Published: August 2010
Contact dermatitis is an acute or chronic immunologic (allergic) or nonimmunologic (irritant) inflammation of the skin usually caused by contact with chemicals but occasionally by biologic or physical agents.1 Of the more than 85, 000 chemicals in our environment, many can be irritants and more than 4350 have been identified as contact allergens. The potential for these substances to cause contact dermatitis varies greatly, and the severity of the dermatitis or eczema, the most common clinical expression, ranges from a mild, short-lived condition to a severe, persistent, job-threatening disease.
The prevalence of contact dermatitis in the general U.S. population has been variably estimated between 1.5% and 5.4%. Contact dermatitis is the third most common reason for patients to seek consultation with a dermatologist, accounting for 9.2 million visits in 2004. It also accounts for 95% of all reported occupational skin diseases.1
Exogenous and endogenous risk factors are listed in Boxes 1 and 2, respectively. Although genetics, gender, and age can be risk factors, the inherent nature, toxicity, and degree of cutaneous exposure to chemicals are probably more important. A history of atopic dermatitis is linked to an increased susceptibility to irritant dermatitis because of a lower threshold for skin irritation, impaired skin barrier function, and slower healing process.2 Wet work and chemical exposure are major precipitating factors for the development of irritant contact dermatitis (ICD) in patients with atopic eczema. Although atopic patients downregulate Th1 cells with a decreased propensity to contact sensitization, allergic contact dermatitis (ACD) is often seen in patients with atopic eczema, and nickel sensitization is increased in atopic patients.3 Other skin conditions with the highest risk of ACD include stasis dermatitis, 1 hand and foot eczemas, and chronic actinic dermatitis.1
|Box 1: Exogenous Factors Influencing Contact Dermatitis
|Cutaneous penetration of chemical|
|Environment (temperature, humidity)|
|Mechanical factors (pressure, friction, abrasion)|
|Properties of the chemical (pH, chemical activity)|
|Other exposure factors: duration, prior or simultaneous exposures, direct versus airborne|
|Box 2: Endogenous Factors Influencing Contact Dermatitis
|Lack of hardening|
|Primary sensitive (hyperirritable) skin|
|Secondary hyperirritability of the skin (status eczematicus)|
|Sensitivity to ultraviolet light|
Irritants cause as much as 80% of cases of contact dermatitis. ICD follows exposure to chemical or physical substances capable of direct damage to the skin.1, 2
There are two major types of ICD. Chronic cumulative (traumiterative, marginal) ICD is the type of contact dermatitis most commonly encountered in clinical practice. Cumulative ICD develops as a result of repeated insults to the skin, where the chemicals involved are often multiple and weak.3 The most common irritants include soap, detergents, surfactants, organic solvents, and oils (Box 3).1 Dry skin with a glazed, parched appearance may be the initial sign; erythema, hyperkeratosis, and fissuring can supervene.3 The second major type is acute ICD, which generally results from a single skin exposure to a strong irritant or caustic chemical (alkalis and acids). Most cases are the result of occupational accidents. Depending on the type of exposure to the irritant, the patient can develop erythema, edema, vesicles, and tissue necrosis.1
|Box 3: Causes of Irritant Contact Dermatitis
|Water and wet work|
ACD is a T cell delayed-type (type IV) hypersensitivity reaction that arises from direct skin exposure to an exogenous allergen. These allergens are low-molecular-weight (<500 Da) lipophilic chemicals called haptens that penetrate the skin and covalently bind to carrier proteins to become fully immunogenic. The new antigen-protein complex is processed by Langerhans cells in the epidermis and then travels to the regional draining lymph nodes and is presented to naïve Th1 cells. There, cytokines such as interleukin 2 and interferon-γ are secreted, leading to clonal proliferation of the newly sensitized memory Th1 cells in the paracortical region of the lymph nodes and are released into the circulation. This is the sensitization phase, which takes 5 to 21 days. On re-exposure to the same antigen, the elicitation phase, the previously sensitized person elicits a clinical dermatitis, usually after 12 to 48 hours.1, 3
The clinical features of ACD are often indistinguishable from those of ICD. In the acute stage, erythematous papules, oozing vesicles, and crusted lesions predominate; these can occur anywhere but are best visualized on the palms, sides of the fingers, periungual areas, and soles. Frequently occurring or persistent episodes of acute contact dermatitis often become chronic, with thickening associated with lichenification, scaling, and fissuring. Postinflammatory hyperpigmentation or hypopigmentation can occur. Pruritus is a hallmark of most forms of contact dermatitis.1 Major causes of ACD are listed in Box 4.
|Box 4: Principal Causes of Allergic Contact Dermatitis*|
|Balsam of Peru|
|Gold sodium thiosulfate|
*Top 10 patients list reactions in North America.
Systemic reactivation of ACD, or systemic contact dermatitis (SCD), occurs when persons with contact allergy to a hapten are exposed systemically to the same hapten via the oral, subcutaneous, transcutaneous, intravenous, inhalation, intra-articular, or intravesical route.1, 3, 5
Clinical features of SCD include flare-up of sites of previous dermatitis or of prior positive patch tests and development of dermatitis in previously unaffected areas, such as vesicular hand eczema, flexural dermatitis, nonspecific maculopapular eruptions, vasculitis-like lesions, and the baboon syndrome, 3 which is a well-demarcated eruption on the buttocks, genital area, and inner thighs. Associated systemic symptoms of headache, nausea, vomiting, arthralgias, and diarrhea can accompany the cutaneous findings.
SCD has primarily been caused by medications (e.g., antibiotics, corticosteroids, iodine, alcohol-containing drugs, nonsteroidal antiinflammatory drugs [NSAIDs], vitamin B, iodine). But metals (nickel, cobalt, chromium, gold, mercury), Myroxylon pereirae (balsam of Peru) from spices and flavorings, and certain foods or food additives (e.g., garlic, onion, herbs, quinine tonic water, propylene glycol) are other causes. A relatively high dose of hapten is usually needed. Other variables include route of administration, bioavailability, individual sensitivity to the allergen, and interaction with amino acids and other allergens.
Diagnostic history and physical examination clues are discussed in the overview of ICD and ACD. The appearance of the lesions often corresponds to whether the patient's dermatitis is acute or chronic at the time of presentation. Most of the diagnostic discussion focuses on ACD, which is easier to diagnose than ICD. A summary of the diagnostic workup is listed in Box 5. The differential diagnosis of contact dermatitis is listed in Box 6.
|Box 5: Diagnostic Workup for Contact Dermatitis
|Box 6: Differential Diagnosis of Contact Dermatitis
|Other Types of Eczema or Dermatitis|
No universally accepted test exists for diagnosing ICD, which is often diagnosed by excluding other types of dermatitis including ACD. Because of the clinical similarity of ACD and ICD, it is important that patients believed to have either disorder undergo patch testing, which is positive in the former and negative in the latter.
Diagnosis of ACD is based on the history; on the appearance, periodicity, and localization of the eruption; and on the clinical course. History is especially important in cases of chronic dermatitis and putative occupational contact dermatitis. History alone may be accurate only 50% of the time, on average, ranging from 80% correct for nickel to 50% for moderately common allergens to about 10% for less-common allergens. Even with obvious causes, the specific allergen might not be known, and ACD to other chemicals may be associated.
Skillful history taking is required to differentiate ACD from contact urticaria and ICD, which is especially difficult in chronic cases. Detailed questioning of the patient about all topical medications (over-the-counter and prescription), systemic medications, cosmetics, lotions and creams, occupation, hobbies, travel, and clothing is also important. A past history of ACD to one or more of the major contact allergens, such as nickel, rubber, topical medicaments, cosmetics (fragrances, preservatives, and dyes), or obvious occupational or avocational exposures such as chrome, epoxy, acrylics, gloves, clothing, first aid creams, preservatives, plants, and other chemicals, can point to inadvertent ACD in another unexplained eruption.1, 3-5
The distribution of dermatitis is often the single most important clue to the diagnosis of ACD. The area of most intense dermatitis usually corresponds to the site of the most intense contact with the allergen. Exceptions exist, such as nail polish allergy, which typically occurs on ectopic sites, especially the eyelids, face, and neck. In addition to the transfer of allergens to distant sites, volatile airborne chemicals can cause dermatitis on exposed body areas. Regional differences in susceptibility to contact allergens exist. The thinner eyelid and genital skin is more susceptible to ACD and ICD. Scalp hair is often protective, with allergic reactions to hair cosmetics involving the upper face, eyelids, postauricular area, and neck. Other areas have higher or lower exposures to allergens that are not always obvious and that are reflected in unusual distributions of dermatitis. Allergens in lotions and creams which are applied all over the body sometimes produce reaction in skin folds and intertriginous areas, where the chemicals tend to concentrate.
Attempting to recognize ACD on the basis of physical examination alone may be only partially accurate. Linear vesicular streaks are commonly seen in poison ivy, oak, and sumac dermatitis, but contact with other plants can give a similar picture. Contact with liquids can also produce linear vesicles. Failure to examine the entire skin can result in misdiagnosis. Eczema on the trunk and arms might in fact represent autoeczematization from contact or stasis dermatitis of the legs. There are significant regional variations in contact dermatitis, and knowledge of substances that cause dermatitis of specific body sites facilitates the diagnosis (Box 7).
|Box 7: Contact Allergen Exposures by Location of Dermatitis1, 2|
|Face, Eyelids, and Neck|
|Trunk and Flexural Areas|
Data from Cao LY, Taylor JS: V Contact Dermatitis and Related Disorders. 2 Dermatology. ACP Medicine. Dale DC, Federman DD, Eds. BC Decker Inc, Hamilton, ON, September 2008. http://www.acpmedicine.com. (accessed August 6, 2009), and Chew AL, Maibach HI: Occupational issues of irritant contact dermatitis. Int Arch Occup Environ Health 2003;76:339-346.
If the history and the clinical presentation reveal one or more risk factors for ACD, patch testing is indicated. The patch test is the only useful and reliable method—the gold standard—for diagnosing ACD, and its proper performance and interpretation require considerable experience.1, 6 The patch test aims to reproduce in miniature the clinical eczematous dermatitis by applying allergens under occlusion on intact skin of patients with suspected contact dermatitis. A positive patch test represents an in vivo visualization of the elicitation phase of contact dermatitis. Patch testing for ACD is not meant to reflect an irritant reaction. The patch test is typically better than relying on history alone, trial and error, or in vitro tests.1, 6
Commercially available individual patch test allergens in a dilute, nonirritating concentration are applied to the upper back for 48 hours. After the patch tests are removed, the sites of the patch tests are evaluated twice, usually after removal at 48 hours and again at 96 hours or beyond. Results at both readings are graded according to intensity of the reaction at the patch test site on a scale of 0 to 3+.1 Relevance of positive reactions to present or past episodes of dermatitis is determined by correlating the patch test results with chemicals, products, and processes encountered in the environment.1
Patch tests should generally not be applied if the patient's dermatitis is active or involves the back. A screening patch test series is typically applied and supplemented by aimed patch testing with other patch test chemicals based on the patient's history and occupation. Limited screening patch test series diagnose only 20% to 50% of a patient's contact allergens, and additional testing is often indicated to more adequately diagnose ACD.
Histopathology is of limited value in diagnosing contact dermatitis. Findings depend on the stage of the process and the nature of the contactant. Most types of eczema show similar histopathologic changes and cannot be distinguished with certainty.1
Identification and elimination of the offending irritant or allergen and protection from further exposure are important in managing contact dermatitis of all causes and types. Patients with ACD must be educated about potential sources of exposure and cross-reacting allergens, and they must be provided with lists of potential products and processes that contain the allergen and a list of nonsensitizing substitutes.1 Examples of allergen alternatives include topical erythromycin or mupirocin as substitutes for neomycin. Neomycin can cross-react with gentamycin and tobramycin. Bacitratin should generally be avoided in neomycin-sensitive patients because of coreactivity.
Reasons for persistence of ACD include unidentified sources of allergens or irritants at home or at work, exposure to cross-reacting allergens, presence of underlying endogenous (e.g., atopic) eczema, and adverse reactions to therapy.
In the case of hand dermatitis, practical management must include protective measures as well as the use of topical corticosteroids and lubrication. The use of vinyl gloves with cotton liners to avoid the accumulation of moisture that often occurs during activities involving exposure to household or other irritants and foods (e.g., peeling or chopping fruits or vegetables) may be helpful.7 In the workplace, verify that gloves are safe to use around machinery before recommending their use. Protective devices themselves can introduce new allergic or irritant hazards in the forms of rubber in gloves and solvents in waterless cleansers. Automation of industrial processes can reduce exposure but is the most expensive preventive measure. Barrier creams are generally a last resort and are probably best used in workers with no dermatitis.
Once dermatitis develops, use of topical treatment is helpful. Topical corticosteroids are the mainstay of ACD therapy; however, their use in ICD is controversial. For mild or moderate localized dermatitis, topical corticosteroids applied twice daily are usually effective within a few days and should be continued for 2 weeks. Lower-potency agents should be applied to the face and intertriginous areas, and higher-potency steroids should be reserved for the extremities and torso. Frequent and prolonged use of topical corticosteroids in fold areas can cause atrophy, telangiectasia, or striae, and their use on the face can also cause steroid rosacea. Topical calcineurin inhibitors (e.g., tacrolimus or pimecrolimus) may be used as an alternative to low-potency topical corticosteroids in chronic ICD.8
Emollients or occlusive dressings may improve barrier repair in dry, lichenified skin.1 Traditional petrolatum-based emollients are accessible and inexpensive, and they have been shown to be as effective as an emollient containing skin-related lipids. To relieve pruritus, a lotion of camphor, menthol, and hydrocortisone (Sarnol HC) is soothing, drying, and antipruritic. Pramoxine, a topical anesthetic in a lotion base (Prax) can also relieve pruritus. Phototherapy with bath PUVA (psoralen plus ultraviolet A) therapy may be helpful for chronic contact dermatitis of the palms and soles.
Most cases of contact dermatitis are effectively managed without the use of systemic corticosteroids. Short courses of systemic corticosteroids are indicated for patients with severe vesiculobullous eruptions of the hands and feet or the face or with severe disseminated ACD, such as poison ivy, sumac, or oak.1 Also systemic drugs such as cyclosporine may be effective, but they should be prescribed for limited periods by those experienced in their use. When dermatitis is complicated with a secondary infection, systemic antibiotics against Staphylococcus aureus and Staphylococcus pyogenes are preferred.1 Sedating antihistamines such as diphenhydramine hydrochloride, hydroxyzine hydrochloride, and doxepin hydrochloride may be administered at night for intense itching.1
Once a contactant has been identified as the causal factor, patients should be educated about avoidance, including everyday practices that can cause or contribute to the contact dermatitis. For ICD, less irritating substances, such as emollients and soap substitutes, should be used rather than soap when washing. Moisturizers are believed to increase hydration or prevent transepidermal water loss, thereby maintaining skin barrier function and reducing the risk of ICD.2
In the occupational arena, strategies for preventing contact dermatitis include administrative measures, environmental measures, and personal measures. Administrative measures include worker education and training regarding specific job hazards. Environmental measures include eliminating hazardous materials or finding substitutes for them, isolating and enclosing the work process, providing exhaust ventilation, and observing good housekeeping. Personal measures include applying emollients, adjusting personal cleansing and hygiene routines, and wearing personal protective equipment.3
The safety of patch testing in pregnancy has not been studied. Although the minute amounts of allergens applied during patch testing appear unlikely to be absorbed in sufficient amounts to harm the fetus, most physicians defer such testing in pregnancy. As with all treatments in pregnant women, the benefits of testing should be weighed against any potential risk.9
Contact dermatitis has been well documented in children, and nickel and rubber allergies appear to be increasing in this age group. Patch testing with a limited series of allergens is indicated in small children with limited back areas.10
Skin hyporeactivity or anergy is not well understood and may be observed in patients taking corticosteroids, immunomodulators, or ultraviolet light therapy and in patients with cancer, sarcoidosis, and viral infections such as human immunodeficiency virus (HIV) and measles.11