Wound Healing. Dhaval Bhavsar, MD Assistant Professor Dept of Plastic, Wound and Burn Surgery KUMC. Dhaval Bhavsar, Wound Healing (Basics)

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1 Wound Healing Dhaval Bhavsar, MD Assistant Professor Dept of Plastic, Wound and Burn Surgery KUMC

2 Skin Largest Organ Provides Protection from elements, Infective organisms Protective sensation When breached infection, loss of thermal regulation

3 Normal Skin

4 Epidermis

5 Dermis

6 What is Wound any break in the skin or an organ caused by violence or surgical incision

7 Wound Healing restoration of continuity after wounding

8 Wound Healing- 3 Classic Phases Inflammation Proliferation Remodeling

9 Hemostasis Clot formation Start point of inflammation

10 Inflammatory phase Starts within 6-8 hrs PMN cells Later Monocytes (Macrophages)

11 Inflammation Reaches its height at hrs Also release growth factors Prepares wound for proliferation

12 Proliferation Fibroplasia Matrix deposition Angiogenesis Re-epithelialization

13 Granulation tissue

14 Fibroplasia Fibroblasts activated fibrocytes Most important cells Secrete- Collagen Glycosaminoglycans Elastin Fibronectin Protease

15 Fibroplasia Fibroblasts increase in number as inflammatory cells decrease Begins 3-5 days after wounding Migrate and proliferate in response to fibronectin, platelet-derived growth factor (PDGF), fibroblast growth factor, transforming growth factor, and C5a

16 Collagen deposition The most important matrix component Deposition starts about 3 rd day and continues for 2-4 weeks depending on wound size Procollagen Tropocollagen Collagen

17 Collagen Deposition Collagen deposition dependent on Age Tension Pressure Stress

18 Matrix Source- fibroblasts Components GAG Heparin Sulfate Chondroitin Sulfate Hyaluronic Acid Dermatan Sulfate

19 Angiogenesis Wound healing requires rich blood supply to sustain newly formed tissue It is evident in erythema (redness) of the new scar Capillary density decreases as the need reduces and scar matures

20 Angiogenesis Macrophages release- Macrophage derived angiogenic factor in response to low tissue oxygen tension Work as chemoattractant Basic FGF and VEGF are also important

21 Angiogenesis Endothelial cells bud arise from capillary ends Produced in line Endothelial cells coalesce and bind fibrin

22 Re-epithelialization Covers the granulation tissue with epidermal cells and completes wound healing Re-establishes the barrier

23 Re-epithelialization Actin-rich protrusions, lamellipodia and filopodia Adhesions at the leading edge Cells move forward by contracting the actin cytoskeleton Coordinated processes of adhesion assembly, disassembly and turnover

24 Epithelial Cell Migration

25 Wound Contraction Centripetal movement of wound edges Maximal rate of contraction mm/day Depends on the degree of tissue laxity and shape of the wound Role of myofibroblast

26 Myofibroblast Lab Invest 2003, 83:

27 Remodeling Collagen remodeling depends on balance between new collagen formation and collagen destruction Collagenase and Matrix metalloproteinase

28 Remodeling Collagen becomes increasingly organized Fibronectin gradually disappears Hyaluronic acid and glycosaminoglycans are replaced by proteoglycans Water is resorbed These events allow collagen fibers to lie closer together, facilitating collagen cross-linking

29 Remodeling Begins approximately 21 days after injury Remodeling may continue indefinitely

30 Strength of Repaired Wound Tensile strength- load capacity per unit area Maximum achieved in 90 days Usually it is 80% of original strength Bursting strength- force required to break a wound regardless of its dimension

31 Clinical Wound Healing Stages are concurrent Epithelial migration 1mm/day Requires intervention if larger than 5 cm

32 Superficial Partial Deep Burn Wound Healing Superficial- primary epithelization Partial- From epithelial appendages Deep partial- slow epithelization from remaining epithelial appendages Deep- Can not epithelize

33

34 Fetal Wound Healing Rapid Efficient Perfect Scar less

35 Fetal Wound Healing Involves mechanisms similar to cell migration and proliferation during embryonic stage of fetal life No inflammation Wound contraction takes place but no scarring

36 Abnormal Healing Hypertrophic scar Keloid Chronic non-healing wound

37 Hypertrophic Scar Imbalance in collagen production and degradation Either over production OR Low degradation Red, elevated scars

38 Hypertrophic Scar Usually along tension lines Contracture occurs more in areas with laxity

39 Keloid African>Asians> Caucasians Comparable to malignant growth Extends beyond wound margins

40 Non healing Wound Wound that fails to progress through an orderly sequence of repair in a timely fashion Arbitrary time point: 3-4 weeks

41 Causes of Delayed Wound Healing Infection Tissue hypoxia Repeated trauma Presence of necrotic tissue or foreign body Systemic causes Diabetes Malnutrition- protein Immunodeficiency

42 Common Non-healing Wounds Diabetic wound Pressure sore Venus ulcer

43 Wound Healing & Nutrition Vitamin C and A Protein Essential amino acids Investigate Serum protein Hemoglobin Micronutrients Mg, Cu, Zn, Fe

44 Tendon Repair Gross Examination Intermediate phase Early phase J Hand Surg [Am] Sep;28(5): Late phase

45 Nerve Repair

46 Bone Repair

47 THANK YOU

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