inflamation and wound healing

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INFLAMMATION AND WOUND HEALING Guided by: Dr Sowmya Kote Dr Ashish Singla Presented by: Dr Hansa kundu:

INFLAMMATION AND WOUND HEALING Guided by: Dr Sowmya Kote Dr Ashish Singla Presented by: Dr Hansa kundu

Contents::

Contents: Introduction History Signs Types :Acute & chronic Acute inflammation: -Vascular events - Cellular events Chemical mediators of inflammation

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Inflammatory cells Fate of acute inflammation Chronic inflammation Granulomatous inflammation Healing: a) Regeneration b) Repair c) Wound Healing: -Healing by First intention -Healing by secondary intention -Factors influencing healing d) Healing in specialized tissues Wound care

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INTRODUCTION DEFINITION: As by Textbook of Pathology by Harsh Mohan Inflammation- It is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cells and tissues.

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• Egyptian papyrus - 3000 B.C. The word inflammation means ‘Burning’ • Celsus (Roman in 1st century A.D.) SIGNS: Rubor - Tumor - Calor - Dolor redness - swelling - heat - pain • Virchow added functio laesa later History

TYPES OF INFLAMMATION:

Acute inflammation “The immediate and early response to an injurious agent” Chronic inflammation “Inflammation of prolonged duration (weeks or months) in which active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously“ TYPES OF INFLAMMATION

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Acute - minutes to days Characterized by fluid and protein PMN’s SG > 1.020 Chronic - weeks to years Lymphocytes and macrophages ACUTE Infection - PMN’s ( Polymorph nuclear Cells) CHRONIC Infection - Mono nuclear Cells EXUDATE

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Exudate •  vascular permeability • high protein & cell debris • Specific Gravity > 1.020 Transudate • normal vascular permeability • low protein (mostly albumin) • Specific Gravity < 1.012 Edema - exudate or transudate ; interstitium or cavity

Acute inflammation :

Acute inflammation i) Vascular events: a) Hemodynamic changes b) Altered vascular permeability ii) Cellular events: a) Exudation of Leucocytes b) Phagocytosis

Vascular events: Hemodynamic Changes :

Vascular events: Hemodynamic Changes Transient vasoconstriction Persistent Progressive Vasodilatation Local Hydrostatic Pressure Slowing/stasis Leucocytic Margi nation

LEWIS EXPERIMENT:

LEWIS EXPERIMENT

ALTERED VASCULAR PERMEABILITY:

ALTERED VASCULAR PERMEABILITY The appearance of inflammatory oedema due to increased vascular permeability of micro vascular bed is explained on the basis of Starling’s hypothesis. In normal conditions fluid balance is maintained by two opposing set of forces: i) Forces that cause outward movement of fluid from microcirculation are intravascular hydrostatic pressure and osmotic pressure of interstitial fluid.

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ii) Forces that cause inward movement of interstitial fluid into circulation are intravascular osmotic pressure and hydrostatic pressure of the interstitial fluid. Whatever little fluid is left in the interstitial compartment is drained away by the lymphatics and thus no oedema occurs normally.

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However, in Inflamed tissues –endothelial lining of microvasculature becomes more leaky. Consequently 1. Intravascular osmotic pressure decreases 2.osmotic pressure of the interstitial fluid increases resulting in excessive outward flow of fluid into the interstitial compartment which is exudative inflammatory oedema.

Fig 3-3:

Fig 3-3

Fig 3-2:

Fig 3-2

MECHANISMS OF INCREASED VASCULAR PERMEABILITY:

MECHANISMS OF INCREASED VASCULAR PERMEABILITY Endothelial cell contraction Junctional retraction Direct endothelial injury (immediate sustained response) Leukocyte-dependent endothelial injury Others

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1) Endothelial cell contraction: Endothelial cells contract Develop gaps and become leaky Release of histamine, bradykinin and other chemical mediators Reversible Short duration(15-30 minutes)

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2) Endothelial cell retraction: Structural reorganization of cytoskeleton of endothelial cells This causes reversible retraction at the intercellular junctions. Lasts for 2-4 hours or more Mediated by cytokines

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3) Direct endothelial injury Endothelial cell necrosis and detachment Result of severe injury or burn Process of thrombosis is initiated. Occurs immediately and lasts until vessel repaired

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4) Endothelial injury mediated by leucocytes: Occurs at sites of leukocyte accumulation Due to leukocyte activation which releases proteolytic enzymes and toxic oxygen

Cellular events: Exudation of leucocytes:

Cellular events: Exudation of leucocytes The escape of leucocytes from the lumen of microvasculature to the interstitial tissue is the most important feature of inflammatory response. Changes in the formed elements of blood Adhesion and Rolling Emigration & Diapedesis Chemo taxis

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SLOWING CONCENTRATION Margination Rolling Adhesion Transmigration

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Selectins CAMS Integrins Mucin-like glycoproteins (Sialyl-Lewis X PSL-1 & ESL-1) Weak and transient binding P-selectin on platelets E-selectins on endothelial cell L-selectin on lymphocytes Results in rolling Integrins upregulated and activated for increased affinity to CAMS Results in firm adhesion

Fig 3-6:

Fig 3-6

Fig 3-9:

Fig 3-9

Leukocyte adhesion deficiency 1 (LAD-1):

Leukocyte adhesion deficiency 1 (LAD-1) Recurrent bacterial infections Inflammatory lesions lack neutrophil infiltrate High numbers of neutrophils in the circulation Neutrophils from patients can roll but do not stick

Mechanism of leukocyte adhesion deficiency 1 (LAD -1):

Mechanism of leukocyte adhesion deficiency 1 (LAD -1) Absence of integrins on neutrophils Mutation in n-terminal region of the integrin  chain inhibits proper integrin assembly

Chediak-Higashi Syndrome:

Chediak-Higashi Syndrome Defect in chemotaxis and lysosomal degranulation into phagosomes

Chronic Granulomatous Disease:

Chronic Granulomatous Disease Defect in NADPH oxidase system Marked decrease in ability to kill microorganisms

Cellular events Phagocytosis :

Cellular events Phagocytosis Phagocytosis (engulfment of solid particulate material by the cells-PMNs ,circulating monocytes , macrophages) Attachment stage (Opsonisation) Opsonins coat target and bind to leukocytes IgG opsonin and its corresponding receptor on the surface of polymorphs and monocytes is Fc fragment of immunoglobulin. C3b opsonin fragment of complement and corresponding receptor for C3b on surface of phagocytic cells

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Engulfment Stage Secretion (Degranulation) stage Killing/degradation O 2 dependent: Reactive O 2 species in lysosomes & EC O 2 independent: Bactericidal permeability agents, lysozyme, MBP, lactoferrin Nitrous oxide mechanism

Chemical mediators of inflammation:

Chemical mediators of inflammation Plasma-derived Circulating precursors Have to be activated Cell-derived Sequestered intracellular Synthesized de novo Most mediators bind to receptors on cell surface but some have direct enzymatic or toxic activity Mediators are tightly regulated

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Chemotactic factors (eg. c5a) Tissue injury Vasoactive mediators (eg. histamine) Increased vascular permeability Recruitment of inflammatory cells Edema PMNs Monos Production of inflammatory mediators Acute inflammation Chronic inflammation

Cell-derived mediators vasoactive amines:

Cell-derived mediators vasoactive amines Histamine Found in mast cells, basophils and platelets Released in response to stimuli Main actions of histamine are- vasodilatation, increased vascular permeability, itching and pain. Serotonin Vasoactive effects similar to histamine Found in platelets Released when platelets aggregate

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ARACHIDONIC ACID METABOLITES Where is it located? AA is a component of cell membrane phospholipids The breakdown of AA into its metabolites produces a variety of biologic effects Metabolites of AA - short-range hormones AA metabolites act locally at site of generation Rapidly decay or are destroyed

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AA is released from the cell membrane by phospholipases which have themselves been activated by various stimuli and/or inflammatory mediators AA metabolism occurs via two major pathways named for the enzymes that initiate the reactions; lipoxygenase and cyclooxygenase

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AA metabolites (eicosanoids) Cyclooxygenases synthesize Prostaglandins Thromboxanes Lipoxygenases synthesize Leukotrienes Lipoxins

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PGG 2  PGH 2 PGI 2 Prostacyclin TXA 2 Thromboxane PGD 2 ; PGE 2 PGF 2 Vasodilatation Inhibits Platelet Aggregation Vasoconstriction Promotes Platelet Aggregation Vasodilatation Edema PGI 2 TXA 2

Fig 3-17:

Fig 3-17

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Participate in every aspect of acute inflammation Effective Anti-inflammatory agents act on AA pathways Aspirin and Non-Steroidal Anti-inflammatory Drugs (NSAID’s) - Cyclooxygenase path Steroids act, in part, by inhibiting Phospholipase A2

Platelet-Activating Factor (PAF):

Platelet-Activating Factor (PAF) Another phospholipid-derived mediator released by phospholipases Induces aggregation of platelets Causes vasoconstriction and bronchoconstriction 100 to 1,000 times more potent than histamine in inducing vasodilation and vascular permeability Enhances leukocyte adhesion, chemotaxis, degranulation and the oxidative burst

Cytokines:

Cytokines Polypeptides that are secreted by activated lymphocytes and activated monocytes. Act to regulate cell behaviors Autocrine, paracrine or endocrine effects These “biological response modifiers” are being actively investigated for therapeutic use in controlling the inflammatory response.

Nitric Oxide:

Nitric Oxide NO is a soluble free radical gas Made by nitric oxide synthetase (NOS) in endothelium (eNOS), macrophages (iNOS), and specific neurons in the brain (nNOS) Broad range of functions and effects that are short range Vasodilatation by relaxing smooth muscle.  platelet aggregation Inhibits mast cells Regulates leukocyte recruitment

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Plasma Mediator Systems - Interaction 1. Kinin 2. Clotting 3. Complement 4. Fibrinolytic

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L,. C5 C5a Plasminogen  Plasmin C3 C3a Fibrin  FibrinSplitProducts Prothrombin  Thrombin Fibrinogen XII Kinin Complement Clotting Fibrinolytic Fibrinopeptides Prekallikrein XIIa Kallikrein High Mol. Wt. Kininogen B r adykinin Plasma Mediator Systems - Interaction

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KININ system: Leads to formation of bradykinin Bradykinin causes Increased vascular permeability Arteriolar dilatation Smooth muscle contraction Bradykinin is short lived (kininases) Vascular actions similar to histamine

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Bradykinin : Potent biomolecule 1. Vasodilatation 2. Increased vascular permeability 3. Contraction of smooth muscle 4. Pain on injection 5. Short life, kininase degrades Factor XII activated by: 1. Plasmin 2. Kallikrein 3. Collagen & basement membrane 4. Activated platelets 5. Co-factor = HMWK Vascular Permeability : - Bradykinin - Fibrionopeptides - Fibrin Split Prod. - Factor Xa - Leukotrienes

Fig. 3-17:

Fig. 3-17

Complement system:

Complement system The activation of complement system can occur either: i) By classic pathway through antigen-antibody complexes. ii) By alternate pathway via non-immunologic agents such as bacterial toxins, cobra venoms and IgA.

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Complement system on activation by either of these two pathways yields anaphylatoxins C3a,C4a, C5a and Membrane Attack Complex (MAC) The actions of anaphylatoxins in inflammation are: a) Release of histamine from mast cells and basophills

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b) Increased vascular permeability causing oedema in tissues. c) C3b augments Phagocytosis d) C5a is chemo tactic for leucocytes e) The action of MAC is to cause pores in the cell membrane of the invading microorganisms.

Fig 3-16:

Fig 3-16

Systemic effects of acute inflammation:

Systemic effects of acute inflammation Fever Leucocytosis Lymphangitis – Lymphadenitis. Shock

Outcomes of Acute Inflammation:

Outcomes of Acute Inflammation Resolution Fibrosis/Healing by scarring Abscess formation Progression to chronic inflammation

Chronic inflammation:

Chronic inflammation Inflammation of prolonged duration in which active inflammation, tissue injury and the healing proceed simultaneously. It can be caused by one of the following three ways: Chronic inflammation following acute inflammation Recurrent attacks of acute inflammation Chronic inflammation starting de novo.

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General features of chronic inflammation: Infiltration with mononuclear cells (macrophages, lymphocytes & plasma cells) Tissue destruction Repair involving angiogenesis and fibrosis Macrophage is the prima donna of chronic inflammation

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TYPES OF CHRONIC INFLAMMATION 1. Non-Specific When the irritant substance produces a non specific chronic inflammatory reaction with formation of granulation tissue and healing by fibrosis e.g. chronic osteomyelitis, chronic ulcer 2. Specific When the injurious agent causes a characteristic histological tissue response e.g. Tuberculosis, leprosy etc

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Key macrophage events 1. Recruitment from circulation 2. Local Proliferation 3. Immobilization 4. Differentiation (microglia, kupffer, alveolar macrophage, osteoclasts). Macrophage prominent role due the large repertoire of products it can produce when activated

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Note that the activated macrophage releases products that are similar to those released by PMNs Fig 3-28

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Antigen Presentation to T cells Lymphocyte Activated Lymphocyte Macrophage Activated macrophage IF N-  IL-1 TNF-  Other inflammatory mediators Fig 3-30

Granulomatous Inflammation:

Granulomatous Inflammation Aggregations of activated, modified (epitheliod) appearance Granuloma – focal collection of Granulomatous inflammation Bacteria Tuberculosis Leprosy Parasites Schistosomiasis Fungi Histoplasmosis Blastomycosis Metal/Dust Berylliosis Silicosis Foreign body Splinter Suture Graft material Sarcoidosis

Granuloma:

Granuloma

Healing:

Healing

Process of healing involves 2 distinct processes:

Process of healing involves 2 distinct processes 1) REGENERATION When healing takes place by proliferation of parenchymal cells & usually results in complete restoration of original tissues

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Depending upon their capacity to divide, cells of the body can be divided into: Labile cells - continuously dividing Epidermis, mucosal epithelium, GI tract epithelium etc Stable cells - low level of replication Hepatocytes, renal tubular epithelium, pancreatic acini Permanent cells - never divide Nerve cells, cardiac myocytes, skeletal muscle

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Regeneration of any type of parenchymal cells involves the following two processes: i) Proliferation of original cells from the margin of injury with migration so as to cover the gap. ii) Proliferation of migrated cells with subsequent differentiation and maturation so as to reconstitute the original tissue.

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2) REPAIR Healing takes place by proliferation of connective tissue elements resulting in fibrosis and scarring. Two processes are involved in repair: i. Granulation tissue formation. ii. Contraction of wounds.

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i) Granulation tissue formation 3 phases: a) phase of inflammation b) phase of clearance c) phase of in growth of Granulation tissue: - Angiogenesis - Fibrous tissue formation

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Angiogenesis - New vessels budding from old Fibrosis, consisting of emigration and proliferation of fibroblasts and deposition of ECM As maturation proceeds, more and more of collagen is formed while the number of active fibroblasts and new blood vessels decreases. This results in formation of inactive looking scar known as cicatrisation. Scar remodeling, tightly regulated by proteases and protease inhibitors

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ii) Wound Contraction The wound starts contracting after 2-3 days and the process is completed by the 14 th day. For mechanism of wound contraction a number of factors have been suggested: Dehydration as a result of removal of fluid by drying of wound was 1 st suggested but without being substantiated. Contraction of collagen was thought to be responsible for contraction.

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Discovery of myofibroblasts appearing in active granulation tissue has resolved the controversy surrounding the mechanism of wound contraction. These cells have features intermediate between those of fibroblasts and smooth cells. Their migration into the wound area and their active contraction decreases the size of the defect.

Wound healing:

Wound healing Healing of skin wounds provides a classical example of combination of regeneration and repair described above. This can be accomplished in one of the following two ways: 1) Healing by first intention 2) Healing by second intention 3) Healing by tertiary intention

Primary Intention:

Primary Intention Wound is clean and sutured closed

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Sequence of events in primary union: 1. Initial hemorrhage 2. Acute inflammatory response 3. Epithelial changes 4. organization 5. Suture tracts

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Clean, uninfected, surgical incision with sutures: 1. Blood clot forms a. < 24 hours – PMNs appear b. 24-48 hrs cut edges of epidermis thicken from basal cell hyperplasia, and epithelium migrates for union c. By day 3 – PMN ’ s replaced by macrophages. Granulation tissue invades & collagen at margins.

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d. Incision filled with granulation tissue. Maximal neovascularization & collagen bridges gap. Epidermis covers & is mature. e. One week – After suture removal wound strength only 10% (compared with unwounded skin) f. Second week – Continued collagen deposition and fibroblast proliferation. PMNs gone. g. First month – Scar with cellular connective tissue and no inflammatory cells. Regressed vascular channels. h. Third month – 70-80% of maximum strength.

Fig 4-17 Healing by first intention:

Fig 4-17 Healing by first intention

Secondary:

Secondary Wound remains open to heal by granulation tissue formation and scar retraction Chosen for bacterial contamination or tissue loss

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Large tissue defect to fill common denominator Differs from primary union in several ways: More fibrin, more debris  more intense inflammation More granulation tissue is formed Wound contraction aided by myofibroblasts

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Sequence of events in secondary union is: 1. Initial hemorrhage 2. Inflammatory phase 3. Epithelial changes 4. Granulation tissue 5.Wound contraction 6. Presence of infection

Fig 4-17 Healing by second intention: Larger injury, abscess, infarction. Process is similar but results in much larger scar and then primary union:

Fig 4-17 Healing by second intention: Larger injury, abscess, infarction. Process is similar but results in much larger scar and then primary union

Tertiary:

Tertiary Delayed primary closure after a few days of open wound healing

Delayed Healing:

Delayed Healing Normal healing – continual increase in mechanical integrity/strength over time with an eventual plateau Delayed – decrease in rate with eventual achievement of normal plateau Nutritional deficiencies, infection, severe trauma Impaired/Chronic – failure to achieve normal mechanical integrity/wound strength Immunocompromised, diabetes, chronic steroid use.

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Factors influencing Healing: A) LOCAL FACTORS - infection - poor blood suplly - foreign bodies - movement - exposure to ionizing radiation - exposure to uv light - type,size and locatio of injury.

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2) SYSTEMIC FACTORS - Age - Nutrition deficiency - Systemic infection - Uncontrolled diabetics - Hematologic abnormalities

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HEALING IN SPECIALISED TISSUES

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Fracture healing : i) Primary union of fractures- Occurs in a few special situations when the ends of fracture are approximated as is done by application of compression clamps. In these cases bony union takes place with the formation of medullary callous without periosteal callus formation. ii) Secondary union- more common

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3 Headings:- a) Procallous formation - hematoma - local inflammatory response - in growth of granulation tissue -callus composed of woven bone and cartilage b) Osseous callous formation c) Remodeling

GI Tissue Healing:

GI Tissue Healing Surgical reanastamosis with sutures or staples Failure of healing – dehiscence, leak, fistula Excessive healing – stricture, stenosis Submucosa provides highest tensile strength Serosa provides a watertight seal via a fibrin seal

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Serosa/mucosa heals without scarring Decrease in strength during wk1 due to collagenolysis, collagenase colon > sm. int Anastamosis should be tension-free, good blood supply, adequate nutritional status, no sepsis

Cartilage Wound Healing:

Cartilage Wound Healing Cartilage is an avascular ECM of proteoglycans, collagen fibers, and water Nutrients diffuse from a hypervascular perichondrium Injury to cartilage have poor healing Superficial – disruption of ECM, injur chondrocytes – no inflammation, ↑ synth of proteoglycans/collagen, poor regeneration Deep – involve underlying bone/tissue. Hemorrhage initiates inflammation and cellular repair. Fibroblasts migrate across granulation tissue to fill defects wihc are eventually undergo chondrification and hyaline cartilage is formed

Tendon Wound Healing:

Tendon Wound Healing Tendons/ligaments – parallel bundles of collagen interspersed by spindle cells Healing: 1. hematoma 2. organization, 3. laying down ECM (collagen types I & III) 4. scar formation Hypovascular tendons heal with less motion and more scarring Mechanical integrity may never reach pre-injury levels

Nerve Wound Healing:

Nerve Wound Healing Nerve injury – neurapraxia (focal demylenation) axonotmesis (disrupted axonal continuity with maintenance of Schwann cell basal lamina) neurotmesis (transection) Healing – 1. survival of axonal cell bodies Wallerian degeneration – phagocytosis of degenerating axons/sheath from the distal stump 2. regeneration of axons from the proximal stump, remyelination 3. migration/connection of regenerating ends to targets

Fetal Wound Healing:

Fetal Wound Healing No scar formation until 3 rd trimester Environment: sterile, temperature stable, fluid Inflammation: reduced 2˚ immaturity of immune system = ? no scarring Growth Factors: absence of TGF- β Matrix: excessive and extended hyaluronic acid production by fibroblasts (stimulated by fetal urine components)

Local wound care:

Local wound care Exam: depth, configuration, extent of necrosis, foreign bodies, infection Irrigation with Normal Saline (iodine, H2O2, and organic antibacterial preps ↓ healing) Debridement, hematoma evacuation Sterilize area/field, edge approximation vs. split thickness skin/allograft vs. rotation/free flaps

Antibiotics:

Antibiotics Utilize for obvious wound infections Erythema, cellulites, swelling, purulence Tailor usage to suspected microbes for the wound location and pt’s immune function

Growth Factor Therapy:

Growth Factor Therapy PDGF-BB is FDA approved for treatment of diabetic foot ulcers Recombinant human GF in a gel suspension Increases healing, decreases healing time

Dressings:

Dressings Mimics epithelial barrier, protection of site Compression provides haemostasis, decreases edema Occlusion controls hydration and allows for oxygenation/gaseous diffusion Occlusion stimulates collagen synthesis and epithelial cell migration Primary- directly on wound Secondary- placed on a primary dressing

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Absorbent - absorbs wound fluid which could lead to maceration and bacterial overgrowth Non adherent - impregnated with paraffin, petroleum jelly or water-soluble jelly. Requires a secondary dressing to seal edges and prevent desiccation/infection (semi) occlusive - Film dressing good for minimally exudative wounds. Waterproof, impervious to microbes, permeable to water vapour and O2.

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Hydrophilic - Aid in absorption Hydrophobic - Waterproof, prevents absorption. Hydrocolloid/hydro gel - absorbent + occlusive. Absorption of exudates leaves a gelatinous mass after dressing removal (a traumatic, can be washed off). Hydro gels are useful for burns because they allow for a high rate of evaporation without decreasing wound hydration.

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Alginates - derived from brown algae. Polysaccharide polymers have a high absorbency. Good for skin loss, open surgical wounds with medium exudation, and full-thickness chronic wounds Absorbable –within wounds as haemostatic agent. Collagen, gelatin, cellulose. Medicated - benzoyl peroxide, zinc oxide, neomycin, bacitracin-zinc. Increase epithelialization.

Skin Grafts:

Skin Grafts Split/partial thickness graft = epidermis + partial dermis Require less vascular supply Full thickness = entire epidermis and dermis Greater mechanical strength, increased resistance to wound contraction, improved cosmetics Auto graft – transplant from another site Allograft – transplant from a living nonidentical donor or cadaver Subject to rejection, may contain pathogens Xeno graft – from another species Subject to rejection, may contain pathogens Preparation of wound bed – debridement of necrotic/fibrinous tissue, control of edema, minimizing exudates', revascularization of wound bed, ↓ bacterial load

Skin Substitutes:

Skin Substitutes Good for extensive wounds with limited availability of auto grafts Now may be used a wound dressing Tissue engineered with living cells Does not require tissue harvesting, readily available, may be sutured or applied topically Promote healing Disadvantages: limited survival, high cost, requires multiple applications Cultured Epithelial Auto grafts – expanded from a biopsy of the pt’s skin and grown into sheets. Not rejected, stimulate epithelialization Can also be obtained from cadavers, donors and cryo preserved

CONCLUSION:

CONCLUSION Human body is subjected to various insults which results in tissue injury and inflammation. Nature responds to these insults maintaining the equilibrium with the external environment. This is accomplished by various by mechanical and chemical events resulting in wound healing. Hence it is essential to know the patho physiology of inflammation and wound healing.

REFERENCES:

REFERENCES Mohan Harsh. Textbook of pathology.4 th ed. New Delhi : Jaypee brothers; 2010.p.114-161 Dey C N, Dey K T. Textbook of pathology.15 th ed. Delhi: Central production; 2007.p.6.1-7.9 Barbul Adrian. Schwartz principles of surgery.8 th ed. New York: Mc Grawhill production;2004.p.240-310.

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