Dermatology · PANCE / PANRE

Allergic and Irritant Contact Dermatitis

Eczematous reaction from skin contact with chemical irritants (ICD) or allergens triggering type IV hypersensitivity (ACD).

Also known as: contact dermatitis, allergic contact dermatitis, irritant contact dermatitis, ACD, ICD, poison ivy

Overview

Inflammatory dermatitis caused by direct contact with an exogenous agent. Two main forms: irritant contact dermatitis (ICD, non-immunologic toxic injury) and allergic contact dermatitis (ACD, T-cell mediated type IV delayed hypersensitivity).

Epidemiology

ICD accounts for ~80% of all contact dermatitis; most common occupational skin disease (hairdressers, healthcare, cleaning, construction, food handling). ACD prevalence ~20%; nickel is the most common allergen worldwide.

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Risk factors

Occupational wet work, frequent hand washing, hand sanitizers
Atopic dermatitis (impaired barrier → predisposes to ICD and sensitization)
Common allergens: nickel, fragrance mix, balsam of Peru, formaldehyde, preservatives (MCI/MI, paraben mix), neomycin, bacitracin, rubber accelerators, p-phenylenediamine (hair dye), urushiol (Toxicodendron — poison ivy/oak/sumac)
Photoallergens: sunscreen chemicals (oxybenzone), NSAIDs (ketoprofen), topical antibiotics

Pathophysiology

ICD: direct cytotoxic injury → barrier disruption → release of pro-inflammatory cytokines (IL-1, TNF-α). No sensitization required; severity dose-dependent. ACD: small molecule hapten penetrates skin, binds carrier protein, presented by Langerhans cells in regional lymph nodes → CD4+ T-cell sensitization (1-3 weeks); re-exposure → CD8+ memory T-cell mediated delayed hypersensitivity (24-72 hours) → eczematous response.

Clinical presentation

Symptoms

ICD: burning, stinging, soreness; pruritus less prominent
ACD: intense pruritus; sometimes burning
Onset of ACD: 24-72 h after re-exposure in sensitized patient; ICD can occur within minutes to hours

Signs / physical exam

Acute: erythema, edema, vesicles, weeping, crusting
Subacute: erythematous scaly papules and plaques
Chronic: lichenification, fissuring, hyperpigmentation
Distribution matches exposure: linear streaks (poison ivy), earlobes/wrist/belt-line (nickel), hands (occupational), face/eyelids (cosmetics, nail polish transfer), scalp/hairline (hair dye), feet (shoe leather/rubber)

Classic findings

Sharp geometric or linear borders matching the contactant; eyelid involvement from airborne or transferred allergens is highly suggestive of ACD.

Differential diagnosis

Atopic dermatitis — Personal/family atopy, flexural distribution, chronic course; AD predisposes to contact dermatitis
Nummular dermatitis — Coin-shaped plaques without exposure history
Tinea — Annular with central clearing and raised scaly border; KOH positive
Cellulitis / erysipelas — Warm, tender, indurated; systemic symptoms; rapid spread; no vesicles
Herpes zoster — Grouped vesicles in dermatomal distribution; prodromal pain
Dyshidrotic eczema — Deep-seated tapioca-like vesicles on palms/soles/lateral fingers; pruritic
Phytophotodermatitis — Streaky linear hyperpigmentation/blistering after lime/celery/citrus exposure + sun (psoralen + UV)

Diagnostic workup

Diagnostic criteria

Clinical pattern + temporal/spatial correlation with exposure; patch test confirms ACD allergen.

Labs

Clinical diagnosis based on history and morphology
Patch testing (gold standard for ACD): T.R.U.E. test or comprehensive panels (NACDG); read at 48 and 96-120 h
Skin biopsy nonspecific (spongiotic dermatitis) — distinguishes from psoriasis or CTCL when atypical

Imaging

Not indicated

Diagnostic algorithm

Feature	Irritant (ICD)	Allergic (ACD)
Mechanism	Direct cytotoxic injury — non-immune	Type IV delayed hypersensitivity (T-cell)
Prior sensitization	Not required	Required (1-3 wk for first exposure)
Onset after exposure	Minutes to hours	24-72 h (memory response)
Predominant symptom	Burning, stinging	Pruritus
Borders	Sharp, matches contactant	May extend beyond contact site (id reaction)
Diagnosis	Clinical + exposure history	Patch testing
Examples	Soap, solvents, wet work, urine/saliva	Nickel, fragrance, neomycin, urushiol, hair dye

Distinguishing features of irritant vs allergic contact dermatitis.

Treatment

First-line

Identify and eliminate offending agent — single most important intervention
Topical corticosteroid potency by site: hydrocortisone 1-2.5% (face, folds), triamcinolone 0.1% (trunk, extremities), clobetasol 0.05% (palms, soles, lichenified plaques) — 1-3 weeks
Topical calcineurin inhibitor (tacrolimus, pimecrolimus) for face/eyelids/folds or steroid-sparing maintenance
Cool compresses (Burow's solution/aluminum acetate) for acute weeping phase
Emollients to restore barrier; gloves and barrier creams for occupational ICD
Oral antihistamine (sedating, e.g., hydroxyzine) at night for sleep — minimal direct effect on itch

Severe / widespread / facial ACD (e.g., poison ivy)

Oral prednisone 0.5-1 mg/kg/day tapered over 2-3 weeks (NOT a Medrol Dose Pack — rebound is common with short tapers <14 days)
Short course IV/IM corticosteroid (e.g., triamcinolone IM) acceptable alternative

Chronic occupational hand dermatitis

Job modification, gloves (vinyl/nitrile over cotton liners), barrier creams, frequent moisturizing
Refractory: phototherapy (narrowband UVB, PUVA), oral alitretinoin (where available), dupilumab

Second-line / adjunct

Antibiotic only if secondary bacterial infection — cephalexin, dicloxacillin
Topical antipruritic: pramoxine, menthol
Refer to occupational medicine for workers' compensation documentation

Complications

Secondary bacterial infection (S. aureus, S. pyogenes)
Post-inflammatory hyperpigmentation, especially Fitzpatrick IV-VI
Chronic occupational hand dermatitis → job loss, disability
Erythroderma in widespread severe cases
Steroid-induced atrophy with prolonged high-potency topical use

PANCE pearls

Linear streaky vesicles after hiking = poison ivy / oak / sumac (urushiol). The fluid in vesicles does NOT spread the rash; new lesions reflect different exposure doses absorbed at different rates.
Eyelid dermatitis from nail polish (tosylamide formaldehyde resin) is classic — patient touches eyes with allergen-coated nails.
Nickel patch testing is positive in ~15-20% of women and ~5% of men; the dimethylglyoxime spot test identifies nickel-releasing metal jewelry.
Topical neomycin and bacitracin are common ACD culprits — avoid prophylactic 'triple antibiotic' on clean wounds; petrolatum is sufficient.
Oral prednisone for poison ivy MUST be tapered ≥14-21 days; shorter courses cause rebound.

References

AAD/ACDS 2020 — American Contact Dermatitis Society Core Allergen Series (Schalock et al., Dermatitis 2020)
NACDG — North American Contact Dermatitis Group Patch-Test Results Periodic Reports (DeKoven et al., Dermatitis)
AAD 2006 — Guidelines of Care for Contact Dermatitis (Bourke et al., J Am Acad Dermatol; updated reference standards)

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