Based on clinical practice scenario (wound care), discuss the extent Literature review

Based on clinical practice scenario (wound care), discuss the extent to which evidence based practice was utilised, including re - Literature review Example These processes encompass the concept of wound care. Wound care is a crucial part of the medical practice. It prevents infection and blood loss, as well as further complications for the patient. There are various techniques which health professionals can apply in order to manage wounds. Such management strategies are supported by various studies and evidence in actual practice. This study shall consider literature and supporting researches in wound care, with particular attention given to patient preference and evidence-based practice. With the variety of applications which can be used for skin care, there is a need to consider the best type of care according to patient response and outcomes. Wound care All injuries trigger a series of events which are involved in healing, characterized by the arrival of platelets and inflammatory cells at the site of injury (Diegelmann and Evans, 2004). These cells also give off signals on the influx of connective tissue cells and on the increase of new blood. Chemical signals for these are the cytokines or growth factors. The fibroblasts are the connective tissues which mark collagen deposition essential for tissue injury (Diegelmann and Evans, 2004). In response to injury, platelets come into contact with exposed collagen. With platelet aggregation, clotting elements are released causing the formation of a fibrin clot at the injured area. The fibrin clot is considered the provisional matrix upon which healing is built on. Platelets facilitate clotting which helps control bleeding and loss of fluids and electrolytes. As well as releasing the cytokines, which initiate healing, these platelets also release the platelet-derived growth factor (PDGF) and transform growth factor-beta (TGF-B). Through the PDGF, chemotaxis of neutrophils, macrophages, smooth muscle cells, and fibroblasts is initiated (Diegelmann and Evans, 2004). These platelets also trigger the mitogenesis of the fibroblasts and smooth muscle cells. The TGF-B also t riggers the healing cascade by drawing in the macrophages and prompting them to release more cytokines (including the fibroblast growth factor-FGF, PDGF, TNFa and the IL-1) (Diegelmann and Evans, 2004). The TGF-B supports the chemotaxis of the fibroblast and the smooth muscle cells; it also regulates collagen and collagenase expression (Diegelmann and Evans, 2004). The overall result of these signals is a strong response of the matrix which then supports the release of cells which help ensure rapid formation of new connective tissue at the injured area during the proliferative stage of healing which follows the inflammatory phase (Diegelmann and Evans, 2004). Within 24 hours of the injury neutrophils are the common markers in the injury site. This neutrophil removes foreign material and bacteria in the wound site. Bacteria send of chemical signals which attract neutrophils, ingesting these through phagocytosis. These neutrophils will fill themselves with bacteria and make up the lau dable pus in the injury site (Diegelmann and Evans, 2004). The mast cell is a market cell crucial to wound healing. These cells give off granules made up of enzymes, histamine, and numerous other active amines; they are also responsible for the signs of inflammation seen around the wound. The active amines in the mast cells trigger nearby vessels to become leaky; this causes the easy passage of mononuclear cells in the injured area (Diegelmann and Evans, 2004). Fluids also gather at the wound site and with this, signs of