Pathology of Acute Skin Inflammation: Urticaria & Eczema

SKIN PATHOLOGY --- ACUTE INFLAMMATORY DERMATOSES Acute lesions last days to weeks. Characterized by inflammation (predominantly mononuclear cells, not neutrophils), oedema, and sometimes epidermal, vascular, or subcutaneous injury. Some resolve; others transition to a chronic phase. --- 1. URTICARIA (Hives) Definition: Common disorder caused by localized mast cell degranulation → dermal microvascular hyperpermeability → erythematous, oedematous, pruritic plaques called wheals . Pathogenesis: Most cases: Type I (immediate) hypersensitivity — antigens bind IgE on mast cells → degranulation Triggers: pollens, foods, drugs, insect venom IgE-independent: opiates and certain antibiotics directly cause mast cell degranulation Hereditary angioedema: inherited deficiency of C1 esterase inhibitor → uncontrolled complement activation → affects lips, throat, eyelids, genitals, distal extremities. Laryngeal involvement can compromise the airway — potentially dangerous In the vast majority of cases, no cause is found despite extensive investigation Morphology (Histology): Subtle findings Sparse superficial perivenular infiltrate of mononuclear cells, rare neutrophils, sometimes eosinophils Superficial dermal oedema → wider-spaced collagen bundles Mast cell degranulation difficult to see on H&E; highlighted by Giemsa stain Clinical Features: Affects any age, but most common 20–40 years Individual lesions develop and fade within hours; episodes can last days to months Ranges from small pruritic papules to large oedematous erythematous plaques Can be localized or generalized Pressure urticaria: lesions only in pressure-bearing areas (feet, buttocks) Persistent lesions may indicate urticarial vasculitis (complement deposition in dermal venules) Treatment: antihistamines; systemic steroids for severe/refractory cases --- 2. ACUTE ECZEMATOUS DERMATITIS Definition: A clinical term covering multiple conditions with varied aetiologies. Presents as red papules with overlying vesicles that ooze and crust. With persistence → raised, scaling plaques. Subtypes: Allergic contact dermatitis — topical allergen exposure (e.g., poison ivy) Atopic dermatitis — genetic defects in keratinocyte barrier function; not purely allergen-driven Drug-related eczematous dermatitis — hypersensitivity to a systemic drug Photoeczematous dermatitis — abnormal reaction to UV or visible light Primary irritant dermatitis — chemical, physical, or mechanical skin damage Pathogenesis (Contact Dermatitis as the model): Allergen (e.g., poison ivy) chemically modifies self-proteins Epidermal Langerhans cells process and present antigen to naive T cells in draining lymph nodes → immunologic memory On re-exposure: memory CD4+ T cells migrate to skin → cytokine release → inflammatory cell recruitment + epidermal damage (delayed-type hypersensitivity) Morphology (Histology): Hallmark: Spongiosis (intercellular epidermal oedema) → synonym: spongiotic dermatitis Oedema fluid splays apart keratinocytes; intercellular bridges become stretched and more visible Superficial perivascular lymphocytic infiltrate Oedema of dermal papillae + mast cell degranulation Eosinophils prominent in drug-induced cases Histology is similar regardless of cause → clinical correlation is essential Clinical Features: Pruritic, oedematous, oozing plaques with vesicles/bullae Persistent antigen exposure → progressive scaling (hyperkeratosis) + epidermal thickening (acanthosis) Scratching/rubbing can produce or worsen lesions → may evolve into Lichen Simplex Chronicus Resolves when offending stimulus is removed "Inside jobs" (internal antigen e.g., ingested food/drug) vs. "outside jobs" (external contact antigen) Atopic dermatitis: strong genetic basis; 80% concordance in identical twins, 20% in fraternal twins. Usually begins in childhood, clears in adulthood. Often coexists with asthma and allergic rhinitis — the atopic triad --- 3. ERYTHEMA MULTIFORME Definition: Uncommon, usually self-limited hypersensitivity disorder triggered by infections or drugs. Triggers: Infections: herpes simplex (most common), Mycoplasma, some fungi Drugs: sulfonamides, penicillin, salicylates, hydantoins, antimalarials Pathogenesis: Skin-homing cytotoxic T cells attack basal cells of skin and mucosae These cells display antigens that cross-react with the inciting drug or microbe Morphology (Histology): Gross: characteristic targetoid lesions — red macule/papule with pale vesicular or eroded center Early: superficial perivascular lymphocytic infiltrate + dermal oedema + lymphocytes along dermoepidermal junction associated with degenerating keratinocytes Later: discrete/confluent zones of basal epidermal necrosis + blister formation Severe form ( Toxic Epidermal Necrolysis ): necrosis extends through full thickness of epidermis Clinical Features: Wide diversity of lesions: macules, papules, vesicles, bullae, and targetoid lesions — hence "multiforme" Infection-associated forms (especially HSV) are less severe Drug-asso