Добавил:
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
Скачиваний:
0
Добавлен:
15.09.2026
Размер:
17 Мб
Скачать
☆
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.