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Wound Healing

Wound Healing

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Wound Healing

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  1. Wound Healing Orlando Canizares, MD Tulane University Health Science Center Division of Plastic & Reconstructive Surgery

  2. Overview • Wound Healing • Phases • Factors Influencing • Adjuncts to Wound Healing • Fetal wound healing • Wound Care • Principles • Dressings • Abnormal Scarring

  3. Phases of Wound Healing • Tissue Injury and Coagulation • Inflammation • Remove devitalized tissue and prevent infection • Early • Late • Fibroproliferative • Balance between scar formation and tissue regeneration • Fibroblast migration • Collagen synthesis • Angiogenesis • Epithelialization • Maturation/Remodeling • Maximize strength and structural integrity • Contraction • Collagen Remodeling

  4. Tissue Injury and Coagulation • Tissue Injury and Coagulation • INJURY (Physical, antigen-antibody reaction, or infection) • Transient (5-10 minute) vasoconstriction • Slows blood flow, aid in hemostasis • Histamine mediated vasodilation and permeability changes • Vessels become lined with leukocytes, platelets and erythrocytes • Leukocyte migration into the wound • Endothelial cells swell and pull away from each other -> allowing serum to enter the wound • Hemostatic factors from platelets, kinins, complement, and prostaglandins send signals to initiate the inflammatory phase • Fibrin, Fibronectin, and plasma help form a clot and stop bleeding

  5. Early Inflammation • Complement Cascade Activation • PMN infiltration • 24-48 hours • Stimulated by: • Complement components (C5a) • Formyl-methionyl peptide products from bacteria • Transforming Growth Factor (TGF)-b

  6. Early InflammationPMNS • Predominant cell type from 24-48 hours • Phagocytosis and debridement • Removal of PMNS does not alter wound healing

  7. Late InflammationMacrophage • Most critical cell type • Predominates after 48-72 hours • Attracted by: • Growth factors (PDGF, TGF-b) • Complement • Clotting components • IgG • Collagen and elastin breakdown products • Leukotriene B4 • Platelet factor IV

  8. Late InflammationMacrophage Functions • Phagocytosis • Primary producer of Growth Factors (PDGF, TGF-b) • Recruitment of fibroblasts (proliferative phase) • Proliferation of extracellular matrix by fibroblasts • Proliferation of endothelial cells (angiogenesis) • Proliferation of smooth muscle cells • This leads to the Fibroproliferative phase

  9. Late InflammationLymphocyte • Appears at 72 hours • Attracted by: • Interleukins • IgG • Complement products • Role yet to be determined

  10. Fibroproliferative • Fibroblasts • Migrate into the wound via ECM • Predominant cell type by day 7 • Collagen synthesis • Begins on days 5-7 • Increases in linear fashion for 2 to 3 weeks • Angiogenesis • Promoted by macrophages (TNF-alpha, FGF, VEGF) • Epithelialization • Mitosis of epithelial cells after 48-72 hours • Modulated by growth factors (EGF, FGF, KGF)

  11. FibroproliferativeExtracellular Matrix • Forms a scaffold for cell migration and growth factor sequestration (fibronectin, proteoglycans, collagen, etc.) • Proteoglycans and Glycosaminoglycans • chondroitin sulfate • heparan sulfate • keratan sulfate • hyaluronic acid (1st to appear)

  12. Collagen • Principle building block of connective tissue • 1/3 of total body protein content

  13. Collagen Types • Type 1 • Bones, skin, and tendons • 90% of total body collagen • Found in all connective tissues except hyaline cartilage and basement membranes • Type 2 • Hyaline cartilage, cartilage-like tissues, and eye tissue

  14. Collagen Types • Type 3 • Skin, arteries, uterus, abdominal wall, fetal tissue • Association with Type I collagen in varying ratios (remodeling phase) • Type 4 • Basement membranes only • Type 5 • Basement membranes, cornea • Skin • Type 1 : Type 3 ratio is 4:1 • Hypertrophic scars/immature scars ratio maybe as high as 2:1

  15. Collagen Metabolism • Dynamic equilibrium • Synthesis (Fibrosis) vs. Degradation (collagenases) • Collagenase activity • Stimulated: PTH, Adrenal corticosteroids, colchicine • Inhibited: Alpha 2-macroglobulin, cysteine, progesterone • Healing wound • 3-5 weeks equilibrium is reached between synthesis and degradation (no net change in quantity)

  16. Angiogenesis • Formation of new blood vessels throughout inflammatory and proliferative phase of wound healing • Initiated by platelets • TGF-b and PDGF • PMN • Macrophages • TNF-alpha, FGF, VEGF • Endothelial Cell • Forms new blood vessels

  17. Epithelialization • Repithelialization begins within hours of injury • Stimulated by • Loss of contact-inhibition • Growth factors • EGF (mitogenesis and chemotaxis) • KGF, FGF (proliferation)

  18. Epithelialization • Epithelium advances across wound with leading edge cells becoming phagocytic • Collagenase (MMP) • Degrades ECM proteins and collagen • Enables migration between dermis and fibrin eschar • Mitosis of epithelial cells 48-72 hours after injury behind leading edge

  19. Maturation/Remodeling • Longest phase: 3 weeks – 1 year • Least understood phase • Wound Contraction and Collagen Remodeling • Wound Contraction • Myofibroblast • Fibroblasts with intracellular actin microfilaments

  20. Maturation/Remodeling • Collagen Remodeling • Type 3 Collagen degraded and replaced with Type 1 • Collagen degradation achieved by Matrix Metalloproteinase (MMP) activity (fibroblasts, PMNs, macrophages) • Collagen reorientation • Larger bundles • Increased intermolecular crosslinks

  21. Tensile Strength • Collagen is the main contributing factor • Load capacity per unit area • (Breaking capacity- force required to break a wound regardless of its dimensions) • Rate of tensile strength increases in wounds vary greatly amongst species, tissues and individuals • All wounds begin to gain strength during the first 14-21 days (~20% strength), variable then after • Strength PEAKs @ 60 days • NEVER reaches pre-injury levels • Most optimal conditions  may reach up to 80%

  22. Predominant Cell Types

  23. Special Characteristics of Fetal Wound Healing • Lack of inflammation • Absence of FGF and TGF-b • Regenerative process with minimal or no scar formation • Collagen deposition is more organized and rapid • Type 3 Collagen (No Type 1) • High in hyaluronic acid • Area of ongoing research

  24. Factors That Influence Wound Healing • Oxygen • Fibroblasts are oxygen-sensitive • Collagen synthesis cannot occur unless the PO2 >40mmHg • Deficiency is the most common cause for wound infection and breakdown • Hematocrit • Mild to moderate anemia does not appear to have a negative influence wound healing (given sufficient oxygenation) • >50% decrease in HCT • some studies report a significant decrease in wound tensile strength • while other studies find no change

  25. Factors That Influence Wound Healing • Smoking • Multifactorial in limiting wound healing • Nicotine • Vasoconstrictive -> decreases proliferation of erythrocytes, macrophages, and fibroblasts • CO • Decreases the oxygen carrying capacity of Hgb • Hydrogen Cyanide • Inhibits oxidative enzymes • Increases blood viscosity, decrease collagen deposition and prostacyclin formation • A single cigarette may cause cutaneous vasoconstriction for up to 90 minutes

  26. Factors That Influence Wound Healing • Mechanical Stress • Affects the quantity, aggregation, and orientation of collagen fibers • Abnormal tension -> blanching, necrosis, dermal rupture, and permanent stretching • Hydration • Well hydrated wounds epithelialize faster • Environmental Temperature • Healing is accelerated at temperatures of 30 C • Tensile strength decrease by 20% in 12C environment

  27. Factors That Influence Wound Healing • Denervation • No direct effect on epithialization or contraction • Loss of sensation and high collagenase activities in skin -> prone to ulcerations • Foreign Bodies (including necrotic tissue) • Delay healing and prolong the inflammatory phase • Nutrition • Delays increases in tensile strength • Edema • May compromise tissue perfusion

  28. Factors That Influence Wound Healing • Oxygen Derived Free Radicals • Degrade Hyaluronic acid and collagen • Destroy cell and organelle membranes • Interfere with enzymatic functions • Age • Tensile strength and wound closure rates decrease with age

  29. Factors That Influence Wound Healing • Infection • Prolongs inflammatory phase, impairs epithiliazation and angiogenesis • Increased collagenolytic activity -> decreased wound strength and contracture • Bacterial counts > 105, b-hemolytic strep • Chemotherapy • Decreases fibroblast production and wound contraction • If started 10-14 days after injury, no significant long term problems, but short term decreased tensile strength • Radiation • Stasis and occlusion of small blood vessels • Decreased tensile strength and collagen deposition • Systemic Diseases • DM • Glycosylated RBCs  Stiffened RBCs & Increased blood viscosity • Glycosylated WBCs  impaired immune function • Renal Dz

  30. Factors That Influence Wound Healing • Steroids • Inhibit wound macrophages • Interfere with fibrogenesis, angiogenesis, and wound contraction • Vitamin A and Anabolic steroids can reverse the effects • Vitamin A • Stimulates collagen deposition and increase wound breaking strength • Topical Vitamin A has been found to accelerate wound reepithealization

  31. Factors That Influence Wound Healing • Vitamin C • Essential cofactor in the synthesis of collagen • Deficiency is associated with immune dysfunction and failed wound healing (Scurvy) • Immature fibroblasts and extracellular material • High concentrations do not accelerate healing

  32. Factors That Influence Wound Healing • Vitamin E • Large doses inhibit wound healing • Decreased tensile strength • Less collagen accumulation • HOWEVER • Antioxidant that neutralizes lipid peroxidation caused by radiation  Decreasing levels of free radicals and peroxidases increases the breaking strength of wounds exposed to preoperative radiation

  33. Factors That Influence Wound Healing • Zinc • Deficiency: • Impairs epithelial and fibroblast proliferation • Decreases B and T cell activity • Only accelerates healing when there is a preexisting deficiency

  34. Factors That Influence Wound Healing • NSAIDs • Decrease collagen synthesis an average of 45% (ordinary therapeutic doses) • Dose-dependent effect mediated through prostaglandins

  35. Adjuncts to Wound Healing • Fibrin-based tissue adhesives • Increase breaking strength, energy absorption, and elasticity in healing wounds

  36. Adjuncts to Wound Healing • Hydrotherapy • Whirlpool • Pulsed Lavage • Stimulates formation of granulation tissue • Clean non draining wounds with healthy granulation tissue should NEVER be subjected to hydrotherapy • Water agitation damages fragile cells

  37. Adjuncts to Wound Healing • Hyperbaric Oxygen • Increases levels of O2 and NO to the wound • Benefit: Amputations, osteoradionecrosis, surgical flaps, skin grafts • None to minimal benefit with necrotizing soft-tissue infections • Wounds require adequate perfusion • Many off-label uses (Benefit? Financial?) • Acne, Migraines, Lupus, Stroke, MS, and many more • Medicare Coverage • 14 Covered Areas (next slide)

  38. Medicare Coverage of HBO • (1)  Acute carbon monoxide intoxication • (2)  Decompression illness • (3)  Gas embolism • (4)  Gas gangrene • (5)  Acute traumatic peripheral ischemia • (6)  Crush injuries • (7)  Progressive necrotizing infections • (8)  Acute peripheral arterial insufficiency • (9)  Preparation and preservation of compromised skin grafts • (10)  Chronic refractory osteomyelitis • (11)  Osteoradionecrosis (ORN) • (12)  Soft tissue radionecrosis (STRN) • (13)  Cyanide poisoning • (14)  Actinomycosis

  39. Adjuncts to Wound Healing

  40. Wound Care General Principles • Cleaning and Irrigation • Need at least 7psi to flush bacteria out of a wound • High pressure can damage wounds and should be reserved only for heavily contaminated wounds • Debridement • Most critical step to produce a wound that will heal rapidly without infection • Non-selective: Dakin solution, Hydrogen Peroxide, etc. • Useful in wounds with heavy contamination • When starts to granulate, start selective • Selective: sharp, enzymatic, autolytic, or biologic

  41. Selective Debridement • Enzymatic • Naturally occurring enzymes that selectively digest devitalized tissue • Collagenase (Santyl), Papain-Urea (Accuzyme), etc. • Autolytic • Uses the body’s own enzymes and moisture to breakdown necrotic tissue • 7-10 days under semi occlusive and occlusive dressings • Ineffective in malnourished patients • Biologic • Maggots • Calcium salts and bactericidal peptides • Separate necrotic from living tissue making surgical debridement easier

  42. Wound Care General Principles • Fundamentals of Surgical Wound Closure • Incision should follow tension lines and natural folds in the skin • Gentle tissue handling • Complete hemostasis • Eliminate tension • Fine sutures and early removal • Evert wound edges • Allow scars to mature before repeat intervention (2 weeks to 2 months scar appearance is the worst) • Scar appearance depends more on type of injury than method of closure • Technical factors of suture placement and removal are more critical than type of suture used • Immobilization of wounds to prevent disruptions and excessive scarring (Adhesive strips after suture removal)

  43. Wound Dressings • Over 2,000 commercially available • Red-Yellow-Black Classification • Created to help choose appropriate dressings in wounds healing by secondary intention • Treat worse colors first • Black -> Yellow -> Red

  44. Dressing Types • Alginates (Aquacel) • Wounds with heavy exudates (dry the wound) • Converts in a sodium salt -> hydrophilic gel occlusive environment • Change when begins to weep exudate • Creams (Silvadene cream) • Opaque, soft solid or thick liquids with a slight drying effect • Wounds with moist weeping lesions • Ointments (bacitracin) • Semisolids that melt at body temperature • Aid in rehydration and topical application of drugs

  45. Dressing Types • Foams (Mepilex) • Hydrophobic polyurethane sheets with a non absorbent adhesive occlusive cover (very absorbent and nonadherent) • Absorb environmental water and slow epitheliaztion • Films (Tegaderm) • Transparent polyurethane membranes with water-resistant adhesives • Conform well, semipermeable to moisture and oxygen, impermeable to bacteria • Promote autolytic debridement • Good for wound monitoring • Can lead to maceration in wounds with a heavy exudate and can tear skin

  46. Dressing Types • Gauze • Highly permeable to air and allow rapid moisture evaporation • Stick to granulation tissue and damage the wound with removal • Painful removal • Lint can harbor bacteria • Hydrocolloids • Completely impermeable • Avoid in anaerobic infections • Comfortable and adhere well (good for high-friction areas) • Good at absorbing exudate • Hydrogels • Starch and water polymers in gels, sheets, or impregnated gauze • Rehydrate wounds (poor for absorbing exudate)