy sites: 29 % prevalence
rate of polyps and cancers.
15 Benign Tumors of the Anorectum
207
5. Infl ammatory bowel diseases: 5 % lesions are
found adjacent to villous adenomas.
6. Endocarditis with Streptococcus agalactiae
increases the risk of villous adenoma.
Majority of colorectal carcinomas follow the
adenoma–carcinoma sequence because of following facts:
1. One third of operated specimen of colorectal
carcinomas contains one or more synchronous
adenoma.
2. Risk of carcinoma increases with the number
of adenomas.
3. Adenoma tissue is frequently found adjacent
to carcinoma.
Risk factors for high-grade dysplasia and
invasive carcinoma include polyp size (38.5 %
for polyps more than 10 mm). Polyp size is the
strongest predictor. Other factors include villous
histology, age more than 60 years, and left-sided
lesions.
15.2.3.2 Epidemiological Facts
Colonoscopic prevalence of adenoma in asymptomatic patient of more than 50 years is 24–47 %.
Prevalence increases with age and is about
50–65 % in patients with more than 75 years of
age.
Adenoma can occur in 30–50 % of patient 6
months to 4 years after polypectomy.
Mean age of adenoma diagnosis is 10 years
earlier than carcinoma. Adenoma grows from
<5 mm to 1 cm in 2–3 years, and progression
from 1 cm adenoma to carcinoma takes 2–5
years. Cancer probability for lesions >1 cm is
3 %, 8 %, and 24 % at 5, 10, and 20 years, respectively. Metastasis occurs only in lesions invading
the muscularis mucosa through the lymphatics
close to it.
Thirty percent of these tumors can be missed
if they are less than 5 mm, and 10 % of these
tumors can be missed if they are 6–9 mm.
Six to nine percent of these adenomas are
advanced, i.e., more than 1 cm in size, high-grade
dysplasia, and appreciable villous tissue. Most
adenocarcinomas arise from adenomas and
removal of adenomas has been found to reduce
the incidence of carcinoma.
Villous adenomas harbor malignancy in
4–40 % of cases, associated with severe degree of
dysplasia, and 40 % of such tumors will recur
despite complete excision (Cho et al. 2008 ).
Invasive carcinoma is missed in 40 % cases. The
risk of malignant transformation is 15–25 % and
40 % if a lesion is >4 cm.
15.2.3.3 Classifi cation
Based on their shape, adenomas are classifi ed as
(a) sessile and (b) pedunculated. Histologically
they are classifi ed into (a) tubular [85–91 %], (b)
villous [5–10 %], and (c) tubulovillous [1 %]
adenomas (O’Brien et al. 1990 ).
Tubular adenomas typically have at least 80 %
dysplastic tubules, which are packed tightly and
extending into the normal appearing lamina propria and only 0–25 % of villous tissue.
Tubulovillous adenomas have more than 20 %
tubular component and 25–75 % villous component.
Villous adenomas consist of at least 80 % villous fronds, which are essentially crypts elongated to twice the normal length or more. These
villous fronds have a lamina propria core surrounded by adenomatous epithelium. These are
rarely less than 1 cm. in size and premalignant
polyps of the gastrointestinal tract. Sixty percent
of adenomas >2 cm and all large fl at adenomas
are villous.
Clinical Presentation
The majority of these lesions are asymptomatic
and are detected during screening colonoscopies.
Symptomatic patients may present with bleeding
per rectum, change in bowel habits, or nonspecifi c abdominal pain. Secretory diarrhea syndrome is rare and is seen in large villous rectal
tumors. They appear smooth surfaced and redder
than the adjacent mucosa, but the surface may
appear nodular as their size increases. Irregular
contour, ulcerations, friability, fi rm/hard consistency, thickening of stalk, and nonlifting of tumor
with submucosal invasion should raise the suspicion of malignancy in adenoma. The size of these
lesions can vary from 1 mm to several centimeters (Fig.
15.3a, b ).
208
ab
Fig. 15.3 ( a , b ) Endoscopic and operative views of tubular polyp
R. Mohan
Complications which adenomas can undergo
include hemorrhage, obstruction, bowel torsion,
and malignant transformation.
15.2.3.4 Investigations
1. Complete blood count.
2. Iron study.
3. Fecal occult blood. Positive only in 20–40 %
adenomas (usually large and distal). Five to
ten percent of patients with positive FOB have
colonic cancers.
4. Double-contrast barium study. It detects ade-
nomas in only 30–50 % of cases depending on
tumor size.
5. CT colonography (virtual colonoscopy).
Detection rate varies from 39 to 93 % depend-
ing on the size of adenoma. It is not as sensi-
tive as endoscopy. It is useful in patients with
incomplete colonoscopy.
6. Endoscopy and endoscopic biopsy. Endo-
scopic evaluation is the most useful and
sensitive investigation for adenomas from
both diagnostic and therapeutic points of
view. Complete colonoscopy is done to rule
out synchronous lesions in the proximal
colon.
15.2.3.5 Treatment
A . Medical care:
(a) Snare polypectomy
Snare polypectomy is possible in the
majority of patients, exception being carcinoma. Polypectomy site should be
marked with methylene blue or India ink.
Follow-up endoscopy following polypectomy should be done at 3 years, if there
are only 3–10 polyps, but if there are
more than 10 lesions with villous and
high-grade dysplasia, it should be less
than 3 years. Low-risk patients with less
than 3 small (<1 cm) polyps with lowgrade dysplasia should have follow-up
endoscopy at 5 years. Earlier colonoscopy
should be done in selected patients with
multiple small polyps and large sessile
adenoma (>2 cm) and those removed
incompletely or in piecemeal, i.e.,
• 3–6 monthly for the fi rst year
• 6–12 monthly for the second year
• Yearly for 2–5 years
Small rectal hyperplastic polyps should
be taken as normal and can have follow-up
endoscopy at 10 years. Malignant adenomas
15 Benign Tumors of the Anorectum
209
Fig. 15.4 Multiple polyps and multiple site involvement
requiring surgical resection
completely excised with favorable differentiation, free margin, and no vascular and
lymphatic invasion need no more treatment
(American College of Gastroenterology
Guidelines).
(b) NSAIDS and COX-2 Inhibitors:
They inhibits prostaglandins and cyclooxygenase activity and decreases the
incidence of polyps. Regression of polyps occurs in FAP with low dose aspirin.
Low dose Aspirin (81 mg) may have
some role in decreasing adenoma recurrence. Sulindac (NSAID) has apoptotic
activity on colonic cells thereby causes
regression of polyps (Luis et al.
2001 ).
B . Surgical treatment:
(a) Indications:
• Large sessile polyps more than 2–3 cm
• Multiple polyps encompassing two
colonic fi elds (Fig. 15.4 )
• Suspicious of malignancy, e.g., lymphovascular invasion, involvement of
deeper third of the submucosa, less
than 2 mm margins, and sessile polyp
removed in piecemeal
Lesions in the lower half of the rectum
can be excised by transanal route. Transanal
endoscopic microscopic surgery (TEMS) is
done for proximal rectal lesions. Sometimes
major resections in the form of anterior
resection or abdominoperineal resection are
indicated for large circumferential, multiple, and invasive tumors (Casdesus
2009 ).
Classical oncological resection for
malignant polyps is recommended in the
following situations:
1. Pedunculated polyps with invasion of
the submucosa wall below the stalk or
lymphovascular invasion.
2. Sessile polyps with invasion of deeper
third of the submucosa. Depth of infi ltration is the main determinant of
lymph node metastasis.
3. Malignant polyps removed with
<2 mm margin.
4. Sessile polyps removed in piecemeal.
(b) Histology
The excised specimen should be histologically assessed for the degree of dysplasia
and presence of in situ carcinoma. The pedicle of a pedunculated adenoma and the base
of a sessile adenoma should be meticulously
assessed for completeness of excision.
On microscopy, adenomatous cells
have hyperchromatic nuclei with cellular
proliferation at all levels. Dysplastic
changes in adenomas are categorized as
low or as high grade. With progression of
dysplasia, nuclear atypia, mitotic fi gures,
and increasing loss of polarity develop,
with mucin-depleted tall columnar cells
containing basally located oval nuclei.
15.2.4 Preventive Measures
• Low-fat intake and red meat. Fat increases biliary sterols which are damaging. Fat intake
should be limited to >25–30 % of energy intake.
210
R. Mohan
Fig. 15.6 Microphotograph of a serrated polyp
hyperchromatic nuclei. There may be focal areas
Fig. 15.5 Serrated polyps
of excess mucous production (Torlakovic and
Snover
1996 ). There may also be varying degrees
of atypia and dysplasia (Lu et al. 2010 ). The nor-
• High fruit and fi ber intake. Fiber inhibits
harmful bacteria and prevents their harmful
effects. About 20–30 g fi ber should be taken
daily.
• Calcium supplements, vitamins, and minerals
impede carcinogenesis.
• Maintain normal body weight.
• Daily exercise.
• Avoid smoking and excessive use of alcohol.
mal mucosal zone of proliferation which is at the
base of the crypts is noted to be located in the
middle or the upper part of the crypts (Torlakovic
and Snover 1996 ) (Fig. 15.6 ).
Serrated polyps are classifi ed into (a) traditional serrated adenoma, (b) mixed polyps, and
(c) sessile serrated adenomas (Bauer and
Papaconstantinou 2008 ). The three variants have
subtle architectural variations, and all three have
malignant potential (Longacre and FenoglioPreiser 1990 ). The sessile serrated adenoma is
considered a precursor to dysplastic serrated ade-
15.2.5 Specifi c Adenomas
15.2.5.1 Serrated Polyps and Adenoma
Serrated polyps appear as pale, nodular, small
lesions and grossly resemble hyperplastic polyps
(Fig. 15.5 ). They are considered by some authors
to be a subtype of hyperplastic polyps or adenomatous polyps, while some others consider
hyperplastic polyps as a subtype of serrated polyps. They can occur as a part of the serrated polyposis syndrome and can potentially undergo
malignant transformation. Microscopic examination of a serrated polyp typically shows serrated
and dilated crypts which may sometimes be oriented horizontally. These dilated crypts demonstrate branching at the base, with small and
normally arranged basilar nuclei and enlarged
noma and also adenocarcinoma (Goldstein et al.
2003 ). This transformation is thought to occur
through the serrated adenoma pathway, which is
distinct from the adenoma–carcinoma sequence
in colorectal cancer, and involves acquired
genetic mutations of the BRAF oncogene and
KRAS (Chan et al. 2003 ).
Traditional serrated adenoma is very rare
(0.5–1.3 %) of colorectal polyps and occurs as a
pedunculated lesion. On microscopy, there is
characteristic epithelial dysplasia and infolding,
with serration of the luminal surface of the crypts.
The nuclei appear elongated and centrally placed.
There may also be pseudostratifi cation and eosinophilic cytoplasm. Mixed polyps demonstrate a
mixture of the serrated architecture seen in hyperplastic polyps and sessile serrated adenoma with
15 Benign Tumors of the Anorectum
211
dysplastic features seen in adenomatous polyps
(Harvey and Ruszkiewicz 2007 ). The sessile ser-
rated adenoma is the most common variant and
constitutes about 15–20 % of serrated adenoma.
They are pale, large, and sessile lesions that are
usually located on the crests of the mucosal folds.
Microscopic features which are characteristic of
both hyperplastic polyps and traditional serrated
polyps are seen, such as dilated crypts and change
of the zone of proliferation (Torlakovic et al.
2003 ). They grow larger than the other variants,
with extension parallel or through the muscularis
mucosae.
Endoscopic visualization techniques such as
chromoendoscopy with indigo carmine staining and
narrow band imaging aid in differentiating between
hyperplastic polyp and sessile serrated adenoma
and also between dysplastic sessile serrated adenoma, traditional serrated adenoma, and mixed
polyp. Characteristic starlike pattern of pits and
honeycomb pattern of capillaries seen in hypertrophic polyp can be differentiated from the irregularly
distributed pits with dilated and elongated capillaries seen in adenoma. Although rates of recurrence
after resection and also rates of progression of the
disease are not very clear, in view of the risk of
malignant transformation, excision of these lesions
is advisable. Most lesions can be removed endoscopically, the sessile lesions being resected using
the saline lift technique and the pedunculated
lesions using a polypectomy snare. Occasionally,
extension of a sessile lesion deeper to the muscularis mucosae may result in incomplete resection, and
these patients require surveillance at shorter intervals. Large polyps which are not amenable for
endoscopic resection should be surgically resected
(Bauer and Papaconstantinou
2008 ).
15.2.5.2 Flat and Depressed
Adenomas
These are not true polyps but are identifi ed by
chromoendoscopy with indigo carmine dye.
These adenomas occur with an incidence of 20 %
and contain cancer more often than polypoid adenomas. Flat adenomas of >1 cm. in size have
29 % incidence of high-grade dysplasia or cancer. Treatment consists of endoscopic polypectomy or operative resection.
Fig. 15.7 Hyperplastic polyp
15.2.6 Nonneoplastic Adenomas
15.2.6.1 Hyperplastic Polyp
Hyperplastic polyps develop as a result of defective epithelial maturation and failure of apoptosis. Although they are considered to be
nondysplastic and nonmalignant, transformation
into an adenomatous polyp, a mixed hyperplastic
and serrated polyp, or a serrated polyp can occur
(Estrada and Spjut 1980 ). Serrated polyps are
considered to be a type of hyperplastic polyp
with potential for malignant transformation.
Hyperplastic polyps occurring as a part of a polyposis syndrome show an increased incidence of
malignant transformation.
They are usually multiple and occur most
commonly in the rectosigmoid region (Fig.
15.7 ).
These are small and nodular lesions, measuring
less than 5 mm in size, appearing pale in contrast to the adjacent mucosa, and have a broad
base (Estrada and Spjut 1980 ). Microscopic
examination shows characteristic hyperplastic,
elongated, and nonbranching mucosal crypts,
with no atypia and containing mature goblet
cells. Chromoendoscopy with indigo carmine
staining and magnifi cation reveals a starlike pit
pattern which helps to distinguish it from the
irregular grove pattern typically seen in adenomatous polyp. On narrow band imaging, a typical honeycomb pattern is seen (Kudo et al. 1994 ).
One of the polyps should be endoscopically or
212
R. Mohan
transanally excised for confi rmation of diagnosis.
Patients should be advised regular colonoscopic
surveillance.
15.2.6.2 Infl ammatory Polyp
Infl ammatory polyps occur in a background of
chronic infl ammation and attempts at repair.
They are pseudopolyps and are usually seen in
ulcerative colitis but may be seen in Crohn’s
disease and in infective colitis. They occur as
multiple lesions with uniform width from their
base to the head, consisting of infl amed regenerating mucosa, with adjacent areas of ulceration.
Infl ammatory polyps do not require any specifi c treatment and the underlying infl ammatory
disease should be treated. The adjacent mucosa
should be evaluated for dysplasia.
15.2.6.3 Hamartomatous Polyps, Juvenile Polyp, and Retention Polyp
Hamartomatous polyps, otherwise called as
juvenile or retention polyps, are localized proliferation of normal and mature intestinal epithelial cells. They occur usually in children, and
the incidence is more common in men (boys)
than in women (girls). They can occur sporadically or as a part of a polyposis syndrome.
Sporadically occurring hamartomatous polyps
are considered nonmalignant, unless histological examination reveals adenomatous components (Mesiya et al. 2005 ). When more than
three of these lesions are noted, a polyposis syndrome should be thought of. Juvenile polyposis
syndrome is a rare autosomal dominant disorder, with multiple such polyps being found
throughout the gastrointestinal tract. There may
be a family history of the disease in 20–50 % of
these patients (Rickert et al.
Patients can present with abdominal pain,
sometimes with bleeding if ulceration has
occurred and occasionally with diarrhea. The
polyp can prolapse out through the anal canal.
Hamartomatous polyps are thought to occur
due to the blockage of colonic glands caused by
mucosal infl ammation or ulceration, leading to
dilatation and proliferation of the gland with the
development of granulation and connective tissue
1979 ).
proliferation. Microscopy examination typically
reveals dilated, mucous-fi lled, cystic-looking
glands, in a highly vascularized background of
fi brous stroma. Although these polyps are not
premalignant, juvenile polyposis syndrome is
considered to be a potentially premalignant
condition (Longo et al.
endoscopic resection followed by a thorough histological examination.
1990 ). Treatment is by
15.2.6.4 Lymphoid Hyperplasia and Lymphoid Polyp
These are benign tumors of lymphoid origin.
Lymphoid hyperplasia is an uncommon, benign
condition that occurs in the rectum and occasionally in the anal canal, due to the presence of lymphoid follicles (Cornes 1961 ). The exact etiology
for this occurrence is not known, but it is possibly
due to an infl ammatory response. However, a
hereditary predisposition has also been noted. In
children, it can present as an acute infl ammatory
response to an infective process. Since the fi rst
report of this condition in 1865, many sporadic
occurrences of this condition have been reported.
The tumors can occur at any age, with a higher
incidence in the third and fourth decades of life.
In children, a higher incidence is noted between
the fi rst and the third years of life, and the incidence in boys is twice that of girls. Because of a
few reported occurrences in twins and in siblings
and an association with familial polyposis, a
hereditary predisposition has also been suggested.
It may be asymptomatic if the location is in the
rectum but can be painful when located in the anal
canal, especially during defecation (Alvear
The tumor can occur as focal nodular, diffuse,
or polypoidal and is noted most commonly in
the distal rectum. The nodules are usually small,
fi rm, and sessile but can occasionally be large and
pedunculated. There may be an umbilication at the
apex or the center of the nodule which may be helpful in making a diagnosis. Histologically, there is a
thin lining of mucosa covering well- differentiated
lymphoid tissue, which had whitish fi brous bands
interspersed between the follicles. In the polypoidal form, the follicles have a well- defi ned germinal
center. The macroscopic and microscopic appearance can resemble that of a malignant lymphoma
1984 ).
15 Benign Tumors of the Anorectum
213
(Symmers 1948 ). Evaluation is done by endoscopy
and biopsy for histological examination, which
usually confi rms the diagnosis. Excision and histological examination is necessary because of its
close resemblance to other malignant tumors. It is
also necessary to differentiate this condition from
multiple polyposis. Local excision is the treatment
of choice and recurrence of disease is rare.
15.3 Benign Mesenchymal Tumors
15.3.1 Lipoma
Lipoma of the rectum is very uncommon, and a
more common site is the perianal region. They usually occur as solitary lesions in contrast to colonic
lipomas which tend to occur as multiple lesions.
Majority (90 %) of these lipomas develop in the
submucosal plane, although a small percentage
(10 %) may develop in the subserosal plane.
Patients may be asymptomatic or may present with
tenesmus when its location is in the distal rectum.
Occasionally, a large lipoma may cause symptoms
of obstruction because of its size. Rarely they can
be a cause for rectal bleed or an intussusception. A
pedunculated lesion may prolapse through the anal
canal (Zurkirchen and Leutenegger 1998 ).
The tumor is soft and well circumscribed on
palpation, with its yellowish color visible through
the overlying mucosa on visualization using a
proctoscope or an endoscope. The overlying
mucosa can be pinched up, and the lesion is usually compressible (Rodriguez et al.
Treatment of a rectal lipoma can be done by
transanal incision and enucleation or endoscopically if it is pedunculated (Nijhawan et al. 1993 ).
A large rectal lipoma may require a transabdominal approach for complete removal.
1990 ).
Fig. 15.8 Fibroma of rectum
occur due to repeated episodes of thrombosis and
strangulation without sloughing out of the covering
mucosa, with the covering columnar epithelium
gradually getting converted into columnar epithelium. It is usually single but can occasionally be
multiple. Generally small in size, it can very slowly
increase in size, over the years. It has a pale and
smooth surface, is usually oval in shape, has a fi rm,
and has minimal mobility. It may be located in the
wall of the distal rectum but may become polypoidal and project into the lumen of the rectum
15.8 ). The surface may become ulcerated,
(Fig.
causing bleeding and may mimic a malignant
lesion (Yadoo and Nathan
Patients complain of tenesmus and sometimes a
sense of heaviness in the rectum. Occasionally the
covering epithelium can ulcerate, and the patient
may present with bleeding per rectum. Evaluation
is by digital rectal examination and proctoscopy.
The diagnosis is to be confi rmed by histology,
especially in patients presenting with ulceration
and bleeding. Treatment is by transanal excision.
1971 ).
15.3.2 Fibroma
Fibroma is an uncommon tumor occurring in the
anorectal region. It can arise in a hypertrophied
anal papilla or due to fi brous infi ltration of a prolapsed internal hemorrhoid. This is thought to
15.3.3 Infl ammatory Fibroid Polyp
and Eosinophilic Granuloma
Infl ammatory fi broid polyp is a term proposed by Helwig and Ranier, for a submucosal
214
R. Mohan
Fig. 15.9 Infl ammatory fi broid polyp
granuloma with eosinophilic infi ltration which
was initially described by Vanek (Vanek 1949 ;
Helwig and Ranier 1953 ). This tumor can rarely
occur in the rectum, presenting as a polypoidal
lesion. It is a benign tumor representing reactive infl ammatory changes with proliferation
of spindle cells and represents a true benign
mesenchymal tumor (Schildhaus et al. 2010 ).
These spindle cells have been found to express
platelet-derived growth factor alpha and contain
activating platelet- derived growth factor alpha
mutations also (Daum et al. 2010 ). They occur
as a solitary tumor, measuring between 2 and
5 cm, arising from the mucosa or the submucosa,
and can be pedunculated or sessile (Fig. 15.9 )
(Hasegawa et al.
1997 ). On microscopy, they
contain a mixture of proliferation of small blood
vessels, fi broblast- like spindle cells, and edematous connective tissue with eosinophils, plasma
cells, macrophages, and mast cell infi ltrates
(Kim and Kim 1988 ; Eslami-Varzaneh et al.
2004 ). Malignant transformation is not known
to occur.
Patients may present with bleeding per rectum, tenesmus, change in bowel habits, and
bowel obstruction (Park et al. 2007 ). Large
tumors can become adherent to adjacent structures such as the sacrum and mimic rectal malignancy (Jin et al. 2013 ). The tumor can be excised
transanally or endoscopically, surgical resection
being required for larger lesions.
15.3.4 Leiomyoma
Leiomyoma can occur uncommonly in the rectum
(Serra et al. 1989 ). They are more common in
females, when compared to males. Small leiomyomas usually are asymptomatic and are sometimes
detected on routine rectal examination. Larger leiomyomas can cause tenesmus, interfere with the
passage of stools, a feeling of fullness in the rectum, and sometimes a frequent desire to defecate.
The tumor can cause obstructive symptoms and is
known to undergo malignant transformation.
The tumors are usually noted to arise from the
internal anal sphincter (Vorobyov et al. 1992 ).
Magnetic resonance imaging and endorectal ultrasonography are imaging modalities which can be
used to evaluate the extent of the tumor. On
endorectal ultrasonography, the tumor appears as a
homogenous, hypoechoic lesion with no invasion
into perirectal tissues (Serra et al. 1989 ). Ulceration,
bleeding from the tumor, and extrarectal fi xity on
imaging are suggestive of malignant transformation. Small leiomyomas can be excised transanally.
If the lesion is extending extrarectally, an extrarectal approach would be a better option. Local excision is also adequate for large leiomyomas, but
there is a higher chance of local recurrence.
15.3.5 Neurofi broma
These are benign tumors arising from the nerve
sheath. They can rarely occur in the anorectal
region. After von Recklinghausen’s fi rst description of multiple subcutaneous neurofi bromatosis
in 1882, disseminated neurofi bromatosis with
visceral involvement was reported in 1930. The
incidence of gastrointestinal involvement has
been reported to be 11–25 % (Pinsk et al.
The disease is also known to occur in the gastrointestinal tract with no other areas of involvement. Neurofi broma can occur as a single lesion
or as a cluster of lesions. Only three cases of solitary neurofi broma arising in the anal canal, with
no other systemic involvements, have been
reported in the literature. While evaluating a
patient with generalized neurofi bromatosis with
associated gastrointestinal bleeding or intestinal
2003 ).