Epidemiology & Risk Factors

  • Epidemiology:
    • Accounts for ~80% of all contact dermatitis cases.
    • Most common occupational skin disorder (especially hand dermatitis).
  • Risk Factors:
    • Occupations with frequent wet work or chemical exposure (e.g., healthcare workers, cleaners, hairdressers, machinists, food handlers). c
    • Pre-existing skin barrier dysfunction (e.g., history of atopic dermatitis).
  • Common Irritants:
    • Physical/Chemical: Soaps, detergents, alcohol-based rubs, solvents, acids/alkalis, water (repeated immersion).
    • Biological: Urine and feces (e.g., diaper dermatitis).

Clinical Features

  • Pathophysiology: Non-immunologic direct cytotoxic damage to the epidermal barrier (does not require prior sensitization).
  • History:
    • Onset: Immediate (strong acids/alkalis) vs. gradual/cumulative (mild irritants like soaps over weeks/months).
    • Symptoms: Burning, stinging, and pain > pruritus (hallmark distinction from allergic contact dermatitis).
  • Physical Examination:
    • Distribution: Sharply demarcated to the exact areas of direct contact (e.g., hands, web spaces, diaper area sparing inguinal creases).
    • Acute: Erythema, edema, dryness, cracking, and occasionally vesicles/bullae with caustic agents.
    • Chronic: Dryness, scaling, hyperkeratosis, painful fissures, and lichenification.

Diagnosis

  • Initial/Screening: Clinical diagnosis based on detailed occupational/exposure Hx and physical exam findings.
  • Confirmatory / Rule-Out:
    • Patch testing: Negative in ICD; used primarily to rule out Type IV hypersensitivity (allergic contact dermatitis).
  • Key Labs: None routinely indicated.
  • Biopsy: Rarely needed; reserved for atypical or treatment-refractory cases. Shows non-specific epidermal necrosis, parakeratosis, and superficial perivascular infiltrate.
  • KOH Prep: Negative for hyphae; performed to exclude dermatophyte infection.

Differential Diagnostics

  • Allergic Contact Dermatitis (ACD):
    • Diff: Type IV hypersensitivity (requires prior sensitization); intense pruritus >> burning/pain; lesions typically spread beyond the margins of direct contact; positive patch test.
  • Dyshidrotic Eczema (Pompholyx):
    • Diff: Recurrent episodes of intensely pruritic, deep-seated “tapioca-pudding” vesicles on the lateral aspects of fingers, palms, and soles; unrelated to chemical exposure.
  • Atopic Dermatitis:
    • Diff: Classic flexural distribution (antecubital and popliteal fossae); personal/family Hx of atopy (asthma, allergic rhinitis); onset typically in early childhood.
  • Tinea Manuum:
    • Diff: Often asymmetric/unilateral (classic “two feet, one hand” syndrome); active scaling border with central clearing; positive KOH prep.
  • Plaque Psoriasis:
    • Diff: Well-demarcated erythematous plaques with thick silvery scale on extensor surfaces (elbows, knees), scalp, or lumbosacral region; associated with nail pitting and Auspitz sign.

Management

  • First-Line:
    • Identify and eliminate exposure to the offending irritant (essential for resolution).
    • Barrier restoration: Frequent application of thick, lipid-rich emollients (e.g., petrolatum-based ointments).
    • Preventive measures: Use of protective barrier gear (e.g., vinyl/nitrile gloves; avoid latex if allergy risk exists), mild soap-free cleansers, and cotton glove liners for prolonged glove use.
  • Second-Line (Active Inflammation / Flares):
    • Topical corticosteroids (TCS):
      • High/mid-potency TCS (e.g., clobetasol, triamcinolone) for thick skin on hands/feet.
      • Low-potency TCS (e.g., hydrocortisone 1-2.5%) for thin skin (face, intertriginous areas).
  • Refractory Cases:
    • Topical calcineurin inhibitors (e.g., tacrolimus, pimecrolimus) to avoid chronic steroid-induced skin atrophy.
    • Phototherapy (PUVA or narrowband UVB) for chronic, severe, treatment-resistant occupational disease.
    • Short course of oral corticosteroids (rarely indicated; reserved for extreme caustic burns).

Complications

  • Secondary bacterial infection: Most commonly impetiginization (Staph aureus or Strep pyogenes); manifests with honey-colored crusting, purulent discharge, or worsening erythema.
  • Cellulitis: Entry of pathogens through deep, painful cutaneous fissures.
  • Chronic disabling dermatitis: Can lead to significant occupational impairment and loss of productivity.
  • Post-inflammatory pigmentary changes: Hyper- or hypopigmentation, particularly in darker skin phototypes.