Download Chapter 96 - Disorders of the Anorectum

CHAPTER 96 Disorders of the
Anorectum
Wendy C.Coates
PERSPECTIVE
Patients visit the emergency department (ED) with a variety of
anorectal complaints. Such problems may be self-limited or may
signify the presence of an underlying medical condition. A high
degree of sensitivity and a professional demeanor should be maintained in interactions with these patients, who may find it difficult
to discuss historical details openly and to describe physical complaints related to this area of the body and its function.
PRINCIPLES OF DISEASE
The anorectum marks the end of the alimentary canal. From its
beginning at the rectosigmoid junction at the level of the third
sacral vertebra (S3), the rectum follows the sacral curvature for 12
to 15 cm and then sharply turns posteriorly and inferiorly at the
puborectalis muscle (Fig. 96-1). Here the anal canal begins its
4-cm course to the anal verge, the orifice whereby stool exits the
body. It is supported by three muscle groups, the levator ani and
the internal and external anal sphincters. Anal valves are located
2 cm proximal to the anal verge at the dentate line. Above the
valves are the anal crypts, which contain mucous glands to provide
lubrication during defecation. These constitute a nidus for abscess
formation, if occluded. Proximal to the crypts are the columns of
Morgagni, where the epithelium of the anal canal changes from
pink columnar (as in the rectum) to squamous.1
The superior, middle, and inferior hemorrhoidal arteries
provide the blood supply to the anorectum. They arise from the
inferior mesenteric, internal iliac, and internal pudendal arteries,
respectively. The superior hemorrhoidal veins drain into the
portal system, and the inferior hemorrhoidal veins drain into the
caval system. Lymphatic drainage is to the inferior mesenteric
nodes above the dentate line and to the inguinal nodes from all
areas of the anorectum.1
Sympathetic and parasympathetic nervous systems function
together to retain the contents of the rectum until evacuation is
desired. Continence is maintained when sympathetic fibers from
L1 to L3 (upper rectum) and presacral nerves (lower rectum)
inhibit contraction of rectal smooth muscle and L5 fibers cause
the internal sphincter to contract. Elimination occurs when parasympathetic fibers from the anterior roots of S2 to S4 cause the
rectal wall to contract and the internal sphincter to relax. Voluntary external sphincter control is mediated by motor branches of
the pudendal nerve (S2, S3) and the perineal branch of S4. The
levator ani is supplied by the pudendal nerve and pelvic branches
of S3 to S4 fibers. Sensory perception of rectal distention involves
a signal pathway from extramural receptors to parasympathetic
fibers from S2 to S4. The abundant sensory nerve endings of the
1276
distal anal epithelium perceive sensations that are transmitted by
the pudendal nerve.1
Defecation begins as the rectum becomes distended, the internal sphincter relaxes, and stool enters the anal canal. At an appropriate time and place, the external sphincter is relaxed to complete
the process of elimination. Sometimes voluntary straining is
needed to assist in the passage of stool. When the Valsalva maneuver is performed, the abdominal muscles contract, the rectal angle
straightens, and the pelvic floor descends. To postpone defecation,
the external sphincter contracts voluntarily. This contraction
relaxes the rectal wall and quells the urge to defecate unless there
is an underlying sphincter disorder or an overwhelming volume
of stool.1
CLINICAL FEATURES
History
A complete history of anorectal and gastrointestinal (GI) symptoms and the presence of systemic disease elucidate the diagnosis
of most anorectal disorders (Box 96-1; Fig. 96-2). Common complaints include bleeding, swelling, pain, itching, and discharge.
Standard historical questions about time and circumstances of
onset, duration, quality, and exposure to radiation should be
asked. Alterations in bowel habits should be noted. These include
changes in color, frequency, or consistency of the stool and the
presence of straining, flatus, and incontinence of solid or liquid
stool. Persons with underlying GI disorders (e.g., Crohn’s disease,
cancer, polyps) are predisposed to atypical presentations of anorectal problems. Similarly, those with underlying systemic diseases
such as acquired immunodeficiency syndrome (AIDS), cancer,
diabetes mellitus, and coagulopathy are prone to develop more
serious complications of standard anorectal conditions. Finally,
patients should be asked directly about sexual practices involving
the anus.2
Rectal Bleeding
The color, amount, and relationship to defecation are important
factors in establishing the cause of rectal bleeding. Approximately
10 to 20% of the population experiences rectal bleeding at some
time.3 Pain and bright red blood signify anal fissures or hemorrhoids. Fissure pain is sharp, sudden in onset, and not associated
with swelling, whereas pain from a prolapsed or thrombosed hemorrhoid is gnawing, continuous, and of more gradual onset. Painless rectal bleeding occurs with internal hemorrhoids, cancer, or
precancerous lesions.
Chapter 96 / Disorders of the Anorectum 1277
whereas melena indicates a very proximal source. Bloody mucus
is associated with cancer, inflammatory bowel disease, and
proctitis.3
Rectosigmoid
junction
S3
Middle valve of
Houston (level
of peritoneal
reflection)
Levator ani
muscle
Puborectalis
muscle
Anorectal
junction
Columns of
Morgagni
External anal
sphincter
Dentate line
Internal anal
sphincter
Patients who report a swelling near the anus or have the sensation
of rectal fullness often list hemorrhoids as their chief complaint.
Painful swellings that bleed usually are thrombosed hemorrhoids,
but other painful lesions such as abscesses, pilonidal disease, and
hidradenitis suppurativa must be considered. Painless, itchy swellings may be caused by condylomata acuminata or secondary
syphilis. A mass protruding through the anal orifice may signal
rectal prolapse. Perianal and rectal carcinoma should be considered in older persons and those with long-standing anorectal
complaints.2
Pain and Itching
Severe, episodic anorectal pain that is not associated with bleeding
or swelling may represent proctalgia fugax or levator ani syndrome. Perianal itching (pruritus ani) is caused by any lesion that
makes hygiene difficult to maintain or may be attributed to certain
foods or medications.
Physical Examination
Anal verge
Figure 96-1. Anorectal anatomy.
BOX 96-1
Swelling and Masses
Medical History in Diagnosis
of Anorectal Disorders
Anorectal History
Pain
Bleeding
Swelling
Itching
Discharge
Urgency
Gastrointestinal History
Change in bowel habits (straining, flatus, color, consistency,
frequency)
Nausea or vomiting
Incontinence of stool
Underlying GI disease (Crohn’s disease, cancer, polyps)
Systemic Disease History
Diabetes mellitus
Coagulopathy
Cancer
HIV infection
Sexual History of the Anus
Penetration
Known STDs
Assault
GI, gastrointestinal; HIV, human immunodeficiency virus; STD, sexually transmitted
disease.
The physical examination should take place in private, with the
patient’s modesty respected. The patient can then relax the external sphincter to facilitate a complete examination. The patient is
placed in the left lateral decubitus position and covered with
a sheet. The buttocks are inspected for dermatologic manifestations of disease and then gently spread apart to expose the anal
orifice. Elements of personal hygiene are noted, in addition to
anatomic disruptions such as fissures, skin tags, lesions, protruding hemorrhoids, or abscesses. The patient is asked to strain; the
integrity of the pelvic floor is assessed, and prolapse of hemorrhoids or rectal mucosa is noted. Next, a well-lubricated gloved
finger is placed flat against the anal opening, exerting gentle pressure until the external sphincter relaxes and allows the finger to
enter the anus. Anal sphincter tone can be assessed by asking the
patient to squeeze the anal muscles against the examining finger.
By sweeping the finger in a circumferential manner, accessible
areas of the anorectum can be examined for masses and areas of
tenderness. The cervix or prostate is palpated through the rectal
wall. A bidigital examination reveals masses and tender areas at
the distal portion of the anal canal and perineum. On withdrawal,
the contents on the glove can be assessed for frank or occult blood,
mucus, or pus.
Direct visualization can be accomplished by anoscopy. With the
patient positioned as described, the lubricated anoscope is inserted
into the anus with the obturator in place. The obturator is removed
to allow a circumferential view of the rectal mucosa. Attention is
directed to sites of bleeding, hemorrhoids, masses, or abnormal
tissue and finally the dentate line and anal epithelium.
SPECIFIC ANORECTAL PROBLEMS
Hemorrhoids
The relationship of bleeding to defecation is important. Visible
blood on the toilet paper usually is caused by anal fissures or
external hemorrhoids; however, minute quantities can result from
any irritating condition. Bright red blood that drips into the toilet
bowl or streaks around the stool is caused by internal hemorrhoids. Blood mixed with stool originates proximal to the rectum,
Perspective
When the Philistines defeated the Israelites, the book of I Samuel
reports the fate of the avengers: “A deadly panic had seized the
whole city, since the hand of God had been very heavy upon it.
Those who escaped death were afflicted with hemorrhoids, and
the outcry from the city went up to the heavens.”4 In 1815 the
1278 PART III ◆ Medicine and Surgery / Section Five • Gastrointestinal System
Pain?
Yes
No
Bleeding?
Bleeding?
Yes
No
Swelling?
Yes
No
Yes
No
Swelling?
Yes
Swelling?
No
Yes
No
Itch?
Itch?
Yes
Yes
Episodic
pain?
Yes
Hemorrhoids
Anal
fissure
Abscess
Pilonidal cyst
Hidradenitis
Proctalgia
fugax
No
D/C?
Urgency?
Yes
No
Yes
Incontinence
Polyps
Adenoma
Hemorrhoids
Condylomata
acuminata
Procidentia
Proctitis
Pruritus
ani
Figure 96-2. Algorithm for anorectal complaints. D/C, discharge.
battle of Waterloo marked the defeat of Napoleon’s army. Speculation purports that the great leader suffered from hemorrhoids at
the time of his defeat.5 Hemorrhoidal disease continues to afflict
modern humans, with a 5% incidence in the U.S. population. Both
sexes are affected, and an increased frequency has been documented among whites, rural dwellers, and those of high socioeconomic status.6
Principles of Disease
Hemorrhoids occur when the anal vascular cushions become
engorged. Rather than forming a continuous ring around the
anal canal, the submucosa forms three distinct cushions of tissue
that are richly supplied with small blood vessels and muscle
fibers. Blood supply to these cushions is from the superior
rectal artery, with some contribution from the middle and inferior
hemorrhoidal arteries, which explains why hemorrhoidal bleeding
is bright red. The muscularis submucosa cushions the anal
canal during defecation to prevent injury and to aid in fecal
continence.7
As the supportive tissue deteriorates, often starting in the third
decade of life, venous distention, prolapse, bleeding, and thrombosis may occur. Some controversy exists about whether straining
and constipation cause these changes by producing venous backflow when intra-abdominal pressure increases.7,8 In pregnant
women, direct pressure on a hemorrhoidal vein can produce
symptomatic hemorrhoids. Up to one third of pregnant women
experience hemorrhoids in the last trimester of pregnancy or the
postpartum period. An increased incidence of thrombosed hemorrhoids is associated with traumatic deliveries.9,10 Some familial
predisposition is recognized, but whether this is a result of genetics
or acquired factors such as diet is unknown.
Hemorrhoids are not varicose veins; they are normal structures
that manifest symptoms when the muscularis submucosa weakens
and the anal cushions are displaced distally.7 Conditions that
increase sphincter tone correlate with a higher prevalence of hemorrhoids.8 Portal hypertension does not cause hemorrhoids in
adults. The incidence of symptomatic hemorrhoids is similar in
patients with and in those without portal hypertension. Rectal
bleeding in patients with portal hypertension may be caused by
rectal varices, which are vascular communications between the
superior and middle hemorrhoidal veins.6,11 A major exception
to this observation occurs in the pediatric population; children
with portal hypertension are susceptible to hemorrhoidal
exacerbations.12,13
Clinical Features
A careful history is needed to confirm the presence of hemorrhoids because many patients use this term to refer to any perianal
condition. Bleeding with defecation is the most common complaint, and unless the hemorrhoids are thrombosed, it usually is
painless. Patients report variable amounts of bright red blood on
the toilet paper or in the toilet bowl. Many complain of swelling,
itching, mucoid discharge, or simply the presence of a moist perianal area. Further history should address recent stool patterns,
such as diarrhea or constipation; chronic medical problems, such
as portal hypertension or bleeding disorders; and a dietary and
family history.
Frequent bowel movements, prolonged sitting, heavy lifting,
and straining while defecating exacerbate hemorrhoidal symptoms. Although straining is cited as a cause of hemorrhoids, it also
may be a result of them when the patient is constipated from
delaying defecation because of fear of pain. Physical examination
should ascertain the type and degree of hemorrhoids. This can be
accomplished by a visual inspection at rest and during straining.
Nonprolapsing hemorrhoids can be visualized on anoscopy as a
focus of bleeding or as they bulge when the patient is asked to
strain while the anoscope is removed. Anoscopy is painful and not
useful in cases of prolapsed or thrombosed hemorrhoids.
Hemorrhoids are classified according to their location and
severity (Table 96-1). External hemorrhoids originate below the
dentate line and receive their blood supply from the inferior hemorrhoidal plexus. They are covered with modified squamous epithelium (anoderm) and resemble the surrounding skin. Two
syndromes are common. First, the veins beneath the skin of
the hemorrhoid become dilated and the surrounding subcutaneous tissue becomes engorged, causing swelling or pressure after
Chapter 96 / Disorders of the Anorectum 1279
A
B
Figure 96-3. Thrombosed hemorrhoids. A, External. B, Internal. Note the engorged external hemorrhoids surrounding the thrombosed internal
hemorrhoids. (A, Courtesy Michelle Lin, MD, Harbor-UCLA Medical Center; B, courtesy Gershon Effron, MD, Sinai Hospital of Baltimore. From
Seidel HM, et al: Mosby’s Guide to Physical Examination, 4th ed. St Louis, Mosby, 1999.)
Table 96-1
BOX 96-2
Types of Hemorrhoids
TYPE
ORIGIN
EPITHELIUM
External
Inferior hemorrhoidal plexus
Proximal to dentate line
Modified squamous
epithelium (anoderm)
Internal
Superior hemorrhoidal plexus
Distal to dentate line
Transitional or columnar
epithelium (mucosa)
Mixed
Superior and inferior
hemorrhoidal plexus
Transitional, columnar,
or modified squamous
epithelium (mucosa and
anoderm)
The WASH Regimen for Management
of Hemorrhoids
Warm water
Analgesic agents
Stool softeners
High-fiber diet
these lesions do not cause pain. Second-degree internal hemorrhoids temporarily prolapse outside the anal canal during defecation but spontaneously return to their normal position at the end
of the bowel movement. Both first- and second-degree hemorrhoids are amenable to medical management. Third-degree internal hemorrhoids prolapse spontaneously or during defecation and
remain outside the body until they are manually replaced into
the anal canal. A throbbing, pressure-like pain may accompany
bleeding and subsides when the hemorrhoids are reduced. Fourthdegree internal hemorrhoids cannot be reduced and are permanently prolapsed. Continued prolapse leads to the formation of a
thrombus with possible progression to gangrene. Definitive treatment for the intense pain and thrombosis is surgical.8,14
Table 96-2
Classification of Internal Hemorrhoids
by Severity
TYPE
PROLAPSE
MODE OF
REDUCTION
First degree
None
N/A
Medical
management
Second
degree
During defecation
Spontaneous
Medical
management
Management
Third degree
May be
spontaneous
or during
defecation
Manual
Medical
management
Optional
surgical repair
Fourth degree
Permanent
Irreducible
Surgical repair
The symptoms of nonthrombosed external and nonprolapsing
internal hemorrhoids can be ameliorated by the standard
regimen—warm water, analgesics, stool softeners, and high-fiber
diet (WASH)—aimed at combating the problems that led to
the hemorrhoids’ formation (Box 96-2). Anal canal pressures
decrease in warm water (40° C). Patients can direct a shower
stream at the area for several minutes or take sitz baths. Mild oral
analgesic agents reduce the pain. Several over-the-counter preparations are available for the treatment of hemorrhoidal symptoms;
however, their use is directed at improved hygiene and temporary
symptom relief rather than correction of the condition.15 The use
of topical anesthetics, corticosteroids, astringents (e.g., witch
hazel), mineral oils, and cocoa butter is controversial. Prolonged
use of topical corticosteroids produces atrophic skin changes and
is discouraged.7 Stool softeners can make the passage of stool
easier, to prevent straining. A high-fiber diet (consumption of
20 to 30 g of dietary fiber per day) produces stool that is passed
more easily.16
Patients with second- or third-degree internal hemorrhoids also
benefit from this regimen; however, permanent resolution of their
symptoms may require surgical intervention (Table 96-3). These
patients can be discharged from the ED with the WASH regimen
and referred to a surgeon for banding, sclerotherapy, or elective
TREATMENT
N/A, not applicable.
defecation. Painless, bright red bleeding may occur. Second, the
veins can become thrombosed as clots form within them (Fig.
96-3A). This produces acute pain and tenderness to palpation. A
bluish discoloration often is noted.
Internal hemorrhoids originate above the dentate line and
receive their blood supply from the superior hemorrhoidal plexus
(Fig. 96-3B). They are covered with a mucosal surface consisting
of transitional or columnar epithelium that looks very different
from the surrounding anoderm. They are classified according to
severity (Table 96-2). Symptoms and signs range from mild, painless bleeding with defecation to irreducible prolapse with unremitting and debilitating pain. First-degree internal hemorrhoids
protrude into the lumen of the anal canal, causing a feeling of
fullness. Because the mucosal wall lacks sensory nerve endings,
1280 PART III ◆ Medicine and Surgery / Section Five • Gastrointestinal System
Anesthetic
Elliptical
incision
A
Remove
clot
B
C
Figure 96-4. Excision of thrombosed external hemorrhoid. A, Field
block with local anesthetic. B, An elliptical incision is made around the
hemorrhoid. C, The thrombosed hemorrhoid is removed. (From Larson
S, et al [eds]: Atlas of Emergency Procedures. St Louis, Mosby, 2001.)
Figure 96-5. Lateral anal fissure. (Courtesy Gershon Effron, MD, Sinai
Hospital of Baltimore. From Seidel HM, et al: Mosby’s Guide to Physical
Examination, 4th ed. St Louis, Mosby, 1999.)
Anal Fissures
Principles of Disease
Table 96-3
Surgical Management of Hemorrhoids
CLASSIFICATION
MANAGEMENT
Thrombosed external hemorrhoids
Excision in emergency department
Second- and third-degree internal
hemorrhoids
Elective surgical repair
Banding
Sclerotherapy
Hemorrhoidectomy
Fourth-degree hemorrhoids
(nonthrombosed)
Nonemergent hemorrhoidectomy
Thrombosed or gangrenous
fourth-degree internal
hemorrhoids
Emergent hemorrhoidectomy
hemorrhoidectomy. Patients with acute, gangrenous, thrombosed
fourth-degree internal hemorrhoids should be referred for emergent hemorrhoidectomy.
Acutely thrombosed external hemorrhoids can be excised (not
incised and drained) in the ED to provide prompt relief within
the first 48 hours after the onset of symptoms (Fig. 96-4). Incision
results in incomplete evacuation of the clot, subsequent rebleeding, swelling, and the formation of a skin tag.8,17 If not excised, the
thrombosed external hemorrhoid resolves spontaneously after
several days when it ulcerates and leaks the dark accumulated
blood, with relief of associated symptoms. Residual skin tags may
persist, making anal hygiene more challenging. In the ED setting,
this procedure is not commonly performed in pediatric patients,
pregnant women, or immunocompromised patients.
Nonsurgical therapy with topical nifedipine (0.3%) and lidocaine (1.5%) gel has been shown to alleviate symptoms when
applied twice daily for 2 weeks. The purported effectiveness of this
regimen for treatment of thrombosed hemorrhoids is related to
the ability of nifedipine to modulate resting sphincter tone and
thereby reduce the associated pain and inflammation. However,
this regimen is not widely used.18
The development of an anal fissure is the most common cause of
intensely painful rectal bleeding of sudden onset. A superficial tear
in the anoderm results when a hard piece of feces is forced through
the anus, usually in patients who are constipated. Although anyone
can experience an anal fissure, it is most common in the 30- to
50-year age bracket.19 It is the most commonly encountered anorectal problem in pediatric patients, especially infants.20,21 Males
and females are affected equally. Most fissures occur along the
posterior midline, where the skeletal muscle fibers that encircle the
anus are weakest. Anterior midline fissures are more common in
women than in men. Fissures that occur elsewhere are more likely
to be associated with systemic disease such as leukemia, Crohn’s
disease, human immunodeficiency virus (HIV) infection, tuberculosis (TB), or syphilis.19 Fissures not treated promptly may
become chronic, with development of a classical “fissure triad” of
deep ulcer, sentinel pile, and enlarged anal papillae (Fig. 96-5). A
sentinel pile forms when the skin at the base of the fissure becomes
edematous and hypertrophic. A resolving sentinel pile can form a
permanent skin tag and may be associated with a fistulous tract.
Clinical Features
The patient reports sudden, searing pain during defecation that
may be accompanied by a small amount of bright red blood in the
stool or on the toilet paper. This is followed by a nagging, burning
sensation that lasts for a few hours from internal sphincter spasm.
Subsequent bowel movements are excruciating, and the external
sphincter can exhibit a reflex spasm. Physical examination must
be performed cautiously to avoid further spasm and pain. The
depth of the fissure, its orientation to the midline, and the presence of a coexisting sentinel pile or edema are noted. Rectal examination during an acute exacerbation often is impossible because
of pain and sphincter spasm.19
Management
Specific measures for the treatment of anal fissures are summarized in Box 96-3. Treatment with the WASH regimen (see Box
Chapter 96 / Disorders of the Anorectum 1281
96-2) focuses on eliminating constipation with a bulking agent,
stool softener, and high-fiber diet. Warm sitz baths and limited use
of topical anesthetics may be helpful. Parental encouragement of
pediatric patients helps prevent encopresis, which can result from
a fear of painful bowel movements. Most acute, uncomplicated
fissures resolve in 2 to 4 weeks. For adult patients with chronic
anal fissures, application of various topical agents aimed at reducing sphincter pressures has been effective.22-24 Hyperbaric oxygen
has been used successfully for adjunctive therapy.25
Lidocaine ointment is effective in treating chronic anal fissures.
In addition, nitroglycerin ointment applied topically to the
anoderm two or three times daily has been shown to relieve the
pain from anal fissures. Although it was not associated with more
rapid healing, patients receiving this therapy have reported a
higher level of comfort during the healing process. The typical side
effect of a vasodilatory headache may be experienced by some
patients.26
Nifedipine gel (0.2%) in combination with lidocaine (1.5%)
applied to the anal area twice daily is effective in promoting
healing and reducing discomfort in the management of anal fissures. The mechanism of healing is thought to be the reduction
of anal canal pressures by local calcium channel blockade.27,28
When the efficacy of calcium channel blockers was compared
directly with that of topical nitrates, the rates of healing and recurrence were similar; however, the incidence of side effects was lower
in one study.29
Injection of botulinum toxin by colorectal surgeons (2.5 to 5.0
units of Botox preparation) is effective in relaxing the sphincter
tone by inhibiting acetylcholinesterase release but may cause temporary, reversible fecal incontinence.24,27,30-33 Injection into the
external (rather than internal) sphincter muscles may reduce this
undesirable side effect. It has not yet been studied as a primary
treatment in the ED or primary care setting. In comparison with
the topical treatments, botulinum toxin may provide some advantages in its rate of permanent healing34; however, the first line of
therapy is still dietary modification and the application of topical
agents because of their cost, ease of application, and benign side
effect profiles.24,33 Long-term treatment of recurrent fissures
BOX 96-3
Abscesses and Fistulae
Principles of Disease
Anorectal abscesses and fistulae occur in otherwise healthy adults
when the mucus-producing glands at the base of the anal crypts
occlude. Abscesses are a manifestation of inflammatory bowel
disease, trauma, cancer, radiation injury, and infection (TB, lymphogranuloma venereum, actinomycosis). Common causative
bacteria are Staphylococcus aureus, Escherichia coli, Streptococcus,
Proteus, and Bacteroides.35 An increased incidence in infants (85%
in male babies) has been reported to be associated with congenital
abnormalities.36
Management
General Approach. Anorectal abscess is an acute disease that naturally progresses to fistula formation in the body’s attempt to drain
the infection spontaneously. Symptoms vary depending on the site
of infection, but incision and drainage constitute the curative
treatment in all cases (Table 96-4). Delay of medical management
may allow extension of the infection and eventual compromise of
the sphincter mechanism.37 Adjunctive antimicrobial therapy is
indicated in patients who are immunocompromised or diabetic
or have valvular heart disease. Tetanus immunization status should
be verified. The sites of anorectal abscess formation are depicted
in Figure 96-6. The difficulty in diagnosis is that pain often precedes physical findings of a mass or fluctuance. Approximately
34% of patients with AIDS develop anorectal abscesses and fistulae, which may include opportunistic organisms in addition to the
usual ones. HIV-infected patients appear to be more likely than
their seronegative cohorts to have an incomplete fistulous tract.
This condition prevents adequate spontaneous drainage, highlighting the urgency of treating these patients promptly. A small
incision is desirable, when possible, because wound healing in
general may be impaired.
Treatment of Specific Abscesses
Treatment of Anal Fissures
Perirectal and Perianal Abscesses. Perirectal and perianal abscesses
are the most common (40-45%) and produce painful swelling at
the anal verge that is worsened by defecating or sitting. Most
patients are afebrile. Physical examination reveals localized tenderness, erythema, swelling, and fluctuance. ED management by
incision and drainage with same-day discharge is possible in
patients who do not have comorbidity (e.g., diabetes mellitus,
extremes of age, compromised immune status). Some patients
• WASH regimen*
• Nitroglycerin ointment (0.4%) bid or tid
• Nifedipine gel (0.2%) bid with lidocaine (1.5%)
• Botulinum toxin (surgical consultation)
• Anal dilation performed with the patient under general
anesthesia
• Surgical excision
*See Box 96-2.
Table 96-4
focuses on reducing resting anal pressures and may require anal
dilation performed with the patient under anesthesia or surgical
correction to reduce the tone of the internal sphincter.19
Types of Abscesses of the Anorectum
FEATURE
PERIANAL
ISCHIORECTAL
INTERSPHINCTERIC
SUPRALEVATOR
POSTANAL
Incidence
40-45%
20-25%
20-25%
<5%
5-10%
Location
Outside and verge
Buttocks
Lower rectum
Above levator ani
Deep to external sphincter
Symptoms
Painful perianal mass
Buttock pain
Rectal fullness
Perianal and buttock pain
Rectal fullness
Pain near coccyx
Fever, ↑ WBCs
−
±
±
+
+
Associated fistula
++
+
+++
+++
−
ED incision and drainage
+
±
−
−
−
ED, emergency department; WBCs, white blood cells; −, does not occur; ±, occurs sometimes; ++, occurs often; +++, usually occurs.
1282 PART III ◆ Medicine and Surgery / Section Five • Gastrointestinal System
Supralevator
abscess
Intersphincteric
abscess
Ischiorectal
abscess
Perianal
abscess
Figure 96-6. Location of common anorectal abscesses. (Adapted from Gordon PH, Nivatvonghs S: Principles and Practice of Surgery for the
Colon, Rectum, and Anus. St Louis, Quality Medical Publishing, 1992.)
may be unable to tolerate the procedure without general or
regional anesthesia. The WASH regimen (see Box 96-2) may
alleviate postprocedure discomfort. Antibiotics are unnecessary
in healthy adult patients except in cases involving associated
cellulitis.38,39
Ischiorectal Abscess. Approximately 20 to 25% of abscesses form
outside the sphincter muscles in the buttocks, and patients report
severe pain. The diagnosis is obvious if an indurated mass is seen
on the buttocks but is more difficult if the abscess is deep. Patients
often have fever and leukocytosis. If there is no induration, a
needle aspirate can confirm the presence of pus. Although many
of these abscesses will require drainage performed with the patient
under general anesthesia, superficial abscesses can be treated in
the ED as for perianal abscess. If the patient is febrile, a short
course of antibiotics, such as cephalexin, may be considered,
beginning with a parenteral dose before drainage, followed by 3
to 7 days of an oral agent.39,40
Intersphincteric Abscess. One fourth of abscesses form in the
space deep to the external sphincter and inferior to the levator ani.
The infection tracks cephalad and may appear to be a mass in the
rectum and can be confused with a thrombosed internal hemorrhoid. Patients report continuous rectal pressure and a throbbing
pain exacerbated by defecation or sitting. They may have fever and
leukocytosis. External evidence of inflammation may be lacking,
but rectal examination reveals an erythematous, indurated, sometimes draining mass. Associated fistulae and inguinal lymphadenopathy are common. Drainage in the operating room is required
so that the entire abscess and fistula network can be evaluated
and treated.35
Supralevator Abscess. Accounting for less than 5% of abscesses,
supralevator abscesses cause perianal and buttock pain associated
with fever and leukocytosis. External evidence of this disease
usually is absent, which often delays the diagnosis. Approximately
23% of patients with this condition are obese or have diabetes
mellitus, and others have concurrent disorders such as Crohn’s
disease, pelvic inflammatory disease, or diverticulitis. A tender
mass may be palpated on rectal or pelvic examination. Emergent
surgical treatment is indicated to drain the abscess and excise the
fistulous network.35,39
Postanal Abscess. Postanal abscesses are uncommon and
occur posterior to the rectum, deep to the external sphincter, and
inferior to the levator ani. Patients experience severe rectal discomfort and coccygeal pain. They usually are febrile and have
continuous pain that does not change with position. Rectal examination is painful, but anal drainage is rare. Many of these abscesses
are missed on initial presentation, and the patient may be misdiagnosed as having lumbosacral strain, proctalgia fugax, sciatica, or
coccygodynia. Patients often return in a few days with an abscess
draining at the skin. Treatment is surgical.
Horseshoe Abscess. Occasionally a large, communicating,
horseshoe-shaped abscess forms in the ischiorectal, intersphincteric, or supralevator space. Surgical management is necessary.
Necrotizing Infection. A delay in management of an anorectal
abscess may lead to the destruction of tissue, especially in diabetic
or immunocompromised patients. Widespread cellulitis, necrotic
tissue, and gas on radiography suggest the possibility of nec­
rotizing fasciitis, Fournier’s gangrene, or tetanus. Wide surgical
débridement, broad-spectrum antibiotics with anaerobic coverage, and tetanus prophylaxis are required.
Treatment of Fistulae
A fistula (Latin for “pipe”) is a connection between two epitheliumlined surfaces. Anorectal fistulae develop in 50 to 67% of patients
with ischiorectal abscesses.37 Other causes include Crohn’s disease,
trauma, foreign body reactions, TB, and cancer. Evidence to
support these diagnoses should be sought because the anorectal
complaint may be the presenting symptom of the underlying
disease. Patients notice a recurrent or persistent perianal discharge
that becomes painful when one of the openings becomes occluded.
Bidigital rectal examination may reveal a tract in the perineum or
canal. Probing of fistulous tracts is not recommended because the
danger of creating a new tract outweighs the benefit of identifying
the path of the existing fistula. Spontaneous resolution of fistula
in ano is rare. Although symptoms resolve when antibiotics are
administered (e.g., ciprofloxacin, metronidazole), they commonly
return as soon as therapy is discontinued. Increasingly, definitive
treatment of the fistulous network at the time of incision and
drainage of the abscess is advocated to prevent ongoing progression of the disease continuum. Fistulectomy and application of
fibrin glue are commonly accepted practices of colorectal surgeons.35,39,40,41 Nonsurgical treatments that have been proposed for
some patients, especially those with Crohn’s disease, are administration of infliximab, a monoclonal antibody, or cyclosporine and
hyperbaric oxygen therapy.37
Chapter 96 / Disorders of the Anorectum 1283
Pilonidal Disease
Principles of Disease
Little nests of hair in the sacrococcygeal area were first described
in 1847 by Anderson (Latin pilus, “hair”; nidus, “nest”), who originally believed the lesions to be scrofula.42 More than 150 years
later, physicians have yet to agree on the cause and best mode of
treatment. Pilonidal abscesses and subsequent sinus tracts afflict
young adults with a 4 : 1 male predominance and are more
common in obese and hirsute persons. The disease is rare in
people older than 40 years, even among those who were affected
in their youth. The lesions arise in the midline of the sacrococcygeal area in the natal cleft and should not be confused with anal
fistulae, perirectal abscesses, hidradenitis suppurativa, or granulomatous diseases (syphilis, TB).43 Much of the current understanding of pilonidal disease comes from the experience in World War
II, when the condition was rampant among jeep drivers and was
therefore dubbed “jeep-driver’s disease.”43,44
The debate between congenital predisposition and acquired
disease seems to favor the latter.44-46 This theory asserts that bacteria enter the usually sterile hair follicle and produce inflammation and edema, thereby occluding the opening to the skin surface.
The contents expand until the hair follicle ruptures, and the material spreads into the subcutaneous fatty tissue, where a foreign
body reaction leads to abscess formation. The purulent material
subsequently tracks cephalad and drains to the skin through a
laterally displaced, epithelialized tract. Diagnosis is made by establishing the presence of a painful, fluctuant area in the presacral
skin. In chronic or recurrent disease, visible or palpable tracts 2 to
5 cm in length may be identified with openings approximately
5 cm above the anus. These sinuses usually contain hairs and cellular debris.43,44
are common. Treatment begins with careful attention to perianal
hygiene, warm compresses, and broad-spectrum antibiotics.
Recently, infliximab has been found to be effective, resulting in
rapid clinical improvement.49 Drainage of isolated lesions may
provide symptomatic relief, but the recurrence rate approaches
40%. Referral to a surgeon for wide excision of tissue involved in
advanced chronic disease may be necessary.50-52
Proctalgia
Perspective
Anorectal pain (proctalgia) that does not arise from one of the
organic disorders described earlier can be severe and difficult
to treat.53,54 The two most common causes are levator ani syndrome and proctalgia fugax. These disorders can be distinguished
by their patterns of affliction. Other causes of pelvic pain, such as
tumors, cauda equina syndrome, and endometriosis, must be
considered.55
Levator Ani Syndrome
A constant, dull pressure in the sacrococcygeal region that is precipitated by defecation or prolonged periods of sitting suggests
levator ani syndrome. The patient usually has tenderness of the
levator muscles, which may be firmly contracted on examination.
It affects both men and women. No standard treatment regimen
has been studied, but anecdotal reports indicate that sitz baths,
levator ani muscle massage, and muscle relaxants can provide
some relief.53,54
Proctalgia Fugax
Treatment options vary, ranging from conservative therapy to
extensive surgical excision.43,44,47 Antibiotics can supplement incision and drainage in cases accompanied by cellulitis but are not
effective as the primary mode of treatment. ED management of
pilonidal disease involves drainage of the acute abscess for relief
of symptoms. To prevent reaccumulation of debris and to minimize inflammation in the midline, a longitudinal incision lateral
to the sacral midline should be made. To decrease the usual 40%
recurrence rate, the patient can be referred for follicle removal and
unroofing of sinus tracts after the acute inflammation subsides
(usually 1 week). An alternate noninvasive strategy of shaving the
hairs in the natal cleft every 3 weeks has been reported. For patients
whose disease is recalcitrant, unroofing and marsupialization or
wide excision techniques are used.47
Proctalgia fugax is an intensely painful spasm in the rectal area
that begins abruptly and lasts for several minutes. It is attributed
to a sudden spasm of the levator muscle complex or the sigmoid
colon. People who frequently visit the toilet are at greatest risk,
and women are more commonly affected than men. A psychogenic predisposition is described by Pilling and colleagues, who
found that professionals, managers, and perfectionists are more
likely to be affected.56
Proctalgia fugax can begin abruptly during sleep, defecation,
urination, or intercourse. The nature of the pain has been compared to a “charley horse.” It lasts less than 30 minutes and may
radiate to the coccyx or perineum. Symptoms during recurrent
episodes are consistent for the affected person, and each patient
has a unique constellation of symptoms.53 Treatment often is
unrewarding, but recommendations include bowel cleansing
regimens, upward manual pressure on the anus, diazepam, and
topical nitrates.54
Hidradenitis Suppurativa
Fecal Incontinence
Perianal hidradenitis suppurativa is an infection of the apocrine
glands. It is most common in young adults and is related to poor
skin hygiene, hyperhidrosis, obesity, acne, diabetes mellitus, and
smoking. The condition commonly is misdiagnosed as pilonidal
disease or fistula in ano. Other considerations in the differential
diagnosis include sebaceous cysts, furuncles, granulomas (from
TB or syphilis), and Crohn’s disease. Occluded apocrine ducts may
be infected with strains of Staphylococcus, Streptococcus, E. coli, or
Proteus. Extension through the dermis spreads the infection to
neighboring ducts, and a network of sinus tracts forms. This cycle
leads to extensive scarring.46,48
Patients report one or more tender, draining pustules in the
perianal area, which may be associated with fever, leukocytosis,
and malaise. Local lymphadenopathy and surrounding cellulitis
Perspective
Management
Fecal incontinence is an embarrassing condition that affects
parous women, elderly persons, and patients with a variety of
neurologic or traumatic disorders. The delicate balance among the
pelvic floor muscles, sphincters, and anorectal sensation is disrupted in this condition. Complete incontinence is the inability to
control passage of solid feces. Partial incontinence is characterized
by loss of control of the passage of flatus or liquid feces.
Principles of Disease
Multiple causes of fecal incontinence have been described (Box
96-4).53,57,58 Injury to muscles and nerves may result from
1284 PART III ◆ Medicine and Surgery / Section Five • Gastrointestinal System
BOX 96-4
Causes of Fecal Incontinence
Traumatic Causes
Iatrogenic (surgical) nerve injury
Spinal cord injury
Obstetric trauma
Sphincter injury
Neurologic Causes
Spinal cord lesions
Dementia
Autonomic neuropathy (e.g., diabetes mellitus)
Obstetric: pudendal nerve damage from stretching during
surgery, Hirschsprung’s disease
Mass Effect
Carcinoma of anal canal
Carcinoma of rectum
Foreign body
Fecal impaction
Hemorrhoids
Medical Causes
Procidentia
Inflammatory disease
Diarrhea
Laxative abuse
Pediatric Patients
Congenital
Meningocele
Myelomeningocele
Spina bifida
After corrective surgery for imperforate anus
Sexual abuse
Encopresis
accidental trauma or surgery for anorectal disorders. Similarly,
injury or stretching during childbirth can cause immediate or
delayed problems. Spinal cord and cauda equina lesions and the
autonomic neuropathy of diabetes mellitus can cause progressive
incontinence. Liquid feces may seep around tumors or foreign
bodies of the rectum or anal canal. A common “foreign body” is
a large impacted stool, as seen in elderly patients or those with
underlying megacolon. Explosive diarrhea from laxative abuse,
inflammation, or infection can temporarily overwhelm a normal
sphincter mechanism. Partial incontinence after surgery to correct
imperforate anus is common.59 Incontinence is a common feature
of congenital neurologic conditions such as meningocele, myelomeningocele, and spina bifida. Encopresis also may develop in
young children (4 to 7 years) experiencing emotional stress.60 In
otherwise healthy children, sexual abuse involving the anus must
be considered.61
Clinical Features
The physical examination should address the local and systemic
factors described previously. The anorectum should be assessed
for masses, hemorrhoids, evidence of previous surgery, and neuromuscular function. The anocutaneous reflex, or “anal wink,” is
elicited by touching the skin near the anus with a pin and observing the resulting constriction. Sphincter function is assessed by
asking the patient to “squeeze” the examiner’s finger.
Management
The approach to management of fecal incontinence depends on
the cause. Structural and inflammatory conditions may be diagnosed with anoscopy. In cases of transient incontinence caused by
BOX 96-5
Causes of Pruritus Ani
Dermatitis
Fecal Irritation
Poor hygiene
Anorectal conditions: fissure, fistula, hemorrhoids, skin tags,
perianal clefts
Systemic: caffeine, tea, beer, spicy foods, citrus fruits, quinidine,
intravenous hydrocortisone, colchicine, tetracycline
Contact Dermatitis
Anesthetic agents, topical corticosteroids, perfumed soap
Systemic Diseases
Dermatologic
Psoriasis, seborrhea
Lichen simplex or lichen sclerosus
Nondermatologic
Chronic renal failure, myxedema, diabetes mellitus,
thyrotoxicosis, polycythemia vera
Vitamin A or D deficiency, iron deficiency
Cancers: Bowen’s, Paget’s, Hodgkin’s diseases
Infections
STDs
Syphilis
HSV infection
HPV infection
Other Infectious Processes
Scabies
Pinworm
Bacterial infection
Fungal infection
HPV, human papillomavirus; HSV, herpes simplex virus; STD, sexually transmitted
disease.
diarrhea, a high-fiber diet along with brief therapy with loperamide or opioids has been shown to solidify stool and enhance
rectal compliance.57
Neuromuscular causes of fecal incontinence can be diagnosed
by anorectal physiologic testing. In addition to conservative
treatment measures described for transient incontinence, Kegel
exercises, biofeedback training, or surgical repair may be
necessary.57,58,62
Pruritus Ani
Principles of Disease
Patients with pruritus ani complain of an uncontrollable urge to
scratch the perianal area. Approximately 1 to 5% of the population
seeks medical attention for this condition during their lifetime.
Others rely on self-treatment to soothe less severe symptoms. The
period of peak incidence is during the fifth and sixth decades of
life, and it occurs more often in men. The condition is more
common in the summer months and is more noticeable at night.
The sensation of itching arises when the richly innervated perianal
skin becomes irritated. Patients scratch vigorously in an effort to
relieve the itching, creating a vicious circle that results in greater
irritation and excoriation. The causes of pruritus ani are summarized in Box 96-5.
The most common cause is the presence of feces on the perianal
skin. Conditions ranging from poor personal hygiene to anatomic
disorders of the anorectum allow feces to accumulate in the area.
Patients may not clean the area thoroughly after defecation. Disruptions in the anorectal anatomy can lead to uncontrollable fecal
accumulation on the perianal skin. Obesity, deep perianal clefts,
copious hair, hemorrhoids, posthemorrhoidal skin tags, rectal
Chapter 96 / Disorders of the Anorectum 1285
mucosal prolapse, anal fissures, and fistulae make the area difficult
to clean effectively. Decreased air circulation from wearing tight
pants or undergarments of synthetic “nonbreathable” fabric may
exacerbate symptoms.63
Foods (e.g., caffeine, spicy or citrus foods, tea, beer) and drugs
(e.g., quinidine, colchicine, tetracycline, intravenous hydrocortisone) augment the irritant quality of the feces by altering its pH.
Perfumed soaps and drugs, especially local anesthetic creams and
ointments, can produce a contact dermatitis. Prolonged use of
hemorrhoidal preparations containing local anesthetic and topical
corticosteroid can exacerbate the symptoms. Other dermatologic
conditions include psoriasis, seborrhea, lichen simplex, and lichen
sclerosus.
Systemic diseases and local infections can produce perianal
itching. Chronic renal failure, diabetes mellitus, thyrotoxicosis,
myxedema, polycythemia vera, deficiency of iron or vitamin A or
D, and certain cancers (Bowen’s disease, Paget’s disease, Hodgkin’s
disease) are systemic causes. Local conditions include pinworms
(Enterobius vermicularis infection), scabies (Sarcoptes scabiei infection), bacterial or fungal infections, and dermatologic manifestations of sexually transmitted diseases (STDs) (e.g., syphilis or
herpes simplex virus [HSV], cytomegalovirus, or human papillomavirus infection).
regarding transmission of STDs and the efficacy of barrier methods
is important.67-69 Semen has a concentrated viral load, and the
damaged epithelium of ulcerated anoderm makes an easy portal
for entry of the virus. Syphilis, gonorrhea, and chlamydial infection have been documented among men who have sex with men.
For this reason, routine STD screening is indicated.67 A summary
of common infections and treatment guidelines is presented in
Table 96-5.
Surgical repair for benign anorectal conditions in HIV-positive
patients should be undertaken early in the course of the disease,
when potential wound healing and overall patient health are at
their best.68 Empirical therapy is indicated for patients who have
recently practiced anal-receptive intercourse and have a rectal discharge. The recommended regimen is a single dose of ceftriaxone
250 mg intramuscularly plus doxycycline 100 mg twice a day orally
for 7 days.67 Patients with anorectal infections should be referred
for HIV testing. The possibility of sexual assault should be considered and managed appropriately.67 The health care provider
should report STDs and new diagnoses of HIV infection in accordance with state and local health department regulations.
Management
Gonorrhea
A careful history and physical examination can identify the cause
of pruritus ani. Important considerations include hygienic care of
the anus, coexisting anorectal or systemic conditions, diet, and
sexual practices.
Pinworms can be identified by applying transparent tape to the
perianal area and attaching it to a glass slide. Visualization of eggs
under the low-power objective of a microscope confirms the diagnosis. The first-line agent is mebendazole (Vermox) 100 mg orally.
An alternative agent is pyrantel pamoate (Antiminth) 1 g orally
(11 mg/kg, to a maximum of 1 g for pediatric patients). The
dose of either may need to be repeated in 2 weeks. Scabies and
pediculosis pubis should be treated with 1% lindane lotion or 5%
permethrin cream. Dermatitis caused by a fungal infection is characterized by sharply demarcated borders and is treated with
clotrimazole or nystatin cream. Definitive treatment of concomitant anorectal conditions (e.g., fissures, fistulae, hemorrhoids, skin
tags, rectal prolapse) can prevent recurrence of pruritus ani.64
Underlying systemic diseases that have perianal manifestations
should be treated. Education on personal hygiene is of the utmost
importance. Patients should be instructed to clean the area thoroughly with lukewarm water after each bowel movement and pat
(rather than rub) it dry with a tissue or towel that is free of chemical irritants. Loose-fitting underwear and exposure to fresh air
may aid in alleviating symptoms. The treatment of acute dermatitis includes a short course of topical corticosteroids,65 calamine
lotion, and systemic antihistamines. Some success with topical
application of capsaicin cream has been reported.62,66 Prevention
of recurrent bouts of pruritus ani requires compliance with
impeccable anal hygiene and minimizing the factors that caused
the initial exacerbation.63
SEXUALLY TRANSMITTED
DISEASES AND PROCTITIS
General Approach
Anorectal transmission of STDs is of particular concern in the
patient with HIV infection. For patients who are sexually active,
the history should ascertain whether sexual practices involve
anal penetration and whether condoms are used. As a means of
public health prevention of disease and patient safety, education
Treatment of Specific Sexually
Transmitted Diseases
Gonorrhea is caused by the gram-negative diplococcus Neisseria
gonorrhoeae. Proctitis (inflammation of the rectum) results
from anal intercourse or autoinoculation from vaginal secretions
and becomes symptomatic after a 5- to 7-day incubation
period. Symptomatic patients report pruritus ani, tenesmus, and
bloody or thick, purulent yellow drainage. Anoscopy reveals proctitis and mucus in the anal crypts. Recovery of the organism
directly from the crypts doubles the likelihood of identifying the
organism on Gram stain. Water should be used to lubricate the
anoscope because many lubricants contain an antibacterial agent.
Signs and symptoms of disseminated gonococcal infection may
include arthritis, skin lesions, perihepatitis, endocarditis, and
meningitis.70
Chlamydial Infection and
Lymphogranuloma Venereum
Infection with Chlamydia trachomatis, an intracellular organism
that is endemic to the tropics, is a common STD in the United
States.67,70 It causes proctitis in people whose sexual practices
include anal intercourse or oral-anal contact. Common signs and
symptoms include mucoid or bloody rectal discharge and tenesmus. Some people are asymptomatic carriers of the organism.
Lymphogranuloma venereum is a more serious manifestation
caused by specific strains of C. trachomatis and starts as a painful
anal or perianal ulceration. Prominent unilateral lymph nodes
coalesce to form a bubo, which must be distinguished from the
granuloma of secondary syphilis. Patients often have systemic
complaints of fever and malaise. Anoscopic examination reveals
an erythematous, friable mucosa. Rectal cultures generally are
unreliable because the organism is intracellular. Diagnosis is best
achieved by immunofluorescent antibody testing. In the final
stage, rectal strictures and rectovaginal fistulae may form.70
Herpes Simplex Virus Infection
Herpes proctitis is caused by both HSV-1 and HSV-2, but HSV-2
is responsible for approximately 90% of cases, especially in the
HIV-positive population.67,70 Herpes genital infections occur in
people whose sexual practices include oral-anal contact or anal
1286 PART III ◆ Medicine and Surgery / Section Five • Gastrointestinal System
Table 96-5
Sexually Transmitted Diseases of the Anorectum
DISEASE OR CONDITION (WITH SPECIFIC
PATHOGEN WHEN KNOWN)
FINDINGS
TREATMENT
LGV
Unilateral inguinal adenopathy
Fever, malaise
Mucoid or bloody discharge
Doxycycline 100 mg PO bid × 21 days
For pregnant patients or those allergic to tetracyclines:
Erythromycin 500 mg PO qid × 21 days
HSV infection
Rectal pain, tenesmus, constipation
Bloody mucoid discharge
Vesicles and ulcerations
Fever, malaise, myalgias, paresthesias
First episode:
Acyclovir 400 mg PO tid 7-10 days or
Acyclovir 200 mg PO 5×/day × 7-10 days
or
Famciclovir 250 mg PO bid × 7-10 days
or
Valacyclovir 1 g PO daily for 7-10 days
Early (primary) syphilis (Treponema pallidum)
Chancre
Tenesmus, pain, mucoid drainage
Inguinal lymphadenopathy
Benzathine penicillin G 2.4 million units IM once
Chancroid (Haemophilus ducreyi)
Inflammatory lesion progresses to ulcer
Inguinal adenitis—bubo
Azithromycin 1 g PO once or
Ceftriaxone 250 mg IM once or
Ciprofloxacin 500 mg PO bid × 3 days or
Erythromycin 500 mg PO tid × 7 days
Idiopathic (usually HIV positive)
Eccentric, deep, poor healing, multiple lesions
Symptomatic relief or surgical referral
Condylomata acuminata (HPV)
Keratinized vegetative growths in anus or skin
Asymptomatic, or pruritus ani, or bleeding
Podofilox 0.5% topically, or cryotherapy
Gonorrhea (Neisseria gonorrhoeae)
Pruritus ani
Tenesmus
Purulent yellow discharge
Ceftriaxone 250 mg IM once or cefixime 400 mg
PO once
Chlamydial infection (Chlamydia trachomatis)
Mucoid or bloody discharge
Tenesmus
Azithromycin 1 g PO once or
Doxycycline 100 mg PO twice per day × 7 days
Syphilis (secondary)
Maculopapular rash
Condyloma latum
Benzathine penicillin G 2.4 million units IM once
Ulcerative Conditions
Nonulcerative Conditions
HIV, human immunodeficiency virus; HPV, human papillomavirus; HSV, herpes simplex virus; IM, intramuscularly; LGV, lymphogranuloma venereum; PO, orally.
intercourse. Symptoms appear 1 to 3 weeks after exposure. Those
with proctitis may have severe rectal pain, bloody mucoid discharge, tenesmus, constipation, sacral paresthesias, or urinary difficulties. Systemic complaints may include fever, malaise, and
myalgias. Physical examination and anoscopy may be impossible
without anesthesia. Single or coalesced vesicles and ulcerations
occur in the perianal area and rectum, and anoscopy reveals an
erythematous, friable, ulcerated rectal mucosa. Chronic mucocutaneous HSV infection is considered diagnostic for AIDS. Definitive diagnosis with viral or immunofluorescent staining relies on
proper collection of fluid and scrapings from the base of the
vesicle.67,70
Syphilis
Syphilis is caused by Treponema pallidum, a motile spirochete.
During anal intercourse, the organism enters the rectal mucosa or
anoderm and forms an ulcer (chancre) within 2 to 6 weeks. The
chancre heralds the primary phase of syphilis and may resemble
an anal fissure. Patients may experience discomfort during defecation, tenesmus, mucoid discharge, and inguinal adenopathy.
Primary syphilis can be confused with lymphoma, but the
diagnosis can be made by visualizing spirochetes on darkfield
microscopy from scrapings taken from the base of the ulcer.70
Serologic testing is useful several weeks after the appearance of the
chancre. Treponemal tests such as the fluorescent treponemal antibody test yield a positive result earlier than does the Venereal
Disease Research Laboratory (VDRL) or rapid plasma reagin
(nontreponemal) test. Patients with AIDS have a high incidence
of neurosyphilis regardless of the stage of syphilis at the time they
seek treatment.71
If the chancre goes unnoticed, patients may have secondary
syphilis on presentation, marked by a maculopapular rash that
characteristically involves the palms and soles. Condyloma latum
is a spirochete-laden, weeping, verrucous lesion in the perianal
area that emits a foul odor. It is easily distinguishable from condyloma acuminatum, which has a drier, more keratinized appearance. Serologic testing results usually are positive. Tertiary syphilis
is rare but may manifest as a rectal gumma with severe perianal
pain and paralysis of the sphincters, which may be mistaken for
anal cancer.67
Chancroid
Chancroid is caused by the gram-negative bacillus Haemophilus
ducreyi and begins as an inflammatory pustule or macule that
ruptures to form an irregularly shaped ulcer. In several days,
painful inguinal adenitis develops. Chancroid often is a diagnosis
of exclusion.
Condyloma Acuminatum
Condyloma acuminatum, the most commonly encountered anorectal STD, is caused by human papillomavirus. These lesions, also
called genital warts, most often are found in homosexual men but
can be seen in heterosexual men, women, and children. The mode
Chapter 96 / Disorders of the Anorectum 1287
Figure 96-7. Condylomata acuminata in a child.
of transmission is primarily through sexual intercourse, but transmission can occur through close personal contact, as often happens
in pediatric cases in which an infected person is changing a diaper
and transmits the virus to the infant because of poor handwashing
techniques. It is incumbent on the evaluating physician to consider sexual abuse in such cases.21 Because one half of HIV-positive
patients have anal warts, HIV testing is recommended in patients
with this diagnosis.67
The pink-to-gray warts are a result of hyperplastic epithelial
growth and appear as vegetative papilliform growths (Fig. 96-7).
They may coalesce to form a massive patch that obscures the anal
verge.33 Many patients are asymptomatic or report pruritus ani, a
“hemorrhoid,” or bleeding. Evaluation should include anoscopy
because the warts often grow within the anal canal. Failure to treat
the internal lesions results in recurrence.67,70 The differential diagnosis includes the condyloma latum of secondary syphilis and
squamous cell carcinoma. Progression to intraepithelial neoplasia
has been reported to be related to the level of immunosuppression.
Preferred treatment is cryotherapy, but outpatient treatment with
0.5% podofilox solution or gel can be successful in limited cases.67
Ulcerative Lesions in the Patient with HIV Infection
The practice of anal intercourse has led to a proliferation of anorectal STDs. Most patients who are HIV seropositive have current
or past infection with an STD, which may be the initial reason for
seeking medical attention. One third of anorectal complaints in
this population fall into three categories: (1) routine proctologic
conditions as seen in the general population, (2) STDs, and (3)
opportunistic infections (Box 96-6). The treatment of routine
conditions and common STDs is similar to that in other patients
except that wound healing may be slower in HIV-infected patients.
In immunocompromised patients, the differential diagnosis of
ulcerative anorectal lesions should include opportunistic infections, lymphoma, and Kaposi’s sarcoma. Patients with AIDS often
exhibit idiopathic anal ulcerations with pain and bleeding. Before
this diagnosis is made, other possible causes of the lesions must
be considered (see Box 96-6). Symptomatic relief can often be
achieved with the WASH regimen (see Box 96-2), but recalcitrant
lesions may require surgical excision.67,70
Radiation Proctitis
Radiation-induced injury of the rectum is often caused by treatment of gynecologic, urologic, and GI malignancies. Immediate
radiation proctitis usually is self-limited and responds to symptomatic treatment. Delayed radiation proctitis can manifest up to
Figure 96-8. Prolapse of the rectum. (Courtesy Gershon Effron, MD,
Sinai Hospital of Baltimore. From Seidel HM, et al: Mosby’s Guide to
Physical Examination, 4th ed. St Louis, Mosby, 1999.)
2 years after the exposure to radiation and may predispose the
patient to subsequent rectal malignancies as a result of damage
to DNA.
Signs and symptoms of radiation proctitis include bleeding
ranging in severity from spotting to hemorrhage, tenesmus, diarrhea, pain, fistula in ano, and rectal strictures. Diagnosis is achieved
by rectal mucosal biopsy, a procedure best performed with the
patient under sedation or anesthesia.
Treatment regimens include the use of anti-inflammatory
agents, botulinum toxin injection, enemas with short-chain fatty
acids, oral sucralfate therapy, hyperbaric oxygen therapy, and sclerosing therapy.72-75 Supportive therapy can be given for symptoms
that the individual patient experiences.
Procidentia
Rectal prolapse, or procidentia, is a disease of persons at the
extremes of age. Prolapse is complete if all bowel layers protrude
and incomplete if only the mucosal layer is involved. In adults,
complete procidentia is most common among older women with
a history of excessive straining while defecating. The cause is a
laxity of attachment structures, and the rectal prolapse often is
accompanied by uterine prolapse or cystocele. Patients report an
anal mass that protrudes during defecation, coughing, or sneezing.
Findings may include fecal incontinence, bloody or mucoid discharge, and a foul odor. In some cases the patient is able to reduce
the prolapse manually, whereas in others the tissue becomes edematous and a red, ulcerated mass protrudes from the anus (Fig.
96-8). Sphincter tone may be weakened. Reduction may be
attempted; when this is successful, the patient should be discharged with agents to relieve constipation. Surgical repair often
is necessary.76,77
In children up to 4 years of age, procidentia often is associated
with chronic constipation or diarrheal disease. However, it may
herald the presence of malnutrition, parasitic infection, or cystic
fibrosis.78 Children usually have a mucosal prolapse. The parent
reports protrusion during defecation with small amounts of
mucus or blood. This condition must be distinguished from
a protruding juvenile polyp and intussusception. Gentle
reduction may be attempted. Conservative medical management
aimed at the cause of procidentia often is successful because of the
self-limited nature of the condition in children. Increasing the
dietary fiber and fluid intake frequently is successful as a first line
of therapy.77,78
1288 PART III ◆ Medicine and Surgery / Section Five • Gastrointestinal System
BOX 96-6
Anorectal Lesions in the Patient
with HIV Disease
Common Conditions
Anal fissure
Abscess and fistula
Hemorrhoids
Pruritus ani
Pilonidal disease
Common STDs
Gonorrhea
Chlamydial infection
Herpes
Chancroid
Syphilis
Condyloma acuminatum
Atypical Conditions
Infectious
TB, CMV infection, actinomycosis, cryptococcosis
Neoplastic
Lymphoma, Kaposi’s sarcoma, squamous cell carcinoma
Other
Idiopathic anal ulcer
CMV, cytomegalovirus; HIV, human immunodeficiency virus; STD, sexually
transmitted disease; TB, tuberculosis.
Anorectal Foreign Bodies
Perspective
Anorectal foreign bodies may result from the use of the anus for
sexual gratification, although they also are found in children, psychiatric patients, and victims of assault or iatrogenic injury. Most
objects are introduced directly into the anus, but some become
lodged there after oral ingestion. It is important to identify and
remove foreign bodies to prevent mucosal lacerations, intestinal
perforation and obstruction, sepsis, and peritonitis.79,80 In many
cases, removal can be done safely in the ED.
Clinical Features
Objects Inserted into the Anus. Rarely, a foreign body such as an
enema tip or broken rectal thermometer is introduced iatrogenically. In most cases the foreign body is placed deliberately by the
patient or a partner for medicinal or sexual purposes. Objects that
are commonly retrieved include fruits and vegetables; household
items, especially those whose dimensions resemble the penis; and
items purchased specifically with an anal erotic intent.80,81 By the
time patients arrive at the ED, sometimes days after the introduction of the foreign body, they have likely tried to remove it at
home. The history of the injury often is reluctantly given or is
vague and inconsistent. The initial ED evaluation, conducted in a
nonjudgmental manner, attempts to ascertain the type of foreign
body involved, how long it has been there, what attempts have
been made to remove it, and whether the patient has fever, abdominal pain, or rectal bleeding. The possibility of assault should be
considered.81
Physical examination of the anorectum begins with an external
examination for signs of trauma followed by digital rectal examination and anoscopy, which may reveal the foreign body, a lax
sphincter, or a mucosal injury. Abdominal examination may
demonstrate signs of perforation or obstruction. The foreign
body may be visible on abdominal radiographs, or its presence
may be inferred by a nonspecific gas pattern, free air, or signs of
intestinal obstruction.80 If perforation is suspected, water-soluble
Figure 96-9. Removal of a foreign body from the rectum.
contrast material can be introduced to delineate radiolucent
foreign bodies.
Orally Ingested Foreign Bodies. Some foreign bodies that are
ingested orally, especially toothpicks and fish or chicken bones,
pass through the GI tract and subsequently become lodged in the
rectum or anal crypts.81 Patients at highest risk for ingested foreign
bodies are children, especially those in the first 2 years of life;
psychiatric patients; and body packers who ingest condoms containing drugs.
Management
Optimal treatment depends on the location and type of object
found.79 In general, objects that are soft and low-lying (less than
10 cm from the anal verge) can be removed safely in the ED. Large,
hard, fragile objects and those that have migrated proximally are
difficult to remove without anal dilation and instrumentation to
assist in the passage through the sacral curve and sphincters. These
are best performed with the patient under general anesthesia.82 As
a rule, however, the patient should remain awake to assist in expulsion by performing the Valsalva maneuver at the appropriate time,
and premedication with a benzodiazepine is helpful to relax both
the sphincter and the patient.81 With the patient in the lithotomy
position, suprapubic pressure can assist in removal (Fig. 96-9).
Other positions may be more appropriate for a particular
foreign body.
Several methods are effective for removal. The easiest is to grasp
an edge of the foreign body with forceps and apply traction while
the patient bears down. Most foreign bodies in the rectum do not
have a convenient place to grasp, and other methods are needed.
A Foley catheter can be placed beside the foreign body and the
balloon inflated proximal to it (Fig. 96-10). This breaks the
suction of the rectal wall mucosa and provides a way to guide the
object out of the rectal vault. Hollow objects may be filled with
plaster of Paris, with an inset, inflated Foley catheter to be used as
a handle.81
Other creative ways to remove foreign bodies in the ED have
been successful, and an individualized strategy for each patient is
essential. After the removal of the foreign body, all patients should
undergo sigmoidoscopy to look for mucosal tears and perforations. Discharge instructions should warn the patient about signs
and symptoms of perforation, peritonitis, and sepsis.80
Chapter 96 / Disorders of the Anorectum 1289
KEY CONCEPTS
■ Patients who seek treatment for nonspecific anorectal
complaints should be evaluated for the presence of
underlying systemic disease (e.g., cancer, diabetes mellitus,
immunodeficiency) because disorders of the anus may herald
associated conditions.
■ Patients with any STD should be evaluated for HIV infection
and questioned about the use of the anus for sexual
purposes.
■ Anorectal conditions can be differentiated according to an
algorithm (see Fig. 96-2) that addresses the presence or
absence of pain, bleeding, swelling, and pruritus, in
combination with an assessment of the patient’s overall
health.
■ Most anorectal conditions can be symptomatically improved
by adherence to the WASH regimen (warm water, analgesics,
stool softeners, high-fiber diet).
Figure 96-10. Foley catheter–assisted removal of a rectal
foreign body.
The references for this chapter can be found online by
accessing the accompanying Expert Consult website.
Chapter 96 / Disorders of the Anorectum 1289.e1
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