Metabolic response to trauma

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Metabolic Response to trauma

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  • The ebb phase is characterized by hypovolemic shock. Cardiac output, oxygen consumption and blood pressure all decrease, thereby reducing tissue perfusion. These mechanisms are usually associated with hemorrhage. Body temperature drops. The reduction in metabolic rate may be a protective mechanism during this period of hemodynamic instability.
    Cuthbertson DP, et al. Adv Clin Chem 1969;12:1-55Welborn MB. In: Rombeau JL, Rolandelli RH, eds. Enteral and Tube Feeding. 3rd ed. Philadelphia, PA: WB Saunders; 1997.
  • The ebb phase is characterized by hypovolemic shock. Cardiac output, oxygen consumption and blood pressure all decrease, thereby reducing tissue perfusion. These mechanisms are usually associated with hemorrhage. Body temperature drops. The reduction in metabolic rate may be a protective mechanism during this period of hemodynamic instability.
    Cuthbertson DP, et al. Adv Clin Chem 1969;12:1-55Welborn MB. In: Rombeau JL, Rolandelli RH, eds. Enteral and Tube Feeding. 3rd ed. Philadelphia, PA: WB Saunders; 1997.
  • Endocrine response in the form of increased catecholamines, glucocorticoids and glycogen, leads to mobilization of tissue energy reserves. These calorie sources include fatty acids and glycerol from lipid reserves, glucose from hepatic glycogen (muscle glycogen can only provide glucose for the involved muscle) and gluconeogenic precursors (eg, amino acids) from muscle.
  • Trauma or critically ill patients should not be overfed. Alterations in serum glucose and lipid levels, development of fatty liver, and electrolyte shifts have been associated with overfeeding.
    Barton RG. Nutr Clin Pract 1994;9:127-139.
  • Delivery of appropriate substrates or macronutients is essential. Patients require at least 100g of glucose per day during metabolic stress to prevent ketosis. During hypermetabolic stress, a carbohydrate level of 30%-40% of total calories is recommended. Glucose intake should not exceed 5 mg/kg/min.
    Barton RG. Nutr Clin Pract 1994;9:127-139.
    ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA.
  • Dietary fat should provide between 20-35% of total calories. Maximum recommended infusion rate when administering intravenous lipids is 1.0-1.5 g/kg/day. Serum triglyceride levels in stressed patients should be monitored to ensure adequate lipid clearance.
    Barton RG. Nutr Clin Pract 1994;9:127-139.
    ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA
  • Protein requirements increase during metabolic stress and are estimated at between 1.2-2.0 g/kg/day, or approximately 20% to 30% of the total calorie intake during stress.
    Barton RG. Nutr Clin Pract 1994;9:127-139.
    ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA
  • Calorie-to-nitrogen ratios can be used to prevent lean body mass from being utilized as a source of energy. Therefore, in the non-stressed patient, less protein is necessary to maintain muscle as compared to the severely stressed patient.
    Nitrogen balance can be affected by the biological value of the protein as well as by growth, caloric balance, sepsis, surgery, activity (bed rest and lack of muscle use can promote nitrogen excretion), and by renal function.
  • Glutamine is one of the few nutrients included in the category of conditionally-essential amino acids.
    Glutamine is the body’s most abundant amino acid and is involved in many physiological functions. Plasma glutamine levels decrease drastically following trauma.
    It has been hypothesized that this drop occurs because glutamine is a preferred substrate for cells of the gastrointestinal cells and white blood cells. Glutamine helps maintain or restore intestinal mucosal integrity.
    Smith RJ, et al. JPEN 1990;14(4 Suppl):94S-99S.
    Pastores SM, et al. Nutrition 1994;10:385-390.
    Calder PC. Clin Nutr 1994;13:2-8.
    Furst P. Eur J Clin Nutr 1994;48:607-616.
    Standen J, Bihari D. Curr Opin Clin Nutr Metab Care 2000;3:149-157.
  • Arginine is also considered a conditionally essential amino acid. Barbul and colleagues showed that arginine supplements increased thymus weight in uninjured rats and decreased thymus involution from trauma.
    (Barbul A, et al. J Surg Res 1980;29:228-235)
    In studies on humans and animals, arginine supplements increased nitrogen retention and immune function and improved wound healing.
    Arginine plays other roles that are not well understood; for instance as a scretagogue (growth hormone), precursor for polyamines and nitric oxide. Therefore, one should avoid providing more than 2% of total calories as arginine.
    Because arginine is considered an immune-enhancing nutrient, it may not be appropriate to feed supplemental arginine to septic or inflammatory patients whose immune system is already stimulated and where addition of arginine supplementation may be detrimental.
    Barbul A. JPEN 1986; 10: 227-238
    It is worth noting that the studies on the use of arginine supplementation were done with patients in the early phase of stress.
  • Micronutrient, trace element, vitamin, and mineral requirements of metabolically stressed patients seem to be elevated above the levels for normal healthy people.
    There are no specific dosage guidelines for micronutrients and trace elements, but there are plausible theories supporting their increased intake.
    This slide lists some of these nutrients along with the rationale for their inclusion.
  • Lesson objectives are:
    Explain the differences between metabolic responses to starvation and trauma.
    Explain the effect of trauma on metabolic rate and substrate utilization.
    Determine calorie and protein requirements during metabolic stress.
    This session will also review macronutrients during metabolic stress, highlighting the role of conditionally-essential nutrients in specific situations.
  • Metabolic response to trauma

    1. 1. Metabolic Response to Trauma Presented by Dr. Mohammed haneef
    2. 2.  INTRODUCTION  ClASSIFICATION  FEATURES OF METABOLIC RESPONSE  FACTORS MEDIATING METABOLIC RESPONSE  CONSEQUENCES OF METABOLIC RESPONSE  FACTORS MODIFYING METABOLIC RESPONSE  APPLIED ASPECTS
    3. 3. • Following accidental or deliberate injury, a characteristic series of changes occurs, both locally at the site of injury and within the body generally; these changes are intended to restore the body to its pre-injury condition. • The magnitude of the metabolic response is generally proportional to the severity of tissue injury and the presence of ongoing stimulation but can be modified by additional factors such as infection • The response to injury has probably evolved to aid recovery,by mobilizing substrates and mechanisms of preventing infection, and by activating repair processes • Although the metabolic response aims to return an individual to health, a major response can damage organs distant to the injured site itself. • In modern surgery, a major goal is to minimize the metabolic response to surgery in order to shorten recovery times.
    4. 4. • Classically, these responses have been described as stress response, a term coined by the scottish chemist CUTHBERTSON in 1932. • Intial response is directed at maintaining adequate substrate suppy to the vital organs, in particular oxygen and energy • When the inflammatory response impairs function of organs or organ systems, the term multiple organ dysfunction syndrome is applied (MODS) • SIRS, systemic infalmatory response syndrome is a the term used to describe the body’s response to infections and noninfectious causes and consists of two or more of the following • Hyper/hypo thermia • Leukopenia/ leukocytosis • Tachycardia • Tachyapnea
    5. 5. Classification • Aller and colleagues propose a modern perspective on the metabolic events associated with the inflammatory response to major trauma • the "ischemia/reperfusion phenotype” –phenotype represents the immediate, nervous system-related alteration in response to injury, in which neuronal and humoral responses and edema formation predominate. This phase is characterized by regulating the metabolic supply to cells via the least elaborate mechanism:diffusion. • the "leukocytic phenotype“ – is characterized as the intermediate (or "immune") phase of the metabolic response to trauma. This phase is characterized by leukocytic and bacterial infiltration of previously damaged tissues, which occurs in an edematous, oxygen-poor environment. The resulting post-shock hypercatabolism and hypermetabolism is related to a hyperdynamic response with increased body temperature, increased oxygen consumption, glycogenolysis,lipolysis, proteolysis and futile substrate cycling • The “ Angeogenic phase “- third ("angiogenic") phenotype is defined as the late (or"endocrine") phase of systemic response to injury. This phase is characterized by a return of oxidative metabolism,favoring angiogenesis in damaged tissues and organs. This process creates a capillary bed that facilitates tissue repair and regeneration
    6. 6. Ebb and Flow phases • Trauma causes major alterations in energy and protein metabolism. • The response to trauma can be divided into the ebb phase and the flow phase. The ebb phase occurs immediately after trauma and lasts from 24-48 hours followed by the flow phase. After this, comes the anabolism phase and finally, the fatty-replacement phase.
    7. 7. • Unmodified metabolic response • Ebb phase -phase of metabolic response to acute stress • Flow phase - phase of metabolic response after operation • Anbolic phase - recovery from operation Time EnergyExpenditure Ebb Phase Ebb Phase Flow Phase Flow Phase
    8. 8. Metabolic Response to Trauma: Ebb Phase (upto 24 hours)• Characterized • Hypovolemic shock • reversible • Irreversible • Release of Catacholamines/ vasoactive hormones • ↑ Cardiac Output • Peripheral Vasoconstriction • ↑ Respiratory Rate • Delivery of Maximum oxygen Levels • ↑ Blood Glucose • Mobilization of free Fatty acids Fonseca : Oral and Maxillofacial Trauma Vol.1
    9. 9. Metabolic Response to Trauma: Flow Phase (may last for weeks)∀↑ Catecholamines ∀↑ basal metabolic Rates ∀↑ Glucocorticoids ∀↑ Glucagon • Release of cytokines, lipid mediators • Acute phase protein production Fonseca : Oral and Maxillofacial Trauma Vol.1
    10. 10. Anabolic phase • Recovery • restoration of lean body mass, weight and well being
    11. 11. Metabolic Response to Trauma Fatty Deposits Liver & Muscle (glycogen) Muscle (amino acids) Fatty Acids Glucose Amino Acids Endocrine Response
    12. 12. • Endocrine response in the form of increased catecholamines, glucocorticoids and glycogen, leads to mobilization of tissue energy reserves. These calorie sources include fatty acids and glycerol from lipid reserves, glucose from hepatic glycogen (muscle glycogen can only provide glucose for the involved muscle) and gluconeogenic precursors (eg, amino acids) from muscle.
    13. 13. Flow phase Phenomenon Effect ↑ catecholamine ↑ glucagon ↑ cortisol ↑ insulin ↑ cardiac output ↑ core body temperature ↑ aldosterone ↑ ADH IL1, IL6, TNF spillage from wound ↑ consumption of glucose, FFA, amino acid ↑ O2 consumption fluid retention systemic inflammatory response N or ↑ glucose N or ↑ FFA normal lactate ↑ CO2 production ↑ heat production multi-organ failure
    14. 14. Metabolic response Sequence of events surgical problem ± infection operation bleeding tissue trauma bacterial contamination necrotic debris local inflammatory response wound healing recovery hypermetabolism muscle wasting immunosuppression organ failure mortality * * mortality food deprivation wound pain infection immobility Ebb phase Flow phase Anabolic phase *acute stress
    15. 15. Comparison of metabolic response between ebb and flow phase Ebb phase Flow phase Blood glucose level ↑ N or ↑ Glucose production N ↑ Free fatty acid level ↑ N or ↑ Insulin concentration ↓ N or ↑ Catecholamine ↑ ↑
    16. 16. Comparison of metabolic response between ebb and flow phase (con’t) Ebb phase Flow phase Glucagon ↑ ↑ Blood lactate level ↑ N Oxygen consumption ↓ ↑ Cardiac output ↑ ↑ Core temperature ↓ ↑
    17. 17. Strategy to attenuate metabolic response to surgery During ebb phase •Prompt fluid and blood replacement to maintain blood pressure •Adequate oxygen supply and ventilation •Cardiovascular support by inotropes •Antibiotics During flow phase •Nutritional support •Warm room temperature •Mobilization •Hemodialysis •Timely intervention for complication
    18. 18. • Neuroendocrine Response • Lipid Derived Mediators • Cytokines
    19. 19. • Upregulation of sympathoadrenal axis • ↑ epinephrine inhibition of Glucose uptake • ↑nor epinephrine promotes glucagon secreation • ↑Vasopressin promotes lipolysis • ↑ dopamine gluconeogenesis • Stimulation of hypothalamic – pituitary axix
    20. 20. Cytokine Mediated response • Polypeptide hormones, protein mediators • Act locally (paracrine)/ systemically (endocrine) • Responsible for • Fever • Leucocytosis • Hypotension • malaise • Important cytokines: • TNF • IL-1 • IL-2 • IL-6 • IL-8 • Released by: • Monocytes • Lymphocytes • Marcophages
    21. 21. Lipid derived mediators • Act by: • Enhanced superoxide production • Enchanced platelet aggregation • Changes in endothelial permeability • Altered pulmonary vascular reactivity
    22. 22. Metabolic Response to Overfeeding • Hyperglycemia • Hypertriglyceridemia • Hypercapnia • Fatty liver • Hypophosphatemia, hypomagnesemia, hypokalemia Trauma or critically ill patients should not be overfed. Alterations in serum glucose and lipid levels, development of fatty liver, and electrolyte shifts have been associated with overfeeding.
    23. 23. Macronutrients during Stress Carbohydrate •At least 100 g/day needed to prevent ketosis •Carbohydrate intake during stress should be between 30%-40% of total calories •Glucose intake should not exceed 5 mg/kg/min Barton RG. Nutr Clin Pract 1994;9:127-139 ASPEN Board of Directors. JPEN 2002; 26 Suppl 1:22SA
    24. 24. Macronutrientes during Stress Fat •Provide 20%-35% of total calories •Maximum recommendation for intravenous lipid infusion: 1.0 -1.5 g/kg/day •Monitor triglyceride level to ensure adequate lipid clearance Barton RG. Nutr Clin Pract 1994;9:127-139 ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA
    25. 25. Macronutrients during Stress Protein •Requirements range from 1.2-2.0 g/kg/day during stress •Comprise 20%-30% of total calories during stress Barton RG. Nutr Clin Pract 1994;9:127-139 ASPEN Board of Directors. JPEN 2002;26 Suppl 1:22SA
    26. 26. Determining Protein Requirements for Hospitalized Patients Stress Level Calorie:Nitrogen Ratio Percent Potein / Total Calories Protein / kg Body Weight No Stress < 15% protein 0.8 g/kg/day Moderate Stress 15-20% protein 1.0-1.2 g/kg/day 1.5-2.0 g/kg/day > 20% protein Severe Stress
    27. 27. • Calorie-to-nitrogen ratios can be used to prevent lean body mass from being utilized as a source of energy. Therefore, in the non-stressed patient, less protein is necessary to maintain muscle as compared to the severely stressed patient. • Nitrogen balance can be affected by the biological value of the protein as well as by growth, caloric balance, sepsis, surgery, activity (bed rest and lack of muscle use can promote nitrogen excretion), and by renal function.
    28. 28. Role of Glutamine in Metabolic Stress •Considered “conditionally essential” for critical patients •Depleted after trauma •Provides fuel for the cells of the immune system and GI tract •Helps maintain or restore intestinal mucosal integrity Smith RJ, et al. JPEN 1990;14(4 Suppl):94S-99S; Pastores SM, et al. Nutrition 1994;10:385-391 Calder PC. Clin Nutr 1994;13:2-8; Furst P. Eur J Clin Nutr 1994;48:607-616 Standen J, Bihari D. Curr Opin Clin Nutr Metab Care 2000;3:149-157
    29. 29. • Glutamine is one of the few nutrients included in the category of conditionally-essential amino acids. • Glutamine is the body’s most abundant amino acid and is involved in many physiological functions. Plasma glutamine levels decrease drastically following trauma. • It has been hypothesized that this drop occurs because glutamine is a preferred substrate for cells of the gastrointestinal cells and white blood cells. • Glutamine helps maintain or restore intestinal mucosal integrity.
    30. 30. Role of Arginine in Metabolic Stress • Provides substrates to immune system • Increases nitrogen retention after metabolic stress • Improves wound healing in animal models • Stimulates secretion of growth hormone and is a precursor for polyamines and nitric oxide • Not appropriate for septic or inflammatory patients. Barbul A. JPEN 1986;10:227-238; Barbul A, et al. J Surg Res 1980;29:228-235
    31. 31. Key Vitamins and Minerals Vitamin A Vitamin C B Vitamins Pyridoxine Zinc Vitamin E Folic Acid, Iron, B12 Wound healing and tissue repair Collagen synthesis, wound healing Metabolism, carbohydrate utilization Essential for protein synthesis Wound healing, immune function, protein synthesis Antioxidant Required for synthesis and replacement of red blood cells
    32. 32. • Micronutrient, trace element, vitamin, and mineral requirements of metabolically stressed patients seem to be elevated above the levels for normal healthy people. • There are no specific dosage guidelines for micronutrients and trace elements, but there are plausible theories supporting their increased intake. • This slide lists some of these nutrients along with the rationale for their inclusion.
    33. 33. Factors influencing the Extent and Duration of the Metabolic Response • Pain and Fear • Surgical Factors: • Type of surgery • Region • Duration • Preoperative support • Extent of the trauma and degree of resuscitation • Post traumatic complications: • Hemorrhage • Hypoxia • Sepsis and Fever • Re-operation • Pre-existing nutritional status • Age and sex • Anaesthetic considerations
    34. 34. Methods to Minimize the Metabolic Response • Replace blood and fluid losses • Maintain Oxygenation • Give adequate nutrition • Provide Analgesia • Avoid Hypothermia
    35. 35. Consequences of the Response • Limiting injury • Initiation of repair processes • Mobilization of substrates • Prevention of infection • Distant organ damage
    36. 36. Strategy to attenuate metabolic response to surgery Principles • No effective strategy to attenuate metabolic response • Supportive measures are available • Perfect surgery is essential
    37. 37. Strategy to attenuate metabolic response to surgery During ebb phase • Prompt fluid and blood replacement to maintain blood pressure • Adequate oxygen supply and ventilation • Cardiovascular support by inotropes • Antibiotics
    38. 38. Strategy to attenuate metabolic response to surgery During flow phase • Nutritional support • Warm room temperature • Mobilization • Hemodialysis • Timely surgery for complication
    39. 39. References • Fonseca trauma Vol.1 • Metabolic response to trauma (The journal of Bone and Joint Surgery) • Clinical aspects of the metabolic response to trauma (The american Journal of Clinical Nutrition: Vol.3, Number 3) • Metabolic response to trauma ( Australian journal of physiotherapy) • Manipulating the metabolic response to injury (British medical bulletin 1999;55 (no.1): 181-195) • The metabolic response to stress: an overview and update (Anesthesiology 73:308-327, 1980)

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