Pathophysiology
- Sustained pressure exceeds capillary perfusion pressure leading to ischemia.
- Reduced blood flow causes tissue hypoxia, impaired nutrient delivery, and waste accumulation.
- Ischemia injures endothelium → increased vascular permeability → inflammation and local edema, further impairing perfusion.
- Prolonged hypoxia causes irreversible cell injury, leading to tissue necrosis
- Shear and friction (contributing factors):
- Shear forces distort and occlude capillaries
- Friction damages superficial skin layers, weakening the barrier - Moisture - Macerates skin, lowers resistance to pressure and shear injury
- Cycle of worsening:
- Necrotic tissue becomes a nidus for infection → further inflammation, delayed healing, deeper ulceration
Grade
These are graded according to the depth of tissue loss;
- Stage 1 – Skin intact but with non-blanching redness.
- Stage 2 – Partial-thickness loss of skin with exposed dermis.
- Stage 3 – Full-thickness loss of skin, in which fat is visible in the ulcer and granulation tissue and rolled wound edges are often present.
- Stage 4 – Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer.
Management
- Prevent further tissue loss by off-loading the affected area
- Prevent further areas of pressure tissue injury
- Provide psychosocial support
- Provide wound care; debridement with infection, non-adhesive absorbable dressings with regular inspection, where available some dressings have debriding properties.
- Analgesia
- Optimise nutrition
- Close follow up in conjunction with community-based CNS