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.
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 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
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.
This document provides an overview of nutrition in surgical patients. It discusses the basics of nutrition including caloric and protein requirements. The importance of nutrition for surgical patients is described along with the complications of malnutrition like infection and poor wound healing. Methods of nutritional assessment involving history, exams, and labs are outlined. Both enteral and parenteral nutrition are covered, including indications, contraindications, administration methods, and potential complications. The take home messages emphasize the importance of meeting caloric needs to avoid complications, using enteral nutrition when possible, and closely monitoring patients on nutrition support.
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.
1) Entero-cutaneous fistulas are abnormal connections between the skin and gastrointestinal tract that allow intestinal contents to drain onto the skin.
2) They are usually caused by surgery, trauma, infection, inflammation or radiation and most commonly involve the small intestine.
3) Treatment involves stabilization, controlling sepsis, optimizing nutrition, identifying the fistula anatomy, and eventually either definitive surgical repair or closure of the fistula tract.
Ventral hernia is protrusion of peritoneal sac through anterior abdominal wall defects except Groin hernias. In this presentation I have discussed Epigastric, Umbilical, Para umbilical, Incisional, Spigelian and Lumbar hernias.
Surgical hemostasis is one of the pillars of modern surgery. Adequate hemostasis in a surgical patient involves a detailed perioperative clinical evaluation and investigation, and various intra operative techniques and options. Ensuring adequate surgical hemostasis reduces morbidity and mortality by modulating the metabolic response to trauma, decreasing the incidence of post operative anemia, reduces rates of surgical site infection and ultimately improving wound healing
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 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
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.
This document provides an overview of nutrition in surgical patients. It discusses the basics of nutrition including caloric and protein requirements. The importance of nutrition for surgical patients is described along with the complications of malnutrition like infection and poor wound healing. Methods of nutritional assessment involving history, exams, and labs are outlined. Both enteral and parenteral nutrition are covered, including indications, contraindications, administration methods, and potential complications. The take home messages emphasize the importance of meeting caloric needs to avoid complications, using enteral nutrition when possible, and closely monitoring patients on nutrition support.
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.
1) Entero-cutaneous fistulas are abnormal connections between the skin and gastrointestinal tract that allow intestinal contents to drain onto the skin.
2) They are usually caused by surgery, trauma, infection, inflammation or radiation and most commonly involve the small intestine.
3) Treatment involves stabilization, controlling sepsis, optimizing nutrition, identifying the fistula anatomy, and eventually either definitive surgical repair or closure of the fistula tract.
Ventral hernia is protrusion of peritoneal sac through anterior abdominal wall defects except Groin hernias. In this presentation I have discussed Epigastric, Umbilical, Para umbilical, Incisional, Spigelian and Lumbar hernias.
Surgical hemostasis is one of the pillars of modern surgery. Adequate hemostasis in a surgical patient involves a detailed perioperative clinical evaluation and investigation, and various intra operative techniques and options. Ensuring adequate surgical hemostasis reduces morbidity and mortality by modulating the metabolic response to trauma, decreasing the incidence of post operative anemia, reduces rates of surgical site infection and ultimately improving wound healing
This document discusses crush injury and crush syndrome. It defines crush syndrome as muscle damage from prolonged pressure that can lead to systemic complications from the release of intracellular muscle contents. Key points include: crush syndrome is a medical emergency requiring aggressive IV fluid resuscitation and bicarbonate to prevent renal failure from myoglobinuria; complications include rhabdomyolysis, hyperkalemia, hypocalcemia, and metabolic acidosis; it commonly results from events causing mass casualties such as earthquakes.
This document discusses the management of open fractures. It begins by defining an open fracture and classifying open fractures using the Gustilo and Tscherne systems. It then outlines the treatment principles of open fractures which include antibiotic prophylaxis, wound debridement, and fracture stabilization. The initial management, primary surgery including further debridement, irrigation, and skeletal stabilization are described. Factors determining limb salvage versus amputation are provided. The document concludes with discussions on external fixation, internal fixation, and wound closure approaches.
This document discusses various types of stomas including colostomies and ileostomies. It describes their indications, techniques for formation, types like end, loop and continent variations, as well as complications and management strategies. Stomas are surgically created openings of the intestinal or urinary tract onto the abdominal wall to divert feces or urine. Proper technique and siting are important to reduce complications.
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.
1. The document discusses the metabolic response to injury, which involves complex physiological and hormonal changes aimed at restoring homeostasis following trauma.
2. It describes the phases of the metabolic response as including an initial "ebb" phase aimed at conserving energy, followed by a "flow" or catabolic phase involving increased metabolism and breakdown of proteins and fat to mobilize energy stores.
3. Key elements of the catabolic flow phase include hypermetabolism, increased protein breakdown in skeletal muscle and liver, insulin resistance, and changes in body composition with loss of muscle mass. Mediators include stress hormones and cytokines.
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.
Advanced Trauma Life Support (ATLS) is a system to rapidly assess and treat trauma patients. It focuses on the initial care of trauma patients, with an emphasis on the first hour known as the "golden hour." The goal of ATLS is to rapidly identify and intervene in life-threatening injuries through a primary and secondary survey, resuscitation, and stabilization of the patient for transfer to the operating room or intensive care unit if needed. ATLS aims to minimize mortality and morbidity through structured training programs for medical professionals in trauma care.
An intestinal stoma is an artificial opening in the abdominal wall that connects the intestinal tract to the outside of the body. There are different types of stomas including ileostomies, colostomies, and urostomies. Ileostomies divert small intestine contents and have a liquid effluent that is discharged continuously. Colostomies divert large intestine contents and have solid, intermittent effluent. Stomas can be temporary or permanent depending on the clinical situation and are constructed in different ways including as an end stoma or loop stoma. Proper stoma care and use of appliances is important for managing stomas.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
Postoperative fever can occur for various reasons depending on the timing. Fever within the first 2 days is usually non-infectious and due to atelectasis. From days 3-4, fever is commonly due to urinary tract infections or deep vein thrombosis. Between days 5-8, surgical site infections become a more frequent cause of fever. Timely diagnosis and treatment of the underlying cause are important for improving patient outcomes.
Whipple's procedure - Indications, Steps, ComplicationsVikas V
The document describes the Whipple procedure, which was first performed by Dr. Allen Whipple in 1935. It involves removing the head of the pancreas, part of the small intestine, the gallbladder, and bile duct. The original procedure was done in two stages but is now typically done in one stage. The document outlines the key steps of the modern Whipple procedure, including mobilizing tissues, dividing vessels, transecting organs, and reconstructing the digestive and biliary systems with anastomoses. Vascular resection of veins like the splenic vein may sometimes be required as well.
This document outlines the principles of amputation, including definitions, indications, types, pre-operative evaluation, operative techniques, post-operative care, and complications. It notes that amputation is an ancient procedure that should be viewed not as a failure of treatment, but as the first step towards allowing a patient to return to a more comfortable life. The document emphasizes the multidisciplinary nature of amputation and importance of both surgical and post-operative care in achieving the best outcomes for patients.
- Intestinal stomas are surgically created openings of the small or large intestine onto the abdominal wall. There are three main types: colostomy, ileostomy, and loop stoma.
- Complications include prolapse, herniation, stenosis, dermatitis from effluent, and obstruction. Dietary advice focuses on reducing gas, bulk and odorous foods. Management involves properly attaching collection bags and monitoring for complications.
The document discusses the principles of fracture management. It covers fracture classification, emergency care including splinting and analgesia, and definitive treatment including closed and open reduction, immobilization methods like casting, traction, and fixation. The goals of treatment are to heal the bone in proper position and alignment to restore function with minimal time, expense and complications.
Damage control surgery involves rapidly controlling hemorrhaging and contamination through temporary closure of injuries to stabilize critically injured patients, followed by resuscitation and definitive repair once physiology is restored. It aims to prevent the lethal triad of hypothermia, acidosis, and coagulopathy. The approach has three stages - initial laparotomy and packing, ICU resuscitation, and planned reoperation once metabolic conditions improve. It has been shown to improve survival rates for severely injured trauma patients compared to traditional surgery.
This document discusses different types of ventral hernias, including umbilical, epigastric, incisional, and paraumbilical hernias. It describes the causes, clinical features, diagnosis, and treatment options for each type. For treatment, it compares open surgical repair techniques like primary closure or mesh placement versus laparoscopic approaches. Complications of surgery like seroma, infection, and injury are also reviewed.
This document provides an overview of ulcers, skin infections, and their management. It begins by defining an ulcer and describing the causes, identification, and types of ulcers including venous, arterial, neuropathic, and malignant ulcers. It then discusses skin infections like impetigo, erysipelas, cellulitis, and infections of hair follicles. Pressure ulcers and their staging system are also covered. The document concludes by describing life-threatening skin infections such as streptococcal gangrene, clostridial myonecrosis, and necrotising fasciitis. Conservative and surgical management approaches are discussed throughout.
- The document classifies open fractures using the Gustilo-Anderson classification system based on wound size, soft tissue injury, and degree of contamination. Grade I fractures have a clean wound less than 1 cm, while Grade III fractures have extensive soft tissue damage or injury over 8 hours old.
- Management of open fractures aims to prevent infection through prompt debridement, antibiotics, splinting, and wound coverage. Early debridement within 5 hours can significantly reduce infection rates compared to later debridement.
- Risk of infection increases with higher fracture grade, from 0-12% for Grade I up to 9-55% for Grade III fractures. Prompt antibiotics, debridement, and wound management seek
Relationship between trauma and diseasesSaid Dessouki
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),
metabolc response by martha, alfred and pascal.pptxAidenJosephat
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.
This document discusses crush injury and crush syndrome. It defines crush syndrome as muscle damage from prolonged pressure that can lead to systemic complications from the release of intracellular muscle contents. Key points include: crush syndrome is a medical emergency requiring aggressive IV fluid resuscitation and bicarbonate to prevent renal failure from myoglobinuria; complications include rhabdomyolysis, hyperkalemia, hypocalcemia, and metabolic acidosis; it commonly results from events causing mass casualties such as earthquakes.
This document discusses the management of open fractures. It begins by defining an open fracture and classifying open fractures using the Gustilo and Tscherne systems. It then outlines the treatment principles of open fractures which include antibiotic prophylaxis, wound debridement, and fracture stabilization. The initial management, primary surgery including further debridement, irrigation, and skeletal stabilization are described. Factors determining limb salvage versus amputation are provided. The document concludes with discussions on external fixation, internal fixation, and wound closure approaches.
This document discusses various types of stomas including colostomies and ileostomies. It describes their indications, techniques for formation, types like end, loop and continent variations, as well as complications and management strategies. Stomas are surgically created openings of the intestinal or urinary tract onto the abdominal wall to divert feces or urine. Proper technique and siting are important to reduce complications.
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.
1. The document discusses the metabolic response to injury, which involves complex physiological and hormonal changes aimed at restoring homeostasis following trauma.
2. It describes the phases of the metabolic response as including an initial "ebb" phase aimed at conserving energy, followed by a "flow" or catabolic phase involving increased metabolism and breakdown of proteins and fat to mobilize energy stores.
3. Key elements of the catabolic flow phase include hypermetabolism, increased protein breakdown in skeletal muscle and liver, insulin resistance, and changes in body composition with loss of muscle mass. Mediators include stress hormones and cytokines.
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.
Advanced Trauma Life Support (ATLS) is a system to rapidly assess and treat trauma patients. It focuses on the initial care of trauma patients, with an emphasis on the first hour known as the "golden hour." The goal of ATLS is to rapidly identify and intervene in life-threatening injuries through a primary and secondary survey, resuscitation, and stabilization of the patient for transfer to the operating room or intensive care unit if needed. ATLS aims to minimize mortality and morbidity through structured training programs for medical professionals in trauma care.
An intestinal stoma is an artificial opening in the abdominal wall that connects the intestinal tract to the outside of the body. There are different types of stomas including ileostomies, colostomies, and urostomies. Ileostomies divert small intestine contents and have a liquid effluent that is discharged continuously. Colostomies divert large intestine contents and have solid, intermittent effluent. Stomas can be temporary or permanent depending on the clinical situation and are constructed in different ways including as an end stoma or loop stoma. Proper stoma care and use of appliances is important for managing stomas.
NECROTISING FASCIITIS- the flesh eating infection
#surgicaleducator #necrotisingfasciitis #surgicaltutor #babysurgeon #usmle
· Dear Viewers
· Greetings from “Surgical Educator”
· Today in this episode I have discussed about Necrotising Fasciitis- the flesh eating infection
· It is common in immunocompromised patients even after trivial trauma.
· I have discussed about the overview,etiology,types,clinical features,complications and treatment of Necrotising Fasciitis
· I hope this video is interesting and also useful to all of you
· You can watch the video in the following links:
· surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
Thank you for watching the video
Postoperative fever can occur for various reasons depending on the timing. Fever within the first 2 days is usually non-infectious and due to atelectasis. From days 3-4, fever is commonly due to urinary tract infections or deep vein thrombosis. Between days 5-8, surgical site infections become a more frequent cause of fever. Timely diagnosis and treatment of the underlying cause are important for improving patient outcomes.
Whipple's procedure - Indications, Steps, ComplicationsVikas V
The document describes the Whipple procedure, which was first performed by Dr. Allen Whipple in 1935. It involves removing the head of the pancreas, part of the small intestine, the gallbladder, and bile duct. The original procedure was done in two stages but is now typically done in one stage. The document outlines the key steps of the modern Whipple procedure, including mobilizing tissues, dividing vessels, transecting organs, and reconstructing the digestive and biliary systems with anastomoses. Vascular resection of veins like the splenic vein may sometimes be required as well.
This document outlines the principles of amputation, including definitions, indications, types, pre-operative evaluation, operative techniques, post-operative care, and complications. It notes that amputation is an ancient procedure that should be viewed not as a failure of treatment, but as the first step towards allowing a patient to return to a more comfortable life. The document emphasizes the multidisciplinary nature of amputation and importance of both surgical and post-operative care in achieving the best outcomes for patients.
- Intestinal stomas are surgically created openings of the small or large intestine onto the abdominal wall. There are three main types: colostomy, ileostomy, and loop stoma.
- Complications include prolapse, herniation, stenosis, dermatitis from effluent, and obstruction. Dietary advice focuses on reducing gas, bulk and odorous foods. Management involves properly attaching collection bags and monitoring for complications.
The document discusses the principles of fracture management. It covers fracture classification, emergency care including splinting and analgesia, and definitive treatment including closed and open reduction, immobilization methods like casting, traction, and fixation. The goals of treatment are to heal the bone in proper position and alignment to restore function with minimal time, expense and complications.
Damage control surgery involves rapidly controlling hemorrhaging and contamination through temporary closure of injuries to stabilize critically injured patients, followed by resuscitation and definitive repair once physiology is restored. It aims to prevent the lethal triad of hypothermia, acidosis, and coagulopathy. The approach has three stages - initial laparotomy and packing, ICU resuscitation, and planned reoperation once metabolic conditions improve. It has been shown to improve survival rates for severely injured trauma patients compared to traditional surgery.
This document discusses different types of ventral hernias, including umbilical, epigastric, incisional, and paraumbilical hernias. It describes the causes, clinical features, diagnosis, and treatment options for each type. For treatment, it compares open surgical repair techniques like primary closure or mesh placement versus laparoscopic approaches. Complications of surgery like seroma, infection, and injury are also reviewed.
This document provides an overview of ulcers, skin infections, and their management. It begins by defining an ulcer and describing the causes, identification, and types of ulcers including venous, arterial, neuropathic, and malignant ulcers. It then discusses skin infections like impetigo, erysipelas, cellulitis, and infections of hair follicles. Pressure ulcers and their staging system are also covered. The document concludes by describing life-threatening skin infections such as streptococcal gangrene, clostridial myonecrosis, and necrotising fasciitis. Conservative and surgical management approaches are discussed throughout.
- The document classifies open fractures using the Gustilo-Anderson classification system based on wound size, soft tissue injury, and degree of contamination. Grade I fractures have a clean wound less than 1 cm, while Grade III fractures have extensive soft tissue damage or injury over 8 hours old.
- Management of open fractures aims to prevent infection through prompt debridement, antibiotics, splinting, and wound coverage. Early debridement within 5 hours can significantly reduce infection rates compared to later debridement.
- Risk of infection increases with higher fracture grade, from 0-12% for Grade I up to 9-55% for Grade III fractures. Prompt antibiotics, debridement, and wound management seek
Relationship between trauma and diseasesSaid Dessouki
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),
metabolc response by martha, alfred and pascal.pptxAidenJosephat
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.
Homeostasis, the internal milieu of the human bodyNoorAlam626605
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.
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 o surgery for aneasthseia.pptxNuunPh
The document discusses the metabolic response to surgery, which aims to maintain homeostasis in the face of surgical trauma. The neuroendocrine and stress response results in hormonal and metabolic changes that mobilize substrates, limit tissue damage, destroy infectious organisms, and activate repair processes. This includes increased levels of cortisol, catecholamines, glucagon, growth hormone, and antidiuretic hormone, which alter carbohydrate, protein, and lipid metabolism. The catabolic response provides energy substrates while postponing anabolism and optimizing host defense. After volume is restored and infection is controlled, the anabolic phase begins with insulin promoting reparative processes and rebuilding of lost proteins and body fat.
The body responds to stress and injury through metabolic and inflammatory responses known as the ebb and flow phases. In the initial ebb phase, metabolism decreases to conserve energy and resources. The subsequent flow phase involves increased metabolism and inflammation to restore function and fight infection. Prolonged or excessive response can lead to organ dysfunction or failure through effects like fluid shifts, immune imbalance, and metabolic changes that impact protein, carbohydrate and fat metabolism. Factors like severity of injury, infection, fluid status, and nutrition influence the response and clinical outcomes.
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.
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.
Metabolic response to trauma - In Perspective of Maxillofacial SurgeryMaxfac Center
Metabolic responses that occur following trauma and its clinical implications to minimize morbidity and mortality.
Mentor: Dr Saikat Saha MDS, OMFS, SIliguri, West Bengal, India
Address: MAXFAC Center for Oral and Maxillofacial and Head & Neck Surgery, Siliguri
Email : maxfacmail@gmail.com
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.
metabolic response to the disease .pptxdeepak160452
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.
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.
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.
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.
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.
Dentistry L8 METABOLIC RESPONSE TO TRAUMA-1.pptxbgjn55kymp
The metabolic response to trauma involves complex metabolic changes mediated by the neuroendocrine system to reduce the effects of injury and return the body to its preinjury state. It occurs in three phases: the ebb phase aims to conserve energy in the initial 24-48 hours after trauma; the flow phase is catabolic for about 7 days due to increased hormones that cause weight loss; and the anabolic recovery phase lasts 2-4 weeks to replace losses and restore the body's preinjury condition.
Dentistry L8 METABOLIC RESPONSE TO TRAUMA-1.pptxbgjn55kymp
The metabolic response to trauma involves complex metabolic changes mediated by the neuroendocrine system to reduce the effects of injury and return the body to its preinjury state. It occurs in three phases: the ebb phase aims to conserve energy in the initial 24-48 hours after trauma; the flow phase is catabolic for about 7 days due to increased stress hormones which cause weight loss; and the anabolic recovery phase lasts 2-4 weeks to replace losses and restore the body's preinjury condition.
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.
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.
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Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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Metabolic Response to Trauma.pptx
1. Presented by:
Dr. Neha Umakant Chodankar
II MDS
Department of OMFS
Metabolic Response to
Trauma
2. Contents
• Introduction
• Detection of Cellular Injury
• Physiologic response to trauma
• CNS Regulation Of Inflammation In Response To Injury---Neuro- endocrine response
• Mediators of Inflammation
• Cell Mediated Inflammation
• Metabolic Changes after Trauma
• Metabolism In Surgical Patients
• Metabolism during Starvation
• Modulation of response
• Nutrition as Therapy
• Conclusion
3. Introduction
• Injury produces profound systemic effects.
• Hormones, the autonomic nervous system, and cytokines all produce
a series of responses that are designed to help defend the body
against the insult of trauma and promote healing.
• Classically, these responses have been described as the stress
response, a term coined by the Scottish chemist Cuthbertson in 1932.
4. • The cascade of interactions and host responses in a severely traumatized
patient follow a recognizable pattern, but the depth and duration of these
changes are variable, and usually depend on the extent of the injury and
the presence of ongoing stimulation.
• Each results in marked variations in the metabolic response, and this
variability persists during the later chronic and recovery phases of the
original injury.
• The body’s initial response to insult (the acute phase) is directed at maintaining
adequate substrate delivery to the vital organs, in particular oxygen and energy.
5. Detection of Cellular Injury
• Mediated by members of damage
associated molecular pattern family
• Systemic inflammatory response
that limit damage and restore
homeostasis:
1. Acute proinflammatory response
- Innate immune system recognize
ligands
2. Anti- inflammatory response
- Modulate proinflammatory phase
and return homeostasis
6. Physiologic response to trauma
• The metabolic response to trauma in humans has been defined in 3 phases:
1) Ebb phase or decreased metabolic rate in early shock phase,
2) Flow phase or catabolic phase,
3) Anabolic phase or recovery
7. Ebb phase
• Develops within the first hours after injury (24-48 hours).
• It is characterized by reconstruction of body’s normal tissue perfusion and
efforts to protect homeostasis.
• In this phase, there is a decrease in total body energy and urinary nitrogen
excretion.
• An early increase is detected in
endocrine hormones such as
catecholamines and cortisol.
8. • As a result of this long lasting
response, the adipose tissue, skin
and other tissues are destructed.
Flow phase
• Defined as an ‘all or nothing’ reaction
• High substrate flow should to target systems is essential.
• Although this response is necessary for survival in the short term, if it
persists over a long period of time or if the response is severe it leads to the
onset of body damage (2-7. days).
9. • The flow phase is an early period catabolism that provides compensating
response to the initial trauma and volume replacement, except most minor
injuries.
• In this phase, the metabolic response is directly related to the supply of
energy and protein substrates in order to protect tissue, damage repair and
critical organ functions.
• The increased body oxygen consumption and metabolic rate are among
these responses.
10. Late anabolic phase:
• The late anabolic phase is the final phase of the recovery period, and is
characterized by
ogradual restoration of body protein and fat stores and
onormalization of positive nitrogen balance after the metabolic response to
trauma is stopped.
• It may take a few weeks to
several months after serious
injury.
11. Phase Duration Role Physiological
Response
Hormonal response
Ebb 24-48hrs Conserve Blood volume and
energy
Repair
BMR
Temperature
CO2
Hypovolemia
Lactic Acidosis
Catecholamines
Cortisol
Aldosterone
Flow
Catabolic 3-10 days Mobilisation of energy stores-
Recovery and Repair
BMR
Temperature
CO2
O2 consumption
Cytokines
Increased Insulin
Glucagon
Cortisol
Insulin resistance
Anabolic 10-60 days Replacement of lost tissue Positive Nitrogen
balance
Growth hormone
IGF
12. Ebb phase Flow phase
Hypometabolic state Hypermetabolic state
Decreased energy expenditure Increased energy expenditure
Cold clammy extremities Warm extremities
Cardiac output below normal Cardiac output increased
Core temp low Core temp elevated
Normal glucose production, elevated
levels
Increased glucose production, normal or
slightly elevated
Insulin conc low Low or elevated
Catecholamines elevated High normal or elevated
Glucagon elevated Elevated
Mediated by central nervous system Mediated by central nervous system and
cytokines
13. CNS Regulation Of Inflammation In Response To
Injury
• DAMPs and inflammatory molecules convey stimulatory signals to CNS via
multiple routes.
• Inflammatory stimuli interact with receptors on brain to generate
proinflammatory mediators (cytokines, chemokines, adhesion molecules,
proteins of complement system, and immune receptors).
• Inflammation can also signal the brain via afferent fibres (vagus nerve).
14. 1.Hypothalamic- pituitary- adrenal
(HPA) axis Release glucocorticoids
2. Sympathetic nervous system
Release catecholamines
• An early response of the
neuroendocrine system -upregulation
of the sympatho-adrenal axis,
Neuro-endocrine response
15. • This causes inhibition of glucose uptake by tissue, which stimulates glucagon
secretion.
• Sympathetic activity promotes
lipolysis within adipose tissue,
which begins to provide an
energy source for
gluconeogenesis.
• Gluconeogenesis in the liver is
stimulated by glucagon.
16.
17.
18. Endocrine Stress Response
Hormone Time Effect
Catecholamines Stress dependent immediate and
continues for 24-48hrs
Hyperglycemia
Raises metabolic rate
Mobilize fatty acids
Haemodynamic stability
ADH Immediate to 1 week Promotes reabsorption of water
Peripheral vasoconstrictor
Renin- Angiotensin Vasoconstrictor
Release of Aldosterone
(conserves Na and eliminates K)
Insulin First few hours: decreased secretion
Later anabolic: increased release of
insulin
Glycolysis
Glycogenesis
Lipogenesis
Proinflammatory activity
Growth hormone Anabolic phase Protein synthesis
Ketogenesis
19. Endocrine Stress Response
Hormone Time Effect
Catecholamines Stress dependent immediate and
continues for 24-48hrs
Hyperglycemia
Raises metabolic rate
Mobilize fatty acids
Haemodynamic stability
ADH Immediate to 1 week Promotes reabsorption of water
Peripheral vasoconstrictor
Renin- Angiotensin Vasoconstrictor
Release of Aldosterone
(conserves Na and eliminates K)
Insulin 2 phases
First few hours: decreased secretion
Later anabolic: increased release of
insulin with peripheral insulin resistance
Glycolysis
Glycogenesis
Lipogenesis
Proinflammatory activity
Growth hormone Anabolic phase Protein synthesis
Ketogenesis
20. Endocrine Stress Response
Hormone Time Effect
Catecholamines Stress dependent immediate and
continues for 24-48hrs
Hyperglycemia
Raises metabolic rate
Mobilize fatty acids
Haemodynamic stability
ADH Immediate to 1 week Promotes reabsorption of water
Peripheral vasoconstrictor
Renin- Angiotensin Vasoconstrictor
Release of Aldosterone
(conserves Na and eliminates K)
Insulin First few hours: decreased secretion
Later anabolic: increased release of
insulin
Glycolysis
Glycogenesis
Lipogenesis
Proinflammatory activity
Growth hormone Anabolic phase Protein synthesis
Ketogenesis
22. Serotonin
• It is monoamine neurotransmitter (5-hydroxytryptamine) derived from
tryptophan
• It is a potent vasoconstrictor
• Released by platelets
• Present in intestinal chromaffin cells & platelets
• Other effects include bronchoconstriction, platelet aggregation
• Unclear role in inflammation
24. Acute Phase Proteins
• Nonspecific markers produced by hepatocytes in response to injury,
infection, inflammation
• Induced by IL-6
25. Cytokines
• Protein mediators, collectively called cytokines, are produced at the site of
injury by diverse circulating immune cells- Monocytes, lymphocytes,
macrophages, and other cells.
• The most important cytokines in trauma are
otumor necrosis factor (TNF),
othe interleukins (IL-1, IL-2, IL-6, and IL-8),
othe interferons, and
ovarious growth factors such as granulocyte-macrophage colony stimulating
factor (GM-CSF), and
oplatelet-derived growth factors (PDGFs).
26. • TNF influences cellular attraction as part of the local inflammatory
response, leukocyte migration, and systemic hypotension.
• It also promotes muscle catabolism, free fatty acid release, and hepatic
synthesis of acute-phase reactants.
27. • Interleukins are polypeptides released from lymphocytes; each is
numbered according to the amino acid sequence that elicits its action.
Circulating free receptors are known for IL-1 and IL-6.
• IL-1 can be detected in the circulation within a few hours after injury
• More profound systemic effects include fever and changes in protein
metabolism.
30. PMNLs
• Catecholamines and glucocorticoids marginalize peripheral PMNs and
recruit them from the bone marrow.
• Capillary endothelial integrity is disrupted, leading to the formation of
edema, defects in oxygen delivery, hypoxic cellular injury, and other
adverse consequences for cellular homeostasis.
31. Metabolic Changes after Trauma
• Oxygen and energy requirements are increased in proportion to the
severity of the trauma.
• It is believed that 40% of the total body energy consumption is used for ion
pumps and transport process.
32. Lipid Metabolism:
• Free fatty acids are primary sources of energy after trauma.
• Triglycerides provide 50-80% of the energy consumed after trauma and
critical illness.
33. • If the patient is given glucose in a dose more than he can oxidize this will
lead to more hepatic steatosis. This phenomenon is more frequent in
septic, diabetic, and obese patients.
• Hepatic ketogenesis is stimulated less in situations where starvation is
together with an illness as compared to starvation alone due to high insulin
levels.
• In this way, glucose is used as an energy source in the peripheral injured
tissues.
34. • The activity of lipoprotein lipase is reduced in fat and muscle by the action
of increased proinflammatory cytokines (TNF) in trauma and sepsis.
• During the ebb phase, plasma fatty acid and glycerol levels increase by
lipolysis. Lipolysis continues in the flow phase and the increased free fatty
acids inhibit glycolysis.
• Fatty acid synthesis is inhibited with the effects of increase in glucagon and
intracellular fatty acids. However, inhibition is not enough in cases of
severe trauma, hemorrhagic shock and sepsis.
35. • The rate of ketogenesis following trauma is inversely proportional to injury
severity. Ketogenesis is reduced in major trauma, shock and sepsis due to
an increase in insulin and increased use of free fatty acids.
• In minor trauma, ketogenesis is increased but this increase will not reach
the level of starvation ketosis.
36. Protein And Amino Acid Metabolism
• In metabolic response to trauma systemic proteolysis begins especially by
the action of glucocorticoids, the catabolism is increased and excretion of
urinary nitrogen rise upto 30 g/day.
37. • This translates to an average of 1.5% daily loss in body mass.
• According to this calculation, a traumatized individual with no oral
nutrition is going to lose 15% of his body mass in 10 days.
• Therefore, amino acids cannot be accepted as long-term fuel reserves, and
excess amounts of protein losses are incompatible with life.
• By gluconeogenesis after posttraumatic protein catabolism, amino acids
are provided for the synthesis of acute phase proteins, albumin, fibrinogen,
glycoproteins, complement factors and similar molecules.
38. • Elective surgery and minor trauma lead to a decrease in protein synthesis
and mild level protein degradation. Severe trauma, burns and sepsis
progress with increased protein catabolism.
• Increase in urinary nitrogen levels and negative nitrogen balance can be
detected at an early stage after injury peaking at day 7. Protein catabolism
may continue upto 3 to 7 weeks
• Protein catabolism is carried out by degradation of skeletal muscle. The
increase in protein metabolism is followed by the increase in flow phase
and parallels to changes in oxygen uptake and heart rate.
39. • Muscle catabolism can be reduced by nutritional support during flow
phase. Protein synthesis can be stimulated, but complete suppression of
muscle catabolism is not possible.
• Net muscle protein recovery can be obtained during the anabolic period of
the disease only with enough exercise and nutritional support.
40. Carbohydrate Metabolism
• Administration of glucose to surgical patients during fasting aims to reduce
proteolysis and to prevent the loss of muscle mass.
• Daily infusion of 50 g of glucose increases fat oxidation and suppresses
ketogenesis.
• In case of excessive glucose administration excessive carbon dioxide
production will occur, resulting in adverse effects in patients with
suboptimal pulmonary function.
• Administration of glucose during fasting reduces protein breakdown for
gluconeogenesis, but this reduction is not sufficient to meet the
requirements in trauma and sepsis.
41. • Other hormonal and proinflammatory factors are effective in protein
degradation under stress conditions, and muscle breakdown is inevitable.
• Administering insulin in increased stress decreases protein breakdown in
muscle tissue. This effect has been found to occur by increasing muscle
protein synthesis and by preventing protein degradation in hepatocytes.
• One of the most important body responses to traumatic stimulation during
critical illness is providing sufficient substrate to organs and cells where
mitochondrial respiration is not possible.
42. • Glucose can be used in hypoxic tissue and inflammatory cells with this
feature. Glucose is also important in recovering wounds
• The severity of injury and tissue damage after trauma parallels
hyperglycemia. In the early period of Ebb phase, glycogen stores, primarily
hepatic, are used only for a period of 12-24 hours.
• In the late phase of trauma, the flow phase, amino acids, lactate, pyruvate
and glycerol is used for renal and hepatic gluconeogenesis.
43. • Increased endogenous glucose synthesis occurs in critical illness. This
situation cannot be completely inhibited by exogenous glucose and insulin
administration.
• Gluconeogenesis is an essential process that is driven by stress hormones
and cytokines. The first metabolic change after trauma is gluconeogenesis.
• The lactate metabolism capacity is normally 150 grams, and increases to
large amounts under stress. Glucose is synthesized from alanine in a similar
manner.
• In this way, the nitrogen that is formed during amino acid metabolism is
introduced to blood stream, and glucose production in the liver is ensured.
44. Physiological Effects Of Insulin And Insulin Resistance In Stress
• The decrease in the normal anabolic effect of insulin, i.e. the development
of insulin resistance, is the main source of a series of reactions in response
to injury and the consequent metabolic state.
• Insulin controls protein metabolism
• Insulin also controls fat metabolism
• The specific signaling pathways in insulin sensitive cells are activated to
provide anabolic reactions such as glycogen storage, protein synthesis in
muscle, or as to block lipolysis in fat cells.
45. • Amino acids, free fatty acids and glucose is released into the bloodstream
from various tissues in stress response. Fat is consumed in the body rather
than glucose.
• It has been reported that by infusing sufficient amount of insulin to keep
glucose within normal range, the remaining metabolism is normalized.
46. • From a clinical point of view, insulin infusion sufficient enough to normalize
glucose levels can be used as the final aim to achieve these reactions and
can be used to achieve glucose control.
• Tight glycemic control will improve the outcomes of critically ill patients
following major trauma.
47. Metabolism In Surgical Patients
• Adequate nutrition of patients who lost weight and will undergo surgical
procedures is critical.
• Patients generally die not due to their present diseases, but because of
secondary complications due to malnutrition.
• In starvation, glucagon and epinephrine stimulate glycogenolysis through
the cAMP pathway, while cortisol and glucagon stimulate gluconeogenesis.
• Factors Affecting Surgical Response ----Age, Nutrition and diet, Anesthesia
and Operative stress
48. • Postoperatively, the utilization of glucose is reduced due to insulin
resistance, with an increase in triglyceride and free fatty acid break down
due to an increase in catecholamine secretion.
• The increase in the use of lipid does not affect glucose management.
However, the relative insulin resistance can be reduced by preoperative
glucose loading.
• The degree of hyperglycemia significantly affects postoperative outcome
and morbidity.
49. Metabolism During Fasting
• Comparable to changes seen in acute
injury
• Average human requires 25-40
kcal/kg/day of carbs, protein, fat
• Normal adult body contains 300-400g
carbs (glycogen) – 75-100g hepatic, 200-
250g muscle (not available systemically
due to deficiency of G6P)
50. • Following the first 24 hours of fasting, liver and kidney glycogen stores will
be depleted, and the glucose demand of tissues is provided by protein
degradation and gluconeogenesis.
• For the first 5 days of fasting, there is upto 75 g/day of protein degradation.
• After the fifth day, the stress hormone response decreases and protein
degradation levels decrease down to 15-20 g/day
Metabolism of Simple Starvation
• Lactate is not sufficient for glucose demands
• Protein must be degraded (75 g/d) for hepatic gluconeogenesis
• Proteolysis occurs from decreased insulin and increased cortisol
• Elevated urinary nitrogen (7 -> 30 g/d)
51. Metabolism of Prolonged Starvation
• Proteolysis is reduced to 20g/d and urinary nitrogen excretion stabilizes to
2-5g/d
• Organs (myocardium, brain, renal cortex, skeletal muscle) adapt to ketone
bodies in 2-24 days
• Kidneys utilize glutamine and glutamate in gluconeogenesis
• Adipose stores provide up to 40% calories (approx 160g FFA and glycerol)
• Stimulated by reduced insulin and increased glucagon and catecholamines
52. Modulation of Response
• Researchers have tested novel therapeutic strategies and options aimed at
selectively inhibiting the undesirable actions of cytokines while allowing
the appropriate responses to be expressed.
• Some effects of cytokines on target tissue have been successfully blocked
by the use of anticytokine antibodies and specific cytokine receptor
antagonists.
• Pharmacologic manipulation of the end-organ response to stress is also
accomplished with some drug classes that act on specific mediators of the
response.
53. • Control of hyperglycemia in critically ill surgical patients has been shown in
a large, prospective, randomized trial to decrease morbidity and mortality.
• Intensive insulin therapy (IIT) requires maintenance of blood glucose levels
below 110 mg/dL.
• Subsequent analysis found that increased mortality from hypoglycemic
events negates the benefits of IIT in clinical practice. Trauma patients,
however, were a subset found to having benefited the most from IIT.
• Further investigation is necessary to determine safe and effective
mechanisms for glycemic control in trauma patients.
54. • Hydrocortisone therapy: In trauma patients there is some evidence that
hydrocortisone therapy attenuates the stress response.
• Further research is needed to establish practical therapeutic strategies,
particularly in traumatic brain injury, in which high-dose steroids have been
associated with an increase in mortality.
• Human activated protein C (drotrecogin alfa [activated]) was one of the
first approved recombinant agents targeting the procoagulant and
generalized inflammatory response that occurs during sepsis.
55. • Pharmacologic manipulation of the response to traumatic injury has been
met with limited success.
• Research continues to attempt to identify agents that protect the patient
from the deleterious effects of the host response.
• Knowing which patient may benefit from a particular medication may be a
function of that individual’s unique DNA.
• Current studies have identified specific genetic polymorphisms that are
predictors of adverse outcomes in severe trauma and sepsis. Future
investigation may help develop individually tailored treatments.
56. Nutrition as Therapy
• The advantages of enteral nutrition over parenteral nutrition have been
clearly demonstrated, and the gastrointestinal tract should be used
whenever possible.
• The traditional preference is to feed patients by the enteral route for
reasons that include
oa reduction of the number of enteric organisms that may be responsible for
bacterial translocation.
ostimulation of the enterocyte brush border and gut associated lymphoid
tissue that is an important protective mechanism against the proliferation
of the offending organisms.
57. • The route of feeding may also have an impact on the production of
cytokines after injury; thus, use of the enteral route may confer an
additional advantage.
• Considerable attention has focused on nutrients that attenuate the
metabolic response to injury.
• Nutrients that appear to enhance the immune system include arginine,
glutamine, and nucleic acids. The immune system may be enhanced by
altering the relative amounts of omega-6 versus omega-3 unsaturated fatty
acids.
• Other nutrients may act as oxidants, preventing damage by free radicals,
such as the common antioxidants vitamins A, C, E, and the trace element
selenium.
58.
59. Conclusion
• Injury produces a series of physiologic changes mediated by local and
systemic agents and systemic effects. The metabolic response aims to
promote substrate delivery to the injured organs and promote healing.
• An understanding of the metabolic response allows the clinician to support
the patient through the physiologic changes associated with the stress
response caused by injury.
• Future research offers the promise of directly tailoring treatment and
modulating the metabolic response to minimize the impact of major
trauma.
60. References
• Oral and Maxillofacial Trauma 4th edition Fonseca
• Schwartz’s Principles of Surgery 11th edition
• Turgay Şimşek et al Response to trauma and metabolic changes:
posttraumatic metabolism Ulusal Cer Derg 2014; 30: 153-9
Editor's Notes
However, some of these responses may be counterproductive.
PIPBy activation of cellular processes designed to restore tissue function & eradicate invading micro-organism.(SIRS)
Compensatory anti inflammatory response syndrome down-regulated to minimize autogenous tissue injury. Prevent excessive pip phase---immunosuppression in critical pts
Cuthbertson first recognized the increases in
basal temperature,
energy expenditure,
oxygen consumption, and
also the loss of potassium and nitrogen.
catecholamines (adrenaline) are responsible for the increase in energy production and consumption.
Anabolic == begins with onset of recovery ..normalizatn of vital signs improved appetite and diuresis
The peak and duration of the response parallel the severity of the trauma.
↑ epinephrine, ↑norepinephrine,
↑vasopressin, and
↑dopamine.
The hypothalamic-pituitary axis is stimulated after the sympathetic nervous system after trauma.
The pituitary releases adrenocorticotropic hormone (corticotropin, or ACTH), which stimulates the adrenal cortex to secrete glucocorticoid hormones such as cortisol and aldosterone.
Severe injury activates the adrenergic system
Norepinephrine and Epinephrine increased 3-4 fold and remain elevated 24-48hrs after injury
Epinephrine causes hepatic glycogenolysis, gluconeogenesis, lipolysis and ketogenesis
Decreases insulin and glucagon secretion Major cause of stress induced hyperglycemia
Insulin
Stress inhibited release + peripheral insulin resistance = hyperglycemia
Tight control of glucose levels especialy in diabetics significantly reduces mortality after injury
Aldosterone
Synthesized, stored, released from the adrenal zona glomerulosa Maintains intravascular volume
Deficiency- hypotension, hyperkalemia
Excess- edema, HTN, hypokalemia, metabolic alkalosis
Growth Hormone
During anabolic -> protein synthesis, fat mobilization, and skeletal cartilage growth occurs
2˚ to release of insulin-like growth factor (IGF1)
Rapidly released or stored in neurons, skin, gastric mucosa, mast cells, basophils and platelets
Increased with hemorrhagic shock, trauma, thermal injury and sepsis
Magnitude of effects are proportional to severity of injury
Kinins increase inhibit gluconeogenesis, renal vasodilation, increases bronchoconstriction
C-reactive protein best reflects inflammation
Affected only by preexisting hepatic failure
Accuracy surpasses that of ESR
They enhance immune cell function and are responsible for the systemic effects of inflammation and sepsis, such as fever, leukocytosis, hypotension,delayed gastric emptying, and malaise.
effects, including the activation of resting T lymphocytes and macrophages, induction of hematopoietic growth factors, stimulation of chemotaxis of neutrophils, and synthesis of collagen and collagenases.
demonstrates the fluctuating levels of cytokine
receptors over time. Quantitative serum cytokine levels,
Monocytes
Downregulation of receptor TNFR
Platelets
Source of eicosanoids and vasoactive mediators
Clot is a chemoattractant for PMNs/monocytes
Modulate PMN endothelium adherence
Migration occurs within 3 hrs of injury
Mediated by serotonin, PAF, PGE2
Eosinophils
Migrate to parasitic infection release cytotoxic granules
Reside in the GI, lung, and GU tissues
Activated by IL-3, GM-CSF, IL-5, PAF, and anaphylatoxins C3a and C5a
Lipids and cytokines (e.g., IL-1, TNF, PAF) then prime these cells for enhanced superoxide anion release and sequestration in end organs.
This derangement can cause MOF
The sympathetic nervous system and catecholamines are mainly responsible from the increase in energy consumption.
In the surgical patients, knowledge of changes in amino acid, lipid, and carbohydrate metabolisms is important in determining the appropriate metabolic and nutritional support.
The energy necessary for the increased gluconeogenesis is provided from either lactate or amino acids in the liver.
Lipolysis is accelerated in the early period because of
The energy released by fat oxidation is the most important energy source for liver cells.
Since glucose is only partially oxidized, and 80-90% of the energy required for gluconeogenesis is derived from fat oxidation
Body lipid stores are durable and in large amounts.
In contrast to what is detected in prolonged fasting, glycolysis and proteolysis continues
The net changes in protein catabolism and synthesis are related to the duration and the level of injury.
tissues in organs such as the liver and kidneys were being preserved while skeletal muscles were particularly used for this purpose
Young men lose more nitrogen, whereas this loss is less in the elderly and women.
Previous physical condition of the patient, factors such as age and gender influence the degree of proteolysis.
During this period, protein turnover gradually decreases.
Protein gain is not due to increased protein synthesis but a consequence of decreased destruction.
During starvation, glucose production is carried out by using the protein storage. The proteolysis in this period mainly takes place in skeletal muscle, however, protein degradation is also observed in solid organs.
Leukocytes, macrophages, and endangered organs cannot perform mitochondrial respiration. Therefore, endogenous glucose production should increase in trauma patients (150% increase as compared to the control value). In this regard, glucose is an essential substrate since in a certain period of glycolysis oxygen is not required and energy supply continues during that period.
(where mitochondria has not yet developed).
The “fat” cannot reach here because capillaries have not yet developed, and they cannot be used as an energy source. Therefore, immune cells, fibroblasts, granulation tissue and brain tissue mainly use glucose.
The increaseed synthesis of glucose is essential for the continuation of human life in critical conditions and is important
Alanine mainly consists of lactate and amino groups in muscle.
Glucose may be synthesized from glycerol that results from adipose tissue destruction (lipolysis)
Insulin is the most important anabolic hormone in the body.
by primarily reducing muscle protein degradation, and supporting protein synthesis in the presence of amino acids.
by stimulating the formation of triglycerides and inhibiting their breakdown.
In all major stress conditions such as major surgery, the effect of insulin increases due to secretion of stress hormones like glucagon, catecholamines, cortisol and growth hormone and the inflammatory reaction generated by cytokines.
Age: As age increases, the hormonal response in the postoperative period lasts longer.
Nutrition and diet: Postoperative metabolic response is increased by preoperative nutritional support. Patients who received nutritional support for prolonged periods have more postoperative insulin resistance.
Anesthesia: The type of anesthesia also affects surgical stress response. LA<GA
Operative stress: Surgical trauma/stress level is one of the factors that affect the magnitude of inflammatory and metabolic response to surgery
Postoperative insulin resistance can be prevented in elective surgery by specific perioperative practices such as preoperative carbohydrate administration, and minimally invasive surgery.
The positive nitrogen balance ensures increase in protein synthesis, and a rapid and progressive increase of weight and muscle force.
Achieving maximum positive nitrogen balance of 4 g/day results in protein synthesis of approximately 25 g/day and body mass gain of 100 g/day (10)
A healthy 70kg adult will use 180 g /d of glucose to support obligate glycolytic cells (neurons, RBCs, PMNs, renal medulla, skeletal m.)
Glucagon, Norepinephrine, vasopressin, Angiotensis II promote utilization of glycogen stores
Glucagon, Epinephrine and cortisol promote gluconeogenesis
The successful management of the metabolic changes that accompany severe trauma influences and may prevent some of the major complications of trauma—
namely impaired immune function,multiple organ failure, and sepsis
Another problem with these therapies is that cytokines are rapidly released after injury, and the administration of antibodies, by necessity, occurs later—after the initiation of the cytokine cascade.
For example, cyclooxygenase inhibitors such as ibuprofen inhibit the production of eicosanoids and may thus blunt the physiologic response to cytokines, such as fever, associated with TNF, IL-1, and IL-6.
It had been initially found to reduce death rates in patients with severe sepsis.
Ongoing surveillance proved that there was no survival benefit in patients with severe sepsis when compared with placebo, and the drug has since been withdrawn from the market.
Recently, a role for supplemental parenteral nutrition has been advocated.
The concept of immunonutrition continues to evolve and, particularly within the last 5 years, the approach to the modulation of nutrition by timing to feed, amounts, route of administration, and composition of the nutritional product have yielded new information regarding how to optimally feed injured and critically ill patients
, mainly cytokines, hormones, and activation of the sympathetic nervous system
However, in the setting of severe trauma, these responses can result in organ injury.
These consequences can produce significant morbidity and mortality.