Wound healing dr sumer

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wound healing

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Wound healing dr sumer

  1. 1. Dr sumer yadav
  2. 2. wound Any violation of live tissue integrity may be regarded as a wound Skin is the largest organ of the human body. Acute wound- orderly and timely reparative process - laceration, puncture, abrasion, avulsion, amputation, contusion Chronic wound – wound not healed in 4 weeks. Venous and arterial ulcers, diabetic ulcers, pressure ulcers.
  3. 3. Three techniques of wound treatment Primary intention- all tissue including skin are closed with suture material. Secondary intention – in which wound is left open and close naturally. Tertiary intention – in which wound is left open for number of days and then closed if it found to be clean.
  4. 4. DEFINITION – wound healing Response of an organism to a physical disruption of a tissue/organ with an aim to repair or reconstitute the defect and to re-establish homeostasis. Can be achieved by 2 processes: scar formation & tissue regeneration. Dynamic balance between these 2 is different in different tissues.
  5. 5. Introduction During healing, a complex cascade of cellular events occur to achieve resurfacing, reconstitution and restoration of tensile strength of injured tissue. 3 classic but overlapping phases occur: inflammation, proliferation & maturation.
  6. 6. Phases of Healing Inflammatory (Reactive) Haemostasis Inflammation Proliferative (Regenerative/Reparative) Epithelial migration proliferation Maturation Maturational (Remodeling) Contraction scarring Remodeling
  7. 7. Early Wound Healing Events (Days 1-4) A. Inflammatory or reactive phase - immediate response to injury - goals: hemostasis, debridement , sealing of the wound Events 1. Increase vascular permeability 2. Chemotaxis 3. Secretion of cytokines 4. Growth factor
  8. 8. Inflammatory Phase Blood vessels are disrupted, resulting in bleeding. Hemostasis is achieved by formation of platelet plug & activation of extrinsic(initiation) & intrinsic clotting(amplification) pathways. Formation of a provisional fibrin matrix. Recruitment of inflammatory cells into the wound by potent chemoattractants.
  9. 9. Inflammatory phase 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.
  10. 10. Inflammatory cells PMN - Migration of PMN stops when wound contamination has been controlled - Don’t survive more than 24 hours - Increase contamination stimulates PMN resulting to delayed wound healing and destruction of tissues. - Not essential for wound healing
  11. 11. Inflammatory cells Macrophages - Orchestrate release of cytokines/ Process of wound healing/ release of growth factors - 24 – 48 hours - Source of TNF /interleukin 1, 6, 8
  12. 12. Macrophage Activities During Wound Healing Activity Mediators Phagocytosis Reactive oxygen species Nitric oxide Débridement Collagenase, elastase Cell recruitment and activation Growth factors: PDGF, TGF-, EGF, IGF Cytokines: TNF-, IL-1, IL-6 Fibronectin Growth factors: TGF-, EGF, PDGF Cytokines: TNF-, IL-1, IFNEnzymes: arginase, collagenase Prostaglandins Nitric oxide Growth factors: FGF, VEGF Cytokines: TNFNitric oxide Matrix synthesis Angiogenesis
  13. 13. Table 8-2 Growth Factors Participating in Wound Healing Growth Factor Plateletderived growth factor (PDGF) Fibroblast growth factor (FGF) Wound Cell Origin Platelets, macrophages, monocytes, smooth muscle cells, endothelial cells Cellular and Biological Effects Chemotaxis: fibroblasts, smooth muscle, monocytes, neutrophils Mitogenesis: fibroblasts, smooth muscle cells Stimulation of angiogenesis Stimulation of collagen synthesis Fibroblasts, endothelial Stimulation of angiogenesis cells, smooth muscle (by stimulation of cells, chondrocytes endothelial cell proliferation and migration) Mitogenesis: mesoderm and neuroectoderm Stimulates fibroblasts,
  14. 14. Wound Healing Keratinocyte growth factor (KGF) Keratinocytes, fibroblasts Significant homology with FGF; stimulates keratinocytes Epidermal growth factor (EGF) Platelets, macrophages, monocytes (also identified in salivary glands, duodenal glands, kidney, and lacrimal glands) Stimulates proliferation and migration of all epithelial cell types Transforming growth factor- B (TGF- B ) Keratinocytes, platelets, macrophages Homology with EGF; binds to EGF receptor Mitogenic and chemotactic for epidermal and endothelial cells Transforming growth factor- alpha (TGFalpha ) (3 isoforms: , , ) 1 2 3 Platelets, T lymphocytes, macrophages, monocytes, neutrophils Stimulates angiogenesis TGFstimulates wound 1 matrix production (fibronectin, collagen glycosaminoglycans); regulation of inflammation TGF- 3 inhibits scar
  15. 15. Late Events in Inflammation Entry of lymphocytes. Appearance of mast cell: aberrant scarring?
  16. 16. Inflammatory cells Lymphocytes - Peak on 7th day - Affects fibroblast - Stimulate cytokines - Not essential for acute wound healing
  17. 17. B. Proliferative phase Goal: granulation tissue formation Events: 1.Angiogenesis 2.Fibroplasia 3.Epithelization
  18. 18. Proliferative Phase Granulation tissue formation (composed of fibroblasts, macrophages and emdothelial cells). Contraction. Re-epithelialization (begins immediately after injury) Decrease collagen synthesis at 4 weeks after injury
  19. 19. Proliferative phase Extracellular matrix - Scaffold for cellular migration - Composed of fibrin, fibrinogen, fibronectin, vitronectin Fibronectin and type 3 collagen = early matrix Type 1 collagen – wound strength later
  20. 20. Proliferative phase Hydroxylation results in stable triple stranded helix Vitamin C, TGF B, IgF 1, IgF 2- increase collagen synthesis Interferon Y , steroids – decreases collagen synthesis
  21. 21. 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.
  22. 22. 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. FGF-1 is most potent angiogenic stimulant identified. Heparin important as cofactor, TGFalpha, beta, prostaglandins also stimulate.
  23. 23. 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 5. Epithelial cells proliferation contributes new cells to the monolayer. Contact inhibition when edges come together. By three keratinocyte functions – migration , proliferation and differentiation.
  24. 24. Remodeling Phase Goal: scar contraction with collagen cross- linking, shrinking and loss of edema Programmed regression of blood vessels & granulation tissue. Wound contraction. Collagen remodeling.
  25. 25. Maturation phase Wound contraction – centripetal movement of full thickness of skin Decreases amount of disorganized scar Wound contracture, physical restriction, limitation of function- result of wound contraction Appearance of stimulated fibroblast known as myofibroblast
  26. 26. Fetal Wound Healing  Younger the fetus less noticeable is the scar  Fetal fibroblasts even in adult transplantation heals with the absence of inflammation  Theory: that wound fibroblasts do not become myofibroblasts until late in gestation.  IL6 is high in adult stimulated fibroblasts compared to fetal stimulated ones with coincides with increased inflammation in adults  Thrombospondin 1 decreases with increase in gestation. It destabilizes matrix contracts in the EC space, facilitates mitogenesis and chemotaxis. Promotes cell associated protease and self supports matrix turnover. Thus inflammation would decrease and there would be less scarring
  27. 27. Collagen 19 types identified. Type 1(80-90%) most common, found in all tissue. The primary collagen in a healed wound. Type 3(10-20%) seen in early phases of wound healing. Type V smooth muscle, Types 2,11 cartilage, Type 4 in BM.
  28. 28. Wound Contraction Begins approximately 4-5 days after wounding by action of myofibroblasts. Represents centripetal movement of the wound edge towards the center of the wound. Maximal contraction occurs for 12-15 days, although it will continue longer if wound remains open.
  29. 29. 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.
  30. 30. Wound Contraction Contraction of a wound across a joint can cause contracture. Can be limited by skin grafts, full better than split thickness. The earlier the graft the less contraction. Splints temporarily slow contraction.
  31. 31. Remodeling After 21 days, net accumulation of collagen becomes stable. Bursting strength is only 15% of normal at this point. Remodeling dramatically increases this. 3-6 weeks after wounding greatest rate of increase, so at 6 weeks we are at 80% to 90% of eventual strength and at 6months 90% of skin breaking strength.
  32. 32. Remodeling 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 mos, so scar revision should not be done prematurely.
  33. 33. Local Factors Iscemia Infection: impairs healing. Smoking: increased platelet adhesiveness, decreased O2 carrying capacity of blood, abnormal collagen. Radiation: endarteritis, abnormal fibroblasts.
  34. 34. Systemic Factors Malnutrition Cancer Old Age Diabetes- impaired neutrophil chemotaxis, phagocytosis. Steroids and immunosuppression suppresses macrophage migration, fibroblast proliferation, collagen accumulation, and angiogenesis. Reversed by Vitamin A 25,000 IU per day.
  35. 35. Inadequate Regeneration CNS injuries Bone nonunion Corneal ulcers
  36. 36. Inadequate Scar Formation Diabetic foot ulcers. Sacral pressure sores. Venous stasis ulcers.
  37. 37. Excessive Regeneration Neuroma Hyperkeratosis in cutaneous psoriasis Adenomatous polyp formation.
  38. 38. Excessive Scar Formation Excessive healing results in a raised, thickened scar, with both functional and cosmetic complications. If it stays within margins of wound it is hypertrophic. Keloids extend beyond the confines of the original injury. Dark skinned, ages of 2-40. Wound in the presternal or deltoid area, wounds that cross langerhans lines.
  39. 39. Keloids and Hypertrophic Scars Keloids more familial Hypertrophic scars develop soon after injury, keloids up to a year later. Hypertrophic scars may subside in time, keloids rarely do. Hypertrophic scars more likely to cause contracture over joint surface.
  40. 40. Keloids and Hypertrophic Scars Both from an overall increase in the quantity of collagen synthesized. Recent evidence suggests that the fibroblasts within keloids are different from those within normal dermis in terms of their responsiveness. No modality of treatment is predictably effective for these lesions.

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