1. Wound Healing Dr. Ranjeet Patil

2. Definition Regeneration Replacement of dead or damaged cells by functioning cells of same structure and function Bones, Liver Repair Replacement of dead or damaged cells by granulation tissue which matures to form scar Function is lost-Lower order cells Skin None Brain, Skeletal muscle, Cardiac muscle

3. Wound closure types Primary First-intention Closure, the wounds are sealed immediately with simple suturing, skin graft placement, or flap closure Closure at end of a surgical procedure. Secondary Spontaneous-intention, no active intent to seal the wound Closes by re-epithelialization, contraction of the wound Highly contaminated wound Tertiary Initially treated by repeated debridement, systemic or topical antibiotics, or negative pressure wound therapy for several days to control infection Surgical intervention, such as suturing, skin graft placement, or flap design, is performed

5. WOUND-HEALING PHASES Inflammation Reactive phase The body's defences are aimed at limiting the amount of damage and preventing further injury Eschar or fibrinous exudate Upto 6 days

6. Inflammation Haemostasis platelet aggregation, degranulation, and activation of the coagulation cascade platelet-derived growth factor (PDGF), transforming growth factor beta (TGF), platelet-activating factor, fibronectin, and serotonin Increased Vascular Permeability

7. Inflammation Inflammation PMN 24 to 48 hours Prostaglandins, complement factors, interleukin-1 (IL-1), tumour necrosis factor alpha (TNF-), TGF, platelet factor 4, bacterial products primary role-phagocytosis of bacteria and tissue debris angiogenesis and collagen synthesis

8. Macrophages 48 to 96 hours – complete healing Phagocytosis Reactive oxygen species, Nitric oxide Debridement Collagenase, elastase Cell recruitment and activation Growth factors: PDGF, TGF, EGF, IGF Cytokines: TNF-, IL-1, IL-6, Fibronectin Matrix synthesis Growth factors: TGF, EGF, PDGF, Cytokines: TNF-, IL-1, Enzymes: arginase, collagenase, Prostaglandins, Nitric oxide Angiogenesis Growth factors: FGF, VEGF , Cytokines: TNF, Nitric oxide

9. T lymphocytes Less numerous than macrophages Peak at about 1 week post injury role in wound healing is not fully defined

10. Proliferation Proliferation Regenerative or reparative phase Consists of re-epithelialization, matrix synthesis, and neovascularization to relieve the ischemia of the trauma itself Granulation tissue 4-14 days

11. Fibroblasts synthesize collagen actively carry out matrix contraction Endothelial cells Formation of new capillaries (angiogenesis)

13. Maturation Remodelling phase Scar contraction with collagen cross-linking, shrinking, and loss of oedema Contracting or advancing edge 8th day- months

14. Remodelling 21 days up to 1 year Collagen remodeling is also characteristic of this phase. Type III collagen is initially laid down, replaced by type I collagen

15. Epithelialization 1st day Rapid mitotic divisions Defect is bridged Layering of the epithelium Keratinisation

19. Abnormalities of Wound Healing

20. Delaying Factors Systemic Age Nutrition Trauma Metabolic diseases Immunosuppression Connective tissue disorders Smoking Local Mechanical injury Infection Edema Ischemia/necrotic tissue Topical agents Ionizing radiation Low oxygen tension Foreign bodies

22. Treatment Treatment of hypertrophic and keloid scars Pressure – local moulds or elasticated garments Silicone gel sheeting (mechanism unknown) Intralesionalsteroid injection (triamcinolone) Excision and steroid injection Excision and postoperative radiation (external beam or brachytherapy) Intralesionalexcision (keloids only) Laser – to reduce redness (which may resolve in any event) Vitamin E or palm oil massage (unproven)

23. Contractures Where scars cross joints or flexion creases, a tight web may form restricting the range of movement at the joint Hyperextension or hyperflexion deformity Treatment may be simple involving multiple Z-plasties

25. Thankyou