Wound healing

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  • The three phases of wound healing are inflammation, proliferation, and maturation. The immediate response to injury is the inflammatory (also called reactive) phase. The body's defences are aimed at limiting the amount of damage and preventing further injury. The proliferative (also called regenerative or reparative) phase is the reparative process and consists of re-epithelialization, matrix synthesis, and neovascularization to relieve the ischemia of the trauma itself. The final maturational (or remodelling) phase is the period of scar contraction with collagen cross-linking, shrinking, and loss of enema. In a large wound such as a pressure sore, the eschar or fibrinous exudate reflects the inflammatory phase, the granulation tissue is part of the proliferative phase, and the contracting or advancing edge is part of the maturational phase. All three phases may occur simultaneously, and the phases with their individual processes may overlap (
  • Exposure of sub endothelial collagen to platelets results in platelet aggregation, degranulation, and activation of the coagulation cascade. Platelet -granules release a number of wound-active substances, such as platelet-derived growth factor (PDGF), transforming growth factor beta (TGF), platelet-activating factor, fibronectin, and serotonin. In addition to achieving haemostasis, the fibrin clot serves as scaffolding for the migration into the wound of inflammatory cells such as polymorphonuclear leukocytes (PMNs, neutrophils) and monocytes.
  • Cellular infiltration after injury follows a characteristic, predetermined sequence (see Fig. 9-1). PMNs are the first infiltrating cells to enter the wound site, peaking at 24 to 48 hours. Increased vascular permeability, local prostaglandin release, and the presence of chemotactic substances, such as complement factors, interleukin-1 (IL-1), tumour necrosis factor alpha (TNF-), TGF, platelet factor 4, or bacterial products, all stimulate neutrophil migrationmacrophages achieve significant numbers in the wound by 48 to 96 hours post injury and remain present until wound healing is complete.
  • 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, IFN- Enzymes: arginase, collagenase Prostaglandins Nitric oxide Angiogenesis Growth factors: FGF, VEGF Cytokines: TNF- Nitric oxide
  • T lymphocytes comprise another population of inflammatory/immune cells that routinely invades the wound. Less numerous than macrophages, T-lymphocyte numbers peak at about 1 week post injury and truly bridge the transition from the inflammatory to the proliferative phase of healing. Although known to be essential to wound healing, the lymphocytes' role in wound healing is not fully defined
  • Fixed basal cells in a zone near the cut edge undergo a series of rapid mitotic divisions, and these cells appear to migrate by moving over one another in a leapfrog fashion until the defect is covered.22 Once the defect is bridged, the migrating epithelial cells lose their flattened appearance, become more columnar in shape, and increase their mitotic activity. Layering of the epithelium is re-established, and the surface layer eventually keratinizes.23
  • Wound healing

    1. 1. Wound Healing<br />Dr. Ranjeet Patil<br />
    2. 2. Definition<br />Regeneration<br />Replacement of dead or damaged cells by functioning cells of same structure and function<br />Bones, Liver<br />Repair<br />Replacement of dead or damaged cells by granulation tissue which matures to form scar<br />Function is lost-Lower order cells<br />Skin<br />None<br />Brain, Skeletal muscle, Cardiac muscle<br />
    3. 3. Wound closure types <br />Primary<br />First-intention<br />Closure, the wounds are sealed immediately with simple suturing, skin graft placement, or flap closure<br />Closure at end of a surgical procedure.<br />Secondary<br />Spontaneous-intention, no active intent to seal the wound<br />Closes by re-epithelialization, contraction of the wound<br />Highly contaminated wound<br />Tertiary <br />Initially treated by repeated debridement, systemic or topical antibiotics, or negative pressure wound therapy for several days to control infection<br />Surgical intervention, such as suturing, skin graft placement, or flap design, is performed<br />
    4. 4.
    5. 5. WOUND-HEALING PHASES<br />Inflammation<br />Reactive phase<br />The body's defences are aimed at limiting the amount of damage and preventing further injury<br />Eschar or fibrinous exudate<br />Upto 6 days<br />
    6. 6. Inflammation<br />Haemostasis<br />platelet aggregation, degranulation, and activation of the coagulation cascade<br />platelet-derived growth factor (PDGF), transforming growth factor beta (TGF), platelet-activating factor, fibronectin, and serotonin<br />Increased Vascular Permeability<br />
    7. 7. Inflammation<br />Inflammation<br />PMN <br />24 to 48 hours<br />Prostaglandins, complement factors, interleukin-1 (IL-1), tumour necrosis factor alpha (TNF-), TGF, platelet factor 4, bacterial products<br />primary role-phagocytosis of bacteria and tissue debris<br />angiogenesis and collagen synthesis <br />
    8. 8. Macrophages <br />48 to 96 hours – complete healing<br />Phagocytosis <br />Reactive oxygen species, Nitric oxide <br />Debridement <br />Collagenase, elastase <br />Cell recruitment and activation <br />Growth factors: PDGF, TGF, EGF, IGF Cytokines: TNF-, IL-1, IL-6, Fibronectin <br />Matrix synthesis <br />Growth factors: TGF, EGF, PDGF, Cytokines: TNF-, IL-1, Enzymes: arginase, collagenase, Prostaglandins, Nitric oxide <br />Angiogenesis <br />Growth factors: FGF, VEGF , Cytokines: TNF, Nitric oxide <br />
    9. 9. T lymphocytes <br />Less numerous than macrophages<br />Peak at about 1 week post injury<br /> role in wound healing is not fully defined<br />
    10. 10. Proliferation<br />Proliferation<br />Regenerative or reparative phase<br />Consists of re-epithelialization, matrix synthesis, and neovascularization to relieve the ischemia of the trauma itself<br />Granulation tissue<br />4-14 days<br />
    11. 11. Fibroblasts<br />synthesize collagen<br />actively carry out matrix contraction<br />Endothelial cells<br />Formation of new capillaries (angiogenesis)<br />
    12. 12.
    13. 13. Maturation <br />Remodelling phase <br />Scar contraction with collagen cross-linking, shrinking, and loss of oedema<br />Contracting or advancing edge<br />8th day- months<br />
    14. 14. Remodelling<br />21 days up to 1 year<br />Collagen remodeling is also characteristic of this phase.<br />Type III collagen is initially laid down, replaced by type I collagen<br />
    15. 15. Epithelialization<br />1st day<br />Rapid mitotic divisions<br />Defect is bridged<br />Layering of the epithelium<br />Keratinisation <br />
    16. 16.
    17. 17.
    18. 18.
    19. 19. Abnormalities of Wound Healing<br />
    20. 20. Delaying Factors<br />Systemic <br />Age <br />Nutrition <br />Trauma <br />Metabolic diseases <br />Immunosuppression <br />Connective tissue disorders <br />Smoking <br />Local <br />Mechanical injury <br />Infection <br />Edema<br />Ischemia/necrotic tissue <br />Topical agents <br />Ionizing radiation <br />Low oxygen tension <br />Foreign bodies <br />
    21. 21. Excess Healing<br /><ul><li>Hepatic cirrhosis, Pulmonary Fibrosis, Scleroderma, Retrolental Fibroplasia, Diabetic Retinopathy, Osteoarthritis</li></ul>Hypertrophic scar<br />Defined as excessive scar tissue that does not extend beyond the boundary of the original incision or wound<br />Prolonged inflammatory phase<br />Keloid<br />Defined as excessive scar tissue that extends beyond the boundaries of the original incision or wound<br />Aetiology is unknown<br />Both hypertrophic and keloid scars shows excess collagen with hypervascularity, but this is more marked in keloids where there is more type B collagen<br />
    22. 22. Treatment<br />Treatment of hypertrophic and keloid scars<br />Pressure – local moulds or elasticated garments<br />Silicone gel sheeting (mechanism unknown)<br />Intralesionalsteroid injection (triamcinolone)<br />Excision and steroid injection<br />Excision and postoperative radiation (external beam or brachytherapy)<br />Intralesionalexcision (keloids only)<br />Laser – to reduce redness (which may resolve in any event)<br />Vitamin E or palm oil massage (unproven)<br />
    23. 23. Contractures<br />Where scars cross joints or flexion creases, a tight web may form restricting the range of movement at the joint<br />Hyperextension or hyperflexion deformity<br />Treatment may be simple involving multiple Z-plasties<br />
    24. 24.
    25. 25. Thankyou<br />

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