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창상치유 ; 학습목표
• 창상의 종류
• 감염위험에 따른 분류
• 폐쇄성창상의 치유과정
• 창상치유에 영향을 주는 전신적 및 국소적요인
• 당뇨병과 창상치유
• Wound dressing의 목적
Wound Healing
• A complex integrated sequence of cellular,
physiologic, and biochemical events initiated by
the stimulus of injury to tissue
Healing process
• The same events, in the same order, occur in every
healing process regardless of the tissue type or the
inciting injury
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.
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
Types of wound closure
• Primary closure
• Delayed primary closure
• Secondary closure
• Closure of partial thickness skin wound
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
Primary closure
Secondary closure
• No active intent to seal the wound
• The wound is closed by reepithelization and
contraction with some deposition of scar tissue
Secondary closure
Delayed primary closure
• Tertiary intention
• Surgical intervention, such as suturing, skin graft
replacement, or flap design, after repeated
debridement and antibiotics therapy
Delayed primary closure
Partial thickness wound healing
TISSUE RESPONSES TO INJURY
• Vascular events
• Cellular events
• Chemical mediators
Vascular events
• Immediate transient vasoconstriction
• active vasodilatation
• permeability change
TISSUE RESPONSES TO INJURY
• Vascular events
• Cellular events
• Chemical mediators
Cellular events
• platelets
• neutrophils
• macrophages
• lymphocytes
• fibroblasts
• endothelial cells
platelets
• Hemostasis
• Release of platelet granules
œ- granules
dense granules
lysosomes
Neutrophils
• Protection against infection
• Intracellular products release
free radicals
cyclooxygenase products
lipooxygenase products
protease, antiprotease
band2 protein
Macrophages
• phagocytosis
• initiation of fibroplasia
• release cellular products
neutral protease, complement factors,
reactive oxygen metabolites,
growth factors, fibronectin,
interleukin 1, enzyme inhibitors
TISSUE RESPONSES TO INJURY
• Vascular events
• Cellular events
• Chemical mediators
Chemical mediators
• Vasoactive agents
• Chemotactic factors
• Cytokines
Vasoactive agents
• Histamin
• Serotonin
• Arachidonic acid
Cytokines in wound healing
• TGF-β
• PDGF
• FGF
• EGF
• IGF-1
• Etc. KGF, CTGF, TNF, interleukins
TGF-β
• platelets, macrophage. fibroblast 에 서 release 되 며 healing
process의 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
PDGF
• 주로 platelets의 α-granule에서 release되며 macrophage,
endothelial cell, fibroblast에서도 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
FGF
• endothelial cell 과 macrophage 에 서
production
• 작용 ;
stimulate endothelial cells to divide and form
new capillaries
chemoattract endothelial cells and fibroblasts
EGF
• keratinocytes에서 release
• 작용 ;
• stimulates mitosis in epidermal cells and
fibroblasts
• increase the secretion of collagenase by
fibroblasts
WOUND HEALING PHASES
• Inflammatory phase
• Proliferative phase
• Maturational phase
Inflammatory phase
• The body’s defenses are aimed at limiting the
amount of damage and preventing further injury
• At the initial time of tissue
disruption, platelets
release coagulation factors
and cytokines to initiate
the healing process
• 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
Proliferative phase
• angiogenesis
• fibroplasia
• epithelization
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
• 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.
Maturational phase ( = remodeling )
• The period of scar contracture with collagen cross-
linking, shrinking, and a loss of edema
• The remodeling phase is
characterized by an
equilibrium between
collagen synthesis and
collagen degradation in an
effort to reestablish the
connective tissue matrix.
MECHANISMS IN WOUND HEALING
• Epithelization
• Contraction
• Connective tissue matrix deposition
Epithelization
1. sealed by clot formation
2. epithelial cell migration across the defect
3. keratinocytes – detatchment, migration,
proliferation, differentiation, stratification
MECHANISMS IN WOUND HEALING
• Epithelization
• Contraction
• Connective tissue matrix deposition
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.
MECHANISMS IN WOUND HEALING
• Epithelization
• Contraction
• Connective tissue matrix deposition
Components of extracellular matrix
• Collagen
• Elastin
• Fibronectin
• Laminin
• Proteoglycans
• Hyaluronic acid
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
FACTORS AFFECTING WOUND
HEALING
• Types of injury
• Age
• Medications
• Host disease factors
• Technical factors
Types of Injury
• Sharp injury
• Crush injury
• Missile injury
• Thermal injury
Aging
• In vitro – decrease in the proliferative potential
of fibroblasts and epithelial cells
• Clinically – heal more slowly with less scarring
Medications
• Steroids & Vitamin A
• Anti-inflammatory agents
• Phenytoin
• Antineoplastic agents
• Anticoagulants
• Vitamin E
Steroids
• Impairing macrophage migration
• Altering neutrophil function
• Inhibit synthesis of procollagen by
fibroblasts
Vitamin A deficiency
• Impair monocyte activation
• Inhibit fibronectin deposition
• Impairment of TGF-β receptors
• Vitamin A directly counteracts the effect of
glucocorticoid
Host disease factors
• Nutrition
• Infection
• Wound hypoxia
• Diabetes
• Jaundice
• Uremia
• Malignancy
• Irradiation
• Denervation
Nutrition
• Protein
• Vitamin C – decrease in rate and quality of
collagen production
• Vitamin K
• Minerals – zinc, copper
Infection
• Bacteria
prolong the inflammatory phase
interfere with epithelization, contraction and
collagen deposition
• Endotoxin
collagen degradation and destruction of
surrounding previously normal tissue
Wound hypoxia
• Oxygen – necessary for normal metabolic cellulat function
• Tissue oxygen level 이 35mmHg 이하로 떨어지면
neutrophil의 bacterial killng, fibroblasts의 replication이
안되며 collagen production에 이상이 온다.
Causes of wound ischemia
• Poor arterial flow - atherosclerosis
• Poor venous flow – venous stasis
• Smoking
• Radiation
• Edema
• Diabetes mellitus
• Vasculitis
• Pressure
Diabetes mellitus
• Tissue hypoxia
artherosclerosis, microvascular abnormality
• Repetitive trauma
Diabetes mellitus
• Susceptable to infection
attenuated inflammatory response
impaired chemotaxis
inefficient bacterial killing
• Impaired lymphocyte and leukocyte function
• Increased collagen degradation and decreased
deposition
Technical Factors
• Surgical technics
• Suture materials
• Wound care
Surgical technique
• Handle gently
• Adequate hemostasis
• Careful apposition of wound edges
Surgical technique: skin incision
• Direction
• Length
• Location
Suture materials
• Absorbable sutures;
• Non-absorbable sutures;
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
Agents to optimize wound healing
• Dressing
• Antibiotics ; controversial
• Debriding agents
• Phamacologic agents
Ideal dressing
• simple, inexpensive, highly absorptive, nonadherent
• achieve moist healing and have antibacterial properties
• less frequent dressing change
• all-in-one dressing
Wound-healing products(1)
• Passive products ; lint
cotton wool
• plugging and concealing wounds
Wound-healing products(2)
• New dressings ; polymeric films,
polymeric foams,
hydrogels,
hydrocolloids
• Classified as interactive dressings, providing a
microenvironment which is conducive to healing
Wound-healing products(3)
• Active products which actively stimulate
healing beyond that of the normal
biological maximum.
Wound_healing_4.ppt
Wound_healing_4.ppt
Wound_healing_4.ppt
Wound_healing_4.ppt

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Wound_healing_4.ppt

  • 1. 창상치유 ; 학습목표 • 창상의 종류 • 감염위험에 따른 분류 • 폐쇄성창상의 치유과정 • 창상치유에 영향을 주는 전신적 및 국소적요인 • 당뇨병과 창상치유 • Wound dressing의 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
  • 9. Secondary closure • No active intent to seal the wound • The wound is closed by reepithelization and contraction with some deposition of scar tissue
  • 11. Delayed primary closure • Tertiary intention • Surgical intervention, such as suturing, skin graft replacement, or flap design, after repeated debridement and antibiotics therapy
  • 14.
  • 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
  • 20.
  • 21. Neutrophils • Protection against infection • Intracellular products release free radicals cyclooxygenase products lipooxygenase products protease, antiprotease band2 protein
  • 22.
  • 23. Macrophages • phagocytosis • initiation of fibroplasia • release cellular products neutral protease, complement factors, reactive oxygen metabolites, growth factors, fibronectin, interleukin 1, enzyme inhibitors
  • 24.
  • 25.
  • 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 에 서 release 되 며 healing process의 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 platelets의 α-granule에서 release되며 macrophage, endothelial cell, fibroblast에서도 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 에 서 production • 작용 ; stimulate endothelial cells to divide and form new capillaries chemoattract endothelial cells and fibroblasts
  • 33. EGF • keratinocytes에서 release • 작용 ; • stimulates mitosis in epidermal cells and fibroblasts • increase the secretion of collagenase by fibroblasts
  • 34.
  • 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.
  • 44.
  • 45.
  • 46.
  • 47.
  • 48.
  • 49.
  • 50.
  • 51.
  • 52.
  • 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
  • 59.
  • 60.
  • 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
  • 62.
  • 63.
  • 64.
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  • 66.
  • 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 neutrophil의 bacterial killng, fibroblasts의 replication이 안되며 collagen production에 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.