Contact dermatitis

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Contact dermatitis encompasses two conditions: allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD). Both conditions frequently coexist, as either condition may disrupt the skin barrier, increasing the risk of allergen sensitization and/or irritant sensitivity. Common allergens that cause ACD include metals, personal care products, plants, latex, preservatives, topical medications, and food and beverages. Common irritants that cause ICD include metals, strong acids or alkalis, soaps, solvents, topical medications, fabrics, and dust. ICD is primarily a clinical diagnosis; ACD requires patch testing. For both conditions, the mainstay of management is to avoid the offending agent and maintain the skin barrier with regular emollient use. Acute symptomatic relief (e.g., cool compresses) may improve comfort. Treatment for ACD also involves topical corticosteroids for localized disease and oral steroids for generalized disease.

Types of contact dermatitis

Approach to suspected contact dermatitis

• Perform a thorough history and examination to evaluate for sources of irritant and/or allergen exposure, including: ^[6]
  • Personal products
  • Home and work environments
  • In children: toys, sports gear, musical instruments, and caregiver personal care products ^[4]
• Suspected ACD
  • Refer for patch testing to confirm diagnosis.
  • Children who cannot undergo patch testing: Consider avoiding common allergens.
• Suspected ICD: Start empiric management of ICD (i.e., irritant avoidance).
• Diagnostic uncertainty or persistent lesions: Refer to a specialist (e.g., dermatologist, allergist) for further evaluation.

ACD and ICD may be difficult to distinguish clinically and often co-exist. Patch testing is indicated if ACD is suspected.^[7]

Differential diagnosis of contact dermatitis^[2][3][6]

• Other types of dermatitis, e.g.:
  • Atopic dermatitis
  • Seborrheic dermatitis
  • Dyshidrotic eczema
  • Nummular dermatitis
  • Dermatitis herpetiformis
  • Stasis dermatitis
• Infections, e.g.:
  • Skin and soft tissue infections
  • Scabies
  • Tinea pedis
• Psoriasis
• Phototoxicity and/or sunburn
• Mycosis fungoides (cutaneous T-cell lymphoma)

Epidemiology

• Adults: 15–20% have a contact allergy to ≥ 1 allergen. ^[8][9]
• Children: rare in the first few months of life; prevalence increases to that of adulthood by adolescence. ^[4][6]
• ♀ > ♂ ^[9]

ACD is one of the most common dermatological diagnoses, and its prevalence is increasing worldwide. ^[8]

Etiology

Common allergens ^[2][6]

• Metals: : nickel , cobalt, chromium ^[4][7]
• Personal care products: perfumes, soaps, cosmetics, diapers, wipes
• Plants: poison ivy, poison oak, poison sumac
• Occupational: gloves , solvents, detergents
• Preservatives: e.g., thimerosal
• Topical medications: hydrocortisone, topical antibiotics (e.g., neomycin), benzocaine ^[2]

Risk factors ^[6][8]

• Congenital risk factors: certain genetic polymorphisms
• Acquired risk factors: other forms of dermatitis (e.g., atopic dermatitis ), occupational exposures

Pathophysiology

ACD is a type IV hypersensitivity reaction.

• First contact with allergen → allergic sensitization
• Repeated contact with allergen → development of a rash after 12–48 hours

Compared to type I–III hypersensitivity reactions, which are antibody-mediated, type IV reactions are mediated by T cells.

Clinical features

• Characteristics of lesions ^[2][4]
  • Acute
    • Intensely pruritic erythematous papules and plaques
    • Vesicles with serous oozing in more severe cases
    • Distinct borders that may extend beyond the site of allergen exposure
  • Chronic: fissures, lichenification, and hyperpigmentation ^[4]
• Distribution
  • Local (reflects areas and shapes of exposures); examples include:
    • Rash where jewelry is worn: suggests nickel allergy
    • Rash on face and eyelids: likely caused by cosmetics
    • Rash in axillae: likely caused by fragrances or deodorant
    • Pruritic papulovesicular rash with a linear pattern on extremities: likely caused by urushiol-producing plants like poison ivy in patients with a history of exposure (urushiol-induced contact dermatitis)
  • Ectopic (lesions at a distance from initial exposure): due to inadvertent transfer of allergen by self or others ^[6]
  • Systemic contact dermatitis ^[6]
    • Can develop after systemic exposure (e.g., ingestion, intravenous) to allergens (e.g., metals or flavorings in foods, medications).
    • Manifestations include generalized dermatitis, flexural and intertriginous dermatitis, and local dermatitis.
  • In children, the lips and feet are commonly affected. ^[4]

Contact dermatitis due to poison oak, poison ivy, or poison sumac is the most likely cause in a patient presenting with erythematous, pruritic, and burning skin lesions in a linear pattern that appear 24 hours after a camping trip.

Diagnosis ^[2]

• Suspect ACD in patients with pruritic lesions in well-demarcated areas of exposure.
• Review the patient's use of personal products as well as their home and work environment to determine the likely allergen.
• All patients require patch testing (gold standard) to confirm the diagnosis. ^[6]

Patch test^[6]

• Indications
  • Suspected ACD
  • Worsening of lesions or poor response to empiric topical corticosteroids ^[6]
  • Additional indications in children ^[4][5]
    • New-onset atopic dermatitis in late childhood or adolescence
    • Prior to initiation of systemic treatment
    • Dermatitis involving the face, hands, feet, and/or perineal area
• Procedure
  • A series of patches fixed with common allergens are applied directly to the skin.
  • Results are commonly read at 48 hours. ^[6][10]
• Interpretation: A positive reaction consists of erythema, papules, and, sometimes, vesicles at the site of the patch(es). ^[11]

Before performing a patch test, avoid or decrease the dosage of systemic immunosuppressants (e.g., systemic corticosteroids). ^[6]

Additional diagnostic studies ^[2]

Consider in selected patients to exclude differential diagnoses of contact dermatitis.

• Bacterial culture: if there is weeping, crusting, exudate
• KOH preparation: if there is erythema and scaling
• Dermoscopy: if concern for scabies
• Punch biopsy: if the diagnosis remains unclear

Management ^[2][6][7]

Approach

• The mainstay of management of ACD for all adults and children is avoiding exposure to allergens.
• In patients with ACD from plants (e.g., poison ivy), wash contaminated skin immediately after exposure. ^[12]
• Treat skin lesions with corticosteroids.
• Provide nonpharmacological symptomatic management, e.g.:
  • Cool compresses
  • Calamine lotion, emollients, colloidal oatmeal baths
  • Wet dressings (e.g., for oozing, crusting lesions)
• Treat bacterial and fungal superinfections as needed; see also:
  • "Treatment of skin and soft tissue infections"
  • “Impetigo”
  • "Treatment of mucocutaneous candidiasis”
• For severe or persistent lesions, refer to dermatology for consideration of additional treatment options. ^[7]

Antihistamines, although commonly used, are generally not effective for treating pruritus associated with ACD. ^[2]

If contact dermatitis worsens despite treatment with topical therapies, consider if ACD has developed due to allergic sensitization to topical medication (e.g., topical corticosteroids, neomycin); patch testing is indicated. ^[6]

Corticosteroid therapy

• Adults
  • Topical corticosteroids are preferred for localized dermatitis.
    • Areas with thin skin (e.g., face, genitals, flexural surfaces): low-potency topical corticosteroids (e.g., desonide) ^[2]
    • Other areas: mid-potency topical corticosteroids (e.g., triamcinolone ) or high-potency topical steroids (e.g., clobetasol ), depending on severity ^[2]
  • Systemic steroids; (e.g., prednisone ) are often required for generalized dermatitis (e.g., affecting > 20% of the body surface area). ^[2][13]. ^[2][6][13]
• Children ^[6]
  • Topical corticosteroids, with potency based on the location and severity of disease ^[14]
    • Use the lowest potency and shortest duration necessary to reduce the risk of adverse effects. ^[15]
    • Avoid ointments.
  • Systemic steroids may be necessary for generalized dermatitis and/or severe symptoms. ^[14]

Avoid long-term use of topical steroids to prevent local skin atrophy and systemic adverse effects. ^[6]

ICD is caused by the direct cytotoxic effect of a causal agent. It is either acute or, more commonly, chronic. ^[3][7][16]

Etiology ^[3][17]

Common irritants

• Chemical irritants, e.g.:
  • Heavy metals
  • Strong acids and alkalis
  • Water, soaps and detergents
  • Solvents, synthetic oils
  • Topical medications
• Physical irritants, e.g.:
  • Friction
  • Certain fabrics that prevent ventilation (e.g., synthetics) or are rough (e.g., wool)
  • Dust (e.g., coal, rock, sawdust)

Risk factors

• Environmental factors, e.g.:
  • Low humidity
  • Frequent exposure to moisture (e.g., frequent handwashing or hand disinfection, food preparation) ^[3]
  • Extreme temperatures (e.g., thermal burns, sunburn, cold injury)
• History of atopy

Clinical features ^[3]

• Skin lesions limited to the area of irritant exposure are characteristic of contact dermatitis.
• The dorsum of the hands are most commonly affected. ^[3][17]
• Additional manifestations in children include: ^[3][6]
  • Irritant diaper dermatitis
  • Perioral dermatitis, due to frequent licking or exposure of cheeks to certain foods

Diagnostics ^[2][3]

• ICD is a diagnosis of exclusion. ^[7]
• A presumptive diagnosis of ICD can be made if symptoms improve by avoiding the irritant.
  • History and examination may help differentiate irritant vs. allergic contact dermatitis.
  • ICD usually resolves within 6 weeks of avoiding the causative agent. ^[18]
• Diagnostic uncertainty
  • Assess for alternative diagnoses (see "Differential diagnoses of contact dermatitis").
  • Refer to a specialist (e.g., dermatologist, allergist) for further evaluation, which may include:
    • Patch testing
    • Dermoscopy
    • Microbiological studies (e.g., KOH preparation, culture of exudate)

As ICD disrupts the skin barrier, patients may present with concurrent atopic dermatitis or ACD. ^[3][7]

Management ^[2][3][6]

Management of ICD is similar in adults and children. Irritant diaper dermatitis and perioral dermatitis are covered separately.

• Avoid exposure to irritants; for occupational exposures, use of PPE and/or job reassignment may be necessary.
• Maintain skin barrier integrity (e.g., with regular use of emollients). ^[7]
• For exposure to severe chemical irritants: ^[7]
  • Immediately irrigate with water and remove contaminated clothing.
  • Treat chemical burns; see "Burns" for details.
• Provide symptomatic relief with cold compresses, calamine lotion, and/or colloidal oatmeal as needed. ^[2]
• Treat bacterial and fungal superinfections (see also “Treatment of skin and soft tissue infections” and “Treatment of mucocutaneous candidiasis”)
• Consider corticosteroids after irritant removal, although their benefit for ICD is not well established. ^[2]
• For severe or persistent lesions, refer to dermatology for consideration of additional treatment options.

Prognosis

• ICD usually resolves within 2–6 weeks of removing the irritant. ^[18]
• For patients with ongoing exposure:
  • Resolution after treatment occurs in only ∼ 30% of patients. ^[18]
  • Spontaneous resolution can occur in patients exposed to mild to moderate irritants (hardening phenomenon). ^[17][19]