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Wound healing

A presentation about Wound Healing.

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Wound healing

  2. 2. DEFINITION  Wound healing refers to the body’s replacement of destroyed tissue by living tissue.  Can be achieved by 2 processes: tissue regeneration &scar formation.  Dynamic balance between these 2 is different in different tissues.
  3. 3. Introduction  During healing, a complex cascade of cellular events occur to achieve resurfacing, reconstitution and restoration of tensile strength of injured tissue.  Wound healing occurs in 3 phases 1. Inflammatory phase 2. Proliferative phase 3. Remodeling phase
  4. 4. Stages of wound healing
  5. 5. I. Inflammatory phase A. Immediate to 2-5 days B. Hemostasis 1. Vasoconstriction – damaged blood vessels constrict 2. Hemostasis is achieved by formation of platelet plug & activation of extrinsic & intrinsic clotting pathways. 3. Formation of a provisional fibrin matrix C. Recruitment of inflammatory cells into the wound by potent chemoattractants
  6. 6. Early Events in Inflammation  Fibrin and fibronectin form a lattice that provides scaffold for migration of inflammatory, endothelial, and mesenchymal cells.  Neutrophilic infiltrate appears: removes dead tissue & prevent infection.  Monocytes/macrophages follow neutrophils: orchestrated production of growth factors & phagocytosis.
  7. 7. Late Events in Inflammation  Entry of lymphocytes.  Appearance of mast cell
  8. 8. II. Proliferative phase A. 2 days to 3 weeks B. Granulation tissue formation (composed of fibroblasts,macrophages and endothelial cell) C. Angiogenesis D. Contraction I. Wound edges pull together to reduce the defect E. Epithelialization I. Epithelial cells migrate across the new tissue to form a barrier between the wound and the environment
  9. 9. Mesenchymal cell proliferation  Fibroblasts are the major mesenchymal cells involved in wound healing, although smooth muscle cells are also involved.  Macrophage products are chemotactic for fibroblasts. PDGF, EGF, TGF, IL-1, lymphocytes are as well.  Replacement of provisional fibrin matrix with type III collagen.
  10. 10. Angiogenesis  Angiogenesis reconstructs vasculature in areas damaged by wounding, stimulated by high lactate levels, acidic pH, decreased O2 tension in tissues.  Recruitment & assembly of bone marrow derived progenitor cells by cytokines is the central theme.  EGF-1 is most potent angiogenic stimulant identified. Heparin is also an important as cofactor, TGF- alpha, beta, prostaglandins also stimulate.
  11. 11. Epithelialization  Basal cell layer thickening, elongation, detachment & migration via interaction with ECM proteins via integrin mediators.  Generation of a provisional BM which includes fibronectin, collagens type 1 and 3  Epithelial cells proliferation contributes new cells to the monolayer. Contact inhibition when edges come together.
  12. 12. III. Remodeling phase A. 3 weeks to 2 years B. New collagen forms which increases the tensile strength of the wound C. 19 types identified. Type 1(80-90%) most common, found in all tissue. The primary collagen in a healed wound. D. Type 3(10-20%) seen in early phases of wound healing. Type V smooth muscle, Types 2,11 cartilage, Type 4 in BM.
  13. 13. Remodelling  The number of intra and intermolecular cross- links between collagen fibers increases dramatically.  A major contributor to the increase in wound breaking strength  Quantity of Type 3 collagen decreases replaced by Type 1 collagen  Remodeling continues for 12 months, so scar revision should not be done prematurely.
  14. 14. Wound Contraction  Begins approximately 4-5 days after wounding by action of myofibroblasts.  Generally occurs in large surface wounds.  Represents centripetal movement of the wound edge towards the centre of the wound.  Maximal contraction occurs for 12-15 days, although it will continue longer if wound remains open.
  15. 15. Wound contraction  The wound edges move toward each other at an average rate of 0.6 to .75 mm/day.  Wound contraction depends on laxity of tissues, so a buttock wound will contract faster than a wound on the scalp or pretibial area.  Wound shape also a factor, square is faster than circular.
  16. 16. Wound Strength  Skin wounds  At the end of first week,wound strength is approximately 10% of unwounded skin  Wound strength increases rapidly over next 4 weeks and then slows down at approximately at third month,reaches a plataue at about 70- 80% of the tensile strength of unwounded skin  Scar tissue is ne ve r as stro ng as the o rig inal tissue !!
  17. 17. Important Growth factors responsible for wound healing  Platelet derived growth factor:  Promotes migration and proliferation of fibroblasts  Is chemotactic for monocytes  Epidermal growth factor  Promotes growth of endothelial, epithelial cells and fibroblasts
  18. 18. Growth factors in wound healing  Fibroblast growth factor:  Promotes synthesis of ECM proteins including fibronectin.  Chemotactic for fibroblasts and endothelial cells  Promotes angiogenesis  Vascular Endothelial Growth Factor (VEGF)  Angiogenesis  Macrophage derived growth factors  IL-1 and TNF  Promote proliferation of fibroblasts and endothelial cells.
  19. 19. Wound healing  Wound healing is accomplished in one of the following two ways: 1. Healing by first intention (primary union) 2. Healing by second intention (secondary union)
  20. 20. Healing by first intention (primary union)  Occurs in clean, incised wounds with good apposition of the edges – particularly planned surgical incisions  (clean wounds – no infections or foreign bodies)  The incision causes only focal disruption of epithelial basement membrane continuity and death of a relatively few epithelial and connective tissue cells.  As a result, epithelial regeneration predominates over fibrosis
  21. 21. Healing by first intention: Sequence of events
  22. 22. Immediate  The narrow incisional space rapidly fills with fibrin clotted blood  Dehydration at the surface produces a scab to cover and protect the healing repair site
  23. 23. Within 24 hrs  Movement and proliferation of epithelial cells across the wound resulting in a thin, but continuous epithelial layer  Early inflammation close to the edges (neutrophils)
  24. 24. 2-3 days  Neutrophils replaced by macrophages  Macrophages remove the blood clot  Proliferation of epithelial cells  Fibroblastic activity
  25. 25. 10-14 days  Scab loose (aka dry clot)  Epithelial covering complete  Fibrous union of edges  Wound still weak  vascularization
  26. 26. By the end of the first month  Scar comprises of a cellular connective tissue devoid of inflammatory infiltrate, covered by intact epidermis  Dermal appendages destroyed in the line of incision are permanently lost  Tensile strength of the wound increases and
  27. 27. Healing by second intention (secondary union)  This occurs in open wounds, particularly when there has been significant loss of tissue, necrosis or large wounds with irregular margins  Regeneration of parenchymal cells cannot completely reconstitute the original architecture  Abundant granulation tissue grows in from the margin to complete the repair  Granulation tissues consists of:  ECM fibroblasts  Macrophages, neutrophils  New blood vessels
  28. 28. Healing by second intention (secondary union) sequence of events
  29. 29. Early
  30. 30. A few days
  31. 31. 1 week Epithelial proliferation Capillary loops (granulations) Scab shed Loose connective Tissue formed by fibroblasts
  32. 32. 2 weeks onwards
  33. 33. Months Full thickness of Epithelium restored Varying depth of Surface depression Thick collagenous Scar tissue becoming Less vascular
  34. 34. Secondary union differs from primary union in several respects 1. inflammatory reaction is more intense 2. larger amounts of granulation tissue formation 3. larger scar 4. ***wound contraction  Myofibroblasts: modified fibroblasts with feature of SMC  defect significantly decreases in size as wound heals.
  35. 35. Factors that influence healing  Classified as A. Systemic and B. Local
  36. 36. Systemic Factors that Delay/Retard Wound Healing  Nutrition  Protein deficiency, Vitamin C deficiency  inhibit collagen synthesis  Zn deficiency (cofactor in type III collagenase)  Metabolic status  diabetes mellitus:  Susceptibility to infection caused by impaired circulation and increased glucose.  Circulatory status  inadequate blood supply  atherosclerosis, vascular defects  Hormones  glucocorticoids inhibit collagen synthesis, decrease inflammation
  37. 37. Local Factors that Delay/Retard Wound Healing  Infection  most important cause of delayed wound healing  Persistent injury and inflammation  Mechanical factors  motion early in healing  Foreign material - like suture material and foreign bodies  Size, location & type of wound  wounds in ↑vascularized areas (face) heal faster than in poorly vasc areas (tendon, feet)  small wounds heal faster than larger  incisions faster than blunt trauma (contusions)
  38. 38. Complications of wound healing 1. Deficient scar formation 2. Excessive formation of repair components 3. Exaggerated contraction
  39. 39. Deficient scar formation Can lead to two types of complications: A. Wound Dehiscence (rupture of wound)  most common after abdominal surgery coughing, vomiting, B. Ulceration - defect in the continuity
  40. 40. Wound Dehiscence
  41. 41. Excessive formation of repair components 1. Keloid / hypertrophic scar (excess collagen) 2. Exuberant granulation or proud flesh (excessive granulation tissue that protrudes above the level of the surrounding skin and impairs the growth of epithelium)
  42. 42. Keloid / hypertrophic scar  Raised scars due to accumulation of excess amounts of collagen ( type III – type I)  Hypertrophic scars do not grow beyond the boundaries of the original wound  Keloids grow beyond the boundaries of the original wound (more serious)
  43. 43. Keloid
  44. 44. Exuberant granulation (proud flesh)  Excessive granulation tissue  Protrudes above surrounding skin  Prevents re -epithelialization
  45. 45. Exaggerated contraction  deformation of surrounding tissue or wound  Can compromise the movement of joints.  most common on  palms, soles, anterior thorax following severe burns