This PPT describes about the Metabolic response to injury as given in Bailey & Love - 26th edition. It will be very useful for Final year MBBS students.
The effect of stress on hormone serum level/cortisol the stress hormone/stress as a cause of endocrine disorders such as diabetes mellitus, thyroid storm, obesity and hyperthyroidism/stress and hormones/Disorders caused by high-stress level/prolactin hormone is affected by stress/is growth hormone affected by stress.
Stress, Food, and Inflammation Psychoneuroimmunology and Nutr.docxcpatriciarpatricia
- Stress, depression, and inflammation are linked through common pathways like sympathetic activity, oxidative stress, and pro-inflammatory cytokines.
- Unhealthy diets high in saturated fat and refined carbs promote inflammation while diets high in omega-3 fatty acids, fruits, vegetables, and whole grains reduce inflammation.
- Stress influences food choices towards unhealthy options and can enhance inflammatory responses to meals, while certain diets like Mediterranean can positively impact mood and inflammation.
This document discusses the impacts of climate change and pollution on cardiovascular health. It finds that high temperatures are associated with increased cardiovascular disease, and implementation of heat-health plans is needed. Air pollution effects may be stronger on high temperature days due to synergistic effects on the cardiovascular system. The biological mechanisms of this interaction are not fully understood but possibly include increased inflammation and oxidative stress from both air pollution and temperature.
The document discusses endocrine issues in critical illness, including the stress response and its effects on glucose levels and insulin resistance. It presents evidence that tight glycemic control with intensive insulin therapy reduces mortality in critically ill patients. The text also examines glucocorticoid physiology and biosynthesis, noting that adrenal insufficiency is common in sepsis and ICU patients. Studies demonstrate improved outcomes with hydrocortisone replacement in patients with septic shock or adrenal insufficiency.
This document provides an overview of obesity, energy balance, inflammation, and other factors related to metabolic health. It discusses how factors like stress, poor diet, lack of activity, and environmental toxins can disrupt metabolic processes and gene expression, leading to issues like insulin resistance, obesity, and disease. The document recommends addressing the root causes of metabolic imbalance through a Mediterranean-style diet high in nutrients and low in inflammation-promoting foods. Regular physical activity and lifestyle factors are also important to maintain metabolic health and gene expression. The goal is to take an integrative, upstream approach to metabolic disorders through nutrition and lifestyle interventions before relying on downstream medical treatments.
Trauma triggers a complex metabolic response aimed at returning the body to homeostasis. This response involves two phases - an initial "ebb phase" characterized by hypometabolism followed by a "flow phase" of hypermetabolism. The hypermetabolic response is mediated by neuroendocrine and inflammatory factors like cortisol, catecholamines, cytokines and growth hormones which increase glucose and lipid metabolism while breaking down skeletal muscle. Understanding and limiting factors like hypothermia, edema and immobilization can reduce complications from this metabolic response.
This PPT describes about the Metabolic response to injury as given in Bailey & Love - 26th edition. It will be very useful for Final year MBBS students.
The effect of stress on hormone serum level/cortisol the stress hormone/stress as a cause of endocrine disorders such as diabetes mellitus, thyroid storm, obesity and hyperthyroidism/stress and hormones/Disorders caused by high-stress level/prolactin hormone is affected by stress/is growth hormone affected by stress.
Stress, Food, and Inflammation Psychoneuroimmunology and Nutr.docxcpatriciarpatricia
- Stress, depression, and inflammation are linked through common pathways like sympathetic activity, oxidative stress, and pro-inflammatory cytokines.
- Unhealthy diets high in saturated fat and refined carbs promote inflammation while diets high in omega-3 fatty acids, fruits, vegetables, and whole grains reduce inflammation.
- Stress influences food choices towards unhealthy options and can enhance inflammatory responses to meals, while certain diets like Mediterranean can positively impact mood and inflammation.
This document discusses the impacts of climate change and pollution on cardiovascular health. It finds that high temperatures are associated with increased cardiovascular disease, and implementation of heat-health plans is needed. Air pollution effects may be stronger on high temperature days due to synergistic effects on the cardiovascular system. The biological mechanisms of this interaction are not fully understood but possibly include increased inflammation and oxidative stress from both air pollution and temperature.
The document discusses endocrine issues in critical illness, including the stress response and its effects on glucose levels and insulin resistance. It presents evidence that tight glycemic control with intensive insulin therapy reduces mortality in critically ill patients. The text also examines glucocorticoid physiology and biosynthesis, noting that adrenal insufficiency is common in sepsis and ICU patients. Studies demonstrate improved outcomes with hydrocortisone replacement in patients with septic shock or adrenal insufficiency.
This document provides an overview of obesity, energy balance, inflammation, and other factors related to metabolic health. It discusses how factors like stress, poor diet, lack of activity, and environmental toxins can disrupt metabolic processes and gene expression, leading to issues like insulin resistance, obesity, and disease. The document recommends addressing the root causes of metabolic imbalance through a Mediterranean-style diet high in nutrients and low in inflammation-promoting foods. Regular physical activity and lifestyle factors are also important to maintain metabolic health and gene expression. The goal is to take an integrative, upstream approach to metabolic disorders through nutrition and lifestyle interventions before relying on downstream medical treatments.
Trauma triggers a complex metabolic response aimed at returning the body to homeostasis. This response involves two phases - an initial "ebb phase" characterized by hypometabolism followed by a "flow phase" of hypermetabolism. The hypermetabolic response is mediated by neuroendocrine and inflammatory factors like cortisol, catecholamines, cytokines and growth hormones which increase glucose and lipid metabolism while breaking down skeletal muscle. Understanding and limiting factors like hypothermia, edema and immobilization can reduce complications from this metabolic response.
The metabolic response to traumatic brain injury (TBI) involves undesirable alterations including disrupted metabolism and a hypercatabolic state. Several key pathways are affected by TBI, including glycolysis, gluconeogenesis, glycogenolysis, and proteolysis. In the brain, inflammation causes increased energy demands, resulting in hyperglycolysis and increased lactate uptake. Peripheral stores such as glycogen are mobilized via lactate and gluconeogenesis to support brain glucose needs. Throughout the body, TBI induces a hypermetabolic state characterized by increased protein breakdown and whole-body catabolism. This leads to severe malnutrition if not addressed through specialized nutrition protocols tailored for TBI patients' high protein and calorie requirements.
Therapeutic angiogenesis using protein and gene therapies offers hope to patients with myocardial ischemia. Current clinical trials are assessing the safety and efficacy of administering growth factors like VEGF and FGF via gene therapy or protein therapy to stimulate new blood vessel growth in the heart. While early phase I studies showed promising results, larger phase II studies using placebo controls did not consistently find significant improvements, demonstrating the need for more research to determine the optimal treatment method, dosage, and administration route.
Relief from hot flushes is one of the most common reasons for visits from mid-life women and represents a major healthcare cost. Hot flushes are associated with poor sleep, depressed mood, decreased quality of life, and may increase risk of cardiovascular disease and poor bone health. A standardized hop extract containing 8-PN (8-prenylnaringenin) at 100 mcg per day provided relief for mild vasomotor symptoms and was well tolerated by menopausal women in clinical studies. 8-PN begins changing hormone balance after a single dose and shows potential benefits for breast health, cardiovascular health, and bone health when consumed as part of a balanced diet and lifestyle.
critical illness and metabolism ICRC 2012.pptxssuser6aa7a3
This document discusses the stress response pattern seen in critically ill patients. It describes the metabolic changes that occur across multiple organ systems as part of the body's adaptive response to critical illness and injury. These include increases in oxygen demand, protein catabolism, and changes in endocrine and immune function. Recognizing the typical ebb and flow phases of this stress response enables clinicians to better predict patient trajectories, guide diagnostic and therapeutic decisions, and identify unexpected deviations from the expected pattern.
This randomized controlled trial compared early initiation of low-dose hydrocortisone therapy versus standard therapy for septic shock in geriatric patients. 120 patients were randomly assigned to receive early hydrocortisone upon initiation of vasopressors or standard therapy where hydrocortisone was given after fluids and vasopressors failed. The primary outcome of 28-day mortality did not significantly differ between groups. Secondary outcomes of ICU stay duration, vasopressor requirement, and mechanical ventilation need also showed no significant differences. While reversal of shock was higher in the early group, more adverse effects like hyperglycemia occurred. The study concluded that early steroids provided limited benefit for outcomes in elderly patients with septic shock.
This document discusses systemic steroid therapy. It begins by introducing steroids and their use as drugs to treat inflammatory disorders. It then describes the hypothalamic-pituitary-adrenal axis that controls endogenous steroid secretion. The main types of endogenous corticosteroids are described as well as their normal daily secretions. The actions of glucocorticoids, mineralocorticoids, and anabolic steroids on various body systems are explained in detail. Finally, examples of systemic steroids are provided along with their common indications for use in therapy.
The document summarizes the body's systemic response to injury. It discusses the immunologic and inflammatory response as well as the neuroendocrine response, which involves the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. The response aims to limit damage, restore homeostasis, and has effects on the cardiovascular and metabolic systems. It occurs in three phases - ebb, flow, and recovery - and involves changes in hormones, metabolism, temperature, and other physiological functions to break down and rebuild energy stores.
This document summarizes a clinical trial that tested the effects of a glutathione patch on cellular physiological function in different organs. The trial found that wearing the patch for 12 hours per day for 4 weeks significantly improved cellular physiological status in the pancreas, liver, gallbladder, intestines, adrenal glands, hypothalamus and pituitary gland, as measured by bioelectrical impedance data. This suggests the patch is effective at enhancing glutathione levels and positively impacting organ function. The technology provides a safe, convenient and affordable way to boost glutathione compared to previous intravenous methods.
The document discusses the relationship between stress, the hypothalamic-pituitary-adrenal (HPA) axis, and immune function. It summarizes that psychological stressors activate the HPA axis and increase glucocorticoid release from the adrenal glands. Prolonged high glucocorticoid levels can damage the hippocampus and impair HPA regulation, sensitizing the stress response. Early life stress may also program the HPA axis and increase risk of mental illnesses. The document reviews evidence that stress and glucocorticoids influence immune function and that CRH antagonists show promise in treating depression and stress-related disorders by regulating abnormal HPA activity.
The document discusses stress and digestive disorders in animals. It defines stress as a systemic state that develops from long-term exposure to stressors. Common stressors include road transportation, climate, crowding, and nutritional deficiencies. Transportation is considered highly stressful and results in increased cortisol, leukocytosis, and dehydration in animals. Prolonged stress can lead to stress-related diseases like anaphylaxis, which is an acute allergic reaction caused by exposure to an antigen. Anaphylaxis causes respiratory distress, anxiety, and collapse. Treatment involves epinephrine and corticosteroids to counter the allergic reaction. The document examines the causes, signs, pathology, and treatment of stress and digestive disorders in
Exercise and the_immune_system--influence_of_nutri_01Daniel Pancho
This document discusses how exercise affects the immune system. It states that moderate exercise enhances the immune system while only intense long-duration exercise impairs it. This impairment is referred to as the "open window" where viruses may more easily invade the body. Nutritional factors and ageing can also influence the immune system's response to exercise. Regular exercise may increase resistance to infections like colds, while overtraining is associated with more respiratory infections.
The document discusses a biotechnology company focused on developing products that regenerate or strengthen the human immune system. It summarizes results showing that the company's drug candidate Homspera stimulates hematopoietic stem cells, increasing white blood cell and platelet production. Studies also suggest Homspera may help resolve neutropenia caused by radiation exposure and chemotherapy by boosting white blood cell counts in irradiated animals.
The document discusses the metabolic response to injury in the body. It describes the graded nature of the response, which is proportional to the severity of injury. The response consists of physiological, metabolic, clinical and laboratory changes. It is mediated by neuroendocrine responses involving stress hormones and cytokines, as well as immune system responses. The metabolic response aims to restore normal health but can sometimes damage distant organs. It follows a pattern known as the Ebb and Flow model, with an initial catabolic phase promoting mobilization of energy stores followed by an anabolic recovery phase. Key catabolic elements include hypermetabolism, alterations in muscle and hepatic protein metabolism, and insulin resistance.
Cell adaptation, injury, and death play important roles in disease pathogenesis according to Rudolph Virchow's theory. Adaptation is a reversible cellular response to stress that allows cells to survive physiological or pathological stimuli. If stress is too severe or prolonged, it can lead to cell injury, which may be reversible or irreversible. The main types of cellular adaptation include hyperplasia, hypertrophy, atrophy, metaplasia, and dystrophy. Cell injury damages intracellular structures and impairs cellular functions. The two main types of cell death are necrosis, which is unregulated, and apoptosis, which is programmed and controlled. Necrosis leads to cell lysis while apoptosis involves fragmentation into apoptotic bodies.
By binding to a new nuclear-associated receptor, opioid
growth factor (OGF), also known by its chemical name
[Met5]-enkephalin, promotes cellular homeostasis.
Serum OGF levels are high in diabetic individuals.
In the animal model, opioid receptor antagonists like
naltrexone (NTX) alleviate many of the consequences of
diabetes
Stress is defined as a state of physiological or psychological strain caused by an adverse stimuli , physical, mental, or emotional, internal or external that tend to disturb the functioning of an organism and which the organism naturally desires to avoid.
International Journal of Pharmaceutical Science Invention (IJPSI)inventionjournals
is an international journal intended for professionals and researchers in all fields of Pahrmaceutical Science. IJPSI publishes research articles and reviews within the whole field Pharmacy and Pharmaceutical Science, new teaching methods, assessment, validation and the impact of new technologies and it will continue to provide information on the latest trends and developments in this ever-expanding subject. The publications of papers are selected through double peer reviewed to ensure originality, relevance, and readability. The articles published in our journal can be accessed online
Metabolic Response To Injury and surgical stressSaurabhJagdale8
The document discusses the metabolic response to injury that occurs following accidental injury, surgery, or other trauma. It describes the physiological and biochemical changes, including alterations in body metabolism, wound healing, and immunity. These changes are mediated by hormones, inflammation-related cytokines, and neural circuits in order to maintain homeostasis. The response involves an initial catabolic phase followed by an anabolic rebuilding phase. Factors that can exacerbate the response are discussed, as well as the importance of avoiding complications and optimizing perioperative care through newer ERAS protocols.
1. General anaesthesia can have both direct and indirect effects on the immune system by impacting the innate immune response, adaptive immune response, cytokine production, neutrophil activity, and immunoglobulin levels.
2. Surgery alone increases pro-inflammatory cytokine levels, but anaesthetic agents may increase or decrease specific cytokine production depending on the agent.
3. Perioperative interventions like mechanical ventilation, blood transfusions, chronic pain, and immunosuppressive drugs for transplant patients can further impact the immune response. Precautions are needed for patients with these factors.
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
Weitere ähnliche Inhalte
Ähnlich wie Respuesta metabólica al Trauma Resumen.pdf
The metabolic response to traumatic brain injury (TBI) involves undesirable alterations including disrupted metabolism and a hypercatabolic state. Several key pathways are affected by TBI, including glycolysis, gluconeogenesis, glycogenolysis, and proteolysis. In the brain, inflammation causes increased energy demands, resulting in hyperglycolysis and increased lactate uptake. Peripheral stores such as glycogen are mobilized via lactate and gluconeogenesis to support brain glucose needs. Throughout the body, TBI induces a hypermetabolic state characterized by increased protein breakdown and whole-body catabolism. This leads to severe malnutrition if not addressed through specialized nutrition protocols tailored for TBI patients' high protein and calorie requirements.
Therapeutic angiogenesis using protein and gene therapies offers hope to patients with myocardial ischemia. Current clinical trials are assessing the safety and efficacy of administering growth factors like VEGF and FGF via gene therapy or protein therapy to stimulate new blood vessel growth in the heart. While early phase I studies showed promising results, larger phase II studies using placebo controls did not consistently find significant improvements, demonstrating the need for more research to determine the optimal treatment method, dosage, and administration route.
Relief from hot flushes is one of the most common reasons for visits from mid-life women and represents a major healthcare cost. Hot flushes are associated with poor sleep, depressed mood, decreased quality of life, and may increase risk of cardiovascular disease and poor bone health. A standardized hop extract containing 8-PN (8-prenylnaringenin) at 100 mcg per day provided relief for mild vasomotor symptoms and was well tolerated by menopausal women in clinical studies. 8-PN begins changing hormone balance after a single dose and shows potential benefits for breast health, cardiovascular health, and bone health when consumed as part of a balanced diet and lifestyle.
critical illness and metabolism ICRC 2012.pptxssuser6aa7a3
This document discusses the stress response pattern seen in critically ill patients. It describes the metabolic changes that occur across multiple organ systems as part of the body's adaptive response to critical illness and injury. These include increases in oxygen demand, protein catabolism, and changes in endocrine and immune function. Recognizing the typical ebb and flow phases of this stress response enables clinicians to better predict patient trajectories, guide diagnostic and therapeutic decisions, and identify unexpected deviations from the expected pattern.
This randomized controlled trial compared early initiation of low-dose hydrocortisone therapy versus standard therapy for septic shock in geriatric patients. 120 patients were randomly assigned to receive early hydrocortisone upon initiation of vasopressors or standard therapy where hydrocortisone was given after fluids and vasopressors failed. The primary outcome of 28-day mortality did not significantly differ between groups. Secondary outcomes of ICU stay duration, vasopressor requirement, and mechanical ventilation need also showed no significant differences. While reversal of shock was higher in the early group, more adverse effects like hyperglycemia occurred. The study concluded that early steroids provided limited benefit for outcomes in elderly patients with septic shock.
This document discusses systemic steroid therapy. It begins by introducing steroids and their use as drugs to treat inflammatory disorders. It then describes the hypothalamic-pituitary-adrenal axis that controls endogenous steroid secretion. The main types of endogenous corticosteroids are described as well as their normal daily secretions. The actions of glucocorticoids, mineralocorticoids, and anabolic steroids on various body systems are explained in detail. Finally, examples of systemic steroids are provided along with their common indications for use in therapy.
The document summarizes the body's systemic response to injury. It discusses the immunologic and inflammatory response as well as the neuroendocrine response, which involves the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. The response aims to limit damage, restore homeostasis, and has effects on the cardiovascular and metabolic systems. It occurs in three phases - ebb, flow, and recovery - and involves changes in hormones, metabolism, temperature, and other physiological functions to break down and rebuild energy stores.
This document summarizes a clinical trial that tested the effects of a glutathione patch on cellular physiological function in different organs. The trial found that wearing the patch for 12 hours per day for 4 weeks significantly improved cellular physiological status in the pancreas, liver, gallbladder, intestines, adrenal glands, hypothalamus and pituitary gland, as measured by bioelectrical impedance data. This suggests the patch is effective at enhancing glutathione levels and positively impacting organ function. The technology provides a safe, convenient and affordable way to boost glutathione compared to previous intravenous methods.
The document discusses the relationship between stress, the hypothalamic-pituitary-adrenal (HPA) axis, and immune function. It summarizes that psychological stressors activate the HPA axis and increase glucocorticoid release from the adrenal glands. Prolonged high glucocorticoid levels can damage the hippocampus and impair HPA regulation, sensitizing the stress response. Early life stress may also program the HPA axis and increase risk of mental illnesses. The document reviews evidence that stress and glucocorticoids influence immune function and that CRH antagonists show promise in treating depression and stress-related disorders by regulating abnormal HPA activity.
The document discusses stress and digestive disorders in animals. It defines stress as a systemic state that develops from long-term exposure to stressors. Common stressors include road transportation, climate, crowding, and nutritional deficiencies. Transportation is considered highly stressful and results in increased cortisol, leukocytosis, and dehydration in animals. Prolonged stress can lead to stress-related diseases like anaphylaxis, which is an acute allergic reaction caused by exposure to an antigen. Anaphylaxis causes respiratory distress, anxiety, and collapse. Treatment involves epinephrine and corticosteroids to counter the allergic reaction. The document examines the causes, signs, pathology, and treatment of stress and digestive disorders in
Exercise and the_immune_system--influence_of_nutri_01Daniel Pancho
This document discusses how exercise affects the immune system. It states that moderate exercise enhances the immune system while only intense long-duration exercise impairs it. This impairment is referred to as the "open window" where viruses may more easily invade the body. Nutritional factors and ageing can also influence the immune system's response to exercise. Regular exercise may increase resistance to infections like colds, while overtraining is associated with more respiratory infections.
The document discusses a biotechnology company focused on developing products that regenerate or strengthen the human immune system. It summarizes results showing that the company's drug candidate Homspera stimulates hematopoietic stem cells, increasing white blood cell and platelet production. Studies also suggest Homspera may help resolve neutropenia caused by radiation exposure and chemotherapy by boosting white blood cell counts in irradiated animals.
The document discusses the metabolic response to injury in the body. It describes the graded nature of the response, which is proportional to the severity of injury. The response consists of physiological, metabolic, clinical and laboratory changes. It is mediated by neuroendocrine responses involving stress hormones and cytokines, as well as immune system responses. The metabolic response aims to restore normal health but can sometimes damage distant organs. It follows a pattern known as the Ebb and Flow model, with an initial catabolic phase promoting mobilization of energy stores followed by an anabolic recovery phase. Key catabolic elements include hypermetabolism, alterations in muscle and hepatic protein metabolism, and insulin resistance.
Cell adaptation, injury, and death play important roles in disease pathogenesis according to Rudolph Virchow's theory. Adaptation is a reversible cellular response to stress that allows cells to survive physiological or pathological stimuli. If stress is too severe or prolonged, it can lead to cell injury, which may be reversible or irreversible. The main types of cellular adaptation include hyperplasia, hypertrophy, atrophy, metaplasia, and dystrophy. Cell injury damages intracellular structures and impairs cellular functions. The two main types of cell death are necrosis, which is unregulated, and apoptosis, which is programmed and controlled. Necrosis leads to cell lysis while apoptosis involves fragmentation into apoptotic bodies.
By binding to a new nuclear-associated receptor, opioid
growth factor (OGF), also known by its chemical name
[Met5]-enkephalin, promotes cellular homeostasis.
Serum OGF levels are high in diabetic individuals.
In the animal model, opioid receptor antagonists like
naltrexone (NTX) alleviate many of the consequences of
diabetes
Stress is defined as a state of physiological or psychological strain caused by an adverse stimuli , physical, mental, or emotional, internal or external that tend to disturb the functioning of an organism and which the organism naturally desires to avoid.
International Journal of Pharmaceutical Science Invention (IJPSI)inventionjournals
is an international journal intended for professionals and researchers in all fields of Pahrmaceutical Science. IJPSI publishes research articles and reviews within the whole field Pharmacy and Pharmaceutical Science, new teaching methods, assessment, validation and the impact of new technologies and it will continue to provide information on the latest trends and developments in this ever-expanding subject. The publications of papers are selected through double peer reviewed to ensure originality, relevance, and readability. The articles published in our journal can be accessed online
Metabolic Response To Injury and surgical stressSaurabhJagdale8
The document discusses the metabolic response to injury that occurs following accidental injury, surgery, or other trauma. It describes the physiological and biochemical changes, including alterations in body metabolism, wound healing, and immunity. These changes are mediated by hormones, inflammation-related cytokines, and neural circuits in order to maintain homeostasis. The response involves an initial catabolic phase followed by an anabolic rebuilding phase. Factors that can exacerbate the response are discussed, as well as the importance of avoiding complications and optimizing perioperative care through newer ERAS protocols.
1. General anaesthesia can have both direct and indirect effects on the immune system by impacting the innate immune response, adaptive immune response, cytokine production, neutrophil activity, and immunoglobulin levels.
2. Surgery alone increases pro-inflammatory cytokine levels, but anaesthetic agents may increase or decrease specific cytokine production depending on the agent.
3. Perioperative interventions like mechanical ventilation, blood transfusions, chronic pain, and immunosuppressive drugs for transplant patients can further impact the immune response. Precautions are needed for patients with these factors.
Ähnlich wie Respuesta metabólica al Trauma Resumen.pdf (20)
Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
Reimagining Your Library Space: How to Increase the Vibes in Your Library No ...Diana Rendina
Librarians are leading the way in creating future-ready citizens – now we need to update our spaces to match. In this session, attendees will get inspiration for transforming their library spaces. You’ll learn how to survey students and patrons, create a focus group, and use design thinking to brainstorm ideas for your space. We’ll discuss budget friendly ways to change your space as well as how to find funding. No matter where you’re at, you’ll find ideas for reimagining your space in this session.
How to Manage Your Lost Opportunities in Odoo 17 CRMCeline George
Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPRAHUL
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
core of India. Mirzapur, with its varied terrains and abundant biodiversity, offers an optimal
environment for investigating the changes in vegetation cover dynamics. Our study utilizes
advanced technologies such as GIS (Geographic Information Systems) and Remote sensing to
analyze the transformations that have taken place over the course of a decade.
The complex relationship between human activities and the environment has been the focus
of extensive research and worry. As the global community grapples with swift urbanization,
population expansion, and economic progress, the effects on natural ecosystems are becoming
more evident. A crucial element of this impact is the alteration of vegetation cover, which plays a
significant role in maintaining the ecological equilibrium of our planet.Land serves as the foundation for all human activities and provides the necessary materials for
these activities. As the most crucial natural resource, its utilization by humans results in different
'Land uses,' which are determined by both human activities and the physical characteristics of the
land.
The utilization of land is impacted by human needs and environmental factors. In countries
like India, rapid population growth and the emphasis on extensive resource exploitation can lead
to significant land degradation, adversely affecting the region's land cover.
Therefore, human intervention has significantly influenced land use patterns over many
centuries, evolving its structure over time and space. In the present era, these changes have
accelerated due to factors such as agriculture and urbanization. Information regarding land use and
cover is essential for various planning and management tasks related to the Earth's surface,
providing crucial environmental data for scientific, resource management, policy purposes, and
diverse human activities.
Accurate understanding of land use and cover is imperative for the development planning
of any area. Consequently, a wide range of professionals, including earth system scientists, land
and water managers, and urban planners, are interested in obtaining data on land use and cover
changes, conversion trends, and other related patterns. The spatial dimensions of land use and
cover support policymakers and scientists in making well-informed decisions, as alterations in
these patterns indicate shifts in economic and social conditions. Monitoring such changes with the
help of Advanced technologies like Remote Sensing and Geographic Information Systems is
crucial for coordinated efforts across different administrative levels. Advanced technologies like
Remote Sensing and Geographic Information Systems
9
Changes in vegetation cover refer to variations in the distribution, composition, and overall
structure of plant communities across different temporal and spatial scales. These changes can
occur natural.
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
1. The Surgically Induced Stress Response
Celeste C. Finnerty, PhD1,2, Nigel Tapiwa Mabvuure, MD1, Arham Ali, MD1, Rosemary A.
Kozar, MD, PhD3, and David N. Herndon, MD1
1Department of Surgery, Shriners Hospitals for Children–Galveston and the University of Texas
Medical Branch, Galveston, Texas
2The Institute for Translational Science and the Sealy Center for Molecular Medicine, The
University of Texas Medical Branch
3Department of Surgery, University of Texas–Houston Health Science Center, Houston, Texas.
Abstract
The stress response to surgery, critical illness, trauma, and burns encompasses derangements of
metabolic and physiological processes which induce perturbations in the inflammatory, acute
phase, hormonal, and genomic responses. Hypermetabolism and hypercatabolism result, leading to
muscle wasting, impaired immune function and wound healing, organ failure, and death. The
surgery-induced stress response is largely similar to that triggered by traumatic injuries; the
duration of the stress response, however, varies according to the severity of injury (surgical or
traumatic). This spectrum of injuries and insults ranges from small lacerations to severe insults
such as large poly-traumatic and burn injuries. Although the stress response to acute trauma
evolved to improve chances of survival following injury, in modern surgical practice the stress
response can be detrimental.
Following surgical or accidental trauma, the nervous system activates the stress response by
sending impulses from the injured site to the hypothalamus. The hypothalamus either
removes its inhibitory tone on the pituitary or releases hormones which stimulate the
production and/or release of pituitary hormones. Pituitary hormones act on their respective
target organ causing the release of hormones such as the stress hormone, cortisol. Elevations
of cortisol, glucagon, catecholamines, and a host of inflammatory cytokines, also exacerbate
the stress response to surgery.
Afferent nerve signals from the injured site and proinflammatory cytokines have the net
effect of increasing the secretion of hormones from the pituitary gland. Increased secretion
of the anterior pituitary hormones corticotrophin (ACTH) and growth hormone (GH) have
particularly significant metabolic consequences. Other anterior pituitary hormones such as
thyrotrophin (TSH) and the gonadotropins (follicle stimulating hormone [FSH] and
luteinizing hormone [LH]) are not as significantly affected.
Agents Generating the Stress Response to Surgery
Cortisol
Corticotrophin-releasing hormone (CRH), released by the hypothalamus, stimulates the
anterior pituitary release of ACTH into the bloodstream. ACTH is a by-product of the
Financial disclosure: The publication of the supplement in which this article appears is supported by an educational grant from Nestle
Healthcare Nutrition. Authors received an honorarium from the Nestle Nutrition Institute for their participation in the North American
Surgical Nutrition Summit.
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2. breakdown of pro-opiomelanocortin. To complete the hypothalamic-pituitary (HPA) axis,
cortisol (the stress hormone) is produced by the adrenal glands following ACTH stimulation.
The HPA axis is regulated by a negative feedback mechanism in which cortisol suppresses
the release of both CRH and ACTH. Cortisol is a catabolic glucocorticoid hormone that
mobilizes energy stores to prepare the body for the fight or flight response to stressors. It
promotes gluconeogenesis in the liver, leading to raised blood glucose levels.
Hyperglycemia reduces the rate of wound healing and is associated with an increase in
infections and other comorbidities including ischemia, sepsis, and death.
During and after surgery the negative feedback mechanisms fail and high levels of both
ACTH and cortisol persist in the blood. In the presence of raised cortisol levels in a severe
stress response, the rate of protein breakdown exceeds that of protein synthesis,1 resulting in
the net catabolism of muscle proteins to provide substrates for gluconeogenesis. Further
substrates for gluconeogenesis are provided through the breakdown of fat. Triglycerides are
catabolized into fatty acids and glycerol, a gluconeogenic substrate.
Growth Hormone
Growth hormone-releasing hormone (GHRH) from the hypothalamus stimulates the anterior
pituitary to release GH. Propagation of the GH initiated signal occurs via the insulinlike
growth factors which regulate growth. Signaling via these effectors regulates catabolism by
increasing protein synthesis, reducing protein catabolism, and promoting lipolysis. Like
cortisol, GH increases blood glucose levels by stimulating glycogenolysis. The
hyperglycemic effect is also increased due to the anti-insulin effects of GH. However, the
increased secretion of GH after surgery is not thought to be important in the perioperative
period.2
Vasopressin
Vasopressin is a major antidiuretic hormone which released from the neurohypophysis.
After surgery, it acts on arginine vasopression (V2) receptors in the kidneys, leading to the
insertion of aquaporins into the renal wall. Aquaporins allow the movement of water from
the renal tubule back into the systemic circulation. Vasopression concentrations can be
raised after surgery by pain alone.
Burn Injury Induces a Genomic and Hormonal Response Analogous to
Trauma
Patients inflicted with burn injury undergo an elaborate hypermetabolic and
hyperinflammatory response that persists for several years postburn.3-5 This effect has been
proven amongst clinical parameters and at the cellular level. A large, prospective study in
977 severely burned children was conducted to document the hypermetabolic response.5
Interesting enough, the results depicted a sustained response, many throughout the 3-year
study period. Predicted resting energy expenditure remained increased in burn patients (P < .
05). Bone mineral content, lean body mass, and fat content decreased in burn patients when
compared with nonburned controls (P < .05). Urinary epinephrine, norepinephrine, and
cortisol increased several-fold in burn patients for 2, 18, and 36 months postburn
respectively (P < .05). Up to a 2,000-fold increase in cytokines IL-6, IL-8, G-CSF, and
MCP-1 was seen immediately postburn and remained significantly elevated for 3 years
compared with controls. Similarly, GM-CSF, INF-γ, TNF-α, IL-1β, IL-2, IL-5, IL-7, IL-10,
and IL-17 showed significant elevations in the serum of burned children (P < .05). Serum
proteins also showed drastic alterations in burn patients. Before increasing to levels in
nonburned controls, α2-macroglobulin remained decreased for 60 days postburn. Similarly,
retinol-binding protein, prealbumin, transferrin, and apolipoprotein A1 underwent marked
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3. decreases compared with controls and remained low for up to 90 days postburn. Conversely,
haptoglobin, α1-acidglycoprotein, and C-reactive protein significantly increased in response
to burn. Serum glucose levels in burn patients took 6 months to return back to normal while
insulin levels remained elevated throughout the study period (P < .05). The results of this
study depicted the extent of involvement of multiple organ systems for up to 3 years
postburn.
The extent and magnitude of severe burn injury was similarly depicted when catecholamine
levels were investigated in 413 burn patients and compared with those of 12 normal, healthy
controls.6 Catecholamine levels were found to be directly proportional to extent of burn
injury, but, in addition, an interesting trend in catecholamine levels were noted as well.
Although epinephrine levels vary over time, they remained elevated for up to 60 days
postburn (P < .05). On the other hand, norepinephrine remained significantly elevated for 2
years in the same burn patients when compared with nonburned controls (P < .05). These
supraphysiologic elevations in urinary catecholamines foster the notion of a hypermetabolic
response in burned patients.
These persistent perturbations of hormonal, acute phase, stress, and inflammatory proteins
contribute to the clinical presentation of the burn stress response. Due to high levels of
catecholamines, the patients are in a tachycardic, nervous, hypermetabolic state, which
increases the stress on the heart. Continuing elevations of cytokines indicates prolonged
immune-inflammatory dysfunction, which is confirmed by the long-term
immunosuppression reported in these patients. Recent investigations have linked the
elevations of particular cytokines IL-6 and MCP-1 to insulin resistance. Severely burned
patients remain insulin resistant for at least 3 years postinjury. The duration of these
responses has led to the interrogation of the transcriptomes of particular tissues—peripheral
blood leukocytes, skin, muscle, and fat. These studies have shown that signaling related to
insulin resistance and protein catabolism is altered in tissue from burned patients for at least
a year post injury7,8
Comparison of transcriptome changes in peripheral blood leukocytes from humans exposed
to experimental endotoxemia, blunt trauma, and severe burn injury showed that many of the
same genes are involved in the response to each insult, however, the duration and magnitude
of the response to burn injury is greatest. This confirmed that a burn injury is in fact an
extreme model of critical illness and trauma. Similarly, burn injury evokes hormonal
changes in line with those seen in patients postoperatively. Increased and sustained levels of
catecholamines, glucagon, and glucocorticoid have been reported in burn patients.9-11
Surgically induced stress most certainly invokes a large, controlled response akin to burn
injury.
Clinical Consequences of the Injury-Induced Metabolic Stress Response
Since Sneve’s early description of the catabolic response in burn patients,12 efforts to define
and modulate the metabolic responses to injury and stress have continued. The
characterization of a 2-phase hypermetabolic response to injury by Cuthbertson, divided the
response to injury into quantifiable events.13 The initial ebb phase, occurring within several
hours of the injury and lasting for 2-3 days, consists of reductions in cardiac output, oxygen
consumption (VO2), the basal metabolic rate, and glucose tolerance. The second flow phase,
beginning after the ebb phase and lasting for days to weeks depending on injury severity, is
characterized by increases in cardiac output, respiratory rate, VO2, hyperglycemica, skeletal
muscle catabolism, and a negative nitrogen balance. Although the ebb and flow phase model
is very simple, and may not adequately describe the metabolic responses induced following
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4. severe or multiple insults, the correlations established between injury and hypermetabolism
continue to guide advancements in surgical care.
Postburn muscle catabolism occurs in conjunction with an increase in metabolic rates.14
Soon after this link was made, Moore15 suggested that following a traumatic injury,
proteolysis and muscle catabolism could be reduced by feeding the patient continuously.
Reversal of preexisting protein deficiencies with long-term parenteral nutrition (PN) was
explored to achieve a reduction of the risk of postsurgical complications.16
The postburn hypermetabolic response is induced by increased serum catecholamine
concentrations and maintenance of ambient temperature or administration of
pharmacotherapeutic agents. Both burn and severe traumatic injuries induce a
hypercatabolic response that, along with a heightened inflammatory response, leads to organ
failure.3 The attenuation of the hypermetabolic response through nutrition and
pharmacologic interventions results in improved patient outcomes.
Traumatic injury induces inflammatory and hormonal responses that alter metabolic
processes, thereby changing nutrition requirements. The stress response to injury evolves
temporally as the patient moves through the ebb and flow phases and eventually into the
rehabilitative period. During each of the periods, nutrition requirements and nutrient intake,
absorption and substrate utilization are different.
Major surgery, critical illness and sepsis, and traumatic and burn injuries induce elevations
in the metabolic rate in an attempt to restore homeostasis. Although initially beneficial, the
exaggerated and prolonged inflammatory, metabolic, and catabolic responses induce clinical
complications, delay recovery, and increase mortality.
Significant basal metabolic rate (BMR) elevations occur in patients with burns over 30% or
more of total body surface area. Inflammatory, hormonal, and stress signaling mechanisms
drive the hypermetabolic response including elevations of circulating catecholamines,
glucocorticoids, and glucagon, with subsequent increases in gluconeogenesis,
glycogenolysis, and protein catabolism. Insulin resistance and peripheral lipolysis develop
as well.
Nutrition and Resuscitative Interventions
Surgical stress may impair metabolism, thereby negatively affecting the body’s ability to
grow, heal, maintain homeostasis, or adapt to the patient’s surroundings. This may also
affect the metabolic pathways through which absorption of nutrients and subsequent break
down leads to generation of energy. Nutrition supplementation is needed to counteract
dietary deficiencies, to augment the reduced function of the alimentary tract, and to support
healing and recovery. Improved understanding of the pathophysiological response to injury
has enabled the development of nutrition supplementation protocols that support recovery
while reducing the effects of muscle catabolism, the major contributor to postsurgery or
trauma adverse outcomes.
To heal following surgery and injury, increased availability of glucose, amino acids, and
other nutrients is needed. Muscle proteolysis facilitates the release of glutamine and alanine
following neuroendocrine and inflammatory signaling. These amino acids are required for
protein synthesis and also serve as the building blocks fueling hepatic gluconeogenesis.
Alanine and ammonia are derived from glutamine in the gut; these compounds are either
used or converted to urea. To limit protein catabolism for the release of these amino acids,
adequate nutrition supplementation is required.
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5. Severely burned patients require fluid resuscitation to prevent hypovolemic shock.
Resuscitation fluid is administered in accordance to the percentage of body surface area
burned and body weight. The best indication of volume status is urinary output. Minimum
target values are 0.5ml/kg/hr for adults and 1ml/kg/hr for children. Pulmonary edema and
cardiac dysfunction can result from over resuscitation and subsequent hypervolemia.
Following severe burn injury, early resuscitation is paramount. When immediate medical
care is not available, oral rehydration with basic electrolyte replacement should be provided.
Due to the increased caloric and protein requirements, early initiation of nutrition support is
also necessary. The severely burned patient may not be able to ingest sufficient nutrition
intake orally, especially with larger burns. Therefore, enteral nutrition delivery is initiated to
enable achievement of requisite nutrition targets. Feeding tubes are recommended in all
patients with burns > 20%. Enteral nutrition should be started and increased to goal as soon
as resuscitation is complete. Adequate carbohydrates are needed to prevent loss of lean body
mass,17 and sufficient fat to prevent a free fatty deficiency. 18 Formulas supplemented with
the anti-inflammatory and immunomodulating omega-3 fatty acids may contribute to better
outcomes after burn injury.19 In general, a high carbohydrate, high protein, low fat enteral
diet supplemented with glutamine and antioxidants has recently been suggested as the
optimal combination.20 Preservation of gut mucosa integrity relies on early resuscitation and
enteral feeding. Without these steps, splanchnic blood flow is diminished, leading to
mucosal atrophy, bacterial overproliferation and translocation, and subsequent development
of sepsis. Because nutrition supplementation alone is inadequate for the prevention of
muscle catabolism, pharmacologic, surgical, or environmental interventions may be needed
as well.
Postburn outcomes can be significantly improved by early excision and wound closure,
prevention of excessive heat loss by elevating ambient temperatures, and early
implementation of nutrition supplementation. Taking these outlined steps results in
attenuation of the postburn hormonal and inflammatory responses, reduced
hypermetabolism, decreased catabolism, and enhanced wound healing resulting in improved
morbidity and decreased mortality.
Interventions to Specifically Modulate the Hypermetabolic Response
Insulin
Insulin is secreted by the β-cells of the pancreas in response to food or raised blood glucose
or protein levels. The net effects of insulin are anabolic: hence it promotes glycogenesis and
the uptake of glucose into muscles and fat. However, during the surgical stress response the
amount of insulin secreted does not adequately meet the body’s increased needs and cells
become resistant to the reduced amount of insulin secreted. The degree of insulin secretion
suppression and resistance is proportional to the scale of the operation.21 This contributes to
a net catabolic state with an uncorrected hyperglycemia. Clinically, this is important as it has
been shown in some studies that patients in whom insulin sensitivity is reduced by 50% after
surgery suffer major complications and severe infections 6- and more than 10-fold,
respectively, compared with controls.22
Large operations and large burn wounds have similar effects on insulin homeostasis.
Therefore, important lessons can be learned from studies in burn patients. Recently, a study
investigating hyperglycemia and insulin resistance in 20 pediatric burn patients was
performed.8 Fasting serum glucose levels persistently remained elevated throughout the
duration of the study period (466 days) in burn patients compared with nonburned controls
(P < .05). In addition, increased fasting insulin levels were observed in burn patients with
peak levels of insulin at around 40-60 days postburn (P < .05). Thereafter, insulin trials have
been proposed in burn patients. One randomized clinical study found that intensive insulin
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6. therapy significantly decreased the incidence of infections and sepsis, improved organ
function, remedied insulin resistance, and reversed the posttraumatic catabolic state.23
Increased fractional synthesis rate of donor site wound protein has also been seen in burn
patients on intensive insulin treatment.24 Furthermore, muscle protein breakdown and
sustained lean body mass were found in burn patients on continuous insulin infusions.
Undoubtedly, euglycemia within a reasonable range decreases morbidity and healing time in
the postoperative patient.
Propranolol
The nonselective β-blocker propranolol has long been used in the trauma setting for the
control of tachycardia. Its use in pediatric burn patients has been studied extensively.25-30 In
a randomized controlled trial, 90 burn patients were given propranolol daily at a dose of 4
mg/kg/day for a duration of 1 year.31 When compared with control burn patients, a
significant reduction in predicted resting energy expenditure, and predicted heart rate were
found. In addition, decreased central fat and central mass as measured by dual image x-ray
analysis (DEXA) studies were found on patients receiving propranolol treatment. Another
study investigated the effects of propranolol given to 171 pediatric burn patients on cardiac
work.27 Decreased heart rate was sustained in patients receiving propranolol after the second
day and persisted throughout the treatment period (P < .001). Propranolol was initiated at a
dose of 1 mg/kg/d in these patients but increased to 4mg/kg/ day to maintain this response. It
is evident from these investigations that propranolol ameliorates the hyperdynamic and
hypercatabolic response seen in burn patients.
Oxandrolone
Oxandrolone is an analogue of testosterone. However, oxandrolone contains only 5% of its
virilizing androgenic effects.32 Oxandrolone has been shown to improve lean body mass in
conditions in which muscle wasting is evident. Burn victims are a subset of this population
as they exhibit peripheral lipolysis and marked extremity muscle wasting. A study analyzing
the effects of oxandrolone with and without exercise in pediatric burn patients was published
in 2007.33 A significant increase in lean body mass and body weight was found in patients
receiving oxandrolone and on exercise therapy compared with treated with placebo and
exercise (P < .05). Another study found that burned children treated with oxandrolone had a
significantly decreased length of intensive care unit stay (0.48 ± 0.02 days/%burn) when
compared with burned children receiving the standard burn care (0.56 ± 0.02 days/%burn).32
The same study showed preserved lean body mass and increased prealbumin and total
protein levels in patients on oxandrolone treatment compared with controls (P < .05). Five-
year outcomes to determine safety and efficacy profiles in burned children treated with
oxandrolone examined 70 children on a dose of oxandrolone 0.1 mg/kd, twice daily. The
results of this trial indicated long-term safety with minimum side effects. Improvements in
muscle strength, cardiac work, and height were observed. The additional outcome of
increased bone mineral content in these burn patients was postulated to occur via an insulin-
like growth factor-1 mediator.34
Exercise
Early ambulation and rehabilitation has remained on the forefront for patients undergoing all
types of surgery. Even patients undergoing cardiac procedures have been recommended
some form of controlled cardiac rehabilitation program. Recently, a 10-year study
investigated the incidence of cardiovascular events in 975 patients post–cardiovascular
surgery while exercising during cardiac rehabilitation.35 These patients underwent various
procedures including percutaneous transluminal coronary angioplasty (PTCA; 75%), post-
cardiac surgery (coronary bypass graft, 13.2%), valvular surgery and other cardiac surgery
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7. (4.2%), and others (7.6%). During the 13,934 patient hours of cardiac monitoring during
exercise, no deaths, acute myocardial infarctions, or cardiac arrests were observed. Exercise
rehabilitation programs can be safely implemented in patients postsurgery safely, provided
pre-exercise evaluation and close monitoring during exercise, at least in the trial period, are
mandated. The effects of exercise on lean body mass, resting energy expenditure, muscle
strength, range of motion, thermoregulation, and quality of life in pediatric burn patients has
extensively been studied.33,34,36-40 Many of these studies initiated an exercise program
approximately 6 months postburn. One such study found increased peak torque in patients in
the exercise arm (EX) vs those treated with the standard of care (SOC; EX, 54.31 ± 44.25%
vs SOC, 12.29 ± 16.49%; P = .02). An increase in lean body mass was also found in the EX
when compared with patients treated with SOC (EX, 8.75 ± 5.65% vs SOC, 2.06 ± 3.17%; P
= .004).37 Exercise in pediatric burn patients improves not only musculoskeletal
composition but also pulmonary function41 and quality of life.42
Intensive Insulin and Glycemic Control
Inadequately controlled blood sugar levels can result in increased morbidity and mortality in
all patients whether diabetic or not. Hyperglycemia is associated with increased
inflammation, infectious complications (including sepsis), ventilator dependence, length of
hospital stay, and mortality. Deleterious consequences on the nervous, immune, respiratory,
and renal systems arise from increased blood sugar levels.43 Low blood sugar is equally
dangerous. Hypoglycemia adversely affects the circulatory and both the autonomic and
central nervous systems. Clinical presentation of hypoglycemia includes fatigue, drowsiness,
dizziness, tachycardia, seizures, and coma. Tight glycemic control is necessary for rapid
wound healing and patient outcome. We and others have shown that in recent years, the
emergence of protocols for tight glycemic control with intensive insulin administration has
reduced complications and improved outcomes in critically ill and severely burned
patients.43 Aggressive glycemic control in line with these intensive insulin protocols reduces
insulin resistance and hyperglycemia. Although most physicians agree that maintenance of
normoglycemia is beneficial, controversy persists regarding establishment of the target
blood glucose levels and protocolization of indications for intensive insulin therapy
initiation.
Summary
The stress response to surgery, critical illness, trauma, and burns encompasses derangements
of metabolic and physiological processes that induce perturbations in the inflammatory,
acute phase, hormonal, and genomic responses. Hypermetabolism and hypercatabolism
result, leading to muscle wasting, impaired immune function and wound healing, organ
failure, and death. Optimal nutrition support is required to insure positive patient outcomes
following surgery, trauma, critical illness, and burn injuries. Amelioration of the systemic
inflammatory, hormonal, and metabolic responses with nutrition supplementation,
pharmacologic interventions, and exercise reduces the impact of the hypermetabolic and
stress responses.
Discussion
Robert Martindale
David, I am very impressed with the work you are doing. Do you start all of these things on
every patient and then sort out who is going to be the best fit? I know you just study
adolescents and children.
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8. David Herndon
I have spent most of my life in performing randomized controlled studies. I do one study at a
time. I would recommend to clinicians that they consider the multicentered long-term
studies that we are doing and participate in them with enthusiasm and zeal so that we can
really change standard of care. If I had my choice, I would give Oxandrolone and
propranolol to a 60% total body surface burn, initiate exercise, and feed at 1500 kilocalories
per meter squared burned. I would do that starting at admission and proceeding for 1 year
post-injury. The diet would be high protein, high sugar, and low fat. I would also give
selenium, zinc, copper and a variety of other minerals that have been proven necessary
under these circumstances. I do not believe that immune enhancing diets have necessarily
been proven yet in these patients.
Rosemary Kozar
I am going to start with a controversial question. You talked about the evils of TPN. What
about the patient that has an ileus that cannot be fed enterally?
David Herndon
I do give supplemental TPN when patients develop an ileus and cannot tolerate enteral
feeding. Their livers do get worse and they are at risk of infection. I change lines every 4–5
days based on an article that I wrote in 1975 and I am true to my principals. Use TPN but
only when really necessary.
Rosemary Kozar
My understanding is that long term, many burn patients become obese. I seem to see this
same phenomenon in my sick trauma patients. What happens with the genetic changes and
alterations and all the things that you talked about with time? It almost seems like they are
reversed. Patients now have low muscle mass and a high percentage of body fat.
David Herndon
We have looked extensively at obesity in burn patients; fat people get fatter after burns, and
thin people get thinner. Unfortunately, it is not easily summarized as everybody gets fat. I
think that exercise and proper nutrition and seeing your patient every couple of months and
addressing such issues on an individualized basis is what is required.
Marco Braga
What percentage of your patients need to be supplemented with parenteral nutrition in order
to cover the nitrogen intake, especially in the early phase after thermal injury? The second
question is what is your opinion about the potential of glutamine in terms of adding it into
enteral nutrition to protect the barrier function?
David Herndon
In answer to the first question, the people that I treat who require parenteral nutrition are
those people who become septic and develop enteral feeding intolerance such that they do
not tolerate oral calories. I did a randomized study in 1980 that showed if we tried to
supplement with parenteral nutrition, we increased morbidity and mortality. It is only in
those patients with an ileus that prevents me from feeding the gut that I use TPN. I have
worked with Doug Wilmore for a long time and I think that glutamine probably is a
conditionally necessary additive in this patient population. I personally have not studied
glutamine but I am looking forward to the multicentered Canadian study addressing that
issue.
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9. Paul Wischmeyer
Our lab is starting to show propranolol can have the very same effects in sepsis models and
perhaps in trauma models that you report in your burn patients. We are thinking of moving
forward to a multicenter trial some day with that. Do you think the effects are only in burn
patients? In our burn unit at least, we start at day 7 post-burn with anabolic agents when the
patients are out of the acute phase. When do you start and why? In response to your answer
on the glutamine question, we have about 57 patients enrolled in Re-Energize study now, so
it will be a little while until we have the answer.
David Herndon
I think that the catecholamine overdrive is common to all types of surgical stress and occurs
in an additive fashion in septic individuals. I think trials are needed for beta blocking agents.
Tachycardia is pathologic and beta-blockers are simple drugs to use. Obviously, you lose
tachycardia as an indicator of hypovolemia or stress. I think that tachycardia is an incredibly
important marker of the prolonged stress response and that it is an adaptive response that has
gone awry. We can and should modulate it appropriately.
Paul Wischmeyer
Should we be waiting until day 7?
David Herndon
Cuthbertson described an ebb and flow response to major catabolic stress. In burn patients,
we do excision and grafting within 24 hours of the time of injury then we start propranolol.
For surgical patients, I think you first have to drain the abscess and get out of the ebb phase
before your start an agent that is going to depress the heart rate.
Beth Taylor
I wanted to bring back your comments to surgery patients and the prolonged stress response.
I think that after patients leave the hospital they continue to have complications from this
prolonged stress response. What type of complications would you see months down the
road? Would they be related to the loss of lean body mass? Should we define “success” not
based on discharge alive from the hospital but rather on one-year mortality? For CMS, if a
patient is readmitted too soon for congestive heart failure, you are not reimbursed. Can we
convince our surgeons that if prescribe a postoperative plan to include nutrition and
exercise, patients we have less readmissions? Maybe in the end we will get support for those
programs from the government?
David Herndon
That is a wonderful discussion. I think you have really identified the area we need to study.
There are postop pressure sores, aspirations, and pneumonias that lead to admission to SNIF
units. I think the time back to work or the time out of work should be an indicator of our
success rate and not just whether we get them out of the hospital alive. I also think we can
make tremendous improvements in world health by concentrating on rehabilitation and
return to work and looking at long-term quality of life outcomes as opposed to short-term
surgical morbidity and mortality outcomes.
David Flum
I want to build on Beth’s question. Tell us about the signs of the hypermetabolic state after
surgery? What can we learn from burns about the length of time after one of these events
when you are hypermetabolic and when you could benefit from nutrition intervention? If
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10. you look at patients who have had colon surgery, about 3 weeks after surgery, they are
taking in only about 40% of their normal caloric load. If you look at bariatric patients, it is
30%. We view this as a success and clearly, these patients are still hypermetabolic. How
long does that last and is their a role for nutrition supplementation either by total load or
specific type that we should be trying in our patients?
David Herndon
I feel that specific long-term outcome studies that are geared toward these end points need to
be done. It is my prejudice and my feeling that this is a huge worldwide health problem that
has been ignored. We should do studies looking at the duration of the catabolic response and
the effect of strength on return to work and quality of life. We should treat those catabolic
phenomena not just with nutrition but with a balanced program that would improve health. I
do think a balanced program compared with standard of care would absolutely shock people
if a proper study were to be done.
Ken Kudsk
In obese patients, probably the best way to break insulin resistance is exercise. Do you break
insulin resistance in your burn patients through exercise? Have you measured that?
David Herndon
We are in the process of writing a manuscript in that regard and the answer is yes. Our
patients are insulin resistant for up to a year or 2 after injury and exercise profoundly
decreases the duration.
Ken Kudsk
I was quite intrigued about your experience using an insulin clamp. Are you using it during
the immediate phase or during the flow phase?
David Herndon
We use a continuous insulin infusion for about 40 days throughout the patient’s hospital
course.
Ken Kudsk
Is that when you see protein balance improved?
David Herndon
Yes, it takes about 30-40 days.
Ken Kudsk
Do you also find that at this point you reduce your glucose intake overall because your
energy expenditure is decreased?
David Herndon
We did see a decrease in resting energy expenditure and a decrease in caloric intake in those
patients who were given insulin. It was marginal but it was statically significant.
Ken Kudsk
Do you think everybody should have his or her metabolic response blunted? The reason that
I ask is, it is not unusual that we will get a young trauma patient who for the first 4–5 days is
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11. tachycardic but otherwise doing well. My concern is that you can miss other diagnoses if
you mask the tachycardic response.
David Herndon
I think that is the critical question that still gives us equipoise to do randomized prospective
trials with beta-blockers. I do not know that in the adult population there has been enough
studies to look at the risk of missed injuries or complications. There are physiologic benefits
to beta-blockade. The question is which patients will have dangerous sequelae if you allow
the catabolic response to persist.
Ken Kudsk
I think with the burn patients, you can predict that they are going to be catabolic for a long
period of time, but with trauma patients, they could go into either group. Either they could
go into the group that recovers very quickly or they could go into the group that stays in
your ICU for a prolonged period of time.
David Herndon
I think that patients who get an additional septic insult will go on to have a prolonged
course. I think the elderly do not bounce back from big operations and critical care
interventions. I think that any therapy needs to be used selectively, even nutrition.
Robert Martindale
I just have a question about the enteral intolerance that we referred to earlier in the
conversation. I am wondering if we can identify high-risk patients who are likely to develop
enteral intolerance. Based what you know about the metabolic response to injury, is there a
role for prophylactic use of motility agents? We tend to use them reactionary when the
problem develops but should we be recommending their use in high risk patients at the same
time we are starting enteral nutrition?
David Herndon
I certainly think there is a place for motility agents and I do not have enough knowledge to
know exactly what that would be. The vast majority of patients with burns can begin on
enteral feeding within 2 hours of time of injury. If you start feeding right away, patients
generally do not get an ileus. I also think there are many people that can be fed through an
ileus.
John Drover
Is there much known about individual genetics determining the metabolic response to
injury? Is there a way of looking at your data to say that there are groups of patients that
respond differently?
David Herndon
I think we can use the genetic response within the first 24 hours of a massive burn to predict
that one individual is going to do worse than another individual. But, what do we do with
that particular kind of information? Do we expend more resources on a person who has a
more distinct genetic response with down regulation of immune system and up regulation of
inflammatory systems and treat them with care that is more assiduous? I think that is
probably what I would do right now but obviously much more data needs to be done in that
regard.
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12. Bob Martindale
I think your point of feeding within a couple of hours of injury really sets home to this
patient population. I know that you published in the ’80s with McDonald that if we feed
early we prevent the progression of ileus and prevent bowel wall edema. It has now taken us
30 years in the ICU setting to learn that again. The general principles learned from surgical
and trauma population have not really caught on yet.
Steve McClave
This persistent catabolic response to the injury that goes out 2 years resembles the persistent
inflammation, immunosuppression, and catabolism (PICS) that Fred Moore has described.
Should we be monitoring for that so that we know if it is still going or if it has been turned
off? How do we best monitor that syndrome?
David Herndon
I have used stable isotope studies. I also think that dual interjectory absorptiometry is useful
and when you get away from the fluid balance problems of the first acute days, it is a good
way of looking at lean body mass vs fat mass, bone mineral density, and bone mineral
content over time. I would encourage each of you to think of using a DEXA scan to follow
your patients over time.
Paul Wischmeyer
Should we be following urinary or plasma cortisol? I have just completed analyzing some
recent data where we could show that there is a longitudinal increase in risk of mortality
from increases in cortisol over time. The patient whose cortisol continued to be persistently
elevated, died.
David Herndon
I think that clearly 24-hour urinary catechols can be measured. I would not follow serum, it
is just not too variable.
Keith Miller
Who should follow patients over time? The multidisciplinary team has been accepted in the
care of the cancer patient, but many times at our burn center, we as the burn surgeons do not
typically follow these patients over time. They go back to their primary care physician.
David Herndon
Well, I really think that is one of the messages that I would like to leave to the next
generation. We should follow our patients until they are completely recovered since we
know best when that occurs.
Acknowledgments
Nigel Mabvuure wishes to acknowledge Restore-Burn and Wound Research for funding his research elective.
Supported was received by grants from the National Institute for Disabilities and Rehabilitation Research
(H133A070026 and H133A70019), the National Institutes of Health (P50-GM60338, R01-GM56687, and T32-
GM8256), and Shriners Hospitals for Children (71001, 71008, 84080, 79135, 8660, 9145, and 8760). Dr Finnerty is
an ITS Career Development Scholar supported, in part, by NIH KL2RR029875 and NIH UL1RR029876. This
study is registered at clinicaltrials.gov: NCT00675714.
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13. References
1. Gore DC, Jahoor F, Wolfe RR, Herndon DN. Acute response of human muscle protein to catabolic
hormones. Ann Surg. 1993; 218(5):679–684. [PubMed: 8239784]
2. Burton D, Nicholson G, Hall G. Endocrine and metabolic response to surgery. Continuing Ed
Anaesthesia Crit Care Pain. 2004; 4(5):144–147.
3. Jeschke MG, Chinkes DL, Finnerty CC, et al. Pathophysiologic response to severe burn injury. Ann
Surg. 2008; 248(3):387–401. [PubMed: 18791359]
4. Wilmore DW, Long JM, Mason AD Jr, Skreen RW, Pruitt BA Jr. Catecholamines: mediator of the
hypermetabolic response to thermal injury. Ann Surg. 1974; 180(4):653–669. [PubMed: 4412350]
5. Jeschke MG, Gauglitz GG, Kulp GA, et al. Long-term persistence of the pathophysiologic response
to severe burn injury. PLoS One. 2011; 6(7):e21245. [PubMed: 21789167]
6. Kulp GA, Herndon DN, Lee JO, Suman OE, Jeschke MG. Extent and magnitude of catecholamine
surge in pediatric burned patients. Shock. 2010; 33(4):369–374. [PubMed: 20407405]
7. Song J, Finnerty CC, Herndon DN, et al. Thermal Injury activates the eEF2K-dependent eEF2
pathway in pediatric patients. JPEN J Parenter Enteral Nutr. 2012; 36(5):596–602. [PubMed:
22269896]
8. Jeschke MG, Finnerty CC, Herndon DN, et al. Severe injury is associated with insulin resistance,
endoplasmic reticulum stress response, and unfolded protein response. Ann Surg. 2012; 255(2):
370–378. [PubMed: 22241293]
9. Hart DW, Wolf SE, Mlcak R, et al. Persistence of muscle catabolism after severe burn. Surgery.
2000; 128(2):312–319. [PubMed: 10923010]
10. Mlcak RP, Jeschke MG, Barrow RE, Herndon DN. The influence of age and gender on resting
energy expenditure in severely burned children. Ann Surg. 2006; 244(1):121–130. [PubMed:
16794397]
11. Norbury, WB. Total Burn Care. 3rd. Saunders Elsevier; Philadelphia, PA: 2007. HD
12. Sneve H. The treatment of burns and skin grafting. JAMA. 1905; 45:1–8.
13. Cuthbertson DP. Post-shock metabolic response (Arris-Gale Lecture to the Royal College of
Surgeons of England). Lancet. 1942; 239:433–437.
14. Cope O, Nardi GL, Quijano M, Rovit RL, Stanbury JB, Wight A. Metabolic rate and thyroid
function following acute thermal trauma in man. Ann Surg. 1953; 137(2):165–174. [PubMed:
13017515]
15. Moore, FD. Metabolic Care of the Surgical Patient. Saunders; Philadelphia, PA: 1959.
16. Dudrick SJ. Early developments and clinical applications of total parenteral nutrition. JPEN J
Parenter Enteral Nutr. 2003; 27(4):291–299. [PubMed: 12903895]
17. Wolfe RR, Allsop JR, Burke JF. Glucose metabolism in man: responses to intravenous glucose
infusion. Metabolism. 1979; 28:210–220. [PubMed: 763155]
18. Rodriguez NA, Jeschke MG, Williams FN, Kamolz LP, Herndon DN. Nutrition in burns Galveston
contributions. JPEN J Parenter Enteral Nutr. 2011; 35:704–714. [PubMed: 21975669]
19. Norbury, WB. Modulation of the hypermetabolic response after burn injury. In: Herndon, DN.,
editor. Total Burn Care. Saunders Elsevier; Philadelphia, PA: 2007. p. 420-433.
20. Hall KL, Shahrokhi S, Jeschke MG. Enteral nutrition support in burn care: a review of current
recommendations as instituted in the Ross Tilley Burn Centre. Nutrients. 2012; 4:1554–1565.
[PubMed: 23201833]
21. Thorell A, Nygren J, Ljungqvist O. Insulin resistance: a marker of surgical stress. Curr Opin Clin
Nutr Metab Care. 1999; 2(1):69–78. [PubMed: 10453333]
22. Sato H, Carvalho G, Sato T, Lattermann R, Matsukawa T, Schricker T. The association of
preoperative glycemic control, intraoperative insulin sensitivity, and outcomes after cardiac
surgery. J Clin Endocrinol Metab. 2010; 95(9):4338–4344. [PubMed: 20631016]
23. Jeschke MG, Kulp GA, Kraft R, et al. Intensive insulin therapy in severely burned pediatric
patients: a prospective randomized trial. Am J Respir Crit Care Med. 2010; 182(3):351–359.
[PubMed: 20395554]
Finnerty et al. Page 13
JPEN J Parenter Enteral Nutr. Author manuscript; available in PMC 2014 September 01.
NIH-PA
Author
Manuscript
NIH-PA
Author
Manuscript
NIH-PA
Author
Manuscript
14. 24. Tuvdendorj D, Zhang XJ, Chinkes DL, et al. Intensive insulin treatment increases donor site
wound protein synthesis in burn patients. Surgery. 2011; 149(4):512–518. [PubMed: 21236451]
25. Olah G, Finnerty CC, Sbrana E, et al. Increased poly(ADP-ribosyl)ation in skeletal muscle tissue
of pediatric patients with severe burn injury: prevention by propranolol treatment. Shock. 2011;
36(1):18–23. [PubMed: 21368715]
26. Kobayashi M, Jeschke MG, Asai A, et al. Propranolol as a modulator of M2b monocytes in
severely burned patients. J Leukoc Biol. 2011; 89(5):797–803. [PubMed: 21330352]
27. Williams FN, Herndon DN, Kulp GA, Jeschke MG. Propranolol decreases cardiac work in a dose-
dependent manner in severely burned children. Surgery. 2011; 149(2):231–239. [PubMed:
20598332]
28. Jeschke MG, Norbury WB, Finnerty CC, Branski LK, Herndon DN. Propranolol does not increase
inflammation, sepsis, or infectious episodes in severely burned children. J Trauma. 2007; 62(3):
676–681. [PubMed: 17414346]
29. Baron PW, Barrow RE, Pierre EJ, Herndon DN. Prolonged use of propranolol safely decreases
cardiac work in burned children. J Burn Care Rehabil. 1997; 18(3):223–227. [PubMed: 9169945]
30. Herndon DN, Barrow RE, Rutan TC, Minifee P, Jahoor F, Wolfe RR. Effect of propranolol
administration on hemodynamic and metabolic responses of burned pediatric patients. Ann Surg.
1988; 208(4):484–492. [PubMed: 3052328]
31. Herndon DN, Rodriguez NA, Diaz EC, et al. Long-term propranolol use in severely burned
pediatric patients: a randomized controlled study. Ann Surg. 2012; 256(3):402–411. [PubMed:
22895351]
32. Jeschke MG, Finnerty CC, Suman OE, Kulp G, Mlcak RP, Herndon DN. The effect of
oxandrolone on the endocrinologic, inflammatory, and hypermetabolic responses during the acute
phase postburn. Ann Surg. 2007; 246(3):351–360. [PubMed: 17717439]
33. Przkora R, Herndon DN, Suman OE. The effects of oxandrolone and exercise on muscle mass and
function in children with severe burns. Pediatrics. 2007; 119(1):e109–e116. [PubMed: 17130281]
34. Porro LJ, Herndon DN, Rodriguez NA, et al. Five-year outcomes after oxandrolone administration
in severely burned children: a randomized clinical trial of safety and efficacy. J Am Coll Surg.
2012; 214(4):489–502. [PubMed: 22463890]
35. Kim C, Moon CJ, Lim MH. Safety of monitoring exercise for early hospital-based cardiac
rehabilitation. Ann Rehabil Med. 2012; 36(2):262–267. [PubMed: 22639752]
36. McEntire SJ, Chinkes DL, Herndon DN, Suman OE. Temperature responses in severely burned
children during exercise in a hot environment. J Burn Care Res. 2010; 31(4):624–630. [PubMed:
20616652]
37. Al-Mousawi AM, Williams FN, Mlcak RP, Jeschke MG, Herndon DN, Suman OE. Effects of
exercise training on resting energy expenditure and lean mass during pediatric burn rehabilitation.
J Burn Care Res. 2010; 31(3):400–408. [PubMed: 20354445]
38. Neugebauer CT, Serghiou M, Herndon DN, Suman OE. Effects of a 12-week rehabilitation
program with music & exercise groups on range of motion in young children with severe burns. J
Burn Care Res. 2008; 29(6):939–948. [PubMed: 18849852]
39. McEntire SJ, Herndon DN, Sanford AP, Suman OE. Thermoregulation during exercise in severely
burned children. Pediatr Rehabil. 2006; 9(1):57–64. [PubMed: 16352508]
40. Celis MM, Suman OE, Huang TT, Yen P, Herndon DN. Effect of a supervised exercise and
physiotherapy program on surgical interventions in children with thermal injury. J Burn Care
Rehabil. 2003; 24(1):57–61. [PubMed: 12543995]
41. Suman OE, Mlcak RP, Herndon DN. Effect of exercise training on pulmonary function in children
with thermal injury. J Burn Care Rehabil. 2002; 23(4):288–293. [PubMed: 12142585]
42. Rosenberg M, Celis MM, Meyer W III, et al. Effects of a hospital based wellness and exercise
program on quality of life of children with severe burns. Burns. 2013; 39(4):599–609. [PubMed:
22985974]
43. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill
patients. N Engl J Med. 2001; 345:1359–1367. [PubMed: 11794168]
Finnerty et al. Page 14
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