dr nikil jain dr nikil jain

DefinitionDefinitionWoundWound --Loss of tissue integrity Loss of tissue integrity that leads to disruption of that leads to disruption of normal anatomic structure & normal anatomic structure & function.function.

Healing Healing --It is referred as It is referred as replacement of destroyed living replacement of destroyed living tissue. It comprises of tissue. It comprises of inflammation & repair .inflammation & repair .

CLASSIFICATIONCLASSIFICATION““Centers for disease control & prevention(CDC) Centers for disease control & prevention(CDC)

using an adaption of American college of using an adaption of American college of surgeonsurgeon’’s wound classification schemas wound classification schema””

Surgical wounds are:Surgical wounds are:I.I.Clean woundsClean woundsII.II.Clean-contaminated woundsClean-contaminated woundsIII.III.Contaminated woundsContaminated woundsIV.IV.Dirty or infected woundsDirty or infected wounds

1.1.Clean woundsClean wounds:-:-An uninfected operative wound in which An uninfected operative wound in which no inflammation is encountered & the no inflammation is encountered & the respiratory, alimentary, genital or respiratory, alimentary, genital or uninfected urinary tracts are not uninfected urinary tracts are not entered. Ex. Incisions made under entered. Ex. Incisions made under aseptic conditions.aseptic conditions.

Closed by primary union & usually are Closed by primary union & usually are not drained.not drained.

Apposition of tissue is maintained Apposition of tissue is maintained until wound tensile strength is until wound tensile strength is sufficient so that sutures or other sufficient so that sutures or other form of tissue apposition are no longer form of tissue apposition are no longer needed.needed.

2.2.Clean-contaminated woundsClean-contaminated wounds:-:-Operative wounds in which the Operative wounds in which the respiratory, alimentary, genital, respiratory, alimentary, genital, or or urinary tracts are entered under urinary tracts are entered under controlled conditions and without controlled conditions and without unusual contamination.unusual contamination.

Appendectomies, cholecystectomies, Appendectomies, cholecystectomies, and hysterectomies fall into this and hysterectomies fall into this category, as well as normally category, as well as normally clean clean wounds which become wounds which become contaminated by contaminated by entry into a entry into a viscus resulting in viscus resulting in minimal spillage of contents.minimal spillage of contents.

3.3.Contaminated woundsContaminated wounds:-:-Open, traumatic wounds or injuries such as Open, traumatic wounds or injuries such as soft tissue lacerations, open soft tissue lacerations, open fractures, fractures, and penetrating wounds; and penetrating wounds; operative operative procedures in which gross procedures in which gross spillage from spillage from the gastrointestinal the gastrointestinal tract occurs; tract occurs; genitourinary or biliary tract procedures genitourinary or biliary tract procedures in the presence of infected urine or bile; in the presence of infected urine or bile; and operations in which a major break in and operations in which a major break in aseptic technique has occurred (as in aseptic technique has occurred (as in emergency open cardiac emergency open cardiac massage)massage)

Microorganisms Microorganisms multiply so rapidly that multiply so rapidly that within 6 hours a contaminated wound within 6 hours a contaminated wound can can become infectedbecome infected..

4.4.Dirty and infected woundsDirty and infected wounds:-:-Heavily contaminated or Heavily contaminated or clinically clinically infected prior to the infected prior to the operation. operation. They include perforated viscera, They include perforated viscera, abscesses, or neglected traumatic abscesses, or neglected traumatic wounds in which wounds in which devitalized tissue devitalized tissue or foreign material or foreign material have been have been retained. Infection retained. Infection present at the present at the time of surgery can increase the time of surgery can increase the infection rate of any wound by an infection rate of any wound by an average of four times.average of four times.

Depending on capacity of cells to divide they can be Depending on capacity of cells to divide they can be grouped as:grouped as:

1.1. Labile cells-Labile cells- multiply through out life multiply through out life under normal physiologic conditionsunder normal physiologic conditions..

2.2. Stable cells-Stable cells- decrease or loose their decrease or loose their ability to proliferate after ability to proliferate after adolescence but retain their capacity adolescence but retain their capacity to multiply in response to stimuli to multiply in response to stimuli through out adult life.through out adult life.

3.3. Permanent cells-Permanent cells- loose their ability to loose their ability to proliferate around the time of birthproliferate around the time of birth..

Wound healingWound healing

Normal wound healingNormal wound healing regeneration or repairregeneration or repairAbnormal wound healingAbnormal wound healingUnregulated excessive healing Unregulated excessive healing Deficiency in healingDeficiency in healing

RegenerationRegeneration-- healing takes place by healing takes place by parenchymal cells and usually results in parenchymal cells and usually results in complete restoration of original complete restoration of original tissues.tissues.

RepairRepair- - when healing takes place by when healing takes place by proliferation of connective tissue proliferation of connective tissue elements results in fibrosis & scarring.elements results in fibrosis & scarring.

Wound healingWound healing3 main mechanisms3 main mechanisms

I.I. Connective tissue matrix Connective tissue matrix depositdeposit

II.II.ContractionContraction

III.III. EpithelizationEpithelization

Acute wounds normally heals Acute wounds normally heals in a very orderly and in a very orderly and efficient manner characterized efficient manner characterized by for distinct, But by for distinct, But overlapping phasesoverlapping phases

I.I.Hemostasis ( coagulation) Hemostasis ( coagulation) II.II.Inflammation Inflammation III.III.ProliferationProliferationIV.IV.RemodelingRemodeling

HemostasisHemostasis:-:-The normal healing response begins the The normal healing response begins the moment the tissue is injured.moment the tissue is injured.

The blood components spill into the site The blood components spill into the site of injury, the platelets come into of injury, the platelets come into contact with exposed collagen and other contact with exposed collagen and other elements of extra cellular matrix.elements of extra cellular matrix.

This contact triggers the platelet to This contact triggers the platelet to release clotting factor as well as release clotting factor as well as essential growth factors and cytokines essential growth factors and cytokines such as platelet derived growth factor such as platelet derived growth factor (PDGF) and transforming growth factor (PDGF) and transforming growth factor beta (TGF)beta (TGF)

The healing cascade begins The healing cascade begins immediately following injury immediately following injury when the platelets come into when the platelets come into contact with exposed contact with exposed collagen.collagen.

Platelet aggregation proceeds, Platelet aggregation proceeds, clotting factor are released clotting factor are released resulting in deposition of a fibrin resulting in deposition of a fibrin clot at the site of injury. clot at the site of injury.

The fibrin clot serves as a The fibrin clot serves as a provisional matrix and sets the stage provisional matrix and sets the stage for the subsequent events of healing. for the subsequent events of healing.

Platelets not only release the Platelets not only release the clotting factors needed to control clotting factors needed to control the bleeding and loss of fluid and the bleeding and loss of fluid and electrolytes but they also provide a electrolytes but they also provide a cascade of chemical signals, known cascade of chemical signals, known as cytokines or growth factors, that as cytokines or growth factors, that initiates the healing response.initiates the healing response.

The two most important signals are The two most important signals are PDGF and TGF-beta.PDGF and TGF-beta.

The PDGF initiates the chemotaxis of The PDGF initiates the chemotaxis of neutrophills, macrophages, smooth neutrophills, macrophages, smooth muscle cells and fibroblasts.muscle cells and fibroblasts.

TGF-beta adds another important TGF-beta adds another important signal for the initiation of signal for the initiation of the healing cascade by the healing cascade by attracting macrophages and attracting macrophages and stimulates them to secrete stimulates them to secrete additional cytokines including additional cytokines including FGF (fibroblast growth factor), FGF (fibroblast growth factor), PDGF, TNF a (tumor necrosis PDGF, TNF a (tumor necrosis alpha) & IL-1 (interleukin 1). alpha) & IL-1 (interleukin 1).

INFLAMMATORY PHASEINFLAMMATORY PHASENeutrophills are the next Neutrophills are the next predominent cell marker in the predominent cell marker in the wound within 24 hours after wound within 24 hours after injury.injury.

The major function of the The major function of the neutrophills is to remove foreign neutrophills is to remove foreign material, bacteria and non-material, bacteria and non-functional host cells and damaged functional host cells and damaged matrix components that may be matrix components that may be present in the wound site.present in the wound site.

Bacteria give of chemical signals Bacteria give of chemical signals attracting neutrophills, which attracting neutrophills, which injures them by the process of injures them by the process of phagocytosis.phagocytosis.

The mast cell is another marker cell The mast cell is another marker cell of interest in wound healing.of interest in wound healing.

Mast cells release granules filled Mast cells release granules filled with enzymes, histamine and other with enzymes, histamine and other active amines and these mediators are active amines and these mediators are responsible for the characteristic responsible for the characteristic signs of inflammation around the signs of inflammation around the wound site.wound site.

The active amines released from the The active amines released from the mast cell, causes surrounding vessels mast cell, causes surrounding vessels to become leaky and thus allow the to become leaky and thus allow the speedy passage of the mononuclear speedy passage of the mononuclear cells into the injury area.cells into the injury area.

By 48 hours after injury, fixed By 48 hours after injury, fixed tissue monocytes become activated tissue monocytes become activated to become wound macrophages.to become wound macrophages.

These specialized wound These specialized wound macrophages are perhaps the most macrophages are perhaps the most essential inflammatory cells essential inflammatory cells involved in the normal healing.involved in the normal healing.

Inhibition of macrophage function Inhibition of macrophage function will delay the healing response.will delay the healing response.

Once activated these wound Once activated these wound macrophages also release PDGF macrophages also release PDGF & TGF beta that further & TGF beta that further attracts fibroblasts and attracts fibroblasts and smooth muscle cells to the smooth muscle cells to the wound site. wound site.

These highly phagocytic macrophages are also These highly phagocytic macrophages are also responsible for removing non functional host responsible for removing non functional host cells, bacteria-filled neutrophills, damaged cells, bacteria-filled neutrophills, damaged matrix, foreign debris and any remaining matrix, foreign debris and any remaining bacteria from wound site.bacteria from wound site.

The presence of wound macrophages is a marker The presence of wound macrophages is a marker that the inflammatory phase is nearing an end that the inflammatory phase is nearing an end and proliferative phase is beginning.and proliferative phase is beginning.

PROLIFERATIVE PHASEPROLIFERATIVE PHASE As this phase progresses, the TGF-As this phase progresses, the TGF-beta released by the platelets, beta released by the platelets, macrophages and T-lymphocytes macrophages and T-lymphocytes becomes a critical signal. becomes a critical signal.

TGF-beta is considered to be a TGF-beta is considered to be a master control signal that regulates master control signal that regulates a host of fibroblasts functions.a host of fibroblasts functions.

TGF-beta has a 3 pronged effect on TGF-beta has a 3 pronged effect on extracellular matrix depositionextracellular matrix deposition . .

First, it increases transcription of First, it increases transcription of the genes for collagen, proteoglycans the genes for collagen, proteoglycans and fibronectin thus increasing the and fibronectin thus increasing the over all production of matrix proteins. over all production of matrix proteins.

At the same time TGF-beta decreases the At the same time TGF-beta decreases the secretion of proteases responsible for secretion of proteases responsible for the breakdown of matrix and it also the breakdown of matrix and it also stimulates the protease inhibitor, stimulates the protease inhibitor, tissue inhibitor of metallo-protease.tissue inhibitor of metallo-protease.

Other cytokines considered to be Other cytokines considered to be important are interleukins fibroblasts important are interleukins fibroblasts growth factors & TNF.growth factors & TNF.

As healing progresses, several As healing progresses, several responses are activated.responses are activated.

The process of epithelization is The process of epithelization is stimulated by presence of EGF stimulated by presence of EGF (epithelial growth factor) and TGF-(epithelial growth factor) and TGF-alpha that are produced by activated alpha that are produced by activated wound macrophages, platelets and wound macrophages, platelets and keratinocytes.keratinocytes.

Once the epithelial bridge is complete Once the epithelial bridge is complete enzymes are released to dissolve the enzymes are released to dissolve the attachment at the base of scab attachment at the base of scab resulting in removal.resulting in removal.

Due to high metabolic activity at Due to high metabolic activity at the wound site there is more demand the wound site there is more demand for oxygen & nutrients. for oxygen & nutrients.

Local factors in the wound micro Local factors in the wound micro environment such as low pH, reduced environment such as low pH, reduced oxygen tension and increased lactate oxygen tension and increased lactate actually initiate the release of actually initiate the release of factors needed to bring in a new factors needed to bring in a new blood supply, this process is called blood supply, this process is called angiogenesis or neovascularization angiogenesis or neovascularization

It is stimulated by vascular It is stimulated by vascular endothelial cell growth factor, endothelial cell growth factor, basic fibroblast growth factor and basic fibroblast growth factor and TGF-beta. TGF-beta.

As this phase progresses the As this phase progresses the predominant cell in the wound site predominant cell in the wound site is fibroblast. is fibroblast.

This cell of mesenchymal origin is This cell of mesenchymal origin is responsible for producing the new responsible for producing the new matrix needed to restore structure matrix needed to restore structure and function.and function.

Fibroblast attach to the cables of Fibroblast attach to the cables of the provisional fibrin matrix and the provisional fibrin matrix and begin to produced collagen.begin to produced collagen.

Finally collagen will mature by the Finally collagen will mature by the process of hydroxylation, process of hydroxylation, glycosylation & cross linking.glycosylation & cross linking.

REMODELING PHASEREMODELING PHASEFinal maturation of collagen Final maturation of collagen occurs during the final remodeling occurs during the final remodeling phase.phase.

This phase is characterized by This phase is characterized by continued synthesis and continued synthesis and degradation of the extra cellular degradation of the extra cellular matrix components trying to matrix components trying to establish a new equilibrium.establish a new equilibrium.

In summary the healing cascade In summary the healing cascade begins with an orderly process of begins with an orderly process of hemostasis & fibrin deposition hemostasis & fibrin deposition which leads to an inflammatory which leads to an inflammatory cell cascade, characterized by cell cascade, characterized by neutrophills, macrophages & neutrophills, macrophages & lymphocytes with in the tissue.lymphocytes with in the tissue.

This is followed by attraction & This is followed by attraction & proliferation of fibroblasts & proliferation of fibroblasts & collagen deposition & finally collagen deposition & finally remodeling by collagen cross remodeling by collagen cross linking & maturation.linking & maturation.

Types of wound healingTypes of wound healing

•Healing by Primary Healing by Primary intentionintention

•Healing by Secondary Healing by Secondary intention.intention.

Primary wound closurePrimary wound closureDef.Def.- - approximate approximate the acutely the acutely disrupted disrupted tissue with tissue with sutures, etc.sutures, etc.

IndicationIndication--clean clean surgical surgical wound, clean wound, clean contaminated contaminated woundwound

Primary wound closurePrimary wound closure

Healing by first intentionHealing by first intention

1. Initial hemorrhage1. Initial hemorrhage:: wound wound is filled with blood is filled with blood which then clots and which then clots and seals the wound seals the wound against dehydration against dehydration and infectionand infection

2. Inflammatory phase2. Inflammatory phase::

3.Epithelial changes3.Epithelial changes::Epidermal cells from both Epidermal cells from both the margins proliferate & the margins proliferate & migrate in the form of migrate in the form of epithelial spurs.epithelial spurs.

A well approximated wound A well approximated wound is covered by a layer of is covered by a layer of epithelium in 48 hrs.epithelium in 48 hrs.

The migrated epidermal The migrated epidermal cells separate the cells separate the underlying viable dermis underlying viable dermis from overlying necrotic from overlying necrotic material & clot, forming material & clot, forming a scab which is cast off.a scab which is cast off.

4. Organization4. Organization::By 3By 3rdrd day fibroblasts day fibroblasts also invade the wound also invade the wound area.area.

By 5By 5thth day new day new collagen fibrils start collagen fibrils start forming.forming.

In 4 weeks, the scar In 4 weeks, the scar tissue with scanty tissue with scanty cellular & vascular cellular & vascular elements, a few elements, a few inflammatory tissue is inflammatory tissue is formed.formed.::

Healing by second Healing by second intentionintention

1.1. Inflammatory phase:Inflammatory phase:2.2. Initial hemorrhage:Initial hemorrhage:

Wound contraction and epithelializationWound contraction and epithelialization

3.Epithelial changes:3.Epithelial changes: epidermal cells epidermal cells migrate in the migrate in the form of form of epithelial spurs epithelial spurs but do not cover but do not cover the surface the surface fully until fully until granulation granulation tissue from base tissue from base has started has started filling the filling the wound spacewound space..

4. Granulation 4. Granulation tissuetissue::

The main bulk of The main bulk of secondary healing is secondary healing is by granulation tissue.by granulation tissue.

5.Wound contraction5.Wound contraction::Important feature of Important feature of secondary healing.secondary healing.

Wound contracts to Wound contracts to one-third to one one-third to one fourth of its original fourth of its original sizesize

Factors influencing wound Factors influencing wound healinghealing

A)A)General factorsGeneral factors 1. Age1. Age 2. Temperature2. Temperature 3. Nutrition: deficiency of3. Nutrition: deficiency of a. Protein a. Protein - - interfere with formation of interfere with formation of

granulation tissue & collagen.granulation tissue & collagen. - wound lacks tensile - wound lacks tensile

strength strength - Synthesis of pro collagen - Synthesis of pro collagen

is hamperedis hampered

Vitamin C deficiency:Vitamin C deficiency:• Results in capillary fragilityResults in capillary fragility• Formation of unstable collagen which is Formation of unstable collagen which is quickly quickly

degraded by collagenolysis.degraded by collagenolysis. Vitamin E:Vitamin E:• Serves as membrane stabilizer & plays an Serves as membrane stabilizer & plays an

important role in lysosome functionimportant role in lysosome function Vitamin A deficiencyVitamin A deficiency::• Decrease collagen synthesis and stabilityDecrease collagen synthesis and stability

Zinc DeficiencyZinc Deficiency:: -DNA & RNA polymerase, are zinc -DNA & RNA polymerase, are zinc dependent.dependent.

-Zinc excess also inhibit healing -Zinc excess also inhibit healing 4. Corticosteroids: 4. Corticosteroids: - suppression of immune system.- suppression of immune system.5. Medicaments:5. Medicaments: warferrin & heparin decrease formation warferrin & heparin decrease formation of fibrin of fibrin

matrix.matrix.6. Diabetes :6. Diabetes : a. a. Increased susceptibility to infections Increased susceptibility to infections due to due to

decreased phagocytic capacity & decreased phagocytic capacity & neutrophil neutrophil

chemotaxis.chemotaxis.

b. Hyperglycemia results in b. Hyperglycemia results in decreased activity of phagocytes & decreased activity of phagocytes & production of abnormal collagen.production of abnormal collagen.

c. Insulin is required for earliest c. Insulin is required for earliest stages of collagen formation.stages of collagen formation.

7.Depressed general resistance; infection7.Depressed general resistance; infection

8.Shock:8.Shock:

9.Malignancy:9.Malignancy:

10. Genetic defects10. Genetic defects 11. Coagulation disorders:11. Coagulation disorders: Formation of poor fibrin network & Formation of poor fibrin network & abnormal abnormal

platelet adhesionplatelet adhesion

12. Smoking:12. Smoking: CO2 binds preferentially to hemoglobinCO2 binds preferentially to hemoglobin nicotine is potent nicotine is potent vasoconstrictor ,associated vasoconstrictor ,associated

with hypercoaguability & with hypercoaguability & predisposes to predisposes to

micro vascular occlusion.micro vascular occlusion.

Local factorsLocal factors1.1. InfectionInfection2.2. MovementMovement3.3. Poor blood supplyPoor blood supply4.4. Presence of foreign bodiesPresence of foreign bodies5.5. Haematoma Haematoma 6.6. oedemaoedema7.7. Surgical causes Surgical causes

Healing of FracturesHealing of Fractures Healing of fractures can be Healing of fractures can be

considered in many stages, in fact it considered in many stages, in fact it is continuous and different stages is continuous and different stages overlap in different areas.overlap in different areas.

Integrity of periosteumIntegrity of periosteum alone can alone can ensure adequate blood supply.ensure adequate blood supply.

1.1. Haematoma formationHaematoma formation:: Due to torn blood vessels. The broken Due to torn blood vessels. The broken

fragments may further damage soft fragments may further damage soft tissues. Haematoma holds the tissues. Haematoma holds the fragments together loosely through fragments together loosely through fibrin network.fibrin network.

2.Inflamatory reaction2.Inflamatory reaction:: Hyperemia of the reaction causes Hyperemia of the reaction causes decalcification of bone adjacent to decalcification of bone adjacent to the fracture. Macrophages phagocytose the fracture. Macrophages phagocytose red cells and debris of soft tissues. red cells and debris of soft tissues. Resorption of necrosed bone is a slow Resorption of necrosed bone is a slow process, it is executed through process, it is executed through osteoclasts and is helped by acid pH osteoclasts and is helped by acid pH which develops in the area.which develops in the area.

3. Organization of granulation tissue3. Organization of granulation tissue Granulation tissue originates from Granulation tissue originates from soft tissues of bone (marrow, soft tissues of bone (marrow, endosteum and periosteum) and from endosteum and periosteum) and from soft tissues around fractured bone.soft tissues around fractured bone.

4. Formation of provisional callus4. Formation of provisional callus: (Latin – : (Latin – hard). hard).

Is hard calcified granulation Is hard calcified granulation tissue uniting the fractured tissue uniting the fractured ends. The formation begins ends. The formation begins between 6th and 10th day.between 6th and 10th day.

The main contribution comes The main contribution comes from the undamaged cells of the from the undamaged cells of the periosteum& endosteum.periosteum& endosteum.

Formation of nonlamellar bone:Formation of nonlamellar bone: Follows intra-membranous ossification.Follows intra-membranous ossification. Osteoid laid by osteoblasts Osteoid laid by osteoblasts subsequently get calcified.subsequently get calcified.

Calcification is helped by alkalinity Calcification is helped by alkalinity of tissues, alkaline phosphatase of tissues, alkaline phosphatase secreted by osteoblasts ,local super secreted by osteoblasts ,local super saturation of calcium derived by saturation of calcium derived by resorption of bony spicules.resorption of bony spicules.

Bony callus predominates whenever Bony callus predominates whenever fracture segments are properly fracture segments are properly immobilizedimmobilized. .

Formation of cartilage:Formation of cartilage: The process is same as The process is same as endochondral ossification.endochondral ossification.

Cartilage formation occurs Cartilage formation occurs prominently in superficial part of prominently in superficial part of callus.callus.

Greater the movement of fractured Greater the movement of fractured fragments or their separation, fragments or their separation, larger the amount of cartilage larger the amount of cartilage formed.formed.

Provisional callus is completely Provisional callus is completely formed in 2 to 3 weeks.formed in 2 to 3 weeks.

5. Formation of definitive callus5. Formation of definitive callus::External callus is removed, intermediate callus External callus is removed, intermediate callus

converted into compact cortical bone and the converted into compact cortical bone and the internal callus is turned into cancellous bone internal callus is turned into cancellous bone &hollowed out to form the marrow cavity.&hollowed out to form the marrow cavity.

Fat & marrow cells reappear in cavity. old & new Fat & marrow cells reappear in cavity. old & new bone are firmly cemented.bone are firmly cemented.

It is a complex process and regulated by hormones It is a complex process and regulated by hormones & growth factors.& growth factors.

Healing of Extraction Healing of Extraction SocketSocket Socket heal by second intention.Socket heal by second intention.Events in 1Events in 1stst week weekWhen a tooth is removed ,socket When a tooth is removed ,socket fills with blood which coagulates fills with blood which coagulates to seal it from oral environment.to seal it from oral environment.

Inflammation & clearance of debris Inflammation & clearance of debris such as bone fragments.such as bone fragments.

Fibroplasia also begins during first Fibroplasia also begins during first week.week.

Epithelium migrates until it meets Epithelium migrates until it meets epithelium from other side or it epithelium from other side or it finds a bed of granulation tissue.finds a bed of granulation tissue.

Osteoclasts accumulate along the Osteoclasts accumulate along the crestal bone.crestal bone.

22ndnd week weekOsteoid deposition along alveolar Osteoid deposition along alveolar bone lining.bone lining.

Epithelium may be fully intact.Epithelium may be fully intact.

33rdrd & 4 & 4thth week weekEpithelization of most socket being Epithelization of most socket being complete .complete .

Resorption of cortical bone from crest Resorption of cortical bone from crest and wall of socket.and wall of socket.

4-6 months4-6 monthsComplete resorption of cortical bone Complete resorption of cortical bone lining.lining.

Epithelium moves toward the crest as Epithelium moves toward the crest as bone fills socket. eventually becoming bone fills socket. eventually becoming level with adjacent crestal gingiva.level with adjacent crestal gingiva.

Radio graphically loss of distinct Radio graphically loss of distinct lamina dura.lamina dura.

Hyperbaric oxygen Hyperbaric oxygen • Beneficial effects:Beneficial effects: 1. Decreased local tissue edema1. Decreased local tissue edema 2. Improved cellular metabolism2. Improved cellular metabolism 3. Improved local tissue oxygen.3. Improved local tissue oxygen. 4. Improved leukocyte-killing ability.4. Improved leukocyte-killing ability. 5. Increased effectiveness of antibiotics5. Increased effectiveness of antibiotics

6. Enhanced uptake of platelet derived 6. Enhanced uptake of platelet derived growth factor.growth factor.7. Promotion of collagen deposition.7. Promotion of collagen deposition.8. Promotion of neoangiogenesis.8. Promotion of neoangiogenesis.9. Enhanced epithelial migration.9. Enhanced epithelial migration.

..

Abnormality in Wound Abnormality in Wound HealingHealing

i.i. Excessive wound healingExcessive wound healing

ii.ii.Inadequate wound Inadequate wound healinghealing

Excessive Wound Excessive Wound HealingHealing5-15% of wounds5-15% of woundsExcessive wound healing can Excessive wound healing can result in Hypertrophic scar result in Hypertrophic scar or Keloid formation.or Keloid formation.

Hypertrophic scarHypertrophic scar:: remain remain within the within the borders of borders of the original the original scarscar

KeloidKeloid - - extend extend beyond the beyond the original scar original scar marginsmargins

Excessive Wound HealingExcessive Wound Healing

Differ clinically and biologicallyDiffer clinically and biologically::

Hypertrophic scarHypertrophic scar - develop in weeks - develop in weeks after injury, regress over period after injury, regress over period of time.of time.

KeloidKeloid - - can develop up to 1 year, can develop up to 1 year, usually do not regress, usually usually do not regress, usually recur after excision.recur after excision.

Inadequate Wound Inadequate Wound HealingHealing•Disrupted normal sequenced of Disrupted normal sequenced of wound healingwound healing

•Chronic wound - pressure ulcer, Chronic wound - pressure ulcer, diabetic ulcer, venous static diabetic ulcer, venous static ulcer, etc.ulcer, etc.