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72
R. A. Malizia and B. T. Valerian
Anal Mass
A. History
- Digital rectal
examination (C)
Physical examination (B)
Appearance
Anoscopy (D)
No
Pain
Ulcerative
Draining
Exophytic
Prolapsed internal
Mucosal
Rectal prolapse (M)
Biopsy (V)
Neoplasm (U)
Complex
Fistula-in-ano (S)
YesNo
Destruction (R)
Condyloma acuminata (Q)
Excisional
hemorrohid (O)
hemorrhoidectomy (P)
Perineal
Rectopexy +/-
sigmoid resection
Conservative
Seton
Advancement flap (T)
Lay open
Fistulotomy (T)
Mucosal
proctectomy (N)
rectosigmoidectomy
management (L)
Yes
anesthesia
D. Exam under
Appearance
Hypertrophied
anal papilla (K)
Ulcerative
Sexually
Hematoma
Thrombosed
Erythematous
Anorectal abscess (E)
Symptomatic
YesNo
disease (I)
transmitted
Antibiotics (J)
external
hemorrhoid (G)
>4 days <4 days
Incision and drainage (F)
Excision (L)
Excisional
thrombectomy (H)
Conservative
management (H)
Fig. 9.1 Algorithm for evaluation and management of anal mass
9 Evaluation andPerioperative: Anal Mass
73
should all be assessed. Evaluation of the
sphincter complex may be performed by having the patient squeeze around a fully inserted
nger. A gentle sweep above the anorectal
ring is warranted for full characterization.
Additionally, bi-digital rectal examination
may provide benecial when assessing the
tract of a stula-in-ano and potential sphincter complex involvement. To conduct this
maneuver, an inserted index nger pushes
outward against the anal mucosa while
simultaneously utilizing the thumb to push
the anal verge in an inward direction. If at
any time unbearable pain is generated, the
examination should be aborted and the
patient should be scheduled for an anorectal
examination under anesthesia.
D. If the patient has tolerated the digital rectal
examination, further internal visualization
should be conducted via anoscopy. A well
lubricated anoscope is inserted into the anal
canal. Circumferential evaluation of the
canal should be conducted. This technique
will help directly visualize the severity of
internal hemorrhoid disease, mucosal abnormalities, ulcerations, internal stulous openings, or internal lesions. If any concern for
inammatory bowel disease or rectal involvement, sigmoidoscopy or formal colonoscopy
may be warranted.
E. An anorectal abscess can form an erythema-
tous, painful, protuberant external anal mass.
Abscess formation can occur in several distinct anatomical locations; including the
supralevator, ischiorectal, intersphincteric,
and perianal spaces. The most prevalent site
for abscess formation is in the perianal space.
Anatomically, numerous anal glands and
ducts empty into anal crypts at the dentate
line. Luminal or glandular obstruction due to
a multitude of etiologies, such as, foreign
body, trauma, prior surgical intervention, or
malignancies, can result in accumulation of
static mucous products resulting in a nidus
for infection. Common clinical manifestations of a perianal abscess are pain, swelling,
constitutional symptoms. Patients may report
foul smelling, purulent drainage if the
abscess has spontaneously drained prior to
evaluation. When evaluating a patient with
these complaints, a thorough history is warranted with careful attention to those areas
previously outlined in the beginning of the
chapter. Physical examination should encompass a careful external examination noting
extent of the erythema and the central location of the abscess. If the abscess has not ruptured, palpation may elicit intense pain and
uctuance. It is important to note, that deep
ischiorectal, intersphincteric and supralevator abscesses may not reveal external ndings. A digital rectal examination may be
attempted assessing for additional areas of
internal uctuance and/or presence of a
stula-in-ano.
F. The management of perianal or supercial
ischiorectal abscesses is incision and drainage. Often times these may be drained under
local anesthetic in the ambulatory setting.
Larger and more complex abscesses should
be drained under anesthesia in the operating
room. If amenable to bedside drainage, the
area of maximal tenderness, uctuance or
drainage should be identied. This region
should then be circumferentially inltrated
with local anesthetic. A cruciate incision
should be conducted over the center of the
lesion. The corners of the incision should be
cut free by scalpel or scissor to ensure adequate drainage. If present, loculations should
be disrupted with gentle, blunt dissection via
clamp or forceps. Copious irrigation should
be utilized to ensure all purulent material has
been removed. The wound site may be temporarily packed. With adequate drainage,
antibiotic coverage is not necessary in the
otherwise healthy individual. The wound site
should be evaluated in follow up to ensure no
evidence of recurrence has occurred.
G. A thrombosed external hemorrhoid may also
present as an acute, painful external anal mass
with associated hematoma. Hemorrhoids are
normal anatomical cushions of vascular tissue
located in the anal canal. Three main cushions
exist in the left lateral, right anterolateral and
right posterolateral regions of the anal canal.
74
R. A. Malizia and B. T. Valerian
External hemorrhoids are located in the distal
aspects of the anal canal, are covered by anoderm, and have somatic innervation.
Classically, external hemorrhoid thrombosis
presents as acute perianal pain with a rm
mass along the anal verge. A bluish/purple
discoloration of the mass may be reported by
the more curious patient. Physical examination should be conducted in the prone jackknife or left lateral decubitus positions. Visual
inspection and digital rectal examination
should be performed. With appropriate pain
relief, anoscopy should be performed in order
to exclude a strangulated, prolapsed internal
hemorrhoid or a large, edematous, perianal
skin tag associated with Crohn’s disease, as
management would differ.
H. Treatment for a thrombosed external hemor-
rhoid is contingent upon timing of presentation. The natural history of a thrombosed
external hemorrhoid is severe, progressive
pain until 48–72h. After this time frame, pain
slowly improves with the start of thrombus
resorption or rupture through the overlying
necrotic skin. Therefore, if a patient presents
within 4days of onset, excisional thrombectomy is warranted. In the ofce, the patient is
placed in the prone jackknife position. A local
anesthetic eld block is applied to region surrounding the thrombosed external hemorrhoid. An elliptical incision is then conducted
encompassing the necrotic skin overlying the
thrombus. The thrombus should then be fully
expressed or removed with forceps.
Hemostasis should be obtained via direct
pressure or other hemostatic agents like silver
nitrate applicators. The skin edges are left
open for adequate drainage. Oral analgesics
and stool softeners may be necessary after
excision. Sitz baths should be conducted at
least three to four times per day, and after
bowel movements. Simple incision and drainage should be avoided in this situation, as it
will be inadequate. If the patient presents outside of the rst 4 days of symptoms, conservative therapy should be offered. This
includes analgesia, stool softeners, Sitz baths
as described above.
I. Several sexually transmitted diseases (STD)
may present as a painful, ulcerative internal
and/or external anal mass. Typically, this
infection occurs through the process of anoreceptive intercourse, although may be an
extension of active genital/perineal disease.
Damage received to the mucosal lining during anoreceptive intercourse allows for the
transmission of pathogens. Patients with
ulcerative STD’s may present with fever,
chills, lethargy, general malaise, rectal/anal
pain, pruritus, discharge, and tender lymphadenopathy. When assessing these complaints, it is pertinent to obtain a very detailed
sexual history as outlined earlier in the chapter. On physical examination, a thorough
examination of the inguinal lymph nodes,
genitalia, perineum and perianal region
should be conducted with notation of lymphadenopathy, lesions or ulcerations. Digital
rectal examination, anoscopy and/or sigmoidoscopy should be performed to evaluate
the internal mucosa of the anal canal and the
rectum for signs of proctitis.
J. Common organisms and viral infections pre-
cipitating the development of ulcerative
lesions include: Lymphogranuloma venereum strains of Chlamydia trachomatis,
Hemophilus ducreyi, Treponema pallidum
and herpes simplex virus. Often these organisms may be difcult to identify with routine
culture. Diagnosis is typically generated by
detailed history, physical examination and
exclusion of other infections. In the case of
Syphilis, caused by Treponema pallidum,
diagnosis is made via either dark-eld
microscopy or a series of serologic testing
including rapid plasma regain, Venereal
Disease Research Laboratory, and the uorescent treponemal antibody absorption test.
Antibiotic therapy is the mainstay of treatment for these ulcerative STD’s.
Unfortunately, herpes simplex virus may
cause recurrent outbreaks due to latency of
the virus. Treatment is based on symptomatic
relief during an outbreak, oral antiviral therapy, and suppressive therapy targeted at
recurrence.
9 Evaluation andPerioperative: Anal Mass
75
K. Hypertrophied anal papillae may present as a
mucosal appearing external anal mass. Often,
development may be associated with a
chronic anal ssure; however, idiopathic
enlargement may occur as well. Clinically,
patients may report a precipitating acute anal
ssure occurring several weeks prior.
Inability to heal this ssure may result in a
chronic state. This continued inammation
and irritation may lead to hypertrophy and
prolapse of the adjacent internal anal papillae. Additional complaints of poor perianal
hygiene, pruritus, and mucous discharge may
be noted. On physical examination, careful
retraction of the buttocks will reveal a bulging mucosal mass. An anal skin tag, often
referred to as a sentinel pile, may also be
present externally. The presence or absence
of a chronic anal ssure should be noted.
Digital rectal examination and anoscopy may
be attempted in the setting of a chronic ssure, but should be performed judiciously in
the ofce if an acute anal ssure is present. If
idiopathic hypertrophy, a biopsy may be warranted if irregularities are identied.
L. Conservative therapy is the mainstay of treat-
ment for benign hypertrophied anal papillae.
If associated with a chronic anal ssure,
treatment should also address the underlying
ssure. Simple mucosal excision may be
warranted if proving symptomatic or if suspicious for malignancy.
M. Full thickness or mucosal rectal prolapse
may also generate a painless, bulging, mucosal anal mass. Careful assessment of bowel
habits, constipation, incontinence, frequency
of prolapse, and obstetrical history in women
should be obtained. Several anatomic factors
may cause full thickness rectal prolapse
including redundancy of the rectum and
weakness of the pelvic oor musculature.
Presenting complaints typically revolve
around a protruding, painless mass. Other
associated features may include rectal fullness, sensation of pressure, incontinence,
excessive straining, and feelings of incomplete defecation. On physical examination,
the rectum may already be prolapsed. If not,
the patient may be placed on a toilet and
made to strain as if having a bowel movement. This should generate prolapse. Full
thickness rectal prolapse is identied by concentric folds of tissue and redundancy to the
rectal wall. Rectal mucosal prolapse has a
more radial appearance to the tissue folds.
Once the prolapsed is reduced, digital rectal
examination should be performed to assess
rectal tone and sphincter strength. In rare
instances, neoplasia can be the cause for prolapse. Endoscopic evaluation may be warranted to evaluate the rectum and distal
colon. Any suspicious lesions should be
biopsied to rule out malignancy.
N. Operative treatment for full thickness rectal
prolapse depends on overall surgical risk. For
low risk individuals, a transabdominal rectopexy with or without resection of the sigmoid
is preferred. A high risk patient might be better served by a perineal proctosigmoidectomy or mucosal proctectomy.
O. Prolapsed internal hemorrhoids may present as
a mucosal appearing external anal mass.
Internal hemorrhoids are located proximal to
the dentate line, covered by columnar epithelium, and have visceral innervation.
Development of internal hemorrhoids is caused
by venous outow obstruction. This progresses
to congestion, swelling and prolapse of the
effected vascular cushion. Common symptoms
include hematochezia with defecation, mucous
discharge, sensation of inadequate rectal emptying, and inability to maintain perianal
hygiene. Please refer to section on thrombosed
external hemorrhoid for specic physical
examination strategies and ndings.
P. Common treatment options for internal hem-
orrhoids depend on the severity of disease.
Grade 1 (no prolapse) and Grade 2 (spontaneously reducing) may benet from conservative medical management and/or rubber
band ligation, sclerotherapy, or infrared
coagulation. It is acceptable for less advanced
Grade 3 (manually reducible) internal hemorrhoids to undergo conservative management illustrated above. However, more
advanced Grade 3 and Grade 4 (irreducible)
76
R. A. Malizia and B. T. Valerian
internal hemorrhoids should undergo excisional hemorrhoidectomy.
Q. Human papilloma virus has been identied
to cause the development of exophytic perianal and anal condyloma acuminata. Roughly
40 subtypes have been shown to play a
causative role in anogenital infection. Of
these, HPV types 6, 11 are the most common
subtypes to generate benign anogenital warts.
Types 16, 18, 31, 33, and 35 can generate
exophytic anogenital lesions, but also confer
a greater risk of dysplasia and carcinoma.
Transmission occurs via sexual intercourse
with a partner manifesting active disease,
subclinical, or asymptomatic infection.
Development of anal warts can occur in the
absence of anoreceptive intercourse.
Bleeding and pruritus may be associated
complaints. Their appearance typically
resembles pink, “cauliower-like” exophytic
lesions. Diagnosis is based on clinical evaluation. A thorough internal examination via
anoscopy is crucial to identify additional
lesions in the anal canal.
R. Treatment consists of destruction of the
lesions. Common techniques for mild disease
include topical applications with imiquimod
or podophyllin, excision, or fulguration with
electrocauterization, or laser therapy. Minor
disease may be eradicated in the ofce setting under local anesthetic. More extensive
disease is best dealt with in the operating
room under intravenous sedation or general
anesthesia. Regardless of the method for
obliteration, continued surveillance is crucial
as recurrent lesions and development of anal
intraepithelial dysplasia may occur.
S. A draining external anal mass may result from
development of a stula-in-ano. A preceding
anorectal abscess can result in the epithelialization of an aberrant tract with extension to
the anus or rectum. Fistula-in- ano often manifest with an internal opening present in the
anal canal or rectum, as well as an external
opening on the perineum. There are several
different classications of stula- in- ano
including; intersphincteric, trans- sphincteric,
suprasphincteric, and extrasphincteric. The
specic details of each type of stula-in-ano
will not be discussed in this chapter. Common
clinical manifestations include spontaneous
drainage, pain with defecation, bleeding, and
perineal pressure. Identication of the external opening(s) on physical examination may
be evidenced by the presence of purulent
drainage, uctuance or granulation tissue.
Digital rectal examination should evaluate for
the presence of an internal opening. Positive
ndings include a raised, nodular region or a
small depression along the normal mucosa.
However, identication of the internal opening may be difcult. Goodsall’s rule may provide a useful predictor for the expected
location of the internal opening. While examining the perineum, a transverse line through
the center of the anus marks the posterior and
anterior perineum. Posterior to this line, the
stula tract typically travels curvilinear, with
the internal opening located in the posterior
midline. Anterior to this line, the tract typically travels in a linear fashion, entering at the
closest anal crypt. Temptation to probe the stula tract should be avoided in the ofce setting. Imaging modalities, such as,
stulography, anorectal ultrasonography, or
MRI, have been described and should be
restricted to more complex or recurrent
disease.
T. The goal of treatment is to identify and suc-
cessfully remove the stula tract, while circumventing damage to the sphincter
complex. Based on the location of the stula,
different surgical treatment options exist.
The lay-open stulotomy technique has been
described for the treatment of low transsphincteric or uncomplicated intersphincteric stulas. For complex stulas denoted by
potential involvement of the sphincter complex, recurrent disease, IBD or an anterior
location in a female patient, the placement of
a seton or endorectal advancement ap may
be recommended.
U. Although relatively uncommon, anal cancer
can present as a painless, ulcerative anal or
perianal mass. These represent roughly only
2.6% of all digestive system malignancies.
9 Evaluation andPerioperative: Anal Mass
77
Brief review of the anal canal and anal margin will be imperative in understanding the
embryological origin of malignancies that
arise in this region. Proximally, the rectum
transitions to the surgical anal canal at the
anorectal ring. This ring denotes the most
superior aspect of the sphincter complex. The
canal extends past the dentate line for 1–2cm
until it reaches the distal border at the intersphincteric groove. From this point distally,
the anal margin extends roughly 5cm in a
circular fashion encompassing the perianal
skin. At the proximal border, the mucosa is
comprised of columnar epithelium. At the
level of the dentate line, a transitional zone of
epithelium develops. Columnar epithelium
begins to transition to squamous epithelium,
which then constitutes the distal aspect of the
anal canal and margin. Although full description and treatment of the numerous anal
malignancies will not be covered in this
chapter, they will be listed based on location.
Malignancies arising in the anal canal are
typically squamous cell, adenocarcinoma,
melanoma, or sarcoma. Those of the anal
margin consist of squamous cell, basal cell,
verrucous, Kaposi’s sarcoma, and lymphoma. Often patients will present with
symptoms of bleeding, anal pain, pressure,
presence of ulceration or a bulging external
mass. When evaluating these complaints, a
detailed history is warranted. A full review
may be found in the beginning of the chapter,
but particular attention should be paid to
growth in size of the lesion, episodes of
incontinence, HPV status, anoreceptive intercourse, immunodeciency disorders, and
smoking status. Physical examination should
include external visual inspection with documentation of vertical and horizontal diameters of the lesion, location, extension into the
anal canal, irregularity, pigmentation, rm-
ness, presence of ulceration. Digital rectal
examination and anoscopy should be conducted circumferentially to evaluate for the
presence of internal lesions. If identied
additional information regarding mobility of
the lesion should be noted. Careful assessment of sphincter involvement should be
documented.
V. All suspicious lesions should be biopsied.
This may be conducted in the prone jackknife position. Local anesthetic should be
applied surrounding the area for biopsy. The
area should be biopsied at the junction of
lesion and normal appearing tissue. The
specimen should be sent for prompt histopathological analysis. Additional use of
imaging modalities may be warranted to further characterize the lesion. Endoanal/
endorectal ultrasonography, computed
tomography, and pelvic magnetic resonance
imaging will provide valuable insight into
extent of the malignancy, sphincter involvement, lymphatic involvement, depth of invasion, and potential metastatic spread. Please
refer to the section covering anal carcinoma
for further treatment details.
Suggested Reading
Wexner SD, Vernava AM. Clinical decision making in
colorectal surgery. NewYork: Igaku-Shoin; 1995.
Beck DE, Wexner SD.Fundamentals of anorectal surgery.
London: W.B.Saunders; 1998.
Beck DE, Roberts PL, Saclarides TJ, Senagore AJ, Stamos
MJ, Wexner SD. The ASCRS textbook of colon and
rectal surgery. NewYork: Springer; 2011.
Safar B, Sands D.Perianal Crohn’s disease. Clin Colon
Rectal Surg. 2007;20(4):28.
CDC.Sexually transmitted diseases treatment guidelines,
2015. Morbid Mortal Weekly Rep. 2015;64:3.
National Comprehensive Cancer Network. Anal
Carcinoma. https://www.nccn.org/professionals/phy-
sician_gls/pdf/anal.pdf. Accessed 07 July 2016.
Part II
Anal Conditions
Anal Conditions: Anal Fissure/ Recurrent Anal Fissure
AlexandraElias andRonG.Landmann
10
Refer to Algorithm in Fig.10.1
A. An anal ssure has a pathognomonic presen-
tation, characterized by pain during defecation (passing glass, knives, razor blades, hot
pokers, or barbed wire), post-defecatory pain
(spasms or clenching lasting 20min to 3h),
fear of defecation, and rectal bleeding
(streaks of blood or drops on toilet paper).
B. Because of the pathognomonic presentation
of an anal ssure, a thorough history focusing on symptoms, dietary habits (i.e. ber
content, ber supplementation, and hydration), and details of defecation (e.g. presence
of constipation or diarrhea, avoidance of defecation, caliber of bowel movements) is the
most important tool for diagnosis. A conrmatory non-invasive physical examination
should be performed to exclude other diagnoses. Perform gentle gluteal spread with
mild anal canal effacement, and visually
inspect for sentinel tag and/or break in ano-
A. Elias
Division of Colon and Rectal Surgery,
Mayo Clinic, Jacksonville, FL, USA
R. G. Landmann (*)
Section of Colon and Rectal Surgery,
Department of Surgical Oncology,
Baptist-MD Anderson Cancer Center,
Jacksonville, FL, USA
e-mail: Landmann.Ron@mayo.edu
derm revealing internal anal sphincter muscle bers, being sure to note the location to
determine whether the ssure is typical or
atypical (Fig.10.2). A typical ssure will be
located in the midline, usually posteriorly
(90%, but can also be located anteriorly), and
will have sharply demarcated edges. An atypical ssure will be located laterally and may
be painless, deep, and/or wet-appearing with
weeping edges. Pruritus ani, which presents
as very supercial excoriated ssures, should
also be excluded.
C. Laboratory evaluation is not indicated for typ-
ical anal ssures. For atypical anal ssures,
biopsy or culture may be indicated to evaluate
for an alternative suspected disease process
(e.g. sexually transmitted infection (STI),
Crohn’s disease, or cancer). Please refer to
chapter 23 for additional information
D. Endoscopic evaluation is not indicated solely
for typical acute anal ssures. For refractory
disease, careful internal examination with
anoscopy and/or exible sigmoidoscopy is
warranted to exclude other pathology. In the
setting of chronic diarrhea or bloody bowel
movements, colonoscopic evaluation for
colitides should be considered. Patients who
require endoscopy for routine colorectal cancer screening or surveillance guidance—
apart from the ssure—should undergo
colonoscopic evaluation as indicated.
© Springer Nature Switzerland AG 2020
S. R. Steele etal. (eds.), Clinical Decision Making in Colorectal Surgery,
https://doi.org/10.1007/978-3-319-65942-8_10
81
82
A. Elias and R. G. Landmann
Fig. 10.1 Algorithm for anal ssure and recurrent anal ssure
Posterior
T: Typical Fissure
A: Atypical Fissure:
Anterior
Fig. 10.2 Fissure type by location
E. An acute ssure is dened as a ssure that has
been present for less than 6weeks. They typically appear as supercial tears and lack the
rolled edges, visible internal sphincter bers
and associated papillae and tags demonstrated
with chronicity. The majority of acute typical
anal ssures will respond to conservative man-
Crohn’s disease
Tuberculosis
Sexually transmitted infections
(e.g. HIV, Herpes, Syphilis)
Leukemia
Anal/low rectal neoplasm
Severe pruritus ani
Intersphincteric abscess
Drugs (i.e. Nicorandil)
agement, which should be utilized as rst line
therapy (refer to section L in algorithm).
F. A chronic anal ssure is dened as a ssure
that has been present for longer than 6weeks.
A 2012 Cochrane review demonstrated only
one-third of patients with chronic ssures
healed without medical or surgical interven-
10 Anal Conditions: Anal Fissure/Recurrent Anal Fissure
83
tion. Medical therapy was effective for nearly
half of patients; however, late recurrences
were common (50%). Surgery may be necessary for chronic ssures refractory to medical
therapies (refer to section M in algorithm).
G. Trauma from large, hard stool or anal pene-
tration may lead to the onset of a ssure. The
anorectal angle puts the posterior midline
anoderm under the highest tensile stress,
which may explain the frequency of ssuring
in this location.
H. Manometry has revealed elevated internal
sphincter pressures in patients with ssures.
While some experts believe sphincter hypertonicity contributes to the formation of a ssure by aggravating the pre-existing relative
ischemia, others argue sphincter hypertonicity is triggered in response to a ssure. Both
topical and injectable medical therapies target sphincter hypertonicity and local tissue
blood ow and perfusion (refer to sections
K and L in algorithm).
Fig. 10.3 Treatment
scheme
Fiber in diet Fiber supplement Hydration
Dietary and Conservative Management
I. Arteriography and laser Doppler owmetry
have demonstrated relative ischemia of the
posterior midline anal canal.
J. The goals of treatment are to resolve pain,
heal the ssure, maintain continence, and minimize recurrence. A 2012 Cochrane Review
recommended conservative management with
long-term dietary modications as rst line
therapy. Ideally, the patient should have soft,
well-formed, easily passable bowel movements. To this end, we recommend a high ber
diet (i.e. fresh fruit, vegetables, bran, whole
grains) with additional ber supplements (e.g.
psyllium, Metamucil®, Konsyl, Beneber®)
and adequate hydration (i.e. 8–10 glasses of
water daily with avoidance of caffeine and
alcohol.). A goal of 20–30g of soluble ber is
recommended. Stool softeners may be used
short-term during the acute convalescence.
Please refer to our treatment scheme
(Fig. 10.3) and summary of treatment comparison trials (Table10.1).
Control Constipation/Diarrhea
Endoscopy for suspected colitis
Reduce Sphincter Tone/Spasms
Sitz baths
Topical Drugs
Nitroglycerin/Rectiv Nifedipine Diltiazem (preferred)
Refractory
Botox Chemical Sphincterotomy
Surgery
Lateral Internal Sphincterotomy Advancement flap