Surgery Basics Flashcards
WOUND HEALING steps(5)
Hemostasis
Inflammation
Proliferation
Maturation
Remodeling
wound healing
Hemostasis
Disruption in tissue integrity
Division of blood vessels
Exposure of extracellular matrix to platelets
-Platelet activation
-Degranulation
-Coagulation activation
Fibrin clot
wound healing
Inflammation
Platelet degranulation releases wound active substances
Platelet Derived Growth Factor (PDGF)
Transforming Growth Factor- 𝛃 (TGFb)
Platelet activating factor
Fibronectin
Serotonin
wound healing
Inflammation/ Neutrophils
Fibrin clot serves as matrix for PMNs and monocytes
Neutrophils
24-48 hours
Chemotactic factors
TNF-𝛼 – angiogenesis and collagen synthesis
Collagenase – matrix and ground substance degradation
Phagocytosis of bacteria and debris
Does not directly promote healing
Inflammatory response
Cleaning
Environment for Macrophages
Environment for vessels and collagen
wound healing
inflammation/Macrophages
Fibrin clot serves as matrix for PMNs and monocytes
Macrophages
48 – 96 hours
Remain through-out process until wound healing complete
Wound debridement and phagocytosis
Cytokine and growth factors
-Cell Proliferation
-Matrix synthesis
-Angiogenesis
wound healing
inflammation/ T-lymphocytes
1 week post injury
Bridge transition from inflammatory to proliferation
Modulation of the wound environment
wound healing
proliferation
Days 4-12
Establish tissue continuity
Fibroblast – recruited by platelet-derived growth factor (PDGF)
Proliferate in wound
Activated by cytokines (from macrophages)
Endothelial cells
Migration from venules
Promote angiogenesis
Matrix (collagen) synthesis
Dependent on oxygen, vascularization, vitamin, cofactors, sterility
Collagen deposition
-Type I – extracellular skin matrix
-Type III – repair of skin
wound healing
Maturation
Reorganization of previously synthesized collagen
Re-establishment of extracellular matrix
-Fibronectin and Type III collagen deposition
-Then Proteoglycans and GAGs deposition
-Finally, type I collagen deposition in the matrix
Tensile strength depends on ratios of collagen types and quality
wound healing
remodeling
Constant turnover of collagen
-Synthesis, lysis and deposition
-Shift of types to type I
Final tensile strength
-Cross-linking of fibril
-6 weeks – 6 months
-Less strength than uninjured tissue
-75-80% strength
wound healing
epithelialization
Final step in tissue integrity
Proliferation and migration of adjacent epithelial cells
Begins day 1
Thickening of epidermal wound edge
Migration across matrix surface
Keratinize after cross-bridging complete
48 hours for reapproximated incised wounds
Days to weeks for larger wounds
WOUND CONTRACTION
Secondary intention only
Myofibroblast
Migrate to wound day 6
Contract to decrease wound size
Fibroblast
Initial contraction in days 1-6
WOUND CLASSIFICATION
acute vs chronic
Acute wound
Recent wound (< 4 weeks duration)
Chronic wound
Any acute wound not healed by 4 weeks
TYPES OF WOUND HEALING
primary/secondary/tertiary
Primary Intention
Closure using suture/material
Clean wounds
Secondary Intention
Healing through tissue granulation
Tissue loss; contamination
Tertiary Intention
Delayed primary closure
Combination of primary and secondary intention
Causes of delayed healing
Advanced age?
Or is it confounded based on co-morbidity
Smoking
Hypoxia, hypoperfusion- Optimal collagen synthesis requires oxygen as a cofactor
Steroids, chemo drugs
Diabetes Mellitus; metabolic disorders
Obesity; nutrition
Infection
delay in healing
Diabetes Mellitus
Impaired inflammation, angiogenesis, collagen synthesis
Vascular related disease
Hypoxia, hypoperfusion
Decreased growth factor production
Impaired leukocyte function
delay iin healing
obesity
Obesity
Independent factor for delayed wound healing
Proinflammatory nature of adipose tissue
Adipokines, cytokines
Related to comorbid conditions
Diabetes mellitus
Vascular disease
Increased tension on repaired surgical wounds
Risk of dehiscence: failure of wound healing
delay in healing
Nutrition
Protein deficiency – impaired collagen synthesis
Caloric deficiency – decreased granulation and matrix formation
Usually requires long-standing impairment
But easily improved with intensive, short-term treatment