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5.1 Wounds, normal wound healing and factors affecting healing (2).pptx

  1. Wound healing and factors affecting healing Dr Preetinder Brar
  2. Wounds, healing and tissue repair 5.1 Describe normal wound healing and factors affecting wound healing 5.2 Elicit, document and present a history in a patient presenting with wounds 5.3 Differentiate various types of wounds, plan and observe management of wounds
  3. Wound healing • Wound healing is a mechanism whereby the body attempts to restore the integrity of the injured part. • However, this falls far short of the regeneration of tissue by pluripotent cells, seen in some amphibians.
  4. Wound healing It is often detrimental, as seen in the problems created by scarring such as • Adhesions, • Keloids, • Contractures and • Cirrhosis of the liver. However, a clean incised wound in a healthy person where there is no skin loss will follow a set pattern.
  5. Wound healing NORMAL WOUND HEALING • This is variously described as taking place in 3 or 4 phases, the most commonly agreed being: 1. The inflammatory phase; 2. The proliferative phase; 3. The remodelling phase (maturing phase).
  6. Normal wound healing • Occasionally, a haemostatic phase is referred to as occurring before the inflammatory phase, or a destructive phase following inflammation consisting of the cellular cleansing of the wound by macrophages.
  7. Normal wound healing • The inflammatory phase begins immediately after wounding and lasts 2-3 days. • Bleeding is followed by vasoconstriction and thrombus formation to limit blood loss. • Platelets stick to the damaged endothelial lining of vessels, releasing adenosine diphosphate (ADP), which causes thrombocytic aggregates to fill the wound.
  8. (a) Early inflammatory phase with platelet-enriched blood clot and dilated vessels.
  9. Normal wound healing • When bleeding stops, the platelets then release several cytokines from their alpha granules.
  10. Normal wound healing 1. Platelet derived growth factor (PDGF), 2. Platelet factor IV and 3. Transforming growth factor beta (TGFβ). • These attract inflammatory cells such as polymorphonuclear lymphocytes (PMN) and macrophages.
  11. Normal wound healing • Platelets and the local injured tissue release vasoactive amines such as 1. Histamine, 2. Serotonin and 3. Prostaglandins, which increase vascular permeability, thereby aiding infiltration of these inflammatory cells.
  12. (b) Late inflammatory phase with increased vascularity and increase in polymorphonuclear cells and lymphocytes (round cells)
  13. Normal wound healing • Macrophages remove devitalised tissue and micro-organisms while regulating fibroblast activity in the proliferative phase of healing. • The initial framework for structural support of cells is provided by fibrin produced by fibrinogen. • A more historical (Latin) description of this phase is described in 4 words: rubor (redness), tumor (swelling), calor (heat) and dolor (pain).
  14. Normal wound healing The proliferative phase lasts from the 3rd day to the 3rd week consists of 1. Fibroblastic activity with the production of collagen and ground substance (glycosaminoglycans and proteoglycans) 2. The growth of new blood vessels as capillary loops (angioneogenesis) 3. Re-epithelialisation of the wound surface.
  15. Normal wound healing • Fibroblasts require vitamin C to produce collagen. • The wound tissue formed in the early part of this phase is called granulation tissue. • In the latter part of this phase, there is an increase in the tensile strength of the wound due to increased collagen, which is at first deposited in a random fashion and consists of type III collagen.
  16. Normal wound healing • This proliferative phase with its increase of collagen deposition is associated with wound contraction, which can considerably reduce the surface area of a wound over the first 3 weeks of healing.
  17. (c) Proliferative phase with capillary buds and fibroblasts.
  18. Normal wound healing The remodelling phase is characterised by maturation of collagen (type I replacing type III until a ratio of 4:1 is achieved). • There is realignment of collagen fibres along the lines of tension, decreased wound vascularity and wound contraction due to fibroblast and myofibroblast activity.
  19. Normal wound healing • This maturation of collagen leads to increased tensile strength in the wound which is maximal at the 12th week post injury and represents approximately 80% of the uninjured skin strength.
  20. (d) Mature contracted scar.
  21. Wounds, healing and tissue repair NORMAL HEALING IN SPECIFIC TISSUES • Bone • Nerve • Tendon
  22. Normal healing in specific tissues Bone • The phases are the same, but periosteal and endosteal proliferation leads to callus formation, which is immature bone consisting of osteoid (mineralised by hydroxyapatite and laid down by osteoblasts). • In the remodelling phase, cortical structure and the medullary cavity are restored.
  23. Normal healing in specific tissues • If fracture ends are accurately opposed and rigidly fixed, callus formation is minimal and primary healing occurs. • If a gap exists, then secondary healing may lead to delayed union, non-union or malunion.
  24. Normal healing in specific tissues Nerve • Distal to the wound, Wallerian degeneration occurs. • Proximally, the traumatic degeneration extends as far as the last node of Ranvier. • The regenerating nerve fibres are attracted to their receptors by neurotropism, which is mediated by growth factors, hormones and other extracellular matrix trophins.
  25. Normal healing in specific tissues • Nerve regeneration is characterised by profuse growth of new nerve fibres which sprout from the cut proximal end. • Overgrowth of these, coupled with poor approximation, may lead to neuroma formation.
  26. Normal healing in specific tissues Tendon • While following the normal pattern of wound healing, there are two main mechanisms whereby nutrients, cells and new vessels reach the severed tendon. 1. Intrinsic, which consist of vincular blood flow and synovial diffusion
  27. Normal healing in specific tissues 2. Extrinsic, which depends on the formation of fibrous adhesions between the tendon and the tendon sheath. • The random nature of the initial collagen produced means that the tendon lacks tensile strength for the first 3-6 weeks.
  28. Normal healing in specific tissues • Active mobilisation prevents adhesions limiting range of motion, but the tendon must be protected by splintage in order to avoid rupture of the repair.
  29. Wound healing ABNORMAL HEALING • Some of the adverse influences on wound healing are listed below:
  30. Factors influencing wound healing • Site of wound • Structures involved • Mechanism of wounding • Incision • Crush • Crush avulsion • Contamination (foreign bodies/bacteria) • Loss of tissue • Other local factors • Vascular insufficiency (arterial or venous) • Previous radiation • Pressure • Systemic factors • Malnutrition or vitamin and mineral deficiencies • Disease (e.g. diabetes mellitus) • Medications (e.g. steroids) • Immune deficiencies (e.g. chemotherapy, AIDS) • smoking
  31. Abnormal healing • Delayed healing may result in loss of function or poor cosmetic outcome. • The aim of treatment is to achieve healing by primary intention and so reduce the inflammatory and proliferative responses.
  32. Classification of wound closure and healing • Primary intention – Wound edges apposed – Normal healing – Minimal scar • Secondary intention – Wound left open – Heals by granulation, contraction and epithelialisation – Increased inflammation and proliferation – Poor scar • Tertiary intention (also called delayed primary intention) – Wound initially left open – Edges later opposed when healing conditions favourable
  33. Abnormal healing Healing by primary intention is also known as healing by first intention. • This occurs when there is apposition of the wound edges and minimal tissue trauma that causes least inflammation and leaves the best scar.
  34. Abnormal healing • Delayed primary intention healing occurs when the wound edges are not opposed immediately, which may be necessary in contaminated or untidy wounds.
  35. Abnormal healing • The inflammatory and proliferative phases of healing have become well advanced when closure of the wound is carried out. • This is also called healing by tertiary intention in some texts and will result in a less satisfactory scar than after healing by primary intention.
  36. Abnormal healing Secondary healing or healing by secondary intention occurs in the wound that is left open and allowed to heal by granulation, contraction and epithelialisation.
  37. THE END