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

9. 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

10. 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

11. Ebb phase:
hrs
fluid retention
elevated counter Regulator hormones
glycogenolysis, Lipolysis

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

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

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

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

16. 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.

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

18. Cytokine Cascade TNF  IL-1 and IL-6.
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.

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

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

21. 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

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

23. 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

24. 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

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

26. 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

27. 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

28. 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

29. 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

30. 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.

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

32. Nutritional Assessment

33. Nutritional Assessment
Who to feed ?
When and How to feed ?
What to feed ?

34. 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

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

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

37. Nutrient Composition
What to feed ?
How much energy ?

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

39. 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.

40. Indirect calorimetry
Metabolic cart

41. Metabolic cart in critical illness
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

42. Predicting REE Harris-Benedict is correct 80-90% of the time
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

43. Predicting REE Multipliers for various disease states attempt
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

44. 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.

45. Nutrient Composition
What ?
Protein.
Carbohydrate.
Fat.

46. 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.

47. 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.

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

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

50. Substrate Provision Carbohydrates:
maximum glucose oxidation rate: mg/kg/min.

51. 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

52. 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

53. 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

54. Effects of IV Lipid in Trauma Patients:
Lipid (n=30) No Lipid (n=27) P
Age ± ± _
ISS ± ± _
Apache II ± ± _
On Ventilator* ± ±
ICU Los* ± ±
Hospital Los* ± ±
Survival / /27
Non-protein kcal/kg ± ± 1
% kcal as Lipid ±
Amino Acids (g/kg-d) ± ± 0.1
* in days, LOS = length of stay
Data expressed means ± SD
Battistella et al. J Trauma 39: 164, 1995

55. 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.

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

57. 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.

58. Questions…?