• Pathophysiology
    • Also known as xerosis cutis or asteatosis; refers to abnormally dry skin.
    • Caused by a defect in the epidermal barrier function leading to ↑ transepidermal water loss (TEWL).
    • Exacerbated by low humidity (winter), harsh soaps, and frequent hot bathing, which strip natural lipids from the stratum corneum.
    • Common in elderly pts due to age-related ↓ in sebaceous and sweat gland function.
  • Clinical Features
    • Dry, rough, and scaly skin, often with fine flakes or cracks.
    • Pruritus is the dominant symptom and can be severe.
    • Common locations: Shins (most frequent), arms, hands, and trunk.
    • Spares areas with high sebaceous gland concentration (e.g., face, axilla, groin).
FeatureXerosisEczema (Atopic Dermatitis)
PathophysiologySimple barrier dysfunction (↓ water)Immune dysregulation (Th2, filaggrin)
Hallmark SymptomSkin tightness, mild pruritusINTENSE pruritus (“the itch that rashes”)
Key SignFine scaling, “cracked” appearanceLichenification (chronic), vesicles (acute)
DistributionGeneralized, esp. anterior shinsFlexural areas (antecubital/popliteal fossae)
Tx FoundationEmollientsEmollients + Topical Corticosteroids for flares
  • High-Yield Associations (Systemic Causes of Xerosis/Pruritus)
  • Treatment
    • First-line: Liberal use of thick moisturizers (emollients), especially those containing ceramides, urea, or lactic acid.
      • Apply immediately after bathing on damp skin to trap moisture (“soak and seal”).
    • Lifestyle Modifications:
      • Use lukewarm water for short baths/showers.
      • Use mild, pH-neutral, non-soap cleansers.
      • Increase ambient humidity with a humidifier.
    • Second-line (for significant inflammation): Low-potency topical corticosteroids (e.g., hydrocortisone).
  • Complications
    • Asteatotic eczema (Eczema craquelé): Inflammation and fissuring develop on xerotic skin, resembling “cracked porcelain.”
    • Secondary bacterial infection (impetiginization) from scratching, typically with S. aureus.