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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Question 1DermatologyMedium
A 45-year-old female develops red itchy linear streaks on her arm 2 days after gardening. The pattern follows where leaves brushed her skin. Which of the following is the most likely diagnosis?
  • AIrritant contact dermatitis
  • BStasis dermatitis
  • CAtopic dermatitis
  • DAllergic contact dermatitis
Reveal answer & full explanation
Correct answer: D — Allergic contact dermatitis
  • AIrritant contact dermatitis
  • BStasis dermatitis
  • CAtopic dermatitis
  • DAllergic contact dermatitis

Why Allergic contact dermatitis is correct

  • Allergic contact dermatitis is a type IV (delayed) hypersensitivity reaction, T-cell mediated, requiring prior sensitization
  • Onset occurs 24–72 hours after re-exposure to the allergen
  • The linear streak pattern following where leaves brushed the skin is characteristic of Toxicodendron (poison ivy/oak/sumac) contact — the urushiol oil causes this linear distribution
  • Treatment: avoid the allergen, topical mid-to-high potency corticosteroids, oral corticosteroids if severe
  • Patch testing identifies the specific causative allergen

Why the others are wrong

  • Irritant contact dermatitis — more common than allergic; non-immunologic (no prior sensitization required); caused by direct cellular damage from soap, detergent, or solvent; typically presents with more burning/stinging rather than pruritus and lacks discrete borders
  • Stasis dermatitis — affects the lower legs in the setting of venous insufficiency; not triggered by plant contact
  • Atopic dermatitis — chronic pruritic eczema in flexural distributions; not caused by plant contact and does not produce linear streaks

Additional high-yield points

  • Most common cause of allergic contact dermatitis in adults: nickel (found in jewelry, snaps, watches)
  • Distinguishing allergic from irritant contact dermatitis: allergic is typically more pruritic with discrete borders; irritant causes more burning/stinging
Question 2DermatologyMedium
A 34-year-old landscaper presents 2 days after clearing brush, reporting an intensely pruritic rash. Examination shows linear streaks of erythema, edema, and vesicles across both forearms, the neck, and the face, involving roughly 25% of the body surface area. The eruption is weeping in several areas. He has no fever and no signs of secondary infection. Which of the following is the most appropriate initial management?
  • AOral hydroxyzine for itch relief
  • BOral prednisone for 2 to 3 weeks
  • COral cephalexin for 7 to 10 days
  • DOral methylprednisolone for 6 days
Reveal answer & full explanation
Correct answer: B — Oral prednisone for 2 to 3 weeks
  • AOral hydroxyzine for itch relief
  • BOral prednisone for 2 to 3 weeks
  • COral cephalexin for 7 to 10 days
  • DOral methylprednisolone for 6 days

Why Oral prednisone for 2 to 3 weeks is correct

  • This is severe, widespread allergic contact dermatitis (urushiol-induced poison ivy), a type IV delayed hypersensitivity reaction, with facial involvement and ~25% BSA, which is beyond what topical therapy can control.
  • Guideline-supported management of severe or widespread ACD is a systemic corticosteroid: oral prednisone 0.5-1 mg/kg/day tapered over 14-21 days. Tapers shorter than 14 days cause rebound dermatitis, so the longer course is required.

Why the others are wrong

  • Oral methylprednisolone for 6 days: a real systemic steroid, but a course under 14 days is the classic poison ivy mistake; rebound flare is common, so the dose pack is inadequate for this severity.
  • Oral cephalexin for 7 to 10 days: an antibiotic, indicated only with secondary bacterial infection. This patient has no purulence, fever, or honey-crusting, so it does not treat the underlying dermatitis.
  • Oral hydroxyzine for itch relief: a sedating antihistamine that may aid sleep, but it has minimal direct antipruritic effect in contact dermatitis and does not address the widespread inflammatory reaction.
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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

FeatureIrritant (ICD)Allergic (ACD)
MechanismDirect cytotoxic injury — non-immuneType IV delayed hypersensitivity (T-cell)
Prior sensitizationNot requiredRequired (1-3 wk for first exposure)
Onset after exposureMinutes to hours24-72 h (memory response)
Predominant symptomBurning, stingingPruritus
BordersSharp, matches contactantMay extend beyond contact site (id reaction)
DiagnosisClinical + exposure historyPatch testing
ExamplesSoap, solvents, wet work, urine/salivaNickel, 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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