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Metabolic and Nutritional Support of the Trauma Patient

Metabolic and Nutritional Support of the Trauma Patient

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Metabolic and Nutritional Support of the Trauma Patient

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  1. Metabolic and Nutritional Support of the Trauma Patient Bradley J. Phillips, MD Burn-Trauma-ICU Adults & Pediatrics

  2. Historical Prospective(Metabolic and Nutritional Support) • “Starve a fever, feed a cold” • 300 BC ,100 AD - Aristotle, Galen -” vital heat “ • 1600’s Harvey, Van Helmont - heat related to circulation, heat is lost due to death • 1920’s Cuthbertson - hypermetabolic response to injury

  3. Metabolic response to injury The metabolic responses to critical illness /trauma evolve over time Metabolic needs reflexed the phase of the injury response Phases of the injury response : ebb,flow, convalescence

  4. Ebb phase: • 24 - 48 hrs • fluid retention • elevated counter Regulator hormones • glycogenolysis, Lipolysis

  5. EBB phase • Decrease cardiac output • Decrease oxygen consumption • Decrease temperature • Increase blood sugar, lactate levels, normal to low Insulin levels

  6. Flow phase: • - Post ebb ,variable time course • Hypermetabolic • muscle catabolism • Hyperglycemia • Elevated Free fatty acids

  7. Flow phase • Increase cardiac output • Increase body temperature • Increase 02 consumption • Increase blood sugar, Insulin

  8. Convalescence / Recovery Phase: • weeks to months • anabolic • decrease in total body edema, • return of GI function • weight gain

  9. Metabolic Response to Injury • Substrate mobilization: • mixed fuel of glucose,protein and Lipid. • Glucose via glycogen then hepatic and renal gluconeogenesis. (lactate, glycerol, alanine). • Protein from peripheral stores to provide alanine and substrates for hepatic acute phase proteins. • Lipid mobilized from peripheral stores via lipolysis to generate free fatty acids and glycerol.

  10. Neuroendocrine Response to Injury Counter Regulatory hormones Glucagon Epinephrine Norepinephrine Growth hormone Cortisol

  11. Cytokine Cascade • Releases from multiple cell types after injury or infection. • TNF  IL-1 and IL-6. • IL-1 > TNF, IL-6 stimulate pituitary - adrenal axis. • Glucocorticoids inhibit cytokine release, reduces cytokine MRNA.

  12. Neuroendocrine/Cytokine Response to Injury • Stimuli • Hemorrhage, ECF loss • Hypoxemia • Pain/anxiety • Change in temperature • Change in substrate availability • Tissue injury

  13. Injury/Stress : Carbohydrate metabolism • glycogenolysis • gluconeogenesis • increase liver production and peripheral uptake • insulin residence • hyperglycemia

  14. Carbohydrate Metabolism in stress HORMONES: counter - regulatory Glucagon, epinephrine, norepinephrine cortisol - counter act hypoglycemia Epinephrine -  glycogenolysis,  gluconeogenesis  glucagon Glucagon -  liver production of glucose, dose not effect clearance Insulin -  production from B cells, resistance Postreceptor Cortisol potentiates other hormones effects glucose,AA and Fatty acid metabolism

  15. Carbohydrate Metabolism in Stress Cytokines: TNF -  hepatic glucose productions,  glucose uptake in peripheral tissue IL - 1 -  plasma glucose -  hepatic production  peripheral glucose transport

  16. Injury/stress : Protein metabolism • Protein catabolism • Protein synthesis is up, but the net rate of brake down is greater. • AA mobilized from skeletal muscle to fuel wound healing , the cellular inflammatory response and acute phase protein production, AA oxidized for fuel • Protein catabolism poorly suppressed by exogenous fuels

  17. Protein Metabolism in stress Hormones - muscle counter regulatory hormones increase muscle protein brake down Cortisol,glucagon and catecholamines -  muscle breakdown GH/IGF-1 -  levels in stress anabolic Insulin - inhibits protein break down

  18. Protein metabolism in Stress Hormones - liver • epinephrine -  APP,  AA transport • glucagon -  APP,  AA transport • cortisol -  AA, enhance other hormone,cytokine effects • GH -  AA transport

  19. Protein Metabolism in Stress • CYTOKINES: • TNF, IL-I - increase protein breakdown in muscle, may inhabit effects of IGF - 1 • IL-6 -  APP production as do IL-I, TNF,IFN • Cytokines and hormones interact to effect protein synthesis in the liver and protein breakdown in muscle

  20. Injury/Stress : Lipid metabolism • Increases fat metabolism ,increased serum FFA,Triglycerides •  clearance of triglycerides,  lipoprotein lipase activity •  Lipolysis •  Synthesis of liver Apolipoproteins and triglycerides - denovo + recycled FFA

  21. Lipid Metabolism in stress • HORMONES: • Effect of counter regulator hormones on lipid metabolism unclear • Epinephrine  Lipolysis in adipose tissue • Glucagon -  FA synthesis in the liver • Cortisol -  FA synthesis in adipose tissue does not effect liver FA synthesis • Insulin -  FA synthesis in hepatocyte

  22. Lipid Metabolism in Stress Cytokines: TNF -  serum triglycerides -  hepatic FFA and triglyceride synthesis,  Lipolysis in adipose tissue  serum FFA; glycerol IL-1, IFN-’s -  Lipolysis,  Lipoprotein Lipase :effect many aspects of hepatic Fatty acid synthesis

  23. Metabolic Response to Injury • Substrate mobilization: • mixed fuel of glucose,protein and Lipid. • Glucose via glycogen then hepatic and renal gluconeogenesis. (lactate, glycerol, alanine). • Protein from peripheral stores to provide alanine and substrates for hepatic acute phase proteins. • Lipid mobilized from peripheral stores via lipolysis to generate free fatty acids and glycerol.

  24. Metabolic Response to Injury Ebb phase - fuel mobilization Flow phase - catabolic Convalescence - anabolic Counter Regulatory hormones Cytokines TNF,IL-1 and IL-6.

  25. Nutritional Assessment

  26. Nutritional Assessment • Who to feed ? • When and How to feed ? • What to feed ?

  27. Nutritional Assessment • Who to feed ? • Only those patients who will benefit • Only those patients whose risks of complications from malnutrition are greater then the risks of nutritional interventions

  28. Nutritional Assessment • Who to feed ? • Malnourished patients > 10% Wgt. Lose. • NPO > 5-7 days. • Patient expected to be NPO > 7-10 days.

  29. Nutritional Support • How: • Use the gut. • It’s natural. • Protects the patient from the TPN Doctor.

  30. Nutrient Composition • What to feed ? • How much energy ?

  31. Hypermetabolism of Injury • Major surgery 10% > baseline. • Trauma 25% > baseline. • Large burn injury 100% > baseline.

  32. Energy Requirements of Injury • Measured need : indirect calorimetry • E.E. = (3.94 x VO2 ) + (1.1 x VCO2 ) • Estimated energy needs: Harris-Benedict • men: EE= 66+(13.8xwgt) + (5xHt) -(6.8xage) • women: EE= 665+ (9.6xwgt) + (1.7xHt) - (4.7xAge) • 25kcal/Kg/day.

  33. Indirect calorimetry Metaboliccart

  34. Indirect Calorimetry Metabolic cart in critical illness • Resting energy expenditure of critically ill patients varies widely over the course of the day and over the course of an illness • Measurements from - 10 % to + 23 % of an “average” REE can be seen within a 24 hour period

  35. Indirect Calorimetry Predicting REE Harris-Benedict is correct 80-90% of the time in healthy, normal volunteers. In 10-14% it over estimates EE In obese normal volunteers it predicts EE correctly in only 40-64% in critically ill patients the Harris-Benedict equation is correct only 50% of the time For most disease processes Harris -Benedict underestimates EE

  36. Indirect Calorimetry Predicting REE Multipliers for various disease states attempt to improve the accuracy of the Harris-Benedict equation These multipliers tend to overestimate EE when compared to indirect calorimetry

  37. Nutrient Composition - Energy • Complications of under feeding ? • Morbidity and mortality of malnutrition • Complications of over feeding? • Hyperglycemia, fatty liver , respiratory failure, immunosuppression,etc . • 25kcal/Kg/day will avoid over or under feeding of most critically ill patients.

  38. Nutrient Composition • What ? • Protein. • Carbohydrate. • Fat.

  39. Substrate Provision Protein: metabolic stress leads to; proteolysis of skeletal muscle,increased Hepatic synthesis of APP,increased use of AA for energy production. Net nitrogen lose • 1.5 gram/kg/day. • > 1.4 gram/kg/day leads to both an increase in protein synthesis and catabolism with no net gain for the patient. • Glutamine, Arginine.

  40. Substrate Provision • Carbohydrates: • Glucose primary fuel for the injury response. • Injury/stress effect ability to oxidize glucose • Stable post-op patient maximum glucose oxidation rate 7mg/kg/min. • Stressed patient maximum glucose oxidation rate 5mg/kg/min.

  41. Substrate Provision • Carbohydrates: • maximum glucose oxidation rate: 5mg/kg/min. • Avoid: over feeding, hyperglycemia (BS < 220 mg/dL).

  42. PREVALENCE OF HYYPRGLECEMIA • IN TPN PATIENTS • 260 TPN patients screened, 102 low risk patients evaluated . 22 % ( 23/102) of low risk patients had BS > 200mg/dl • Glucose infusion:mg/Kg/min < 4 4.1 - 5 > 5 • Patients BS > 200 mg/dl 0 (0 %) 5 (11 %) 18 (50 %) • Patients BS < 200 mg/dl 18 41 19 • Rosemarin DK, et al, Nutri. Clin Pract, 1996;11:151-6

  43. Substrate Provision • Carbohydrates: • maximum glucose oxidation rate: 5mg/kg/min.

  44. Substrate Provision- lipid Lipid: Fat metabolism is increased in stress, increased lipolysis, increased fatty acid oxidation, increased production and release from the liver . Lipid administration prevents essential fatty acid deficiency ,spares protein. Lipid administration has cardiopulmonary and immunologic effects

  45. Substrate Provision • Lipids: • Provide EFA’s. • Provide calories that avoid hyperglycemia. • Mixed fuel may enhance protein sparing. • Cardiovascular effects. • Immunologic effects. • giving lipid in low concentrations and slowly <0.1 gr/kg/hr of iv lipid

  46. Substrate Provision • Lipids: • Cardiopulmonary effects. Alterations in diffusion,shunting and oxygenation • Immunologic effects. Overload REE system,impair neutrophil chemotaxis, modulate eicosanoid production • Effects can be modulated by : choice of lipid; giving lipid in low concentrations and slowly; <0.11gr/kg/hr of iv lipid

  47. Effects of IV Lipid in Trauma Patients: Trauma Patients Lipid (n=30) No Lipid (n=27) P Age 33 ± 10 32 ± 9 _ ISS 27 ± 8 30 ± 9 _ Apache II 25 ± 6 22 ± 5 _ On Ventilator* 27 ± 21 15 ± 12 0.01 ICU Los* 29 ± 22 18 ± 12 0.02 Hospital Los* 39 ± 24 27 ± 16 0.03 Survival 30/30 25/27 Non-protein kcal/kg 29 ± 2 22 ± 1 % kcal as Lipid 25 ± 4 0 Amino Acids (g/kg-d) 1.6 ± 0.2 1.5 ± 0.1 * in days, LOS = length of stay Data expressed means ± SD Battistella et al. J Trauma 39: 164, 1995

  48. Conclusion • N.S. essential to Rx/avoid malnutrition and its complication. • N.S. only helpful for patients at risk and if given correctly. • Avoid over feeding. • Avoid hyperglycemia. • Lipid at low concentrations, given slowly.

  49. Nutritional Support • Energy - 25 kcal/kg/day • Glucose - Do not exceed 5mg/kg/min • Protein - 1.5 gr/kg/day • Lipid - Do not exceed 0.11 gr/kg/hr

  50. Conclusion • Metabolic response to injury evolve over time . • Responses are under hormonal and cytokine control • Hypermetabolism after injury is variable. • Nitrogen loss, muscle wasting and hyperglycemia. • Outcome from injury can be enhanced by the judicious use of nutritional support.