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study of the use of topical capsaicin (0.006%) it was found to relieve anal itching in 70% of
the patients treated without significant side effects.
16,17
Topical tacrolimus is known to produce a burning itch as a side effect by indirectly activating TRPV1, a transient receptor potential channel. Tacrolimus works by competitiveirritation and patients reported pruritus ani relief after 4 weeks of topical administration;
however, the relapse rate was 75%.
18,19
9.4.3 Anal Tattooing
In cases of refractory pruritus ani, anal tattooing with intradermal and subcutaneous
injection of the perianal region with 1% methylene blue, bupivacaine, and lidocaine is
indicated. The mechanism of action seems to be the destruction of sensory nerve endings
by the injection of the dye, causing hypoesthesia of the perianal region. A preparation of
10mL 1% methylene blue, 5 mL saline solution, 7.5 mL 0.25% bupivacaine with epinephrine (1/200,000), and 7.5 mL 0.5% lidocaine is infiltrated using a small gauge needle to
cover the affected perianal skin up to the dentate line. Patients must be informed that this
tattoo is permanent.
7,20–22
9.5 Secondary Causes of Pruritus
9.5.1 Local Irritation
The process is generally initiated by increased moisture associated with hemorrhoids, fistulas, physical activity, and anal fissures. No controlled trials have been done to examine
food or diet as a cause of pruritus ani, but anal leakage is related to dietary factors like
caffeine, alcohol, chocolate, citrus fruit, tomatoes, and spicy foods.
23
Patients with altered
bowel habits after an episode of constipation or diarrhea often complain of irritation of the
anal margin and usually clean the anal area excessively.
7
Pruritus ani can be caused by an
excess of sweat and moisture; an overabundance of hair round the anus; some soaps, perfumes, or creams, which can initiate an allergic response to one or more ingredients; and
the use of wet wipes containing several chemicals, including alcohol and other astringents
that damage the perianal skin and increase the moisture around the area. Patients often
react to this worsening irritation by increasing their local hygiene and thus a deleterious
feedback loop is created. In some cases sedative antihistamines or antidepressants are
used.
11
9.6 Anorectal Diseases
9.6.1 Hemorrhoids
Hemorrhoids affect 10 million persons per year24and more than 50% of the US population
over the age of 50 years have experienced the condition
25
; it is the most common pruritus-
related anorectal disease.
23
Internal hemorrhoids originate from the inferior hemorrhoid
venous plexus above the dentate line and are covered by mucosa, while external
118 ANORECTAL DISORDERS
hemorrhoids are located below the dentate line and drain via inferior rectal veins into the
pudendal vessels and then into the internal iliac vein. These vessels are covered by anoderm that is comprised of modified squamous epithelium. External hemorrhoids usually
do not cause symptoms unless thrombosis occurs, in which case the patient experiences
acute pain.
26
As a result, these tissues contain pain fibers and affect how patients present
and are treated.
24
The pathophysiology of hemorrhoid development includes sliding anal cushion, hyper
perfusion of hemorrhoid plexus, vascular abnormality, tissue inflammation, and internal
rectal prolapse (rectal redundancy). Goligher’s classification includes: grade I, nonprolapsing hemorrhoids; grade II, prolapsing hemorrhoids on straining, but reduce spontaneously; grade III, prolapsing hemorrhoids requiring manual reduction; and grade IV,
nonreducible prolapsing hemorrhoids, including acutely thrombosed or incarcerated
hemorrhoids.
26
The most common clinical presentations of symptomatic hemorrhoids
include pruritus, painless rectal bleeding, fecal soilage, perianal irritation, or mucus loops.
For the diagnosis of hemorrhoids a clinical history is very important, including a rectal
examination and anoscopy. If it can be determined that red blood clearly comes from
hemorrhoids an anoscopy is enough, but if there is doubt a colonoscopy should be carried
out or at least a flexible sigmoidosocopy.
27
The different grades of hemorrhoid may lead to
different approaches to treatment.
28
Treatment is often divided into nonsurgical management, office procedures, and surgical management utilizing an operating room. The decision on how to treat depends on many factors including the degree of symptoms, age, and
other medical conditions.
Medical therapy is most appropriate for first-degree hemorrhoids. The cornerstone of
medicaltherapy is adequate intake of fiber and water. Topical corticosteroidsand analgesics
are useful for managing pruritus ani and perianal skin irritation due to poor hygiene, mucus
discharge, or fecal seepage. Prolonged use of potent corticoid preparations may be harmful
and should be avoidedbecause they are associated with corticaldamage to the perianal skin.
Nonoperative techniques for ablating hemorrhoids include injection sclerotherapy, diathermy coagulation, bipolar coagulation, infrared coagulation, and rubber band, which
are appropriate for second-and third-degreehemorrhoidsbut are also indicated when medical treatment of first-degreehemorrhoids has failed.Complications are infrequentand usually minor.
24,29,30
Traditional hemorrhoidectomy is more effective for grade III hemorrhoids;
ideally the operation should remove the internal and external components of hemorrhoids
completely to reduce recurrence, it can be performed with a variety of surgicaldevices, none
of which display a clear advantage over the others.
31
Systematic reviews demonstrated
slightlylower complication rates and higher long-term recurrence rates with stapled hemorrhoidopexy compared with standard hemorrhoidectomy.
32,33
9.6.2 Anal Fissure
Anal fissures are linear splits in the anal mucosa. In 90% of cases most fissures are
posterior and midline and are related to constipation or anal trauma, fissures in lateral
positions should raise suspicion for disease processes such a Crohn’s diseases,
Chapter 9 • Pruritus Ani 119
tuberculosis, HIV, dermatologic conditions, and anal carcinoma.30Acute fissures frequently resolve within a few weeks, chronic fissures persist longer than 8–12 weeks; a
chronic anal fissure is maintained as a nonhealing ulcer by sphincter spasm and consequent ischemia. Patients with an anterior fissure are more likely to have occult external
sphincter injury and impaired external sphincter function compared with patients with
a posterior fissure.
34
Painful defecation and rectal bleeding are common symptoms,
but also present are itch and discomfort.
The initial management of typical fissures is described in
Table 9.2. Treatment for
chronic anal fissure is typically directed toward relieving spasm, and as such it is a predominantly medical condition, with surgery reserved for medically refractory cases, to
avoid the complications risk. Anal fissures treated with lateral internal sphincterotomy
(surgery) or 0.2% nitroglycerin for 10 weeks achieved higher rates of fissure healing
(96% vs 67% at 5weeks) but also demonstrates a significantly higher rate of minor fecal
incontinence (44% vs 0%).
35
9.6.3 Infectious
There are infections associated with pruritus ani. The intertriginous eruption by Candida
spp. is responsible for 10% of pruritus ani. Diffuse, marginated, erythematous, often macerated plaques, which are frequently painful, characterize it, but itching may be predominant. These manifestations are localized in the inguinal and perianal region, esp ecially in
patients with risk factors.
4,36
Mycotic flora is seen in proctological patients with and without
pruritus ani; the presence of dermatophytes has always been associated with pruritus ani.
37
The risk factors associated are the use of topical steroids, systemic antibiotic treatments,
and diabetic or immunosuppressed patients. Preferred treatments are antifungal powder,
lotion, or cream, depending on the moisture levels of the perianal region. Systemic antifungal treatment with fluconazole or itraconazole is indicated for severe infections.
4,37
Parasitic infections are other conditions that are associated with pruritus ani, esp ecially Enterobius vermicularis (pinworms). Perianal itching is the cardinal symptom of
a pinworm infestation.
38
Anal parasites are considered to be the most frequent cause of
pruritus ani at a pediatric age,
38
although they are less frequent in adults because of its
infectious cycle, anus-hand-mouth. However, in endemic areas with poor living conditions and overcrowding, the prevalence increases in adults. In the United States, approximately 20% of children will develop pinworm at some point in their lives because the
parasite is easily spread through the fecal-oral route.
39
Table 9.2 Initial Measures to Treat Anal Fissures
Increase the fiber and water intake 20–35g per day
Use fiber supplements Psyllium, methylcellulose
Sits baths 10–15 min, two times daily
Topic analgesics Lidocaine
Topical vasodilators Nifedipine or nitroglycerin
120 ANORECTAL DISORDERS
In pinworm pruritus ani occurs at n ight and causes an inflammation reaction due to
the presence of adult worms and e ggs on the perianal skin. If the host scratches the eggs
become lodged under the fingernails, thereby augmenting transmissi on, and secondary
bacterial infection may occur if excoriation is severe.
38
In patients with nocturnal itching
a clear cellophane tape can be applied to the anus and then examined for worms and
eggs to make the diagnosis. The goal of pharm acotherapy is to eradicate the infestation
and it is thus important to empirically cover the entire household simultaneously. The
preferred treatment is with oral alb endazo le or mebendazole, whic h is used as first-line
treatme nt; a single dose (100 mg) of mebendazole results in a mean cure rate of 95%, but
a second dose is often given after 1–2 weeks to help prevent recurrences due to reinfection.
40
An oral dose of albendazole (400 mg) plus a topical albendazole preparation
relieves perianal itching in 100%.
41
Itching, irritation, and excoriation should be treated
symptomatically.
9.6.4 Psychological Causes
In some cases pruritus ani may be a manifestation of depression or psychological disturbance. Common mood disorders, such as anxiety, stress, and certain personality traits
may contribute.
13
Although it seems arbitrary to systematically ascribe psychogenic etiologies to idiopathic pruritus ani, even though psychological factors may be present in
individual patients.
42
References
1. Chaudhry V, Bastawrous A. Idiopathic pruritus ani. Semin Colon Rectal Surg. 2003;14(4):196–202.
2. Hanno R, Murphy P. Pruritus ani. Classification and management. Dermatol Clin. 1987;5(4):811–816.
3. Markell KW, Billingham RP. Pruritus ani: etiology and management. Surg Clin North Am. 2010;90
(1):125–135.
4. Zuccati G, Lotti T, Mastrolorenzo A, et al. Pruritus ani. Dermatol Ther. 2005;1(4):355–363.
5. Ringkamp M, Schepers RJ, Shimada SG, et al. A role for nociceptive, myelinated nerve fibers in itch
sensation. J Neurosci. 2011;31(42):14841–14849.
6. Twycross R, Greaves MW, Handwerker H, et al. Itch: scratching more than the surface. QJM. 2003;96
(1):7–26.
7. Ansari P. Pruritus ani. Clin Colon Rectal Surg. 2016;29(1):38 –42.
8. Song S-G, Kim S-H. Pruritus ani. Contemp Coloproctol. 2011;27(2):54–57.
9. Farouk R, Duthie GS, Pryde A, et al. Abnormal transient internal sphincter relaxation in idiopathic
pruritus ani: physiological evidence from ambulatory monitoring. Br J Surg. 1994;81:603–606.
10. Allan A, Ambrose NS, Silverman S, et al. Phisiological study of pruritus ani. Br J Surg. 1987;50:19–23.
11. Swamiappan M. Anogenital pruritus—an overview. J Clin Diagn Res. 2016;10(4):WE01–WE03.
12. Al-Ghnaniem R, Short K, Pullen A, Fuller LC, Rennie JALA. 1% hydrocortisone ointment is an effective
treatment of pruritus ani: a pilot randomized controlled crossover trial. J Color Dis. 2007;22(12):1463.
13. Siddiqi S, Vijay V, Ward M, Mahendran R, Warren S. Pruritus ani. Ann R Coll Surg Engl. 2008;90
(6):457–463.
Chapter 9 • Pruritus Ani 121
14. Foxx-Orenstein AE, Umar SB, Crowell MD. Common anorectal disorders. Gastroenterol Hepatol.
2014;10(5):294–301.
15. Nasseri YY, Osborne MC. Pruritus ani: diagnosis and treatment. Gastroenterol Clin North Am. 2013;
42(4):801–813.
16. Lysy J, Sistiery-Ittah M, Israelit Y, et al. Topical capsaicin—a novel and effective treatment for idio-
pathic intractable pruritus ani: a randomised, placebo controlled, crossover study. Gut. 2003;52
(9):1323–1326.
17. Anand. Capsaicin and menthol in the treatment of itch and pain: recently cloned receptors provide the
key. Gut. 2003;52:1233–1235.
18. Ucak H, Demir B, Cicek D, Dertlioglu SB, Akkurt ZM, Ucmak DHN. Efficacy of topical tacrolimus for
the treatment of persistent pruritus ani in patients with atopic dermatitis. J Dermatolog Treat. 2013;
(6):454–457.
19. Suys E. Randomized study of topical tacrolimus ointment as possible treatment for resistant idio-
pathic pruritus ani. J Am Acad Dermatol. 2012;66(2):327–328.
20. Mentes BB, Akin M, Leventoglu S, Gultekin FA, Oguz M. Intradermal methylene blue injection for the
treatment of intractable idiopathic pruritus ani: results of 30 cases. Tech Coloproctol. 2004 Mar;
8(1):11–14.
21. Botterill ID, Sagar PM. Intra-dermal methylene blue, hydrocortisone and lignocaine for chronic,
intractable pruritus ani. Colorectal Dis. 2002;4(2):144–146.
22. Samalavicius NE, Poskus T, Gupta RK, Lunevicius R. Long-term results of single intradermal 1% meth-
ylene blue injection for intractable idiopathic pruritus ani: a prospective study. Tech Coloproctol. 2012
Aug;16(4):295–299.
23. Daniel GL, Longo WE, Vernava 3rd AM. Pruritus ani. Causes and concerns. Dis Colon Rectum. 1994
Jul;37(7):670–674.
24. Sanchez C, Chinn BT. Hemorrhoids. Clin Colon Rectal Surg. 2011;24(1):5–13.
25. Rivadeneira DE, Steele SR, Ternent C, et al. Practice parameters for the management of hemorrhoids.
Dis Colon Rectum. 2011;54(9):1059–1064.
26. Clinical Practice Committee. American Gastroenterological Association medical position statement:
diagnosis and treatment of hemorrhoids. Gastroenterology. 2004;126(5):1461–1462.
27. Lohsiriwat V. Treatment of hemorrhoids: a coloproctologist’s view. World J Gastroenterol. 2015;
21(31):9245–9252.
28. Lohsiriwat V. Hemorrhoids: from basic pathophysiology to clinical management. W
orld J Gastroen-
terol. 2012;18(17):2009–2017.
29. Ganz RA. The evaluation and treatment of hemorrhoids: a guide for the gastroenterologist. Clin Gas-
troenterol Hepatol. 2013;11(6):593–603.
30. Wald A, Bharucha AE, Cosman BC, Whitehead WE. ACG clinical guideline: management of benign
anorectal disorders. Am J Gastroenterol. 2014;109(8):1141– 1157.
31. Nienhuijs S, de Hingh I. Conventional versus Ligasure hemorrhoidectomy for patients with symptom-
atic hemorrhoids. Cochrane Database Syst Rev. 2009;(1):CD006761.
32. Jayaraman S, Colquhoun PH, Malthaner RA. Stapled hemorrhoidopexy is associated with a higher
long-term recurrence rate of internal hemorrhoids compared with conventional excisional hemorrhoid surgery. Dis Colon Rectum. 2007;50:1297–1305.
33. Tjandra JJ, Chan MK. Systematic review on the procedure for prolapse and hemorrhoids (stapled
hemorrhoidopexy). Dis Colon Rectum. 2007;50:878–892.
34. Jenkins JT, Urie A, Molloy RG. Anterior anal fissures are associated with occult sphincter injury and
abnormal sphincter function. Color Dis. 2008 Mar;10(3):280–285.
122 ANORECTAL DISORDERS
35. Parellada C. Randomized, prospective trial comparing 0.2 percent isosorbide dinitrate ointment with
sphincterotomy in treatment of chronic anal fissure: a two-year follow-up. Dis Colon Rectum. 2004;(4).
36. Zuccati G, Lotti T, Mastrolorenzo A, Rapaccini A, Tiradritti L. Pruritus ani. Dermatol Ther.
2005;18:355–362.
37. Dodi G, Pirone E, Bettin A, et al. The mycotic flora in proctological patients with and without pruritus
ani. Br J Surg. 1985 Dec;72(12):967– 969.
38. Jones JE. Pinworms. Am Fam Physician. 1988;(38):159–164.
39. Stermer E, Sukhotnic I, Shaoul R. Pruritus ani: an approach to an itching condition. J Pediatr Gastro-
enterol Nutr. 2009;48(5):513–516.
40. Truscott J, Abebe A, Donkers K, Segers D. Recognizing common parasitic infestations. JAAPA. 2017;30
(5):1–6.
41. Shivaram PS, Panda C, Rout N, Mishra AP. Anal albendazole application for pruritus ani in threadworm
infestation. J Trop Pediatr. 2005;51(6):386.
42. Laurent A, Boucharlat J, Bosson JL, Derry A, Imbert R. Psychological assessment of patients with idi-
opathic pruritus ani. Psychother Psychosom. 1997;66(3):163–166.
Chapter 9 • Pruritus Ani 123
10
Infectious Proctitis
Andreia Albuquerque
FA C U L T Y OF MEDI C I N E OF TH E U N I VE R S I T Y OF P O R T O, P O R T O , P O R T U GA L H O M ER T O N A N AL
NE O P L A SI A S E RV I C E ( H A N S ), H O M ER T O N U N I V E R SI T Y HOS P I T A L, L O N DO N , UN I T E D K I N G D OM
10.1 Definition and General Concepts
Proctitis is an inflammation of the rectum, typically involving the last 15 cm
1
and can have
noninfectious (e.g., inflammatory bowel disease, radiation proctitis) or infectious causes.
Most of the infections are sexually transmitted diseases (STDs) and common pathogens
are Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum, and herpes simplex virus (HSV).
1–3
Other pathogens also exist, although they are less frequently
described, like cytomegalovirus (CMV ) and amebiasis. Transmission can occur during
sexual anal intercourse. Men who have sex with men (MSM) are a high-risk group, but
other practices and routes of infection can also be implicated.
In some studies gonorrhea and chlamydia were the most frequent causes of proctitis in
MSM, followed by herpes and syphilis,
4
but in other settings HSV was the most common
pathogen implicated in HIV-positive MSM.
5
HIV-positive MSM frequently have multiple
infections compared with HIV-negative MSM.
5
In developed countries outbreaks of lymphogranuloma venereum (LGV) in MSM with
proctitis as the form of presentation
6
have been reported. There are several symptoms that
suggest proctitis; however, in many cases, patients can be asymptomatic.
7
The pathogen’s
primary infection site is related to the patient’s symptoms. In cases involving the rectum,
few sensory nerve endings are present, so frequently there are no symptoms (e.g., gonorrhea and chlamydia). Infections of the stratified squamous epithelium of the perianal area
and anal verge are more commonly painful (e.g., in HSV).
8
The presence of anal or perianal ulcers in a young sexually active patient is frequently associated with HSV or syphilis,
and HIV should always also be excluded.
9
In this chapter, proctitis due to chlamydia, gonorrhea, HSV, syphilis, CMV, and
Entamoeba histolytica will be described in more detail (
Table 10.1).
10.2 Herpes Simplex Virus
There are two types of HSV: type 1 (HSV-I) and type 2 (HSV-2). Most cases of HSV proctitis
are caused by HSV-2,
10
but the first-episode of anog enital herpes due to HSV-1 is signif-
icantly increased among younger MSM and heterosexual women.
11
Herpetic infections
can be primary or a reactivation.
1
In 20% of the cases infection has a chronic and
Anorectal Disorders.
https://doi.org/10.1016/B978-0-12-815346-8.00010-2
© 2019 Elsevier Inc. All rights reserved.
125
Table 10.1 Causes of Infectious Proctitis
Etiology Symptoms Endoscopy/Anoscopy Diagnostic Tests Therapy
Herpes simplex
virus type 1 and
type 2
Severe pain,
tenesmus,
constipation, anal
discharge, sacral
paresthesia,
difficulty urinating
Ulcers, purulent exudate Herpes simplex virus
DNA detection in rectal
biopsies or exudate
from lesions
Acyclovir 400 mg orally
three times daily, acyclovir
200mg orally five times
daily, valacyclovir 1g orally
twice daily or famciclovir
250mg orally three times a
day for 7–10 days (CDC) or
5–10days (European
guidelines)
Neisseria
gonorrhoeae
Most patients
asymptomatic
Tenesmus, pruritus,
thick purulent anal
discharge
Thick purulent anal
discharge, friability,
erythema
NAATs
Culture for
antimicrobial sensitivity
(treatment failure)
Ceftriaxone 250mg IM +
azithromycin 1g orally
single dose (CDC)
Ceftriaxone 500mg IM +
azithromycin 2g single
dose (European guidelines)
Treponema
pallidum
Primary syphilis:
chancre, discharge,
bleeding, pain,
itching
Secondary syphilis:
discharge, bleeding,
pain, anorectal
condylomata lata
Mucous membrane,
friability, erythema,
ulceration
Nontreponemal tests
(e.g., VDRL, RPR):
screening and
monitoring therapy
response
Treponemal test (e.g.,
FTA-ABS): confirmation
of diagnosis
Benzathine penicillin G 2.4
million units IM single dose
Chlamydia
trachomatis
serovars D-K
Most asymptomatic
Pain, discharge,
rectal bleeding
Friability, ulceration,
mild erythema
NAATs Azithromycin 1 g orally
once or doxycycline
100mg orally twice a day
for 7 days
Chlamydia
trachomatis
serovars L1, L2,
or L3
Pain, rectal bleeding,
fever, tenesmus
Normal or mild
erythematous, friable
mucosa, deep ulcers,
granulomas,
mucopurulent exudates,
strictures
NAATs Doxycycline 100mg orally
twice daily for 21 days
Cytomegalovirus Most asymptomatic
Mononucleosis-like
illness with rectal
bleeding, after
unprotected anal
intercourse
Mucositis, ulceration,
polypoid, and mass
lesions
PCR in blood and
mucosa or
immunohistochemistry
of the mucosa
Ganciclovir 5 mg/kg IV
twice daily for 2–3 weeks
or foscarnet 90 mg/kg IV
twice daily
Entamoeba
histolytica
Bloody diarrhea,
fever and abdominal
pain
Edematous mucosa,
ulcers
Antigen assays, PCR,
serology
Metronidazole 750mg
orally
three
times daily for
5–10days plus
paromomycin 10mg/kg/
day three times daily for 5–
10days or diloxanide
furoate 500mg three times
daily for 10 days orally
CDC, Centers for Disease Control and prevention; FTA-ABS, fluorescent treponemal antibody absorption; IM, intramuscular; IV,
intravenous; NAATs, Nucleic acid amplification tests; PCR, polymerase chain reaction; RPR, rapid plasma reagin; VDRL, venereal disease
research laboratory.
recurrent course.12Sexual transmission can occur duri ng anal intercourse or oral-anal
contact, especially in MSM.
7
The seroprevalence for HSV-1 and/or HSV-2 in MSM is
around 95%.
10
HSV proctitis is more common in HIV-positive MSM5and the incubation period is
around 1–3 weeks after exposure.
1
Severe pain, tenesmus, constipation, anal discharge,
sacral paresthesia, and difficulty urinating can be the presenting symptoms.
1,2
Only
one-third of the MSM have external ulceration.
5
Ulcers and purulent exudate can be seen
in the endoscopy/proctoscopy
1
(Fig. 10.1A–C). The biopsies in the ulcer’s base can reveal
nuclear inclusions or multinucleate cells.
1
HSV DNA detection from rectal biopsies or exudate from lesions is a rapid detection
method with high sensitivity and specificity, and it should be used routinely for diagnosis.
13,14
Serology is of limited value for acute infection diagnosis. The detection of IgG antibodies indicates previous infection and IgM is unreliable for diagnosing acute infection,
although seroconversion might be an indicator of a primary infection.
The Centers for Disease Control and Prevention (CDC) STDs treatment guide lines
9
(published in 2015) recommended treating the first genital HSV infection (there are no
specific recommendations for HSV proctitis) with either acyclovir 400mg orally three
times daily, acyclovir 200 mg orally five times daily, valacyclovir 1 g orally twice daily, or
famciclovir 250 mg orally three times a day for 7–10 days. These drugs can help control
the symptoms (first episode or recurrences) and decrease the duration of viral shedding,
but they do not eradicate the virus nor interfere with subsequent recurrences.
2
The 2017
European guidelines for the management of genital herpes
14
suggested treatment with the
same drugs for 5–10 days. Patients with proctitis due to HSV should be screened for HIV,
and abstinence is recommended when lesions are present.
2
HIV-positive patients can
have prolonged or more severe episodes and HSV shedding is increased.
9
10.3 Gonorrhea
Gonorrhea is caused by N. gonorrhoeae, and common infection routes are oral-anal, anal
sexual intercourse, and, in women, cervical/urethral dissemination. MSM and women are
high-risk groups.
1,2
FIG. 10.1 Immunocompetent women presenting with symptoms of pain and rectal bleeding. (A) Proctoscopy
revealing an ulcer extending from the pectin line to the distal rectum. (B) Extensive ulceration in the perianal area. (C)
Perianal area 14 days after acyclovir therapy was started.
Chapter 10 • Infectious Proctitis 127
The incubation period is around 5–7 days, but most patients are asymptomatic.7Tenesmus, pruritus, and a typically thick purulent anal discharge in the anoscopy can be
reported.
1,2
Other findings in the anoscopy, like friability and erythema, are nonspecific.
2
N. gonorrhoeae can be detected by nucleic acid amplification tests (NAATs) or by culture. The culture should be performed for antimicrobial sensitivity testing in patients with
treatment failure. Gram-negative diplococci are suggestive of a diagnosis, but microscopy
sensitivity is low in rectal infection
15
; therefore, it is not recommended in the rectum.
9
NAATs can provide results quicker, with higher sensitivity and are the first option in rectal
infections,
15
although no information on antibiotic susceptibility is provided.
The CDC recommended intramuscular (IM) ceftriaxone 250 mg plus azithromycin 1 g
orally in a single dose (similar for HIV-positive and negative patient s) as first-line therapy
for uncomplicated rectal infections (cure rates are 99.2%).
9
Doxycycline 100 mg orally
twice a day for 7 days can be used in cases of azithromycin allergy. This regimen can treat
both gonorrhea and chlamydia, co-infections are commonly seen. No test-of-cure is
needed for uncomplicated rectal infection treated with any of the recommended or alternative regimens, but patients should be re-tested 3 months after treatment (re-infection
risk). Testing for other STDs, including chlamydia, syphilis, and HIV, should also be done.
There is a threefold risk of HIV infection in MSM with gonorrhea.
2
The 2012 European
guidelines on the diagnosis and treatment of gonorrhea in adults recommended the same
drug regimen, but with different doses: ceftriaxone 500 mg IM as a single dose plus with
azithromycin 2 g as single oral dose.
15
If the patient is asymptotic a NAAT should be done
and in cases where there are persistent symptoms a culture is recommended with antimicrobial sensitivity testing.
15
Sexual partners need to be tested and treated.
9,15
Patients
should abstain from sexual activity for 7 days after they and their partners have completed
treatment and symptoms have resolved.
10.4 Syphilis
Syphilis is an infection due to T. pallidum with several different stages of the disease.
Acquired syphilis is divided into early and late stages. Early syphilis includes primary, secondary, and early latent syphilis. The European Centre for Disease Prevention and Control
defines early syphilis as syphilis acquired <1 year previously and for the World Health
Organization it is <2 years previously. Late syphilis includes late latent and tertiary
syphilis.
16
In acquired disease, transmission occurs through sexual contact12and most cases of
primary and secondary syphilis are in MSM. Mucocutaneous lesions predispose to infection and they are uncommon after the first year of infection.
9
Anorectal involvement can be seen in the primary and secondary stages. In primary
syphilis, painless anal ulcers can appear 2–6 weeks after infection, typically as an isolated
anal or rectal ulcer (chancre) with indurated edges and a clean base. One or multiple
lesions can be present,
1
usually with concomitant regional lymphadenopathy. Perianal
involvement can be seen, especially in MSM (
Fig. 10.2). Proctitis with or without
128 ANORECTAL DISORDERS
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