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1.Wound healing.pptx
- 1. WOUND HEALING SAMUEL GETAHUN, R1 Moderator:Dr.Yohannes Plastic and reconstructive surgeon 3/31/2023 wound healing 1
- 2. Contents Classification ofwounds Wound healing Phases of wound healing Factors affecting wound healing Healing in specific tissues Chronic wounds 3/31/2023 wound healing 2
- 3. CLASSIFICATION OF WOUNDS Closed vs open Based on: The level of cleanliness Degree of clinical risk of infection Duration of healing Clinical healing pattern and The risk for tetanus 3/31/2023 wound healing 3
- 4. CLOSED Intact epithelialsurface Skin cover not completely breeched e.g. – contusion, bruise, hematoma OPEN Complete break of the epithelial surface e.g. – abrasion , laceration, puncture, degloved wound, bites 3/31/2023 wound healing 4
- 5. Based on levelof cleanliness TIDY Incised Clean No devitalized tissue Tendon and neurovascular injuries Primary closure UNTIDY Crushed Contaminated Devitalized tissue Tissue loss Fractures are common Secondary or tertiary 3/31/2023 wound healing 5
- 6. Based on degreeof clinical risk of infection 3/31/2023 wound healing 6
- 7. Based on clinicalhealing pattern Healing by: Primary intention Secondary intention Tertiary intention 3/31/2023 wound healing 7
- 8. Based on durationof healing Acute wounds Heal in a predictable pattern and time frame Mostly few complications Chronic wounds Failure to epithelialize and close in a reasonable time, mostly >3mo 3/31/2023 wound healing 8
- 9. Based on riskfor tetanus 3/31/2023 wound healing 9
- 10. WOUND HEALING 3/31/2023 wound healing 10 Complex biologic process of restoring normal tissue continuity Repair or reconstruction of a defect in an organ or tissue, commonly the skin. Starts immediately after being wounded.
- 11. PHASES OF WOUNDHEALING 3/31/2023 wound healing 11
- 12. Hemostasis and inflammation Precedes and initiates inflammation PMNs are the first infiltrating cells, peaking at 24 to 48 hours. 48-96hrs post wounding macrophages invade the wound. About 1wk post injury T-lymphocytes invade the wound 3/31/2023 wound healing 12
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- 14. Proliferative phase From4th day to roughly 21st day of injury Fibroblasts, epithelial and endothelial cells are the important cells Angiogenesis , granulation tissue formation , epithelialization and contraction occurs. Balance b/n scar formation & tissue regeneration 3/31/2023 wound healing 14
- 15. EPITHELIALIZATION proliferation andmigration of epithelial cells adjacent to the wound Starts with in 1 day of injury. Marginal and fixed basal cells migrate to the surface of the wound and bridge the defect which eventually keratinizes. 3/31/2023 wound healing 15
- 16. Maturation and remodeling Starts at the fibroblastic phase and continues 6-12 months post injury Maximize the strength & structural integrity Re-organization of previously synthesized collagen. Finally forms mature, avascular and acellular scar. 3/31/2023 wound healing 16
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- 19. Factors affecting woundhealing Systemic Local Age Nutrition Trauma Metabolic diseases Hypoxia, anemia and hypo perfusion Immunosuppression Smoking Mechanical injury Infection Ischemia/necrotic tissue Ionizing radiation Foreign bodies 3/31/2023 wound healing 19
- 20. Healing in specifictissues GI Tract begins with reapposition of the bowel ends. Some of the differences in healing are, Mesothelial (serosal) and mucosal healing can occur without scarring. Significant decrease in marginal strength in the 1st week Collagenase is expressed markedly in the colon compared to the small bowel. Failure of healing results in dehiscence, leaks, and fistulas. Excessive healing results in stricture and stenosis of the lumen. 3/31/2023 wound healing 20
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- 22. BONE Inflammation Hematoma Liquefaction and degradation Revascularization Soft callus stage Hard callus stage Remodeling 3/31/2023 wound healing 22
- 23. CARTILAGE Healing responsedepends on the depth of injury. Superficial cartilage injuries are slow to heal and result in persistent structural defects. Deep injuries involve underlying bone and soft tissue resulting in structural and functional integrity of the injured site. 3/31/2023 wound healing 23
- 24. TENDON Tendon vasculaturehas an effect on healing. Tenocytes are metabolically very active and retain a large regenerative potential. Restoration of mechanical integrity may never be equal to that of the undamaged tendon. 3/31/2023 wound healing 24
- 25. NERVE Three typesof nerve injuries- Neurapraxia Axonotmesis Neurotmesis 3/31/2023 wound healing 25
- 26. Chronic wounds Woundsthat have not healed in 3 months. Unresponsiveness to normal regulatory signals. Fibroblasts from chronic wounds have decreased proliferative potential. Malignant transformation of chronic ulcers can occur in any long-standing wound (Marjolin’s ulcer). 3/31/2023 wound healing 26
- 27. Ischemic arterial ulcers Due to lack of blood supply painful at presentation. Commonly present at the most distal portions of the extremities. 3/31/2023 wound healing 27
- 28. VENOUS STASIS ULCERS Due to venous stasis and hydrostatic back pressure. Leads to Venous hypertension and capillary damage Fails to re-epithelialize despite the presence of adequate granulation tissue. 3/31/2023 wound healing 28
- 29. DIABETIC WOUNDS 2ryto neuropathy, foot deformity, and ischemia. Neuropathy is both sensory and motor Sensory- unrecognized injury Motor (Charcot’s foot)- collapse or dislocation of the IP or MTP joints Micro- and macrovascular circulatory 3/31/2023 wound healing 29
- 30. Pressure ulcers Localizedarea of tissue necrosis. Accelerated in the presence of friction, shear forces, and moisture. Stages- Non-blanching erythema Partial thickness skin loss Full thickness skin loss Full thickness skin loss involving muscle and bone 3/31/2023 wound healing 30
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- 32. Hypertrophic scars Doesnot extend beyond the boundary Across areas of tension and flexor surfaces, which tend to be at right angles to joints or skin creases. Develop within 4 weeks after trauma. 3/31/2023 wound healing 32
- 33. KELOIDS • Extends beyondthe boundaries of the original incision or wound • 3 months- years after initial insult. • Higher incidence in the skin of earlobes, the deltoid, presternal and upper back region. 3/31/2023 wound healing 33
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- 36. CONTRACTUES Where scarscross joints , a tight web may form restricting the range of movement at the joint. can cause hyperextension or hyperflexion deformity 3/31/2023 wound healing 36
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Editor's Notes
- #8 -healing occurs in closed wounds in which the edges are approximated, such as a clean skin incision closed with sutures. -The incisional defect re-epithelializes rapidly, and matrix deposition seals the defect. 2. Second intention healing occurs when the wound edges are not apposed, Granulation tissue fills the wound, and the wound contracts and re-epithelializes. 3. Delayed primary or third intention healing -open wound is secondarily closed several days after injury eg.after removal of a ruptured appendix Left open initially Edges approximated 4-6 days later….For contaminated wounds …skin Grafts and flaps may be reqiured
- #9 -Acute wounds transition through the stages of wound healing as a linear pathway, with clear start- and endpoints -Chronic wounds are arrested in one of these stages, usually the inflammatory stage, and cannot progress further -- The presence of necrotic tissue, foreign material and bacteria result in the abnormal production of metalloproteases which alter the balance of inflammation and impair the function of the cytokines
- #10 -Tetanus toxoid (0.5 mL intramuscularly) and tetanus immune globulin (250 units intramuscularly) should be given to patients with puncture wounds who have received less than three doses of tetanus toxoid or whose immunization status is uncertain. -Patients sustaining wounds not classified as clean or minor should also undergo passive immunization with TIG -Human TIG in high risk ( un-immunized )…..Commence active immunization ( T toxoid) -Previously immunized- booster >10 years needs a booster dose booster <10 years- no treatment in low
- #11 be divided into overlapping phases defined by characteristic cellular populations and biochemical activities
- #13 -Exposure of subendothelial collagen to platelets results in platelet aggregation, degranulation, and activation of the coagulation cascade -the fibrin clot serves as scaffolding for the migration into the wound of inflammatory cells -Increased vascular permeability, local prostaglandin release, and the presence of chemotactic substances all stimulate neutrophil migration -primary role of neutrophils is phagocytosis of bacteria and tissue debris. are also a major source of cytokines early during inflammation, especially TNF-α3 which may have a significant influence on subsequent angiogenesis --role of lymphocytes in wound healing is not fully defined. Depletion of most wound T lymphocytes decreases wound strength and collagen content -selective depletion of the CD8+ suppressor subset of T lymphocytes enhances wound healing. However, depletion of the CD4+ helper subset has no effect
- #14 -Macrophages also play a significant role in regulating angiogenesis and matrix deposition and remodeling. oxygen radical and nitric oxide synthesis. Their most pivotal function is activation and recruitment of other cells via mediators -The healing progression of chronic wounds usually becomes arrested in this inflammatory stage. - The presence of necrotic tissue, foreign material and bacteria result in the abnormal production of metalloproteases which alter the balance of inflammation and impair the function of the cytokines
- #15 During this phase tissue continuity reestablished n Characterized by Epithelialization Fibroplasia & Vascularization Endothelial cells also proliferate extensively participate in angiogenesis -strongest chemotactic factor for fibroblasts is PDGF.-Fibroblasts are transformed from local mesenchymal cells, are usually present in the wound within 24 hrs,…10th day . -They attach to the fibrin matrix of the clot, multiply, and produce glycoprotein and mucopolysaccharides, which make up ground substance. -Fibroblasts isolated from wounds synthesize more collagen than nonwound fibroblasts, they proliferate less, and they actively carry out matrix contraction -Fibroblasts synthesize collagen, the primary structural protein of the body ,production begins on the 2nd day, when it is secreted as an amorphous gel devoid of strength. Maximum collagen production does not begin until day five and continues for at least six weeks .The developing collagen matrix stimulates angiogenesis. -fibroblasts produce myofibroblasts, are present in the wound by the fifth day and have characteristics of smooth muscle cells with the ability to contract .Pulling the edges of the wound together is dependent upon tissue mobility. Myofibroblastic cells are lost via apoptosis as repair resolves to form scar. -In this phase the fibrin matrix is replaced by granulation tissue , which is composed of fibroblasts, macrophages and endothelial cells which form extracellular matrix and new blood vessels.
- #16 -Fixed basal cells in a zone near the cut edge undergo a series of rapid mitotic divisions, and these cells appear to migrate by moving over one another until the defect is covered -Re-epithelialization is complete in less than 48 hours in the case of approximated incised wounds, but may take substantially longer in the case of larger wounds, where there is a significant epidermal/dermal defect -The stimuli remain incompletely defined; however, it appears that it is mediated by a combination of a loss of contact inhibition; exposure to constituents of the extracellular matrix, particularly fibronectin; and cytokines Involves a sequence of changes in wound keratinocytes—detachment, migration, proliferation, differentiation, and stratification.
- #17 Wound strength and mechanical integrity in the fresh wound are determined by both the quantity and quality of the newly deposited collagen -Key elements of maturation include collagen cross-linking, collagen remodeling, wound contraction and repigmentation --remodeling is characterized by the process of wound contraction by myofibroblasts and collagen remodeling i.e type ІІІ collagen initially laid down by fibroblast will be changed to type І collagen in few months. -fibronectin and collagen type III constitute the early matrix scaffolding; glycosaminoglycans and proteoglycans represent the next significant matrix components; and collagen type I is the final matrix.
- #18 By several weeks post injury the amount of collagen in the wound reaches its plateau , but tensile strength continue increase for several month.
- #20 -the supply of cutaneous nerves and blood vessels decreases with age, and loss of collagen and ability to produce more collagen. -Diabetes is associated with vasculopathy, neuropathy and immunopathy -chemotherapy have effect on wound healing, through its effects on vascular endothelial growth factor (VEGF). VEGF is an important factor contributing to angiogenesis during the early stages of wound healing, - Bacteria produce inflammatory mediators that inhibit the inflammatory phase of wound healing and prevent epithelialization -steroid Healing especially when given in the first 3 days after wounding a deficiency in inflammatory cell function. Diminishing the supply of cytokines, Macrophage migration,….fibroblast proliferation, collagen accumulation, and angiogenesis Reversed by -supplemental vitamin A 25,000 IU/day.OR Topical --
- #21 -Injuries to all parts of the GIT under go the same sequence of healing as cutaneous wounds -submucosa is the layer that imparts the greatest tensile strength and greatest suture-holding capacity, -serosal healing is essential for quickly achieving a watertight seal from the luminal side. technical=handsutured vs. stapled, continuous vs. interrupted sutures, absorbable vs. nonabsorbable sutures, or single- vs. two-layer closure --in the first week due to early and marked collagenolysis.
- #22 Collagenase activity occurs early in the healing process and during the first 3-5ds collagen break down far exceeds collagen synthesis.
- #23 -healing resemble those observed in dermal healing, but some d\c •hematoma formation consists of an accumulation of blood at the fracture site, which also contains devitalized soft tissue, N dead bone, -The next stage accomplishes the liquefaction and degradation of nonviable products at the fracture site. normal bone adjacent to the injury site can then undergo revascularization, with new blood vessels growing into the fracture site. •3 to 4 days after injury, soft tissue forms a bridge between the fractured bone segments ,Clinically, soft callus formation phase is characterized by the end of pain and inflammatory signs N serves as an internal splint, preventing damage to the newly laid blood vessels and achieving a fibrocartilaginous union. formed externally along the bone shaft and internally within the marrow• -hard callus stage consists of mineralization of the soft callus and conversion to bone. This may take up to 2 to 3 months and leads to complete bony union. -remodeling phase. excessive callus is reabsorbed and the marrow cavity is recanalized.
- #24 . cartilage is very avascular and depends on diffusion for transmittal of nutrients across the matrix. hypervascular perichondrium contributes to the nutrition. --in deep-exposure of bone n soft ts leads to the exposure of vascular channels of the surrounding damaged tissue that may help in the formation of granulation tissue. Hemorrhage allows for the initiation of the inflammatory response and the subsequent mediator activation of cellular function for repair. - Gradually, hyaline cartilage is formed, which restores the structural and functional integrity of the injured site.
- #25 -Tendons and ligaments can be subjected to a variety of injuries, such as laceration, rupture, and contusion. Due to the mobility of the underlying bone or muscles, the damaged ends usually separate. -Tendon and ligament healing progresses in a similar fashion as in other areas of the body. Matrix is characterized by accumulation of type I and III collagen along with increased water, DNA, and glycosaminoglycan content. As the collagen fibers are organized, transmission of forces across the damaged portion can occur.
- #26 -neurapraxia (focal demyelination), axonotmesis (interruption of axonal continuity but preservation of Schwann cell basal lamina), and neurotmesis (complete transection). --Following (a) survival of axonal cell bodies; (b) regeneration of axons that grow across the transected nerve to reach the distal stump; and (c) migration and connection of the regenerating nerve ends to the appropriate nerve ends or organ targets. - Phagocytes remove the degenerating axons and myelin sheath from the distal stump (Wallerian degeneration). -Schwann cells ensheathe and help in remyelinating the regenerating axons. - Functional units are formed when the regenerating axons connect with the appropriate end targets. -Several factors play a role in nerve healing, such as growth factors, cell adhesion molecules, and nonneuronal cells and receptors.
- #27 -wounds that have failed to proceed through the orderly process that produces satisfactory anatomic and functional integrity or that have proceeded through the repair process without producing an adequate anatomic and functional result. -Skin ulcers, usually occur in traumatized or vascular compromised soft tissue, are the major component of chronic wounds. -Malignant wounds are differentiated clinically from nonmalignant wounds by the presence of overturned wound edges. suspected malignant transformations, biopsy of the wound edges must be performed to rule out malignancy. Cancers arising de novo in chronic wounds include both squamous and basal cell carcinomas.
- #28 -associated with other symptoms of peripheral vascular disease, such as intermittent claudication, rest pain, night pain, and color or trophic changes. -On examination, there may be diminished or absent pulses with decreased ankle-brachial index and poor formation of granulation tissue. signs of peripheral ischemia, such as dryness of skin, hair loss, scaling, and pallor. -wound is shallow with smooth margins, and a pale base and surrounding skin may be present. -prevention is extremely important in the approach. ??? FOR WHO AND HOW==READ IT
- #29 -are commonly painless. venous obstruction lead to abnormally directed flow from the deep to superficial venous systems via the perforating veins. -The most common site of incompetent perforators is 5 to 10 cm above the medial malleolus -.Congestion and pooling of blood in the superficial veins leads to venous hypertension, is associated with vessels that are abnormally permeable, leading to the accumulation of water, large proteins (including fibrinogen), and extravasated red blood cells into the interstitial space . -The “white cell trap theory” postulates that the macromolecules are thought to trap growth factors and matrix material making them unavailable for tissue repair and the perivascular fibrin cuff may decrease the delivery of oxygen and nutrients leading to skin hypoxia and cell death resulting in the venous ulcer lead to extravasation of hemoglobin causing pruritus and skin damage. Lipodermatosclerosis -neutrophils adhere to the capillary endothelium and cause plugging with diminished dermal blood flow. -Chronic venous ulcers usually are due to the incompetence of the deep venous system and most common being above the medial malleolus, over Cockett’s perforator.
- #30 -60% to 70% of diabetic ulcers are due to neuropathy, 15% to 20% are due to ischemia, and another 15% to 20% combination of both. Tx= Achievement of adequate blood sugar levels. Eradication of the infectious source. débridement of all necrotic or infected tissue. orthotic shoes or casts. Topical PDGF and granulocyte-macrophage colony-stimulating factor. Prevention and specifically foot care. Skin allo grafts -from ill-fitting shoes, foreign bodies, or other trauma. and is 2ry to persistently high glucose levels.
- #31 -develops when soft tissue is compressed between a bony prominence and an external surface -pressure causes capillary collapse and impedes the delivery of nutrients to body tissues -Other contributory factors include immobility, altered activity levels, altered mental status, chronic conditions, and altered nutritional status -tx= débridement of all necrotic tissue, maintenance of a favorable moist wound environment that will facilitate healing, relief of pressure, and addressing host issues such as nutritional, metabolic, and circulatory status. -recurrence rates are extremely high, owing to the population at risk and the inability to fully address the causative mechanisms.
- #32 -Clinically, excess healing can be as significant as wound failure. It is likely that more operative interventions are required for correction of the morbidity associated with excessive healing than are required for wound failure. -The clinical manifestations of exuberant healing are protean and differ in the skin (mutilating or debilitating scars, burn contractions), tendons (frozen repairs), the GI tract (strictures or stenoses), solid organs (cirrhosis, pulmonary fibrosis), or the peritoneal cavity (adhesive disease).
- #33 -risk of HTS increases if epithelialization takes longer than 21 days. Rarely elevated more than 4 mm above the skin. -usually occur across areas of tension and flexor surfaces, which tend to be at right angles to joints or skin creases BOTH- abundance of collagen and glycoprotein deposition. -HTS-collagen bundles are flatter and more random, and the fibers are in a wavy pattern -immune system appears to be involved in the formation of both HTSs and keloids
- #34 -benign fibrous growths present in scar tissue that form because of altered wound healing, with overproduction of extracellular matrix and dermal fibroblasts that have a high mitotic rate Keloidal fibroblasts have normal proliferation parameters but synthesize collagen at a rate 20 times greater than that observed in normal dermal fibroblasts, and 3 times higher than fibroblasts derived from HTS soft to rubbery or hard consistency. rarely extend into underlying subcutaneous tissues -surgical intervention can lead to recurrence, often with a worse result -collagen bundles are virtually nonexistent, and the fibers are connected haphazardly in loose sheets with a random orientation to the epithelium -erexpression of growth factors, such as transforming growth factor-beta (TGF-beta), vascular endothelial growth factor (VEGF), and connective tissue growth factor (CTGF) appear to play a role in the formation of these lesions.TGF-beta is a regulator of fibroblast proliferation and collagen synthesis. In normal wound healing, transforming growth factor-beta (TGF-beta) activity diminishes upon the completion of wound repair, but in keloids TGF-beta is overproduced and poorly regulated
- #37 or flexion creases