Eczema & Contact Dermatitis
A boards-focused walkthrough of eczematous (spongiotic) dermatitis — atopic dermatitis (filaggrin loss-of-function + Th2/IgE), and irritant vs allergic (Type IV) contact dermatitis — emphasizing classic morphology buzzwords, distribution by age, patch-test diagnosis, next-best-step management, and the eczema herpeticum emergency. Includes a comparison table, two vignettes, and the standard ACID hypersensitivity mnemonic.
Overview & Pathophysiology
Eczema (eczematous/spongiotic dermatitis) is a reaction pattern, not a single disease. Shared histology: spongiosis (intercellular epidermal edema) with a lymphocytic infiltrate. Clinically it evolves: acute (erythema, vesicles, weeping) → subacute (scale, crust) → chronic (lichenification, fissuring), all driven by intense pruritus.
Divide by cause:
- Atopic dermatitis (AD) — endogenous. Skin-barrier defect from filaggrin (FLG) loss-of-function mutations plus Th2-skewed immunity (IL-4, IL-13, with IL-5 driving eosinophils and IL-31 driving itch) → elevated IgE. Part of the atopic triad (atopic dermatitis, asthma, allergic rhinitis) and the atopic march.
- Contact dermatitis — exogenous.
- Irritant (ICD): non-immune direct cytotoxic injury (the most common contact dermatitis).
- Allergic (ACD): Type IV (delayed, T-cell–mediated) hypersensitivity to a hapten.
Boards test you on distribution + morphology to name the entity, then a next-best-step in diagnosis (patch test) or management (steroid potency, when to go systemic).
- "The itch that rashes" — pruritus precedes lesions; the scratch–itch cycle produces lichenification.
- Distribution by age:
- Infants: face/cheeks, scalp, extensor surfaces, trunk — classically spares the diaper area (occluded, moist).
- Children/adults: flexural — antecubital & popliteal fossae, neck, wrists, ankles.
- Associated signs: Dennie–Morgan infraorbital folds, allergic shiners, keratosis pilaris, ichthyosis vulgaris, palmar hyperlinearity, white dermographism.
- Labs: ↑ IgE and eosinophilia support atopy, but diagnosis is clinical (Hanifin–Rajka criteria).
- Complications (high-yield):
- S. aureus superinfection → honey-colored crust / impetiginization.
- Eczema herpeticum (disseminated HSV) → dermatologic emergency.
- Widespread molluscum; eczema vaccinatum risk with smallpox (vaccinia) exposure.
Irritant vs Allergic vs Atopic
| Feature | Irritant CD | Allergic CD | Atopic dermatitis |
|---|---|---|---|
| Mechanism | Direct toxicity (non-immune) | Type IV delayed hypersensitivity | Barrier defect + Th2/IgE |
| Prior sensitization | Not needed | Required | N/A |
| Onset after exposure | Minutes–hours | 24–72 h (on re-exposure) | Chronic, relapsing |
| Location | Strictly at contact site | Contact site ± spread beyond | Flexural (age-dependent) |
| Predominant symptom | Burning/stinging | Itch | Intense itch |
| Classic triggers | Soaps, solvents, water, diapers | Nickel, urushiol, neomycin, PPD | Endogenous / atopy |
| Diagnosis | History / clinical | Patch test | Clinical |
- ACD = Type IV (delayed, cell-mediated): a sensitization phase (Langerhans/dendritic cells present hapten to T cells) then elicitation on re-exposure at 48–72 h.
- Nickel = most common ACD allergen (earring backs, belt buckles, jean studs, phone/watch).
- Urushiol = poison ivy/oak/sumac (Toxicodendron) → linear/streaky vesicles; "leaves of three." Blister fluid does NOT spread it; new lesions reflect dose/timing of the original contact.
- Other classics: neomycin/bacitracin (won't heal with the antibiotic ointment), balsam of Peru, fragrance, para-phenylenediamine (PPD) in hair dye / "black henna," potassium dichromate (cement, tanned leather), thimerosal.
- Patch testing identifies the allergen (applied for 48 h, read at 48 h and again at 72–96 h) — distinct from prick/scratch testing for Type I / IgE allergy.
- Occupational hand dermatitis is most often irritant.
Vignette: A 22-year-old develops intensely pruritic linear streaks of vesicles and bullae on the forearms 2 days after a weekend camping trip. Lesions weep and crust; no systemic symptoms.
Diagnosis: Allergic contact dermatitis to urushiol (poison ivy) — a Type IV delayed hypersensitivity. The linear array is the giveaway (skin brushing the plant).
Next best step:
- Localized disease: high-potency topical corticosteroid (e.g., clobetasol) + wash skin/clothing/tools to remove residual urushiol.
- Severe/extensive (>20% BSA) or face/genital involvement: oral prednisone taper over 2–3 weeks — short bursts cause rebound.
- Oral sedating antihistamines for sleep; cool compresses for weeping lesions.
Avoid topical antihistamines/anesthetics (e.g., diphenhydramine, benzocaine) — they can themselves sensitize.
Vignette: A 3-year-old with known atopic dermatitis develops rapid onset of monomorphic, "punched-out" vesicles and erosions with hemorrhagic crust over eczematous skin, plus fever and malaise.
Diagnosis: Eczema herpeticum — disseminated HSV (usually HSV-1) infection of eczematous skin (Kaposi varicelliform eruption). Tzanck smear shows multinucleated giant cells; PCR/DFA confirms.
Next best step:
- Start systemic acyclovir promptly (IV if severe, systemically ill, or periocular) — do not delay for culture results.
- Ophthalmology consult if lesions are near the eye (herpetic keratitis → blindness risk).
- Cover concurrent S. aureus superinfection if suspected.
This is a dermatologic emergency; untreated disseminated HSV can be fatal. Distinguish from honey-crusted bacterial impetiginization.
- Foundation for all eczema: liberal emollients, lukewarm soak-and-smear baths, gentle non-soap cleansers, trigger/irritant avoidance; for ICD/ACD, identify and remove the contactant (curative for contact dermatitis).
- First-line anti-inflammatory: topical corticosteroids, potency matched to site — low potency for face/eyelids/folds, mid–high potency for body and lichenified plaques.
- Steroid-sparing: topical calcineurin inhibitors (tacrolimus, pimecrolimus) for face/eyelids/intertriginous areas; crisaborole (topical PDE-4 inhibitor).
- Superinfection: anti-staph therapy; dilute bleach baths reduce colonization.
- Moderate–severe/refractory AD: phototherapy; systemic dupilumab (anti–IL-4Rα, blocks IL-4/IL-13 signaling) or JAK inhibitors.
- ACD-specific: patch test to name the allergen; strict avoidance.
Standard Gell–Coombs mnemonic — ACID (Types I→IV):
- A — Type I: Anaphylactic / atopic (IgE) → urticaria, anaphylaxis, atopy (links to atopic dermatitis).
- C — Type II: Cytotoxic (IgG/IgM vs a cell-surface/matrix antigen).
- I — Type III: Immune complex (antigen–antibody deposition).
- D — Type IV: Delayed, cell-mediated (T cells) → allergic contact dermatitis, PPD/TB skin test, poison ivy.
Bottom line: Allergic contact dermatitis = the "D" (Type IV, delayed, T-cell), reactions read at 48–72 h. Atopic dermatitis is a chronic Th2/IgE-associated condition (the Type I / atopy family) — not a Type IV reaction.
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