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Wound Healing:

Wound Healing By: Dr. Avinash Prakash “A surgeon’s role in wound management is to create an environment in which the healing process can proceed in an optimal fashion. “


HISTORY OF WOUND HEALING The earliest accounts of wound healing date back to about 2000 B.C The treatment of acute and chronic wounds is an ancient area of specialization in medical practice, with a long and eventful clinical history that traces its origins to ancient Egypt and Greece .


The Ebers Papyrus, circa 1500 BC , details the use of lint (absorbent) animal grease (Barrier), and honey (antibiotic ) as topical treatments for wounds HISTORY OF WOUND HEALING


HISTORY OF WOUND HEALING Galen of Pergamum ( a Greek surgeon who served Roman gladiators in 120–201 A.D ) emphasized the importance of maintaining a moist environment to ensure adequate healing. Ambriose Paré ( French surgeon who served in that role for french kings. He is considered a pioneer in surgical techniques and battlefield medicine 1510-20 ) He found that a simply dressed gunshot wounds heal faster and are less painful than when treated with boiling oil, the previously accepted method.


Ignaz Philipp Semmelweis ( 1818-1865) advocated need for washing hands Joseph Lister (1865- a British surgeon and a pioneer of antiseptic surgery ) began soaking his instruments in phenol and spraying the operating rooms, reducing the mortality rates from 50 to 15%. Wood Johnson(1876): – Antiseptic dressing (cotton gauze impregnated with iodoform ). HISTORY OF WOUND HEALING


Introduction The repair of tissue damage can be broadly separated into two processes, regeneration and healing . Regeneration “ is a perfect restoration of the pre-existing tissue architecture in the absence of scar formation ” Wound healing “ is the effort of injured tissues to restore normal function and structural integrity after injury “

Phases of Wound Healing:

Phases of Wound Healing • Inflammatory phase: hemo-stasis & inflammation • Proliferative phase • Maturation and Remodelling – Epithelialization – Contraction

Inflammatory phase::

Inflammatory phase: • “ The body defenses are aimed at limiting the amount of damage and preventing further injury” Hemostasis & Inflammation : hemostasis precedes and initiates inflammation Local VC ; RBC & platelets adhere Exposed IV & V collagen leads to platelet ,aggregation( vWF ),degranulation Clotting cascade initiated “ fibrin clot ” : serves as scaffolding for the migration of inflammatory cells ( PMN, Monocytes)

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↑Vas Permeability: Platelet activation α granules ( PDGF,TGF-Beta, IGF-I, fibronectin , fibrinogen, thrombo-spondin , vWF ) Dense bodies ( Serotonin) Mast cells adhere to endothelium Histamine Serotonin clinical findings of inflammation, rubor (redness), calor (heat), dolor (pain ) & tumor (swelling),

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PMN migration : peak 24-48 hrs Phagocytosis of bacteria & debris Cytokines ( TNF-alpha ) Protease Macrophages : peak 48-96 hrs, “ Macrophage is the one cell that is truly central to wound healing” Phagocytosis Cytokines and GF ( TGF- Beta , VEGF,IGF-I, EGF, lactate ,) Regulate cell proliferation , matrix synthesis ,angiogenesis T – Lymphocytes : peak 1 week Bridge the transition from inflammatory to proliferative phase Not fully defined

Proliferative phase:Days 4-12:

Proliferative phase: Days 4-12 Fibro-genesis Angio-genesis

Proliferative phase::

Proliferative phase: Continuity is re-established PDGF recruits fibroblasts which proliferate then gets activated ( by cytokines and GF from macrophages ) – matrix synthesis and remodelling Accumulated Lactate : regulate collagen synthesis Endothelial cells proliferate – Migrate from nearby intact venules – Angiogenesis of capillaries • Regulated by cytokines/GFs (VEGF, TNF-a, TGF-ß)


Fibrogenesis The proliferative phase begins with degradation of the initial fibrin-platelet provisional matrix. During f ibrogenesis , fibroblasts synthesize and deposit the matrix at the wound site As fibroblasts proliferate, they become predominant cell types by 3 to 5 days in clean, non infected wounds. The initial fibrin matrix is replaced by a provisional matrix of fibronectin and hyaluron , which facilitates fibroblast migration.

Angiogenesis :

Angiogenesis Process of new blood vessel formation Macrophage orchestrates angiogenesis during the inflammatory phase. 1. Degradation of the BM of post-capillary venules 2. Migration of cells through this gap promoted by FGF, PDGF, and TGF-β 3.Tubule or lumen formation involving cell-cell and cell-matrix interactions. 4.Deposition of BM resulting in capillary maturation.

Maturation and Remodelling:

Maturation and Remodelling •” The period of scar contracture with collagen cross-linking, shrinking, and a loss of edema “ Wound strength depends upon the quality& quantity of deposited collagen It begins in the fibroblastic phase • Early matrix – fibronectin and collagen type III • Fibroplastic phase – reorganization of collagen – Collagenolysis by collagenase a matrix metaloproteinase (MMPs) • Second matrix- GAGs &proteoglycans • Final matrix – collagen type I – Deposited over several weeks, but tensile strength keeps on increasing over months

Maturation and Remodeling:

Maturation and Remodeling • Fibril formation & cross-linking Decrease collagen solubility – Increase strength – Increase resistance • Remodelling 6- 12 months The remodeling phase is resulting in a scar which is avascular, mature, acellular ECM “ Mechanical strength never reaches uninjured levels”


Epithelialization • begins within Day 1 – proliferation and migration of epithelial cells adjacent to wound • Marginal basal cells lose their dermal attachment, enlarge, flatten, and migrate across the matrix (leapfrog) to cover the defect • Once covered, epithelial cells become more columnar , increase mitotic activity and re-establish the layered epithelium • In 48 hours ( approximated incised wounds )

Wound Contraction:

Wound Contraction All wounds contract Myofibroblasts contain a smooth muscle actin in thick bundles called stress fibers – May be responsible for contraction – Increases from day 7-21, fades after 4 wks • Movement &reorganization of the skeleton- wound contraction

Connective Tissue Disorders :

Connective Tissue Disorders Cutis hyperelastica defect in collagen formation Thin, friable skin, prominent veins, easy bruising, poor wound healing, abnormal scar formation, recurrent hernias, EHLER-DANLOS

Marfan Syndrome:

Marfan Syndrome – defect in fibrillin (assoc with elastic fibres) tall stature, arachnodactyly, lax ligaments, hyper extensible skin, myopia, scoliosis, pectus excavatum, ascending aortic aneurysm, prone to hernias

Osteogenesis Imperfecta –:

Osteogenesis Imperfecta – collagen Type I mutation, 4subtypes – Osteopenia/brittle bones, low muscle mass, hernias, lax ligaments, dermal thinning, increased bruising, normal scarring, blue sclera

Epidermolysis Bullosa:

Epidermolysis Bullosa – epidermis &dermis lack the protein anchors that hold them together, resulting in extremely fragile skin subtypes: simplex (epidermis), junctional (BM), dystrophic (dermis) – Tissue separation and blistering – Oral erosions and oesophageal obstruction cause poor nutrition

Acrodematitis Enteropathica:

Acrodematitis Enteropathica – inability to absorb zinc via cell surface binding and cellular translocation, AR – Zinc is a cofactor for DNA polymerase, RT – Impaired granulation tissue formation, erythematous pustular dermatitis periorificial (around the natural orifices) and acral (in the limbs) dermatitis, alopecia (loss of hair), and diarrhoea.

Factors Affecting Wound Healing:

Factors Affecting Wound Healing Systemic Age: Dermal collagen content decreases with aging Nutrition: Arginine deficiency results in decreased wound-breaking strength and wound collagen, Vitamin A increases the inflammatory response in wound healing Vitamin C is required for the conversion of proline and lysine to hydroxyproline and hydroxylysine Zinc deficiency leads to decreased fibroblast proliferation

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Trauma Metabolic diseases :DM, uremia Immunosuppression: glucocorticoids reduce collagen synthesis and wound strength. Connective tissue disorders Smoking

Local :

Mechanical injury Infection: Inactive precursors of MMPs are activated by bacterial proteinases Edema Ischemia/necrotic tissue Ionizing radiation: Causes endothelial cell injury with endarteritis Low oxygen tension: profoundly deleterious effect on all aspects of wound healing. Foreign bodies Local

Excess Healing:

Excess Healing Hypertrophic scars Usually develop within 4 weeks of trauma Collagen bundles are wavy pattern Stay within the original wound , elevated less than 4 mm Occur across areas of tension/flexing Often regress Tx: excision + corticosteroids


Keloids 15x more common in pts with dark skin pigmentation Develop 3 months –years after trauma Collagen fibres are larger, random & not bundled Expand beyond wound edges , can become large


keloid Rarely regress Excision alone (45-100% recurrence) Excision + corticosteroid injections Topical silicone Radiation (10 to 100% recurrence when used alone) Topical retinoids IFN- γ Chemo therapy (5FU,bleomycin) + external compression

Classification of Surgical Wounds:

Type of wound Features Clean No hollow viscus entered Primary wound closure Elective procedure Clean contaminated Hollow viscus entered but controlled No inflammation Primary wound closure Contaminated Uncontrolled spillage from viscus Inflammation apparent Major break in aseptic technique Dirty 1. Untreated, uncontrolled spillage from viscus 2.Pus in operative wound 3.Open suppurative wound, severe inflammation Classification of Surgical Wounds

Classification of Wound healing :

Classification of Wound healing Primary intention Secondary intention Tertiary intention

Primary closure:

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

Secondary closure:

Secondary closure No active intent to seal the wound The wound is closed by reepithelization and contraction with some deposition of scar tissue

Delayed primary closure:

Delayed primary closure Tertiary intention Surgical intervention, such as suturing, skin graft replacement, or flap design, after repeated debridement and antibiotics therapy

Treatment of Wounds:

Treatment of Wounds Local Care Antibiotics Dressings Skin Replacements Growth Factor Therapy

Treatment of Wounds:

Treatment of Wounds ANTIBIOTICS Should be used only when there is an obvious wound infection . S igns of infection to look for include erythema, cellulitis, swelling, and purulent discharge. Indiscriminate use of antibiotics should be avoided to prevent emergence of multidrug resistant bacteria. .

Treatment of Wounds:

Treatment of Wounds DRESSING : The main purpose of wound dressings is to provide the ideal environment for wound healing. The dressing should facilitate the major changes taking place during healing to produce an optimally healed wound.

Desired Characteristics of Wound Dressings:

Desired Characteristics of Wound Dressings - Promote wound healing (maintain moist environment) -Conformability -Pain control -Odor control -Non-allergenic and nonirritating -Permeability to gas -non traumatic removal -Cost-effectiveness -Convenience Treatment of Wounds

Treatment of Wounds:

Treatment of Wounds MECHANICAL DEVICES: Augments and improves on certain functions of dressings, in particular the absorption of exudates and control of odor. The vacuum-assisted closure system assists in wound closure by applying localized negative pressure to the surface and margins of the wound. The negative pressure therapy is applied to a special foam dressing cut to the dimensions of the wound and positioned in the wound cavity or over a flap or graft. This form of therapy has been found to be effective for chronic open wounds (diabetic ulcers and stages 3 and 4 pressure ulcers), acute and traumatic wounds, flaps and grafts.

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Treatment of Wounds

Treatment of Wounds:

Treatment of Wounds SKIN REPLACEMENTS Skin grafts have long been used to treat both acute and chronic wounds. Split- or partial-thickness grafts consist of the epidermis plus part of the dermis, full-thickness grafts retain the entire epidermis and dermis. It resists wound contraction better & resulting in improved cosmesis

Treatment of Wounds:

Treatment of Wounds SKIN REPLACEMENTS Skin Substitutes :” tissue engineering combines novel materials with living cells to provide functional skin substitutes, providing a bridge between dressings and skin grafts.” advantages readily available, not requiring painful harvest, and they may be applied freely or with surgical suturing. They promote healing, either by stimulating host cytokine generation or by providing cells that may also produce growth factors locally. Disadvantages include limited survival, high cost , and the need for multiple applications .

Treatment of Wounds:

Treatment of Wounds SKIN REPLACEMENTS Skin Substitutes The acellular (e.g., native collagen or synthetic material) component acts as a scaffold, promotes cell migration and growth, and activates tissue regeneration and remodeling. The cellular elements re-establish lost tissue and associated function , synthesize extracellular matrix components, produce essential mediators such as cytokines and growth factors, and promote proliferation and migration. Bioengineered skin substitutes have evolved from keratinocyte monolayers to dermal equivalents to split-thickness products with a pseudoepidermis and, most recently, to products containing both epidermal and dermal components that resemble the three-dimensional structure and function of normal skin .

Treatment of Wounds:

Treatment of Wounds GROWTH FACTOR THERAPY Autologous growth factors are harvested from the patient's own platelets, yielding an unpredictable combination and concentration of factors, which are then applied to the wound. Recombinant molecular biologic means permit the purification of high concentrations of individual growth factors. At present, only platelet-derived growth factor BB ( PDGF-BB ) is currently approved by the FDA for treatment of diabetic foot ulcers. A great deal more needs to be discovered about the concentration, temporal release, and receptor cell population before growth factor therapy is to make a consistent impact on wound healing.

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“Treat the WHOLE patient and not just the HOLE in the patient”

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