Wound Healing & Wound Care

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  • Very thorough review of wounds and their progression, including difficult wounds. An important point to make however, is that honey and not just Manuka, has anti-inflammatory and antimicrobial properties to speed wound healing. The use of Thyme Honey in a hospital setting at Limoges France by Prof. Descottes, validated the efficacy in vivo. He conducted parallel treatments on the same wound using pharmacological products or honey for 25 years and the results were faster and better healing with honey usage. There are other monofloral honeys that are also known and documented to possess highly effective healing properties, namely raw honey that hasn't been heated or highly filtered. For more info on recent studies, http://beehealthyfarms.blogspot.fr
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Wound Healing & Wound Care

  1. 1. Wound Healing & Wound Care Souvik Adhikari Postdoctoral Trainee
  2. 2. DEFINITION <ul><li>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. </li></ul><ul><li>Can be achieved by 2 processes: scar formation & tissue regeneration. </li></ul><ul><li>Dynamic balance between these 2 is different in different tissues. </li></ul>
  3. 3. Introduction <ul><li>During healing, a complex cascade of cellular events occur to achieve resurfacing, reconstitution and restoration of tensile strength of injured tissue. </li></ul><ul><li>3 classic but overlapping phases occur: inflammation, proliferation & maturation. </li></ul>
  4. 4. Early Wound Healing Events (Days 1-4)
  5. 5. Stages of Wound Healing
  6. 6. Inflammatory Phase <ul><li>Blood vessels are disrupted, resulting in bleeding. Hemostasis is achieved by formation of platelet plug & activation of extrinsic & intrinsic clotting pathways. </li></ul><ul><li>Formation of a provisional fibrin matrix. </li></ul><ul><li>Recruitment of inflammatory cells into the wound by potent chemoattractants. </li></ul>
  7. 8. Early Events in Inflammation <ul><li>Fibrin and fibronectin form a lattice that provides scaffold for migration of inflammatory, endothelial, and mesenchymal cells. </li></ul><ul><li>Neutrophilic infiltrate appears: removes dead tissue & prevent infection. </li></ul><ul><li>Monocytes/macrophages follow neutrophils: orchestrated production of growth factors & phagocytosis. </li></ul>
  8. 13. Late Events in Inflammation <ul><li>Entry of lymphocytes. </li></ul><ul><li>Appearance of mast cell: aberrant scarring? </li></ul>
  9. 14. Intermediate Events (Days 4-21)
  10. 15. Proliferative Phase <ul><li>Granulation tissue formation (composed of fibroblasts, macrophages and emdothelial cells). </li></ul><ul><li>Contraction. </li></ul><ul><li>Re-epithelialization (begins immediately after injury) </li></ul>
  11. 17. Mesenchymal cell proliferation <ul><li>Fibroblasts are the major mesenchymal cells involved in wound healing, although smooth muscle cells are also involved. </li></ul><ul><li>Macrophage products are chemotactic for fibroblasts. PDGF, EGF, TGF, IL-1, lymphocytes are as well. </li></ul><ul><li>Replacement of provisional fibrin matrix with type III collagen. </li></ul>
  12. 18. Angiogenesis <ul><li>Angiogenesis reconstructs vasculature in areas damaged by wounding, stimulated by high lactate levels, acidic pH, decreased O2 tension in tissues. </li></ul><ul><li>Recruitment & assembly of bone marrow derived progenitor cells by cytokines is the central theme. </li></ul><ul><li>FGF-1 is most potent angiogenic stimulant identified. Heparin important as cofactor, TGF-alpha, beta, prostaglandins also stimulate. </li></ul>
  13. 20. Epithelialization <ul><li>Basal cell layer thickening, elongation, detachment & migration via interaction with ECM proteins via integrin mediators. </li></ul><ul><li>Generation of a provisional BM which includes fibronectin, collagens type 1 and 5. </li></ul><ul><li>Epithelial cells proliferation contributes new cells to the monolayer. Contact inhibition when edges come together. </li></ul>
  14. 22. Late Wound Healing Events (Days 21-1 yr)
  15. 23. Remodeling Phase <ul><li>Programmed regression of blood vessels & granulation tissue. </li></ul><ul><li>Wound contraction. </li></ul><ul><li>Collagen remodeling. </li></ul>
  16. 26. Collagen <ul><li>19 types identified. Type 1(80-90%) most common, found in all tissue. The primary collagen in a healed wound. </li></ul><ul><li>Type 3(10-20%) seen in early phases of wound healing. Type V smooth muscle, Types 2,11 cartilage, Type 4 in BM. </li></ul>
  17. 28. Wound Contraction <ul><li>Begins approximately 4-5 days after wounding by action of myofibroblasts. </li></ul><ul><li>Represents centripetal movement of the wound edge towards the center of the wound. </li></ul><ul><li>Maximal contraction occurs for 12-15 days, although it will continue longer if wound remains open. </li></ul>
  18. 29. Wound Contraction <ul><li>The wound edges move toward each other at an average rate of 0.6 to .75 mm/day. </li></ul><ul><li>Wound contraction depends on laxity of tissues, so a buttock wound will contract faster than a wound on the scalp or pretibial area. </li></ul><ul><li>Wound shape also a factor, square is faster than circular. </li></ul>
  19. 30. Wound Contraction <ul><li>Contraction of a wound across a joint can cause contracture. </li></ul><ul><li>Can be limited by skin grafts, full better than split thickness. </li></ul><ul><li>The earlier the graft the less contraction. </li></ul><ul><li>Splints temporarily slow contraction. </li></ul>
  20. 31. Remodeling <ul><li>After 21 days, net accumulation of collagen becomes stable. Bursting strength is only 15% of normal at this point. Remodeling dramatically increases this. </li></ul><ul><li>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. </li></ul>
  21. 32. Remodeling <ul><li>The number of intra and intermolecular cross-links between collagen fibers increases dramatically. </li></ul><ul><li>A major contributor to the increase in wound breaking strength. </li></ul><ul><li>Quantity of Type 3 collagen decreases replaced by Type 1 collagen </li></ul><ul><li>Remodeling continues for 12 mos, so scar revision should not be done prematurely. </li></ul>
  22. 34. Disturbances in Wound Healing
  23. 35. Local Factors <ul><li>Infection: impairs healing. </li></ul><ul><li>Smoking: increased platelet adhesiveness, decreased O2 carrying capacity of blood, abnormal collagen. </li></ul><ul><li>Radiation: endarteritis, abnormal fibroblasts. </li></ul>
  24. 36. Systemic Factors <ul><li>Malnutrition </li></ul><ul><li>Cancer </li></ul><ul><li>Old Age </li></ul><ul><li>Diabetes- impaired neutrophil chemotaxis, phagocytosis. </li></ul><ul><li>Steroids and immunosuppression suppresses macrophage migration, fibroblast proliferation, collagen accumulation, and angiogenesis. Reversed by Vitamin A 25,000 IU per day. </li></ul>
  25. 37. Abnormal Response to Injury
  26. 38. Inadequate Regeneration <ul><li>CNS injuries </li></ul><ul><li>Bone nonunion </li></ul><ul><li>Corneal ulcers </li></ul>
  27. 39. Inadequate Scar Formation <ul><li>Diabetic foot ulcers. </li></ul><ul><li>Sacral pressure sores. </li></ul><ul><li>Venous stasis ulcers. </li></ul>
  28. 40. Excessive Regeneration <ul><li>Neuroma </li></ul><ul><li>Hyperkeratosis in cutaneous psoriasis </li></ul><ul><li>Adenomatous polyp formation. </li></ul>
  29. 41. Excessive Scar Formation <ul><li>Excessive healing results in a raised, thickened scar, with both functional and cosmetic complications. </li></ul><ul><li>If it stays within margins of wound it is hypertrophic. Keloids extend beyond the confines of the original injury. </li></ul><ul><li>Dark skinned, ages of 2-40. Wound in the presternal or deltoid area, wounds that cross langerhans lines. </li></ul>
  30. 42. Keloids and Hypertrophic Scars <ul><li>Keloids more familial </li></ul><ul><li>Hypertrophic scars develop soon after injury, keloids up to a year later. </li></ul><ul><li>Hypertrophic scars may subside in time, keloids rarely do. </li></ul><ul><li>Hypertrophic scars more likely to cause contracture over joint surface. </li></ul>
  31. 43. Keloids and Hypertrophic Scars <ul><li>Both from an overall increase in the quantity of collagen synthesized. </li></ul><ul><li>Recent evidence suggests that the fibroblasts within keloids are different from those within normal dermis in terms of their responsiveness. </li></ul><ul><li>No modality of treatment is predictably effective for these lesions. </li></ul>
  32. 44. Wound Care
  33. 45. Basics <ul><li>Optimize systemic parameters </li></ul><ul><li>Debride nonviable tissue </li></ul><ul><li>Reduce wound bioburden </li></ul><ul><li>Optimize blood flow </li></ul><ul><li>Reduce edema </li></ul><ul><li>Use dressings appropriately </li></ul><ul><li>Use pharmacologic therapy </li></ul><ul><li>Close wounds with grafts/flaps as indicated </li></ul>
  34. 46. Optimize systemic parameters <ul><li>Age: cannot be reversed, usage of growth factors, aggressive optimization of systemic parameters & supplementation. </li></ul><ul><li>Avoidance of ischemia & malnutrition. </li></ul><ul><li>Correction of diabetes, removal of FB. </li></ul><ul><li>Avoidance of steroids, alcohol, smoking. </li></ul><ul><li>Avoidance of reperfusion injury: total contact casting, compression therapy. </li></ul>
  35. 47. Debridement & Reduction of Bioburden <ul><li>Surface irrigation with saline. </li></ul><ul><li>Debridement: surgical, enzymatic (papain with urea, collagenase), mechanical (pressurized water jet), autolytic, maggots. </li></ul><ul><li>Antibiotics: cellulitis, decreased rate of healing, increased pain, straw colored oozing from skin, contaminated wounds, mechanical implants. </li></ul><ul><li>Removal of FB. </li></ul>
  36. 48. Optimize blood flow & oxygen supply <ul><li>Warmth </li></ul><ul><li>Hydration </li></ul><ul><li>Surgical revascularization </li></ul><ul><li>Hyperbaric O2 therapy: limb salvage. </li></ul>
  37. 49. Reduce edema <ul><li>Elevation </li></ul><ul><li>Compression </li></ul><ul><li>Negative pressure wound therapy: removes pericellular transudate & wound exudate as well as deleterious enzymes. Cannot be used in ischemic, badly infected or inadequately debrided wounds or in malignancy. </li></ul>
  38. 50. Dressings <ul><li>Absorption characteristics: none – films, low – hydrogels, moderate - hydrocolloids, high – foams, alginates, collagen. </li></ul><ul><li>Hydrogels (eg. starch) rehydrate wounds (benefit in small amounts of eschar, infected wounds). </li></ul><ul><li>Hydrocolloids promote wound debridement by autolysis. </li></ul><ul><li>Antimicrobial dressings: silver, cadexomer iodine, mupirocin, neomycin. </li></ul>
  39. 51. Skin Substitutes <ul><li>Autologous keratinocyte sheets. </li></ul><ul><li>Biobrane </li></ul><ul><li>Oasis </li></ul><ul><li>Alloderm </li></ul><ul><li>Integra (sites prone to contracture, coverage of tendons, bone, surgical hardware) </li></ul><ul><li>TransCyte </li></ul><ul><li>Dermagraft </li></ul><ul><li>Orcel </li></ul>
  40. 52. Pharmacologic therapy <ul><li>Antimicrobials </li></ul><ul><li>PDGF </li></ul><ul><li>EGF </li></ul><ul><li>VEGF </li></ul><ul><li>Vit A: steroid use </li></ul><ul><li>Absolutely of no use in normally healing wounds </li></ul>
  41. 53. Flaps & Grafts <ul><li>Radiation wounds require flaps. </li></ul><ul><li>Chronic nonhealing ulcers. </li></ul><ul><li>Extensive areas of ulceration. </li></ul><ul><li>Major soft tissue loss. </li></ul><ul><li>Other therapies: electrical stimulation for recalcitrant ulcers. </li></ul>
  42. 54. Recent Developments <ul><li>Manuka honey (apitherapy) in venous leg ulcers. </li></ul><ul><li>Hyperbranched polyglycerol electrospun nanofibers. </li></ul><ul><li>Androstenediol in steroid inhibited healing. </li></ul><ul><li>GM-CSF hydrogel in deep 2 nd deg burns. </li></ul><ul><li>LASER therapy enhances tissue repair? </li></ul><ul><li>Nitric oxide containing nanoparticles. </li></ul>
  43. 55. THANK YOU

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