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Woundhealing 120305164816-phpapp02(3)

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Wound Healing
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Page 1: Woundhealing 120305164816-phpapp02(3)

Wound Healing

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Wound Healing Types:

Primary Healing – Occurring when a wound is closed within a few hours of its creation. Wound edges are surgically or mechanically approximated, and collagen metabolism provides long-term strength.Delayed Primary Healing – Occurs when a poorly delineated wound is left open to protect against wound infection. The open wound allows for the natural host defense to debride the wound before closure.Secondary Healing – Occurs when an open full thickness wound is allowed to close by wound contraction and epithelialization.Healing of Partial-Thickness Wounds – Occurs when a partial-thickness wound is closed primarily by epithelialization. This wound healing involves the superficial portion of the dermis. There is minimal collagen deposition, and an absence of wound contraction.

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Phases of Wound Healing

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Whether wounds are closed by primary intention, subject to delayed primary closure or left to heal by secondary intention1, the wound healing process is a dynamic one which can be divided into three phases. It is critical to remember that wound healing is not linear and often wounds can progress both forwards and back through the phases depending uponintrinsic and extrinsic forces at work within the patient

The phases of wound healing are:•Inflammatory phase•Proliferation phase•Maturation phase

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The inflammatory phase is the body’s natural response to injury. After initial wounding, the blood vessels in the wound bed contract and a clot is formed. Once haemostasis has been achieved, blood vessels then dilate to allow essential cells; antibodies, white blood cells,growth factors, enzymes and nutrients to reach the wounded area. This leads to a rise inexudate levels so the surrounding skin needs to be monitored for signs of maceration. It is at this stage that the characteristic signs of inflammation can be seen; erythema, heat, oedema, pain and functional disturbance. The predominant cells at work here are the phagocytic cells; ‘neutrophils and macrophages’; mounting a host response andautolysing any devitalised ‘necrotic / sloughy’ tissue.

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During proliferation, the wound is ‘rebuilt’ with new granulation tissue which is comprised of collagen and extracellular matrix and into which a new network of blood vessels develop, a process known as ‘angiogenesis’. Healthy granulation tissue is dependent upon the fibroblast receiving sufficient levels of oxygen and nutrients supplied by the blood vessels. Healthy granulation tissue is granular and uneven in texture; it does not bleed easily and is pink / red in colour. The colour and condition of the granulation tissue is often an indicator of how the wound is healing. Dark granulation tissue can be indicative of poor perfusion, ischaemia and / or infection. Epithelial cells finally resurface the wound, a process known as ‘epithelialisation’.

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Maturation is the final phase and occurs onc the wound has closed. This phase involves remodelling of collagen from type III to type I. Cellular activity reduces and the number of blood vessels in the wounded area regress and decrease.

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Factor affecting on wound healing

Two types of factor influence the wound healing :

A. Local feature : 1. infection.

2. Poor blood supply.

3. Movement.

4. Foreign body.

5. Exposure to ultraviolet ray.

6. Types , size and local of injury.

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Factor affecting wound healing

Systemic feature: Age.Infection.Nutrition :arginine and vita A. Hypoxia.Anemia.Hypo perfusion.Metabolic disorder : D.M. And uremia .Steroid and radiation.

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Complication of wound healing Infection.Epidermal cyst formation.Pigmentation.Deficient scar formation.Incision hernia.Hypertrophied scars and keloid formation.Extensive contraction.Neoplasia.

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Effects Main origin Abbreviation Growth factor

Granulation tissue formation.

•Macrophages.•Salivary gland.•Keratinocytes.

EGF Epidermal growth factor

•Hepatocyte and epithelial cell proliferation.•Expression of antimicrobial peptides.•Expression of chemotactic cytokines.

•Activated macrophages•T-lymphocytes•Keratinocytes

TGF-α Transforming growth factor-α

Epithelial and endothelial cell proliferationHepatocyte motility

Mesenchymal cells

HGF Hepatocyte growth factor

Vascular permeabilityEndothelial cell proliferation

Mesenchymal cells

VEGF Vascular endothelial growth factor

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Granulocyte, macrophage, fibroblast and smooth muscle cell chemotaxisGranulocyte, macrophage and fibroblast activationFibroblast, endothelial cell and smooth muscle cell

•Platelets•Macrophages•Endothelial cells•Smooth muscle cells•Keratinocytes

PDGF Platelet derived growth factor

Fibroblast chemotaxisFibroblast and keratinocyte proliferationKeratinocyte migrationAngiogenesis

MacrophagesMast cellsT-lymphocytesEndothelial cellsFibroblasts

FGF-1, -2 Fibroblast growth factor 1 and 2

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