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Understanding Wound Inflammation Tissue Viability, United Lincolnshire Hospital NHS Trust, Boston, Lincolnshire

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Understanding Wound Inflammation Tissue Viability, United Lincolnshire Hospital NHS Trust, Boston, Lincolnshire KNOWLEDGE WOUND CARE SUPPLEMENT Mark Collier, BA, ONC, RGN, RCNT, RNT, lead nurse/consultant, Understanding wound inflammation tissue viability, United Lincolnshire Hospital NHS Trust, Boston, Lincolnshire Inflammation is the first stage in the wound-healing contact with mature collagen they are activated and Mark Collier describes the process. It is normally followed by two further clump together. During this process, granules from process of wound phases: regeneration (sometimes also referred to as within the cell cytoplasm are released and liberate other inflammation proliferation) and maturation. Inflammation is enzymes, adenosine triphosphate (ATP), serotonin and and the clinical signs characterised by the classic signs of heat and growth factors – such as platelet-derived growth factor associated with it redness, pain and swelling, raised temperature and and epidermal growth factor – which further potentiate fever. The overall function of inflammation is to platelet aggregation (Krasner, 1990). neutralise and destroy any toxic agents at the site of KEY WORDS an injury and to restore tissue homeostasis. Leucocytes There are five types of leucocyte that are Inflammation classified by the presence or absence of granules in the Phagocytosis Wound healing involves cellular activity and the release cytoplasm of the cell. They include lymphocytes, Wound healing of biologically active substances, such as growth neutrophils and macrophages. factors, enzymes, carbohydrates and proteins (Krasner, Their function is the phagocytosis (engulfment and 1990). However, the quality and extent of the digestion) of bacteria, fungi and viruses in the blood. REFERENCES inflammatory response in a wound will be dependent on They also detoxify poisonous proteins that may have Calvin, M. (1998) Cutaneous wound repair. Wounds; 10: the severity of the patient’s injury as well as their been produced as a result of allergic reactions and 1, 12–32. general health, for example, their nutritional state, cellular injury (Calvin, 1998). Collier, M. (2002) Limited hydration and existing comorbidity. resources in wound management: Lymphocytes These white blood cells have a specific a reality for some. Journal of Community Nursing; 16: 3, 38–42. Inflammation Recently, it has been acknowledged immune response. The response is slower but more Cox, D. (1993) Growth factors in that inflammation can be subdivided into two distinct accurate than that of other white cells. Lymphocytes can wound healing. Journal of Wound components: early and late inflammation (Calvin, 1998). be differentiated into T (thymus-maturing) and B (bone- Care; 2: 6, 339–342. This division is important for understanding the process maturing) cells (Kingsley, 2002). Davidson, J., Broadley, K. (1991) of wound healing since delayed healing of chronic The response of experimental wounds to endogenous and wounds often results from an imbalance in the wound Neutrophils Also known as granulocytes, neutrophils exogenous growth factors. In: that prevents progression from one phase to another in target bacteria. Neutrophil infiltration of the wound-bed Janssen, H. et al (eds) Wound a predictable manner (Lazarus et al, 1994). peaks at approximately 24 hours and declines over the Healing. Petersfield, Hampshire: next few days. Neutrophils live for about 24 hours Wrightson Biomedical Publishing. Falanga, V. et al (1994) Workshop Chronic wounds A chronic wound may be defined (Slavin, 1996). on the pathogenesis of chronic as any wound that is failing to heal as anticipated or that wounds. Journal of Investigative has been stuck in any one phase of wound healing for a Macrophages Macrophages have a lifespan of between Dermatology; 102: 1, 125–127. period of six weeks or more (Collier, 2002). Chronic several months and two years, although the number wounds result from an alteration in one or more of the present in a wound starts to decrease at the end of the phases of normal wound healing and may be caused by inflammatory process as a result of apoptosis cellular imbalances. Examples of such cellular (programmed cell death). In the absence of imbalances are increased levels of enzymes or matrix macrophages, tissue debridement will be incomplete metalloproteinases (MMPs), a decreased number of and the influx of fibroblasts to the wound will be available ‘active’ macrophages and/or a decreased significantly reduced. Fibroblasts are responsible for number of ‘active’ growth factors (Calvin, 1998). It is most of the collagen and elastin synthesis and, now thought that most chronic wounds, such as chronic therefore, play a vital role in wound healing. leg ulcers, are stuck in the phase known as early The major influences that macrophages have on inflammation (Falanga et al, 1994). wound healing may be summarised as: ■ Phagocytosing damaged tissue and bacteria; Cells involved in the inflammatory process ■ Producing chemotaxins for continuing white-cell Platelets Platelets are the cells that initiate wound recruitment; healing. They originate in the bone marrow, have a life ■ Releasing proteases that break down necrotic tissue; expectancy of between eight and 12 days and are filled ■ Making cytokines to regulate new tissue formation with cytokines that directly influence the activity of (Calvin, 1998); leucocytes (white blood cells) during the wound- ■ Producing interleukin-6. The interleukin family is a healing process. group of multifunctional cytokines with wide-ranging Platelets are released from damaged blood vessels effect in the wound-healing process. Interleukin-6 is and flow into the wound. When the platelets come into specifically associated with the immune response of the NT 24 June 2003 Vol 99 No 25 www.nursingtimes.net 63 SUPPLEMENT WOUND CARE KNOWLEDGE REFERENCES Hart, J. (1999) Growth factors. In: Glover, D., Miller, M. (eds) Wound Management. London: NT Books. Herbert, L. (1997) Caring for the Vascular Patient. Edinburgh: Churchill Livingstone. Johnston, S., Unsworth, J. (2001) The immunological system and inflammatory phase of wound healing and the pyrexia also been identified as playing an important role in the surgical practice. Surgery; (raised temperature) experienced by patients (Johnston transition from the inflammatory phase to the 19: 1, i–iv. and Unsworth, 2001); regenerative/proliferative phase of wound healing. In Kingsley, A. (2002) Wound ■ The release of matrix metalloproteinases (MMPs), total, the inflammatory phase of wound healing is healing and potential therapeutic options. Professional Nurse; which actively break down proteins and inhibit growth thought to last for five days (Calvin, 1998). 17: 9, 539–544. factors. MMPs assist with the clearance of the damaged Krasner, D. (1990) Chronic Wound extracellular matrix (Kingsley, 2002). Pathophysiological explanation of the ‘classic Care: A Clinical Source Book for signs’ of inflammation Following injury and Professionals. Wayne, PA: Health Management Publications. Growth factors The term ‘growth factor’ is used to endothelial damage, there is an initial vasoconstriction Lazarus, G. et al (1994) describe a variety of proteins that are involved in around the wound site followed by a rapid dilation of the Definitions and guidelines for the coordinating the various processes that occur during arterioles and precapillary sphincters (cuffs of smooth assessment of wounds and normal wound healing (Davidson and Broadley, 1991). muscle that regulate the flow of blood into the capillaries), evaluation of healing. Archives of Put simply, growth factors may be considered as the key resulting in reduced vascular resistance (Herbert, 1997). Dermatology; 130: 4, 489–493. Morison, M. et al (1997) Nursing substances that activate the cells involved with the A number of chemical mediators are released, which Management of Chronic Wounds. inflammatory process. There are several types of growth help to stimulate dilation and therefore increase capillary London: Mosby. factor involved with inflammation, including: permeability and cellular migration. These include: Slavin, J. (1996) The role of ■ Platelet-derived growth factor; histamine, prostaglandins (released from mast cells), cytokines in wound healing. ■ Journal of Pathology; 178: 1, 5–10. Epidermal growth factor; bradykinin (released from damaged epithelial cells) and ■ Angiogenesis growth factor; nitric oxide. ■ Basic fibroblastic growth factor; As a result of the increased blood flow – causing the ■ Transforming growth factor (Hart, 1999; Calvin, 1998; classic signs of heat and redness (hyperaemia) – there Krasner, 1990). is an increase in capillary hydrostatic pressure. This The overall functions of growth factors can be reduces the effectiveness of the normal blood osmotic summarised as follows: pressure and increases the permeability of the ■ Angiogenic – stimulating the growth of new transient capillaries. The increased permeability leads to protein- blood vessels to support the wound-healing process; rich fluid leaking into the interstitial tissue spaces. ■ Chemotatic – attracting various cell types involved in As fluid moves out of the capillaries the viscosity of wound healing to the wound-bed; the blood increases, slowing down blood flow. As the ■ Mitogenic – stimulating cellular proliferation; blood flow slows down, red blood cells clump together ■ Influencing the synthesis of cytokines by forcing white cells to move towards the endothelium of neighbouring cells; the vessels resulting in swelling and pain. ■ Regulating the synthesis and degradation of the There is an increased demand
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