wound healing & wound care
Post on 07-May-2015
Embed Size (px)
- 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.
- 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).
- 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.
- 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.
- 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.
- 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
- 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
- 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
- Surgical revascularization
- Hyperbaric O2 therapy: limb salvage.
49. Reduce edema
- 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.
- Absorption characteristics: none fi