Wound Healing

• Haemostasis • Inflammation • Proliferation • Remodelling

Neutrophils (clean up) and macrophages (direct activity for proliferation phase)

Produce collagen and extra cellular matrix for granulation tissue

Release histamine to increase vascular permeability

Debridement of wound, regulation of chemical mediators and growth factors seen in inflammation and proliferation phase

Activate platelets during haemostatis and produce new blood vessels following vascular injury.

Injury to tissue, skin intact

Damage to the epidermal skin layer

Injury through body structures

Torn skin/tissues

Injury to the epidermal layer

Epidermal and dermal layer involvement

All three layers and possible muscle/bone involvement

Keratinocytes

Melanocytes

Macrophages, lymphocytes, angiocytes and fibroblasts

Minimal contraction, suture closes edges

Fills with a fibrin clot, wound is left open due to an increased risk of infection if closed due to debris. Results with a prolonged inflammation stage

E.g injury to abdomen, could t suture due to swelling, left open until primary intention can be achieved

Prolonged and ineffective inflammation, Slow/poor granulation, Unable to produce/poor epithelium, Hypertrophy of fibrosis (scarring)

There is a protease imbalance, increased MMP and decreased TIMP (tissue inhibitor metallproteases) which are released by local cells

Collagen

Increased WBC, collagen and extra cellular matrix

Cell - cell communication by chemotaxis - direct migration of a cell in response to a stimulus.