Nursing Assignment on Wound Care
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This nursing assignment discusses the inflammatory phase of wound healing, the roles of growth factors and cytokines, and how malnourishment can cause wounds to stall. It also provides insights on carbohydrates, fats, proteins, and vitamins that can help in wound healing.
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Running head: NURSING ASSIGNMENT ON WOUND CARE
Nursing Assignment on Wound Care
Name of the student
Name of the university
Author note
Nursing Assignment on Wound Care
Name of the student
Name of the university
Author note
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1NURSING 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
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
2NURSING ASSIGNMENT ON WOUND CARE
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
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
3NURSING ASSIGNMENT ON WOUND CARE
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).
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).
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4NURSING ASSIGNMENT ON WOUND CARE
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
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
5NURSING ASSIGNMENT ON WOUND CARE
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.
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.
6NURSING ASSIGNMENT ON WOUND CARE
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
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
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7NURSING ASSIGNMENT ON WOUND CARE
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.
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.
8NURSING ASSIGNMENT ON WOUND CARE
9NURSING ASSIGNMENT ON WOUND CARE
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. (6th ed.). Osborne Park, W.A.: Silver Chain Nursing
Association.
Clark, R. A. (2013). The molecular and cellular biology of wound repair. (2nd 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. (3rd 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
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. (6th ed.). Osborne Park, W.A.: Silver Chain Nursing
Association.
Clark, R. A. (2013). The molecular and cellular biology of wound repair. (2nd 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. (3rd 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
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10NURSING ASSIGNMENT ON WOUND CARE
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:
http://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
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:
http://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
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