wound healing & wound care

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Wound Healing & Wound Care Souvik Adhikari Postdoctoral Trainee

Author: souvik-adhikari

Post on 07-May-2015




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  • 1.Wound Healing & Wound Care Souvik Adhikari Postdoctoral Trainee


  • 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.

3. 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.

4. Early Wound Healing Events (Days 1-4) 5. Stages of Wound Healing 6. Inflammatory Phase

  • Blood vessels are disrupted, resulting in bleeding. Hemostasis is achieved by formation of platelet plug & activation of extrinsic & intrinsic clotting pathways.
  • Formation of a provisional fibrin matrix.
  • Recruitment of inflammatory cells into the wound by potent chemoattractants.

7. 8. Early Events in Inflammation

  • 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.

9. 10. 11. 12. 13. Late Events in Inflammation

  • Entry of lymphocytes.
  • Appearance of mast cell: aberrant scarring?

14. Intermediate Events (Days 4-21) 15. Proliferative Phase

  • Granulation tissue formation (composed of fibroblasts, macrophages and emdothelial cells).
  • Contraction.
  • Re-epithelialization (begins immediately after injury)

16. 17. 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.

18. 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, TGF-alpha, beta, prostaglandins also stimulate.

19. 20. 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.

21. 22. Late Wound Healing Events (Days 21-1 yr) 23. Remodeling Phase

  • Programmed regression of blood vessels & granulation tissue.
  • Wound contraction.
  • Collagen remodeling.

24. 25. 26. 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.

27. 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. 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. 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. 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. 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. 34. Disturbances in Wound Healing 35. Local Factors

  • Infection: impairs healing.
  • Smoking: increased platelet adhesiveness, decreased O2 carrying capacity of blood, abnormal collagen.
  • Radiation: endarteritis, abnormal fibroblasts.

36. 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.

37. Abnormal Response to Injury 38. Inadequate Regeneration

  • CNS injuries
  • Bone nonunion
  • Corneal ulcers

39. Inadequate Scar Formation

  • Diabetic foot ulcers.
  • Sacral pressure sores.
  • Venous stasis ulcers.

40. Excessive Regeneration

  • Neuroma
  • Hyperkeratosis in cutaneous psoriasis
  • Adenomatous polyp formation.

41. 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.

42. 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.

43. 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.

44. Wound Care 45. Basics

  • Optimize systemic parameters
  • Debride nonviable tissue
  • Reduce wound bioburden
  • Optimize blood flow
  • Reduce edema
  • Use dressings appropriately
  • Use pharmacologic therapy
  • Close wounds with grafts/flaps as indicated

46. Optimize systemic parameters

  • Age: cannot be reversed, usage of growth factors, aggressive optimization of systemic parameters & supplementation.
  • Avoidance of ischemia & malnutrition.
  • Correction of diabetes, removal of FB.
  • Avoidance of steroids, alcohol, smoking.
  • Avoidance of reperfusion injury: total contact casting, compression therapy.

47. Debridement & Reduction of Bioburden

  • Surface irrigation with saline.
  • Debridement: surgical, enzymatic (papain with urea, collagenase), mechanical (pressurized water jet), autolytic, maggots.
  • Antibiotics: cellulitis, decreased rate of healing, increased pain, straw colored oozing from skin, contaminated wounds, mechanical implants.
  • Removal of FB.

48. Optimize blood flow & oxygen supply

  • Warmth
  • Hydration
  • Surgical revascularization
  • Hyperbaric O2 therapy: limb salvage.

49. Reduce edema

  • Elevation
  • Compression
  • 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.

50. Dressings

  • Absorption characteristics: none films, low hydrogels, moderate - hydrocolloids, high foams, alginates, collagen.
  • Hydrogels (eg. starch) rehydrate wounds (benefit in small amounts of eschar, infected wounds).
  • Hydrocolloids promote wound debridement by autolysis.
  • Antimicrobial dressings: silver, cadexomer iodine, mupirocin, neomycin.

51. Skin Substitutes

  • Autologous keratinocyte sheets.
  • Biobrane
  • Oasis
  • Alloderm
  • Integra (sites prone to contracture, coverage of tendons, bone, surgical hardware)
  • TransCyte
  • Dermagraft
  • Orcel

52. Pharmacologic therapy

  • Antimicrobials
  • PDGF
  • EGF
  • VEGF
  • Vit A: steroid use
  • Absolutely of no use in normally healing wounds

53. Flaps & Grafts

  • Radiation wounds require flaps.
  • Chronic nonhealing ulcers.
  • Extensive areas of ulceration.
  • Major soft tissue loss.
  • Other therapies: electrical stimulation for recalcitrant ulcers.

54. Recent Developments

  • Manuka honey (apitherapy) in venous leg ulcers.
  • Hyperbranched polyglycerol electrospun nanofibers.
  • Androstenediol in steroid inhibited healing.
  • GM-CSF hydrogel in deep 2 nddeg burns.
  • LASER therapy enhances tissue repair?
  • Nitric oxide containing nanoparticles.