1. 창상치유 ; 학습목표 창상의 종류 감염위험에 따른 분류 폐쇄성창상의 치유과정 창상치유에 영향을 주는 전신적 및 국소적요인 당뇨병과 창상치유 Wound dressing 의 목적

2. Wound Healing A complex integrated sequence of cellular, physiologic, and biochemical events initiated by the stimulus of injury to tissue

3. Healing process The same events, in the same order, occur in every healing process regardless of the tissue type or the inciting injury

4. Healing process The activation of basic cellular processes of inflammation, cell proliferation, and growth as well as regulation of these processes once repair is complete.

5. Healing process All repair occurs with an overlapping series of orchestrated events to limit the damage and restore the function and integrity of the structure

6. Types of wound closure Primary closure Delayed primary closure Secondary closure Closure of partial thickness skin wound

7. Primary closure First intention closure Immediately sealed wounds with simple suturing, skin graft placement, or flap closure Eg. emergency laceration repair, closure of the surgical wound

8. Primary closure

9. Secondary closure No active intent to seal the wound The wound is closed by reepithelization and contraction with some deposition of scar tissue

10. Secondary closure

11. Delayed primary closure Tertiary intention Surgical intervention, such as suturing, skin graft replacement, or flap design, after repeated debridement and antibiotics therapy

12. Delayed primary closure

13. Partial thickness wound healing

15. TISSUE RESPONSES TO INJURY Vascular events Cellular events Chemical mediators

16. Vascular events Immediate transient vasoconstriction active vasodilatation permeability change

17. TISSUE RESPONSES TO INJURY Vascular events Cellular events Chemical mediators

18. Cellular events platelets neutrophils macrophages lymphocytes fibroblasts endothelial cells

19. platelets Hemostasis Release of platelet granules œ- granules dense granules lysosomes

21. Neutrophils Protection against infection Intracellular products release free radicals cyclooxygenase products lipooxygenase products protease, antiprotease band2 protein

23. Macrophages phagocytosis initiation of fibroplasia release cellular products neutral protease, complement factors, reactive oxygen metabolites, growth factors, fibronectin, interleukin 1, enzyme inhibitors

26. TISSUE RESPONSES TO INJURY Vascular events Cellular events Chemical mediators

27. Chemical mediators Vasoactive agents Chemotactic factors Cytokines

28. Vasoactive agents Histamin Serotonin Arachidonic acid

29. Cytokines in wound healing TGF-β PDGF FGF EGF IGF-1 Etc. KGF, CTGF, TNF, interleukins

30. TGF-β platelets, macrophage. fibroblast 에서 release 되며 healing process 의 모든 과정에 영향을 준다. 작용 ; stimulates the deposition of collagen and other matrix components inhibits collagenase activity blocks plasminogen inhibitor enhance angiogenesis chemotactic for fibroblasts, monocytes, and macrophages

31. PDGF 주로 platelets 의 α-granule 에서 release 되며 macrophage, endothelial cell, fibroblast 에서도 release 작용 ; attract the neutrophil, macrophage, and fibroblast to the wound powerful mitogen of the neutrophil, macrophage, and fibroblast stimulate fibroblasts to synthesize new extracellula matrix increase the amount of fibroblast-secreted collagenase

32. FGF endothelial cell 과 macrophage 에서 production 작용 ; stimulate endothelial cells to divide and form new capillaries chemoattract endothelial cells and fibroblasts

33. EGF keratinocytes 에서 release 작용 ; stimulates mitosis in epidermal cells and fibroblasts increase the secretion of collagenase by fibroblasts

35. WOUND HEALING PHASES Inflammatory phase Proliferative phase Maturational phase

36. Inflammatory phase The body’s defenses are aimed at limiting the amount of damage and preventing further injury

37. At the initial time of tissue disruption, platelets release coagulation factors and cytokines to initiate the healing process

38. Within the first day following tissue injury, neutrophils attatch to surrounding vessel walls and then move through the vessel walls to migrate to the wound site

39. Proliferative phase angiogenesis fibroplasia epithelization

40. Angiogenesis The process of new blood vessel formation to support a healing wound environment Stimulants ; tissue hypoxia – major stimulus TNF-α, heparin, VEGF, FGF-1, FGF-2

41. The fibroplasia phase is characterized by movement of wound macrophages into the site of injury, which in turn attract fibroblasts. The fibroblasts then repair the site by producing new connective tissue matrix.

42. Maturational phase ( = remodeling ) The period of scar contracture with collagen cross- linking, shrinking, and a loss of edema

43. The remodeling phase is characterized by an equilibrium between collagen synthesis and collagen degradation in an effort to reestablish the connective tissue matrix.

53. MECHANISMS IN WOUND HEALING Epithelization Contraction Connective tissue matrix deposition

54. Epithelization 1.sealed by clot formation 2.epithelial cell migration across the defect 3.keratinocytes – detatchment, migration, proliferation, differentiation, stratification

55. MECHANISMS IN WOUND HEALING Epithelization Contraction Connective tissue matrix deposition

56. Contraction Inward movement of the edges of the injured tissue Begins between days 8 and 10 after injury Fibroblast and extracellular matrix control the process.

57. MECHANISMS IN WOUND HEALING Epithelization Contraction Connective tissue matrix deposition

58. Components of extracellular matrix Collagen Elastin Fibronectin Laminin Proteoglycans Hyaluronic acid

61. Synthesis of collagen 1.Combination of aminoacid to form chains 2.Chains associate to form molecules 3.Molecules associate to form fibrils 4.Fibrils aggregate into fibers or bundles

67. FACTORS AFFECTING WOUND HEALING Types of injury Age Medications Host disease factors Technical factors

68. Types of Injury Sharp injury Crush injury Missile injury Thermal injury

69. Aging In vitro – decrease in the proliferative potential of fibroblasts and epithelial cells Clinically – heal more slowly with less scarring

70. Medications Steroids & Vitamin A Anti-inflammatory agents Phenytoin Antineoplastic agents Anticoagulants Vitamin E

71. Steroids Impairing macrophage migration Altering neutrophil function Inhibit synthesis of procollagen by fibroblasts

72. Vitamin A deficiency Impair monocyte activation Inhibit fibronectin deposition Impairment of TGF-β receptors Vitamin A directly counteracts the effect of glucocorticoid

73. Host disease factors Nutrition Infection Wound hypoxia Diabetes Jaundice Uremia Malignancy Irradiation Denervation

74. Nutrition Protein Vitamin C – decrease in rate and quality of collagen production Vitamin K Minerals – zinc, copper

75. Infection Bacteria prolong the inflammatory phase interfere with epithelization, contraction and collagen deposition Endotoxin collagen degradation and destruction of surrounding previously normal tissue

76. Wound hypoxia Oxygen – necessary for normal metabolic cellulat function Tissue oxygen level 이 35mmHg 이하로 떨어지면 neutrophil 의 bacterial killng, fibroblasts 의 replication 이 안되며 collagen production 에 이상이 온다.

77. Causes of wound ischemia Poor arterial flow - atherosclerosis Poor venous flow – venous stasis Smoking Radiation Edema Diabetes mellitus Vasculitis Pressure

78. Diabetes mellitus Tissue hypoxia artherosclerosis, microvascular abnormality Repetitive trauma

79. Diabetes mellitus Susceptable to infection attenuated inflammatory response impaired chemotaxis inefficient bacterial killing Impaired lymphocyte and leukocyte function Increased collagen degradation and decreased deposition

80. Technical Factors Surgical technics Suture materials Wound care

81. Surgical technique Handle gently Adequate hemostasis Careful apposition of wound edges

82. Surgical technique: skin incision Direction Length Location

83. Suture materials Absorbable sutures; Non-absorbable sutures;

84. Principles of wound management: open wound Clean the wound effectively Achieve moist wound healing Minimize the periwound edema Prevent new pressure insult or wound soilage Maintain adequate tissue oxygenation

85. Agents to optimize wound healing Dressing Antibiotics ; controversial Debriding agents Phamacologic agents

86. Ideal dressing simple, inexpensive, highly absorptive, nonadherent achieve moist healing and have antibacterial properties less frequent dressing change all-in-one dressing

87. Wound-healing products(1) Passive products ; lint cotton wool plugging and concealing wounds

88. Wound-healing products(2) New dressings ; polymeric films, polymeric foams, hydrogels, hydrocolloids Classified as interactive dressings, providing a microenvironment which is conducive to healing

89. Wound-healing products(3) Active products which actively stimulate healing beyond that of the normal biological maximum.