W
OUND HEALI
NG
MBBS, Resident Plastic surgery, HMC, Peshawar
ansoorKhanM
Complex & dynamic process of restoring cellular structures & tissue layers
SCARING
Full thickness wounds
EPITHELIZATION
Partial thickness wounds
HEALING
Phases of wound healing
Inflammatory phase (day1-4)
Limit blood loss
Debridement
Sealing the wound
Inflammatoryphase
Haemostasis Inflammation
Vessel damage ---- bleeding---- platelet plug ---- thromboxane A2 --- Vascular contraction and coagulation pathway activation ---
fibrin frame work deposition
Haemostasis(Activated by intrinsic & extrinsic pathways)
Inflammation
Serotonin/Histamine --- increased vascular permeability
TGF– neutrophil chemotaxis, starts 6-8 hrs, max in 24 hrs
Monocyte/ Macrophage– max 3-4 days
Phagocytosis, cytokines (IL-1, TNF), mediators (TGF, PDGF, FGF)
Activated by platelet secretary products (PDGF, TGF, FGF, Serotonin, Histamine)
Proliferative Phase (day 4-21)
Filling wound gap with granulation
tissue
EVENTS
Fibroplasia, angiogenesis, contraction, re-
epithelization
FIBROPLASIA
Chemotactic TGF, PDGF, EGF, IL-1 Fibroblasts peaks at 7th day Collagen & Matrix deposition, Wound contraction 10-
21 days
ANGIOGENESIS
Hypoxia, lactic acidosis, and FGF-1 (most potent), heparin, TGF, prostaglandin
Endothelial cells proliferation
EPITHELIALIZATION
Basal layers thickens, elongates and cells detaches and migrates
Tailoring the way reality lives
Phase (day 21-2years)
Shrinkage Loss of oedema Strength Scare contraction
EVENTS
Regression of vessels & granulation tissueWound contraction
Collagen remodelling (replacing collagen III with I)Maximum strength at the 12 week
WOUND CONTRACTION
Begin in the proliferative phase (4-5th day)Continues throughout the healing process
Maximum 10-21 dayBrings edges close at a rate of 0.6-0.75mm/day
Depends on the laxity of the skin
LOCAL FACTORSVenn diagram
RISK FACTORS RISK FACTORS SYSTEMIC RISK FACTORSRISK FACTORS RISK
FACTORS
ISCHEMIA
Wound healing is a highly energy dependant process
Sugar is the main fuel for wound
healing
ISCHEMIA
So it take a rich blood supply to heal a wound
ISCHEMIA
Initial response neo-vascularization
Persistent ischemia results in apoptosis
“”
INFECTIONCollagenase production and destruction of collagen
FOREIGN BODIESActs a physical barrier Asylum for bacteria Inability to contract Prevent epithelization
HYPOTHERMIA
Vasoconstriction and decreased blood supply
PAINAdrenaline surge causing vasoconstriction
Keep the wounds wet, warm and comfortable “ ”
SMOKING
VasoconstrictionWhich is not transient— 1 cigarette for 90 min 1 pack for whole day
Carboxihemoglobin--- O2 carrying capacity.
Subcutaneous PO2
SMOKING
1 pack/ day--- 3 times increased chances of flap or graft loss
2 packs/day--- 6 times increased chances of loss of flaps and grafts
SMOKING
STEROIDSLysosomal stabalization--- impaired phagocytosis
Impairment of chemotaxis of microphages
Fibroblast genome inhibition--- decreased collagen, decreased strength and increased dehiscence
HEALING SLOWS DOWN WITH AGING
CUTIS LAXA SYNDROME
EHLER-DANLOS SYNDROME
OSTEOGENESIS IMPERFECTA
FETAL WOUND HEALING(SCARLESS)
ADULT: collagen production, remodelling, scar formation
FETAL: Altered growth substances (Tenascin etc), absence of inflammation, deposition of hyaluronic acid rich matrix and deposition of organized collagen leading to regeneration