ICD-9: 692.9 ○ ICD-10: L24
ACD is a systemic disease defined by hapten-specific T-cell–mediated inflammation.
One of the most frequent, vexing, and costly skin problems.
An eczematous (papules, vesicles, pruritic) dermatitis.
Due to reexposure to a substance to which the individual has been sensitized.
Accounts for 7% of occupationally related illnesses in the United States, but data suggest that the actual incidence rate is 10–50 times greater than reported in the U.S. Bureau of Labor Statistics data. Nonoccupational ACD is estimated to be three times greater than occupational ACD.
All ages but uncommon in young children and in individuals older than 70 years.
One of the most important causes of disability in industry.
ACD is a classic, delayed, cell-mediated hypersensitivity reaction. Exposure to a strong sensitizer results in sensitization in a week or so, while exposure to a weak allergen may take months to years for sensitization. Sensitized T cells circulate in the blood and home to the skin wherever the specific allergen is presented. Thus, all skin is hypersensitive to the contact allergen.
Contact allergens are diverse and range from metal salts to antibiotics, dyes to plant products. Thus, allergens are found in jewelry, personal care products, topical medications, plants, house remedies, and chemicals the individual may come in contact with at work. The most common allergens in the United States are listed in Table 2-2.
TABLE 2-2TOP-ELEVEN CONTACT ALLERGENS (NORTH AMERICAN CONTACT DERMATITIS GROUP) AND OTHER COMMON CONTACT ALLERGENSa |Favorite Table|Download (.pdf) TABLE 2-2 TOP-ELEVEN CONTACT ALLERGENS (NORTH AMERICAN CONTACT DERMATITIS GROUP) AND OTHER COMMON CONTACT ALLERGENSa
|Allergen ||Principal Sources of Contact |
Balsam of Peru
Sodium gold thiosulfate
Methyldibromo glutaronitrile, phenoxyethanol
Metals in clothing, jewelry, catalyzing agentse
Usually contained in creams, ointments
Disinfectant, curing agents, plastics
Cement, galvanization, industrial oils, cooling agents, eyeshades
Parahydroxybenzoic acid ester
Black or dark dyes of textiles, printer’s ink
Conserving agent in foodstuffs
Solvents, shoe polish, printer’s ink
Cement, antioxidants, industrial oils, matches, leather
Plants, e.g., poison ivy
The eruption starts in a sensitized individual 48 h or days after contact with the allergen; repeated exposures lead to a crescendo reaction, i.e., the eruption worsens. Site of the eruption is confined to site of exposure.
Intense pruritus; in severe reactions, also stinging and pain.
“Acute illness” syndrome, including fever, but only in severe ACD (e.g., poison ivy, see below).
Acute. Well-demarcated erythema and edema with superimposed closely spaced papules or nonumbilicated vesicles (Fig. 2-5); in severe reactions, bullae, confluent erosions exuding serum, and crusts. The same reaction can occur after several weeks at sites not exposed.
Acute allergic contact dermatitis on the lips due to lipstick The patient was hypersensitive to eosin. Note bright erythema, microvesiculation. At close inspection, a papular component can be discerned. At this stage, there is still sharp margination.
Subacute. Plaques of mild erythema showing small, dry scales, sometimes associated with small, red, pointed or rounded erythematous firm papules and scales (Figs. 2-6 and 2-7).
Allergic contact dermatitis of hands: chromates Confluent papules, vesicles, erosions, and crusts on the dorsum of the left hand in a construction worker who was allergic to chromates.
Allergic contact dermatitis due to nickel, subacute Note a mix of papular, vesicular, and crusted lesions and loss of sharp margination. The patient was a retired watchmaker who used a metal clasp on the dorsum of the left hand while repairing watches. He was known to be allergic to nickel.
Chronic. Plaques of lichenification (thickening of the epidermis with deepening of the skin lines in parallel or rhomboidal pattern), scaling with satellite, small, firm, rounded or flat-topped papules, excoriations, and pigmentation.
Initially, confined to area of contact with allergen [e.g., earlobe (earrings), dorsum of foot (shoes), wrist (watch or watchband), collar-like (necklace), and lips (lipstick)]. Often linear, with artificial patterns, an “outside job.” Plant contact often results in linear lesions (e.g., Rhus dermatitis, see below). Initially confined to site of contact, later spreading beyond.
Extent. Isolated, localized to one region (e.g., shoe dermatitis), or generalized (e.g., plant dermatitis).
The duration of ACD varies, resolving in some 1–2 weeks, but gets worse as long as allergen continues to come into contact with the skin.
Acute. Erythema → papules → vesicles → erosions → crusts → scaling.
Note: In the acute forms of contact dermatitis, papules occur only in ACD, not in ICD (see Table 2-3).
TABLE 2-3DIFFERENCES BETWEEN IRRITANT AND ALLERGIC CONTACT DERMATITISa |Favorite Table|Download (.pdf) TABLE 2-3 DIFFERENCES BETWEEN IRRITANT AND ALLERGIC CONTACT DERMATITISa
| || ||Irritant CD ||Allergic CD |
|Symptoms ||Acute ||Stinging, smarting → itching ||Itching → pain |
| ||Chronic ||Itching/pain ||Itching/pain |
|Lesions ||Acute ||Erythema → vesicles → erosions → crusts → scaling ||Erythema → papules →vesicles → erosions → crust → scaling |
| ||Chronic ||Papules, plaques, fissures, scaling, crusts ||Papules, plaques, scaling, crusts |
|Margination and site ||Acute ||Sharp, strictly confined to site of exposure ||Sharp, confined to site of exposure but spreading in the periphery; usually tiny papules; may become generalized |
| ||Chronic ||Ill defined ||Ill defined, spreads |
|Evolution ||Acute ||Rapid (few hours after exposure) ||Not so rapid (12–72 h after exposure) |
| ||Chronic ||Months to years of repeated exposure ||Months or longer; exacerbation after every reexposure |
|Causative agents || ||Dependent on concentration of agent and state of skin barrier; occurs only above threshold level ||Relatively independent of amount applied, usually very low concentrations, sufficient but depends on degree of sensitization |
|Incidence || ||May occur in practically everyone ||Occurs only in the sensitized |
Chronic. Papules → scaling → lichenification → excoriations.
Note: ACD is always confined to the site of exposure to allergen. Margination is originally sharp, but it spreads in the periphery beyond the actual site of exposure. In case of strong sensitization spreading to other parts of the body and generalization. The main differences between toxic irritant and ACD are summarized in Table 2-3.
Acute. Prototype of spongiotic dermatitis, with intercellular edema (spongiosis), lymphocytes and eosinophils in the epidermis, and monocyte and histiocyte infiltration in the dermis.
Chronic. Also spongiosis plus acanthosis, elongation and broadening of papillae; hyperkeratosis; and a lymphocytic infiltrate.
In ACD, sensitization is present on every part of the skin; therefore, application of the allergen to any area of normal skin provokes an eczematous reaction. A positive patch test shows erythema and papules, as well as possibly vesicles confined to the test site. Patch tests should be delayed until the dermatitis has subsided for at least 2 weeks and should be performed on a previously uninvolved site (see “Clinical Tests,” Introduction).
Diagnosis and Differential Diagnosis
By history and clinical findings, including evaluation of site and distribution. Histopathology may be helpful; verification of offending agent (allergen) by patch test. Exclude ICD (Table 2-3), atopic dermatitis (AD), seborrheic dermatitis (SD) (face), psoriasis (palms and soles), epidermal dermatophytosis (KOH), fixed drug eruption, and erysipelas phytophotodermatitis.
Allergic Contact Dermatitis Due to Plants
Termed allergic phytodermatitis (APD).
Occurs in sensitized individuals after exposure to a wide variety of plant allergens.
Characterized by an acute, very pruritic, eczematous dermatitis, often in a linear arrangement.
In the United States, poison ivy/oak are by far the most common plants implicated.
Note: Phytophotodermatitis is a different entity; it is a photosensitivity reaction occurring in any individual with a photosensitizing plant-derived chemical on the skin and subsequent sun exposure (see Section 10).
Epidemiology and Etiology
All ages. Very young and very old are less likely to be sensitized. Sensitization is lifelong.
Pentadecylcatechols, present in the Anacardiaceae plant family, are the most common sensitizers in the United States. They cross-react with other phenolic compounds such as resorcinol, hexylresorcinol, and hydroxyquinones.
Anacardiaceae Family. Poison ivy (Toxicodendron radicans), poison oak (T. quercifolium, T. diversilobum). Also poison sumac (T. vernix). Plants related to poison ivy group: Brazilian pepper, cashew nut tree, ginkgo tree, Indian marker nut tree, lacquer tree, mango tree, and rengas tree.
Poison ivy occurs throughout the United States (except extreme southwest) and southern Canada; poison oak on the west coast. Poison sumac and poison dogwood in woody, swampy areas.
Telephone and electrical workers working outdoors. Leaves, stems, seeds, flowers, berries, and roots contain milky sap that turns to a black resin on exposure to air. Cashew oil, unroasted cashew nuts (heat destroys hapten); cashew oil in wood (Haitian voodoo dolls, swizzle sticks); resins; printer’s ink. Mango rind. Marking nut tree of India: laundry marker (dhobi itch). Furniture lacquer from Japanese lacquer tree.
APD usually occurs in the spring, summer, and fall; can occur year-round if exposed to stems or roots. In southwest of the United States, occurs year-round.
All Toxicodendron plants contain identical allergens. Oleoresins are present in milky sap in leaves, stems, seeds, flowers, berries, and roots and are called urushiol. The haptens are the pentadecylcatechols (1,2-dihydroxybenzenes with a 15-carbon side chain in position three). Washing with soap and water removes oleoresins.
More than 70% of people can be sensitized. Dark-skinned individuals are less susceptible to APD. After first exposure (sensitization), dermatitis occurs 7–12 days later. In a previously sensitized person (may be many decades before), dermatitis occurs in <12 h after reexposure.
Note: Blister fluid does not contain hapten and cannot spread the dermatitis.
Poison Ivy/oak Dermatitis. Direct plant exposure: plant brushes against exposed skin giving rise to linear lesions (Fig. 2-8); resin usually is not able to penetrate the thick stratum corneum of palms/soles.
Allergic phytodermatitis of leg: poison ivy Linear vesicular lesions with erythema and edema on the calf at sites of direct contact of the skin 5 days after exposure with the poison ivy leaf.
Food-Containing Urushiol. Unpeeled mango or unroasted cashew nuts expose lips. Mucous membranes uncommonly experience APD, but ingestion of urushiol can produce ACD of the anus and perineum.
Pruritus, mild to severe. Often sensed before any detectable skin changes. Pain in some cases.
Sleep deprivation due to pruritus.
Initially, well-demarcated patches of erythema, characteristic linear lesions (Fig. 2-8); → papules and edematous plaques; may be severe especially on face and/or genitals, resembling cellulitis (Fig. 2-9) → microvesiculation → vesicles and/or bullae (Figs. 2-8 and 2-10) → erosions, crusts. Postinflammatory hyperpigmentation common in darker skinned individuals.
Allergic phytodermatitis of the face: poison ivy Extremely pruritic, erythema, edema, and microvesiculation in the periorbital and perioral area in a previously sensitized young man, occurring 3 days after exposure.
Acute allergic phytodermatitis, bullous This eruption occurred in a patient who had walked barefoot through a forest. It later spread as a papular eruption to the rest of the body. Similar lesions were present on the other foot and lower leg. Differential diagnosis included acute bullous contact dermatitis to caterpillars. Phytophotodermatitis was excluded because at the time of exposure, there was a heavily clouded sky and a papular eruption occurred later on. Caterpillar dermatitis was excluded because of the multiplicity of the lesions and because upon patch testing, the patient was positive to Toxicodendron haptens. Note, patch testing to urushiol is no longer done to avoid sensitization of patients.
Distribution. Most commonly on exposed extremities, where contact with the plant occurs; blotting can transfer to any exposed site; palms/soles usually spared; however, lateral fingers can be involved.
Clothing-Protected Sites. Oleoresin can penetrate damp clothing onto covered skin; wearing clothing previously contaminated with resin can reexpose the skin.
Nonexposed Sites. “Id”-like reaction or some systemic absorption can be associated with disseminated urticarial, erythema multiforme-like, or scarlatiniform lesions away from sites of exposure in some individuals with well-established APD.
Patch Tests with Pentadecylcatechols
Contraindicated as it can sensitize individual to hapten.
By history and clinical findings only.
ACD to other allergens, phytophotodermatitis (see Section 10), soft-tissue infection (cellulitis, erysipelas), AD, inflammatory dermatophytosis, early herpes zoster, and fixed drug eruption.
Other Special Forms of ACD
After systemic exposure to an allergen to which the individual had prior ACD
A delayed T-cell–mediated reaction
Examples: ACD to ethylenediamine → subsequent reaction to aminophylline (which contains ethylene diamine); poison ivy dermatitis → subsequent reaction to ingestion of cashew nuts; also antibiotics, sulfonamides, propylene glycol, metal ions, sorbic acid, fragrances
Contact with airborne allergens in exposed body sites, notably the face (Fig. 2-11); also including eyelids, “V” of the neck, arms, and legs
In contrast to airborne ICD, papular from the beginning, extremely itchy
Prolnged repetitive exposure leads to dry, lichenified ACD with erosions and crusting (Fig. 2-11)
Due to plant allergens, especially from compositae, natural resins, woods, and essential oils volatizing from aroma therapy
Airborne allergic contact dermatitis of the face Extremely itchy, confluent, papular, erosive, and crusted/scaly lesions with lichenification on the forehead, nose, and cheeks following exposure to pinewood dust.
Identify and remove the etiologic agent.
Topical glucocorticoid ointments/gels (classes I–III). Larger vesicles may be drained, but tops should not be removed. Wet dressings with cloths soaked in Burow’s solution changed every 2–3 h. Airborne ACD may require systemic treatment. Pimecrolimus and tacrolimus are effective in ACD but to a lesser degree than glucocorticoids.
Glucocorticoids are indicated if severe and in airborne ACD. Prednisone beginning at 70 mg (adults), tapering by 5–10 mg/d over a 1- to 2-week period. In airborne ACD where complete avoidance of allergen may be impossible, immunosuppression with oral cyclosporine may become necessary.