Wound Healing

1. Wound Healing April 2012 Bystrzonowski N, Singh M www.setpras.org

2. Learning Objectives • Understand the anatomy of the skin and its functions • Understand the different types of wound healing • Understand the different stages of wound healing • Be aware of factors influencing wound healing

3. Relevant Anatomy • Skin Epidermis Hair Follicle Dermal Papillae Dermis Sebaceous Gland Erector Pili Merocrine Sweat Gland Hypodermis (subcutaneous fat)

4. Relevant Anatomy • Layers of the Epidermis • The epidermis is composed of several layers: • From superficial to deep: • Stratum Corneum -Acellular keratin layer • Stratum Lucidum -Dead cells without nuceli • Stratum Granulsoum -Cell cytoplasm contains keratin granules • Stratum Spinosum -Cells connected by desmosomes appear “spiny” • Stratum Germinativum -Basal layer connected to basement membrane

5. Introduction • Functions of the skin include: • Mechanical protection • Sensation • Barrier to infection • Immune surveillance • Thermoregulation • Vitamin D metabolism

6. Types of Wound Healing • Types: • Primary • Delayed Primary • Secondary

7. Types of Wound Healing • Primary Wound Healing: • Wound is closed directly soon after the injury e.g. suturing an incised wound • Advantages: • Faster healing time • Simplifies wound care/fewer dressing changes • Vital structures covered • Disadvantages/Contraindications: • Infected wound • Old wound • Too much tension

8. Types of Wound Healing • Delayed Primary Wound Healing: • Wound is closed after a few days e.g. allowing infection to clear from a dehisced wound before proceeding to closing it • Advantages: • Allows infection to settle prior to closure • Disadvantages/Contraindications: • Often have worse cosmetic result

9. Types of Wound Healing • Secondary Wound Healing: • Also known as secondary intention, wound is left to heal without approximation e.g. defects too large to suture together • Advantages: • Useful if wound too large to close • Contraction of scar over time can produce good results • Disadvantages/Contraindications: • May have worse cosmetic result • Larger amount of granulation tissue • Open wound requires patients to maintain dressings for longer • Increased risks of infection

10. Epithelialisation • Process in which epithelial cells migrate and replicate via mitosis and traverse wound • Main method in wounds that involve superficial dermis and epidermis • Wound contracture not common component • Typically occurs over 48 hours in well opposed wounds

11. Wound Healing

12. Stages of Wound Healing • 1. Haemostasis • Immediately after injury to the skin, can last for few days • Small vessels constrict • Platelet aggregation triggering clotting cascade releasing growth factors and cytokines • Fibrin matrix stabilizes the wound and provides a scaffold

13. Stages of Wound Healing • 2. Inflammation • PMN leucocytes accumulate and transform into MACs • Mast cells degranulate, releasing histamine and other mediators of vasodilation & cell migration • Vasoactive substances make small vessels permeable to inflammatory mediators • Chemotaxis  PMN leucocytes digest bacteria, debris and necrotic tissue with enzymes • Healing of chronic wounds usually becomes arrested at this stage

14. Stages of Wound Healing • 3. Proliferation • Subphases within this phase: • Fibroplasia, matrix deposition, angiogenesis, re-epithelialization • Days 5-7 fibroblasts migrate, laying down type I & III collagen • Tropocollagenprocollagen (triple helix)secreted into extracellular space peptide cleavage collagen fibres • Angiogenesis – new vasculature formed involving endothelial cells

15. Stages of Wound Healing • 3. Proliferation • Fibroblast growth factor and vascular endothelial growth factor modulate angiogenesis • Re-epithelialisation – cells spread from periphery of wound within 24 hours • Cells divide in 48-72 hours resulting in thin epithelial cell layer, bridging the wound • All above can last up to 4 weeks

16. Stages of Wound Healing • 4. Remodelling • After 3rd week, can last up to years • Collagen is degraded and deposited • Contraction occurs from proliferation of fibroblasts (myofibroblasts) • Max tensile strength achieved by 12th week and resultant scar has only about 75% of original tensile strength1 • Scar maturation may take up to 18 months

17. Cells of Wound Healing Platelets PMNs Macrophages Lymphocytes Fibroblasts Capillaries 0 2 4 6 8 10 12 14 16 Days

18. Wound Healing • Factors Affecting Wound Healing2: • Systemic Factors Local Factors • Congenital • Ehlers Danlos • PseudoxanthomaElasticum • EpidermolysisBullosa • Acquried • Nutrition • Drugs: steroids & NSAIDS • Age • Smoking • Endocrine abnormalities (DM, neuropathy) • Infection • Radiation • Poor blood supply (fibroblasts are O2 sensitive) • Trauma • Denervated tissue (some evidence)

19. Tendon Healing • 1. Inflammation • Inflammatory cells and growth factors • 2. Proliferation • Fibroblasts secrete collagen, random arrangement, lacks tensile strength • 3. Remodelling • Tendon structure becomes organised, early movement can limit fibrous attachments to tendon sheath

20. Bone Healing • 1. Haematoma formation • 2. Inflammation • Macrophages and osteoblasts enter haematoma • 3. Proliferation • Soft callus – collagen deposition in haematoma • Hard callus – calcification of cartilaginous callus • 4. Remodelling • Restoration of normal structure

21. Conclusions • The skin is composed of several layers • It has many functions such as immune surveillance and Vitamin D metabolism • Wound healing typically follows set stages: • Haemostasis • Inflammation • Proliferation • Remodelling

22. References • 1. Brown, D, Borschel G. Michigan Manual of Plastic Surgery. Philadelphia: Lippincott, Williams and Wilkins; 2004 • 2. Diegelmann RF, Evans MC. Wound healing: An overview of acute, fibrotic and Delayed healing. Frontiers in Bioscience 2004;9: 283-289