NUR1101 : Nursing Assignment On Wound Care

Introduction:

By the truest definition, a wound is considered as a breakdown of the protective layers of the skin, leading to loss of epithelial continuity. Wounds develop from a blow or a cut or friction or any kind of traumatic injury to the skin or underlying soft tissues. Healing of wounds is a dynamic process that is usually divided into three different phases: Inflammatory phase, Proliferative phase and Maturation phase. Inflammation begins the healing through a wide variety of systems of attack and destruction targeting all invading pathogens (Clark, 2013). During this phase, blood vessels at the site of the wound carry several phagocytic cells, growth factors, cytokines and nutrients to promote the healing process. The wound in the inflammatory stage faces danger if disabled from progressing to proliferation and finally maturation. Progression could be slowed down or even stopped by many obstacles, such as lack of essential nutrients in the blood. However, malnutrition can be prevented or controlled by a wide choice of supplements and nutrients, giving the individual hope for recovery (Carville, 2012). The following discussion aims to provide a detailed understanding of the inflammatory process of wound healing, elucidate the roles of several factors involved in the process and assess the risks of malnutrition in preventing the progression of the healing process.

Goal of the Inflammatory Phase of Wound Healing

Inflammatory phase accounts for the first and foremost response of the body to an injury. It is one of the body’s natural defence mechanisms to instigate healing in the areas of injury from trauma, illness or disease. Following an incident, responses to the injury will move into action immediately to re-instate the normal continuity of the skin (Darby et al., 2014). Inflammation encourages the appropriate cells to arrive to the injured area and clean the area of bacteria, pathogens and debris. Inflammation is responsible for the bleeding control and for the prevention of infection at the site of injury. Normal healing of a wound without interruption follows an ordered unidirectional sequence. During the initial stage of wound healing, platelets play a significant role in clot formation and establishment of homeostasis. Once homeostasis is achieved, various inflammatory cells such as natural killer (NK) cells, neutrophils, lymphocytes come into the play. Tissue damage evokes inflammatory stimuli which activate the NK cells (Tanno et al., 2015). T-lymphocytes play a crucial role in healing cutaneous wounds. T-lymphocytes that utilise the NK cells to clear the pathogens are responsive to antigens and express some proteins to attract cytokines to the ECM. The fluid engorgement brings in these cells through the blood vessels to the site of the wound which then expresses characteristic signs of inflammation such as oedema, warmth, irritation and pain, resulting from the action of the white blood cells (WBCs), cytokines, growth factors and nutrients. Production of chemo-attractant molecules at the site of injury keeps the kinetics of the inflammatory cell infiltration.

Cellular Processes during Inflammatory Phase

The inflammatory phase is consisted of haemostasis, chemotaxis and increase in vascular permeability. It limits any further damage to the wound, forms clot at the site to prevent further blood loss, clears the site of any cellular debris, pathogens and bacteria and fosters the infiltration of the phagocytic cells. It involves both a vascular as well as a cellular response to the injury. Immediately after the injury, vasoconstriction occurs at the site of the wound, mediated by inflammatory factors such as epinephrine, norepinephrine, thromboxanes and prostaglandin. After that, the platelets coalesce at the site, forms the fibrin which is well-known as the blood clot formation. The aggregated platelets attach to the exposed collagen surfaces and get activated. Once activated, the platelets degranulate and release several chemotactic factors and growth factors such as Platelet Derived Growth Factors (PDGF), serotonin and histamine. Histamine causes vasodilation and results in oedema (I de la Torre, 2017). This enables the PDGFs to attract other cells that are necessary for the healing process. These cells include several white blood cells (WBCs) or leukocytes such as neutrophills, macrophages and lymphocytes. Neutrophils are the first cells to enter the site of injury and fight infections. The neutrophils phagocytise the cellular remains and the harmful bacteria. Once in the wound, the neutrophils attract the macrophages that engulf the necrotic debris of the wounds and activate fibroblast responses. Fibroblasts break down the fibrin clot, reform extra-cellular matrix (ECM) and collagen structures to provide the necessary support to the tissues associated with the wound healing (Bainbridge, 2013). Helper-T lymphocytes secrete the cytokines that are responsible for generating more T-cells and involving them at the site of injury to enhance the inflammatory response through activation of macrophages. Macrophages are the major cellular players involved in the process of wound healing (Koh & DiPietro, 2011). Macrophages secrete a type of metalloprotease that promotes autolysis the necrotic tissues (McCarty & Percival, 2013). They boost the defence system of the host, promote inflammation at the site of injury, remove cellular debris by phagocytosis and restore the epithelial tissues. The entire inflammatory process lasts for about a week (Velnar, Bailey & Smrkolj, 2009). If under unavoidable circumstances, the wound does not progress through the phases of Inflammation, Proliferation and Maturation within approximately three months it would be classified as chronic (Holloway et al., 2012).

Roles of Growth Factors or Cytokines during Inflammatory Phase of Wound Healing

The complex process of wound healing is executed with the help of regulatory factors including growth factors, cytokines and chemokines. There are five growth factor families that influence the tissue repair process. The platelet degranulation process releases various different kinds of cytokines and growth factors that play key roles in initiating the wound healing process (Pakyari et al., 2013). These include PDGF, fibroblast growth factor (FGF), epidermal growth factor (EGF), platelet derived angiogenesis factor (PDAF), TGF-β, serotonin, thromboxane, histamine, prostaglandin and bradykinin. The growth factors released into the site of the wound, diffuse inside the surrounding tissues and initiate the chemotactic process to draw the inflammatory cells to the injury site (Gouin & Kiecolt-Glaser, 2012). After this chemotaxis, the cells are activated by several mediators. Macrophages, in turn, activate T-lymphocytes to produce interferon- which acts on the macrophages in a paracrine manner to stimulate the secretion of two other cytokines, namely tumor necrosis factor-α (TNF-α) and interleukin-1 (IL1). These factors facilitate granulation and further epithelialisation (Murray et al., 2015).

Malnourishment: a factor that may cause wound to stall in the inflammatory phase  

The nutritional status of the individual affects the process of wound healing since it requires a definite amount of protein, energy, vitamins and minerals to effectively fulfil the complex procedure. Without a balanced diet containing all the daily requirements, it is difficult for the body and tissues to remain healthy, especially as the individual ages. Impediments in nutritional deficiencies hamper the progression of the wound healing from one phase to the next and prolonged stalling may result in development of chronic wound conditions. Thus, delayed wound healing in malnourished individuals results in non-healing chronic wounds (Posthauer, Dorner & Collins, 2010). Chronic wounds are potential cause of higher morbidity and mortality. This poses a serious threat and generates a clinical concern. Although, managing the nutrition intake may help alter the results and treat the wounds effectively. There are many reasons why a person would lack nutrients, however, the most common would be the inability to absorb or metabolize nutrients, long-term illnesses, anorexia and aging.  For people under a certain care, there are many tools that can be used to document the client’s daily intake and history thus allowing the practitioner to teach, encourage and implement a care plan to improve their nutritional intake. Many supplements are now available to help support the nutrient uptake. Arginine or L-arginine, is an amino acid that is made in the body. It is extensively used as a supplement to help improve chronic wounds effectively (Leigh et al., 2012). Carbohydrate, protein and fat are the primary source of energy in food. If a person is malnourished, that means they do not consume adequate amount of calories by food. In order to maintain the physical processes, their body utilizes the entire source of protein present on their diet and deplete their muscle mass to generate energy. Therefore, malnourished individuals must include adequate energy supplements in their diets to avoid further catabolism and improve anabolism.

Carbohydrates

This can be achieved by consuming adequate amount of carbohydrates that provide the essential energy required for the cellular processes, prevent gluconeogenesis and muscle loss (Posthauer, Dorner & Collins, 2010). Prevention of muscle wasting leads to prevention of loss of subcutaneous tissues and thereby improves wound healing effectively. Foods that are rich in carbohydrates include all fruits, grains, cereals, breads and many vegetables.

Fats

The most effective sources of energy are fats and triglycerides. Foods that are rich in healthy fats include meat, dairy, eggs and vegetable oils. Energy can be gained through essential fatty acids (EFA) which are found as linoleic fatty acids in vegetable sources such as flax seed oil or Borage oil or as linolenic within marine products such as fish oil. Similarly, nuts, grains and fish contain EFA. These nutrients provide a supply of energy to the cells that support proliferation, phagocytic activity and prostaglandin secretion in tissue repair (Carville, 2012).

Proteins

Proteins are the building blocks of the muscles and the only nutrient that consists of nitrogen and amino acids. Proteins are associated with wound repair enzyme synthesis, cellular duplication, collagen synthesis, producing antibody components which are essential for immune response generation and the completion of the initial phase of inflammatory wound healing process (Leigh et al., 2012). Protein sources are present in foods such as meat, egg, dairy, legumes, grains and beans.

Vitamins

Vitamin C influences the activation procedure of the WBCs and macrophages surrounding the wound. Thus, Vitamin C deficiency would cause delayed healing and reduce the power of resistance towards any infection through the injury. Vitamin C is also required for the collagen production which aids wound healing. Foods that are rich in Vitamin C include citrus fruits such as berries, grapes, oranges and vegetables such as tomatoes, bell peppers and broccoli. All the Vitamin B complexes are associated with promoting wound healing process. Such as, Vitamin B6 or pyridoxine which is mostly found in green leafy vegetables and legumes aid red blood cell production and compensates for the blood loss due to the trauma. Thiamine and riboflavin are two other vitamins that are essential for the process of collagenation (Posthauer, Dorner & Collins, 2010).

Conclusion:

Inflammation has been demonstrated as the beginning and finish of an exchange of chemicals and proteins to keep any pathogens at bay that might enter the body through an injury, trauma or disease. The first line of defense is the white blood cells that are quickly activated followed by the chemical messengers. Both the chemokines and pathogens activate the platelets and histamine. The tissues will be expanded and filling with fluid to allow the neutrophils to pass through and destroy any foreign particles. Thus, the inflammatory phase encourages the appropriate cells to arrive to the injured area and clean the area of bacteria, pathogens and debris. While the purpose of inflammatory phase of wound healing is to destroy the foreign particles and protect the body, the need for the individual to help nourish the body and tissues is vital. Adequate nutrition is mandatory for achieving optimal wound healing. Malnourished individuals often fail to possess the essential nutrients required for a wound to heal effectively and develop a chronic wound. If nutrient status is maintained and properly balanced, the strength and energy given to the white blood cells will prevent a wound from becoming chronic.

References:

Bainbridge, P. (2013). Wound healing and the role of fibroblasts. Journal of wound care, 22(8). 407-412. doi: 10.12968/jowc.2013.22.8.407

Carville, K. (2012). Wound care manual. (6^th ed.). Osborne Park, W.A.: Silver Chain Nursing Association.

Clark, R. A. (2013). The molecular and cellular biology of wound repair. (2^nd ed.). Springer Science & Business Media.

Darby, I. A., Laverdet, B., Bonté, F., & Desmoulière, A. (2014). Fibroblasts and myofibroblasts in wound healing. Clinical, cosmetic and investigational dermatology, 7, 301. doi:  10.2147/CCID.S50046

Gouin, J. P., & Kiecolt-Glaser, J. K. (2012). The impact of psychological stress on wound healing: methods and mechanisms. Critical Care Nursing Clinics, 24(2), 201-213. doi: 10.1016/j.ccell.2012.03.006

Holloway, S., Harding, K.,Stechmiller, J. K.,Schultz, G. (2012).Wound Care Essentials: Practice Principles. (3^rd ed.). Philadelphia, PA 19106 USA: Lippincott Williams & Wilkins.

I de la Torre, J. (2017). Chronic wounds. Medscape, Retrieved from: https://emedicine.medscape.com/article/1298452

Koh, T. J., & DiPietro, L. A. (2011). Inflammation and wound healing: The role of the macrophage. Expert reviews in molecular medicine, 13. 2-6. doi: 10.1017/S1462399411001943

Leigh, B., Desneves, K., Rafferty, J., Pearce, L., King, S., Woodward, M. C., … & Crowe, T. C. (2012). The effect of different doses of an arginine-containing supplement on the healing of pressure ulcers. journal of wound care, 21(3), 150-156. doi: 10.12968/jowc.2012.21.3.150 

McCarty, S. M., & Percival, S. L. (2013). Proteases and delayed wound healing. Advances in wound care, 2(8), 438-447. doi:  10.1089/wound.2012.0370

Murray, R. Z., Röhl, J., Zaharia, A., & Rudolph, M. (2015). The role of inflammation in cutaneous repair. Wound Practice & Research, 23(1). 8-15. Retrieved from: https://www.woundsaustralia.com.au/journal/2301_02pdf

Pakyari, M., Farrokhi, A., Maharlooei, M. K., & Ghahary, A. (2013). Critical role of transforming growth factor beta in different phases of wound healing. Advances in wound care, 2(5), 215-224. doi:  10.1089/wound.2012.0406

Posthauer, M. E., Dorner, B., & Collins, N. (2010). Nutrition: a critical component of wound healing. Advances in skin & wound care, 23(12), 560-572. doi: 10.1097/01.ASW.0000391185. 81963 

Tanno, H., Kawakami, K., Ritsu, M., Kanno, E., Suzuki, A., Kamimatsuno, R., … & Maruyama, R. (2015). Contribution of invariant natural killer T cells to skin wound healing. The American Journal of Pathology, 185(12), 3248-3257. doi: 10.1016/j.apath.2015.08.012

Velnar, T., Bailey, T., & Smrkolj, V. (2009). The wound healing process: an overview of the cellular and molecular mechanisms. Journal of International Medical Research, 37(5), 1528-1542. doi: 10.1177/147323000903700531