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