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Summary Table

Feature	Details
Risk Factors	Occupational exposure (healthcare workers, hairdressers, construction workers, cleaners, florists), atopic dermatitis history (predisposes to irritant type), repeated wet work, use of jewelry/cosmetics/fragrances, exposure to plants (poison ivy, poison oak)
Etiology	Two main types: (1) Irritant contact dermatitis from direct cytotoxic damage by a chemical agent without immune sensitization; (2) Allergic contact dermatitis from a Type IV (delayed-type) hypersensitivity reaction to a hapten
Patient Presentation	Pruritic, erythematous, eczematous rash localized to the area of contact with the offending agent; may present acutely with vesicles/bullae or chronically with lichenification and scaling
Classic Physical Exam	Well-demarcated, geometric, or linear distribution that mirrors the shape of the contactant (e.g., watch band pattern on the wrist, linear streaks from plant exposure, periumbilical rash from a nickel belt buckle); vesicles on an erythematous base in acute cases
Key Diagnostic Results	Clinical diagnosis based on morphology and distribution; epicutaneous patch testing is the gold standard confirmatory test for allergic contact dermatitis; skin biopsy shows spongiotic dermatitis (nondiagnostic but supportive)
Management	Identify and remove the offending agent (most important step); topical corticosteroids for localized disease; systemic corticosteroids (oral prednisone) for severe or widespread involvement; emollients and barrier repair
Keywords	"Well-demarcated rash," "geometric distribution," "linear vesicular streaks," "nickel allergy," "rubber gloves," "poison ivy," "patch test positive," "occupation-related rash," "Type IV hypersensitivity"

1. Pathophysiology

Contact dermatitis is broadly divided into two mechanistically distinct categories, and understanding the difference between them is central to answering exam questions correctly.

Irritant contact dermatitis (ICD) accounts for roughly 80% of all contact dermatitis cases. It results from direct chemical or physical damage to the epidermal barrier without requiring prior immune sensitization. When a substance such as a detergent, solvent, acid, alkali, or even prolonged water exposure disrupts the stratum corneum, it triggers release of pro-inflammatory cytokines (IL-1, TNF-alpha) from damaged keratinocytes. This innate immune activation produces localized inflammation. Because no adaptive immune memory is involved, ICD can occur on the very first exposure to the irritant, and the severity is dose-dependent: higher concentration and longer duration of contact produce worse disease. This is why healthcare workers with frequent handwashing and glove use are a classic at-risk population.

Allergic contact dermatitis (ACD) accounts for the remaining 20% and is a Type IV (delayed-type) hypersensitivity reaction mediated by sensitized T-lymphocytes. The process occurs in two phases. During the sensitization phase, a low-molecular-weight chemical (hapten) penetrates the skin, binds to carrier proteins, and is taken up by Langerhans cells (epidermal dendritic cells). These antigen-presenting cells migrate to regional lymph nodes where they present the hapten-protein complex to naive T cells via MHC class II. This generates memory T cells, a process that typically takes 10 to 14 days on first exposure. During the elicitation phase, re-exposure to the same hapten activates these memory T cells, which release inflammatory cytokines (IFN-gamma, IL-17) within 24 to 72 hours, producing the classic eczematous eruption. This delayed onset is the hallmark that separates it from Type I (immediate) hypersensitivity reactions and is a frequently tested concept.

The clinical appearance directly follows from the pathophysiology. Spongiosis (intercellular edema within the epidermis) is the histologic hallmark of eczematous dermatitis and explains the vesicle formation in acute cases. In chronic or repeated exposure, persistent inflammation leads to epidermal hyperplasia and lichenification (thickened, leathery skin with accentuated skin markings). The geometric, well-demarcated distribution of the rash corresponds to the exact area of skin that contacted the offending substance, which is the single most important clinical clue on examination.

2. Classification and Clinical Manifestation

Classification by Mechanism

Type	Mechanism	Onset	Sensitization Required	Dose-Dependent	Classic Example
Irritant Contact Dermatitis	Direct cytotoxic damage to keratinocytes	Minutes to hours (acute) or cumulative over weeks (chronic)	No	Yes	Detergents, solvents, wet work, acids/alkalis
Allergic Contact Dermatitis	Type IV delayed hypersensitivity via sensitized T cells	24 to 72 hours after re-exposure	Yes (prior sensitization phase of 10 to 14 days)	No (even trace amounts can trigger)	Nickel, urushiol (poison ivy), fragrances, neomycin, rubber accelerators

Classification by Chronicity

Stage	Timeline	Clinical Features
Acute	Hours to days	Erythema, edema, vesicles, bullae, oozing, weeping; intensely pruritic
Subacute	Days to weeks	Erythema, scaling, crusting; vesicles may still be present but less prominent
Chronic	Weeks to months	Lichenification, fissuring, scaling, hyperpigmentation or hypopigmentation; pruritus may become the dominant symptom

Common Allergens and Their Typical Distribution

Allergen	Source	Classic Distribution
Nickel	Jewelry, belt buckles, watchbands, bra clasps	Earlobes, periumbilical area, wrist, dorsal feet (from shoe eyelets)
Urushiol	Poison ivy, poison oak, poison sumac	Linear vesicular streaks on exposed extremities
Rubber accelerators (thiuram, carbamates)	Latex/rubber gloves	Dorsal hands with sparing of the palms
Fragrance mix / Balsam of Peru	Cosmetics, perfumes, deodorants	Face, neck, axillae
Neomycin / Bacitracin	Topical antibiotic ointments	Periorbital area, lower extremities (applied to wounds)
Potassium dichromate	Cement, leather	Hands and feet (construction workers, shoe dermatitis)
p-Phenylenediamine (PPD)	Hair dye, temporary tattoos	Scalp margin, forehead, ears, neck
Formaldehyde	Nail polish, fabric finishes	Periorbital area (transferred by fingers), eyelids

3. Diagnostic Workup

Test	Role	Key Findings
Clinical history and physical exam	Best initial diagnostic approach	Geometric, well-demarcated rash corresponding to area of contact; temporal correlation with exposure
Epicutaneous (patch) testing	Gold standard for allergic contact dermatitis	Standardized allergens applied to upper back under occlusion for 48 hours; read at 48 and 96 hours; positive result shows localized eczematous reaction at the test site
Skin biopsy	Supportive but not confirmatory	Spongiotic dermatitis with perivascular lymphocytic infiltrate; cannot distinguish ICD from ACD histologically
Serum IgE / Skin prick testing	Not indicated	These tests evaluate Type I hypersensitivity; contact dermatitis is Type IV; ordering these is a common distractor

The diagnosis of contact dermatitis is primarily clinical. The best initial step is a thorough history focusing on temporal relationship between exposure and rash onset, occupation, hobbies, new products (soaps, cosmetics, jewelry, topical medications), and the anatomic distribution of the eruption. A rash that is sharply demarcated and geometrically matches the shape of a contactant is essentially diagnostic.

When the offending agent is not obvious from history alone, or when the dermatitis is recurrent and the trigger is unclear, the next step is epicutaneous patch testing. This is the gold standard for confirming allergic contact dermatitis. The procedure involves applying a panel of standardized allergens (commonly the TRUE Test or an expanded series) to adhesive patches placed on the upper back. The patches remain in place under occlusion for 48 hours, then are removed for an initial reading. A second reading at 96 hours (sometimes also at 7 days) is essential because some reactions are delayed and may be missed on the 48-hour reading alone. A positive result shows erythema, papules, and vesicles localized to the site of a tested allergen.

It is important to understand what patch testing does not do: it does not diagnose irritant contact dermatitis. ICD is a clinical and exclusion-based diagnosis. If patch testing is negative but the clinical picture strongly suggests contact dermatitis, ICD is the likely diagnosis.

Skin biopsy is rarely needed. It shows spongiotic dermatitis (epidermal intercellular edema) with a perivascular lymphocytic and sometimes eosinophilic infiltrate. However, this pattern is shared across all forms of eczematous dermatitis (atopic dermatitis, nummular eczema, dyshidrotic eczema), so biopsy cannot distinguish between subtypes. It is useful mainly to exclude other diagnoses such as psoriasis, dermatophytosis, or cutaneous T-cell lymphoma.

A common exam trap is offering serum IgE levels or skin prick testing as an answer choice. These modalities evaluate Type I (IgE-mediated) hypersensitivity and have no role in the workup of contact dermatitis, which is Type IV. Selecting these reflects a misunderstanding of the underlying immunologic mechanism.

4. Management and Treatment

Severity	Treatment	Details
All cases	Allergen/irritant avoidance	Identify and eliminate the offending agent; this is the single most important intervention
Mild, localized	Mid-to-high potency topical corticosteroids	Triamcinolone 0.1% ointment or betamethasone valerate 0.1% applied twice daily for 2 to 3 weeks; use low-potency agents (hydrocortisone 1 to 2.5%) on the face, groin, and axillae
Severe or widespread	Systemic corticosteroids	Prednisone 0.5 to 1 mg/kg/day orally, tapered over 2 to 3 weeks; short courses (5 to 7 days) risk rebound dermatitis, particularly with poison ivy/oak
Adjunctive	Emollients and barrier creams	Petrolatum-based emollients to restore skin barrier; cool compresses and calamine lotion for symptomatic relief of vesicular/weeping lesions
Refractory or chronic	Topical calcineurin inhibitors	Tacrolimus 0.1% ointment or pimecrolimus 1% cream; useful as steroid-sparing agents, especially for facial and intertriginous dermatitis
Severe, recalcitrant	Phototherapy or systemic immunosuppressants	Narrowband UVB phototherapy; azathioprine, mycophenolate, or cyclosporine in select chronic cases unresponsive to first-line therapy

The cornerstone of management for both irritant and allergic contact dermatitis is identification and strict avoidance of the causative agent. Without this step, no pharmacologic therapy will produce lasting improvement. For occupational exposures, this may involve changes in workplace practice, use of protective equipment (e.g., nitrile gloves instead of latex for rubber-allergic patients), or in some cases, job modification.

For localized, mild-to-moderate disease, topical corticosteroids are first-line pharmacotherapy. A mid-potency agent such as triamcinolone acetonide 0.1% ointment applied twice daily for 2 to 3 weeks is appropriate for the trunk and extremities. For thickened, lichenified plaques, a high-potency agent (clobetasol propionate 0.05%) may be used for a limited duration of 2 weeks. On thin-skinned areas (face, eyelids, groin, axillae), only low-potency agents such as hydrocortisone 1 to 2.5% should be used to avoid steroid atrophy. Ointment vehicles are preferred over creams because they provide better occlusion and fewer additives that might themselves be irritating or sensitizing.

For severe, widespread, or rapidly progressing disease, systemic corticosteroids are indicated. The classic scenario tested on exams is extensive poison ivy dermatitis with involvement of the face, genitals, or more than 20% body surface area. The standard regimen is oral prednisone at 0.5 to 1 mg/kg/day (typically starting at 40 to 60 mg daily), tapered gradually over 2 to 3 weeks. A critical teaching point is that a short burst of 5 to 7 days without a taper is insufficient for poison ivy and frequently leads to rebound dermatitis once the steroid is discontinued, because urushiol can persist in the skin and the immune response outlasts the short course. This rebound phenomenon is a commonly tested concept.

Topical calcineurin inhibitors (tacrolimus, pimecrolimus) are second-line agents that work by inhibiting T-cell activation and cytokine release. They are particularly valuable as steroid-sparing agents for chronic dermatitis on the face and intertriginous areas where prolonged corticosteroid use carries a high risk of skin atrophy, telangiectasia, and striae.

Wet dressings and cool compresses applied with Burow solution (aluminum acetate) are helpful adjuncts for acute vesicular, weeping lesions. They promote drying and provide symptomatic relief from pruritus.

For patients with known contact allergy, long-term counseling on avoidance strategies is essential. Patients allergic to nickel should be advised to use nickel-free jewelry or apply clear nail polish as a barrier coating on metal surfaces. Patients allergic to rubber chemicals should switch to nitrile or vinyl gloves. Providing patients with a written list of cross-reacting substances and alternative products is a practical and testable concept in the outpatient management of ACD.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Atopic dermatitis	Pruritic, eczematous plaques; can affect similar body areas (hands, flexural surfaces)	Atopic dermatitis has a flexural distribution (antecubital and popliteal fossae), begins in early childhood, and is associated with asthma/allergic rhinitis; contact dermatitis has a geometric, exposure-matched distribution and no atopic triad
Nummular eczema	Round, coin-shaped eczematous plaques that may vesiculate and crust	Lesions are scattered, not confined to a contact zone; typically on the lower extremities; no clear temporal relationship to an irritant or allergen
Seborrheic dermatitis	Erythematous, scaly patches on the face	Distribution follows sebaceous gland-rich areas (nasolabial folds, scalp, eyebrows, retroauricular); greasy, yellowish scale; not related to external contact
Tinea corporis	Annular, erythematous, pruritic plaque with scaling	Has a raised, advancing border with central clearing; KOH preparation shows septate hyphae; distribution is not geometric/exposure-dependent
Psoriasis	Well-demarcated, scaly plaques	Silvery-white scale, Auspitz sign (pinpoint bleeding on scale removal); favors extensor surfaces (elbows, knees), scalp, and gluteal cleft; not pruritic in many cases
Scabies	Intensely pruritic eruption affecting the hands and wrists	Distribution favors interdigital web spaces, wrists, waistline, and genitalia; lesions are papular with characteristic burrows; worsens at night; found in multiple household members
Drug eruption (fixed drug eruption or morbilliform rash)	Erythematous, pruritic rash with temporal relationship to a new exposure	Distribution is widespread and symmetric, not confined to a contact zone; fixed drug eruption recurs at the exact same site with re-exposure to the offending drug
Latex allergy (Type I)	Rash related to glove exposure	Type I latex allergy is IgE-mediated with immediate urticaria (wheals) within minutes, potentially with anaphylaxis; contact dermatitis from rubber is delayed (24 to 72 hours) and eczematous, not urticarial

6. Traps and High-Yield Pearls

The most common way students lose points on contact dermatitis questions is by failing to distinguish Type I from Type IV hypersensitivity in the setting of latex or rubber exposure. A question describing a healthcare worker with an urticarial rash appearing within minutes of donning gloves is testing latex allergy (Type I, IgE-mediated), not contact dermatitis. Conversely, a delayed eczematous eruption appearing 48 to 72 hours after glove use, with sparing of the palms and involvement of the dorsal hands, points to allergic contact dermatitis from rubber accelerator chemicals (Type IV). Choosing the wrong hypersensitivity mechanism leads to selecting the wrong diagnostic test (skin prick test and serum IgE for Type I versus patch testing for Type IV).

A second major trap involves the duration of systemic steroid therapy for poison ivy. Vignettes will describe a patient who was given a short, 5-to-7-day course of prednisone and now returns with a flare of the same dermatitis. The correct interpretation is rebound from an inadequately tapered course, and the next best step is to restart prednisone with a proper 2-to-3-week taper, not to order further diagnostic testing.

Another tested concept is the distinction between irritant and allergic contact dermatitis on clinical grounds. ICD tends to produce a burning or stinging sensation and develops rapidly after exposure, while ACD is predominantly pruritic and has a delayed onset. ICD is dose-dependent (a small amount of a weak irritant may produce no reaction), while ACD can be triggered by even trace quantities of the allergen once sensitization has occurred.

Finally, be alert to vignettes involving eyelid dermatitis caused by allergens transferred from the fingers (e.g., nail polish containing formaldehyde resin or tosylamide). The contactant never directly touches the eyelid, which can mislead students into considering atopic dermatitis or seborrheic dermatitis. The key clue is that the rash is on the eyelids (thin, highly permeable skin) while the hands (thicker stratum corneum) are spared, and the patient recently started using a new nail product.

The core competency being tested across all contact dermatitis questions is pattern recognition: matching a well-demarcated, geometrically distributed eczematous rash to the correct external exposure, selecting the appropriate diagnostic test based on the underlying immune mechanism, and prescribing a steroid regimen of adequate duration.

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