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ANAL AND PERIANAL REGION 51
AB
FIGURE 10-3 “Triangle” island flap. A, Diamond-shaped defects are created by excision of scar tissue. B, Triangular flaps are moved into the
defects and sutured in place.
anal canal. Gras may be congured as a triangle (Fig. 10-3A and B)
or a “house” ap (Fig. 10-4A and B). Care must be taken to ensure
that the length of the ap is no longer than its width. Beveling the
lateral aspects of the ap is helpful to maintain an adequate blood
supply. Extensive dissection into the perirectal fat is occasionally
required. e gra is mobilized into the anal canal and secured with
absorbable 3-0 sutures. Multiple aps can be constructed for severe
stenosis, although they probably should be limited to two aps.
For more severe strictures associated with even greater loss of
anoderm, a rotational-type “S” plasty (Fig. 10-5A and B) may be
required. is operation is the procedure of choice for the mucosal
ectropion that occurs as the Whitehead deformity aer an injudicious hemorrhoidectomy.
An algorithm for the treatment of anal stenosis is presented in
Figure 10-6.
Postoperative Complications of Anoplasty
e two most common postoperative complications that will lead to
failure of anoplasty are infection and hematoma. Other complications
include ap necrosis from loss of blood supply, suture dehiscence
from excessive suture line tension, donor site problems, restenosis,
and ectropion if a mucosal ap is advanced too far. Meticulous surgical technique and appropriate bowel preparation is required. For
procedures such as simple anotomy and lateral sphincterotomy,
bowel preparation is limited to phosphate enemas preoperatively. For
more extensive procedures, a restricted, low-roughage diet must be
adhered to for 3 days, followed by oral cathartic agents, as well as
oral and intravenous antibiotics. Postoperatively, patients undergoing
A
B
FIGURE 10-4 “House” island flap. A, Excision of scar leaves a rectan-
gular defect. A “house-shaped” flap is outlined. B, The flap is advanced
into the anus to cover the defect. Its site of origin is closed directly.
Cause and ManageMent of anal stenosis52
AB
FIGURE 10-5 Rotational flap (S-plasty). A, Circumferential scar tissue is excised, leaving a ring-shaped defect. S-shaped incisions are marked. B, The
flaps created by the incisions are rotated to cover the defect.
Severe symptoms
Anal stenosis
Mild to moderate
symptoms
FIGURE 10-6 An algorithm for the treatment of anal stenosis. PLIS, Partial lateral internal sphincterotomy.
anoplasty should be maintained on a high-ber diet and bulking
agents. Long-term dietary management may be required.
Postoperative follow-up of patients undergoing anal stenosis sur-
gery should include the following elements:
1. Oce visits to assess wound healing and bowel function
2. Examination to ensure patients do not have an impaction and are
not having diarrhea as a result of inappropriate use of laxatives
(the best dilators are normal postoperative bowel movements)
3. Occasional gentle dilatation with use of the index nger or a
small sigmoidoscope
4. Follow-up until wound healing is complete
A nal issue that occasionally may be encountered is a high
anal stenosis, extending from the dentate line to the anorectal ring.
Sphincterotomy, either single or multiple, may be quite useful for this
cohort. For these patients, the involvement of mucosa and not anoderm appears to confer an improved prognosis.
Dilation
Simple stricture
Anotomy ± PLIS
Anoplasty (Y-V, island,
Extensive stricture
Conservative
management with bulk
fiber agents
Gentle dilation
house advancement
flaps, S-plasty)
S u g g e S t e d R e a d i n g
Christensen MA, Pitsch RM, Cali RI, etal. House advancement pedicle ap
for anal stenosis. Dis Colon Rectum. 1992;35:201–203.
Corman ML. Colon and Rectal Surgery. 6th ed. Philadelphia: Lippincott; 2012.
Milsom JW, Mazier WP. Classication and management of postsurgical anal
stenosis. Surg Gynecol Obstet. 1986;163:60–64.
Oliver GC, Rubin RJ. Anoplasty. In: Fielding LP, Goldberg SM, eds. Rob &
Smith’s Operative Surgery: Surgery of the Colon, Rectum and Anus. 5th ed.
London: Butterworth-Heinemann; 1993.
Pidala MJ, Slezak FA, Porter JA. Island ap anoplasty for anal canal stenosis
and mucosal ectropion. Am Surg. 1994;3:194–196.
M A
P W
Jennifer Blumetti and Jose R. Cintron
BACKGROUND AND EPIDEMIOLOGY
Anal warts (condyloma acuminata) occur as a result of infection with
the human papillomavirus (HPV). According to the Centers for Disease Control and Prevention, HPV infection aects approximately 20
million people and more than 50% of all sexually active individuals.
High-risk populations such as homosexual men can have a prevalence of HPV approaching 95%. Overall, approximately 5 million
new cases of anal or genital warts occur every year.
HPV is a human-specic, double-stranded DNA virus that is
incorporated into the genome of epithelial keratinocytes. It has an
incubation period of 1 to 6 months. More than 90% of genital warts
are caused by the HPV subtypes 6 and 11, although other subtypes
such as 16, 18, 31, 33, and 35 also may be involved. ese latter subtypes are more oen associated with squamous cell cancer. Infection with HPV occurs through direct contact with the virus, most
commonly via sexual contact, although transmission also can occur
through nonsexual contact. Perianal infection with the virus can
occur in the absence of anoreceptive intercourse. e virus is present
in secretions at the base of the scrotum and the vagina and can track
along the perineum to the perianal skin, and thus condoms do not
necessarily provide protection from HPV infection. Groups at high
risk for HPV infection and subsequent condyloma include those who
test positive for human immunodeciency virus (HIV; up to 30%
prevalence) and those who are immunosuppressed. Up to a 4% incidence of anal condyloma occurs aer kidney transplantation.
Recently, vaccines have been developed to prevent HPV infection.
Two commonly used vaccines that are clinically available are eective against the strains that cause squamous cell cancers (subtypes 16
and 18). One vaccine (Gardasil, Merck and Co, Whitehouse Station,
N.J.) is also eective against the subtypes that cause almost all cases
of condylomatous disease (subtypes 6 and 11). e vaccines are typically given to children of both sexes starting at age 11 years and can
be given up until the age of 26 years. It is recommended that they be
administered to high-risk groups (i.e., young homosexual men, HIVpositive persons). Persons who have already been infected with HPV
can still receive the vaccine, which should provide protection against
strains other than those with which they are infected.
PRESENTATION OF DISEASE AND DIAGNOSIS
Patients with perianal or anal condyloma present with pruritus, burning, discharge, bleeding, diculty with perianal hygiene, and palpable lesions. Persons with intra-anal or larger lesions may note changes
in bowel habits or tenesmus. In most patients, the diagnosis is made
upon physical examination. Examination should include anoscopy or
proctoscopy because the disease can be seen internally in more than
75% of patients. Patients also should be evaluated for genital warts,
including a penile examination in men and examination of the vulva,
vagina, and cervix in women. High-resolution anoscopy (HRA) can
be performed as an adjunct to physical examination and endoscopy,
as well as for treatment of microscopic HPV disease. To perform
HRA, the perianal region and anal canal are covered with a 3% acetic
acid solution and viewed through an operating colposcope or microscope. Areas infected with HPV will become acetowhite. Lugol’s solution can then be applied to dierentiate between low-grade lesions,
normal tissue (which will appear black), or high-grade lesions (which
will appear yellow or mahogany). is procedure facilitates targeted
biopsies or ablation of these areas.
Upon examination, condyloma have a “cauliower-like” appearance and vary in size from small, single lesions to large coalesced
masses (Fig. 11-1). ey vary in color from pink to gray-white, can
be at, sessile, pedunculated, or exophytic, and can range in size from
a millimeter to large fungating lesions measuring several centimeters.
Microscopically, condyloma appear to have ngerlike projections
in the epidermis with acanthosis, parakeratosis, and hyperkeratosis
(Fig. 11-2). Koilocytes—that is, large polygonal shaped squamous
cells with shrunken nuclei within a large cytoplasmic vacuole—
are also commonly seen. Condylomas themselves typically do not
undergo malignant degeneration because they are usually caused
by low-risk HPV subtypes. Condylomas can be associated with lowgrade dysplasia. e high-risk HPV subtypes (16 and 18) are associated with high-grade dysplasia and cancer.
For patients at high risk for anal HPV disease (such as HIV-positive and homosexual men), screening using an anal Papanicolaou
(Pap) smear has become common. is procedure is performed by
inserting a swab or cytology brush into the anal canal and rotating
it to collect cells, which are then placed on a slide and evaluated in
a similar manner to a cervical Pap smear. Results are then classied
as a normal, low-grade squamous intraepithelial lesion, a high-grade
squamous intraepithelial lesion, squamous cell cancer, or atypical
cells of undetermined signicance. High-resolution anoscopy can
then be used for further evaluation and treatment of the anal Pap
smear ndings.
TREATMENT OF ANAL CONDYLOMA
Many methods of treatment are available for anal condyloma. e
choice of treatment depends on several factors, including location
(intra-anal vs. perianal) and the volume of disease that is present.
Treatment is aimed at removing the visible manifestations of the disease and not eradication of the underlying HPV. Close follow-up is
necessary to treat recurrent visible disease early. HIV status should
not aect choice of treatment, although it is important to note that
in immunocompromised patients the treatment may be less eective
and recurrence rates may be higher than in patients whose immune
system is not compromised. Treatment can be divided into medical
53
ManageMent of anal and Perianal Warts54
FIGURE 11-1 Gross appearance of condyloma acuminatum. Small-
volume disease may be treated in the office.
Medical Therapies
Podophyllum-Based Therapies: Podophyllin and Podofilox
Podophyllum is a cytotoxic agent derived from the resin of the Podophyllum emodi or Podophyllum peltatum plant. e active compo-
nent is podophyllotoxin, which blocks polymerization of tubules
into microtubules, leading to an arrest of mitosis and thus resulting
in destruction of the warts. However, podophyllum can damage surrounding normal skin, so care must be taken to limit the area of treatment to the aected area only. e unpuried resin, podophyllin, can
be applied by a provider directly to the wart as a 10% to 25% solution
in a tincture of benzoin. Patients are then instructed to wash it o
aer 6 hours. Advantages of podophyllin are that it is easy to apply
and is inexpensive. Disadvantages are that it should not be applied
to internal lesions and it can be extremely irritating to the surrounding skin, with subsequent dermatitis, scarring, or possible necrosis.
Podophyllin is teratogenic and cannot be used in pregnant women.
In large amounts it can cause systemic toxic eects. Podophyllin typically requires multiple treatments with repeated oce visits, and its
eectiveness in treating longstanding condyloma is poor because of
poor penetration into keratinized lesions. Overall recurrence rates of
up to 65% have been reported, and thus this therapy is used less frequently than other options for the treatment of condyloma.
Podolox is puried podophyllotoxin in the form of a 0.5% gel
or solution that patients apply themselves. It is applied directly
to the warts twice daily for 3 days, followed by no therapy for 4
days; this regimen can be repeated up to four times. Total volume
applied should not exceed 0.5 mL/day. Benets of podolox are
that it can be applied at home and does not need to be washed o.
Patients are cautioned to avoid application to normal skin because
it can be irritating, and it cannot be used internally because of
increased systemic absorption. Ecacy is better than for podophyllin, with 37% to 88% clearance rates, but it has up to a 38%
recurrence rate.
FIGURE 11-2 Microscopic appearance of condyloma acuminatum.
Arrows denote koilocytes.
TABLE 11-1: Tr eatment of Anal and Perianal Warts
Topical Treatments Ablative Treatments
Patient applied Oce based
Podophilox (cytotoxic) Cryotherapy
5FU (cytotoxic) Excision
Imiquimod (immunomodulator) Electrocautery
Polyphenon (immunomodulator)
Physician applied Operative
Trichloracetic acid (cytotoxic) Excision
Bichloracetic acid (cytotoxic) Electrocautery
Podophyllin (cytotoxic) Laser ablation
5FU, Fluorouracil.
(cytotoxic or immunologic) or physically ablative therapies and can
be categorized as patient-applied therapies versus physician-directed
therapies (Table 11-1)
Trichloracetic and Bichloracetic Acid
Trichloracetic and bichloracetic acid are physician-provided agents
that cause tissue sloughing due to chemical coagulation of proteins.
Topical solutions (50% to 90%) are applied directly to the warts and
allowed to dry. Application can be repeated weekly. ese acids also
can be applied intra-anally. Disadvantages include pain and burning
at the site and scarring if applied excessively. In addition, weekly visits and multiple applications are needed. Sodium bicarbonate, talc,
or soap can negate the pain caused by overapplication. Clearance of
condyloma with trichloracetic or bichloracetic acid has been demonstrated in up to 70% of patients, with recurrence rates up to 36%.
Trichloracetic acid has been shown to be less eective and have more
adverse eects on local skin than cryotherapy in a randomized trial.
Imiquimod
Imiquimod is an immune modulator that acts by inducing interferon and tumor necrosis factor-α release, thereby activating the
host immune system to clear HPV infection by both innate and
cell-mediated pathways. Imiquimod is prescribed as a 5% cream,
which is applied at night three times weekly and then washed o in
the morning, and it can be used for up to 16 weeks. Adverse eects
include local skin reactions such as erythema, induration, burning,
itching, erosions, and ulceration. Successful eradication of the condyloma is achieved in up to 70% of patients, usually within 8 to 10
weeks. Imiquimod can be successfully utilized in patients with HIV,
including those with a low CD4 count or a high viral load. Although
some clinicians were concerned that the use of imiquimod in patients
who had undergone a transplant might lead to rejection as a result of
immune stimulation, this has not proven to be the case, and imiquimod can be used safely in this population. Treatment with imiquimod
aer ablation of condyloma may be useful in maintaining sustained
clearance of disease.
Other Medical Treatments
Chemotherapeutic agents such as fluorouracil (5FU) have been
used in the treatment of anal condyloma. 5FU is an antimetabolite that inhibits DNA synthesis. It is applied as a 5% cream and
administered daily or every other day for up to 10 weeks. Adverse
effects include dermatitis or mucositis, and it cannot be used by
pregnant women because of its teratogenic effects. The few randomized studies that have been performed on the use of 5FU
cream to treat condyloma have suggested that clearance can occur
in up to 50% of patients within 3 months of treatment, with a 50%
recurrence rate.
Interferon alpha can be given as an intralesional injection in doses
from 1 to 2 million units per lesion, with a maximum dose of 5 million units at one time. It can be given up to three times per week for
3 to 8 weeks. e dose is limited because of adverse eects such as
fevers, myalgia, headache, fatigue, and leukopenia. High cost and the
need for repeated visits, along with recurrence rates of up to 40%,
have restricted its popularity.
Sinecatechins ointment (Polyphenon E), derived from green
tea, is a newer agent that stimulates the immune system by releasing interferon and tumor necrosis factor-α. It is approved for use in
immunocompetent patients. is ointment is applied three times
daily for up to a maximum of 16 weeks. Adverse eects are typically
mild, and clearance rates are similar to those of other topical agents.
Ablative Therapies
ANAL AND PERIANAL REGION 55
FIGURE 11-3 A Buschke-Löwenstein tumor that has undergone
malignant degeneration. (Photo courtesy Luay Ailabouni, MD.)
Wide surgical excision is also the treatment of choice for giant
condylomas, also called Buschke-Löwenstein tumors or verrucous
carcinomas. ese rare lesions behave in a locally destructive manner but histologically may appear similar to a benign condyloma
(Fig. 11.3). Given the large size of these lesions and the need for wide
excision, coverage of the defect with a cutaneous ap or skin gra
may be necessary. ese tumors require aggressive treatment because
malignant degeneration may occur in up to 50% of cases, and they
can recur in up to 66% of cases.
Cryotherapy
Cryotherapy consists of the application of liquid nitrogen to the
condyloma for 10 to 20 seconds. It can be applied using a cottontipped applicator or a spray device. e liquid nitrogen destroys the
condyloma by inducing epidermal and dermal cytolysis, inducing
inammation and triggering a cell-mediated immune response.
It is typically administered every 1 to 2 weeks, with most condylomas clearing by three treatment cycles. Adverse eects include
pain, blistering, hypo- or hyperpigmentation, and ulcer formation.
Although an anesthetic typically is not used, topical anesthetics
can be added to ease moderate pain associated with the treatment.
Clearance rates can be up to 88%, but the recurrence rate can be as
high as 21% to 39%. Cryotherapy is typically reserved for smallvolume disease because larger lesions may not be cleared with this
modality alone.
Surgical Excision/Fulguration
Surgical excision and fulguration is typically performed with use of
a local or regional anesthetic, depending on the size of the lesions.
Lidocaine with epinephrine can be injected subcutaneously to elevate
the warts and allow preservation of the healthy skin. Excision can
then be performed with ne scissors or cautery. Although most condylomas are benign, representative lesions should be sent for histologic testing to rule out dysplasia or malignancy. Electrocautery can
then be applied to the remaining lesions, aer which the lesions are
curetted and cautery is reapplied until a white coagulum is seen. Care
should be taken to avoid wide excision or extensive coagulation in
larger or circumferential perianal lesions because this practice can
lead to anal stenosis. e advantage of surgical excision is that the
condyloma, including large lesions, can be treated at one setting. e
major complications of surgical excision are pain and scarring. Success rates with surgical excision and fulguration have been reported
in up to 94% of patients, although recurrence rates can be as high as
29%.
Laser
A carbon dioxide laser has been used to treat anal condyloma, with
postoperative pain similar to that for surgical excision/fulguration.
Success rates up to 95% have been reported with the laser, but it
has lost favor because of its expense and the eects of vaporized
HPV. ese eects include a risk of transmission of HPV, with cases
of laryngeal papillomatosis reported. Use of goggles, masks, and
smoke evacuators is standard practice when the laser is used for
treatment.
Recurrent Disease
Recurrence of anal and perianal condyloma is a signicant issue.
Ablative and directed topical treatments treat only the visible disease, and as a result, intact virus remains in normal-appearing tissues. Recurrence rates, which can be up to 70% depending on the
modality of treatment, can be due to persistent HPV or re-infection. HIV-positive patients with low CD4 counts have been shown
to have higher recurrence rates than do persons with higher CD4
counts. Close surveillance allows treatment of recurrences when
they are small, many of which appear in the rst 3 months aer
the initial treatment. e addition of an immune modulator such
as imiquimod aer ablative therapies is appealing, and one study
showed that this approach resulted in better clearance than ablative
treatments alone.
Treatment Algorithm
Treatment of anal and perianal condyloma should be individualized
based on the disease burden and the willingness of the patient to apply
his or her own treatment. Patients should also be counseled regarding
the need for multiple treatments and the possibility of using multiple
treatment modalities. An algorithm is provided (Fig. 11-4).
ManageMent of anal and Perianal Warts56
Condyloma
Minimal condyloma Moderate/severe or large Recurrent
Patient directed:
• Imiquimod
• Podofilox
Physician directed in office:
• Scissors excision
• Cautery
• Cryotherapy
• Trichloracetic acid
• Bichloracetic acid
• Podophyllin
FIGURE 11-4 Authors’ proposed treatment algorithm. 5FU, Fluorouracil.
Operating room:
• Excision
• Electrocautery
• Laser ablation
CONCLUSION
HPV infection with resultant anal and perianal condyloma is a
common condition with a diverse presentation. Multiple treatment
modalities are available, but recurrence rates are high. Treatment
should be individualized, and close follow-up is important early aer
treatment.
S u g g e S t e d R e a d i n g
Centers for Disease Control and Prevention. Human papillomavirus (HPV).
< www.cdc.gov/std/hpv/ >; December 9, 2015.
Chang GJ, Welton ML. Human papillomavirus, condylomata acuminata, and
anal neoplasia. Clin Colon Rectal Surg. 2004;17(4):221–230.
Echenique I, Phillips BR. Anal warts and anal intradermal neoplasia. Clin
Colon Rectal Surg. 2011;24:31–38.
Gormley RH, Kovarik CL. Human papillomavirus-related genital dis-
ease in the immunocompromised host, Part 1. J Am Acad Dermatol.
2012;66(6):867.e1–e14.
Small volume:
• Repeat in office
treatments
• Imiquimod
• Interferon
•Topical 5FU
Gormley RH, Kovarik CL. Human papillomavirus-related genital dis-
ease in the immunocompromised host, Part 2. J Am Acad Dermatol.
2012;66(6):883.e1–883.e17.
Scheinfeld N, Lehman DS. An evidence based review of medical and surgical
treatments of genital warts. Dermatol Online J. 2013;19(6):18559.
Schiller JT, Castellsague X, Garland SM. A review of clinical trials of hu-
man papillomavirus prophylactic vaccines. Vaccine. 2012;30(suppl 5):
F123–F138.
Schofer H, Van Ophoven A, Henke U, etal. Randomized comparative trial
on the sustained ecacy of topical imiquimod 5% cream versus conventional ablative methods in external anogenital warts. Eur J Dermatol.
2006;16:642–648.
Uribe N, Rueda C, Lopez M, etal. Management of giant anal condyloma by
wide local excision and anoplasty. Colorect Dis. 2012;14:1394–1397.
Wiley DJ, Douglas J, Beutner K, etal. External genital warts: diagnosis, treat-
ment and prevention. Clin Infect Dis. 2002;35(suppl 2):S210–S224.
Large volume:
•
Repeat electrocautery
wed by imiquimod
• Follo
A V
I
Victor L. Modesto and Lester Gottesman
he anorectum is being used with increased frequency for sexual
fulllment. In both sexes this practice has resulted in an increase
T
in the incidence and variety of sexually transmitted diseases (STDs).
e lifestyle that is oen associated with men who have sex with men
(MSM) is a denite risk factor for STDs, although monogamous MSM
have no higher risk for STDs than do monogamous heterosexuals.
Anorectal venereal infections also aict women who practice
anal receptive intercourse (ARI). Heterosexual anal intercourse confers a much greater risk of human immunodeciency virus (HIV)
transmission than does vaginal intercourse and is far more common
than generally realized; more than 10% to 30% of American women
and their male partners engage in the act regularly.
e multiple organisms found in the area, only some of which are
pathogenic, oen hamper the diagnosis and treatment of STDs.
e rising incidence of infectious proctitides, especially in MSM,
warrants consideration of infectious causes when proctitis is diagnosed. e symptoms mimic inammatory bowel disease (IBD), and
thus the history and physical examination should address sexual habits, including ARI, as well as anogenital lesions and lymphadenopathy.
BACTERIAL INFECTIONS
Gonorrhea
Gonorrhea is caused by Neisseria gonorrhoeae, a gram-negative intra-
cellular diplococcus. It is the most common bacterial STD aecting
the anorectum. Anoreceptive transmission, aer a 5- to 7-day incubation period, causes proctitis and cystitis. In women, gonorrhea can
result from ARI autoinoculation of vaginal gonorrhea into the lower
rectum. Asymptomatic gonococcal proctitis occurs frequently and
can only be detected by laboratory testing.
When symptoms occur, patients present with severe tenesmus,
pruritus, and bloody or mucoid rectal discharge. e initial infection, if untreated, can progress on rare occasions to more advanced
disease, such as perihepatitis, meningitis, endocarditis, and probably
the most common disseminated form, gonococcal arthritis.
A thick, yellow, mucopurulent discharge with or without proctitis
is highly suggestive of gonorrhea. One classic nding is the ability to
express the mucopus from the anal crypts by applying gentle external
pressure while the anoscope is in place.
In symptomatic men, polymorphonuclear leukocytes with intracellular Gram-negative diplococci seen on Gram stains of urethral
specimens are diagnostic. Gram stains of rectal specimens, however,
are insucient for detection of infection.
Although nucleic acid amplication tests (NAATs) have not been
approved by the U.S. Food and Drug Administration (FDA) for use
on rectal specimens, they are in fact being used with increasing
frequency in this clinical context and are more sensitive than cultures. Many laboratories have now established performance criteria
for the utilization of NAATs on rectal swab specimens.
Cultures using modied ayer-Martin agar with antimicrobial
susceptibility testing are still the “gold standard” and are recommended in all cases of treatment failures.
Preferred Clinical Approach
Empiric treatment is started based on clinical suspicion while awaiting denitive culture results. Screening 3 months aer treatment is
an important part of the management because 35% of patients will
experience a recurrence. Treatment of all sexual contacts decreases
the recurrence rate.
e Centers for Disease Control and Prevention no longer recommends use of oral cephalosporins for the treatment of gonococcal
infections. For uncomplicated gonococcal infections of the rectum,
the recommended regimen is a single dose of ceriaxone, 250 mg
intramuscular (IM) plus a single dose of azithromycin, 1 g orally or
doxycycline, 100 mg orally twice a day for 7 days. Alternative regimens include a single dose of cexime, 400 mg orally plus a single
dose of azithromycin, 1 g orally or doxycycline, 100 mg orally twice
a day for 7 days. Because concomitant chlamydia infections are common, a single dose of azithromycin, 1 g, is added. For patients with
documented severe cephalosporin allergies, a single oral dose of
azithromycin, 2 g, is to be used. All patients should be followed up
with a test of cure 1 week later. With close follow-up and treatment of
all sexual partners, a 95% cure rate is a reasonable expectation. Evaluation for other sexually transmitted pathogens, such as syphilis and
HIV, is also required because multiple organisms are oen present.
Guidance by regional public health services regarding the prevalence
of emerging resistant strains of gonorrhea help determine therapeutic
choices.
Chlamydia trachomatis and Lymphogranuloma venereum
Chlamydia infection is one of the most common STDs in the United
States. Approximately 4 million chlamydial infections occur yearly.
e incidence in both men and women who practice ARI is rising.
Approximately 70% of rectal chlamydia infections are asymptomatic,
thereby providing a reservoir for future infections.
Chlamydia proctitis typically occurs within 10 days of penetrating
anal sexual contact and may coexist with other STDs, especially gonorrhea. Up to 15% of asymptomatic MSM harbor chlamydia organisms. Fieen immunotypes are known; serovars D through K are
responsible for C. proctitis, and serovars L1, L2, and L3 are responsible for Lymphogranuloma venereum (LGV).
57
AnorectAl VenereAl InfectIons58
Aer either ARI or oral-anal intercourse, non-LGV proctitis presents with pain, tenesmus, and fever. Examination reveals erythematous rectal mucosa, but mucosal ulcerations are rare. Inguinal and/or
femoral nodes may be enlarged and matted (“buboes”). Patients with
LGV also experience pain and tenesmus, but with associated mucosal ulcerations and a more pronounced friability resembling Crohnrelated proctitis. e inguinal lymphadenopathy plays an important
role in dierentiating LGV from Crohn-related proctitis. Untreated
disease can progress to ulceration, causing rectovaginal or rectovesical stulas, abscesses, and, as a late nding, rectal strictures mimicking rectal cancer. Because of similarities between LGV and IBD,
LGV should be considered as a dierential diagnosis in patients with
proctitis or IBD-related symptoms, especially among HIV-positive
men. LGV also may exhibit extraintestinal manifestations, including
reactive arthritis and hepatitis.
Among MSM infected with rectal gonorrhea or chlamydia, a history of two additional prior rectal infections was associated with an
eightfold increased risk of HIV. erefore, HIV testing should be
considered.
Anorectal Chlamydia trachomatis infections can be diagnosed by
NAATs even though these tests do not carry an FDA indication for use
on rectal swabs. As in the case of anorectal gonococcal infections, an
increasing number of laboratories are validating the use of NAATs for
C. trachomatis detection on rectal swab specimens. Aptima Combo 2
(Hologic Inc., Marlborough, Mass.) is a transcription-mediated assay that
has the advantage of detecting both N. gonorrhoeae and C. trachomatis.
For LGV, chlamydia serology is supportive of the diagnosis when
the complement xation titers are greater than 1:64. Genital lesion
swabs or lymph node aspirates can be tested either by culture, direct
immunouorescence, or nucleic acid detection.
Biopsy reveals infectious proctitis with crypt abscesses, infectious
granuloma, and giant cells. e presence of granulomas can lead to
an erroneous diagnosis of Crohn-related proctitis.
Preferred Clinical Approach
Presumptive treatment for both N. gonorrhoeae and C. trachomatis
co-infection remains the standard of care. Recommended regimens
are a single dose of azithromycin, 1 g orally, or doxycycline, 100 mg
orally twice a day for 7 days.
e alternative regimens are erythromycin base, 500 mg orally
twice a day for 7 days, or erythromycin ethylsuccinate, 800 mg orally
four times a day for 7 days, or levooxacin, 500 mg orally once daily
for 7 days, or ooxacin, 300 mg orally twice a day for 7 days.
For LGV, the recommended treatment is doxycycline, 100 mg
orally twice a day for 21 days, and the alternative regimen is erythromycin base, 500 mg by mouth four times a day for 21 days.
Azithromycin, 1 g orally once weekly for 3 weeks, could also be
used based on its antimicrobial susceptibility activity. A test of cure
should be performed at least 4 weeks aer completion of therapy.
Treatment of the strictures is oen complicated because they can
be multiple and of varying segments. Many extend to the splenic exure and must be dierentiated from IBD, ischemia, and cancer.
e treatment of symptomatic strictures should initially include
a 3-week course of the appropriate antibiotics. Proximal diversion or
sphincter-saving excisional surgery may be the only alternative for
treatment failures. Asymptomatic strictures require no treatment.
Chancroid
Chancroid is caused by Haemophilus ducreyi, a small gram-negative,
nonmotile, non–spore-forming aerobic bacillus. It is characterized by
painful adenopathy, multiple perianal abscesses, and tender genital or
anorectal ulcers. e presence of painful “kissing ulcers” is typical of
this infection. Because of the so nature of the ulcers, distinguishing
them from herpes or syphilis is dicult. Lymphadenopathy (bubo
formation) is present in approximately 50% of cases, and sometimes
the lymph nodes become suppurative. Chancroid is common in
developing countries and facilitates HIV transmission. Eective and
early treatment is therefore an important part of any strategy to control the spread of HIV infection. Diagnosis is determined primarily
by culture of a specimen obtained by a swab from the base of the
genital ulcer. Several dierent media have been used, but GC agar
(Life Technologies [GIBCO], Grand Island, N.Y.) has the highest
sensitivity (80%) for the isolation of H. ducreyi. No FDA-approved
polymerase chain reaction test for H. ducreyi is available. Testing for
herpes simplex virus (HSV) and syphilis should also be performed.
Preferred Clinical Approach
e recommended treatment regimens include azithromycin, 1 g
orally (single dose); Doxycycline 100 mg orally twice a day for
7 days; alternative therapy includes: Erythromycin base 500 mg
orally four times a day for 7 days or Levooxacin 500 mg orally
once daily for 7 days or Ooxacin 300 mg orally twice a day for
7 days. Treatment should be started based on clinical suspicion
while awaiting culture results. Resolution of the adenopathy lags
behind resolution of the ulcers.
Granuloma Inguinale
Granuloma inguinale is a chronic glaucomatous infection caused by
Klebsiella granulomatis, a gram-negative intracellular bacterium. e
disease is insidious, with several months passing before red, shiny,
hard masses develop on the genitals or around the anorectum. Scarring can lead to stenosis of the anorectum. e bacterium is dicult
to culture. Tissue crush preparation or biopsy conrms the diagnosis
with the presence of the dark-staining Donovan bodies. No FDAapproved molecular assays exist for K. granulomatis. e dierential
diagnosis includes carcinoma, secondary syphilis, and amebiasis.
is disease is fairly rare in the United States.
Preferred Clinical Approach
Recommended regimens are Azithromycin 1 g orally once per week
or 500 mg daily for at least 3 weeks and until all lesions have completely healed. Alternative regimens are all to be prescribed for a
minimum of 3 weeks or until all lesions have healed and consist of
Doxycycline 100 mg orally twice a day or trimethoprim-sulfamethoxazole, one double-strength tablet (160 mg/800 mg) orally twice a day,
or ciprooxacin, 750 mg orally twice a day, or erythromycin base, 500
mg orally four times a day.
Syphilis (“The Great Masquerader”)
e organism that causes syphilis (Treponema pallidum) enters the anus
during ARI, and anal ulcers usually appear within 2 to 6 weeks but may
occur up to 3 months later. In 10% to 20% of cases, the primary lesion,
referred to as a chancre, may be hidden within the anal canal. e chancre is usually at the anal verge and typically is painless. In some instances,
especially if the lesion becomes secondarily infected, it may cause exquisite pain and be mistaken for an anal ssure. Unlike classic ssures, the
lesion may be situated o the midline, peripherally on the anal skin or
proximally above the dentate line. Multiple chancres may be present.
When chancres are not treated, the ulcer heals spontaneously in
3 to 4 weeks. is stage is followed “classically” 2 to 10 weeks later by
secondary lesions in the guise of a diuse red maculopapular rash on
the palms of the hands and soles of the feet.
Secondary syphilis also may present as a pale brown or pink at
verrucous lesion called condyloma latum, which is a large perianal
mass composed of many raised smooth warts, which tend to secrete
mucus and are associated with pruritus and a foul odor. ese lesions
are highly infectious and can coexist with primary chancre. e
ANAL AND PERIANAL REGION 59
dierential diagnosis includes condyloma acuminatum, which is
oen more desiccated and keratinized. Spirochetes are usually demonstrated in condyloma latum on modied Steiner silver staining.
Both primary and secondary lesions are infectious.
Proctitis in the absence of anogenital lesions, mimicking IBD, has
also been reported. Rectal syphilis with painless inguinal adenopathy
has been mistaken for lymphoma because both diseases present with
rubbery inguinal lymphadenopathy and submucosal rectal irregularities. In contrast, genital ulcers are associated with painful adenopathy.
Syphilitic rectal gummas are exceedingly rare and can be confused
with malignant growths. Like lymphoma, rectal syphilis is generally
accompanied by tenesmus, mucoid discharge, and rectal pain.
In one third of patients, anal syphilis proceeds to a spontaneous
cure, with an additional third remaining latent. About a third of the
cases will progress to late or tertiary syphilis, which can occur several
years aer primary or secondary disease. Asymptomatic central nervous system involvement is demonstrated in up to 25% of patients
with late or latent syphilis. Because syphilis is a systemic infectious
disease, central nervous system involvement (neurosyphilis) can
occur at any stage of infection. Ideally, a sample of the cerebrospinal
uid should be obtained for examination. Syphilitic ocular involvement is almost pathognomonic of neurosyphilis and needs to be
treated as neurosyphilis.
Because of the variable manifestations of syphilitic ulcers, any
ulcer in MSM must be viewed with suspicion. Women with anal
ulcers should be questioned regarding ARI. Anoscopy with modied Steiner silver staining of scrapings from the base of the chancre reveals early syphilis. Biopsy may demonstrate spirochetes on a
Treponema pallidum immunohistochemical stain. T. pallidum cannot
be isolated by culture.
Indirect diagnoses can be based on serologic tests that are dened
as treponemal or nontreponemal. Nontreponemal tests include
Venereal Disease Research Laboratory (VDRL) and the rapid plasma
reagin tests, which vary according to disease activity; hence titers can
reect persistent disease or responsiveness to treatment. e VDRL
is used predominantly for screening, and false-positive results have
been reported with rheumatologic disorders, Epstein-Barr virus,
infections, and cancer.
T. pallidum–specic assays usually use the uorescent treponemal
antibody absorption test (FTA-ABS). e FTA-ABS becomes positive
earlier than nontreponemal tests and is conrmatory for syphilis.
Preferred Clinical Approach
e treatment of primary and secondary syphilis is a single dose of
long-acting benzathine penicillin (Bicillin), 2.4 million units IM,
regardless of HIV status. For patients with early latent syphilis (dened
as evidence of infection acquired during the preceding 12 months), a
single dose of benzathine penicillin is still recommended. However, if
the latent period is greater than 1 year or is of unknown duration, then
the patient is classied as having late latent syphilis and the 2.4 million
units injection of benzathine penicillin is repeated every week for 3
consecutive weeks for delivery of a total of 7.2 million units.
By denition, patients with latent syphilis have serologic evidence
of infection but are asymptomatic, and the objective of treatment is
the prevention of complications.
Tertiary syphilis is dened by the presence of gummas and cardiovascular complications without neurologic involvement. e recommended treatment regimen is the same as for late latent or latent
syphilis of undetermined duration. Benzathine penicillin G, 2.4 million units IM, is administered once a week for 3 weeks.
Neurosyphilis is treated with aqueous penicillin G, 18 to 24 million units every 24 hours for 10 to 14 days. An alternative regimen is
procaine penicillin, 2.4 million units IM once daily plus probenecid,
500 mg orally four times a day, both for 10 to 14 days.
In nonpregnant patients who are allergic to penicillin, doxycycline 100 mg by mouth twice a day has been used for many years with
good results.
Pregnant patients and patients with HIV disease who are allergic to penicillin should always be treated with penicillin aer
desensitization.
In all patients, a fourfold drop in the rapid plasma reagin titer is
needed to document a successful treatment response.
VIRAL INFECTIONS
Herpes Simplex Virus
Recently, HSV infections of the anorectal region have become more
frequent. HSV is transmitted either through ARI or oral-anal sex.
Most HSVs are caused by HSV-2, but recently a signicant proportion has been caused by HSV-1, especially among younger MSM
and heterosexual women. Once local inoculation occurs, the virus
is transported along the peripheral nerves to the neuronal nucleus.
is viral invasion of the neurons leads to a latency state that is not
well understood.
e risk of recurrence with genital herpes is 60% for persons
infected with HSV-1 and 90% in persons infected with HSV-2. Cellmediated responses appear to be more important in controlling the
severity of mucocutaneous outbreaks of the virus, which explains the
severe infections observed in HIV-positive patients.
HSV infection begins 4 to 21 days aer ARI. e infection usually presents with severe, constant pain in the anorectal region and
proctitis. Proctitis is usually associated with anal intercourse, and
diagnostic suspicion should be raised by perianal vesicles or painful oral/anogenital ulcerations. Proctitis can be severe, manifesting
as constipation, tenesmus, and a mucopurulent discharge. e pain is
so intense that it leads to inhibition of the desire to defecate (psychogenic constipation), with subsequent fecal impaction. Systemic manifestations include fever, chills, and malaise. Occasionally, bilateral
tender inguinal lymphadenopathy may occur. Neurologic symptoms
due to the sacral nerve root involvement, such as paresthesia, neuralgia, and pain radiating down the posterior thighs, may be observed.
Dyspareunia, urinary retention, and impotence also may occur. e
clinical course generally lasts 7 to 21 days; recurrent infections are
mild and rarely associated with systemic symptoms. e disease is
highly contagious from the rst appearance of the vesicles until perianal re-epithelialization is complete.
During the acute phase, the anorectum is oen exquisitely tender, and thus accurate examination requires induction of topical or
regional anesthesia. Inspection may reveal acute lesions ranging from
small vesicles with red areolae to large ruptured vesicles of aphthous
coalesced ulcers on the perianal skin or in the anal canal. Shallow
perianal ulcers may coalesce and extend to the sacrococcygeal area in
a buttery distribution.
Anoscopy reveals friable epithelium, ulceration, and mucopurulent discharge. Proctoscopy reveals friable mucosa, diuse ulcerations, and occasional vesicles and pustules limited to the distal 10
cm of the rectum (the extent to which the ejaculum can reach).
Viral cultures of a suspicious vesicle are positive in up to 90% of
clinical infections. Scraping of the ulcerations stained with Giemsa
stain reveal the multinucleated giant cells typical of herpes infection
(Tzanck preparation). A direct biopsy may also reveal the typical
giant cells or intranuclear inclusion bodies.
Anogenital ulcers associated with both HSV and syphilis can
lead to a 1.5-fold to sevenfold increase in HIV transmission as a
result of the mucosal barrier breach, and therefore HIV testing is
recommended.
Preferred Clinical Approach
Treatment includes both the acute infection and suppressive therapy
to diminish recurrence. Management of the acute infection includes
palliative measures, such as sitz baths, stool soeners, and analgesics.
AnorectAl VenereAl InfectIons60
No eective cure for HSV infection is known. Antiviral agents,
particularly acyclovir, shorten the clinical course, decrease the severity, and suppress HSV infection in most patients. Spread can happen
even with treated patients, so both partners need lifelong surveillance. Newer agents such as valacyclovir and famciclovir (Famvir)
have superior bioavailability in oral formulations. Acyclovir is available in topical (5%), oral, and intravenous formulations.
e recommended regimens for an initial dose of HSV include
acyclovir, 400 mg orally three times a day for 7 to 10 days; acyclovir,
200 mg orally ve times daily for 7 to 10 days; famciclovir, 250 mg
orally twice a day for 7 to 10 days; or valacyclovir, 1 g orally twice a
day for 7 to 10 days.
Eective episodic treatment of recurrent disease is most eective
when administered within 1 day of lesion outbreaks and may require
that the patient take acyclovir, 400 mg orally three times a day or 800
mg orally twice a day, both for 5 days; famciclovir, 125 mg orally twice
a day for 5 days; valacyclovir, 500 mg orally twice a day for 3 to 5 days;
or valacyclovir, 1 g orally every day for 5 days.
For patients with recurrent outbreaks, consider suppressive therapy with acyclovir, 400 mg orally twice a day; famciclovir, 250 g orally
twice a day; or valacyclovir, either 500 mg or 1 g orally every day
indenitely.
Condylomata Acuminata
Condylomata acuminata (anal and perianal warts) is the most common STD treated by colon and rectal surgeons and the most common STD worldwide because almost 80% of the world’s population is
exposed to human papillomavirus (HPV) by age 50 years. HPV infection has been identied as a denite human carcinogen for six types
of cancer: cervix, penis, vulva, vagina, anus, and the oropharynx.
e disease is caused by HPV, of which more than 150 types have
been identied, each exhibiting some tissue and disease specicity.
HPV types 6 and 11 are most commonly associated with benign,
exophytic condyloma acuminata of the anogenital region, as well as
low-grade dysphasia. Types 16 and 18 have been associated with anogenital condyloma and the more severe forms of dysplasia, including invasive squamous cell carcinoma. HPV typing is thus required
to assess the malignant potential of the HPV lesion and to identify
patients who require closer surveillance. MSM (in whom HPV is
prevalent) are at increased risk for the development of invasive anal
carcinoma, especially if they are infected with HIV.
Typical patients are MSM, although lesions in the perianal region
may be seen in heterosexual men, women, and even children. e
primary mode of transmission of anogenital HPV infection is sexual
intercourse, although spread also may occur through close nonsexual contact. e mode of spread is shedding of active viral particles
from anal condylomata, which then are spread by contact of uid to
another mucocutaneous area.
Clinical Manifestations
Aer a 1- to 3-month period of incubation, condylomata acuminata
are easily recognizable as either pinhead-sized lesions or projecting,
cauliower-like masses. Individual warts may be sessile or pedunculated; they have a tendency to grow in radial rows that may become
conuent and form almost an entire sheet around the anal orice,
sometimes obscuring the anal aperture. Symptoms may include pruritus ani, bleeding, discharge, persistent perianal wetness, and pain.
Some patients report having a lump or mass. Condyloma are conned to the perianal area in only 6% of symptomatic MSM, whereas
both perianal and intra-anal lesions are noted in 84% of symptomatic MSM. Furthermore, 10% of symptomatic patients have only
intra-anal condyloma, emphasizing the importance of anoscopy.
e condylomas are usually conned below the dentate line except
in immunocompromised patients. Topical application of acetic acid
(5%) enhances visualization. Without coincidental treatment of the
concomitant anal canal condyloma acuminata, treatment of perianal
disease is doomed to failure.
A variant of anal condyloma is the giant condyloma acuminatum
(Buschke-Löewenstein tumor, also known as verrucous carcinoma).
Clinically, it appears as a rapidly growing, fungating squamous cell
carcinoma that histologically shows no evidence of invasion. e
aggressive nature of the lesion may cause multiple sinuses or stulous
tracts that can invade fascia, muscle, or rectum and cause inammation, infection, and hemorrhage. Microscopically, the lesions bear a
strong resemblance to condyloma acuminatum, and there is no evidence of invasion of lymphatics or blood vessels or other histopathologic criteria of malignancy. e treatment for verrucous carcinoma
is surgical, and the extent of the operation should be individualized.
Wide local excision with clear margins is recommended. If the anal
sphincter is involved, an abdominoperineal resection should be performed because it oers the only hope of a permanent cure.
Treatment
Anal and perianal warts are notorious for their recurrence. All
patients should undergo anoscopy, proctosigmoidoscopy, and either
vaginal or penile examination. Treatment includes excisional therapy, immunotherapy, and destructive therapy. Recurrence rates range
from 10% to 75%. Accuracy in determining recurrence rates is not
easily achieved because it is oen dicult to distinguish cases of
true recurrence from reinfection. e prevalence of anal squamous
intraepithelial lesions is high among HIV-positive MSM and to a
lesser extent among HIV-negative MSM. e natural history of anal
intraepithelial neoplasm (AIN) has not been fully established, which
prevents clinicians from dening clear management protocols. e
treatment choices are either aggressive removal of all atypical epithelium with high-resolution anoscopy or removal of only grossly
suspicious lesions and observation. However, 80% of anal cancers
are linked to HPV. Treatment options are limited by morbidity and
high recurrence rates. Early detection may permit better tolerance of
therapy. erefore, persons who engage in ARI should have high-resolution anoscopy, anal cytology, and aggressive biopsy of abnormal
areas because of a high prevalence of AIN, especially in HIV-positive
or immunocompromised persons. Women with cervical intraepithelial neoplasia III or cervical cancer also should be evaluated for AIN.
e quadrivalent or 9-valent HPV vaccine (HPV4; Gardasil,
Merck & Co., Inc., Kenilworth, N.J.) has recently demonstrated
ecacy in the prevention of AIN II and AIN III, especially among
MSM, with 77.5% eectiveness. Vaccination of males and females
ages 9 to 26 years has been recommended to reduce the incidence of
vaginal, vulvar, oral, and anogenital cancer.
Preferred Clinical Approach
Electrocautery
Most patients are treated in the oce setting, with more extensive
disease reserved for the operating room. In the oce, patients are
placed in the prone jackknife position; pulse oximetry is used, and
the buttocks are held apart by adhesive tape. Intravenous sedation
can be used depending on the need; however, a local anesthetic is
administered to all patients, with a lidocaine-Marcaine preparation
mixed with sodium bicarbonate to eliminate the burning sensation
associated with administration. A headlight is used for good direct
lighting, and a 3% to 5% solution of acetic acid is applied to the anal
area for better visualization. Acetic acid causes hydrolysis of the keratin and staining of the anal condylomata a whitish color. erefore,
the HPV-infected lesions are prone to acetowhitening and stand out
from the surrounding mucosa or skin.
Either a circumferential block is administered or each wart is individually injected, depending on the extensiveness of the disease. Excision of several condyloma should be performed for histopathologic
evaluation, especially if the lesion appears suspicious for neoplasm.