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 the number of episodic flares, lengthening symptom-free periods and prevention of excoriations Develop coping strategies and expectations for patients/caregivers

Patient Assessment

The pattern of dermatitis and its trigger factors influence the clinical classification and therapy. An approach to assessing patients with dermatitis is shown in Figure 1.

Atopic Dermatitis

Clinical Presentation

Atopic dermatitis presents as an intensely pruritic acute, subacute or chronic eruption seen in characteristic patterns in infants, children and adults. The diagnosis is purely clinical; the symptoms and signs of atopic dermatitis are numerous, but usually nonspecific. Itch is the main symptom. There is no primary skin lesion in atopic dermatitis; the clinical presentation of eczematous skin lesions represents skin changes induced by constant scratching and excoriations.16 The skin is typically dry and the lesions scaly, though they may be vesicular, weeping or oozing in the acute stage. Clinical presentation supports both debated theories as to the chronology of pruritus and lesions: itch may precede visible skin lesions and/or erythema, and inflammation may evoke pruritus.17 Various triggers such as stress result in appearance of erythema followed by itch, then vasodilation and inflammation due to scratching. The pruritus may be focal or generalized if skin is dry and may be most intense during the evening and at night. It is usually intermittent and leads to vigorous itch- scratch cycles, commonly with secondary bacterial infection of excoriated lesions.9

Although atopic dermatitis can affect any area of the body, it preferentially affects the flexures and the face. Distribution of lesions depends on the age of the patient, with infantile, childhood, adolescent and adult phases. In babies aged less than 6 months, the face and scalp are the sites most commonly affected, and redness and chapping of a baby's cheeks can be the earliest sign.3 This chapping usually begins at 2–3 months and persists for 2 years. Remission usually occurs between 2 and 4 years of age. Subsequently, a chronically relapsing dermatitis begins, located on the extensor sides of the extremities but also on the flexural areas. The most common sites are the antecubital and popliteal fossae.3 It can also be located around the mouth, eyelids, neck and hands. The lips can be dry and scaly. Visual signs of chronic atopic dermatitis include less redness, increased dryness and early lichenification (thickened skin, hyperpigmentation and accentuation of skin furrows due to repeated rubbing and scratching). Involvement of the back of the arms and the front of the legs is https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 3/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis seen first, and later a transition occurs to the elbows and knee folds. Frictional areas such as wrists and ankles are regular sites, and localization may occur to the toes. Occlusive footwear causing excessive sweating and drying of the feet may exacerbate the condition. Children aged 4–6 years usually develop symmetric eczema on flexural areas, hands, feet, and the back of the thigh. As the child reaches adulthood, recurrent outbreaks diminish or disappear. In adolescents and adults, the involvement may be generalized, but flexural accentuation is the hallmark of clinical disease. Adults typically exhibit lesions on the face, upper body and flexural areas.18

In addition to the classical patterns, there are site-specific variants. Eyelid eczema is common in 21% of adolescents and is associated with hay fever and exposure to aeroantigens such as house dust mites. The infra-auricular and retro-auricular sites of the ears are particularly prone to fissuring, as a reaction to minor trauma.3

Areas of predisposition may be related to the thickness of the stratum corneum and variations in exposure to irritants and allergens at different body sites: thinnest areas are genitals and eyelids, often subject to rubbing, followed by flexor forearms and posterior auricular.3 Other parts of the face and flexures have a thin epidermal barrier with decreased barrier function. In the areas most vulnerable to penetration, the disease persists longer.3

Other minor features exhibited by atopic patients include recurrent conjunctivitis, cheilitis (chapped lips), infraorbital folds (Dennie-Morgan lines), recurrent infections (especially viral) and impaired cell- mediated immunity.16 See photo, Atopic Dermatitis.

The diagnosis of atopic dermatitis is based on essential and supporting features. Essential features must be present and include pruritus and dermatitis (typical morphology, age-specific features and chronic or relapsing history). Supporting features are present in most cases and include early onset, family history and high IgE reactivity. Other associated features are too nonspecific to be diagnostic. Conditions which must be included in the differential diagnosis are: scabies, contact dermatitis, ichthyosis, cutaneous T-cell lymphoma, psoriasis, photosensitivity, immune deficiency and erythroderma due to other causes.19

Photo 1: Atopic Dermatitis

Dr. P. Marazzi/Science Photo Library

Risk and Aggravating Factors

Genetics: Atopic dermatitis patients have an increased personal or family history of atopic syndrome, including type 1 allergies (immediate hypersensitivity), hay fever, asthma and chronic allergic rhinitis/conjunctivitis and are genetically predisposed.19

Environmental Allergens: Excessive use of soaps, detergents and shampoos irritate the skin and disturb the skin barrier. Alcohol and astringents in skin care products can be drying and their use https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 4/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis should be limited.20 Central heating, insulation, air conditioning and inadequate ventilation may increase exposure to environmental antigens such as house dust mites, molds, pollens and furry pets. Global warming and increased use of fertilizer may enhance density and allergenic potency of pollen from trees and grains.2 The influence of these environmental and lifestyle factors may account for increased incidence in individuals of higher socioeconomic status.4

Climate: The influence of climate is shown in Asians with atopic syndrome who live in humid tropical climates and do not manifest cutaneous symptoms until they move to colder, drier countries.2 A seasonal variation is due to several contributing factors: environmental allergens cause relapses in summer, while climatic influences may cause clearing in summer sun and worsening in the dry, cold air of winter. Dryness of the skin (xerosis) with water content below 10% is crucial for induction of itch and scratching.17 Heat worsens the skin condition.

Sweating: Any stimulus to sweating (thermal, emotional) is a typical hallmark and the most common trigger of itch. Acetylcholine may be involved and there may be a decreased threshold for sweat stimulation.17

Physiologic Stress: Stress associated with demanding modern lifestyles appears to enhance skin irritability and contributes to the itch-scratch cycle and sleep disturbances.7,2 The alteration in skin appearance due to scratching escalates the emotional reaction to coping with the disease.21

Dietary Influences: Although patients with atopic dermatitis are more likely to have food allergies, food ingestion as a causal factor in atopic dermatitis flares is uncommon. Current evidence does not support eliminating cow's milk from the diet to improve atopic dermatitis. Some evidence suggests that elimination of eggs might benefit patients with atopic dermatitis who have suspected egg allergy and are sensitized to eggs, but more research is needed.22 More detailed information about this controversy is documented in the literature.23,24,25,26,27 See also Nonpharmacologic Therapy.

Irritants: Disinfectants, solvents and allergens in skin care products play an important role. Issues of irritation extend to clothing fabrics and products. Intolerance to wool is a hallmark of atopy. Coarse- textured fabrics, liquid or sheet fabric softeners (which cause fibres to plump up and stay erect) and bleach should be avoided.

Infections: Atopic patients have an increased propensity for cutaneous viral infections including herpes simplex, molluscum contagiosum and warts, fungal infections such as dermatophytosis, pityriasis (tinea) versicolor and candidiasis, and bacterial infections such as S. aureus.25

Itch-scratch cycle: Severe pruritus elicits reflexive scratching, resulting in a vicious cycle of itch and scratch.

Contact Dermatitis

Clinical Presentation

Cutaneous responses are dependent on the particular chemical, the duration and nature of the contact, and individual host susceptibility. Despite different pathogeneses, the allergic and irritant forms have similar clinical appearances, especially in the chronic forms. The clinical presentation of contact dermatitis is determined by the severity and acuteness of the inflammation. The area involved usually reflects the pattern of the contacting substance and may have sharp, well-demarcated linear margins or unusual geographic shapes. It may spread to distant sites through lymphocytes. Contact substances may be transferred from the primary site by touch to distant areas, especially the eyelids and neck, which are very reactive sites. The face may display a reaction to substances applied to the scalp. Allergic contact dermatitis and irritant contact dermatitis are predominant causes of periorbital dermatitis.28 Scalp, palms and sole areas are more resistant. The distribution of the lesions may provide clues to the irritant or allergen trigger.

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 5/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis Acute reactions are often red, edematous papules in the early phase, which become vesicles and bullae that ooze if the reaction is severe enough. Chronic reactions produce an entirely different clinical picture in which primary lesions are minimal, and secondary changes such as dryness, lichenification, pigment changes, hyperkeratosis or thickening, excoriation and fissuring predominate. As with other forms of acute and chronic dermatitis, itching is the primary symptom.29

Irritant Contact Dermatitis: Acute irritant contact dermatitis reactions usually reach their peak within minutes to hours after exposure and then start to heal. Symptoms of an acute reaction to mild irritants include burning, stinging and soreness at the site and physical signs of the reaction include erythema, vesiculation and oozing. Strong irritants produce blistering, erosions and ulcers. Acute reactions will have sharply demarcated borders and will generally be asymmetrical. Cumulative irritant contact dermatitis is a consequence of multiple subthreshold skin insults without sufficient time in between for complete restoration of skin barrier function. It may be due to a variety of stimuli or frequent repetition of one factor, especially if occupational. Clinical symptoms will develop only after cumulative damage exceeds the threshold, and the lesions may be less well demarcated. Hand dermatitis occurs principally on the fingers, web spaces and dorsa of the hand. Palms are spared and dryness, erythema and scaling are early features. It often begins on the fourth finger, beneath a ring.9 Long- term glove occlusion and the accumulation of barrier damage from hand washing, even when mild hand cleansers are employed, may lead to cumulative skin irritation.30

Allergic Contact Dermatitis: This is a pruritic eczematous reaction which in its mild form is similar to exposure to an irritant. A typical allergic reaction consists of grouped or linear tense vesicles and blisters, and in severe involvement, marked edema, particularly on the face and in periorbital and genital areas. The acute form can also have a diffuse patchy distribution depending on the allergen (for example, body washes and shampoos that get rinsed over the body) and/or the development of disseminated auto-sensitization (acute, generalized dermatitis arising in response to a prior localized inflammatory reaction). The suspected diagnosis is based on clinical symptoms, a plausible contact to allergens and a suitable history of dermatitis. Differential diagnoses should be considered only after careful exclusion of any causal contact sensitization. Careful diagnosis by patch testing is of great importance. Modifications of the standardized test procedure are the strip patch test and the repeated open application test.31

Common Contact Allergens

A list of contact allergens is presented in Table 1. The most common contact allergens include plants of the Rhus genus, nickel, rubber, ethylenediamine (a stabilizer in many topical preparations) and paraphenylenediamine (an ingredient in black hair dye and industrial chemicals).32 Nearly any chemical can produce contact dermatitis. Small molecules are most likely to be sensitizers since they penetrate the epidermis more readily. The possibility of cross-sensitization with other chemicals is an important consideration. The most notable are listed in Table 2. Cross-sensitization may prohibit use of critically important systemically administered drugs.9

Table 1: Common Causes of Contact Dermatitis Type of Substance Source Dermatitis

Allergic contact Aloe vera Topical medications and dermatitis cosmetics

Bacitracin Topical antibiotic creams, eye and ear preparations

Balsam of Peru Cough syrups, flavourings

Benzocaine Topical antibiotic creams, eye and ear preparations

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Type of Substance Source Dermatitis

Cetylstearyl alcohols Topical medications, cosmetics, paste bandages

Chromium salts Potassium dichromate electroplating, cement, leather tanning agents, detergents, dyes

Cobalt chloride Cements, metal plating, pigments in paints

Ethylenediamine Dyes, fungicides, medications

Formaldehyde Germicides, plastics, clothing, glue, adhesives

Fragrances Topical medications, baby products, cosmetics, household products

Lanolin Topical medications, bath oils and cosmetics

Latex Rubber products, e.g., gloves, catheters, balloons, plants, medical devices, tires, conveyor belts

Methylisothiazolinone Baby wipes

Neomycin Topical antibiotic creams, eye and ear preparations

Nickel Metal alloys, hairpins, jewelry, zippers, hair dyes

Paraphenylenediamine Hair and clothing dyes, chemical photographic use

Potassium dichromate Cement, leather, household cleansers, bleaches

Quaternium 15 Preservative in topical medications and cosmetics

Rhus genus Poison ivy, poison oak, mangos

Rosins (gum and wood) Topical medications

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 7/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis

Type of Substance Source Dermatitis

Rubber accelerators Rubber products (ostomy (mercaptos/carbamates/thiurams) products, bandages, latex products, toys, condoms, diaphragms, goggles, pacifiers)

Topical antihistamines Topical medications

Irritant contact Acids Solvents dermatitis

Alkalis Surfactants

Enzymes Wet cement

Oxidants Hydrogen peroxide, household bleach

33,34 Table 2: Cross-sensitizers with Common Contact Allergens Sensitizers Cross-sensitizers

Ethylenediamine Aminophylline, ethylenediamine antihistamines

Latex Bananas, kiwi, pineapple, chestnuts, avocados, apricots, cherries, grapes, passion fruit, potatoes, peaches, tomatoes (occasionally other fruits and nuts). Alert healthcare practitioners prior to procedures.

Local anesthetics (ester type, Para-amino-containing compounds (widely used in e.g., benzocaine) topicals): parabens, some oral hypoglycemics, sulfonamides, thiazide diuretics

Neomycin Aminoglycosides (gentamicin, tobramcyin), framycetin

Rhus Lacquers from China and Japan, mangos, cashews and ginkgo

Allergens of Note

Plants

Toxicodendron plants, also known as Rhus and poison ivy account for the largest number of cases of allergic contact dermatitis. The typical warning to avoid contact is “Leaflets three, let it be.” The leaves, stems, seeds, flowers, berries and roots of plants contain milky sap that turns into a black varnish-like substance on exposure to air. Once the solvent evaporates, the allergen (urushiol) remains and is antigenic indefinitely, even if the plant has died.33 Sensitization is immediate with the formation of a complex protein in the skin that is not removed through washing. Sensitization and dermatitis occur after 7–10 days, and re-exposure produces a reaction within 8 hours to 2 days. Streaks of erythema or papules, vesicles and bullae in linear arrangement are a characteristic clinical presentation and accompany itching and edema as key

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 8/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis features.12 Urushiol is nonvolatile. Smoke may carry the poison in dispersed form.33 See Table 1 and Table 2.

Latex

Natural rubber latex, sourced in southeast Asia, is a leading cause of immunologic contact urticaria, and can cause IgE-mediated skin-related findings as well as acute respiratory symptoms and even anaphylaxis. Delayed contact allergy may exist more commonly than previously noted, particularly in atopic individuals. Immediate latex allergy (irritant contact dermatitis) is not the same as the more common, less severe T cell-mediated delayed hypersensitivity reaction seen clinically as allergic contact dermatitis.34

Added ingredients to rubber products may cause allergic contact dermatitis: accelerators in the rubber product make it more functional, antioxidants and antiozonants (parapheylenediamine) delay degradation, and other chemicals increase softness and pliability. Allergic contact dermatitis is due to carbamates and thiurams in rubber gloves, mercaptos and parapheylenediamine in shoes, industrial materials and tires, and thioureas in neoprene (used in medical and sporting goods).34 See Table 1 and Table 2.

Metals

Metals are the most common contact allergens; nickel is the most common cause of metal allergy and in most series ranks as the most commonly positive of all screening allergens.35 Nickel allergy can result in both cutaneous and systemic manifestations.36 Reactions to gold, chrome and cobalt are also frequently seen. Cross-sensitization to other metals can occur, e.g., nickel and palladium. Cobalt, nickel and chromium may induce co-reactions and other substances may contain them (cobalt in cement). Usually, the metals must be in solution for allergic contact, but can be liberated by sweat. Nickel, palladium and titanium are the most common metal allergens in contact dermatitis due to eyeglass frames.37 Metals can also be ingested (dietary nickel) or due to sources such as orthopedic implants.35 Irritant contact dermatitis to metals is common in workers exposed to metal salts, dust or fumes.35

Antibiotics

Topical antibiotics used long-term on skin with impaired protective barrier leads to increased risk of hypersensitivity. Groups at a high risk of contact sensitivity include: patients with chronic venous insufficiency, chronic ulcers or chronic otitis externa, or individuals with occupational exposure to antibiotics (e.g., human medicine and veterinary medicine practitioners, pharmaceutical industry workers, cattle breeders). When long-term therapy with topical antibiotics in these patients fails to result in improvement, allergic reactions to topical antibiotics should be considered. Cross-sensitivity, which is frequently associated with topical aminoglycoside antibiotics, poses a significant problem.38

Bacitracin is an antibiotic used in several types of consumer products, including cosmetics and ophthalmic and skin ointments. Bacitracin was the ninth most common contact allergen detected in 2003, causing more than 9% of positive reactions among 5812 patients with suspected contact dermatitis.39 Because bacitracin is used on wounds and is often inappropriately applied to fungal infections, the diagnosis of contact dermatitis can often be elusive. Reactions may be attributed to a slow-healing wound or worsening infection that is treated, ironically, with more topical antibiotic agents. Due to the significant prevalence of bacitracin allergy, the American Contact Dermatitis Society warns it should not be used routinely.39 Clinical affect, scientific evidence, and need for medical cost containment all advocate the discontinuation of routine usage of bacitracin in clean wounds. Table 3 reports changes in common allergic responses, which reflects routine usage.

Antihistamines

Topical antihistamines have been reported to cause contact dermatitis. Doxepin cream was the most commonly implicated topical preparation. A causal relationship is often difficult to recognize because the reaction may be similar to the disease being treated with the antihistamine preparation. Cross-reactivity within the same class of medication is likely but not certain.40 https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 9/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis Preservatives

Many preservatives can cause allergic contact dermatitis (e.g., parabens, formaldehyde). Methylisothiazolinone is a preservative commonly found in baby wipes. Incidence of allergy to this chemical is rising with increasing use and some jurisdictions are calling for a ban on its use. It has been suggested that it is common enough to be included in the standardized series of allergens used in patch testing.41 In Canada, concentration of methylisothiazolinone used alone is limited to 100 ppm, however this is 25 times the limit allowed when it is used in combination with methylchloroisothiazolinone (see Diaper Dermatitis for more information).42

Emulsifiers

Sorbitan sesquioleate and/or sorbitan monooleate are emulsifiers in many topical corticosteroid products. One study and its follow up found incidence rates for allergic contact dermatitis due to these chemicals of 8.9% and 4.1% respectively. The authors suggest that given the presence of sorbitans in many topical corticosteroid formulations, allergy to these chemicals should be considered when patients do not improve as expected with topical corticosteroid therapy.43

39 Table 3: Most Common Patch-test Responses in Patients with Suspected Contact Dermatitis Substance Percentage of Patients Exhibiting Reaction

Nickel sulfate 16.2%

Balsam of Peru 12.3%

Neomycin 11.5%

Fragrance mix 10.9%

Thimerosal 10.8%

Sodium gold thiosulfate 10.5%

Formaldehyde 9.2%

Quaternium 15 9.2%

Bacitracin 9.2%

Cobalt chloride 7.6%

Risk and Aggravating Factors

Consort Contact Dermatitis: Skin-to-skin contact can result in transfer of potential contact allergens from one sex partner to the other and may result from lubricants, hygiene products, seminal fluids, and rubber in diaphragms and condoms.14

Impaired Cell-mediated Immunity: Risk is reduced with impairment of cell-mediated immunity, such as AIDS, lymphomas or atopic dermatitis. Atopic patients are more likely to develop pustular reactions when exposed to nickel.14

Diet: It has been suggested that diet may play a role in allergic contact dermatitis. Approximately 30–50% of patients with latex allergy have hypersensitivity to certain fruits. Presence in food of nickel (e.g., from water, cooking utensils) or balsam of Peru (e.g., wine, https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 10/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis candy chocolate, curry) can aggravate allergic contact dermatitis; eliminating these items from the diet may alleviate symptoms.44

Ethnicity: The incidence of contact dermatitis in Caucasians is greater than blacks due to their greater skin reactivity; however, blacks experience a higher incidence of paraphenylenediamine allergy. Caucasians have a looser packing of skin layers and fewer intercellular lipids, making their skin more permeable to irritants and allergens.45

Gender: Although women develop contact dermatitis more often than men, it is primarily because women are more frequently exposed to irritants, allergens and wet work, and not because of differences in skin reactivity.45

Body Site: Eyelid contact dermatitis may be due to mascara, cosmetic preservatives, nail polish, hair cosmetics, eyeliner, ophthalmic medications, adhesives in false eyelashes, eyelash curlers, paper products, plants, airborne materials and dyes. The chest and abdomen are sites for allergy to metals and elastic objects, and genital areas are susceptible to dermatitis from hygiene products, contraceptives, condoms and seminal fluid. Nails exhibit contact dermatitis from acrylate applications, hardeners, enamels, hydroquinone in bleaching creams, weed killers, insecticides and physical trauma.46

Climate: Seasonal variation occurs with increased prevalence during winter months and exposure to cold, dry air.32

Occupation: Individuals at risk of contact dermatitis are often those who are exposed to these substances occupationally or as part of their daily routine. Exposure to organic solvents together with detergents may increase the risk of acquiring occupational contact dermatitis.47 Rhus dermatitis is seen less often in dark-skinned individuals, more commonly in younger persons, and is a hazard for outdoor workers and enthusiasts.

Latex allergy (from rubber gloves and other sources) is common in healthcare practitioners. The medical community is also at risk of contact dermatitis due to occupational substances, including mucolytics, dressings, adhesive removers, gowns, scrub solutions, formaldehyde and glutaraldehyde, mercury (dentists) as well as active drugs such as anesthetics, essential oils, antibiotics and inactive ingredients including aluminum, petrolatum, oils (olive, castor and sesame) and lanolin.48

Other occupations that can increase the risk of contact dermatitis include photography, textile work, printing industry, agricultural work, office work (carbon sources), bakery work and hairdressing.49 Hand dermatitis as a subtype of contact dermatitis is often seen in healthcare practitioners, hairdressers and dishwashers, especially in those who have atopic dermatitis. Susceptibility is greater among younger people. Bakers and chefs may experience food contact dermatitis due to sorbic acid preservatives, antioxidants, flavour ingredients (peppermint, cinnamon, anise, coriander, garlic, sesame, cashew) and food additives, such as dyes, and benzoyl peroxide.50 Plant allergy may include extracts used in medications such as balsam of Peru, rosin and benzoin.51

Ultraviolet Light: Photocontact dermatitis requires exposure to UV light and may occur due to irritant or allergic causes. Irritant reactions (phototoxic) can occur in anyone due to substances like psoralens, whereas photoallergic contact dermatitis occurs only after an individual with sensitivities is exposed to an allergen. Fragrances and sunscreen chemicals are causes of photocontact dermatitis.52

Stasis Dermatitis

Clinical Presentation

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 11/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis Stasis dermatitis, which occurs due to venous insufficiency, is seen on the lower leg. Acute changes consist of inflammation, edema, pigmentation and ulceration. The eruption may be erythematous and oozing, with marked inflammation. Chronic stasis results in scaling, discoloration and lichenification and is accompanied by edema due to venous disease. This may result in fibrosis, producing hardening and induration of soft tissue. Pigmentation is invariably present in the early stages due to dermal extravasation of red blood cells following small venule rupture. Superficial ulceration may result from acute inflammation and may heal or progress to deeper ulcers. Superficial venous varicosities may also be present.9

Differential Diagnosis of Dermatitis

Table 4 outlines other conditions that should be considered in the differential diagnosis of eczematous dermatitis.

Table 4: Differential Diagnosis of Eczematous Dermatitis Infections and infestations Papulosquamous conditions

Scabies (see Parasitic Skin Psoriasis (see Psoriasis) Infections: Lice and Scabies)

Candidiasis (see Fungal Skin Seborrheic dermatitis (see Dandruff Infections) and Seborrheic Dermatitis)

Herpes (see Viral Skin Rashes) Neoplasms

Tinea (see Fungal Skin Infections) Cutaneous T cell lymphoma

Staphylococcus aureus infections Photosensitivity (see Prevention and (impetigo) (see Bacterial Skin Treatment of Sun-induced Skin Infections: Impetigo, Furuncles Damage) and Carbuncles)

Metabolic diseases Immunodeficiencies

Fatty acid deficiencies

Differentiating Features of Atopic, Contact and Stasis Dermatitis

Table 5 outlines the differentiating features of common dermatitis subtypes.

Table 5: Differentiating Features of Subtypes of Dermatitis Trigger Goals of Condition Duration/Location Description Factors Therapy

Atopic 2 months; chest, Cycles of itching Extreme heat or Decrease dermatitis face, neck, diaper and scratching. cold, rapid trigger area Red, raised temperature factors and blisters with changes, pruritus oozing, dry skin sweating, Suppress irritant or inflammation occlusive 2 y; scalp, neck, clothing (wool Lubricate extremities or nylon), soaps skin and detergents, https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 12/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis

Tgreigagseesr, GAloleavliast eof environmental anxiety Condition Duration/Location Description Factors Therapy allergens, 4–10 y; scattered— Less acute and anxiety, neck, wrist, elbow, oozing; dry infections knee papules, thickening, periorbital edema and erythema

12–20 y; flexor Dry, thickened, areas, hands hyperpigmented plaques

Contact Irritant/allergic: In Unusual patterns Irritant: Time Decrease dermatitis contact area resembling and contact (irritant Allergic: May contacting concentration of exposure to and generalize substance irritant irritants and allergic) Acute: Red, Allergic: allergens blisters, oozing, Sensitization to If dry, wet it may erode allergen If wet, dry it Chronic: Dry, thick, fissured

Dry skin Lower legs (shins), Mild to moderate: Increasing age, Replace dorsa of hands, Dry skin with fine decreased water in the forearms scale; diffuse or humidity, skin and the round patches increased environment Severe: Cracks indoor heat, and fissures in cold, dry, winter diamond pattern air, contact with with redness soaps and irritants, hypothyroidism

Hand Irritant: Sides of the Redness, Repeated Decrease dermatitis fingers, less often dryness, contact with contact throughout palms chapping; small primary irritants, exposure Allergic: Back of the vesicles; excess soap and water, hands sweating solvents and detergents Family history of atopic dermatitis or psoriasis

Stasis Lower leg, proximal Acute: Venous Decrease dermatitis to medial Inflammation, insufficiency, triggers, bed Malleolus edema, and edema, rest and pigmentation and upright posture, elevation, ulceration hot, humid compression Chronic: Scaling, environment, of leg discoloration, sensitizers lichenification

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 13/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis Drug-induced Dermatitis

Eczematous eruptions can also occur with many drugs given either topically or systemically. Cross- sensitivity may occur with structurally related drugs administered by either route. Common sensitizers include antibiotics, phenothiazines and the ester group of anesthetics. As a rule, the eruption starts shortly after administration of the drug, if previous sensitization has occurred. Patch testing with the responsible drug will give positive results. Table 6 lists drugs that commonly evoke eczematous reactions.53

53 Table 6: Drugs that Commonly Cause Eczematous Eruptions Antibiotics chloramphenicol clioquinol gentamicin neomycin penicillin streptomycin sulfonamides

Antihistamines promethazine

Antipsychotics phenothiazines, e.g., chlorpromazine, fluphenazine, perphenazine, prochlorperazine, trifluoperazine

Beta-blockers metoprolol propranolol timolol

Calcium channel blockers54,55 amlodipine diltiazem felodipine nifedipine verapamil

Diuretics thiazide diuretics

Sulfonylureas chlorpropamide tolbutamide

Miscellaneous aminophylline carbamazepine chloral hydrate cyanocobalamin fluorouracil idoxuridine minoxidil nitroglycerin nystatin procainamide https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 14/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis quinine quinidine

Severe or Complicated Dermatitis

Atopic dermatitis that is acute and vesicular, or if moderate to severe (defined as: generalized to more than 30% of the body surface area (BSA), continues to involve larger body areas, remains unresponsive, becomes secondarily infected or interferes with activities of daily life or sleep patterns) requires further assessment and treatment by an appropriate healthcare practitioner. Parameters for assessing severity of atopic dermatitis include: Eczema Area Severity Index (EASI)56 score (a tool used to measure the severity and extent of atopic dermatitis in order to assess clinical response to treatment), quality of life measurement tools (e.g., Dermatology Life Quality Index),56 sleep disturbances, itch (diary), redness, scale, dryness and amount of emollient used. If there is uncertainty about the diagnosis, of if there is suspicion of wide spread herpes simplex, an appropriate healthcare practitioner should be consulted.57

Contact or stasis dermatitis that spreads to distant sites or becomes generalized to more than 30% of BSA, is acute and nonresponsive within a few days, includes edema that persists or increases within a few days, is chronic and nonresponsive within 7–10 days or interferes with quality of life is considered severe or complicated and requires further assessment and treatment by an appropriate healthcare practitioner. To identify the cause of allergic contact dermatitis, practitioners generally use the patch test during which standard concentrations of known substances are applied to the skin and the reactions monitored. Provocative and open use tests may be used after patch testing to distinguish an allergic from an irritant response. Other tests include prick tests and intradermal tests.58

Nonpharmacologic Therapy

Atopic and Contact Dermatitis

Avoidance of irritants and aggravating factors is key. A thorough history is essential to identify the cause, especially any previous treatments that may have exacerbated symptoms or cross-reacted with the irritant or allergen.

Environmental factors that can modulate the effect of irritants include temperature, humidity and texture of fabrics. Intense sun exposure should be avoided. Temperature in home and work environments should be temperate with moderate humidity to minimize sweating and reduce problems related to heat and perspiration. Air conditioning in the summer and a cool air humidifier in the winter may be helpful. If a humidifier is not available, a bowl of water in the room will enhance ambient humidity.

New clothing should be laundered prior to wearing to remove formaldehyde and other chemicals.20 Occlusive clothing should be avoided and loose-fitting cotton or cotton blend garments substituted for nylon, and corduroy for wool. Many blended fabrics are well tolerated. Texture or roughness, rather than fabric type (natural vs. synthetic) determine tolerability and skin irritancy.20,59,60 Liquid fabric softeners or dryer sheets should be avoided because plumping up fibres and making them erect increases irritancy. Bleach in the rinse also irritates and should be avoided. A dilute vinegar rinse can be substituted. Use of liquid rather than powder detergent can result in more complete rinsing; adding a second rinse cycle may facilitate removal of residual powder detergent.

Swimming may be a better tolerated sport than those involving intense perspiration or physical contact and may improve dermatitis. Bathing may also remove allergens from the skin surface and reduce colonization by S. aureus. Despite a drying or irritating effect, swimming in chlorinated pools results in clinical improvement in some atopic patients. Rather than simply rinsing off after swimming, gentle cleansers should be used to effectively remove the chlorine or bromine, and then moisturizer should be applied.20

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 15/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis Wearing cotton gloves or mittens prevents scratching and secondary infections and allows healing of affected hands. They can be used as a barrier against irritants such as newsprint when reading the paper, and can also allow children to play or perform normal activities, with good acceptance. Keeping fingernails clean and short is essential.

A diet that excludes specific foods is not recommended for patients with atopic dermatitis without confirmed food allergy.57 Intervention is indicated in only about 10–15% of atopic children, when the disease is of sufficient severity and there is a strong suspicion that certain food(s) aggravate the condition. Restrictions in diet should not have a greater effect on quality of life than the disease. Risks of dietary restriction must be kept in mind: such diets may lead to malnutrition and deficiencies, carry the risk of anaphylactic reactions upon rechallenge to a restricted food, and challenge the psychological and social well-being of the child.7 If foods aggravate atopic dermatitis, they represent only a fraction of the expression of the disease. Exclusion of foods in pregnancy or breastfeeding to prevent development of atopic dermatitis is not recommended.57 The benefit of breastfeeding is recognized; patients should be advised that exclusive breastfeeding for the first 3 months or more may help prevent the development of atopic dermatitis where there is a family history of atopy.20 Hydrolyzed formulas should not be offered to infants in preference to breast milk for prevention of atopic dermatitis. The introduction of any specific solid food (soft, mashed consistency to prevent choking) should not be delayed beyond 6 months of age. Later introduction of peanut, fish or egg does not prevent, and may even increase, the risk of developing food allergy. Skin or specific IgE blood testing before a first ingestion is discouraged due to the high false-positive rate. Regular ingestion (several times weekly) of newly introduced foods is important to maintain tolerance.61 Maternal use of probiotics during pregnancy and maternal and/or infant use during breastfeeding may be helpful in reducing the development of atopic dermatitis in the child.62,63,64,65 Strain and dose of probiotic is not consistent across studies. There is insufficient evidence to recommend the use of probiotics for treatment of established eczema.66,67

Wet dressing solutions used in atopic and contact dermatitis may include ordinary tap water or saline, in addition to pharmacologic solutions containing astringent and/or antiseptic compounds. The action of a wet dressing is primarily physical, and thus water or physiologic saline are the solutions of choice as they are convenient, inexpensive and pose no problems of sensitivity or damage to healing wounds. Note that the technique used in applying wet dressings determines the effect on the skin: used as compresses, they are drying, whereas used as soaks, they are hydrating. The rule of thumb for application of wet dressings is “If it is wet, dry it (compress); if it is dry, wet it (soak).”

Wet dressings as compresses cool and dry the skin through evaporation. They reduce inflammatory blood flow, cleanse the skin of exudates, crusts and debris and help maintain drainage of infected areas through vasoconstriction. They are indicated in acute eczematous conditions with oozing and crusting, which can be seen in atopic, contact or stasis dermatitis. The solution should be tepid or room temperature, although cold solution is effective in relieving itch in skin that is otherwise not symptomatic. A nonirritating gauze or thin cloth is soaked with solution, then wrung gently so it remains wet but not dripping. The compress is applied to the skin, removed, remoistened and reapplied every few minutes for 20–30 minute periods, 4–6 times daily (“a minute on, a minute off”). After removal, a lotion may be applied to the skin, but avoid occlusion with an ointment. Powders are not applied to any exudative lesion as they crust, causing bleeding on removal and increased risk of infection.

Wet dressings as soaks soften hardened crusts in scaling conditions usually apparent in chronic atopic, contact or stasis dermatitis, and can hydrate the skin. To apply a soak, saturate the cloth and apply to the area for 15–20 minutes without removal. This procedure occludes and breaks down underlying tissue. Soaks are never used for acute, exudating dermatitis as they may macerate the skin, further damaging barrier function. Chronic contact dermatitis that is dry or fissured should be soaked for 5 minutes rather than compressed before application of an occlusive emollient.

Wet-wrap therapy with or without a topical corticosteroid can be recommended for patients with moderate to severe atopic dermatitis and/or recalcitrant disease to decrease disease severity and water loss during flares. It may be performed on an ambulatory or inpatient basis. Most use a technique of a topical agent covered by a wetted first layer of tubular bandages, gauze, or a cotton suit, followed by a dry second/outside layer. For more generalized disease, 2 layers of nonirritating clothing can be similarly prepared. Rationale includes occluding the topical agent for increased penetration, decreasing water loss, and providing a physical barrier against scratching. The wrap can be worn for several hours up to 24 hours at a time, depending on patient tolerance. Most suggest several days of use, although a few https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 16/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis studies continued for up to 2 weeks. Use of topical corticosteroids under the wet wraps seems to be more efficacious than using only moisturizers with the wraps. Care should be taken if mid- to higher- potency corticosteroids are applied under the wraps, as absorption is increased and may cause hypothalamic-pituitary-adrenal axis suppression, especially if used widely on the skin. Temporary decreases in early morning serum cortisol levels have been reported, although short courses of use have not been associated with prolonged adrenal suppression. The potential for increased risk of infection has been raised with the use of mid- to higher-potency topical corticosteroids in wet-wrap therapy, although the data are sparse and conflicting regarding its actual occurrence.68

In the case of atopic dermatitis, control of trigger factors and anxiety is a major strategy. Control of exposure to environmental inhaled allergens is important. Direct contact with allergens and irritants should be reduced. Limit soap cleansing to axillae and groin, using mild soaps, creams or soapless cleansers (Table 8). Restrict showers to once weekly, if possible. Use bathing to rehydrate the skin and follow with liberal use of emollients to prevent evaporation. Water temperature should be warm, not hot.

If contact dermatitis is acute, some principles should be kept in mind. The affected area should be washed immediately and thoroughly. If wet or oozing, compresses with saline or tap water can be applied (1 minute on, 1 minute off for 20–30 minutes) 4–6 times daily. Protect the damaged skin against secondary infection until the acute stage subsides. Do not allow debris due to oozing, scaling and crusting to accumulate (see Nonpharmacologic Therapy, Wet Dressings).

Patients with contact dermatitis should avoid touching the following with bare hands: fruit juices, raw meat, fish and vegetables, especially raw onions and garlic; detergents, turpentine and kerosenes; hair tonics and shampoos. Remove rings when washing hands, as trapped soap may produce flares. Use an unscented soap or hand cleanser free of colour, antiseptics, deodorants, vitamins and tar. Wash hands with lukewarm water and use soap sparingly. Rinse hands thoroughly and dry with clean towel, especially between fingers. Wash as infrequently as possible, no more than 2–3 times daily. Hands can be protected with plastic or vinyl gloves worn with cotton liners, but rubber gloves should be avoided. In hand dermatitis, avoid activity that involves friction, pressure, squeezing or twisting. A low nickel diet for vesicular hand dermatitis can be helpful in select nickel-sensitive cases.69 Avoid adhesive bandages. Chronic hand dermatitis often becomes secondarily infected, especially if fissured, and should be managed appropriately. Despite lack of evidence, small, noninfected fissures can be closed with cyanoacrylate glue (e.g., Superglue). Occlusive dressings such as kitchen plastic wrap (overnight) may expedite healing.

Stasis Dermatitis

Local treatment of stasis dermatitis varies with the state of inflammation. Apply only those topical medications considered essential as patients with stasis dermatitis are readily sensitized; 80% of patients with chronic stasis dermatitis are at risk of contact dermatitis. Ointment bases are the most common inciting agents.70

The reduction of edema is important and achieved through bed rest and elevation of the extremity. After edema subsides, compressive support in the form of an elastic bandage should be applied. After the dermatitis is healed, advise the life-long use of elastic compression stockings.9

Pharmacologic Therapy

For comparative ingredients of nonprescription products, consult the Compendium of Products for Minor Ailments—Cough, Cold and Allergy Products; Skin Care Products: Dermatitis and Dry Skin, First Aid.

For further information on the pharmacologic treatment of atopic dermatitis, consult Compendium of Therapeutic Choices: Atopic Dermatitis.

Bath Products

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 17/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis In most dermatitis conditions, dryness at some stage initiates or exacerbates the symptoms. The primary means of correcting dryness is to add water to the skin and then to apply a hydrophobic substance to keep it there. The benefits of hydration and moisturizers to help restore and maintain normal barrier function cannot be overemphasized. Since wet skin is more permeable to water, it is essential that the skin be covered within the first few minutes to prevent evaporation. Appropriate use of hydration together with occlusive bases or moisturizers will help re-establish and maintain the skin's barrier function. Bathing can have differing effects on the skin depending on the manner in which it is carried out. Bathing with water can hydrate the skin and remove scale, crust, irritants, and allergens, which can be helpful for patients with atopic dermatitis. However, if the water is left to evaporate from the skin, greater transepidermal water loss occurs.71 Bathing is suggested for patients with atopic dermatitis as part of treatment and maintenance; however, there is no standard for the frequency or duration of bathing appropriate for atopic dermatitis. However, it is generally recommended that up to once-daily bathing be performed to remove serous crust; the duration should be limited to short periods of time (e.g., 5–10 minutes) with use of warm water. Moisturizers should be applied soon after bathing to improve skin hydration. Hydration of the face or neck can be achieved by applying a wet washcloth or towel to the involved area. Isolated areas such as hands and feet can be treated with soaks in basins. For the treatment of patients with atopic dermatitis, there is insufficient evidence for clear recommendations on the addition of oils, emollients and most other additives to bath water, or the use of acidic spring water.72

Despite lack of evidence it is generally thought that bath oils applied during or after bathing may help to reduce the rate of water loss through the epidermis; however, they are less effective than lotions and creams applied directly to wet skin since they are diluted with water and are in contact with the skin for a short time period, and most of the deposited oil is wiped off when towel drying. If added at the beginning of the bath, they may prevent rather than enhance hydration and thus should be added near the end of the bath to trap water in the skin. Bath oils give a false sense of lubrication and can make the bathtub slippery. Most bath oils combine mineral or vegetable oils with surfactants that disperse oil through the bath. Concentrations of surfactants (e.g., sodium lauryl sulfate) above 4% reduce the affinity of oil for the skin. Avoid products with fragrance and lanolin. Oil used as a single ingredient will float on top of the water. Bath oil capsules enclose small amounts of oil in soft, flexible gelatin capsules that dissolve in hot water but may necessitate a higher water temperature than desirable and often contain a higher percentage of fragrance. Olive oil is an inexpensive natural product that may be applied directly to rehydrated skin after bathing.

Avoid bath salts. They are highly fragranced and soften water by raising the alkalinity. This may cause itching or redness on sensitive skin. Avoid detergent bubble baths if skin is dry or itchy.

Colloidal oatmeal preparations contain starch and protein and are effective antipruritics. Addition of oatmeal products may be soothing but does not promote increased water absorption. For dry skin, they are not as effective as oils in trapping water to maintain hydration unless the oilated versions are used. Bathing in colloidal oatmeal baths is useful when large body areas are involved.69

Soaps are made from animal or vegetable fat and alkali and consist of surfactants that interact with stratum corneum proteins and lipids in a manner that causes damage, dry skin, and irritation. Most soaps are alkaline in pH, whereas the skin’s normal pH is 4–5.5. Fatty acid plus sodium or potassium hydroxide produce a water-soluble soap. Toilet soaps are usually made from palmitic, stearic or oleic acids. Hard sodium soaps are suitable for bars, flakes and powders while more soluble potassium soaps are used for liquid preparations. Softer and more water-soluble, transparent soaps (or glycerin soaps) do not last long or lather well. They claim to be less drying or irritating than alkaline opaque soaps. However, objective clinical evaluations are lacking.

Soapless cleansers are surfactants and synthetic detergents often recommended for better tolerance, although this is based on only a few clinical studies. They lack lipid and are available in lotion and gel forms. Soapless lotions can be applied liberally and have a foaming action. Removed gently, they leave a thin film on the skin to aid in water retention. No good evidence demonstrates that addition of neutral fats or cold cream to the soapless cleanser counteracts the drying effect. It is improbable that a simple cleansing agent can achieve the 2 opposing tasks (cleansing of the skin and deposition of fat on the skin), especially since the soap is rinsed off. Limited use of soapless cleansers (that are neutral to low pH, hypoallergenic and fragrance free) is recommended.

Excessive washing may remove lipids and water that normally keep the stratum corneum soft and pliable. Choice of soap depends on the type of dermatitis. Avoid soap in acute atopic or contact https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 18/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis dermatitis. For chronic dermatitis and for dry skin, a mild, nonalkaline soap, an aqueous cream or a soap-free cleanser can be used alternately (Table 8). Soap is applied only to intact skin, without rubbing or massaging. Sufficient water should be used to rinse away all traces of soap.

Moisturizers

Breakdown of the skin barrier, the first event in the development of atopic dermatitis, results in xerosis (dry skin), one of the cardinal clinical features. This provides a rationale for the use of a complete moisturizing therapy regimen to combat xerosis and transepidermal water loss (TEWL) in atopic dermatitis and related skin barrier breakdown conditions such as irritant contact dermatitis.73 The main purpose of moisturizer therapy is to restore the epidermal barrier, which is composed of corneocytes, extracellular proteins, and a lipid-rich matrix (ceramides, fatty acids, and cholesterol). Barrier damage is directly correlated to the severity of dermatitis. Use of moisturizers leads to the integrity of the epidermal barrier and a consequent reduction of both TEWL and penetration of irritant substances.

Patients with atopic dermatitis require ongoing moisturizer therapy. Clinical trials have shown that they lessen symptoms and signs of atopic dermatitis, including pruritus, erythema, fissuring, and lichenification.72 Moisturizers can themselves result in some reduction in inflammation and atopic dermatitis severity. There is strong evidence that their use can also reduce the need for pharmacologic intervention. Moisturizers are first-line therapy for mild disease and an important part of the treatment regimen for moderate and severe disease. They also play a key role in maintenance treatment and prevention of flares.72

Skin protection creams or “barrier” creams (usually silicone-based) may be used in the occupational setting to help prevent irritant contact dermatitis. The protective efficacy depends on the amount of product applied per unit skin surface area. The actual amounts applied and the resulting dose per unit area have been reported to be lower than recommended. Some products may show no protective efficacy when used at doses close to those practically applied at workplaces.74 In 1 study, 2 of 6 protective creams failed to prevent solvent-induced cumulative skin irritation, which emphasizes the lack of comparative efficacy among barrier creams.75 Antioxidant creams have been shown to effectively protect the skin from chemical-induced irritation.76 Unfortunately low adherence to skin protective measures that combine creams and other approaches has been reported after 1 year.77

Moisturizers are generally classified by their mechanism of action as emollients, occlusives, or humectants. Newer agents containing ceramides may be classed as barrier repair agents.

Emollients

Emollients are semisolid bases designed to control dryness by slowing evaporation and lubricating the stratum corneum. They may contain glycol, glyceryl stearate, and soy sterols which lubricate and soften the skin. These products cannot keep skin soft and flexible without the required concentration of water in the skin and function only to trap existing moisture. Very little water from emollients is absorbed by the skin; most water in the emollients evaporates when the product is applied and therefore they should be applied while the skin is still damp from bathing. Emollients include lotions, creams and ointments. Most are oil-in-water or water-in-oil emulsions. The higher the oil content, the greater the occlusion and the less drying through evaporation. Ointments are therefore the most occlusive and have the fewest additives, though in a hot, humid environment their use may lead to trapping of sweat with subsequent irritation of the skin. Users may not tolerate oil or water-in-oil products because the greasy texture increases discomfort. Greasy applications are unsuitable for acute oozing dermatitis. In contrast, evaporating water from oil-in-water creams or more liquid oil-in-water lotions produces a cooling effect which alleviates pruritus. A smaller amount of oil content is left as a residual film to protect hydration. Lotions contain more water than creams and may be drying due to the effects of evaporation. Obtain products in the largest size available because they usually need to be applied several times a day on a long-term basis.

Scrutinize the emollient product for other ingredients, as some preservatives, stabilizers, emulsifiers and fragrances may aggravate atopic, allergic or stasis dermatitis (e.g., lanolin, parabens, cresols, sodium lauryl sulfate, cetylstearyl alcohols and fragrance). Choose an emollient for its drying or lubricating properties as suitable for the stage of dermatitis. For an acute, wet dermatitis that has been compressed, https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 19/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis apply a lotion after oozing stops, to facilitate dryness. In less acute, drier dermatitis, an oil-in-water emulsion base is appropriate. In chronic, very dry or scaly dermatitis, a water-in-oil emulsion gives maximum lubrication. Hairy areas may require gels or lotions.

Occlusives

Occlusive agents (petrolatum, dimethicone, mineral oil) form a layer on the skin that retards evaporation of water. Petrolatum provides an occlusive effect but is cosmetically unacceptable as it feels greasy and does not wash off easily. It is sometimes used as a sealer after hydrating the skin; however, it is effective only when used in conjunction with hydration. Due to its highly occlusive properties, it can cause maceration and overgrowth of bacteria or yeast if used on acutely inflamed and oozing lesions. Petrolatum is discussed further as an alternative for diaper dermatitis (see Diaper Dermatitis).

Humectants/Hydrating Agents

Humectants are ingredients with hygroscopic properties to attract and hold water in the skin. Emollients to which humectants have been added may be called hydrating agents. Examples include alpha- hydroxy acids, glycerin, phospholipids, propylene glycol and urea. Some ingredients such as urea also soften keratin. Because they draw water and hydrate the skin, they are more efficacious for dry skin than emollients, which merely trap water present on the skin. Regular use of hydrating agents decreases the need for topical corticosteroids.78,79

Alpha-hydroxy acids (e.g., lactic, citric, glycolic, malic, pyruvic and glucuronic acids) may increase biosynthesis of mucopolysaccharides, contributing to the natural control of keratinization. Concentrations of 2–5% applied twice daily are best for use on larger areas or on the whole body as these compounds may produce irritation at concentrations of 10% or higher.80 Alpha-hydroxy acids affect keratinization at the lowest levels of the stratum corneum, where they affect corneocyte cohesion and new stratum corneum formation. In addition, they increase dermal mucopolysaccharides and collagen formation. Products such as lactic acid have been shown to increase skin surface lipids, extensibility and firmness of the skin, improving skin barrier function.20

Glycerin is a humectant that helps keep the product moist and facilitates spreading. In optimal concentrations of 50% or less, glycerin helps retard water evaporation, keeping it in close contact with the skin. There is no evidence that glycerin is absorbed through the skin.

Phospholipid products contain lecithin, which hydrolyzes to yield oleic, palmitic and stearic fatty acids. Lecithin is a water-binding agent that occurs naturally in the skin. Each phospholipid molecule forms a complex with 15 molecules of water. Water is drawn to and kept in the skin for hydration, keeping it soft and resilient. These preparations may also contain mineral oil, glycerin and lanolin.

Propylene glycol is a viscous, colourless, odourless, hygroscopic liquid used as a solvent and vehicle for water-insoluble or unstable compounds. The pH may vary from 4–8 with these products and an acid pH may result in an irritant reaction. A small percentage of patients may be hypersensitive to propylene glycol.

Urea works mainly by drawing water into the stratum corneum, though there are claims of keratolytic, antifungal, antipruritic, anesthetic and anti-infective properties. It is used mainly in atopic dermatitis for xerosis, as application on open, excoriated areas results in burning and discomfort. It can improve skin barrier function and reduce skin susceptibility to irritants. The concentration of urea determines its effect. Concentrations of 10% hydrate dry skin and 15% accelerate fibrin digestion. Concentrations of 20–30% are antipruritic, break down keratin, decrease the thickness of the stratum corneum and are used in scaling conditions such as ichthyosis. Concentrations of 40% are proteolytic and may be used to dissolve and peel dystrophic nails. Urea is sometimes combined with other active ingredients, such as corticosteroids, anthralin and benzoyl peroxide, to accelerate skin penetration. Combinations with hydrocortisone are useful for the dry itching skin of atopic dermatitis.81

Barrier Repair Products

Recognition of the role of disrupted ceramide content in barrier dysfunction led to the development of barrier repair therapies that aim to restore appropriate ceramide balance. In one study, a ceramide- dominant product was as effective as a mid-potency topical corticosteroid after 28 days.82 The use of https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 20/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis barrier repair products containing key stratum corneum lipids, including ceramides may make it possible to reduce the use of topical corticosteroids and immunosuppressive agents such as tacrolimus and pimecrolimus.

Tar Preparations

Topical coal tar derivatives have been used for many years in the treatment of inflammatory skin diseases. Coal tar activates the aryl hydrocarbon receptor signaling pathway, resulting in enhanced epidermal differentiation, increased levels of filaggrin, and inhibition of a major atopic dermatitis cytokine pathway.83 Prior to the widespread use of corticosteroids, crude coal tar extracts were used to reduce inflammation in atopic dermatitis. Despite limited evidence of efficacy, tar preparations72 may be used to reduce the need for corticosteroids in chronic maintenance therapy of atopic dermatitis. Their effect is not felt to be as potent as corticosteroids but they are long lasting with few side effects. Coal tar is primarily used in scalp preparations, compounded in cream bases that are generally used at night to increase adherence. Patients should cover the head with a shower cap to limit staining, and rinse out in the morning. Coal tar products should not be used on inflamed skin due to irritating effects. Cosmetically, they are less acceptable due to staining and unpleasant smell.20

Topical Corticosteroids

Topical corticosteroids are the mainstay of treatment for atopic dermatitis and first-line treatment for patients with allergic contact dermatitis. They reduce inflammation and pruritus and are useful for both the acute and chronic phases of atopic and contact dermatitis. Their mechanism is complex, affecting multiple resident and infiltrating cells primarily by suppressing inflammatory genes.

A large number of topical corticosteroids are available, ranging in potency from low to extremely high. A variety of factors should be considered when choosing a particular topical corticosteroid, including patient age, areas of the body to which the medication will be applied, and other patient factors such as degree of xerosis, patient preference, and cost of medication. Low-potency choices are recommended for areas of thinner skin (particularly the face and eyelids) and high-potency products are indicated for thickened and lichenified lesions in other locations. Choice of vehicle for the corticosteroid is also important. Vehicles include lotions, solutions, gels, sprays, foams, and oils. In general, ointments are considered more potent and more occlusive and contain less preservatives than creams and lotions. Creams are better tolerated in excessive heat or humidity; lotions are less effective and contribute to xerosis. Solutions are used on the scalp or hairy areas, but the alcohol content may irritate inflamed or excoriated lesions.

As a general rule, the lowest potency corticosteroid that is effective should be used. Therapy should not exceed a 2-week course. Lack of response to low-potency agents such as hydrocortisone may indicate the need for stronger corticosteroids except on the face and in skin folds, where low-potency agents like hydrocortisone remain the drugs of choice.84,85 Using a topical corticosteroid too low in potency may sometimes result in persistence or worsening of atopic dermatitis. In such cases, after a 2-week trial, institute a stepped-care approach, beginning with a mid-to-high potency corticosteroid until control is achieved, and then reducing to a lower-potency agent. Discontinuing a mid- to high-potency corticosteroid without tapering to a lower-potency corticosteroid may result in rebound flaring of atopic dermatitis. Some patients may not respond to corticosteroid therapy due to superinfection.20 When topical corticosteroids are used, any coexisting infection should be treated promptly.

Application of topical corticosteroids to wet skin has not been demonstrated to be better than application to dry skin for children with atopic dermatitis.86 However, in cases where topical corticosteroid alone is inadequate, this ‘‘soak and smear’’ technique may improve response.72,87 Severe or complicated dermatitis may require treatment with stronger corticosteroids. Resistant cases may sometimes respond to the addition of occlusion to the application of the corticosteroid, but this approach should be used with caution and is generally reserved for dermatitis of the hands or feet.

Patients with atopic dermatitis should be advised to continue with moisturizer therapy during treatment with topical corticosteroids. Topical corticosteroids should be used once daily although if insufficient for control, twice daily can be used. Twice weekly maintenance therapy is recommended in patients with https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 21/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis moderate to severe atopic dermatitis experiencing frequent relapses and is more effective than use of moisturizers alone for prevention of flares.72 There is insufficient evidence to know whether it is more beneficial to apply moisturizers before or after topical corticosteroids. A small, randomized study showed no difference over 2 weeks between patients who applied moisturizer before topical corticosteroids and those who did the reverse.88 Many sources suggest moisturizer be applied 30 minutes before topical corticosteroid but this is based on low-level evidence or consensus recommendations and is not universally accepted. Practicality and patient adherence are key factors to consider when deciding on order of application.89

Physical examination for cutaneous side effects is recommended during long-term, potent corticosteroid therapy. Consider the potential for both topical and systemic side effects, including possible hypothalamic-pituitary-adrenal axis suppression, particularly in children. Patient fears of side effects associated with the use of topical corticosteroids for atopic dermatitis should be recognized and addressed to improve adherence and avoid undertreatment. Despite widespread use, with correct education, adverse effects are infrequent with appropriately used mid- to high-potency corticosteroids. Over time, antiproliferative effects (e.g., skin thinning), poor wound healing, hypopigmentation, secondary infections and acne may occur, particularly on the face and in the intertriginous areas. Perioral dermatitis may occur on the face, characterized by erythema, scaling and follicular papules and pustules around the mouth or eye creases. Discontinue the corticosteroid if this occurs, and taper using hydrocortisone. Hydrocortisone is always the drug of choice in these sites. Use of “steroid sparers” such as emollients, occlusives and hydrators help to reduce total corticosteroid exposure, thereby reducing the risk of adverse effects.

It is possible to develop an allergic sensitivity to corticosteroid preparations themselves which appears paradoxical due to the anti-inflammatory effects of the corticosteroids. However, delayed-type reaction to corticosteroids do occur.90 Reported incidence rates in positive patch test results ranged from 0.5%– 3% for various topical corticosteroids in one study.91 Nonresponding eczema, development of subacute contact dermatitis, systemically reactivated allergic contact dermatitis or maculopapular exanthems can be a clinical symptom of a delayed-type hypersensitivity reaction to corticosteroids. The anti- inflammatory nature of corticosteroids makes the diagnosis of allergy more difficult, but it should be considered in patients suffering from intractable dermatitis. Immediate-type hypersensitivity reactions to corticosteroids remain uncommon.

Systemic Corticosteroids

Systemic agents are reserved for severe, acute cases, such as extensive poison ivy/oak; when treating poison ivy/oak, a prolonged course of oral therapy with a slow taper is often required. In general, prolonged use of oral agents for other causes is to be avoided due to adverse effects including diabetes, hypertension, growth retardation, lymphopenia, bone loss, glaucoma/cataracts, and development of Cushing syndrome.92

Topical Calcineurin Inhibitors

Topical calcineurin inhibitors (TCIs) such as tacrolimus and pimecrolimus are analogues of cyclosporine and have anti-inflammatory effects. They are highly effective in improving dermatitis and pruritus. Tacrolimus was effective in the treatment of corticosteroid-resistant allergic contact dermatitis in one study93 and as effective as a moderate-potency corticosteroid in another.94 Tacrolimus and pimecrolimus have both been shown to be effective for treatment of atopic dermatitis in children and adults.72,95 There is some evidence that tacrolimus may have a greater effect than pimecrolimus over time.95,96,97,98 Topical calcineurin inhibitors may not be as effective as moderate- to high-potency topical corticosteroids in the treatment of atopic dermatitis.95 Use of TCI therapy 2–3 times weekly between atopic dermatitis flares is recommended on flare-prone areas to help prevent relapses and decrease the amount of topical corticosteroid needed.72

The most common adverse effect reported for TCIs is burning and stinging at the application site, particularly if the skin is acutely inflamed. Treatment with topical corticosteroids to reduce inflammation prior to instituting TCI therapy may help minimize these reactions.72 Concerns about increased risk of https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 22/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis infections due to immunosuppression may warrant avoiding use on actively infected skin. There is insufficient evidence to support concerns about any link between use of TCIs and risk of malignancy. Routine bloodwork is not recommended.57,72

TCIs are usually considered second-line therapy when topical corticosteroid therapy is ineffective or not tolerated. The major advantage of TCIs is their safety profile and tolerability. They are recommended as steroid-sparing options for long-term topical treatment. They may be safely used in sensitive or thin- skinned areas such as the face, anogenital region and skin folds. 72

Topical Anti-Infectives

Atopic individuals are predisposed to skin infections because of a compromised physical barrier. S. aureus is found in more than 90% of atopic dermatitis. A systematic review examined 26 randomized controlled trials that used a variety of antistaphylococcal treatments in the management of atopic dermatitis, including oral antibiotics, antibacterial soaps, topical antibiotics or antiseptics, special textiles and combinations of topical corticosteroids with antibacterials. While reduction of S. aureus counts on the skin was reported with some interventions, no trials showed improvement in eczema control. The poor quality of many of the studies and low patient numbers make this evidence difficult to interpret.99 Topical antimicrobial preparations are not generally recommended in the treatment of atopic dermatitis. They can be associated with contact dermatitis, and there is concern that their use could promote wider antimicrobial drug resistance. Oral antibiotics are not indicated for routine treatment in noninfected atopic dermatitis.72

Bleach baths may be helpful in cases of moderate to severe disease with frequent bacterial infections, particularly for maintenance because the majority of patients do not show clearance of the bacteria. Development of bacterial resistance is less of a concern with use of dilute bleach compared with the use of topical and systemic antibiotics. Topical hypochlorite products are also available but are more expensive and have not been studied specifically.72

Treatment with antifungal agents is sometimes used to address dermatophyte pathogens such as Malassezia in atopic dermatitis, but the response to these is less effective than treatment with topical corticosteroids.20

Antihistamines

Pruritus is the hallmark of atopic dermatitis and a frequent symptom of contact dermatitis. The itch- scratch cycle complicates atopic dermatitis and should be aborted. Oral antihistamines act by blocking H1-receptors, thereby reducing pruritus caused by histamine. However, pruritus associated with atopic dermatitis is thought to be caused by mediators other than histamine, which is not the key factor.100 Certain subgroups of patients may benefit from antihistamines for other reasons. The first subgroup are those with sleep disturbances. The benefit of antihistamines comes from their side effects. First- generation antihistamines cause drowsiness which may help patients with atopic or contact dermatitis (adults and children) by promoting sleep or affecting sleep disturbances in the presence of pruritus. In these situations, first-generation antihistamines should be used before going to sleep.100 For a second subgroup with comorbid conditions of the atopic diathesis, including allergic rhinitis, chronic urticaria, dermographism or allergen-induced asthma, second-generation antihistamines such as loratadine and desloratadine can be tried. Fexofenadine has demonstrated a small but significant reduction in pruritus in atopic dermatitis, and may be the first option for patients who do not fall into the previous 2 subgroups.101 See Allergic Rhinitis for more information regarding oral antihistamines.

Topical antihistamines are strong contact sensitizers. In addition, due to the ionization that occurs topically, they are not efficacious when applied to normal skin unless to mucous membranes. They have demonstrated little utility and for these reasons, and due to the increased efficacy of other agents, they should be avoided.

An approach to the treatment of atopic dermatitis is shown in Figure 2. An approach to the treatment of contact dermatitis is shown in Figure 3. https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 23/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis

Natural Health Products

Natural remedies may not be harmless and should not be recommended over traditional, standardized and proven therapies. At this time, there are little data to support the majority of complementary therapies tried for atopic dermatitis management. Chinese herbal therapy (or traditional Chinese medicine) has been the most extensively studied. Anti-eczematous efficacy of traditional Chinese herbal medicines was found in one study.102 While it may have some benefit for lesions, the results from randomized controlled trials of oral therapy are conflicting, and reports of serious hepatotoxicity raise potential safety concerns. Some preparations have been reported to cause fatal toxic reactions, and adulteration with other substances such as corticosteroids has also been reported.103,104 The individualized and dynamic nature of this intervention (a different herb is added or subtracted depending on the patient) also poses challenges to performing controlled studies. Acupuncture alone or in conjunction with traditional Chinese medicine decreases signs and symptoms of atopic dermatitis, but the evidence is confined to small studies of limited quality.105,106

The disturbed epidermal barrier function of atopic dermatitis has been linked to altered metabolism of unsaturated fatty acids. This is the theoretical rationale for treatment with essential fatty acids such as gamma-linolenic acid (evening primrose oil). Use is characterized by a low incidence of side effects but also low efficacy in adults, with results in children no better than placebo. Two potential problems associated with use of evening primrose oil are its high cost and the lack of product standardization; adulterated brands may simply contain corn oil. Its use is clinically unsubstantiated and should not be recommended.7 A Cochrane review found no improvement in symptoms of atopic eczema or quality of life with use of borage oil or evening primrose oil compared with placebo.107

Massage therapy may improve symptoms of atopic dermatitis and associated patient and parental anxiety levels. While it is a safe intervention, studies to date are small and of limited quality, precluding recommendation at this time.108,109 Other complementary therapies lacking sufficient evidence include: aromatherapy, homeopathy, naturopathy,110 acupressure111 and autologous blood injections.112

In the case of allergic contact dermatitis due to nickel sensitivity, some effects of nickel may be eliminated or reduced by supplementing with divalent essential metals as there is some evidence that nickel dermatitis improved following oral administration of zinc sulfate.113,114

Monitoring of Therapy

Table 7 provides a monitoring framework for patients with dermatitis, which should be individualized. Parameters should be monitored by the patient or the caregiver, and a diary can be used. Therapy should be appropriately tapered in response to improvement or resolution. The healthcare practitioner should be responsible for ensuring that the treatment plan remains on schedule and is effective, and no adverse effects are occurring. Changes in symptoms due to treatment can be correlated with alterations in trigger factors such as irritants and foods. Stress, anxiety or depression levels should be tracked if they are suspected aggravating factors, and may lessen as skin symptoms improve.

Table 7: Monitoring of Therapy for Atopic, Contact or Stasis Dermatitis Type of Parameter Timeframe/Degree of Actionsa Dermatitis Change

Acute Inflammation Decrease by 50% within 7– Taper therapy in (redness, 10 days response to resolution: swelling, pain, if endpoints not warmth) achieved, consider additional or different therapy. Surface area No progression involved

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 24/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis Extension to other None sites or generalization

Blister formation No new blisters after 1–2 days

Itch/scratching Control to tolerable level within 7–10 days

Disruption of Restoration of normal sleep or daily patterns within 2–3 wk activities

Stress, anxiety, Re-establish normal pattern depression within 2–3 wk

Chronic Changes in Control by 4–8 wk If endpoints not inflammation, achieved, consider scaling, dryness, additional or different itch, scratching therapy.

Progression of No progression of severity severity

Recurrent Lengthening of symptom-free episodes periods throughout therapy

Lichenification No further lichenification throughout therapy

Acute and Allergic reactions None If allergic reaction chronic occurs, discontinue therapy.

Severe dryness, Minimal If severe, decrease irritation (e.g., Should disappear, diminish dose, concentration or redness, or be controlled with frequency of use. inflammation, continued use If still no improvement, stinging) consider different therapy.

a Patients should monitor all parameters daily while on drug therapy. Healthcare practitioners should monitor all parameters after 7–10 days for acute dermatitis and after 2–3 weeks for chronic dermatitis.

Algorithms

Figure 1: Assessment of Patients with Dermatitis

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Abbreviations: BSA = body surface area

Figure 2: Treatment of Atopic Dermatitis

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Figure 3: Treatment of Contact Dermatitis

https://www.myrDxtxr.ucag/p rTinat/nbelwe/documents/MA_CHAPTER/en/psc1056 27/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis Drug Table

Table 8: Selected Self-care Topical Products for Dermatitisa

Drug/C ostb Dosage Adverse Effects Comments

Drug Class: Barrier repair products

ceramides/c holesterol/f ree Apply thin After application, Do not apply within 4 h prior fatty acids layer to a temporary to radiation therapy. EpiCeram Skin Barrier affected area tingling sensation Emulsion, others BID or prn may occur (lasting 10–15 min). $$

Drug Class: Bath Products

bath oils After bath Allergic Acts as a barrier to reduce Keri Oil, others apply 5 mL sensitization may water loss. of oil in 50 occur due to $ mL water lanolin, fragrance with a cotton and other contact swab while sensitizers. the skin is May make the still damp bathtub slippery.

colloidal oatmeal As per Can clump and Provides relief for itching Aveeno Bath product clog drain. skin. Preparations, generics instructions; May contain oils and can act must be as an emollient. $ properly dispersed in water to be effective

Drug Class: Cleansers

opaque soaps Rinse well Drying. May contain moisturizers. Lowila, others after washing Use fragrance-free soap if In atopic possible. $ patients, restrict to axillae and groin

soapless cleansers Apply and Minor irritation Thin layer of product is left on Spectro Jel, others rinse seen rarely. skin allowing for retention of water. $

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Drug/C ostb Dosage Adverse Effects Comments

transparent soaps Rinse well May be less More water soluble but not as Pears, Neutrogena, others after washing drying than effective as other cleansers. In atopic opaque soaps. Use fragrance-free soap if $ patients, possible. restrict to axillae and groin

Drug Class: Corticosteroids, topical

hydrocortisone 0.5%, 1% Apply thin Mild to severe Temporary relief of redness, cream, lotion, ointment layer skin irritation. pain, swelling and itch. Cortate, Emo-Cort, sparingly Rarely, Prevex HC, generics BID–TID hypersensitivity PRN reactions. $ Reassess after 2 wk

Drug Class: Emollientsc

emollients Examples: Apply PRN Allergic Retards evaporation of water. glycol, glyceryl stearate, several times sensitization may As oil content increases soy sterols daily, occur if contains becomes more occlusive. Glaxal Base, Keri Lotion, preferably lanolin, selected Use fragrance-free products if Lubriderm, Neutrogena while skin is preservatives, possible. Cream damp fragrance and other contact $ sensitizers.

Drug Class: Humectants/Hydrating agentsc

humectants Examples: Apply PRN Allergic Humectants are usually alpha-hydroxy acids several times sensitization may incorporated into an emollient (glycolic acid, lactic acid), daily, occur if contains base to form hydrating glycerin, phospholipids preferably lanolin, selected agents. The emollient base (lecithin), propylene while skin is preservatives, prevents water evaporation glycol, urea damp fragrance and and the humectants attract Dermal Therapy, Lac- other contact water into skin. Hydrin, Neostrata, Uremol sensitizers.

$

Drug Class: Occlusivesc

occlusives Examples: Apply PRN Well tolerated, Used to protect against petrolatum, dimethicone, several times usually less irritants such as chemicals, mineral oil daily stinging than with detergents, polishes and Barriere, Complex 15, emollient creams water. Moisturel, Prevex, or lotions or Also useful for prevention and Vaseline humectant- treatment of occupational containing hand eczema. $ hydrating agents

https://www.myrxtx.ca/print/new/documents/MA_CHAPTER/en/psc1056 29/34 9/2/2017 Atopic, Contact, and Stasis Dermatitis a For more information on the use of topical corticosteroids consult the Compendium of Therapeutic Choices: Atopic Dermatitis. b Cost of smallest available pack size; includes drug cost only. c Most moisturizers contain combinations of emollients, humectants and occlusives. Legend: $ <$10 $$ $10–20

Suggested Readings

Cury Martins J, Martins C, Aoki V et al. Topical tacrolimus for atopic dermatitis. Cochrane Database Syst Rev 2015;7:CD009864.

Eichenfield LF, Tom WL, Chamlin SL et al. Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol 2014;70:338-51.

Eichenfield LF, Tom WL, Berger TG et al. Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol 2014;71:116-32.

Lynde C, Guenther L, Diepgen TL et al. Canadian hand dermatitis management guidelines. J Cutan Med Surg 2010;14:267-84.

Saji D, Asiniwasis R, Skotnicki-Grant S. A look at epidermal barrier function in atopic dermatitis: physiologic lipid replacement and the role of ceramides. Skin Therapy Lett 2012;17:6-9.

Scottish Intercollegiate Guidelines Network. Management of atopic eczema in primary care: a national clinical guideline. Edinburgh: SIGN; 2011. Available from: www.sign.ac.uk/pdf/sign125.pdf.

Sidbury R, Davis DM, Cohen DE et al. Guidelines of care for the management of atopic dermatitis: section 3. Management and treatment with phototherapy and systemic agents. J Am Acad Dermatol 2014;71:327-49.

Sidbury R, Tom WL, Bergman JN et al. Guidelines of care for the management of atopic dermatitis: section 4. Prevention of disease flares and use of adjunctive therapies and approaches. J Am Acad Dermatol 2014;71:1218-33.

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