Egyptians-

first to differentiate bet. Infected and non infected wounds

 1650 B.C. Edwin Smith Surgical Papyrus -48

different types of wounds

 They used honey ,lint and grease for treating

wounds
 Galen- importance of moist environment

Louis Pasteur (1822-1895) germ theory of disease Joseph Lister used phenol for soaking his surgical instruments 1960-1970 s development of polymeric dressings

WOUND bodily injury in which there is disruption of normal continuity of structures WOUND HEALING restoration of tissue continuity after injury ,involves wound closure and restoration of function Galen identified primary intentions of wound healing and secondary

FIRST INTENTION - clean ,well perfused ,incised surgical wounds - casual wounds ,minimum destruction of tissue ,edges are closely apposed SECOND INTENTION - large wounds ,significant loss or destruction of tissue - edges cannot be apposed e.g. gaping wounds with lacerated edges, leg ulcers ,highly suppurative wounds

y 1. Inflammation y 2. New tissue formation (proliferation) y 3. Matrix formation and remodeling

Localized protective tissue response due to injury or destruction of tissues

 Acute inflammatory response  Early inflammation  Late inflammation

From the onset of injury to fourth day of healing

 Generates an environment for the formation of

granulation tissue
 Results in removing the debris and necrotic

tissue from the injured area and local reduction of infection

Characterized

by clot formation both in damaged vessels and wound , providing a matrix of fibrin ,fibronectin, vWF, thrombospondin

Facilitate migration of cells into the wound  Stimulate fibroblast proliferation  Shields mitogenic and chemo tactic

factors

from inhibitors

Hemostasis is achieved by platelet mediated

vasoconstriction

Platelet releases biologically active substance s

,that stimulate ECM and cell migration e.g., PDGF ,PF4 , TGF alpha, TGF beta,

Activation

of classical and alternative complement cascades leading to the formation of anphylotoxins C3a , C5a . stimulate release of vaseactive mediators e.g., histamine ,LTC4 ,LTD 4 etc.

Anaphylotoxins

 Early inflammation neutrophil rich.  Attracted by leukocyte chemo tactic factors like

fibrinopeptides ,fibrin lysis ,C5a,LTB4,PAF,PAF,TNF-A,PDGF,

 Main function

products

phagocytosis, release of toxic oxygen intermediates

 Neutrophil infiltration stops in few days, transition

occurs to late inflammation but lengthens in contaminated wounds

Accumulation of macrophages Functions

  

eliminate deleterious materials generate chemo tactic factors releases collagenases ,growth and regulatory factors

e.g. PDGF,FGF,TGF a ,TGF b ,IL -1  critical to the formation of granulation tissue

Macrophage deletion leads to lack of wound

debridement and delay in fibroblast recruitment and proliferation and in matrix synthesis
These

growth and chemotactic factors are necessary for granulation tissue formation and transition to proliferative phase

Starts 5 days of post injury and lasts for 10-14

days  formation of granulation tissue -cells get embedded in loose matrix of collagen type 1 and 3 ,fibrin ,fibronectin and proteoglycans
Fibroblasts construct new extra cellular matrix I

n which macrophages ,blood vessels and fibroblsast get embedded

Endothelial cells form new blood vessels ,which

supply nutrients and oxygen to the wound

Cutaneous wound repair re epithelialization and

granulation tissue formation

Reconstitution of the cells of the epidermis Process starts within hours Source of keratinocytes

partial thickness wounds margin ,hair follicles and ducts of sweat glands full thickness wounds - only source wound margin

y Three phases

1 Fibroplasia 2 Wound contraction 3 Angiogenesis Fibroplasia y Fibroblast recruitment and synthesis of both collagenous and non collagenous matrix

undergo transformation into myofibroblasts Loose ECM 1 aides adhesion of fibroblasts 2 stimulation of migration of fibroblasts 3 supports and orientation to the collagen fibrils ,helps in wound contraction ECM synthesis stops under the influence of interferon gamma
Fibroblast

Wound contraction
y Day 7- 14 y Reduction of all or part of skin defect ,by

centripetal movement of undamaged skin

y Two theories

1 myofibroblast theory cell contraction 2 fibroblast theory cell traction

 New blood vessel formation starts with

fibroplasia
Commences 2 to 3 days after injury Capillaries bud from preexisting functioning

small venules
Macrophages secrete powerful angiogenic stimuli

like FGF,TNF a ,IL-8,lactic acid ,low oxygen tension

Commences with granulation tissue formation

and lasts for months and years

Granulation tissue is replaced by scar tissue Scar tissue is functionally inferior and only

reaching 70 -80 % of original tensile strength

Tensile strength increases due to

1 Increase in collagen deposition 2 Realignment of collagen into large bundle

y DIAGNOSIS is the most important thing y Factors influencing wound healing

1 Patients age , 2 Nutritional status , 3 underlying chronic conditions , 4 Any drug regime 5 Any infections

y Ageing Affects all stages of wound healing y Onset of inflammation is delayed and lasts longer y Cell

proliferation and metabolism, rate of

capillary growth decreases

y Decreased fibroblast activity results in decreased

amount of collagen ,cross linkage and tensile strength

Malnutrition or deficiency of nutrients like zinc

,vit C, iron delay wound healing

Impair immune resistance Increased risk of infection Increased risk of complications ,prolonged

recovery and hospital stay .

Parameters weight ,height, loss of weight

(unintentional) and appetite ,any reduced activity and any diseases like chronic diarrhea and vomiting Measurements
 serum albumin ,  serum transferrin ,  triceps skin fold thickness

Diabetes ,arteriosclerosis and chronic venous

insufficiency
 impair vascular supply and causes tissue hypoxia

Anti inflammatory drugs  Glucocorticoids, cytotoxics, anticoagulants

,immunosuppressive ,pencillamne ,HRT

Delay wound healing by prolonging the

inflammatory response ,which further causes the tissue damage. Susceptibility of infection increases
 presence of necrotic tissue  foreign particles  hematoma in the wound

Wound closure Primary Secondary Acute

causes Chronic

stages of healing

1 thermal 1 diabetic 2 post operative 2 pressure ulcers 3 mechanical 3 leg ulcers

stages of healing Inflammation proliferation 1 granulation 2 epithelial 3 slough 4 necrotic 5 infected remodeling

1. Erythema 2. Presence of pus 3. Excess exudates 4. Odour 5. Change in pain 6. Pyrexia 7. Delayed healing 8. Friable granulation tissue 9. Pocketing at the base of wound

 Swab taken from wound surface showing more than

105 bacteria per gram

Numerous ways ,can be assessed by invasive

and non invasive methods Invasive  histogy , biochemical analysis ,angiography, Non invasive  wound area, wound depth, wound volume,

of wound dressing is to provide optimum environment for the healing of wound Mimics the barrier function of efpithelium and provide hemostasis Improving the gas and solute exchange between blood and tissue Cannot sterilize a wound but provides conditions for reducing the pathogenic overload and delivers antimicrobial agents
Function

1. Primary and secondary dressings 2. Absorbent dressings 3. Non adherent dressings 4. Occlusive /semi occlusive dressings 5. Hydrophilic/Hydrophobic dressings 6. Hydrocolloid and Hydrogel dressings 7. Absorbable materials 8. Medicated dressings

Primary dressing

placed in direct contact with wound provide absorptive capacity ,desication and infection Secondary dressing placed over primary dressing further protection ,absorptive capacity ,compression and occlusion

Imbibe exudate without inebriation Cotton ,wool ,sponge and moss have been used Other absorbent dressings chitin ,chitosan

,alginates ,pectin ,gelatin karaya gums Nonadherent dressings Designed not to stick to wound Gauze is impregnated with paraffin, petroleum jelly ofr KY jelly A secondary dressing should be always used ,to prevent desiccation and entrance of pathogens

Provide

an environment for a clean,minimally exudative wound

Negative pressure- assisted wound closure

y Subatmospheric pressure is applied to wide variety

of wounds y Helps in removal of chronic edema ,increase in blood flow ,and growth of granulation tissue

Hydrophilic /hydrophobic

hydrophilic desinged to absorb the exudate hydrophobic renders the dressig water proof Hydrocolloid and hydrogel dressings combine the benefits od occlusion and absorbency form complex structures with the dispersion medium increase epidermal healing by 30-36% compared with untreated partial thickness wounds

Absorbable materials

degraded invivo Used as hemostats Eg collagen, gelatin,oxidized cellulose Medicated dressings Enhance epidermal resurfacing eg benzoyl peroxidecream , cod liver oil ,allantoin ,zinc oxide treatment,shark liver oil

Exuding wounds

-hydrocolloids and hydrogel ,absorbent dressings Cavity wounds -non adherent dressings with secondary dressing ,hydrogels , hydrocolloids ,medicated dressings Sloughy wounds -hydrogels ,hydrocolloids ,mechanical debridement, absorbent dressings Infected wounds -General infection control measures like hand washing ,systemic and topical anti microbial s

Necrotic wounds

-hydrogels ,hydrocolloids ,mechanical debridement Malodourous wounds -activated charcoal dressings ,sugar paste,metronidazole gels Malignant/fungating wounds -control bleeding ,analgesia,debridement,care surrounding skin Oedematous wounds -compression bandages ,exercise,elevation of limb

Change from occlusive to non occlusive Light pressure dressings Topical application of corticosteroids eg

terracortril Allowing to heal by itself

Surrounding skin care

Paste bandages and hydrated dressings

 Venous ulcers- compression bandages ,paste bandages

,elevation ,exercise  Arterial ulcers paste bandages ,exercise,compression bandages are contraindicated  Mixed artreial and venous ulcers- treat as arterial ulcers with light compression bandages  Pressure ulcers relieve pressure and appropriate dressings  Burns and scalds cold running water ,antimicrobials topical and systemic ,emollients  Diabetic ulcers- foot care ,therapeutic shoes etc

Keloids  Scars that grow beyond the borders of original wounds and rarely regress with time  -sites above the clavicles ,upper extrmeties ,face like pinna Hypertrophied scars  -Scars grow within the borders and frequently regress spontaneously  -Sites any where in the body  -mediated by TGF b activation ,leading to excessive collagen deposition versus degradation

THANK U..