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Atopic, Contact, and Stasis Dermatitis 9/2/2017 Atopic, Contact, and Stasis Dermatitis Atopic, Contact, and Stasis Dermatitis Debra Sibbald, BScPhm, ACPR, MA (Adult Education), PhD (Education) Date of Revision: February 2017 Introduction Dermatitis is a nonspecific term describing both acute and chronic skin reactions with corresponding clinical patterns and history. Although the word eczema (boiling over) has been used synonymously with atopic dermatitis, most dermatologists use the term dermatitis to describe an acute, nonspecific skin reaction that exhibits swelling, erythema, scaling, vesicles and crusts. Atopic dermatitis is a chronic inflammatory skin disease caused by mucocutaneous barrier dysfunction. Contact dermatitis is an inflammatory skin reaction caused by exposure to allergens or irritants. Stasis dermatitis is inflammation of the skin of the lower legs caused by chronic venous insufficiency. Skin changes in dermatitis reflect the pattern of inflammatory response. The appearance is similar in all forms of dermatitis, regardless of cause. When the reaction is acute, the earliest and mildest changes are erythema (redness) caused by engorgement and dilatation of the small blood vessels and, usually, swelling (edema) resulting from leakage of fluid from blood vessels and accumulation in tissues. If swelling is severe, skin cells form vesicles that fill with edema fluid; this process is called vesiculation or blistering. Breakage of blisters results in oozing or weeping and evaporation of this fluid causes crusting and scaling. Dermatitis may progress to a chronic stage where the skin becomes dry, fissured and cracked. With prolonged itching and scratching it thickens, and the normal skin markings become more prominent. This process is called lichenification. The skin may show damage from scratching (linear or punctate scarring) and hyperpigmentation or hypopigmentation.1 Pathophysiology Atopic Dermatitis Atopic dermatitis, allergic rhinitis/conjunctivitis and allergic bronchial asthma belong to the atopic syndrome, or atopic diathesis, which is a mucocutaneous barrier dysfunction.2 Atopic dermatitis is a chronic inflammatory skin disease associated with cutaneous and mucous membranes hyper-reactivity to environmental triggers that are innocuous to nonatopic individuals.3 Atopic dermatitis affects 10–20% of the population. The disease is genetically associated, with a risk of 70% if both parents are afflicted, and a higher risk of inheritance from mother than father. While the genetic link may contribute to increased incidence in Asians or black Caribbeans, this is evident only if living in dry, cold climates.4 It is significantly more common in those of higher socioeconomic status, children from small families and those who live in privately owned properties, possibly reflecting the influence of lifestyle, home furnishing and education.4 Eighty to 85% of patients with atopic dermatitis have high levels of total IgE, which correlate with the severity of clinical disease. Children with mild to moderate disease have much lower levels than those with severe disease.5 The IgE trigger causes an eczema-type reaction rather than a classic urticarial reaction. Eosinophils are involved in producing pro-inflammatory products in the skin and mucous membranes. Twenty percent of patients show normal IgE levels and lack specific sensitization against inhalant and food allergens. Genetic impairment of the epidermal barrier has been proposed as a cause of atopic dermatitis. Evidence supports the classical concept of atopic dermatitis as a continuum that begins with impaired epidermal barrier and penetration of environmental factors causing eczema in about 20% of individuals, primarily female and with normal IgE. Sensitization to allergens and infections progresses to atopic dermatitis, leading to scratching and ensuing tissue damage. This causes https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 1/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis sensitization to self-proteins and the “autoallergic” stage of atopic dermatitis which is associated with high levels of IgE and the concomitant risk of development of asthma.6 Atopic dermatitis is predominantly a disease of childhood.4 It begins in infancy but is rarely present at birth, and decreases in intensity with age. In approximately 80% of cases the problem develops during the first year of life, and in up to 90% of cases the onset occurs before 5 years of age.7 In children younger than 2 years, there may be a stronger male-to-female ratio, but this is reversed after age 2, with a slight female preponderance. Increased disease chronicity in females may be responsible.4 Incidence of occupational allergic and irritant contact dermatitis is increased in patients with atopic dermatitis. In adults and children, Staphylococcus aureus colonization is high, whereas adult skin is more heavily colonized with Malassezia yeasts.8 Contact Dermatitis Contact dermatitis is a pattern of inflammatory responses in the skin that occurs through contact with external factors. The clinical picture is a polymorphic pattern of skin inflammation characterized by a wide range of clinical features, including itching, swelling, redness and scaling. Contact dermatitis is a common occupational disease and is also caused by cosmetics, skin care products and other chemicals such as textile dyes in clothing and outdoor plants. Aggravating factors play a large role since the extent and severity varies with: the frequency and duration of exposure; presence of infected, inflamed or burned skin; degree of allergic sensitivity and mechanical factors such as pressure, friction and excessive perspiration, which may intensify the dermatitis.9 Extremes in temperature, humidity, sweating and occlusion can lower the threshold for irritation.10 Secondary infection with bacteria or fungi is more likely in dermatitic skin.10 Contact dermatitis occurs from infancy onwards and is divided into 2 categories: allergic contact dermatitis (20% of patients) and irritant contact dermatitis (80% of patients). Lower incidence among children is due to limited exposure to allergens.11 Allergic contact dermatitis is a delayed or T cell-driven hypersensitivity immune reaction mediated by lymphocytes previously sensitized by exposure to contact allergens, or haptens. Allergenic substances must be processed within the epidermis by the Langerhans cells that migrate to regional lymph nodes. Here, antigen is conjugated with proteins processed by T lymphocytes, which become specifically reactive to the presented antigen, initiating a sequence of cytokine-mediated events and inflammatory response.12 The reactivity of the skin is a result of balance between T lymphocyte hypersensitivity and suppressor cells which invoke allergen tolerance.12 Most of these cellular reactions produce sensitization in only a small percentage of those exposed. The incubation period after initial sensitization is 5–21 days and 12–48 hours after subsequent re-exposure, but the reaction may continue to develop for several weeks.9 Predisposition to develop allergic contact dermatitis is genetic. Allergic contact dermatitis decreases with age since the skin of people over 65 is less reactive to allergens, due to diminished immune function that occurs with age.11 However, older patients also have impaired epidermal barrier function and slower skin recovery after an insult. In the elderly, eczematous erythroderma (severe widespread redness of the skin) is common.13 Elderly patients may acquire allergy to topical preparations used to treat stasis or contact dermatitis.14 Primary irritant contact dermatitis is a nonallergic reaction resulting from activation of the innate immune system by the direct cytotoxic effect produced by exposure to any substance including chemical, physical or biologic agents, if the concentration and duration of contact are sufficient. Mild irritants such as soaps, detergents and most solvents require repeated or sustained contact to produce inflammation. Strong irritants such as acids and alkalis may injure the skin immediately. Irritant effects may be considerably enhanced by occlusion. The majority of cases are related to occupation, in particular jobs that involve work with water or exposure to irritant substances. Hand dermatitis results from frequent washing of the hands which damages the skin through a combination of mechanisms: increased skin permeability from alkali-induced damage to the keratin, removal of lipids and amino acids from the skin, and alteration of the skin's buffering capacity. Intensification may also be produced by irritants such as waxes, polishes and turpentine and through excoriation or rubbing.12 Hand dermatitis may affect 1 in 9 adults in any https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 2/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis given year, predominating in females with a ratio greater than 5:1.15 Diaper dermatitis is common and is discussed in Diaper Dermatitis. Stasis Dermatitis Stasis dermatitis results from chronic venous insufficiency and is commonly seen in middle-aged or elderly patients, more frequently in women than in men. Approximately one-third of patients have a previous history of deep vein thrombophlebitis related to trauma, pregnancy, surgery or prolonged illness.9 Goals of Therapy Eliminate individual trigger factors or contact exposure to irritants and allergens Restore barrier function Provide symptomatic relief while decreasing skin lesions Implement preventive measures focusing on decreasing
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