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Wound Healing and the Problem Wound

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  1. Wound Healing and the Problem Wound Frederick N. Eko, MD Senior Fellow Division of Plastic Surgery Tulane University School of Medicine

  2. History of Wound Healing • 1700 BC Papyrus: Lint/animal grease/honey • 100 BC Egypt: Wound closure preserved soul • 1000 AD Gun Powder • 1500 AD Hot Oil • 20th Century Scientific Method

  3. Wounds • Customize • Shotgun approach not acceptable • No two patients OR wounds are identical 58y DM, Neuropathy: unaware of R foot gangrene

  4. Wounds

  5. Wounds • Reconstructive Ladder • Simple to Complex Formal Debridement, Elevation/ABI’s Appropriate IV ABX, Wound Vac, Skin Graft

  6. Review of Wound Healing • Three basic types of healing • Primary • Delayed Primary • Secondary

  7. Primary • Wound surfaces opposed • Healing without complications • Minimal new tissue • Results optimal

  8. Delayed Primary • Left open initially • Edges approximated 4-6 days later

  9. Secondary • Surfaces not approximated • Defect filled by granulation • Covered with epithelium • Less functional • More sensitive to thermal and mechanical injury

  10. Secondary Wound Healing

  11. Secondary Wound Healing

  12. Secondary Wound Healing

  13. Three Phases of Wound Healing • Inflammatory Phase • Proliferative Phase • Remodeling Phase

  14. Three Phases of Wound Healing • Inflammatory Phase • Proliferative Phase • Begins when wound is covered by epithelium • Production of collagen is hallmark • 7 days to 6 weeks • Remodeling Phase (Maturation Phase)

  15. Inflammatory Phase • Hemostasis and Inflammation • Days 4 - 6 • Exposed collagen activates clotting cascade and inflammatory phase • Fibrin clot = scaffolding and concentrate cytokines and growth factors

  16. Inflammatory: Granulocytes • First 48 hours (Neutrophils) • Attracted by inflammatory mediators • Oxygen-derived free radicals • Non-specific

  17. Inflammatory: Macrophages • Monocytes • attracted to area by complement • Activated by: • fibrin • foreign body material • exposure to hypoxic and acidotic environment • Reached maximum after 24 hours • Remain for weeks

  18. Inflammatory: Macrophages • Activated Macrophage: • Essential for progression onto Proliferative Phase • Mediate: • Angiogenesis: FGF, PDGF, TGF-ɑ & β and TNF-ɑ • Fibroplasia: IL’s, EGF and TNF • Synthesize NO • Secrete collagenases

  19. Inflammatory Phase

  20. Inflammatory Phase

  21. Inflammatory Phase

  22. Three Phases of Wound Healing • Inflammatory Phase • Proliferative Phase • Remodeling Phase

  23. Proliferative Phase • Epithelization, Angiogenesis and Provisional Matrix Formation • Begins when wound is covered by epithelium • Day 4 through 14 • Production of collagen is hallmark • 7 days to 6 weeks

  24. Epithelialization • Basal epithelial cells at the wound margin flatten (mobilize) and migrate into the open wound • Basal cells at margin multiply (mitosis) in horizontal direction • Basal cells behind margin undergo vertical growth (differentiation)

  25. Proliferative: Fibroblast • Work horse of wound repair • Produce Granulation Tissue: • Main signals are PDGF and EGF • Collagen type III • Glycosaminoglycans • Fibronectin • Elastin fibers • Tissue fibroblasts become myofibroblasts induced by TGF-β1

  26. Wound Contraction • Actual contraction with pulling of edges toward center making wounds smaller • Myofibroblast: contractile properties • Surrounding skin stretched, thinned • Original dermal thickness maintained • No hair follicles, sweat glands

  27. Epithelialization/Contraction

  28. Epithelialization

  29. Collagen Homeostasis • After Wounding (Optimal Healing) • Days 3 - 7 • Collagen production begins • Days 7 – 42 • Synthesis with a net GAIN of collagen • Initial increase in tensile strength due to increased amount of collagen • Days 42+ • Remodeling with No net collagen gain

  30. Collagen • Normal Skin • collagen ratio 4 : 1 Type I/III • Hypertrophic Scar • collagen ratio 2 : 1 Type I/III

  31. Proliferative Phase

  32. Three Phases of Wound Healing • Inflammatory Phase • Proliferative Phase • Remodeling Phase

  33. Maturation Phase • Random to organized fibrils • Day 8 through years • Type III replaced by type I • Wound may increase in strength for up to 2 years after injury • Collagen organization • Cross linking of collagen

  34. Maturation Phase

  35. Impaired Wound Healing

  36. Wound Healing • To treat the wound, you have to treat the patient • Optimize the patient • Circulatory • Pulmonary • Nutrition • Associated diseases or conditions

  37. Oxygen • Fibroblasts are oxygen-sensitive • PO2 < 40 mmHg collagen synthesis cannot take place • Decreased PO2: most common cause of wound infection • Healing is Energy Dependent • Proliferative Phase has greatly increased metabolism and protein synthesis

  38. Hypoxia: • Endothelium responds with vasodilation • Capillary leak • Fibrin deposition • TNF-a induction and apoptosis

  39. Edema • Increased tissue pressure • Compromise perfusion • Cell death and tissue ulceration

  40. Infection • Decreased tissue PO2 and prolongs the inflammatory phase • Impaired angiogenesis and epithelialization • Increased collagenase activity

  41. Nutrition • Low protein levels prolong inflammatory phase • Impaired fibroplasia • Of the essential amino • Methionine is critical • Hydration • A well hydrated wound will epithelialize faster than a dry one • Occlusive wound dressings hasten epithelial repair and control the proliferation of granulation tissue

  42. Temperature • Wound healing is accelerated at environmental temperatures of 30°C • Tensile strength decreases by 20% in a cold (12°C) wound environment • Denervation • Denervation has no effect on either wound contraction or epithelialization

  43. Diabetes Mellitus • Larger arteries, rather than the arterioles, are typically affected • Sorbitol accumulation • Increased dermal vascular permeability and pericapillary albumin deposition • Impaired oxygen and nutrient delivery • Stiffened red blood cells and increased blood viscosity • affinity of glycosylated hemoglobin for oxygen contributing to low O2 delivery • impaired phagocytosis and bacterial killing • neuropathy

  44. Radiation Therapy • Acute radiation injury • stasis and occlusion of small vessels • fibrosis and necrosis of capillaries • decrease in wound tensile strength • direct, permanent, adverse effect on fibroblast • may be progressive • fibroblast defects are the central problem in the healing of chronic radiation injury