Skin Environmental - Pathology

Physical damage

Low temperature damage

• Prolonged cold can cause ice crystal formation and vascular injury resultic in damage to tissue due to increased intracellular salt concentration
• Slow chilling can cause vasoconstriction, cellular damage -> secondary vasodilation and increased permeability -> oedema
• Severe and persistent cold causes vasoconstriction, increase in blood viscosity and tissue anoxia
• Lesions may occur in wet or hypoglycaemic neonates or animals recently moved from warm to cold environment
• Areas affected are extremities
• Lesions consist of gangrene and necrotic tissue

High temperature damage

• May result from excessive heat, liquids, flames, friction, lightning, electricity
• Partial or full thickness burns (first, second and third degree burns)
• Full thickness burns:
  • Total destruction of skin and adnexa
  • Has to be repaired by grafting
  • Life threatening
• Partial thickness burns:
  • Some structures preserved -> regeneration may occur
  • Grossly:
    • Erythema (capillary dilation)
    • Oedema (increased permeability of capillaries)
    • Vesicles
  • Microscopically:
    • Coagulation necrosis of epidermis
    • Subepidermal vesiculation
    • Necrosis of adnexa
    • Degenerated subepidermal collagen
    • May involve large numbers of neutrophils if secondary ifection is present

Sunlight damage

• Transient erythema may develop into sunburn erythema (warmth, swelling, pain)
• Diffusion of inflammatory mediators (e.g. cytokines) from damaged keratinocytes and endothelial cells
• Photooxidation of existing melanin -> pigment darkening
• Melanogenesis
• Immune responses of skin are reduced by UV light

Solar dermatosis and neoplasia

• Caused by chronic sunlight damage
• Damaged tissue generates free radicals than may damage nucleis acids and proteins
• If damage repaired prior to mitosis - no lasting effect
• If mitosis occurs before repair, post-mitotic repair is prone to faults and DNA mutations may result in neoplasia

Solar dermatitis

• Particularly in white animals and where little or no hair is present
• Grossly:
  • Erythema, scaling and crusting
  • -> Wrinkled nand thickened skin
  • Squamous cell carcinoma or haemangiosarcoma/haemangioma may develop
• Microscopically:
  • Dyskeratotic cells
  • Intercellular oedema
  • Vacuolated keratinocytes
  • Followed by hyperkeratosis, parakeratosis and acanthosis
  • Endothelial swelling
  • Haemorrhage
  • Hyperplasia
  • Dermal fibrosis
  • Dogs may develop actinic comedones

Photoenhanced dermatoses

• Many immune-mediated cutaneous disease are made worse by sunlight
  • Lupus erythematosus
  • Dermatomyositis
  • Pemphigus erythematosus
• Vasculitis in extremities, especially white-haired horses
• Grossly:
  • Erythematous, well circumscribed crusted lesions or hyperkeratotic plaques
• Microscopically:
  • Vasculitis of superficial dermal vessels
  • Thrombi may be seen