Skin & Subcutaneous Tissue

Contact dermatitis: irritant vs allergic

Clinical Overview and When to Suspect Contact Dermatitis

— Irritant contact dermatitis (ICD): ~80% of cases. Non-immunologic, direct cytotoxic injury to the epidermal barrier. Occurs in anyone with sufficient exposure (dose- and time-dependent).

— Allergic contact dermatitis (ACD): ~20% of cases. Type IV (delayed) T-cell hypersensitivity requiring prior sensitization. Occurs only in sensitized individuals; small exposures suffice.

— Sharply demarcated eczematous rash localized to an anatomic area of contact (hand, dorsum of foot, periumbilical, neck, eyelids).

— Pattern matches an exposure: linear streaks (plants), rectangular patch on wrist (watchband), earlobes (nickel earrings), waistline (belt buckle), dorsum of feet (shoe rubber/leather), face/eyelids (cosmetics, nail polish transfer).

— New chronic hand dermatitis in a healthcare worker, hairdresser, food handler, mechanic, or cleaner → think occupational ICD, the most common occupational skin disease in the US.

— Family medicine clerkship favorite: outpatient diagnosis, identification of the trigger, return-to-work counseling, and workers' compensation documentation.

— Misdiagnosis as tinea, cellulitis, or atopic dermatitis leads to inappropriate antifungals/antibiotics and treatment failure.

Contact dermatitis (CD) is an inflammatory eczematous reaction of the skin caused by direct exposure to an external agent, broadly split into two mechanistically distinct entities tested side-by-side on Step 3.

When to suspect in ambulatory practice:

Why it matters for Step 3:

Board pearl: A pruritic, vesicular, weeping dermatitis with fuzzy borders that spreads beyond the obvious contact area favors ACD; a burning/stinging, sharply demarcated dry/fissured plaque confined exactly to the area of contact favors ICD. The "rash that itches more than burns" with vesicles = allergic; the "rash that burns more than itches" and is dry/cracked = irritant.

Step 3 management anchor: definitive treatment for both subtypes is identification and avoidance of the offending agent—pharmacotherapy is adjunctive, not curative.

Presentation Patterns and Key History

— ICD: onset within minutes to hours of exposure (acute strong irritant like bleach) OR insidious over weeks–months with repeated low-grade exposure (cumulative ICD from frequent handwashing).

— ACD: onset 24–72 hours after re-exposure in a sensitized patient; first sensitization may take 10–14 days of initial contact before any rash appears.

— ICD: burning, stinging, soreness > itch; skin feels "raw" or "chapped."

— ACD: intense pruritus dominates; patients describe weeping vesicles and an urge to scratch.

— Occupation and specific tasks (wet work >2 h/day is a major ICD risk).

— New personal care products in the last 2–6 weeks (shampoo, deodorant, sunscreen, nail polish, hair dye).

— Jewelry (nickel), watchbands, belt buckles, eyeglass frames, snaps on jeans (periumbilical nickel dermatitis).

— Topical medications: neomycin, bacitracin, benzocaine, diphenhydramine cream—classic ACD culprits applied to wounds.

— Plants: poison ivy/oak/sumac (urushiol), with linear streaks as the giveaway.

— Fragrances and preservatives (methylisothiazolinone, formaldehyde releasers, parabens)—in wipes, cosmetics, paints.

— Hobbies (gardening, leatherwork, epoxy, hair dye with paraphenylenediamine).

— Hand-hygiene frequency (post-pandemic ICD spike in healthcare workers).

Temporal pattern is the single most useful historical clue:

Symptom quality:

Targeted history checklist (FM-style):

Key distinction: If the same area flares every time a particular product is used with a 1–3 day lag, suspect ACD; if many products and water exposures all cause similar discomfort, suspect ICD (impaired barrier).

Board pearl: Periumbilical dermatitis in a teenager = nickel ACD from jeans snap. Bilateral dorsal foot dermatitis sparing toe webs = shoe/rubber ACD. Eyelid dermatitis with normal hands = think transfer dermatitis (nail polish, shampoo) or airborne ACD (fragrance).

Step 3 management: Always ask about secondary gain or workers' comp claims—document exposures objectively without prejudging causation.

Physical Exam Findings

— Hands (dorsum > palms in ACD; web spaces and volar wrist in ICD wet-work).

— Face/eyelids: cosmetics, airborne allergens, shampoos.

— Neck: necklaces (nickel/gold), perfume ("atomizer sign" on lateral neck).

— Axillae: deodorants (vault) vs textile dye (periphery).

— Feet: shoe leather/rubber (dorsum, sparing interdigital).

— Anogenital: wipes (methylisothiazolinone), topical anesthetics.

— Acute: erythema, edema, vesicles/bullae, weeping, crust. ACD vesicles are typically grouped on an erythematous base.

— Subacute: scaling, crusting, fissures, less weeping.

— Chronic: lichenification, hyperkeratosis, fissures, hyperpigmentation (esp. skin of color).

— Sharply demarcated, geometric borders matching exposure (glove cuff line).

— Glazed, parched, fissured skin; minimal vesiculation.

— No spread beyond contact area.

— Ill-defined borders, often with id reaction or autoeczematization at distant sites.

— Vesicles and bullae prominent.

— Linear streaks (rhus dermatitis from urushiol).

— Pattern crosses anatomic units (e.g., hand AND eyelid from transfer).

— Usually normal. Fever, expanding erythema, lymphangitic streaking, or pain out of proportion should redirect you toward cellulitis or necrotizing infection—not CD.

— Generalized erythroderma with systemic symptoms → consider systemic contact dermatitis (e.g., systemic nickel, balsam of Peru in foods) or DRESS.

Distribution is diagnostic. Always map the rash to the suspected contact.

Morphology by acuity:

ICD-favoring exam:

ACD-favoring exam:

Vital signs / systemic assessment:

Key distinction: Cellulitis is warm, tender, unilateral, often febrile, lacks pruritus; CD is pruritic, bilateral if exposure bilateral, afebrile, and usually with vesicles or scaling. Misdiagnosing bilateral lower-leg stasis/contact dermatitis as cellulitis is a top inpatient overdiagnosis—Step 3 loves this.

Board pearl: "Outside job, inside job"—rash patterns matching exogenous contact (geometric, linear, on exposed areas) = contact dermatitis; symmetric flexural rash = atopic dermatitis.

Diagnostic Workup — Initial Evaluation

— Detailed exposure history + exam is the test. Have the patient bring in all products used on the affected area (the "brown bag" approach) and review ingredient labels.

— Photograph the rash distribution—pattern recognition is often diagnostic.

— KOH prep if scaling/annular lesions to exclude tinea (particularly tinea manuum and tinea pedis presenting as unilateral hand or "two feet–one hand" pattern).

— Bacterial swab + culture only if honey-crusted or pustular (impetiginization, secondary S. aureus).

— Wood's lamp if pigmentary changes suggest erythrasma or vitiligo mimic.

— Generalized eruption with systemic symptoms → CBC, LFTs, eosinophil count (rule out DRESS), peripheral smear.

— Severe recalcitrant hand dermatitis → check for atopy markers if dual diagnosis with atopic dermatitis is suspected (serum IgE, history of asthma/rhinitis).

— TSH and ferritin if chronic pruritus without clear contact pattern.

— Skin biopsy. Histology of ICD vs ACD overlaps significantly (spongiotic dermatitis in both); biopsy is reserved for atypical or treatment-resistant cases to rule out psoriasis, mycosis fungoides, or porphyria cutanea tarda.

— Specific IgE or RAST testing—useless for ACD because ACD is type IV, not IgE-mediated.

— Prick testing—appropriate for contact urticaria (type I, e.g., latex), not ACD.

Contact dermatitis is a clinical diagnosis. No lab confirms acute disease; the workup centers on excluding mimics and identifying the trigger.

First-line ambulatory workup:

When to consider broader labs:

What NOT to order routinely:

Key distinction: Latex allergy can be type I (immediate urticaria/anaphylaxis—use prick test or serum IgE) OR type IV (delayed, from rubber accelerators like thiuram, carbamates—use patch test). Step 3 may test which test for which mechanism.

Step 3 management: Document occupational exposures with dates—required for OSHA Form 300 workplace injury logs and workers' compensation claims.

Diagnostic Workup — Patch Testing

— Indication: suspected ACD that is chronic, recurrent, recalcitrant, occupationally limiting, or of unclear allergen.

— Not useful for ICD (no immunologic memory to detect).

— Standardized allergen panels (e.g., T.R.U.E. test screens ~35 allergens; the American Contact Dermatitis Society Core 80 is broader).

— Allergens applied to upper back under occlusive chambers.

— Three visits over a week:

– Day 0: apply patches.

– Day 2 (48 h): remove and read.

– Day 4–7 (72–168 h): second reading—essential, as some allergens (neomycin, corticosteroids, gold) react only at delayed read.

— Hold systemic steroids >10 mg prednisone for ≥1 week; hold topical steroids on the back for ≥1 week; hold UV exposure to back for 1 week.

— Antihistamines are OK (don't affect type IV reactions).

Patch testing is the gold standard for ACD and the single highest-yield concept tested.

Procedure:

Reading (ICDRG scale): + (erythema/papules), ++ (vesicles), +++ (bullae/ulceration), IR (irritant reaction—decrescendo over time vs allergic crescendo).

Clinical relevance: A positive patch test must be matched to the patient's exposure to be meaningful ("present, past, or possible relevance"). Relevance assessment is a key Step 3 concept—a positive nickel patch test in a patient with foot dermatitis from rubber boots is not the answer.

Pre-test counseling:

Top 10 North American allergens (rotate yearly): nickel, methylisothiazolinone, fragrance mix, formaldehyde, Myroxylon pereirae (balsam of Peru), neomycin, bacitracin, cobalt, paraphenylenediamine (PPD), quaternium-15.

Board pearl: Nickel is the #1 contact allergen in the US, especially in women; Myroxylon pereirae (balsam of Peru) cross-reacts with cinnamates and fragrance—patients may flare from foods (cinnamon, citrus, tomatoes, colas).

Key distinction: Irritant patch reactions fade by 96 h; allergic reactions persist or intensify—this crescendo pattern is the test favorite.

Risk Stratification and First-Line Management Logic

— Mild–moderate, localized (<10% BSA):

– Allergen/irritant identification and avoidance (the cure).

– Mid- to high-potency topical corticosteroid (TCS) for 2–4 weeks.

– Bland emollients (petrolatum, ceramide creams) to restore barrier.

– Cool wet compresses (Burow's solution—aluminum acetate) for weeping vesicular phase.

— Severe, widespread (>20% BSA), facial, or disabling:

– Systemic corticosteroids: prednisone 0.5–1 mg/kg/day, tapered over 2–3 weeks. Avoid short tapers (<14 days)—rebound is classic, especially in rhus dermatitis (poison ivy).

– Consider hospitalization if bullous, infected, or unable to function.

— Face, eyelids, intertriginous areas, genitalia: use low-potency TCS (hydrocortisone 1–2.5%) or steroid-sparing topical calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus 1%) to avoid atrophy, striae, and steroid rosacea.

— Hands/feet (thick skin): high-potency TCS (clobetasol 0.05%) often required, sometimes under occlusion.

— Wash exposed skin with soap and water within 10 minutes of urushiol exposure (poison ivy)—after that, oils are absorbed.

— Launder clothing and pet fur after plant exposure; urushiol persists for years on surfaces.

— Use vinyl gloves for wet work (latex/rubber can be the allergen); cotton glove liner under vinyl for hand dermatitis.

— Switch to fragrance-free, preservative-minimal products; consider databases (CAMP, SkinSAFE) to generate safe product lists.

Severity-based management ladder for outpatient CD:

Special anatomic considerations:

Patient counseling pillars:

Step 3 management: For rhus dermatitis (poison ivy) with face/genital involvement or >20% BSA, the answer is oral prednisone tapered over 14–21 days, NOT a Medrol Dosepak—too short, leads to rebound.

Board pearl: "Soak and smear"—15-min cool water soak followed by immediate application of high-potency TCS to wet skin enhances penetration in severe acute dermatitis.

Pharmacotherapy — First-Line Regimens

— Class I (super-high potency): clobetasol propionate 0.05%, betamethasone dipropionate augmented 0.05%—for palms, soles, lichenified plaques; max 2 weeks, no face/folds.

— Class II–III (high potency): mometasone 0.1%, triamcinolone 0.5%, fluocinonide 0.05%—trunk, extremities.

— Class IV–V (mid): triamcinolone 0.1%, hydrocortisone valerate—trunk/extremities, longer durations.

— Class VI–VII (low): hydrocortisone 1–2.5%, desonide 0.05%—face, eyelids, genitals, infants, axillae.

— Apply twice daily for 2–4 weeks; use fingertip unit (FTU) dosing—1 FTU covers ~2 adult palms.

— Ointments (petrolatum-based): most potent, best for dry/lichenified skin; avoid in intertriginous (occlusive).

— Creams: versatile, weepy/oozing areas.

— Lotions/solutions/foams: scalp and hairy areas.

— Tacrolimus 0.1% (adults), 0.03% (≥2 yr); pimecrolimus 1%.

— Steroid-sparing—first-line for face, eyelids, genitals, or chronic CD requiring maintenance.

— Black box warning (theoretical lymphoma risk); counsel patients honestly—real-world data have not confirmed risk.

— Side effect: transient burning on application.

— Sedating antihistamines (hydroxyzine, diphenhydramine) at bedtime for sleep/pruritus.

— Non-sedating antihistamines (cetirizine, loratadine): limited benefit in ACD/ICD (not histamine-mediated), but commonly tried.

— Wet wraps with topical steroid under damp dressing for severe acute flare.

— Treat secondary infection with cephalexin or doxycycline; mupirocin for localized impetiginization.

Topical corticosteroids (TCS): cornerstone of therapy.

Vehicle matters:

Topical calcineurin inhibitors (TCIs):

Crisaborole 2% (PDE-4 inhibitor) and topical ruxolitinib (JAK inhibitor): newer steroid-sparing options, mostly approved for atopic dermatitis but used off-label for chronic CD.

Adjuncts:

Board pearl: Topical antihistamines (diphenhydramine cream) and topical anesthetics (benzocaine) can themselves cause ACD—never recommend for CD itch.

Step 3 management: Document TCS potency, anatomic site, and duration—prescribing clobetasol for eyelid CD is a wrong-answer trap.

Systemic Therapy and Refractory Management

— Acute severe ACD covering >20% BSA.

— Involvement of face, eyes, or genitals with significant edema.

— Severe poison ivy/oak with bullae.

— Failure of high-potency topical therapy.

— Prednisone 0.5–1 mg/kg/day (typically 40–60 mg) for 5–7 days, then taper over total 14–21 days.

— Methylprednisolone dose-pack (6-day taper) inadequate—causes rebound.

— IM triamcinolone acetonide 40–60 mg is an alternative single-dose option (depot effect ~2–4 weeks).

— Hyperglycemia in diabetics—check glucose, may need transient insulin adjustment.

— Mood changes, insomnia, GI upset—consider PPI if high risk.

— Avoid in active untreated infection (TB, HSV keratitis).

— Bone density not a concern for short courses; not needed to add bisphosphonates.

— Phototherapy: narrowband UVB or PUVA—hand/foot units widely used.

— Systemic immunomodulators: methotrexate, cyclosporine, azathioprine, mycophenolate—dermatology referral.

— Dupilumab (anti-IL-4Rα) and JAK inhibitors (upadacitinib, abrocitinib): emerging evidence, especially when overlap with atopic dermatitis.

— Alitretinoin (9-cis-retinoic acid): approved in Europe for chronic hand eczema; not FDA-approved in US.

— Workplace modification: substitute irritants, provide protective gloves (nitrile rather than latex), institute hand-hygiene protocols using lukewarm water and pH-balanced cleansers.

— Workers' compensation documentation: occupational disease, not injury—requires causation letter.

— Consider job change if dermatitis persists >2 years despite optimization (poor prognosis in hairdressers, healthcare workers, food handlers).

Indications for systemic corticosteroids:

Regimen:

Steroid risk counseling (Step 3 favorite):

Refractory chronic ACD (esp. occupational hand dermatitis):

Occupational management:

CCS pearl: For severe poison ivy presenting in clinic—order prednisone 60 mg PO daily × 7 days, then 40 mg × 7 days, then 20 mg × 7 days, prescribe clobetasol 0.05% ointment BID to affected areas (avoiding face/folds), hydroxyzine 25 mg qhs PRN itch, and follow-up in 7–10 days. Advance the clock by 1 week.

Special Populations — Elderly and Renal/Hepatic Impairment

— Thin, atrophic skin (senile xerosis) increases susceptibility to ICD from soaps, urinary incontinence (incontinence-associated dermatitis), and frequent washing.

— Increased ACD prevalence from chronic application of OTC topicals (neomycin, bacitracin, lanolin) to leg ulcers and venous stasis areas—suspect ACD in any non-healing venous ulcer with surrounding eczema.

— Use low-potency TCS on thin elderly skin; high-potency agents accelerate steroid atrophy, purpura, and tearing.

— Systemic steroids: monitor for hyperglycemia, hypertension exacerbation, delirium, fluid retention, osteoporotic fractures; consider GI prophylaxis if NSAID co-use.

— Topical NSAIDs, neomycin, bacitracin, ophthalmic preparations (preservatives like benzalkonium, thimerosal)—common in elderly.

— Transdermal medication patches (clonidine, lidocaine, fentanyl, nitroglycerin) cause local ACD at adhesive sites—rotate sites.

— Topical therapy: minimal systemic absorption from intact skin; safe.

— Avoid high-potency TCS over large areas of denuded skin (HPA suppression, hyperglycemia).

— Systemic prednisone: no dose adjustment needed; monitor for fluid overload and BP.

— Antihistamines: hydroxyzine and cetirizine accumulate in renal failure—reduce dose (cetirizine 5 mg if CrCl <30).

— Prednisone requires hepatic conversion to prednisolone—generally still effective but monitor.

— Methotrexate, azathioprine, cyclosporine: hepatic monitoring essential; avoid in Child-Pugh B/C.

— Topical calcineurin inhibitors: minimal absorption; safe.

— Long-term care residents: incontinence-associated dermatitis is ICD—barrier creams (zinc oxide, dimethicone), scheduled toileting, skin pH-balanced cleansers.

— Caregivers must apply emollients; assess medication adherence and ability to self-apply—failure here is often the reason for "treatment failure."

Elderly considerations:

Polypharmacy and drug-related ACD:

Renal impairment:

Hepatic impairment:

Functional and care-setting considerations:

Board pearl: Chronic leg dermatitis around a venous ulcer that worsens with each new topical = iatrogenic ACD; switch to plain petrolatum, patch test once healed.

Step 3 management: Always reconcile transdermal patches at every visit—site rotation and skin inspection are part of safe prescribing.

Special Populations — Pregnancy, Pediatrics, and Occupational Groups

— Topical corticosteroids: low-to-mid potency preferred; high-potency agents (clobetasol) in large doses (>300 g over pregnancy) associated with low birth weight—use sparingly.

— Topical calcineurin inhibitors: limited data; use only if benefit outweighs risk.

— Systemic prednisone: acceptable in pregnancy for severe disease; first-trimester high-dose linked to small increased risk of oral clefts (controversial)—avoid if possible, use lowest effective dose.

— Avoid methotrexate (teratogen, abortifacient), mycophenolate, retinoids.

— Antihistamines in pregnancy: loratadine and cetirizine are preferred; diphenhydramine for short-term use.

— Most common pediatric ACD allergens: nickel (earrings, belts, snaps), fragrance, neomycin, balsam of Peru, lanolin, methylisothiazolinone (wet wipes—"diaper wipe dermatitis").

— Diaper dermatitis: classic ICD sparing the inguinal folds (contrast with candidal dermatitis which involves folds and has satellite pustules).

— Treat with frequent diaper changes, barrier paste (zinc oxide), brief low-potency TCS if severe; nystatin if candidal.

— Tacrolimus 0.03% for children ≥2 years; pimecrolimus ≥2 years.

— Avoid high-potency TCS on infants (larger BSA-to-volume ratio, increased absorption, HPA suppression risk).

— Healthcare workers: glove allergens (thiuram, carbamates), antiseptics (chlorhexidine), frequent handwashing → cumulative ICD.

— Hairdressers: PPD (hair dye), glyceryl monothioglycolate (perms), nickel (scissors), wet work.

— Construction: chromate in cement (ACD), epoxy resin, wet cement (alkaline ICD with chemical burns).

— Food handlers: garlic, onion, citrus (protein contact dermatitis), wet work.

— Florists: sesquiterpene lactones (Compositae family—chrysanthemum, daisy).

Pregnancy:

Pediatrics:

Occupational groups (high-risk):

Key distinction: Diaper rash that spares the folds = ICD; diaper rash in the folds with satellite lesions = candidiasis; diaper rash with sharply demarcated psoriasiform plaques = inverse psoriasis.

Board pearl: A pediatric patient with periumbilical, ear lobe, and wrist dermatitis = nickel ACD—the trio of jeans snap, earrings, and watch.

Complications and Adverse Outcomes

— Secondary bacterial infection (impetiginization): S. aureus most common, honey-colored crusts, expanding erythema. Treat with cephalexin or doxycycline (if MRSA risk); mupirocin for localized cases.

— Eczema herpeticum: monomorphic punched-out vesicles, fever, lymphadenopathy—emergency. Start IV/PO acyclovir, ophthalmology if periocular.

— Cellulitis vs CD: a critical Step 3 distinction—bilateral lower-leg "cellulitis" is almost always stasis/contact dermatitis. Don't reflexively give vancomycin.

— Lichenification and post-inflammatory hyperpigmentation/hypopigmentation—more pronounced in skin of color; counsel that pigment may take months to normalize.

— Chronic hand eczema: disabling occupational disease, leading cause of dermatologic disability claims; ~50% of patients have persistent symptoms at 10 years.

— Job loss and financial impact in hairdressers, healthcare workers, construction workers; ~25% change occupations.

— Quality of life decrements comparable to severe psoriasis or atopic dermatitis.

— Topical: atrophy, telangiectasia, striae, perioral dermatitis, steroid rosacea, tachyphylaxis, topical steroid withdrawal (TSW) syndrome with overuse.

— Systemic short courses: hyperglycemia, mood lability, insomnia, GI upset, AVN of femoral head (rare but reported), HPA suppression with rebound.

— Inhaled fluticasone/budesonide: rarely associated with ACD via inhalation aerosol.

— Topical corticosteroids themselves are contact allergens (~5% of patch-test populations). Suspect when dermatitis worsens with steroid application. Classes (Coopman): A, B, C, D1, D2—cross-react within groups. Test with tixocortol-21-pivalate, budesonide.

— Patients sensitized to a contact allergen develop dermatitis upon systemic exposure (oral, IV, inhaled). Examples: nickel (food, orthopedic implants), balsam of Peru (foods), gold, mercury, formaldehyde. Presents as widespread eczema, baboon syndrome (SDRIFE), dyshidrotic flare.

Acute complications:

Chronic complications:

Steroid-related complications (iatrogenic):

Sensitization to topical treatments:

Systemic contact dermatitis (SCD):

Board pearl: Worsening eczema with each TCS application = suspect ACD to the steroid or its vehicle (propylene glycol, sorbitan sesquioleate). Patch test.

When to Escalate — Referral, Inpatient, or Specialty Care

— Chronic or recurrent CD without identified trigger.

— Recalcitrant disease despite 4–6 weeks of appropriate topical therapy.

— Suspected occupational dermatitis requiring patch testing and impairment documentation.

— Facial, genital, or hand involvement impairing function.

— Concern for steroid allergy or steroid-sparing therapy initiation.

— Pediatric CD with widespread or atypical features.

— Suspected contact urticaria (type I) overlapping with ACD—e.g., latex.

— Drug eruption with systemic features.

— Workplace causation needs formal evaluation.

— Reasonable accommodations under ADA must be coordinated.

— Workers' comp impairment rating required (AMA Guides).

— Severe bullous reaction with secondary infection, cellulitis, or sepsis.

— Eczema herpeticum—admit for IV acyclovir if extensive, febrile, or periocular.

— Erythroderma (>90% BSA) from systemic CD or progression—admit for fluid/electrolyte/temperature management.

— Anaphylaxis (latex contact urticaria progression) → ED, epinephrine.

— Inability to maintain oral intake or self-care due to severe disease.

— Stevens-Johnson syndrome/TEN mimics with mucosal involvement—STAT dermatology and burn unit consult.

— Periocular CD with conjunctivitis or vision changes.

— Suspected ophthalmic medication ACD (neomycin, brimonidine, dorzolamide preservatives).

Refer to dermatology when:

Refer to allergy/immunology when:

Refer to occupational medicine when:

Indications for ED/inpatient management:

Ophthalmology consult:

CCS pearl: Patient with severe periocular swelling from rhus dermatitis but no vision changes → manage outpatient with oral prednisone taper, cool compresses, ophthalmic lubricants, low-potency TCS to eyelids (avoid the eye). Advance the clock and reassess; consult ophthalmology only if vision is affected or unable to open eyes.

Step 3 management: A clear referral plan with rationale in the note is expected; for occupational cases include "patient to return for patch testing in 2–4 weeks after acute flare controlled and off systemic steroids ≥1 week."

Board pearl: Mucosal involvement, targetoid lesions, Nikolsky sign, or fever with rash should trigger immediate concern for SJS/TEN, DRESS, or AGEP—not contact dermatitis.

Key Differentials — Same-Category (Eczematous) Mimics

— Symmetric flexural distribution (antecubital, popliteal), personal/family history of atopy (asthma, allergic rhinitis), onset in childhood.

— Chronic relapsing course; elevated IgE.

— Overlap: adult atopic patients have ↑ susceptibility to ICD because of impaired filaggrin/barrier; dual diagnosis common, especially in hand dermatitis.

— Coin-shaped, well-circumscribed plaques on extremities (especially shins/dorsal hands); often follows dry skin or minor trauma.

— Distinguish from ACD by absence of exposure pattern.

— Deep-seated, tapioca-like vesicles on palms, soles, lateral fingers; intensely pruritic, episodic.

— Often confused with hand ACD; patch testing helps. Triggers: stress, heat, nickel ingestion (systemic CD overlap).

— Bilateral lower-leg dermatitis in patients with venous insufficiency; hemosiderin staining, varicosities, edema.

— Frequently misdiagnosed as bilateral cellulitis—Step 3 favorite.

— Often complicated by ACD to topical antibiotics or fragrances applied chronically.

— Greasy, yellow scale on scalp, nasolabial folds, eyebrows, retroauricular area, central chest.

— Responds to antifungal shampoos (ketoconazole) and low-potency TCS.

— Sharply demarcated, silvery-scaled plaques; nail pitting/onycholysis; family history.

— Palmar psoriasis vs chronic hand ACD can be tricky—biopsy and patch test help.

— End-stage from chronic scratching—thickened, lichenified plaques; often on neck, ankles, scrotum/vulva. May coexist with any pruritic dermatitis including CD.

Atopic dermatitis (AD):

Nummular eczema:

Dyshidrotic eczema (pompholyx):

Stasis dermatitis:

Seborrheic dermatitis:

Psoriasis (inverse or palmoplantar):

Lichen simplex chronicus:

Key distinction: AD = symmetric, flexural, atopic history, childhood onset. ACD = asymmetric or patterned, matches exposure, adult onset possible. ICD = acute onset after irritant exposure or chronic wet-work, burning > itch.

Board pearl: "Two feet, one hand" tinea masquerades as bilateral foot dermatitis with hand dermatitis—KOH scrapings clinch tinea over CD.

Key Differentials — Non-Eczematous Mimics

— Unilateral, warm, tender, expanding erythema with fever and leukocytosis; lymphangitic streaking common.

— Bilateral lower-leg "cellulitis" is almost always stasis or contact dermatitis—avoid empiric antibiotics; ALT score or NEW HAvUN criteria may help.

— Annular, raised, scaly border with central clearing; KOH positive.

— "Tinea incognito" if treated with TCS—loses scale, becomes pustular.

— Intensely pruritic, worse at night; burrows in web spaces, wrists, areolae, genitals; household members itch.

— Treat with permethrin 5% (× 2, one week apart) or oral ivermectin.

— Persistent eczematous patches in non-sun-exposed (bathing trunk) distribution; refractory to TCS.

— Suspect in any "eczema" >6 months in older adult without clear trigger—biopsy with TCR gene rearrangement.

— Tense bullae on erythematous base; elderly; positive Nikolsky negative; ELISA for BP180/BP230.

— Pre-bullous pemphigoid presents as urticarial eczematous plaques.

— Fever, eosinophilia, LFT abnormalities, mucosal involvement, target lesions—not simple CD.

— Sun-exposed area distribution (face, V of neck, dorsal hands)—sparing under chin, behind ears.

— Phototoxic = sunburn-like (NSAIDs, doxycycline, furosemide); photoallergic = eczematous (sunscreens with oxybenzone, fragrances, NSAIDs).

— Plant phytophotodermatitis (lime juice, celery, parsnip + sun = "margarita dermatitis") = linear streaks with hyperpigmentation.

— Site-specific patterns; appropriate serology/PCR.

Cellulitis / erysipelas:

Tinea (dermatophytosis):

Scabies:

Cutaneous T-cell lymphoma (mycosis fungoides):

Bullous pemphigoid:

Drug eruptions (DRESS, SJS/TEN, AGEP):

Photoallergic / phototoxic reactions:

Erysipeloid, herpes zoster, erythema migrans:

Key distinction: Phytophotodermatitis leaves striking post-inflammatory hyperpigmentation in bizarre handprint or drip patterns—often misdiagnosed as child abuse or ACD; the lime-juice-and-sun history is diagnostic.

Board pearl: Any "contact dermatitis" that fails to clear with appropriate avoidance and topical therapy after 6–8 weeks deserves a biopsy to exclude CTCL or other infiltrative disease.

Secondary Prevention and Long-Term Plan

— Provide patient with an allergen alert card and access to safe-product databases (American Contact Dermatitis Society CAMP [Contact Allergen Management Program], SkinSAFE).

— Train patient to read INCI (International Nomenclature of Cosmetic Ingredients) labels.

— Communicate allergens to dentist, surgeons (implants, sutures), tattoo artists, hairdressers.

— Document allergies in EMR allergy list (e.g., "nickel—ACD," "neomycin—ACD") to prevent inadvertent re-exposure (e.g., perioperative topical antibiotics).

— Workplace controls (hierarchy): elimination > substitution > engineering > administrative > PPE.

— Glove selection: nitrile or vinyl for chemicals; cotton liner inside; change frequently to avoid sweat-occlusion ICD.

— Skin care regimen:

– Lukewarm water (not hot) hand-washing.

– Mild syndet or pH-balanced cleansers; avoid antibacterial soaps with triclosan if irritated.

— Apply emollient (petrolatum, ceramide cream) after every wash and before work.

– Remove rings before wet work (trap moisture, irritants).

— Alcohol-based hand sanitizers are less irritating than soap-and-water in many studies (counterintuitive Step 3 point).

— "Hypoallergenic" and "natural" labels are not regulated—do not equate with safe.

— Cross-reactions: nickel ↔ cobalt; PPD ↔ sulfonamides, azo dyes; balsam of Peru ↔ fragrance, cinnamon, citrus peel.

— Lifelong avoidance for ACD; barrier maintenance daily for ICD.

— Document "fitness for duty" only after dermatitis controlled and protective measures in place.

— Consider OSHA-mandated workplace assessments, MSDS review.

The cornerstone is sustained avoidance—the only true cure for both ICD and ACD.

For confirmed ACD (post-patch testing):

For ICD (especially occupational):

Patient education topics:

Occupational re-entry planning:

Step 3 management: Add the allergen to the EMR allergy field with reaction type "contact dermatitis"—prevents future systemic exposure (e.g., perioperative neomycin irrigation).

Board pearl: Nickel-allergic patients with knee or hip implants generally do not need stainless-steel-free implants unless they have peri-implant dermatitis or chronic pain—the patch test is not predictive enough to drive surgical choice.

Follow-Up, Monitoring, and Counseling

— Mild–moderate CD: reassess in 2–4 weeks; if not improving, reconsider diagnosis, escalate potency, evaluate for ACD.

— Severe CD on systemic steroids: 1–2 week follow-up to assess response, taper, monitor BP/glucose.

— Chronic occupational CD: quarterly visits for first year, then biannually if stable.

— Post-patch testing: dedicated visit 4–6 weeks after testing to review results, relevance, and individualized avoidance plan.

— Disease severity: BSA, Investigator Global Assessment, DLQI (Dermatology Life Quality Index), hand-specific scores (HECSI).

— Side effects of long-term TCS: skin atrophy, telangiectasia, striae—inspect at each visit.

— Systemic immunosuppressants: per agent (CBC, LFTs, BP, creatinine, lipids, BUN).

— Mental health: chronic pruritus and disability are strongly associated with depression and anxiety—screen with PHQ-9.

— Skin care routine (the "emollient prescription"): apply at least twice daily, after bathing, to entire affected area; petrolatum is cheap and effective.

— Trigger avoidance: written allergen list, safe-product brands.

— Realistic timeline: even after trigger removal, dermatitis may take 4–8 weeks to clear; chronic occupational cases longer.

— Sun protection during post-inflammatory hyperpigmentation phase to minimize pigment lock.

— If unable to avoid workplace allergen, reasonable accommodations under ADA (job modification, PPE, transfer).

— Provide written work restrictions: "no exposure to X, must wear nitrile gloves for wet work >15 min."

— Vaccinations: live vaccines (MMR, varicella, zoster live) deferred during high-dose systemic steroids (>20 mg prednisone × ≥14 days)—use recombinant zoster (Shingrix).

— Bone health if recurrent steroid courses: vitamin D, calcium, DEXA if cumulative high-dose.

Follow-up cadence (ambulatory):

Monitoring parameters:

Counseling priorities:

Return-to-work and ADA:

Preventive health integration (FM-style):

Board pearl: Patients with chronic hand dermatitis benefit most from emollient adherence—prescribe a 1-pound (450 g) jar of petrolatum and instruct daily use; compliance jumps when access is easy.

Step 3 management: Always document shared decision-making for steroid use, occupational decisions, and patch-testing referrals.

Ethical, Legal, and Patient Safety Considerations

— Discuss risks and benefits of systemic steroids for a self-limited dermatologic problem; some patients (athletes subject to drug testing, those with brittle diabetes) may decline.

— Off-label use of tacrolimus, dupilumab, JAK inhibitors—document discussion of black box warnings and uncertain long-term safety.

— Patch testing: explain that false positives, false negatives, and "angry-back syndrome" can occur, and that a positive test must be clinically relevant.

— Causation letters require objective documentation of exposures, temporal correlation, patch test relevance.

— Avoid premature attribution—Step 3 may test the family physician's role: gather objective data, refer to occupational medicine, avoid serving as both treating physician and adjudicator if conflict of interest.

— Confidentiality: workers' comp reports release some PHI to employers—inform the patient.

— Phytophotodermatitis can mimic intentional injury (handprint-shaped hyperpigmentation in children). Misdiagnosis as child abuse vs failure to recognize true abuse are both harms—dermatology consult and careful history (lime juice, parsnips, sun exposure) before reporting; consult child protection per state law if any concern remains.

— Conversely, suspicious patterns of "burns" or chemical injuries in vulnerable patients (children, elderly, disabled) warrant reporting per state mandates.

— Document contact allergies in EMR allergy list with reaction = "contact dermatitis"—prevents perioperative neomycin/bacitracin irrigation, dental nickel exposure, ophthalmic preservative exposure.

— Communicate allergen list to surgeons, dentists, anesthesiologists at the time of any procedure scheduling.

— Discharge instructions after ED visit for severe rhus dermatitis must include the full prednisone taper (not a 6-day dosepak) and primary care follow-up in 7–10 days.

— Cosmetic ingredient transparency is limited in US (FDA does not pre-approve cosmetics); advocate for evidence-based product choices.

— Methylisothiazolinone epidemic in wet wipes led to EU concentration limits—US lags.

Informed consent and patient autonomy:

Occupational and workers' compensation:

Mandatory reporting and child safety:

Transition-of-care safety:

Public health and product regulation:

Board pearl: A bizarre, drip-pattern hyperpigmentation on a child's arm after a beach picnic with margaritas = phytophotodermatitis, not abuse—history first.

Step 3 management: Always reconcile EMR allergy lists at every visit and before any procedure.

High-Yield Associations and Rapid-Fire Facts

— Jeans snap/earrings/watch → nickel.

— Hair dye, black henna tattoos → PPD (cross-reacts with sulfonamides, benzocaine, azo dyes).

— Cement/leather tanning → chromate (potassium dichromate).

— Rubber gloves, condoms → thiuram, carbamates, mercaptobenzothiazole.

— Topical antibiotics → neomycin, bacitracin.

— Topical anesthetics → benzocaine (cross-reacts with PPD, sulfonamides).

— Adhesives, plywood, nail polish → formaldehyde, tosylamide formaldehyde resin.

— Sunscreens → oxybenzone (benzophenone-3).

— Plants → urushiol (Toxicodendron); sesquiterpene lactones (Compositae).

— Antiseptics → chlorhexidine, povidone-iodine.

— Nickel ↔ cobalt ↔ palladium.

— PPD ↔ benzocaine ↔ sulfonamides ↔ azo dyes ↔ procaine.

— Balsam of Peru ↔ cinnamates ↔ fragrance ↔ propolis ↔ citrus peel, tomatoes, colas.

— Thiuram ↔ disulfiram (avoid Antabuse in thiuram-allergic patients).

— Hapten + skin protein → Langerhans cell uptake → MHC II presentation → naïve T-cell sensitization in lymph node (10–14 days).

— Re-exposure → memory Th1 (CD4) and CD8 T-cells → cytokine release (IFN-γ, IL-17) → eczematous reaction (24–72 h).

— Direct keratinocyte damage → release of IL-1α, TNF-α, IL-8 → neutrophilic infiltrate → barrier disruption.

— No sensitization phase; magnitude proportional to exposure.

Top US contact allergens (NACDG most recent): nickel sulfate (#1), methylisothiazolinone, fragrance mix I/II, formaldehyde, balsam of Peru (Myroxylon pereirae), neomycin, bacitracin, cobalt chloride, paraphenylenediamine (PPD), quaternium-15.

Classic exposure–allergen pairings:

Cross-reactivity webs (favorite test material):

Type IV hypersensitivity mechanism:

ICD pathophysiology:

Histology: spongiotic dermatitis (intercellular edema) for both; eosinophils more in ACD, neutrophils more in ICD—but overlap.

Board pearl: Disulfiram (Antabuse) for alcohol use disorder can cause a generalized eczematous flare in patients sensitized to thiuram (rubber)—classic high-yield trivia.

Key distinction: Latex glove dermatitis—type I (latex protein) = urticaria/anaphylaxis; type IV (rubber accelerators) = eczematous ACD. Different tests, different management.

Board Question Stem Patterns

— 17-year-old girl with pruritic, lichenified, hyperpigmented patches around the umbilicus and ear lobes for 3 months. Best next step? → Avoid jeans with metal snaps and nickel earrings; consider patch test if persistent. Wrong answers: oral antifungal, oral antihistamine, biopsy.

— Patient returns from hiking with linear vesicular rash on arms, face, and genitals. → Oral prednisone 60 mg/day tapered over 14–21 days. Wrong answer: methylprednisolone dose pack (rebound).

— Healthcare worker with dry, fissured, burning dermatitis on dorsal hands, sparing palms, worse after shifts. → Diagnosis: irritant contact dermatitis from frequent handwashing. Management: nitrile gloves, emollient after each wash, switch to alcohol sanitizer (less irritating than soap and water with prolonged use), mid-potency TCS for flares.

— Elderly woman with chronic venous ulcer treated with neomycin ointment now has surrounding eczematous rash. → Stop neomycin, switch to petrolatum, refer for patch testing once acute flare resolved.

— Elderly man with bilateral lower-leg erythema, hyperpigmentation, itch, afebrile. → Stasis dermatitis (not cellulitis); treat with compression, mid-potency TCS, leg elevation; avoid antibiotics.

— Patient develops scalp and facial eczematous rash 48 h after coloring hair. → PPD ACD; counsel avoidance, cross-reactivity with sulfonamides and benzocaine.

— Woman with bilateral eyelid eczema. → Transfer dermatitis from nail polish (tosylamide formaldehyde resin) or shampoo/conditioner.

— Periumbilical lichenified plaque in a 12-year-old. → Nickel ACD from jeans snap; cover snap with iron-on patch or duct tape.

— Erythematous rash sparing inguinal folds → ICD; barrier paste + frequent changes. With folds and satellite pustules → candidiasis.

— Reaction at 48 h fades by 96 h → irritant reaction, not allergic.

Stem 1 — Nickel ACD:

Stem 2 — Rhus dermatitis (poison ivy):

Stem 3 — Occupational ICD:

Stem 4 — Neomycin ACD over leg ulcer:

Stem 5 — Stasis dermatitis misdiagnosed as cellulitis:

Stem 6 — PPD hair dye reaction:

Stem 7 — Eyelid dermatitis with normal hands:

Stem 8 — Periumbilical rash in child:

Stem 9 — Pediatric diaper dermatitis:

Stem 10 — Patch test interpretation:

Board pearl: Stem clues to ACD: vesicles, asymmetry, exposure timeline, occupational/cosmetic history, response failure to antifungals or antibiotics.

Step 3 management: When the stem asks "next best step" for confirmed CD → identify and avoid trigger beats any drug answer.

One-Line Recap

Contact dermatitis is a clinical diagnosis split into irritant (non-immunologic, dose-dependent, anyone exposed) and allergic (type IV hypersensitivity, requires prior sensitization), and management hinges on identification and avoidance of the trigger, with topical corticosteroids and—when severe—a properly tapered systemic course as adjuncts.

— ICD = direct cytotoxic barrier damage from chemical/physical irritants; burns more than itches; pattern matches exposure precisely.

— ACD = sensitized memory T-cell response 24–72 h after re-exposure; itches more than burns; spreads beyond exposure site; patch testing is the gold-standard confirmatory test.

— Rhus dermatitis needs a 14–21 day prednisone taper—NOT a 6-day dose pack.

— Bilateral lower-leg "cellulitis" is almost always stasis/contact dermatitis—avoid empiric antibiotics.

— Topical neomycin, bacitracin, benzocaine, diphenhydramine are themselves common ACD culprits—don't recommend for CD itch.

— Diaper rash sparing folds = ICD; involving folds with satellite lesions = candidiasis.

— Periumbilical + earlobe + wrist dermatitis in a teen = nickel.

Mechanism in one sentence each:

Top-tier US allergens to memorize: nickel, methylisothiazolinone, fragrance, formaldehyde, balsam of Peru, neomycin, bacitracin, cobalt, PPD, quaternium-15.

Highest-yield Step 3 traps:

Definitive Step 3 management framework: identify exposure → educate avoidance → barrier repair with emollients → topical corticosteroid (potency matched to anatomic site) → systemic steroids for severe/widespread disease → patch testing for chronic or recurrent ACD → document allergens in EMR and counsel on cross-reactivity → follow-up in 2–4 weeks to confirm response and reassess diagnosis.

Board pearl: The single most therapeutic intervention in contact dermatitis is the history, not the prescription pad.