METABOLIC RESPONSE TO TRAUMA.pptx
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The document discusses the metabolic response to trauma, which refers to adaptive changes that maintain homeostasis after injury. It outlines the triggers, components, and sequelae of the metabolic response. The components include sympathetic nervous system activation, endocrine responses like increased cortisol and growth hormone, and cytokine responses from interleukins and tumor necrosis factor. Prolonged or accentuated metabolic responses can harm surgical patients by increasing energy needs, reducing immunity, and impairing wound healing. The response can be attenuated by measures like fluid replacement, analgesia, nutritional support, and prompt infection treatment.
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metabolc response by martha, alfred and pascal.pptx
Following injury or trauma, the body undergoes a metabolic response involving two phases - an initial "ebb phase" lasting 24-48 hours where metabolic rate decreases to conserve energy, followed by a "flow phase" where metabolism increases to aid recovery. During the flow phase, hormones and cytokines induce catabolism, breaking down skeletal muscle and liver proteins which leads to loss of fat and muscle mass over 3-10 days. This hypermetabolic state involves insulin resistance and alters body composition through the mobilization of energy stores for repair.
Metabolic response to trauma
The document discusses the metabolic response to trauma and injury. It begins by outlining the objectives of understanding the metabolic response and how it can be minimized through elective or emergency surgical procedures. It then describes the physiological changes that occur such as increases in temperature, heart rate, and metabolic rate. These changes are mediated by the neuroendocrine stress response and proinflammatory cytokines. The document outlines the ebb and flow phases of metabolic response, describing the catabolic effects in the ebb phase and hypermetabolic effects in the flow phase. Key aspects of the metabolic response include hypermetabolism, insulin resistance, protein catabolism, and changes in body composition. Methods to minimize the metabolic response include fluid resuscitation, oxygen
Metabolic response to injury
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.
Relationship between trauma and diseases
The document discusses the relationship between trauma and diseases. It covers several key points:
1) Trauma can indirectly impact diseases by activating or accelerating latent conditions, especially if accompanied by infection, reduced exercise, weight gain or overeating.
2) Major injuries are associated with an inflammatory response that can lead to multiple organ failure and death if not properly treated.
3) The metabolic response to trauma involves neuroendocrine and immune system changes that mobilize energy stores and substrates. This response aims to aid recovery but can damage distant organs if severe.
4) Specific diseases that can be impacted by trauma include post-traumatic stress disorder, diabetes, rhabdomyolysis (muscle breakdown),
Metabolic stress response
The document outlines the metabolic response to trauma, including its initiators, mediators, phases, and components. The metabolic response is the body's attempt to maintain homeostasis following injury. It is initiated by factors like pain, infection, and hypoxia. It is mediated by the neuroendocrine and immune systems through the release of hormones and cytokines. The response occurs in ebb and flow phases and results in hypermetabolism, protein catabolism, insulin resistance, and other physiological changes aimed at repairing damage and restoring normal function.
Metabolic response to injury
The document summarizes the metabolic response to trauma and injury. It describes the ebb and flow phases identified by Cuthbertson in the 1930s. The ebb phase lasts less than 24 hours and aims to conserve circulating volume and energy stores. The flow phase lasts 3-10 days and involves mobilizing stores for repair through hypermetabolism, increased protein breakdown, and insulin resistance. Nutritional, hormonal, and biologic interventions can help attenuate this catabolic response to injury and promote anabolism.
Metabolic response to trauma
The document discusses the metabolic response that occurs following injury or trauma to the body. It describes how there is an initial ebb phase characterized by shock, followed by a longer flow phase with increased metabolism and hormone levels. The metabolic response aims to restore homeostasis but can also cause organ damage. Factors like infection, nutrition, and inflammation can modify this response. Managing the response through fluid resuscitation, oxygen delivery, and minimizing stressors can improve outcomes.
Metabolic response to injury
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.
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metabolc response by martha, alfred and pascal.pptx
Following injury or trauma, the body undergoes a metabolic response involving two phases - an initial "ebb phase" lasting 24-48 hours where metabolic rate decreases to conserve energy, followed by a "flow phase" where metabolism increases to aid recovery. During the flow phase, hormones and cytokines induce catabolism, breaking down skeletal muscle and liver proteins which leads to loss of fat and muscle mass over 3-10 days. This hypermetabolic state involves insulin resistance and alters body composition through the mobilization of energy stores for repair.
Metabolic response to trauma
The document discusses the metabolic response to trauma and injury. It begins by outlining the objectives of understanding the metabolic response and how it can be minimized through elective or emergency surgical procedures. It then describes the physiological changes that occur such as increases in temperature, heart rate, and metabolic rate. These changes are mediated by the neuroendocrine stress response and proinflammatory cytokines. The document outlines the ebb and flow phases of metabolic response, describing the catabolic effects in the ebb phase and hypermetabolic effects in the flow phase. Key aspects of the metabolic response include hypermetabolism, insulin resistance, protein catabolism, and changes in body composition. Methods to minimize the metabolic response include fluid resuscitation, oxygen
Metabolic response to injury
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.
Relationship between trauma and diseases
The document discusses the relationship between trauma and diseases. It covers several key points:
1) Trauma can indirectly impact diseases by activating or accelerating latent conditions, especially if accompanied by infection, reduced exercise, weight gain or overeating.
2) Major injuries are associated with an inflammatory response that can lead to multiple organ failure and death if not properly treated.
3) The metabolic response to trauma involves neuroendocrine and immune system changes that mobilize energy stores and substrates. This response aims to aid recovery but can damage distant organs if severe.
4) Specific diseases that can be impacted by trauma include post-traumatic stress disorder, diabetes, rhabdomyolysis (muscle breakdown),
Metabolic stress response
The document outlines the metabolic response to trauma, including its initiators, mediators, phases, and components. The metabolic response is the body's attempt to maintain homeostasis following injury. It is initiated by factors like pain, infection, and hypoxia. It is mediated by the neuroendocrine and immune systems through the release of hormones and cytokines. The response occurs in ebb and flow phases and results in hypermetabolism, protein catabolism, insulin resistance, and other physiological changes aimed at repairing damage and restoring normal function.
Metabolic response to injury
The document summarizes the metabolic response to trauma and injury. It describes the ebb and flow phases identified by Cuthbertson in the 1930s. The ebb phase lasts less than 24 hours and aims to conserve circulating volume and energy stores. The flow phase lasts 3-10 days and involves mobilizing stores for repair through hypermetabolism, increased protein breakdown, and insulin resistance. Nutritional, hormonal, and biologic interventions can help attenuate this catabolic response to injury and promote anabolism.
Metabolic response to trauma
The document discusses the metabolic response that occurs following injury or trauma to the body. It describes how there is an initial ebb phase characterized by shock, followed by a longer flow phase with increased metabolism and hormone levels. The metabolic response aims to restore homeostasis but can also cause organ damage. Factors like infection, nutrition, and inflammation can modify this response. Managing the response through fluid resuscitation, oxygen delivery, and minimizing stressors can improve outcomes.
Metabolic response to injury
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.
Metabolicresponsetoinjury drneerajjain
This document discusses the metabolic response to trauma and injury. It describes how injury disrupts homeostasis and causes physiological, metabolic and clinical changes as the body attempts to restore homeostasis. The stress response is mediated by hormones like cortisol and cytokines which cause hypermetabolism, increased protein breakdown, and insulin resistance. These changes are initially beneficial for survival but can become harmful if prolonged. Modern trauma and critical care aims to minimize this response through techniques like early feeding and pain control to promote recovery.
Metabolic Response To Injury and surgical stress
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.
Metabolic Response to Trauma.pptx
The document discusses the metabolic response to trauma in three phases: ebb, flow, and anabolic. The ebb phase is characterized by decreased metabolism and energy expenditure. The flow phase sees increased metabolism and catabolism as the body mobilizes resources. The anabolic phase involves tissue repair and recovery of lost mass. Key hormonal and inflammatory responses that regulate metabolism are also described, including increased catecholamines, cortisol, cytokines and the stress response they induce.
Metabolic Response to Injury.pptx
This document discusses the metabolic response to injury, including the classical concepts of homeostasis and the physiological changes that occur during injury and recovery. It describes the ebb and flow phases of the metabolic response, characterized initially by catabolism to provide substrates for survival, followed by a catabolic phase and later anabolic phase for repair. Key aspects of the response include hypermetabolism, insulin resistance, protein catabolism and redistribution, and the acute phase protein response in the liver. Avoiding unnecessary factors like continued bleeding, hypothermia, underperfusion and immobilization can help minimize the metabolic stress response to injury.
08.Metaboliasfasdfc Response to Trauma.ppt
The metabolic response to injury leads to increased energy expenditure and protein catabolism. This response is mediated by the acute inflammatory response, the endothelium, nerve stimulation, and hormones from the endocrine system. The consequences include limiting injury, initiating repair, and mobilizing substrates. Compared to starvation, trauma does not allow the body to conserve fuels and proteins. The severity of injury determines the degree of metabolic response. Nutrition can modify this response by providing adequate calories, protein, vitamins, and minerals tailored to the patient's needs and stress level.
Homeostasis, the internal milieu of the human body
This document discusses homeostasis and the body's response to injury. It covers several key points:
1. Homeostasis refers to maintaining a constant internal environment. The body has complex coordinated physiological processes to maintain homeostasis.
2. Following major trauma or sepsis, the body exhibits a systemic inflammatory response and loses homeostasis. Medical intervention is needed to return the patient to homeostasis.
3. The response to injury is graded - more severe injuries cause a greater physiological and immunological response. This includes fever, increased metabolism and catabolism.
4. Several factors mediate the metabolic response, including neuroendocrine hormones and cytokines. The response aims to provide substrates for survival but can become harmful if prolonged.
Metabolic Response To Injury
The document summarizes the metabolic response to injury, including its graded nature, components, mediators, phases, and factors that exacerbate or can be avoided. The response involves physiological, metabolic, clinical, and laboratory changes mediated by neuroendocrine and immune system factors. It progresses through ebb and flow phases involving catabolic elements like hypermetabolism and muscle/liver protein alterations. Avoidable exacerbating factors include continuing hemorrhage, hypothermia, tissue edema, underperfusion, starvation, and immobility. The response can be modulated through techniques like minimal access surgery, early mobilization, epidural analgesia, and avoiding prolonged fasting and excessive fluids.
metabolic response to trauma.pptx
1. The document provides tips for using a PowerPoint presentation on metabolic response to trauma. It suggests freely editing the presentation, asking students questions about blank slides, and repeating the process for active learning.
2. The metabolic response to trauma involves physiological neuroendocrine reflexes that restore homeostasis. Trauma stimulates sensors which activate the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. This increases stress hormones like cortisol and catecholamines.
3. The metabolic effects include hypermetabolism, hyperglycemia, increased protein breakdown and gluconeogenesis from protein. This supports the body during injury but causes negative nitrogen balance.
overview on "Metabolic response to injury"
The document summarizes the body's metabolic response to injury and trauma. It discusses how the response is mediated by both the neuroendocrine and immune systems through hormones and cytokines. The response aims to mobilize energy stores and nutrients to support healing, but can become maladaptive. The response proceeds in ebb and flow phases, with an initial catabolic phase followed by an anabolic recovery phase. Factors like continuing bleeding, hypothermia, edema, underperfusion, starvation, and immobility can compound the response and inhibit recovery. Maintaining homeostasis through careful fluid management, analgesia, feeding, and early mobilization can help optimize the response and enhance recovery.
Metabolic Response to Injury
The document summarizes the metabolic response to injury, which occurs in two phases - the ebb phase and the flow phase. The ebb phase occurs in the first 24-48 hours and is characterized by decreased metabolic rate and circulation. The flow phase involves increased metabolism and mobilization of energy stores for recovery. Key aspects of the flow phase include hypermetabolism, muscle wasting through increased protein degradation, acute phase protein response in the liver, and insulin resistance in tissues. The response aims to prioritize resources towards vital organs and wound healing.
Metabolic response to trauma.pptx
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.
Metabolic response to injury
The document discusses the metabolic response to injury, including key concepts like homeostasis and the graded nature of injury response. It describes the "ebb and flow" model where the initial ebb phase conserves energy and the hypermetabolic flow phase mobilizes resources for repair. Major mediators that drive the catabolic response are increased metabolism, altered protein metabolism in muscles and liver, and insulin resistance. Factors like ongoing hemorrhage, hypothermia, edema, underperfusion, starvation, and immobility can compound this response. The goal is to control these avoidable factors to benefit patient recovery.
Metabolic response to trauma
The document discusses the metabolic response to trauma and injury. It describes how the response is graded based on the severity of the stressor, from elective surgery to severe sepsis. The response involves two phases - an ebb phase of catabolism followed by a flow phase of hypermetabolism and mobilization of energy stores for recovery. Key elements of the flow phase include hypermetabolism, alterations in muscle and liver protein, and insulin resistance. The response has physiological, metabolic, clinical and laboratory components and leads to losses of fat and muscle mass if not addressed. Early enteral nutrition and minimizing the neuroendocrine stress response can help maintain weight and nitrogen balance.
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The document discusses the body's metabolic response to trauma on multiple levels. It begins by defining trauma and distinguishing between physical and psychological trauma. It then outlines the neuroendocrine response to trauma, including increased levels of catecholamines, cortisol, aldosterone, and other hormones. This hormonal response leads to catabolic effects on the body as it breaks down tissues to provide energy. The document also discusses mediators of the metabolic response like cytokines and their effects. Finally, it notes implications for therapy focus on supporting the body through the metabolic response phases until recovery.
metabolic response to the disease .pptx
1. Injury causes a metabolic stress response with multiple stages. Initially pro-inflammatory cytokines are released locally, then systemically if the injury is severe enough to cause SIRS.
2. This leads to a hypermetabolic "flow" phase involving increased heart rate, temperature and catabolism. Muscle and liver protein are broken down, increasing urinary nitrogen and acute phase proteins.
3. The response aims to mobilize energy stores for repair but can become dysregulated, causing further damage. Avoiding dehydration, fasting and infection can help limit the response's severity.
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This document discusses various topics related to nutrition support for critically ill patients. It covers causes of injury and metabolic stress, phases of the stress response, differences between starvation and stress-induced metabolic changes, major causes of death, and considerations for providing nutrition support to critically ill patients with conditions like infection, trauma, burns, and obesity or undergoing surgery. Key points emphasized include the importance of early initiation of nutrition support to minimize complications, meeting calorie and protein needs while avoiding overfeeding, and managing fluid, electrolytes and glycemic control.
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The document discusses the metabolic response to injury, which aims to restore tissue function and eradicate microorganisms. It covers homeostasis, the components and mediators of the injury response, and its phases. The response involves increased cardiac output, ventilation, and membrane transport. It is graded based on injury severity. Mediators include neuroendocrine hormones and cytokines. The response has catabolic and anabolic phases to mobilize and replace lost resources. Factors like immobilization, sepsis, and hypothermia can exacerbate it, while avoiding continuing hemorrhage, hypothermia, and tissue issues can reduce its negative impacts.
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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.
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This document discusses the metabolic response to trauma and injury. It describes how injury disrupts homeostasis and causes physiological, metabolic and clinical changes as the body attempts to restore homeostasis. The stress response is mediated by hormones like cortisol and cytokines which cause hypermetabolism, increased protein breakdown, and insulin resistance. These changes are initially beneficial for survival but can become harmful if prolonged. Modern trauma and critical care aims to minimize this response through techniques like early feeding and pain control to promote recovery.
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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.
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This document discusses the metabolic response to injury, including the classical concepts of homeostasis and the physiological changes that occur during injury and recovery. It describes the ebb and flow phases of the metabolic response, characterized initially by catabolism to provide substrates for survival, followed by a catabolic phase and later anabolic phase for repair. Key aspects of the response include hypermetabolism, insulin resistance, protein catabolism and redistribution, and the acute phase protein response in the liver. Avoiding unnecessary factors like continued bleeding, hypothermia, underperfusion and immobilization can help minimize the metabolic stress response to injury.
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The metabolic response to injury leads to increased energy expenditure and protein catabolism. This response is mediated by the acute inflammatory response, the endothelium, nerve stimulation, and hormones from the endocrine system. The consequences include limiting injury, initiating repair, and mobilizing substrates. Compared to starvation, trauma does not allow the body to conserve fuels and proteins. The severity of injury determines the degree of metabolic response. Nutrition can modify this response by providing adequate calories, protein, vitamins, and minerals tailored to the patient's needs and stress level.
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This document discusses homeostasis and the body's response to injury. It covers several key points:
1. Homeostasis refers to maintaining a constant internal environment. The body has complex coordinated physiological processes to maintain homeostasis.
2. Following major trauma or sepsis, the body exhibits a systemic inflammatory response and loses homeostasis. Medical intervention is needed to return the patient to homeostasis.
3. The response to injury is graded - more severe injuries cause a greater physiological and immunological response. This includes fever, increased metabolism and catabolism.
4. Several factors mediate the metabolic response, including neuroendocrine hormones and cytokines. The response aims to provide substrates for survival but can become harmful if prolonged.
Metabolic Response To Injury
The document summarizes the metabolic response to injury, including its graded nature, components, mediators, phases, and factors that exacerbate or can be avoided. The response involves physiological, metabolic, clinical, and laboratory changes mediated by neuroendocrine and immune system factors. It progresses through ebb and flow phases involving catabolic elements like hypermetabolism and muscle/liver protein alterations. Avoidable exacerbating factors include continuing hemorrhage, hypothermia, tissue edema, underperfusion, starvation, and immobility. The response can be modulated through techniques like minimal access surgery, early mobilization, epidural analgesia, and avoiding prolonged fasting and excessive fluids.
metabolic response to trauma.pptx
1. The document provides tips for using a PowerPoint presentation on metabolic response to trauma. It suggests freely editing the presentation, asking students questions about blank slides, and repeating the process for active learning.
2. The metabolic response to trauma involves physiological neuroendocrine reflexes that restore homeostasis. Trauma stimulates sensors which activate the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. This increases stress hormones like cortisol and catecholamines.
3. The metabolic effects include hypermetabolism, hyperglycemia, increased protein breakdown and gluconeogenesis from protein. This supports the body during injury but causes negative nitrogen balance.
overview on "Metabolic response to injury"
The document summarizes the body's metabolic response to injury and trauma. It discusses how the response is mediated by both the neuroendocrine and immune systems through hormones and cytokines. The response aims to mobilize energy stores and nutrients to support healing, but can become maladaptive. The response proceeds in ebb and flow phases, with an initial catabolic phase followed by an anabolic recovery phase. Factors like continuing bleeding, hypothermia, edema, underperfusion, starvation, and immobility can compound the response and inhibit recovery. Maintaining homeostasis through careful fluid management, analgesia, feeding, and early mobilization can help optimize the response and enhance recovery.
Metabolic Response to Injury
The document summarizes the metabolic response to injury, which occurs in two phases - the ebb phase and the flow phase. The ebb phase occurs in the first 24-48 hours and is characterized by decreased metabolic rate and circulation. The flow phase involves increased metabolism and mobilization of energy stores for recovery. Key aspects of the flow phase include hypermetabolism, muscle wasting through increased protein degradation, acute phase protein response in the liver, and insulin resistance in tissues. The response aims to prioritize resources towards vital organs and wound healing.
Metabolic response to trauma.pptx
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.
Metabolic response to injury
The document discusses the metabolic response to injury, including key concepts like homeostasis and the graded nature of injury response. It describes the "ebb and flow" model where the initial ebb phase conserves energy and the hypermetabolic flow phase mobilizes resources for repair. Major mediators that drive the catabolic response are increased metabolism, altered protein metabolism in muscles and liver, and insulin resistance. Factors like ongoing hemorrhage, hypothermia, edema, underperfusion, starvation, and immobility can compound this response. The goal is to control these avoidable factors to benefit patient recovery.
Metabolic response to trauma
The document discusses the metabolic response to trauma and injury. It describes how the response is graded based on the severity of the stressor, from elective surgery to severe sepsis. The response involves two phases - an ebb phase of catabolism followed by a flow phase of hypermetabolism and mobilization of energy stores for recovery. Key elements of the flow phase include hypermetabolism, alterations in muscle and liver protein, and insulin resistance. The response has physiological, metabolic, clinical and laboratory components and leads to losses of fat and muscle mass if not addressed. Early enteral nutrition and minimizing the neuroendocrine stress response can help maintain weight and nitrogen balance.
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The document discusses the body's metabolic response to trauma on multiple levels. It begins by defining trauma and distinguishing between physical and psychological trauma. It then outlines the neuroendocrine response to trauma, including increased levels of catecholamines, cortisol, aldosterone, and other hormones. This hormonal response leads to catabolic effects on the body as it breaks down tissues to provide energy. The document also discusses mediators of the metabolic response like cytokines and their effects. Finally, it notes implications for therapy focus on supporting the body through the metabolic response phases until recovery.
metabolic response to the disease .pptx
1. Injury causes a metabolic stress response with multiple stages. Initially pro-inflammatory cytokines are released locally, then systemically if the injury is severe enough to cause SIRS.
2. This leads to a hypermetabolic "flow" phase involving increased heart rate, temperature and catabolism. Muscle and liver protein are broken down, increasing urinary nitrogen and acute phase proteins.
3. The response aims to mobilize energy stores for repair but can become dysregulated, causing further damage. Avoiding dehydration, fasting and infection can help limit the response's severity.
MEDICAL NUTRITION THERAPY FOR METABOLIC STRESS
This document discusses various topics related to nutrition support for critically ill patients. It covers causes of injury and metabolic stress, phases of the stress response, differences between starvation and stress-induced metabolic changes, major causes of death, and considerations for providing nutrition support to critically ill patients with conditions like infection, trauma, burns, and obesity or undergoing surgery. Key points emphasized include the importance of early initiation of nutrition support to minimize complications, meeting calorie and protein needs while avoiding overfeeding, and managing fluid, electrolytes and glycemic control.
Metabolic respons to injury
The document discusses the metabolic response to injury, which aims to restore tissue function and eradicate microorganisms. It covers homeostasis, the components and mediators of the injury response, and its phases. The response involves increased cardiac output, ventilation, and membrane transport. It is graded based on injury severity. Mediators include neuroendocrine hormones and cytokines. The response has catabolic and anabolic phases to mobilize and replace lost resources. Factors like immobilization, sepsis, and hypothermia can exacerbate it, while avoiding continuing hemorrhage, hypothermia, and tissue issues can reduce its negative impacts.
critical illness and metabolism ICRC 2012.pptx
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.
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Principle of Organ Transplantation.pptx
The document provides an overview of organ transplantation, including:
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- A historical background of major transplant milestones from the 1950s onward including the first successful kidney, liver, lung, and heart transplants.
- Details about transplant immunology, the immune response to foreign organs, and ways to suppress the immune system like with immunosuppressant drugs.
- The types of organ rejection such as hyperacute, acute, and chronic rejection.
- Considerations for organ donation, procurement, preservation, and transplantation.
- Complications after transplantation like infection and potential future directions.
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- Prognosis is best when the injury
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Day case surgery.pptx
Day case surgery, also known as ambulatory surgery, involves planned admission and discharge of a patient within 12 hours for a surgical procedure. It provides several benefits over traditional inpatient surgery such as shorter hospital stays, lower infection rates, and more efficient use of healthcare resources. Common procedures performed as day cases include hernia repairs, cataract removal, and tonsillectomies. Careful patient selection and optimization, as well as coordinated perioperative management involving preoperative assessment and education, regional anesthesia when possible, early mobilization and feeding, and established discharge criteria are important for success. Day case surgery allows for treatment of more patients while maintaining high quality care.
Deep Vein Thrombosis.pptx
This document provides an overview of deep vein thrombosis (DVT) and pulmonary embolism (PE). It covers the definition, epidemiology, risk factors, clinical features, investigations, management including prevention, treatment and anticoagulation. DVT occurs when a blood clot forms in a deep vein, usually in the legs, while PE is a complication that can occur when part of the clot breaks off and travels to the lungs. The document outlines Virchow's triad of factors that contribute to clot formation and discusses various diagnostic tests and therapeutic approaches for DVT and PE.
Fluid and Electrolyte Management in Surgery.ppt
This document provides an outline and introduction to fluid and electrolyte management in surgery. It discusses the normal distribution and balance of body water and electrolytes like sodium, potassium, calcium and magnesium. It describes various fluid and electrolyte disorders that can occur including volume disturbances, concentration disturbances and composition disturbances. It covers causes, clinical features and treatment of conditions like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia and acid-base imbalances. The document emphasizes the importance of fluid and electrolyte management in the perioperative care of surgical patients.
PAIN MANAGEMENT.ppt
This document discusses pain from multiple perspectives:
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- Different types of pain like acute, chronic, neuropathic, and referred pain are described.
- Pain assessment and various scales used to evaluate pain are outlined.
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Nutrition in surgery
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METABOLIC RESPONSE TO TRAUMA.pptx
- 1. METABOLIC RESPONSE TO TRAUMA By Dr. Olofin.K.E
- 2. Outline • Introduction • Historical Perspectives • Triggers of metabolic response to trauma • Components of metabolic response to trauma • Sequelae of metabolic response to trauma in the surgical patient • Factors affecting severity of response • Attenuation of metabolic responses to trauma • Conclusion
- 3. Introduction • Metabolic response to trauma (MRT) refers to adaptive defensive changes aimed at maintaining homeostasis after a traumatic event. • Core objectives of these changes include maintaining circulation, providing energy, repair of wound and restoration of normal function.
- 4. • Responses to trauma can however have adverse effects on the patient if prolonged and accentuated. • Control of these responses can improve the overall outcome in surgical patients.
- 5. Historical Perspectives • 1932- Cuthbertson described in detail the metabolic response of four patients with lower limb injuries • 2 phases were described-the ebb and flow phases
- 6. Triggers of Metabolic response to Trauma 1. Pain from damaged tissues 2. Hypovolemia/Heamorrhage/Hypoxia 3. Infection 4. Inflammatory reaction 5. Acidosis 6. Starvation 7. Hypothermia 8. Anxiety
- 7. Components of Metabolic Response to Trauma • Sympathetic Nervous System Activation • Endocrine reponse • Cytokine response
- 8. Sympathetic Nervous System response Response • Rise in norepinephrine release from adrenal medulla and presynaptic nerve endinngs Effects • Cardiovascular effects – tachycardia, hypertension, redistribution of blood flow, activation of the renin- angiotensin system • GIT-Reduced intestinal motility • Respiratory System- Bronchodilation • Pancreas- Reduces insulin secretion and raises glucagon secretion
- 9. Endocrine Responses Endocrine organ changes • Hypothalamic-pituitary- adrenal system- Rise in ACTH and Growth hormone secretion • Posterior Pituitary gland- arginine vasopressin secretion • Adrenal Cortex-Rise in cortisol and aldosterone • Pancreas-increase in insulin and glucagon secretion Effects • Rise in plasma cortisol, GH increases lipolysis, gluconeogenesis and decreased cellular glucose uptake • AVP- Increases water reabsorbtion in the collecting ducts • Aldosterone increases Na reabsorbtion • Cortisol and glucagon-Insulin antagonism
- 10. Cytokine Mediated Responses Cytokine Effects TNF-alpha Neutrophil activation, upregulation of adhesion molecules, increased capillary permeability, fever IL-1 Neutrophil and T-lymphocyte proliferation, increased capillary permeability, proteolysis and fever IL-2 Increases antibody-dependent cell mediated toxicity, proliferation of activated T4 cells IL-4 Increases B-cell and T4 type 2 cells IL-6 Stimulates acute phase protein production in the liver- C-reactive protein, serum amyloid A protein, Factor VIII, vWF, Fibrinogen IL-10 Anti-inflammatory IL-12 Increases production of IL-2, TNF-b, INF-g
- 11. Sequelae of metabolic response to trauma/Relevance to surgical patient • Increased energy requirement • Reduced immunity • Increase susceptibility to venous thromboembolism • Impaired wound healing • Weight loss • Fatigue
- 12. Factors Influencing Response • Nature and severity of injury • Nutritional status of patient • Age • Sex • Environmental temperature
- 13. Attenuation of Metabolic Response Pre/Per-operative measures • Allaying of fear and anxiety • Prompt replacement of blood and fluid loss • Regional anaesthesia (epidural) when appropriate • Adequate analgesia • Minimally invasive surgeries (laparoscopic surgeries) • Pre-operative nutritional support (arginine, glutamine, fish oil) • Antibiotic prophylaxis Post operative measures • Fluid and electrolyte balance • Adequate analgesia • Early enteral feeding • Perenteral nutritional support • Prompt treatment of infections
- 14. Conclusion • Metabolic response to trauma aims to restore homeostasis after a traumatic event, it also has the propensity of causing unwanted effects. • Measures that reduce its intensity should be taken to reduce morbidity and mortality, and of course improve treatment outcome.
- 15. Thank you!
- 16. References • Principles and Practice of Surgery, 4th Edition • The Stress Response to Trauma and Surgery by JP Desborom, British Journal of Anaesthesia,2000. 85(107-109) • Textbook of anaesthesia, Aitkenhead 4th Edition • Physiological response to Trauma, Infection and Surgery, www.surgical-trauma.co.uk