Chapter 053. Eczema and Dermatitis (Part 2)

Figure 53-1Atopic dermatitis.Hyperpigmentation, lichenification, and scaling in the antecubital fossae are seen in this patient with atopic dermatitis. (Courtesy of Robert Swerlick, MD; with permission.)Atopic Dermatitis: Treatment Therapy of AD should include avoidance of cutaneous irritants, adequate moisturizing through the application of emollients, judicious use of topical antiinflammatory agents, and prompt treatment of secondary infection. Patients should be instructed to bathe no more often than daily using warm or cool water, and to use only mild bath soap. Immediately after bathing while the skin is still moist, a topical anti-inflammatory agent in a cream or ointment base should be...
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Chapter 053. Eczema and Dermatitis (Part 2) Chapter 053. Eczema and Dermatitis (Part 2)Figure 53-1 Atopic dermatitis. Hyperpigmentation, lichenification, and scaling in the antecubital fossae areseen in this patient with atopic dermatitis. (Courtesy of Robert Swerlick, MD; withpermission.) Atopic Dermatitis: Treatment Therapy of AD should include avoidance of cutaneous irritants, adequatemoisturizing through the application of emollients, judicious use of topical anti-inflammatory agents, and prompt treatment of secondary infection. Patients shouldbe instructed to bathe no more often than daily using warm or cool water, and touse only mild bath soap. Immediately after bathing while the skin is still moist, atopical anti-inflammatory agent in a cream or ointment base should be applied toareas of dermatitis, and all other skin areas should be lubricated with amoisturizer. Approximately 30 g of a topical agent is required to cover the entirebody surface of an average adult. Low- to midpotency topical glucocorticoids are employed in mosttreatment regimens for AD. Skin atrophy and the potential for systemic absorptionare constant concerns, especially with more potent agents. Low-potency topicalglucocorticoids or non-glucocorticoid anti-inflammatory agents should be selectedfor use on the face and intertriginous areas to minimize the risk of skin atrophy.Two non-glucocorticoid anti-inflammatory agents are now available, tacrolimusointment and pimecrolimus cream. These agents are macrolideimmunosuppressants that are approved by the U.S. Food and Drug Administration(FDA) for topical use in AD. Reports of broader effectiveness appear in theliterature. These agents do not cause skin atrophy, nor do they suppress thehypothalamic-pituitary-adrenal axis. Recently, however, concerns have emergedregarding the potential for lymphomas in patients treated with these agents. Thus,caution should be exercised when considering these agents. Currently, they arealso more costly than topical glucocorticoids. Secondary infection of eczematous skin may lead to exacerbation of AD.Crusted and weeping skin lesions may be infected with S. aureus. When secondaryinfection is suspected, eczematous lesions should be cultured and patients treatedwith systemic antibiotics active against S. aureus. The initial use of penicillinase-resistant penicillins or cephalosporins is preferable. Dicloxacillin or cephalexin(250 mg qid for 7–10 days) is generally adequate; however, antibiotic selectionmust be directed by culture results and clinical response. More than 50% of S.aureus (SA) isolates are now methacillin resistant (MR) in some communities—community acquired MRSA (CA-MRSA). Current recommendations for thetreatment of CA-MRSA infection in adults include trimethoprim/sulfamethoxazole(1–2 double strength bid), minocycline (100 mg bid), doxycycline (100 mg bid),or clindamycin (300–450 mg qid). Duration of therapy should be 7–10 days.Inducible resistance may limit clindamycins usefulness. The latter can be detectedby the double-disc diffusion test, which should be ordered if the isolate iserythromycin-resistant and clindamycin-sensitive. As an adjunct, the use oftriclosan-containing antibacterial washes and intermittent nasal mupirocin may beuseful. Control of pruritus is essential for treatment, since AD often represents anitch that rashes. Antihistamines are most often used to control pruritus, and mildsedation may be responsible for their antipruritic action. Sedation may also limittheir usefulness; however, when used at bedtime, sedating antihistamines mayimprove the patients sleep. Unlike their effects in urticaria, nonsedatingantihistamines and selective H2 blockers are of little use in controlling the pruritusof AD. Treatment with systemic glucocorticoids should be limited to severeexacerbations unresponsive to topical therapy. In the patient with chronic AD,therapy with systemic glucocorticoids will generally clear the skin only briefly,and cessation of the systemic therapy will invariably be accompanied by return, ifnot worsening, of the dermatitis. Patients who do not respond to conventionaltherapies should be considered for patch testing to rule out allergic contactdermatitis. The role of dietary allergens in atopic dermatitis is controversial, andthere is little evidence they play any role outside of infancy. Immunotherapy withaeroallergens has not proven useful in AD.