wound and wound healing
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WOUND HEALINGIKEM O.M.OUTLINEINTRODUCTIONCAUSES OF TISSUE DAMAGETYPES OF WOUNDSSTAGES OF WOUND HEALING TYPES OF WOUND HEALING SURGICAL SIGNIFICANCE OF WOUND HEALING FACTORS AFFECTING WOUND HEALING COMPLICATIONS OF WOUND HEALING CONCLUSIONREFERENCES
INTRODUCTIONA wound is defined as a breakdown in the protective function of the skin; the loss of continuity of epithelium, with or without loss of underlying connective tissue as a result of trauma, infection or pathological process (Leaper & Harding, 1998) ulcerWound healing is a complex sequence of overlapping events which are often described separately for ease of explanation but in reality form a continuum often referred to as the healing cascade (Diegelmann and Evans,2004).
CAUSES OF TISSUE DAMAGEMechanical AgentsChemical AgentsRadiant Energy Pathogenic Micro-OrganismsCLASSIFICATION OF TYPES OF WOUNDBased on the durationBased on breach of the epitheliumBased on hygieneBASED ON DURATIONACUTEAn acute wound is one that proceeds through an orderly and timely reparative process to establish sustained anatomic and functional integrityCHRONICA chronic wound is one that has failed to proceed through an orderly and timely reparative process to produce anatomic and functional integrity or has proceeded through the repair process without establishing a sustained anatomic and functional result.BASED ON BREACH OF EPITHELIUMCLOSED- Contusion/BruiseOPEN- Abrasion Incision Laceration Puncture/Penetrating/Peforating Avulsion AmputationIllustration showing closed wounds
Illustration showing types of open wounds
STAGES OF WOUND HEALINGConsist of 3 highly integrated and overlapping phases: InflammatoryProliferative or FibroblasticMaturation or Remodelling These phases and their physiological functions must occur in the proper sequence, at a specific time and duration at an optimal intensityINFLAMMATORY PHASECharacterized by haemostasis and inflammation.Collagen exposed as a result of the wound activates the clotting cascade, initiating the inflammatory phase. The exposed cell membranes release thromboxane A2 & prostaglandin 2- which are potent vasoconstrictors.The clot that forms is made of collagen, platelets, thrombin, and fibronectin, and these factors release cytokines and growth factors that initiate the inflammatory response. The fibrin clot serves as a scaffold for cells, such as neutrophils, monocytes, fibroblasts, and endothelial cells and also to concentrate cytokines and growth factors.INFLAMMATORY PHASEChemotaxis and ActivationImmediately after the clot is formed, a cellular distress signal is sent out and neutrophils are the first responders.Inflammatory mediators and prostaglandins cause vasodilation to allow invasion of neutrophils (chemotaxis) by Interleukin (IL)-1, Tumor Necrosis Factor (TNF-), Transforming Growth Factor (TGF-), Platelet Factor-4 (PF4), and bacterial products. Monocytes in the nearby tissue and in the blood will be attracted and transform into macrophages, usually around 48 to 96 hours after injury.INFLAMMATORY PHASENeutrophils aid in clearing the wound of invading bacteria and cellular debris by release of proteolytic enzymes that will digest bacteria and nonviable tissue. Numerous enzymes and cytokines are secreted by the macrophage, including collagenases, which debride the wound; Interleukins and TNF-, which stimulate fibroblasts and promote angiogenesis; and TGF, which stimulates keratinocytesPROLIFERATIVE/FIBROBLASTIC PHASE (4-14Days)Epithelialization, angiogenesis, granulation tissue formation, and collagen deposition are the principal steps in this phase.The stimulus for epithelial proliferation and chemotaxis is epidermal growth factor (EGF) and TGF- produced by activated platelets and macrophages.IL-1 and TNF- upregulate the expression of keratinocyte growth factor (KGF) gene in fibroblasts leading to synthesis and secretion of KGF-1, KGF-2, and IL-6, which simulate neighbouring keratinocytes to migrate in the wound area, proliferate, and differentiate in the epidermis.
PROLIFERATIVE/FIBROBLASTIC PHASE (4-14Days)Angiogenesis, stimulated by TNF-, is marked by endothelial cell migration and capillary formation. The migration of capillaries into the wound bed is critical for proper wound healing. Fibroblasts migrate into the wound site from the surrounding tissue, become activated, and begin synthesizing collagen and proliferate.Platelet-derived growth factor (PDGF) and EGF are the main signals to fibroblasts and are derived from platelets and macrophages.PROLIFERATIVE/FIBROBLASTIC PHASE (4-14Days)Fibroblasts already located in the wound site will begin synthesizing collagen and transform into myofibroblasts for wound contraction (induced by macrophage-secreted TGF-); they have less proliferation compared with the fibroblasts coming in from the wound periphery. In response to PDGF, fibroblasts begin synthesizing a provisional matrix composed of collagen type III, glycosaminoglycans, and fibronectin.1MATURATION/REMODELLING STAGE (Day8-1Yr)The main feature of this phase is the deposition of collagen in an organized and well-mannered network.Collagen synthesis will continue for at least 4 to 5 weeks after wounding. The collagen that is initially laid down is thinner than collagen in uninjured skin and is orientated parallel to the skin.Over time, the initial collagen threads are reabsorbed and deposited thicker and organized along the stress lines.These changes are also accompanied by a wound with an increased tensile strength.
MATURATION/REMODELLING STAGE (Day8-1Yr)The collagen found in granulation tissue is biochemically different from collagen from uninjured skin. Granulation tissue collagen has a greater hydroxylation and glycosylation of lysine residues, and this increase of glycosylation correlates with the thinner fibre size.The collagen in the scar (even after a year of maturing) will never become as organized the collagen found in uninjured skin. Wound strength also never returns to 100 percent. At 1 week, the wound has only 3 percent of its final strength; at 3 weeks, 30 percent; and at 3 months (and beyond), approximately 80 percent.SUMMARY OF WOUND HEALING
TYPES OF WOUND HEALING HEALING BY PRIMARY INTENTION (PRIMARY CLOSURE)Describes the process of wound closure within hours of injury and is possible where the wound edges remain in proximity to each other and there is little or no tissue loss or damage.
HEALING BY SECONDARY INTENTION (SECONDARY CLOSURE)A process were healing takes place by contraction and reepithelialisation as a result of more extensive tissue lossTYPES OF WOUND HEALINGDELAYED PRIMARY WOUND CLOSURE (TERTIARY INTENTION)Wound closure occurs when wound closure is delayed for 36 days due to adverse local conditions such as poor vascularity, uncontrolled bleeding or risk of infection (Gottrup, 1999). Once conditions improve, wounds are closed. Delayed primary closure is therefore a compromise between immediate primary closure and allowing local wound conditions to improve prior to delayed closure.BONE HEALINGOsteoblasts and osteoclasts are involved in the reconstitution and remodeling of boneOsteoblasts are derived from periosteum, endosteum and circulating pluripotent mesenchymal cellsOsteoclasts are derived from monocytes. In the repair of bone, the phenomena of haematoma formation, absorption of debris and structural tissue production proceed with the modification that osteoblasts, take the place of the fibroblasts and lay down matrix which calcify . While osteoclasts function to resorb necrotic bone and bone that needs to be remodeled.SURGICAL SIGNIFICANCE OF WOUND HEALINGThe surgeon can create conditions that augment or impede the natural wound healing process.Adherence to surgical principles facilitate optimal wound healing, with re establishment of tissue continuity minimization of scar size and restoration of function.The surgeons goal with respect to scar formation is not to prevent a scar, but to produce a scar that minimizes any compromise of function and looks as inconspicuous as possible
FACTORS AFFECTING WOUND HEALINGLOCALIschaemiaInfectionForeign bodySurgical TechniqueImmobilization and TraumaFACTORS AFFECTING WOUND HEALINGSYSTEMICSevere Constitutional Diseases-Diabetes Mellitus, Chronic Nephritis , Congestive Cardiac Failure , Chronic Liver Disease and Syphilitic lesions, Cancer HormonesAge
Nutritional Factors- Vitamins A&C, Protein Deficiency:(Arginine & Glutamine), Trace Elements Deficiencies: Zinc deficiencyCytotoxic agentsSmokingCOMPLICATIONS OF WOUND HEALINGInfectionKeloid formationHyperpigmentationImplantation cystsNeoplasiaWeak scarsCicatrization
CONCLUSIONWound healing is a complex process performed by cells that are programmed to achieve wound closure.Although the process of wound healing appears to be simple, advances in molecular science have provided a greater understanding of the complex interactions involved. Understanding of these dynamic physiological processes improves treatment outcome and better patient care.REFERENCESBadoe et al, Principles and practice of surgery including pathology in the tropics: wound and wound healing. Pages 57-66, 2009.George Broughton II, Jeffrey E. Janis, Christopher E. Attinger. Wound Healing: An Overview. (Plast. Reconstr. Surg. 117: 1e-S, 2006.)Leaper DJ and Harding KG. Wounds: Biology and Management. Oxford University Press. 1998Madeleine Flanagan, Wound Healing and Skin Integrity principles and practices: physiology of wound healing. Pages 33-49, Wiley Blackwell 2009