Atopic Dermatitis

Competency:
The resident should be able to: 1. Identify the characteristic features of atopic dermatitis: pruritus, morphology and distribution, and chronic relapsing course 2. Identify factors that worsen atopic dermatitis (drying, chemical irritants, heat, allergens and physical trauma) 3. Plan appropriate treatment of atopic dermatitis (emollients, corticosteroids, antibiotics, and allergen elimination when appropriate) 4. Recognize that children with atopic dermatitis are prone to recurrent infections, particularly with Staphylococcus aureus, herpes simplex and skin fungi, such as Trichophyton sp.

Case:
A one year old girl is seen in your clinic for a rash that wont go away. Mom reports that the patient first presented with the rash on her cheeks at around 2 months of age- she says it started as little bumps, but soon became red and cracked. She notes that as her daughter started crawling, the rash spread to the knees and elbows. Mom has attempted to treat her daughters condition with over the counter moisturizing lotions, to no avail. Although she initially thought the rash got slightly better, she does not note any lasting improvement. In fact, mom is worried that the rash is getting worse, as her daughter has become more irritable and is starting to develop red and white pimples on the affected areas. The patient does not have any significant past medical history, although family history is significant for a brother with asthma. Mom and baby are both obviously distressed, and are looking to you for a diagnosis and some relief. How should you begin?

Questions:
1. 2. 3. 4. 5. How is atopic dermatitis diagnosed? What factors trigger exacerbation of atopic dermatitis? What is the initial management of atopic dermatitis? How does one make the classification of severe atopic dermatitis? If a patient is recalcitrant to treatment, what other diagnoses should be considered in the differential? What other therapies might be instituted by an AD specialist?

How is atopic dermatitis diagnosed?

Atopic dermatitis is a chronic skin condition in which the skin becomes extremely itchy and inflamed, causing redness, swelling, cracking, weeping, crusting, and scaling. Atopic dermatitis is often referred to as eczema, which is a general term for many types of dermatitis. Atopic dermatitis is the most common type of eczema. Major features: (all must be present) Pruritus Chronic or chronically relapsing dermatitis Typical distribution Adults: flexural lichenification and linearity Infants/Children: facial and extensor involvement Infants: cheeks, chin, elbows, knees Children: popliteal/antecubital fossae, neck, wrists, hands, ankles Personal/family history of atopy (asthma, allergic rhinitis, atopic dermatitis)

Minor features: (if no atopic history, need three or more minor features) Xerosis Ichthyosis Early age of onset Palmar hyperlinearity Susceptibility to cutaneous infection Infraorbital fold (Dennie-Morgan line) Nipple eczema Cheilitis Immediate Type 1 skin test response Keratoconus Anterior subcapsular cataracts It is essential to obtain the following information from the history and exam: History: pruritic nature Age of onset Duration of illness Triggers (including nocturnal exacerbation) Infections Problems with foods, irritants, or aeroallergens Seasonal variation Eye complications Environmental exposures Chronicity Distribution of rash Exam: morphology/distribution Diffuse xerosis Erythema Excoriation Papulation Crusting/oozing/pustules (infection) Scaling Lichenification Steroid complications- striae/atrophy

Although laboratory evaluation is not essential to the diagnosis of AD, it can serve useful when developing a management strategy. Lab: Elevated IgE + eosinophilia (not routinely tested, as it is of little clinical utility) Prick skin testing (to identify offending allergens) In vitro testing (RAST). Not generally recommended, but may be helpful when clinical suspicion for allergy is high, but skin is too inflamed for prick testing. If there is suspicion of infection on the basis of physical exam, culture for staph aureus, Tzanck smear for herpes simplex, or KOH prep for dermatophytes. (Note: >90% of patients with chronic AD are colonized with Staph Aureus)

What factors trigger exacerbation of atopic dermatitis?

Potential triggers, such as irritants, allergens, and emotional stressors, should be identified and eliminated as a component of first-line therapy for AD. Not all patients with AD are triggered by every stimulus. Many patients experience exacerbations by some triggers and not by others. It is the clinicians role to identify, through history and other evaluations, each patients specific triggers. Irritants: Lipid solvents Disinfectants Occupational irritants Household fluids Dust mites Furry animals Pollens Molds Human dander Viral infections Staph aureus Fungi -Pityrosporum -Candida -Dermatophytes Foods (contact irritant > vasodilator > allergen) Psyche (stress) Climate (most patients are better in summer than winter, but extreme heat and sweating may trigger AD flares) Hormones (e.g., menstrual cycle, early pregnancy) Isomorphic/Koebner response (ability of scratching or trauma to induce a rash)

Contact and aeroallergens:

Microbial agents:

Others:

Of all triggers, the isomorphic response is the most important exacerbating factor of AD to aggressively address with the patient. All patients should be aware of the itch-scratch-rash cycle, and be counseled as to the importance of resisting the urge to scratch.

What is the initial treatment of atopic dermatitis?

Treatment is directed at symptom relief and reduction of cutaneous inflammation. All patients require skin hydration in combination with an effective emollient. In this regard, ointments are generally preferable to cream preparations.

Topical Steroid Therapy: Mild AD1% or 2.5% hydrocortisone to affected areas (AA) after baths, up to BID Moderate ADSevere AD2.5% HC to AA on face and intertriginous areas Medium potency corticosteroid (0.1% triamcinolone) to other areas frequent bathing up to TID followed by 2.5% HC to face/intertriginous areas and 0.1% triamcinolone to AA on trunk/extremities more potent topical steroids up to 1 week PRN under supervision wet dressings for hydration, medication penetration antihistamines (especially for nocturnal pruritus)

Topical Tacrolimus/ Pimecrolimus: Also useful as an alternative first-line therapy, especially for face/intertriginous skin, in the pediatric population, or for large % of BSA affected. Initiate treatment after acute flare has been treated by topical steroid to avoid painful stinging/burning. Not associated with the side-effects of long-term topical steroid use, but are potent immunosupressants in their systemic formulations. Therefore, one should take care not to apply these medications to inflamed/excoriated skin, as doing so increases the risk of systemic absorption. The manufacturer recommends restricting these agents to 6 weeks of continuous use. Infection: Systemic antimicrobial therapy for S. aureus (macrolides, cephalosporins, penicillinase-resistant penicillins) Important to obtain sensitivity, especially since community-acquired drug-resistant staph aureus is becoming more prevalent. Anti-viral/anti-fungal therapy for herpes simplex/dermatophyte infection Response to Therapy: Complete response- uncommon over short term unless there is a clear cut trigger that can be eliminated Partial response- most common, with reduction in pruritus and extent of disease. Require long-term follow-up for adjustments in treatment plan. Treatment failure- these patients require complete reassessment to confirm diagnosis and consider alternative approaches. Monitor patients response to therapy Adjust medications and skin care according to severity of illness Step-up Rx for flare-ups, and step-down when AD under control

How does one make the classification of severe atopic dermatitis?

Any of the below satisfy the criteria for severe atopic dermatitis: Percentage of skin involvement>20% BSA not responsive to first line tx >10% if includes intertriginous areas, eyelids, or hands

Extensive skin involvement with erythroderma and risk for exfoliation Requiring ongoing or frequent treatment with high-potency topical glucocorticoids or systemic steroids Requiring hospitalization for severe eczema or AD-related infections

Ocular infections/complications Significant disruption of quality of life (sleepless nights, missed work/school, etc.)

If a patient is recalcitrant to treatment, what other diagnoses should be considered in the differential? What other therapies might be instituted by an AD specialist?
Things to consider: Most pts present with AD below the age of 5 years If >16 years, evaluate for contact dermatitis with history and patch test if needed If presenting as adult, important to consider cutaneous T cell lymphoma Uncommon for AD to present < 6 weeks of age Any eczematoid rash dating from 1st month of life should be evaluated for possibility of immunodeficiency, especially if history of infections/FTT AD does not exclusively affect diaper area consider contact dermatitis/ candida Difficult to distinguish AD from seborrheic dermatitis in infants Differentiate on basis of rash distribution Consider iatrogenic causes- pt may be having a type 4 hypersensitivity reaction to topical therapy Dont forget about super-infection!

Consideration of other Conditions that may be confused for atopic dermatitis: Other forms of eczemaSeborrheic dermatitis Contact dermatitis Nummular eczema Dyshidrotic eczema Irritant dermatitis Wiskott-Aldrich syndrome DiGeorge syndrome SCID Ataxia Telangiectasia Hyperimmunoglobulinemia E syndrome Dermatophytosis Scabies Recurrent S. aureus and herpes simplex infections HIV disease Phenylketonuria Tyrosinemia Histidinemia Cutaneous T-cell lymphoma Histiocytosis X Sezary Syndrome

Immunodeficiencies-

Infections-

Metabolic-

Neoplastic-

Other chronic inflammatory skin conditions- psoriasis Pts who are non-responsive to first-line therapy are highly challenging. Some 2nd-line/alternative therapies include: Wet dressings and Occlusion- take care to avoid maceration and exacerbation of skin disease or infection.

Short course of oral systemic steroids (important to taper dose in conjunction with application of topical steroids in order to avoid rebound flare) UBV or PUVA as an adjunct in recalcitrant AD (under supervision of dermatologist) Hospitalization should be carried out before the institution of other anti-inflammatory or immunologic therapies. In many cases, removal from environmental triggers or emotional stressors, intense patient education, and assurance of compliance with therapy results in sustained improvement. Skin clearing will then allow for skin testing and further evaluation. Other investigational treatments include allergen immunotherapy, interferon-gamma, systemic cyclosporine, and PDE inhibitors. References: Atopic dermatitis. Habif: Clinical Dermatology, 3rd Ed. 1996 Clinical features of atopic dermatitis. Immunology and Allergy Clinics of North America. Volume 22. Number 1. February 2002. Disease management of atopic dermatitis: a practice parameter. Annals of Allergy, Asthma, and Immunology. Volume 79. Number 3. September 1997. The clinical spectrum of atopic dermatitis. Journal of Allergy and Clinical Immunology. 104:S90. 1999.