Contact dermatitis

Meet the patient

A 34-year-old theatre nurse has had itchy, fissured hands for nine months, worse since the hospital switched glove supplier. The finger webs are glazed and cracked, the sides of the fingers studded with deep vesicles, and a course of potent topical steroid settled it for a fortnight before it bounced straight back. She is on the verge of leaving nursing altogether.[22][25]

Three questions decide her consultation, and they are the three that decide every contact dermatitis: is this irritant, allergic, or both?, what is she touching?, and will patch testing change her management? Hold those three and the rest of the page slots into place.[1]

Two diseases under one eczematous mask

Contact dermatitis is among the commonest reasons people see a dermatologist and the commonest occupational skin disease in the world — and it wears one mask, eczema (erythema, vesicles, weeping and crusting acutely; dryness, scaling, lichenification and fissuring chronically), while hiding two completely different mechanisms underneath.[1][21]

The split is mechanistic before it is morphological. Irritant contact dermatitis (ICD) is a non-immunological, cytotoxic injury to keratinocytes and the epidermal barrier — water, detergents, solvents, acids, alkalis, wet work, friction. Anyone will get it given a big enough dose, the severity tracks exposure and barrier quality, and there is no immunological memory. Allergic contact dermatitis (ACD) is a cell-mediated type IV delayed hypersensitivity to a low-molecular-weight hapten, and it demands prior sensitisation — first exposure primes, re-exposure flares 24 to 72 hours later, and once primed even picomolar doses can elicit a reaction.[5][6][3]

The classic trap: in real life ICD and ACD coexist constantly. The atopic nurse with wet-work irritant hands who then becomes sensitised to the thiurams in her gloves has both at once — and the irritancy actively helps the allergy by prizing open the barrier and driving hapten through it. Treat one and miss the other, and the patient returns.[1][3]

Shiny and immediate, vesicular and delayed — the face-off

This is the single bedside discriminator an examiner wants, and it is a sentence, not a list: shiny, glazed, painful and immediate is irritant; vesicular, linear, itchy and delayed is allergic. Morphology only suggests the split — it never proves it — but it sets your pre-test probability before you ever patch-test.[1]

Meet the hapten — sensitise first, elicit later

ACD runs as two acts, and the names are viva gold: sensitisation, then elicitation. There is no flare without a prior silent priming — often years earlier, often unremembered.[3][4]

Act 1 — sensitisation. A hapten under 500 Da crosses the stratum corneum, binds endogenous carrier protein to become a complete antigen, and is taken up by epidermal Langerhans cells and dermal dendritic cells. Those cells migrate to the draining lymph nodes and present haptenated peptide on MHC class I and II, generating hapten-specific effector-memory CD8+ and Th1-biased CD4+ T-cells (IFN-γ, IL-2) and long-lived central-memory cells. Innate signalling — TLR engagement, IL-1β and IL-18 via the NLRP3 inflammasome, oxidative stress — licenses that priming.[3][4]

Act 2 — elicitation. Re-exposure recruits those hapten-specific T-cells back to the skin within 24 to 72 hours; they release cytokines that drive spongiosis, vesiculation and the eczematous reaction you see. This is why the rash is delayed, and why it is specific — only a patient already primed to that hapten flares.[3]

Etymology for viva gold: hapten comes from the Greek haptein, 'to fasten' — the molecule fastens itself to a carrier protein to become a complete antigen. Eczema is from ekzein, 'to boil over', which is exactly what spongiotic vesicles look like. Urushiol, the poison-ivy hapten, takes its name from urushi, the Japanese lacquer tree.[3]

Why the barrier is the whole game

The stratum corneum and its lipid matrix — ceramides, cholesterol and free fatty acids — are the principal barrier to both irritants and haptens. Repeated wet work, surfactants and solvents strip surface lipid and corneodesmosomes, raising transepidermal water loss and percutaneous absorption; that is the mechanistic heart of irritant dermatitis and the reason barrier repair (emollients, cotton liners, soap substitution) is genuinely therapeutic, not cosmetic. Atopic skin carries an intrinsically compromised barrier (filaggrin defects) and is markedly predisposed to both ICD and ACD — a fact that explains half the hand-eczema clinic.[7][1]

Where it sits tells you what caused it

Distribution is the highest-yield bedside skill in this topic — the site maps to the allergen before you ever patch-test. A geography lesson beats a biopsy almost every time.[1]

Three variants that change the question

Systemic contact dermatitis is the flare that follows oral re-exposure to a hapten the patient was sensitised to through the skin — classically oral nickel in a nickel-allergic patient, producing vesicular hand dermatitis or a generalised maculopapular eruption. The baboon syndrome variant is the unforgettable one: well-demarcated flexural and anogenital erythema.[23]

Photocontact dermatitis needs UV co-exposure, and you split it the same way you split the rest: phototoxic is dose-related, sunburn-like, with no immune memory; photoallergic is cell-mediated, eczematous, and needs prior sensitisation. The usual culprits are NSAIDs, quinolones, tetracyclines, sulphonamides, phenothiazines and plant furocoumarins. When you meet it, screen for underlying lupus or drug photosensitivity — the light is not always the whole story.[28]

Protein contact dermatitis is the one juniors miss: a chronic eczema with an immediate type I component (urticaria and itching within minutes) on contact with proteins — foods, animal dander, latex — classic in food-handlers and veterinary workers. The immediate reaction sitting on top of the eczema is the tell.[2]

The allergen rogues' gallery

Memorise allergens in clusters, not lists — examiners reward the category and the one-line reason. Lifetime patch-test positivity in the general population sits around 20 percent, and ACD clusters in women of working age. In rough order of frequency on the European and North American baseline series:[10]

The metal trio — nickel, cobalt, chromate. Nickel is the commonest contact allergen on earth; piercings are the dominant sensitiser, sensitisation is lifelong, and patch tests stay positive for decades. Chromate (potassium dichromate in wet cement and tanned leather) is the construction-worker classic, and cobalt rides along with nickel in about half of nickel-positive patients, lurking in tools, alloys and even vitamin B12. Combined chromate, cobalt and wet-cement irritancy is the bricklayer's hand dermatitis.[11][12]

The regulation that worked. The European Nickel Directive (1994, enforced 2001) caps nickel release from prolonged-skin-contact items at under 0.2 µg/cm²/week for post-assemblies and under 0.5 µg/cm²/week for other items — and meta-analysis confirms a sharp fall in sensitisation among young EU women afterwards, with earlobe-piercing sensitisation rates above 25 percent collapsing once the rule bit. Threshold elicitation lives in the low µg/cm²/week range, which is exactly where the regulation drew the line.[13][12]

The fragrance trap — it is the oxidised terpene, not the bottle. Fragrance mix I (cinnamal, cinnamyl alcohol, eugenol, isoeugenol, geraniol, hydroxycitronellal, oakmoss and Evernia prunastri) and mix II (citral, citronellol, coumarin, farnesol, hexyl cinnamal, Lyral) are the screening batteries — but the real sensitisers are the oxidised hydroperoxides of linalool and limonene, which form autoxidatively on storage of citrus and lavender oils and in finished cosmetics, and are far more sensitising than the parent terpenes. Balsam of Peru (Myroxylon pereirae) cross-reacts with many natural fragrances and with cinnamon, vanilla and clove. Clinically: face and eyelid dermatitis from cosmetics, axillary dermatitis from deodorants, periumbilical and facial patterns from stored fragranced products.[14][15][2]

The preservative epidemic — MI. Methylisothiazolinone caused a global wave of sensitisation through cosmetics and household products in the 2010s and is now banned in leave-on cosmetics in the EU. Formaldehyde and its releasers (quaternium-15, imidazolidinyl urea) are the other preservatives to know.[16][17]

Rubber, hair dye, and the medicament trap. Rubber accelerators (thiurams, carbamates, mercaptobenzothiazole) in natural-rubber and nitrile gloves drive healthcare-worker hand dermatitis. PPD in permanent hair dye and black henna tattoos — concentrations often well above regulatory limits — causes severe, vesiculobullous, oedematous scalp and facial flares and cross-reacts with the whole para-amino family: sulphonamides, benzocaine, PABA sunscreens and azo dyes. Topical antibiotics (neomycin, bacitracin, gentamicin) sensitise through chronic wounds, stasis eczema, leg ulcers and otitis externa; neomycin cross-reacts with the other aminoglycosides, so allergy means avoiding them all.[18][19]

The steroid you prescribed is now the allergen. Topical corticosteroid allergy is under-recognised — suspect it when eczema fails to respond to or paradoxically worsens with a potent topical steroid. The Coopman classification (A, B, C, D1, D2) groups cross-reacting molecules; tixocortol pivalate (group A) and budesonide (groups B and D) are the screening markers, and hydrocortisone (group A) allergy is the commonest. Screen for it deliberately — it is a fellowship favourite.[18]

Acrylates, resins, plants and implants. Methacrylates sensitise through nail products, dentistry and artificial nails; (meth)acrylates and epoxy resin affect printers, builders and orthopaedic or dental workers. Plants deliver the classic hapten urushiol (poison ivy, oak and sumac), plus Primula obconica, Compositae (chrysanthemum, daisy) and tulipalin (tulip fingers). Metals and bone cements (methyl methacrylate), surgical glues and tapes in biomedical devices and implants can drive eczematous or persistent dermatitis overlying the hardware — trouble from within.[24]

Patch testing — 48 hours on, read at 72

Patch testing is the diagnostic gold standard for ACD, and the fellowship expects you to run it like a protocol, not a guess. The European Society of Contact Dermatitis guideline fixes the technique, the reading days and the interpretation.[8]

Technique in four lines. Hapten allergens are applied under occlusion in aluminium (Finn) chambers on the upper back in the right vehicle (petrolatum, water) at the right concentration; the panel is removed at 48 hours (D2); readings are taken at D2, D3 or D4, and D7 — because metals, corticosteroids and some drugs react late. Supplementary series (occupational, cosmetic, fragrance, dental, drug, plant) are layered on by history, and the patient's own products, appropriately diluted, are tested when relevant.[8][1]

The ICDRG scale — read every reaction the same way

The International Contact Dermatitis Research Group scale (recently clarified and modified) grades each chamber so two observers speak the same language:[9]

• IR — irritant reaction: discrete glazed erythema or a follicular pattern; not allergic.
• ?+ — faint macular erythema only; doubtful.
• + — erythema, infiltration, possibly papules; weak positive.
• ++ — erythema, infiltration, papules and vesicles; strong positive.
• +++ — a bullous reaction; extreme positive.[9][1]

The baseline-to-extended ladder

Screen with the baseline, extend with the history. Start with the commercial ready-to-use baseline panel (TRUE Test) or the fuller European baseline series in Finn chambers, then add supplementary series — occupational, cosmetic, fragrance, dental, drug, plant — guided by the exposure history, and finish with the patient's own products at appropriate dilution. A baseline-only test in a hairdresser misses the hairdressing series; the ladder exists because the baseline cannot cover every trade.[8][1]

Relevance, and why the test lies

A positive reaction must be interpreted for relevance — present, past or unknown — against the history and exposure; a positive test that does not explain the dermatitis is of limited value, and 'past' relevance does not close the case.[1]

Occupational dermatitis — the medicolegal dimension

Contact dermatitis is the commonest occupational skin disease, and your notes are evidence in a compensation claim. The high-risk trades read like a roll-call of wet and chemical work: healthcare workers, hairdressers, mechanics, construction workers (wet-cement chromate), food handlers, printers, cleaners and metalworkers.[21]

Irritant wet-work dermatitis is the commonest occupational form; occupational ACD is most often to rubber accelerators, chromate, epoxy, acrylates or biocides. Hand dermatitis in these trades is disabling and frequently ends careers, so document causation, exposure, the temporal relationship and functional impairment meticulously, refer early to occupational health, modify the workplace, and prescribe the correct PPE — the right gloves (nitrile for wet work, cotton liners for sweating, latex avoidance where sensitised), barrier creams and soap substitution. Early intervention improves prognosis; delay risks chronicity and permanent occupational disability.[21][22]

Hand eczema — the composite phenotype

Hand eczema deserves its own heading because it is common, disabling, and almost always multifactorial — not one disease. The Lancet review frames it as a composite phenotype where atopic, irritant, allergic and vesicular (pompholyx) components overlap, which is why a single 'diagnosis' rarely fits and why patch testing is mandatory in chronic hand disease.[25]

Classification combines morphology (recurrent vesicular, hyperkeratotic, fissured, atopic) with cause (irritant, allergic, atopic, protein, mixed); severity is graded with the Hand Eczema Severity Index (HECSI), and the quality-of-life and occupational impact is major. Management integrates strict irritant avoidance, emollients and soap substitution, potent topical corticosteroids, and — for severe refractory disease — systemic therapy.[25]

Severe chronic hand eczema now has two systemic options, and both demand respect. Alitretinoin is a systemic retinoid effective for severe refractory chronic hand eczema — and it is highly teratogenic, so a pregnancy-prevention programme is mandatory, with lipids and TSH checked every two months. Dupilumab (IL-4 receptor alpha blockade) has phase IIb proof-of-concept evidence in severe chronic hand eczema with inadequate response or intolerance to alitretinoin, and is increasingly used in severe recalcitrant disease. These are not first-line; they sit above potent topical steroids, phototherapy and the classic immunosuppressants.[27][26]

Differential — what eczema is not contact

The differential of any eczematous eruption is wide, so be deliberate. Run through atopic dermatitis (flexural, atopic background, often coexistent and predisposing), seborrhoeic dermatitis, nummular or discoid eczema, asteatotic eczema, dyshidrotic (pompholyx) eczema, stasis dermatitis (venous), tinea (confirm the dermatophyte on microscopy and culture, and remember the dermatophytid 'id' reaction), psoriasis (including palmar and plantar pustulosis), scabies, drug eruptions and dermatitis herpetiformis. When the diagnosis is uncertain, a biopsy and skin scrapings help — and a high index of suspicion for contact allergy should trigger patch testing in any chronic, asymmetric or site-typical eczema.[1]

Paediatric ACD — under-recognised, not rare

ACD in children is missed because nobody looks for it. Nickel (jewellery, buttons, piercings), footwear allergens and preservatives (MI) are the common culprits in younger children; adolescents add cosmetics, hair dyes (PPD) and acrylates in nail products. Patch testing in children uses an age-appropriate selection and reduced concentrations — the baseline series is adapted, and the family's own products are often tested. Atopic dermatitis is a strong predisposing factor, which is why the atopic child with a persistent, localised, asymmetric eczema deserves patch testing, not just another emollient.[29]

Treat the cause, not just the itch — the management ladder

Management rests on three pillars in this order: identify and remove the cause, restore the barrier, and treat the inflammation. Reverse the order and you lose the patient — the steroid settles the itch, the cause stays, and it bounces back, exactly like the nurse at the top of the page.[19][20]

Pillar 1 — find it and remove it

This is the cornerstone and the most effective intervention you have. Patient education must be specific and written: name the allergen and its synonyms, list the products to avoid including hidden sources, explain the cross-reacting agents, hand over safe alternatives, and give a patient-information leaflet. For irritant and wet-work dermatitis the prescription is a behaviour change — reduce wet work, switch to a soap substitute, use lukewarm water, pat dry, apply emollients regularly, and wear the right gloves: nitrile for wet work, cotton liners for sweating, latex avoidance where sensitised. Workplace and household modification is non-negotiable in occupational cases.[1]

Pillar 2 — restore the barrier

Frequent bland, fragrance-free emollients and high-lipid barrier ointments rebuild the stratum corneum and cut flare frequency; a soap substitute or emollient wash replaces the irritant surfactants that caused half the problem. This is not the dull bit — it is the disease-modifying bit.[7]

Pillar 3 — treat the inflammation

Topical corticosteroids are stepped by potency and site: mild on the face and flexures, potent on the hands and trunk, once to twice daily during flares and tapered as inflammation settles — avoid prolonged potent steroids (atrophy, telangiectasia). Topical calcineurin inhibitors (tacrolimus, pimecrolimus) are the steroid-sparing choice on the face and eyelids. Wet-wrap therapy and short systemic corticosteroid courses (a prednisolone taper over two to three weeks) are reserved for severe acute flares or widespread involvement. Phototherapy (narrowband UVB or PUVA) serves chronic, widespread or treatment-resistant disease, and the systemic agents for genuinely refractory disease are azathioprine, methotrexate, ciclosporin, mycophenolate mofetil, dupilumab and alitretinoin (the last for severe chronic hand eczema). Treat secondary infection with antistaphylococcal antibiotics or antiseptics when it is clinically present.[26][27]

The fellowship dose reference

These are the systemic and biologic doses examiners expect verbatim, and every one carries a monitoring burden you must name alongside the number.[1]

Prevention — regulation that actually worked

Prevention is a primary-care and public-health act, and dermatology has two of the cleanest worked examples in medicine. The European Nickel Directive and the MI bans in leave-on cosmetics are population-level interventions that measurably cut sensitisation — proof that regulating a sensitiser at source beats chasing it patient by patient. Workplace controls (PPE, hazard substitution, health surveillance), atopic skin care from childhood, and patient education on wet-work reduction and emollients complete the preventive layer. Intervene early in occupational dermatitis and the prognosis improves; delay and you get chronicity and permanent disability.[11][16][21]

How patients come to harm — the preventable list

• Erythroderma from widespread contact dermatitis, admitted late for temperature, fluid and electrolyte management — the preventable admission.[1]
• Severe facial, eyelid or genital ACD with secondary infection or functional impairment, under-treated because nobody reached for systemic corticosteroid early.[1]
• Chronic hand eczema labelled 'just eczema' and never patch-tested, ending an occupation and a compensation claim.[25][22]
• Alitretinoin given to a woman of childbearing potential without a pregnancy-prevention programme — a preventable teratogenic disaster.[27]
• Topical corticosteroid allergy missed because nobody questioned eczema worsening on the steroid — the cause was the treatment.[18]
• A patch test read only at D2 and called negative, missing the late-reacting metal or corticosteroid.[8]
• Occupational causation left undocumented, and with it the patient's compensation rights.[21]

The memory devices, and the mantra

The mantra: tell irritant from allergic at the bedside, patch-test before you commit, and treat the cause — not just the itch.[1]

Ward-round test — three stems, thirty seconds each