Acute And Chronic Wounds 6th Edition
Nichele Seibel
Sports injuries are divided into two broad categories, acute and chronic injuries. Acute injuries happen suddenly, such as when a person falls, receives a blow, or twists a joint, while chronic injuries usually result from overuse of one area of the body and develop gradually over time. Examples of acute injuries are sprains and dislocations, while some common chronic injuries are shin splints and stress fractures.
Treatment for a sports injury depends on the type of injury, but minor ones can usually be treated at home by resting, icing, compressing, and elevating (R-I-C-E) the injured part of the body. For more serious injuries, you will need to see a health care provider, and you may need to be set up for a course of physical therapy for rehabilitation and/or fitted for a cast, splint, or brace. In some cases, you may need surgery. A rehabilitation program that includes exercise and other types of therapy is usually recommended before resuming the sport or activity that caused the injury.
The cause of an acute sports injury is a force of impact that is greater than the body part can withstand, while a chronic injury is typically due to repeating the same motion over and over again. Sometimes, overuse injuries can degrade tissues and joints and set the stage for an acute injury.
Do you understand the difference between acute and chronic wounds? If you answered that acute wounds are wounds that have been present for a shorter duration of time, you are correct--but there are many other differences in acute and chronic wounds that are not as obvious and must be taken into account when planning care.
Hemostasis: This is the clot that is formed initially at the site of injury to control bleeding. It is comprised mainly of platelets. The endothelium of blood vessels that are exposed by the injury stimulate platelets to release certain factors, which result in vasoconstriction and initiation of the clotting cascade. Thrombin, prostaglandins, growth factors and other cytokines are released at the site of the injury, whose job it is to attract inflammatory cells to the area, as well as increase their production and migration. Many conditions can interfere with the formation of a clot during hemostasis, such as venous insufficiency, diabetes, thrombocytopenia and other blood dyscrasias. Conditions such as these may lead to poor wound healing, therefore careful management of these conditions will be important in the normal process of wound healing.
Inflammation: Within hours of clot formation, neutrophils travel to the site of injury and adhere themselves to the endothelial cell walls of the damaged vasculature. These neutrophils provide protection against infection as they phagocytize bacteria, dead tissue and any foreign material present. Neutrophils also produce inflammatory mediators that activate and recruit fibroblasts and epithelial cells to the injury site. When neutrophils are depleted they are replaced by macrophages, which help to rid the wound of devitalized tissue and produce elastase and collagenase. Macrophages also prompt an ending of the inflammatory phase and the beginning of the proliferative phase of wound healing. Unfortunately, inflammatory mediators can cause tissue damage and may sometimes prolong the inflammatory phase of healing. Therefore, any process which increases neutrophils (and thus inflammatory mediators) can lead to prolongation of the inflammatory phase, which may be evident to the astute clinician as an increase in exudate. When wounds are stalled in the inflammatory phase, proper management of exudate is an important step in assisting wounds with moving on to the proliferative phase.
Proliferation: During this stage, the wound decreases in size and fills with new connective tissue (contraction, granulation and epithelialization). Granulation tissue is composed of fibroblasts, macrophages, blood vessels, immature collagen and an extracellular matrix. As macrophages begin to decrease in number, other cells, including keratinocytes, fibroblasts and endothelial cells, begin to produce and release growth factors and continue to multiply. As granulation tissue grows, it stimulates collagen production and fibroblasts, which provide the new scaffolding by promoting the migration of endothelial cells and fibroblasts into the wound. The growth of granulation tissue results in filling of the wound and narrowing of wound margins. Eventually the wound closes off and forms a scar. During the proliferation phase, maintenance of a moist wound environment and protection of newly growing tissues is crucial. Any process or condition that interferes with either of these may result in prolongation of the proliferation phase.
Remodeling: In this phase, collagen remodels, proliferates and matures, a process that can take many months. Tensile strength increases but will never achieve the strength present before the injury occurred. At best, tensile strength may be 80%.
Why is it that some wounds progress smoothly and rapidly through the phases of healing, while others stall and become trapped, most often in the inflammatory phase? Although no two wounds are the same, factors that predispose to a chronic wound are similar.
About The Author
Laurie Swezey RN, BSN, CWOCN, CWS, FACCWS, is a Certified Wound Therapist and enterostomal therapist, founder and president of WoundEducators.com, and advocate of incorporating digital and computer technology into the field of wound care.
Acute wounds normally heal in an orderly and efficient manner, and progress smoothly through the four distinct, but overlapping phases of wound healing: haemostasis, inflammation, proliferation and remodelling (Figure 23.1).1,2,3 In contrast, chronic wounds will similarly begin the healing process, but will have prolonged inflammatory, proliferative, or remodelling phases, resulting in tissue fibrosis and in non-healing ulcers.4 the process of wound healing is complex and involves a variety of specialized cells, such as platelets, macrophages, fibroblasts, epithelial and endothelial cells. These cells interact with each other and with the extracellular matrix. In addition to the various cellular interactions, healing is also influenced by the action of proteins and glycoproteins, such as cytokines, chemokines, growth factors, inhibitors, and their receptors. Each stage of wound healing has certain milestones that must occur in order for normal healing to progress. In order to identify the differences inherent in chronic wounds that prevent healing, it is important to review the process of healing in normal wounds
Growth factors are also released from the platelet alpha granules, and include platelet derived growth factor (PDGF), transforming growth factor beta (TGF-β), transforming growth factor alpha (TGF-α), basic fibroblast growth factor (bFGF), insulin-like growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF). Major growth factor families are presented in Table 23.1. Neutrophils and monocytes are then recruited by PDGF and TGF-β from the vasculature to initiate the inflammatory response. A breakdown fragment generated from complement, C5a, and a bacterial waste product, f-Met-Leu-Phe, also provide additional chemotactic signals for the recruitment of neutrophils to the site of injury. Meanwhile, endothelial cells are activated by VEGF, TGF-α and bFGF to initiate angiogenesis. Fibroblasts are then activated and recruited by PDGF to migrate to the wound site and begin production of collagen and glycosaminoglycans, proteins in the extracellular matrix which facilitate cellular migration and interactions with the matrix supporting framework. Thus, the healing process begins with hemostasis, platelet deposition at the site of injury, and interactions of soluble mediators and growth factors with the extracellular matrix to set the stage for subsequent healing events.1,2,7
Inflammation, the next stage of wound healing occurs within the first 24 hours after injury and can last for up to 2 weeks in normal wounds and significantly longer in chronic non-healing wounds (Figure 23.3). Mast cells release granules filled with enzymes, histamine and other active amines, which are responsible for the characteristic signs of inflammation, the rubor (redness), calor (heat), tumor (swelling) and dolor (pain) around the wound site. Neutrophils, monocytes, and macrophages are the key cells during the inflammatory phase. They cleanse the wound of infection and debris and release soluble mediators such as proinflammatory cytokines (including IL-1, IL-6, IL-8, and TNF-α), and growth factors (such as PDGF, TGF-β, TGF-α, IGF-1, and FGF) that are involved in the recruitment and activation of fibroblasts and epithelial cells in preparation for the next phase in healing. Cytokines that play important roles in regulating inflammation in wound healing are described in Table 23.2.
In addition to the growth factors and cytokines, a third important group of small regulatory proteins, listed in Table 23.3, has been identified, and are collectively named chemokines, from a contraction of chemoattractive cytokine(s).8,9,10 the structural and functional similarities among chemokines were not initially appreciated, and this has led to an idiosyncratic nomenclature consisting of many acronyms that were based on their biological functions, (e.g., monocyte chemo-attractant protein-1 (MCP-1), macrophage inflammatory protein-1, MIP-1), their source for isolation (platelet factor-4, PF-4) or their biochemical properties (interferon-inducible protein of 10 kD a (IP-10), or regulated upon activation normal T-cell expressed and secreted, RANTES). As their biochemical properties were established, it was recognized that the approximately 40 chemokines could be grouped into four major classes based on the pattern of cysteine residues located near the N-terminus. In fact, there has been a recent trend to re-establish a more organized nomenclature system based on these four major classes. In general, chemokines have two primary functions: 1) they regulate the trafficking of leukocyte populations during normal health and development, and 2) they direct the recruitment and activation of neutrophils, lymphocytes, macro-phages, eosinophils and basophils during inflammation.
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