Contact Dermatitis
Virginia P. Arcangelo
Dermatitis is an alteration in skin reactivity caused by exposure to an external agent. It is a combination of genetic and environmental factors. It can occur after a single exposure or multiple exposures to an agent or in response to an allergen. The resulting dermatitis usually appears as an inflammatory process. According to the American Academy of Dermatology, contact dermatitis is a common problem and results in approximately 5.7 million visits to health care providers each year. Almost any substance can be a potential irritant. Diaper dermatitis (sometimes called diaper rash) is the most common form of irritant contact dermatitis (ICD) in childhood.
CAUSES
Two types of contact dermatitis are irritant and allergic dermatitis. ICD results from exposure to any agent that has a toxic effect on the skin. Allergic contact dermatitis (ACD) results from exposure to an antigen that causes an immunologic response. Atopic dermatitis (eczema), a form of allergic dermatitis characterized as a pruritic, chronic inflammatory condition, affects between 5% and 10% of the population in the United States (Goodheart, 2008). It most often begins in childhood.
PATHOPHYSIOLOGY
ICD is not an allergic response. It is a result of damage to the water-protein-lipid matrix of the outer layer of skin. It appears as an erythematous, scaly eruption resulting from friction, exposure to a chemical, or a thermal injury. The severity of the reaction depends on the condition of the skin, the concentration and the toxicity of the irritant, and the length of exposure. The reaction appears only in the area exposed to the irritant.
ACD (e.g., poison ivy) is an immunologically mediated response to an allergen (antigen). During the initial sensitization phase, the host is immunized to the allergen. After reexposure, a more rapid and potent secondary immune response occurs. The second phase manifests in ACD, and T cells are key mediators of the reaction. On activation, T cells release cytokines, chemokines, and cytotoxins, causing stimulation of local blood vessels; recruitment of immune cells, such as macrophages and eosinophils; and subsequent amplification of the sensitization response. Within 5 to 7 days after sensitization, there is visual evidence of the response. On subsequent exposures, however, dermatitis may develop within 6 to 18 hours. Hypersensitivity can occur after one exposure or after years of repeated exposures. Contact dermatitis may spread extensively beyond the area of contact.
In atopic dermatitis, there are high concentrations of serum immunoglobulin (Ig) E, decreased numbers of immunoregulatory T cells, defective antibody-dependent cellular cytotoxicity, and decreased cell-mediated immunity. The pathogenesis of atopic dermatitis involves genetic factors, skin barrier defects, and immune dysregulation. The genetics of atopic dermatitis is an area of intense research and plays a significant role in IgE production and allergic sensitization. More recently, the association of atopic dermatitis with filaggrin (FLG) gene mutations suggests the role of skin barrier defects in the pathogenesis of atopic dermatitis. FLG is a protein essential to the normal barrier function of the skin. Deficiency in FLG may contribute to the physical barrier defects in atopic dermatitis and predispose patients to increased transepidermal water loss, infection, and inflammation associated with the exposure of cutaneous immune cells to allergens.
PHARMACOGENOMICS
A genetic basis for atopic dermatitis has long been recognized with a family history of disease as a risk factor. Before characterization of the human genome, heritability studies combined with family-based linkage studies supported the definition of atopic dermatitis as a complex trait in which interactions between genes and environmental factors and the interplay between multiple genes contribute to disease manifestation. The gene encoding FLG has been most consistently replicated as associated with atopic dermatitis. Most gene studies to date have focused on adaptive and innate immune response genes, but there is increasing interest in skin barrier dysfunction genes (Barnes, 2010).
DIAGNOSTIC CRITERIA
ICD and ACD appear as linear streaks of papules, vesicles, and blisters that are very pruritic. In ICD, the lesions are found only in the area of exposure to the irritant. In ACD, the lesions are usually more diffuse, and they may present over an underlying area of edema.
Lesions in atopic dermatitis include papules, erythema, excoriations, and lichenification. In infants, the face, chest, legs, and arms are the most commonly involved areas; lesions are scaly and red and may be crusted patches and plaques. In children, the most common sites are the antecubital and popliteal fossae, the neck, wrists, ankles, eyelids, scalp, and behind the ears. Lesions are usually lichenified because of constant scratching. In adults, the neck, antecubital and popliteal fossae, face, wrist, and forearms are the most commonly involved areas. Lesions may appear as poorly defined, pruritic, erythematous papules and plaques. This may present specific therapeutic opportunities; however, at this time, maintaining a normal epidermal barrier is key.
INITIATING DRUG THERAPY
The most effective form of treatment for contact dermatitis is prevention. The patient must become aware of the causes or triggers and plan ways to avoid them. Before initiating therapy, the practitioner first needs to determine the severity of the problem. If the symptoms are mild, cool compresses may offer relief, and baths with colloidal oatmeal may offer relief from pruritus. Compresses of Burow solution are effective for drying the vesicles and bullae that may be associated with contact dermatitis. If these treatments fail or if the dermatitis is more extensive, drug therapy is initiated.
Before initiating drug therapy, delivery of the drug to the skin, protection/barrier function, and cosmetic acceptability must be considered. Ointment and gels offer the best delivery and protection barrier. Creams are less greasy but less effective. Lotions are dilute creams. Solutions are alcohol-based liquids and are useful for treating the scalp because they do not coat the hair.
Moisturizers used generously and frequently increase skin hydration, and their lipid component improves the damaged skin barrier. Lipid-rich moisturizers both prevent and treat ICD.
Barrier creams containing dimethicone or perfluoropolyethers, cotton liners, and softened fabrics help to prevent ICD.
Goals of Drug Therapy
The goals of drug therapy for dermatitis are as follows:
Restoration of a normal epidermal barrier
Treatment of inflammation of skin
Control of itching
The mainstays of therapy for contact dermatitis are topical corticosteroids. There are also topical immunosuppressives available. Systemic corticosteroids are recommended for widespread symptoms, and antihistamines are used for relieving intense pruritus.
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. Topical calcineurin inhibitors (e.g., tacrolimus or pimecrolimus) may be used as an alternative to low-potency topical corticosteroids in chronic ICD.
Emollients or occlusive dressings may improve barrier repair in dry, lichenified skin. 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.
Topical Corticosteroids
Topical steroidal therapy is safer than systemic steroidal therapy. Steroidal agents are effective for smaller outbreaks. Because of their anti-inflammatory and antimitotic actions, they reduce inflammation and the buildup of scale.
Topical corticosteroids are classified according to potency (Table 11.1), with the fluorinated agents being more potent. Ideally, the least potent topical corticosteroid should be used for the shortest possible time in treating dermatitis. Topical corticosteroids should be avoided if there are additional bacterial, viral, or fungal skin infections, and they are not recommended for prophylaxis.
Dosage
Treatment may be initiated with an intermediate- or high-potency topical corticosteroid. A lower-potency corticosteroid may be used after the symptoms subside. As a rule, short-term therapy with more potent topical corticosteroids is preferred to longer-term therapy with less potent corticosteroids. Low-potency corticosteroids should be used in the facial and intertriginous regions because fluorinated and high-potency
corticosteroids applied to the face may cause atrophy of the tissue or trigger steroidal rosacea. If it is necessary to use either type of agent, use should be limited to a very brief time. The maximum recommended length of treatment with topical corticosteroids is 2 weeks for adults and 1 week for children.
corticosteroids applied to the face may cause atrophy of the tissue or trigger steroidal rosacea. If it is necessary to use either type of agent, use should be limited to a very brief time. The maximum recommended length of treatment with topical corticosteroids is 2 weeks for adults and 1 week for children.
TABLE 11.1 Classification of Topical Corticosteroids by Potency | ||||||||||||
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