Successfully reported this slideshow.

Wound Healing & Wound Care

202

Share

Upcoming SlideShare
Wound and wound healing
Wound and wound healing
Loading in …3
×
1 of 55
1 of 55

More Related Content

Related Books

Free with a 14 day trial from Scribd

See all

Related Audiobooks

Free with a 14 day trial from Scribd

See all

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

×