TextbookDermatologyContact Dermatitis

Contact Dermatitis

Inflammatory skin reaction caused by direct contact with an external substance. Two main types: irritant contact dermatitis (ICD, ~80%) caused by direct chemical damage, and allergic contact dermatitis (ACD, ~20%) caused by a type IV delayed hypersensitivity reaction. Occupational dermatitis is the most common occupational skin disease.

Key Facts

Irritant contact dermatitis (ICD): ~80% of cases; direct chemical damage — no immune sensitisation needed; dose-dependent Allergic contact dermatitis (ACD): ~20% of cases; type IV (delayed) hypersensitivity — requires prior sensitisation; not dose-dependent Common allergens: nickel (most common), fragrance mix, colophony, chromate, rubber chemicals, hair dye (PPD), preservatives Patch testing: gold standard for diagnosing ACD — allergens applied for 48h, read at 48h and 96h; performed in dermatology clinic Occupational dermatitis: most common occupational skin disease; healthcare, hairdressers, construction, food industry RIDDOR reportable: occupational dermatitis is reportable under RIDDOR regulations Allergen avoidance: the most important management step for ACD — sustained improvement with successful avoidance Latex allergy: type I (immediate/IgE) or type IV (delayed/ACD) — important in healthcare workers

Overview

Key Facts

Contact dermatitis is common and underdiagnosed. Distinguishing ICD from ACD requires patch testing. Identifying and avoiding the causative agent is the single most effective intervention.

Epidemiology

  • Lifetime prevalence: ~15–20% of general population
  • Accounts for ~5–7% of dermatology referrals
  • Occupational dermatitis: most common occupational skin disease
  • Healthcare workers, hairdressers, food handlers most affected

Aetiology

ICD triggers: water, detergents, solvents, friction, alkalis, acids, wet work ACD common allergens: nickel (jewellery, belt buckles), chromate (cement), PPD (hair dye), fragrances, preservatives (MI/MCI), rubber chemicals, colophony (adhesives, plasters), epoxy resin

Pathophysiology

ICD: direct cytotoxic damage to keratinocytes → innate immune response → inflammation. No sensitisation required. Damage is dose-dependent. ACD: hapten penetrates skin → processed by Langerhans cells → presented to T-cells in draining lymph nodes → sensitisation (1–2 weeks). Re-exposure → T-cell mediated type IV hypersensitivity → eczematous reaction at 24–72 hours.

Clinical Presentation

Irritant Contact Dermatitis

  • Well-demarcated erythema at contact site
  • Dryness, fissuring, glazed appearance
  • Burning/stinging more than itch
  • Hands most commonly affected (wet work)
  • Onset: immediate or cumulative with repeated exposure

Allergic Contact Dermatitis

  • Eczematous: erythema, vesicles, weeping, crusting
  • Pruritus is prominent
  • Distribution reflects contactant (e.g. wrist = watch/nickel; periorbital = nail varnish via transfer)
  • Onset: 24–72 hours after exposure (delayed type IV)
  • May spread beyond contact site (id reaction)

Red Flags

  • Occupational pattern (worse at work, improves on holiday)
  • Distribution suggesting specific allergen
  • Failure to respond to treatment (unidentified allergen/irritant)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Atopic eczemaFlexural, personal/family atopy, onset in childhoodClinical, IgE
PsoriasisWell-demarcated, silvery scale, nail changesClinical
Tinea manuumUnilateral hand involvement, leading edgeSkin scraping, KOH
ScabiesBurrows, finger webs, nocturnal itch, contactsDermoscopy

Diagnosis / Investigation

Patch Testing (for ACD)

  • Gold standard: European baseline series (28+ allergens) + extended series based on occupation/exposure
  • Method: allergens applied to back in Finn chambers for 48 hours; read at 48 hours and 96 hours
  • Grading: +, ++, +++ (erythema through to vesicles/bullae); IR = irritant reaction
  • Stop topical steroids 1 week before, oral steroids 4 weeks before

Additional

  • Skin biopsy: rarely needed; shows spongiotic dermatitis (indistinguishable from atopic eczema)
  • IgE (total/specific): to exclude atopic component
  • RAST/skin prick testing: for type I latex allergy (NOT for type IV ACD)

Management

Allergen/Irritant Avoidance

  • Identify and avoid causative agent — most important step
  • Substitution: alternative materials, products
  • Protective equipment: gloves (but avoid latex if latex-allergic; use nitrile)
  • Occupational health: workplace assessment, RIDDOR reporting

Pharmacological

  • Emollients: foundation of care (as per eczema)
  • Topical corticosteroids: potent (betamethasone valerate 0.1%) for body; mild (hydrocortisone 1%) for face/flexures
  • Topical calcineurin inhibitors: for face/sensitive areas
  • Severe acute ACD: short course oral prednisolone 0.5mg/kg for 5–7 days (e.g. severe poison ivy/plant dermatitis)

Referral Criteria

  • Dermatology: for patch testing if ACD suspected
  • Occupational health: suspected occupational dermatitis
  • Urgent: severe widespread ACD not responding to topical treatment

Prognosis

  • ACD: excellent if allergen identified and avoided — complete resolution expected
  • ICD: improves with irritant avoidance; chronic exposure leads to persistent disease
  • Occupational dermatitis: ~25% change occupation; ~50% have persistent symptoms at 5 years
  • Poor prognostic factors: continued exposure, hand involvement, atopic background

Other Relevant Information

ICD vs ACD Comparison

FeatureICDACD
MechanismDirect chemical damageType IV hypersensitivity
SensitisationNot requiredRequired (prior exposure)
Dose-dependentYesNo (small amount can trigger)
Patch testingNegativePositive
DistributionConfined to contact areaMay spread beyond
OnsetImmediate or cumulative24–72 hours

Common Allergens and Sources

AllergenSource
NickelJewellery, belt buckles, coins
ChromateCement, leather
PPDHair dye
FragrancesCosmetics, toiletries
Rubber chemicalsGloves, shoes
ColophonyPlasters, adhesives