Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1185_Библиотеки_им_академика_М_И_Перельмана
.pdf
250 C.O. Finne
FIGURE 16-10. This patient had a reaction to topical clotrimazole in
use for 1 week.
Skin scrapings may be submitted for fungus culture, and if
available examined by KOH prep for hyphae. Most colorectal
offices are not set up for KOH prep and rarely are we trained
in this technique, therefore culture is probably more reliable.
Treatment of Pruritus Ani
A general strategy is presented in Table 16-7. Directed treatment
for a specific, curable diagnosis is the ideal, and diagnostic
efforts should be directed to avoid overlooking curable disease.
Many investigators have alluded to the importance of controlling seepage and fecal contamination of the skin. Diet may
directly contribute to itching and it is prudent to give patients
a list of potential foods implicated in itching for an elimination trial. Patients with loose stools may benefit from the
addition of fiber to absorb moisture and add bulk and improve
emptying with defecation. Many patients who have tried fiber
without benefit may benefit from judicious use of Imodium®
or Lomotil® to lessen frequency and firm up stools.
Questran®, in varied doses, has been helpful in my practice to
firm loose stools.
FIGURE 16-11. Scattered lesions, especially when accompanied by
severe symptoms suggest herpes virus infection. Herpes simplex
type 1 was cultured from the base of these ulcerations that were
9 days old at the time of this picture. Treatment caused prompt resolution of symptoms.
Environmental factors should be altered as much as possible with removal of irritants such as soaps, perfumes, dyes in
clothes or wiping tissues, alcohol- or witch hazel-containing
agents, and moisture. Dove® is free of conventional soap and
is the preferred bathing agent. Bidets are not common in the
United States, but detachable shower heads are common and
inexpensive and when equipped with long tubing and handle
may be a useful item for cleansing the perianal skin and anal
canal and eliminating soap residues by flushing with water in
the squatting position. Subsequent drying with a hair dryer
can eliminate moisture, and application of an athlete’s foot
powder or barrier cream will lubricate and prevent maceration
of the skin in the cleft and anal canal. Zeasorb® is an alternate lubricating, drying agent in powder form. Cornstarch is
to be avoided because it is culture medium for yeast.
Cornmeal agar is used to identify different species of yeast
57
in the laboratory.
Dilute white vinegar (1 tablespoon in an
8-ounce glass of water) on a cotton ball is a cheap effective
nonsoapy cleanser that can be kept at the toilet when bathing
is not handy. Burow’s solution, 1:40 (Domeboro® tablet one
in 12 ounces of water, or one in 6 ounces for 1:20) is another
nonirritating cleanser that can be kept refrigerated in a plastic
squeeze bottle and used in lieu of soap or plain water. Burow’s

16. Perianal Dermatology and Pruritus Ani 251
FIGURE 16-13. Skin punch biopsy tools come in various sizes up to
1 cm in diameter (2, 3, and 5 mm pictured). They may be purchased
as autoclavable sets which may be sterilized and reused, or for the
occasional user, disposable punches are supplied in individually
wrapped sterile packages. One advantage of the disposable instruments is that they are always sharp.
FIGURE 16-12. LS has a distinctive appearance with cigarette paper
thinning and wrinkling of the skin. It almost always involves the
labial skin and perineum, making it easy to recognize. Biopsy is
characteristic and is especially indicated for any areas that are raised,
ulcerated, or unresponsive to treatment because of a 5% risk of
squamous cell carcinoma developing within its distribution.
may be used as an antibacterial soak for 5–15 minutes and
then dried. Balneol® is a commercially available mineral
oil–based preparation that can be kept in a pocket and
squeezed onto toilet paper to make a soothing cleansing agent
when using public facilities. Breaks in the skin caused by
scratching or over-vigorous cleansing efforts must be
avoided, so an attempt to control symptoms with application
of topical anesthetics, menthol, phenol, camphor, or a combination of ingredients may be appropriate. These agents may
be used in combination with topical steroids, topical antifungal agents, and topical antibacterials. Doxepin (Sinequan®
TABLE 16-6. Differential diagnosis of groin adenopathy
Benign reactive (shoeless walking)
Lymphoma
Carcinoma (penis,vulva, anal canal)
Sarcoidosis
Syphilis (nontender)
Leishmaniasis
Chancroid (tender)
Herpes genitalis (tender)
Lymphogranuloma venereum
orally) is available topically as an effective antihistamine
(Zonalon®), but orally is 1000 times more potent than
diphenhydramine (Benadryl®) for elimination of itching and
may a useful adjunct at bedtime to avoid nocturnal scratching.
Nocturnal scratching, of which the patient may be unaware, is
probably a significant contributing factor in most cases of
idiopathic pruritus ani. Patients who are awakened by the urge
to scratch should be instructed to gently cleanse the area to
eliminate any fecal seepage and reapply their steroid or barrier cream (whichever is in effect at the time) but not to
scratch. Pepper creams may be useful in breaking the overwhelming urge to scratch by substituting a more powerful
temporary burning stimulus.
No data exist on the influence of clothes or other fomites on
pruritus, but from a practical standpoint, loose underwear that
TABLE 16-7. Treatment of pruritus ani
1. Specific directed treatment for a diagnosis
2. Eliminate offending agent [contact irritant (perfume, soap, toilet paper),
organism]
3. Eliminate scratching (especially nocturnal)
4. Control symptoms
5. Hygienic measures (Dove® soap, detachable shower head, hair dryer to
dry)
6. Withdraw inappropriate steroids
7. Treat infection (silver sulfadiazine cream, gentamicin or clindamycin
topically, nystatin, clotrimazole)
8. Protect skin [barrier creams, powders (especially athlete’s foot powder)]
9. Correct anal disease (fissure, hemorrhoids)
10. Judicious use of appropriate steroids
11. Emphasize control as a chronic condition
12. Reassess diagnosis if response to treatment is not appropriate
13. Anal tattooing in extreme cases

252 C.O. Finne
allows air circulation and promotes dryness makes sense.
Fresh clothes should be used daily that have been laundered
without perfume, perhaps with the addition of a small amount
of chlorine bleach to secure lowered bacterial counts.
Patients who come to the office with acute moderate to
severe changes of the skin are treated by application of
Berwick’s dye (combination of gentian violet and brilliant
green) which has alcohol content and stings, often relieving
the itch. The dye is dried with compressed air or a hair dryer.
Benzoin tincture is applied over top of this as a barrier and
dried similarly. This preparation will stay in place for several
days if only water is used to cleanse and gives excellent temporary relief of symptoms and allows reepithelialization of
broken skin. Berwick’s is suitable as an office applied remedy
but is generally not for home application.
Patients who have mild to moderate symptoms with minimal skin changes will often respond to topical 1% hydrocortisone cream which can be combined with menthol,
0.5%–1.0%, and topical antibiotics (gentamicin, clindamycin,
or bacitracin) or antifungals (clotrimazole, nystatin). This
preparation is applied at night and in the morning after
bathing, being used daily until symptoms subside. Thereupon
a tapering regimen is instituted, ending with substitution of a
barrier cream such as Calmoseptine® to keep the skin
covered. Elimination of the steroids and substitution of an
innocuous agent to maintain attention to the hygiene is an
important goal. Patients with thickened skin and chronic moderate or severe changes should be approached with higher
intensity therapy, with a medium or high potency steroid for a
limited, defined period of time (Table 16-8; nonsteroidal topical therapies are listed in Table 16-9). My preference is to
prescribe brand names when dealing with topical steroids
because of the vehicle in which it is delivered, and the particular salt matter as to potency (Table 16-8). For instance,
betamethasone as Diprolene® is more than 1000 times
more potent than Valisone® cream, with Valisone® ointment
TABLE 16-8. Relative potency of topical steroids (descending order)
Group 1 (most potent) Group 4
Betamethasone dipropionate Desoximetasone 0.05%
0.05% (Diprolene®) (Topicort LP®)
Clobetasol propionate Flurandrenolide 0.05% (Cordran®)
0.05% (Temovate®)
Group 2 Group 5
Desoximetasone 0.25% Betamethasone valerate cream
(Topicort®) 0.1% (Valisone®)
Fluocinonide 0.05% (Lidex®) Hydrocortisone butyrate 0.1%
(Locoid®)
Triamcinolone acetonide 0.1%
(Kenalog®)
Group 3 Group 6 (least potent)
Betamethasone valerate Alclometasone dipropionate
ointment 0.1% (Valisone®) 0.05% (Aclovate®)
Triamcinolone acetonide Hydrocortisone 1%
0.5% (Aristocort®)
TABLE 16-9. Nonsteroidal topical therapy for itching
Berwick’s dye (crystal violet 1% + brilliant green 1% + 95% ethanol 50% +
distilled H
Burow’s solution 1:40
Calmoseptine®
Camphor® (0.1%–3%)
Capsaicin (Zostrix® 0.025%, Dolorac® 0.25%)
Cold compress (ice cube)
Doxepin 5% (Zonalon®)
EMLA (eutectic mixture of local anesthetics)
Hot compress (120˚F)
Macrolide topical agents (Tacrolimus and Pimecrolimus)
Menthol (0.125%–1%)
Phenol (0.125%–2%)
Pramoxine
Shake lotions (calamine + additives)
Topical “caines”
O q.s.ad. 100%) with benzoin barrier
2
somewhere in between. These differences can lead to a great
deal of confusion when prescribing by generic name without
spelling out every tiny detail. Emphasize to patients that a
high-potency steroid should be used for a limited period of
time, generally 4–8 weeks. When normalization of the skin
has been achieved, switch them to a mild steroid such as
hydrocortisone 1% or Locoid® 0.1% with tapering frequency
of application down to once or twice a week or to total elimination. Patients who have frankly eroded or denuded skin
may benefit from topical antibiotics. Silver sulfadiazine
cream to which hydrocortisone or triamcinolone and menthol
have been added may be soothing and promote regrowth of
epidermis over ulcerated areas while suppressing the inflammation that can cause fissuring in the skin.
Skin atrophy is a serious problem with prolonged use of
potent steroids, but each of the steroid preparations differs in
its tendency to cause trouble. Creams cause comparatively
greater atrophy than ointment preparations containing identi-
58
cal ingredients.
Newer, double-ester, nonfluorinated steroids
may prove to be less atrophogenic than the older prepara-
58,59
tions,
but the package stuffers for prednicarbate and
mometasone furoate still quote 8% and 6% incidence of mild
skin atrophy for these compounds. Macrolide topical immune
modulators (tacrolimus and pimecrolimus) seem to be free of
the problem of skin atrophy, a fact that enhances their appeal
for use on the apposed skin of the cleft.
may have some intrinsic antifungal activity as well.
60
These compounds
61
I have
had a very limited, good anecdotal experience with these
compounds, but there are currently no published data on
topical macrolide use in pruritus ani. Table 16-10 lists the
TABLE 16-10. Adverse reactions to topical steroids
Skin atrophy with telangiectasia, pseudoscars, purpura, striae, spontaneous
bleeding
Tinea, impetigo, scabies incognito
Allergic contact dermatitis
Systemic absorption with adrenal suppression
Burning, itching, dryness from vehicle
Rebound worsening after withdrawal

16. Perianal Dermatology and Pruritus Ani 253
potential complications of topical steroids, which are not to be
taken lightly, and are all the more important because they are
preventable complications of treatment excess.
Anal Tattooing
Every practice has a small number of patients who respond
poorly to treatment and whose symptoms are severe enough
to alter life and happiness. These refractory patients may benefit from a technique originally described by a Russian surgeon, but espoused in the United States by Wolloch and
Dintsman
relief after one treatment, one requiring a second injection to
obtain a good result. Eusebio et al.
with complete relief, 8 with incomplete relief but much
improved, and 2 who were not improved, but who had presented with burning, not itching. Three cases of skin necrosis
resulted in modification of their technique, and treatment of
11 subsequent patients was without complication with good
result.
and subcutaneous injection of the following solution with the
patient under intravenous sedation in the prone jackknife
position: 10 mL 1% methylene blue + 5 mL normal saline +
7.5 mL 0.25% bupivacaine with epinephrine (1/200,000)
+ 7.5 mL 0.5% lidocaine. Farouk and Lee
patients treated with a similar volume to the modified technique
of Eusebio et al. Five patients got substantial relief of symptoms with follow-up of 2–5 years. Three of the six required a
repeat injection at 1, 3, and 5 years after the initial treatment.
trating the skin with the same solution as Eusebio et al. using
a modified technique. I use a 30- or 27-gauge needle and infiltrate the skin as I would for cutaneous anesthesia with multiple injection sites sufficient to cover the perianal-involved
skin up to the dentate line (Figure 16-14). All four of my
patients have gotten results lasting at least 1 year, during
which time all have had relative cutaneous hypoesthesia.
They describe the sensation as having the side of one’s face
numb after a dental block. Certain individuals have found this
sensation very disagreeable, so I am careful to warn them
in detail before treatment. The skin changes of severe pruritus in
all cases rapidly and dramatically regressed and resolved.
In one case with return of skin sensation at about a year, the
pruritus returned and required topical therapy to be reinstituted, but was milder and did not require repeat injection. The
response of these patients during the time of hypalgesia lends
some credence to the idea of skin trauma from nocturnal
scratching of which patients are not aware.
Conclusion
Skin conditions around the anus are common and often poorly
diagnosed and treated. The appearance of a lesion is rarely
pathognomonic, but may place it into a diagnostic category
62
who described nine patients, eight of whom got
63
reported 23 patients: 13
64
The modified technique consists of the intradermal
65
reported six
I have personally used this technique on four patients, infil-
FIGURE 16-14. Tattooing with methylene blue is a simple technique
to treat intractable itching that does not respond to traditional vigorous therapy. Patients experience hypalgesia and numbness of the
perianal skin that can be bothersome, but rapid resolution of itching
occurs and the chronic skin changes normalize quickly.
that can be either treated or investigated in a systematic way
to arrive at a logical successful outcome. Follow-up of treatment plans, reevaluation of patients with chronic conditions,
and reconsideration of ongoing prescriptions should be standard practice and help to avoid the pitfall of misdiagnosis.
References
1. Daniel GL, Longo WE, Vernava AM 3rd. Pruritus ani. Causes
and concerns. Dis Colon Rectum 1994;37(7):670–674.
2. Corman ML. Colon and Rectal Surgery. 2nd ed. Philadelphia:
Lippincott; 1989:287.
3. Verbov J. Pruritus ani and its management: a study and reappraisal. Clin Exp Dermatol 1984;9(1):46–52.
4. Quine WV. Quiddities: An Intermittently Philosophical
Dictionary. Cambridge: Harvard University Press; 1987.
5. Bernhard JD. Itch: mechanisms and management of pruritus.
New York: McGraw-Hill; 1994.
6. Stamos MJ, Hicks TC, eds. Pruritus Ani: Diagnosis and
Treatment. New York: Thieme Medical Publishers; 1998.

254 C.O. Finne
7. Sherertz EF. Clinical pearl: symptomatic dermatographism as a
cause of genital pruritus. J Am Acad Dermatol 1994;31(6):
1040–1041.
8. Bernhard JD, Kligman AM, Shelley WB. Dermographic pruritus:
invisible dermographism. J Am Acad Dermatol 1995;33(2 pt 1):
322.
9. Caplan RM. The irritant role of feces in the genesis of perianal
itch. Gastroenterology 1966;50(1):19–23.
10. Smith LE, Henrichs D, McCullah RD. Prospective studies on the
etiology and treatment of pruritus ani. Dis Colon Rectum
1982;25(4):358–363.
11. Allan A, Ambrose NS, Silverman S, Keighley MR. Physiological
study of pruritus ani. Br J Surg 1987;74(7):576–579.
12. Farouk R, Duthie GS, Pryde A, Bartolo DC. Abnormal transient
internal sphincter relaxation in idiopathic pruritus ani: physiological evidence from ambulatory monitoring. Br J Surg
1994;81(4):603–606.
13. Eyers AA, Thomson JP. Pruritus ani: is anal sphincter dysfunction important in aetiology? Br Med J 1979;2(6204):1549–1551.
14. Dodi G, Pirone E, Bettin A, et al. The mycotic flora in proctological patients with and without pruritus ani. Br J Surg 1985;
72(12):967–969.
15. Alexander S. Dermatological aspects of anorectal disease. Clin
Gastroenterol 1975;4(3):651–657.
16. Pirone E, Infantino A, Masin A, et al. Can proctological procedures resolve perianal pruritus and mycosis? A prospective study
of 23 cases. Int J Colorectal Dis 1992;7(1):18–20.
17. Bowyer A, McColl I. A study of 200 patients with pruritus ani.
Proc R Soc Med 1970;63(suppl):96–98.
17A. Weismann K, Sand Petersen C, Roder B. Pruritus ani caused by
heto-hoemolytic streptocacel Acta Derm Venereal 1996;76:415.
18. Bowyer A, McColl I. Erythrasma and pruritus ani. Acta Derm
Venereol 1971;51(6):444–447.
19. Sindhuphak W, MacDonald E, Smith EB. Erythrasma.
Overlooked or misdiagnosed? Int J Dermatol 1985;24(2):95–96.
20. Baral J. Pruritus ani and Staphylococcus aureus. J Am Acad
Dermatol 1983;9(6):962.
21. Dasan S, Neill SM, Donaldson DR, Scott HJ. Treatment of persistent pruritus ani in a combined colorectal and dermatological
clinic. Br J Surg 1999;86(10):1337–1340.
22. Habif TP. Clinical Dermatology: A Color Guide to Diagnosis
and Therapy. 3rd ed. St. Louis: Mosby; 1996.
23. Harrington CI, Lewis FM, McDonagh AJ, Gawkrodger DJ.
Dermatological causes of pruritus ani. BMJ 1992;305(6859):955.
24. Bruynzeel DP. Dermatological causes of pruritus ani. BMJ
1992;305(6859):955.
25. Lochridge E Jr. Pruritis ani: perianal psoriasis. South Med J
1969;62(4):450–452.
26. Meffert JJ, Davis BM, Grimwood RE. Lichen sclerosus. J Am
Acad Dermatol 1995;32(3):393–416; quiz 7–8.
27. Neill SM, Tatnall FM, Cox NH. Guidelines for the management
of lichen sclerosus. Br J Dermatol 2002;147(4):640–649.
28. Wong YW, Powell J, Oxon MA. Lichen sclerosus. A review.
Minerva Med 2002;93(2):95–99.
29. Powell JJ, Wojnarowska F. Lichen sclerosus. Lancet 1999;353
(9166):1777–1783.
30. Carli P, De Magnis A, Mannone F, Botti E, Taddei G, Cattaneo A.
Vulvar carcinoma associated with lichen sclerosus. Experience at
the Florence, Italy, Vulvar Clinic. J Reprod Med 2003;48(5):
313–318.
31. Carli P, Cattaneo A, De Magnis A, Biggeri A, Taddei G,
Giannotti B. Squamous cell carcinoma arising in vulval lichen
sclerosus: a longitudinal cohort study. Eur J Cancer Prev 1995;
4(6):491–495.
32. Byren I, Venning V, Edwards A. Carcinoma of the vulva and
asymptomatic lichen sclerosus. Genitourin Med 1993;69(4):
323–324.
33. Assmann T, Becker-Wegerich P, Grewe M, Megahed M, Ruzicka
T. Tacrolimus ointment for the treatment of vulvar lichen sclerosus. J Am Acad Dermatol 2003;48(6):935–937.
34. Bohm M, Frieling U, Luger TA, Bonsmann G. Successful treatment of anogenital lichen sclerosus with topical tacrolimus. Arch
Dermatol 2003;139(7):922–924.
35. Friend WG. The cause and treatment of idiopathic pruritus ani.
Dis Colon Rectum 1977;20(1):40–42.
36. Akl K. Yogurt-induced pruritus ani in a child. Eur J Pediatr
1992;151(11):867.
37. Murie JA, Sim AJ, Mackenzie I. The importance of pain, pruritus and soiling as symptoms of haemorrhoids and their response
to haemorrhoidectomy or rubber band ligation. Br J Surg
1981;68(4):247–249.
38. Koblenzer CS. Psychologic and psychiatric aspects of itching.
In: Bernhard JD, ed. Itch: Mechanisms and Management of
Pruritus. New York: McGraw-Hill; 1994:347–365.
39. Andrews D, Grunau VJ. An uncommon adverse effect following
bolus administration of intravenous dexamethasone. J Can Dent
Assoc 1986;52(4):309–311.
40. Kligman AM, Frosch PJ. Steroid addiction. Int J Dermatol
1979;18(1):23–31.
41. Goldman L, Kitzmiller KW. Perianal atrophoderma from topical
corticosteroids. Arch Dermatol 1973;107(4):611–612.
42. Alexander-Williams J. Pruritus ani. Br Med J (Clin Res Ed)
1983;287(6386):159–160.
43. Rohde H. Routine anal cleansing, so-called hemorrhoids, and
perianal dermatitis: cause and effect? Dis Colon Rectum 2000;
43(4):561–563.
44. Thorp MA, Oliver SP, Kruger J, Prescott CA. Determination of
the lowest dilution of aluminium acetate solution able to inhibit
in vitro growth of organisms commonly found in chronic suppurative otitis media. J Laryngol Otol 2000;114(11):830–831.
45. Thorp MA, Kruger J, Oliver S, Nilssen EL, Prescott CA. The
antibacterial activity of acetic acid and Burow’s solution as topical otological preparations. J Laryngol Otol 1998;112(10):
925–928.
46. Thorp MA, Gardiner IB, Prescott CA. Burow’s solution in the
treatment of active mucosal chronic suppurative otitis media:
determining an effective dilution. J Laryngol Otol 2000;114(6):
432–436.
47. Dibb WL. In vitro efficacy of Otic Domeboro against Pseudo-
monas aeruginosa. Undersea Biomed Res 1985;12(3): 307–313.
48. Sarmiento JM, Wolff BG, Burgart LJ, Frizelle FA, Ilstrup DM.
Paget’s disease of the perianal region: an aggressive disease? Dis
Colon Rectum 1997;40(10):1187–1194.
49. Jensen SL, Sjolin KE, Shokouh-Amiri MH, Hagen K, Harling H.
Paget’s disease of the anal margin. Br J Surg 1988;75(11):1089–1092.
50. Helwig EB, Graham JH. Anogenital (extramammary) Paget’s
disease. A clinicopathological study. Cancer 1963;16:387–403.
51. Marchesa P, Fazio VW, Oliart S, Goldblum JR, Lavery IC.
Perianal Bowen’s disease: a clinicopathologic study of 47 patients.
Dis Colon Rectum 1997;40(11):1286–1293.

16. Perianal Dermatology and Pruritus Ani 255
52. Chang GJ, Berry JM, Jay N, Palefsky JM, Welton ML. Surgical
treatment of high-grade anal squamous intraepithelial lesions: a
prospective study. Dis Colon Rectum 2002;45(4):453–458.
53. Goldstone SE, Winkler B, Ufford LJ, Alt E, Palefsky JM. High
prevalence of anal squamous intraepithelial lesions and squamous-cell carcinoma in men who have sex with men as seen in a
surgical practice. Dis Colon Rectum 2001;44(5):690–698.
54. Goldman S, Glimelius B, Pahlman L. Anorectal malignant
melanoma in Sweden. Report of 49 patients. Dis Colon Rectum
1990;33(10):874–877.
55. Brady MS, Kavolius JP, Quan SH. Anorectal melanoma. A
64-year experience at Memorial Sloan-Kettering Cancer Center.
Dis Colon Rectum 1995;38(2):146–151.
56. Enker WE, Heilwell M, Janov AJ, et al. Improved survival in epidermoid carcinoma of the anus in association with preoperative
multidisciplinary therapy. Arch Surg 1986;121(12):1386–1390.
57. McClatchey KD. Clinical Laboratory Medicine. 2nd ed.
Philadelphia: Lippincott Williams & Wilkins; 2002.
58. Kerscher MJ, Korting HC. Comparative atrophogenicity potential of medium and highly potent topical glucocorticoids in
cream and ointment according to ultrasound analysis. Skin
Pharmacol 1992;5(2):77–80.
59. Kerscher MJ, Hart H, Korting HC, Stalleicken D. In vivo assessment of the atrophogenic potency of mometasone furoate, a
newly developed chlorinated potent topical glucocorticoid as
compared to other topical glucocorticoids old and new. Int J Clin
Pharmacol Ther 1995;33(4):187–189.
60. Robinson N, Singri P, Gordon KB. Safety of the new macrolide
immunomodulators. Semin Cutan Med Surg 2001;20(4):242–249.
61. Ling MR. Topical tacrolimus and pimecrolimus: future directions. Semin Cutan Med Surg 2001;20(4):268–274.
62. Wolloch Y, Dintsman M. A simple and effective method of treatment for intractable pruritus ani. Am J Proctol Gastroenterol
Colon Rectal Surg 1979;30(1):34–36.
63. Eusebio EB, Graham J, Mody N. Treatment of intractable pruritus ani. Dis Colon Rectum 1990;33(9):770–772.
64. Eusebio EB. New treatment of intractable pruritus ani. Dis Colon
Rectum 1991;34(3):289.
65. Farouk R, Lee PW. Intradermal methylene blue injection for the
treatment of intractable idiopathic pruritus ani. Br J Surg
1997;84(5):670.

17
Sexually Transmitted Diseases
Charles B. Whitlow and Lester Gottesman
There are more than 25 diseases spread primarily by sexual
means with an annual incidence of approximately 15 million
cases in the United States.
major sexually transmitted diseases (STDs) was estimated to
be 17 billion dollars. In the United Kingdom, the incidence of
STDs has increased substantially over the past 6 years and has
led to a new government strategy to counteract these
increases.
by STDs. Infections of the distal anal canal, anoderm, and
perianal skin are similar to lesions in other parts of the genitalia and perineum caused by the same organisms. These are
typically the result of anal receptive intercourse but in some
instances represent contiguous spread from genital infections. Proctitis from sexually transmitted organisms is almost
always from anal intercourse. Direct or indirect fecal–oral
contact produces infection with organisms that cause proctocolitis or enteritis but are generally thought of as food or
waterborne diseases instead of STDs. Included in this group
are Entamoeba histolytica, Campylobacter, Shigella,
Giardia lamblia, and hepatitis A. Although it seems that
male homosexual activity and the use of the anorectum for
sexual gratification is increasing, data regarding the frequency of these behaviors both past and present are limited.
Current estimates are that less than 2% of adult males regularly practice anal receptive intercourse and between 2% to
10% participate in homosexual activity at any point in their
life.
tive intercourse “with some degree of regularity” and females
seem to be more likely than men to have unprotected anal
intercourse.
STDs of the anorectum is caused by several factors. 1) The
signs and symptoms of infection are more organ related than
organism related so that no symptom or symptom complex or
physical finding is diagnostic for many STDs. 2) The presence of more than one organism is not uncommon, especially
with anogenital ulcerations. 3) Determining true pathogen
from colonizing organisms may be difficult. 4) Lastly, there is
2,3
Site and route of infection determine the symptoms caused
4
Between 5% and 10% of females engage in anal recep-
4
Difficulty in correct diagnosis and appropriate treatment of
1
In 1994, the overall cost related to
a lack of rapid sensitive diagnostic tests for many STDs so
that empiric treatment is frequently required.
This chapter discusses the STDs that are most often seen by
colorectal surgeons. Entire texts are devoted to the STDs;
however, we will confine most of our comments to the diagnosis, treatment, and prevention of the anorectal component
of these infections. Infections, which manifest as one of the
colitides, are covered in Chapter 43.
Overview of Anorectal Immunology
The optimal state of health of the anus requires the integrity
of the skin which acts as the primary protection against
invasive pathogens. The mucosa shed from the rectum contains immunoglobulin A which traps foreign antigens and
expels them with stool, preventing them from reaching
the anorectal crypt cells.
by the Langerhans, or dendritic cells which communicate
with the T cells through a complicated mechanism and essentially prime the T cells to identify foreign cells.
allows the entire complement of cell-mediated immunity to
destroy that which is alien. Although study of anal immunology is still in its infancy, it seems that certain pathogens may
alter the balance of cellular elements. It is known that whereas
human papilloma virus (HPV) increases Langerhans cells,
human immunodeficiency virus (HIV) may damage their
effectiveness. In addition, pathogens such as HPV and herpes
simplex virus (HSV) invade into the host cell, combining with
cellular elements or the genome, thus evading surveillance
mechanisms. In addition, in the case of HPV, the identifying
foreign antigens are placed onto the frame of the new virus
near the epidermis, where the virus normally sheds and where
an attack by the host has little value.
HIV is known to deplete cell-mediated immunity by depletion of T cells and destruction of Langerhans cells. This
allows, through unknown mechanisms, propagation of oncogenic processes such as HPV to become dysplastic. The exact
switches are not understood but seem to be related to the
5
Cellular immunity is controlled
6
This then
7
256

17. Sexually Transmitted Diseases 257
coexistence of perhaps HSV and the highly active antiretroviral therapy (HAART) drugs.
Breakdown of the mucous complex protecting the rectum is
seen in various diseases contracted through anal intercourse.
The physical act of intercourse abrades the mucous lining and
delivers pathogens directly to the crypt and columnar cells
allowing for easy entry. Depending on their mechanism of
action, they may burrow into the cells (ameba) or proliferate
on the cells without damaging them (G. neisseria). Invasive
pathogens (LGV) unleash nefarious cytokines that can destroy
the cell. The immune response is usually too late to contain an
acute attack. In the case of recurrent viral attacks (HPV,
HSV), it seems that the level of functioning T cells may have
an impact on recurrence of warts or herpes outbreaks. The
mechanics of anoreceptive intercourse, as compared with
vaginal intercourse, almost always results in denuding of the
protecting cellular and mucous layer of the anus and rectum.
Latex allergies, with condom use, may also be seen causing
severe invasive and erosive proctitis and should be in the differential of a caustic burn to the rectum after sexual anoreceptive intercourse.
Diagnosis and Management of
Bacterial Pathogens
Gonorrhea
Neisseria gonorrhoeae, the Gram-negative diplococcus
(Figure 17-1) responsible for gonorrhea, was first described by
Albert Neisser in 1879 from exudates from urethritis and cer-
8
vicitis.
ing the anorectum. Whereas gonorrhea rates decreased over
the last several decades, in the mid-1990s the incidence slowly
increased to the current rate of about 650,000 cases per year.
Similar recent increases have been noted in Canada and the
United Kingdom.
It is probably the most common bacterial STD affect-
9
Peak incidence for all forms of gonorrhea
is in the late teens for females and early 20s for males.
African-Americans have a 30-fold higher rate of infection
than white Americans.
Infection from N. gonorrhoeae occurs in columnar,
cuboidal, or noncornified epithelial lined cells of the urethra,
endocervix, rectum, and pharynx and is frequently asymptomatic. The incubation period ranges from 3 days to 2 weeks.
Untreated infection may lead to disseminated gonococcal
infection with transient bacteremia, arthritis, and dermatitis.
Rare but severe sequelae include endocarditis and meningitis.
Anorectal transmission in homosexual males and some
females is by anoreceptive intercourse with an infected partner.
Thirty-five to fifty percent of women with gonococcal cervicitis
have concomitant rectal infection which is believed to be from
10
contiguous spread from the genital infection.
Oral-anal sex has
been suggested as another mode of anorectal gonococcal infec-
11
tion.
A large percentage of patients who culture positive for
rectal gonorrhea are asymptomatic—up to 50% of males and
95% of females. Asymptomatic rectal infection constitutes the
main reservoir of gonococcal disease in homosexual men.
Symptomatic anorectal gonococcal infection results in
pruritus, tenesmus, bloody discharge, mucopurulent discharge, and/or severe pain. External inspection of the anus is
generally unremarkable; however, nonspecific erythema and
superficial ulceration may occur (Figure 17-2). Anoscopy
reveals a thick purulent discharge, which classically is
expressed from the anal crypts as pressure is applied externally on the anus. Nonspecific proctitis may be present with
erythema, edema, friability, and pus. Diagnosis is confirmed
by culture on selective media (Thayer-Martin or Modified
New York City) incubated in a CO
Gram’s stain of directly visualized discharge.
-rich environment and
2
12
The use of
lubricants other than water may introduce antibacterial agents
during anoscopy and decrease diagnostic yield. Nonculture
detection of gonorrhea is being used more frequently especially in urethral and cervical infections. Nucleic acid amplification tests (NAATs) such as polymerase chain reaction
FIGURE 17-1. Gram-negative intracellular diplococcus.
FIGURE 17-2. Anorectal gonorrhea.

258 C.B. Whitlow and L. Gottesman
(PCR) and ligase chain reaction (LCR) and nonamplified
DNA probes provide sensitivities of greater than 95% but do
not provide antibiotic susceptibility data. There are no
NAATs currently licensed for detection of rectal gonorrhea.
Because of the prevalence of penicillinase-producing
N. gonorrhoeae starting in the 1970s, penicillin G is no longer
the drug of choice for gonorrhea. The most current recommended treatment regimens from the Centers for Disease
Control (CDC) were published in 2002 and are listed in Table
17-1. Since publication of these guidelines, cefixime has
become unavailable in the United States. Alternative regimens include spectinomycin (2 g as a single intramuscular
injection), other cephalosporins (ceftizoxime, cefoxitin, and
cefotaxime), and other quinolones. Only a few isolates
reported by the Gonococcal Isolate Surveillance Report in the
past 10 years showed decreased susceptibility to the
cephalosporins listed in Table 17-1.
15
Quinolone-resistant
N. gonorrhoeae (QRNG) have been detected in the past
decade with increasing frequency in Asia and the Pacific. In
the United States, this is particularly important in Hawaii
(where QRNG may account for as much as 14% of gonorrhea
isolates) and California. In the United Kingdom, the overall
rate of QRNG was reported at 9.8% for 2002.
16
Concurrent
HIV infection does not alter treatment for anorectal gonorrhea. Because of the high rate of concomitant infection with
chlamydia, patients treated for gonococcal infections should
be given appropriate treatment for chlamydia at the same visit
or measures to rule out chlamydial infection should be taken.
Routine follow-up at 3 months is no longer necessary
because current treatment provides near 100% efficacy.
Patients with persistent symptoms after treatment should be
followed and cultured as should those treated with nonstandard antibiotics. Sexual partners from the past 60 days should
be treated and patient should abstain from intercourse until
treatment is completed and symptoms resolved.
Chlamydia/Lymphogranuloma Venereum
Anorectal transmission of chlamydia is through anoreceptive intercourse although secondary involvement can occur as
a late manifestation of genital infection. Different serovars of
13
C. trachomatis produce differing clinical illness. Serovars D
through K [non–lymphogranuloma venereum (LGV)] are
responsible for proctitis and common genital infections.
Lymphogranuloma venereum is caused by LGV serovars
L1–L3. The incubation period for chlamydia is 5 days to 2
weeks. Non-LGV serovars are less invasive and cause mild
proctitis (manifested by tenesmus, pain, and discharge) but
asymptomatic infection is common. LGV serovars produce a
much more aggressive infection with perianal, anal, and rectal
ulceration. The proctitis produced can be difficult to distinguish from Crohn’s disease (including microscopic findings of
granulomas) with resulting rectal pain and discharge.
Anoscopy and sigmoidoscopy demonstrate friable rectal
mucosa, which is more severe in appearance (and extends
above the rectum in some cases) in LGV strains.
18–20
abscesses, fistulas, and stricturing may also occur. Lymphadenopathy develops in draining nodal basins—iliac, perirectal,
inguinal, and femoral—several weeks after initial infection.
Large indurated matted nodes (Figure 17-3) and overlying
erythema may produce a clinical picture similar to syphilis.
Diagnosis of chlamydia as the causative agent in proctitis
can be difficult. Proper specimen collection increases diagnostic yield and consists of a cotton or Dacron swab with an
inert shaft (plastic or metal). Specimen for tissue culture
should be transported on specific medium and kept refrigerated or on ice until inoculated onto culture plates. Specimens
that are to be tested by a nonculture technique are transported
and stored in accordance with the test manufacturer’s guidelines. In patients with a clinical presentation consistent with
chlamydia proctitis, rectal Gram’s stain showing polymorphonuclear leukocytes without visible gonococci is presumptive for a diagnosis of chlamydia.
20
Tissue culture for
chlamydia is relatively insensitive and is not widely available
because of cost and technical requirements.
21
Perianal
Chlamydia trachomatis is an obligate intracellular bacterium
that is sexually transmitted and results in clinical infections
that are similar to those caused by N. gonorrhoeae.
Simultaneous infection with both organisms is common.
Chlamydia is the most frequently reported STD in the United
States with an annual incidence of about 3 million cases per
17
year.
Aggressive screening programs are credited with the
decline of the chlamydia infection rate from its peak of more
than 4 million per year in the early 1970s.
TABLE 17-1. Treatment of anorectal gonococcal infection
One of the following as a single dose:
Ceftriaxone 125 mg intramuscularly
Ciprofloxacin 500 mg orally
Ofloxacin 400 mg orally
Levofloxacin 250 mg orally
Cefixime 400 mg orally
14
FIGURE 17-3. Inguinal adenopathy of LGV.

17. Sexually Transmitted Diseases 259
Antigen detection by direct fluorescent antibody (DFA) or
enzyme immunoassay DFA is highly specific, widely
available, and does not require rapid transportation or refrigeration. A trained microscopist is needed for interpretation.
As with gonorrhea, newer NAATs are available. Their use is
increasing in genital infection but unproven for anorectal
chlamydia. A pilot study using both PCR and LCR techniques
showed that these techniques can be effective for making this
diagnosis but there are few additional data on the use of
NAATs in anorectal chlamydia.
22
The two recommended treatment regimens for rectal
chlamydia (non-LGV) are azithromycin, 1 g orally as a single
dose or doxycycline, 100 mg orally, twice a day for 7 days.
14
Alternative regimens include erythromycin (less effective,
more gastrointestinal side effects), ofloxacin (7-day course,
more expensive), or levofloxacin (7-day course, no data on
efficacy). Treatment of LGV is with doxycycline or erythromycin for 21 days. In patients with HIV and LGV, prolonged
therapy may be required. Management of sexual contacts is
the same as for gonorrhea. Abstinence from sexual intercourse should last until 7 days after treatment with
azithromycin or completion of 7 days of doxycycline.
Syphilis
Syphilis is an STD caused by the spirochete Treponema pal-
lidum that can present in one of several progressive stages—
primary (chancre or proctitis), secondary (condyloma lata), or
tertiary. The incidence of syphilis had its recent peak of 107
cases per 100,000 people in the United States in 1991, but
decreased to 2.2 per 100,000 in 2001, meaning that only 6103
cases were reported. A slight increase in primary and secondary syphilis cases reported occurred in 2002.
rates have led to a national plan for eliminating syphilis.
The primary stage of anorectal syphilis appears within 2–10
weeks of exposure via anal intercourse. The chancre begins as a
small papule that eventually ulcerates. Anal ulcers are frequently painful (in contrast to genital ulcers) and without exudates. They may be single or multiple (Figures 17-4 and 17-5)
and located on the perianal skin, in the anal canal, or distal rectum. Differentiation from idiopathic anal fissures may be difficult. Painless but prominent lymphadenopathy is common.
Proctitis from syphilis may occur with or without chancres.
Untreated lesions in this stage will usually heal in several weeks.
Hematogenous dissemination of untreated syphilis leads to
a secondary stage that occurs 4–10 weeks after primary lesions
appear. Nonspecific systemic symptoms from this infection
include fever, malaise, arthralgias, weight loss, sore throat, and
headache. A maculopapular rash is seen on the trunk and
extremities. Condyloma lata, another secondary manifestation,
are gray or whitish, wart-like lesions that appear adjacent to
the primary chancre and are laden with spirochetes. Untreated,
the symptoms of syphilis usually resolve after 3–12 weeks—
of these patients, approximately one-fourth will have a relapse
of symptoms in the first year. This is called early latent
syphilis.
23
These low
24
FIGURE 17-4. Solitary anal chancre.
Diagnosis in the primary or secondary stage is made by
visualization of spirochetes on dark-field microscopic
examination of scrapings from chancres (Figure 17-6).
Alternatively, spirochetes may be demonstrated on WarthinStarry silver stain of biopsy specimens. A direct fluorescent
antibody test for T. pallidum (DFA-TP) is performed by some
laboratories.
18,25
Serologic tests, rapid plasma reagin (RPR)
and Venereal Disease Research Laboratory (VDRL), have a
false-negative rate of up to 25% in primary syphilis and are
18
FIGURE 17-5. Multiple anal chancres.
Соседние файлы в папке Библиотека им академика М.И. Перельмана
