Metabolic and Nutritional Support
of the Trauma Patient
Bradley J. Phillips, MD
Burn-Trauma-ICU
Adults & Pediatrics
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
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
Ebb phase:
24 - 48 hrs
fluid retention
elevated counter Regulator hormones
glycogenolysis, Lipolysis
EBB phase
– Decrease cardiac output
– Decrease oxygen consumption
– Decrease temperature
– Increase blood sugar, lactate levels, normal
to low Insulin levels
Flow phase:
- Post ebb ,variable time course
– Hypermetabolic
– muscle catabolism
– Hyperglycemia
– Elevated Free fatty acids
Flow phase
•
•
•
•
Increase cardiac output
Increase body temperature
Increase 02 consumption
Increase blood sugar, Insulin
Convalescence / Recovery Phase:
– weeks to months
– anabolic
– decrease in total body edema,
– return of GI function
– weight gain
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.
Neuroendocrine Response to
Injury
Counter Regulatory hormones
Glucagon
Epinephrine
Norepinephrine
Growth hormone
Cortisol
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.
Neuroendocrine/Cytokine
Response to Injury
• Stimuli
– Hemorrhage, ECF loss
– Hypoxemia
– Pain/anxiety
– Change in temperature
– Change in substrate availability
– Tissue injury
Injury/Stress : Carbohydrate
metabolism
– glycogenolysis
– gluconeogenesis
– increase liver production and peripheral
uptake
– insulin residence
– hyperglycemia
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
Carbohydrate Metabolism in
Stress
Cytokines:
TNF -  hepatic glucose productions,  glucose
uptake in peripheral tissue
IL - 1 -  plasma glucose -  hepatic production 
peripheral glucose transport
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
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
-
Protein metabolism in Stress
Hormones - liver
– epinephrine -  APP,  AA transport
– glucagon -  APP,  AA transport
– cortisol -  AA, enhance other hormone,cytokine
effects
– GH -  AA transport
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
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
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
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
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.
Metabolic Response to Injury
Ebb phase - fuel mobilization
Flow phase - catabolic
Convalescence - anabolic
Counter Regulatory hormones
Cytokines TNF,IL-1 and IL-6.
Nutritional Assessment
Nutritional Assessment
• Who to feed ?
• When and How to feed ?
• What to feed ?
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
Nutritional Assessment
• Who to feed ?
• Malnourished patients > 10% Wgt. Lose.
• NPO > 5-7 days.
• Patient expected to be NPO > 7-10 days.
Nutritional Support
• How:
– Use the gut.
– It’s natural.
– Protects the patient from the TPN Doctor.
Nutrient Composition
• What to feed ?
• How much energy ?
Hypermetabolism of Injury
• Major surgery 10% > baseline.
• Trauma 25% > baseline.
• Large burn injury 100% > baseline.
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.
• Indirect calorimetry
Metabolic cart
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
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
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
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.
Nutrient Composition
• What ?
• Protein.
• Carbohydrate.
• Fat.
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.
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.
Substrate Provision
• Carbohydrates:
– maximum glucose oxidation rate:
5mg/kg/min.
– Avoid: over feeding, hyperglycemia (BS < 220
mg/dL).
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
Patients BS > 200 mg/dl
Patients BS < 200 mg/dl
<4
0 (0 %)
18
Rosemarin DK, et al, Nutri. Clin Pract, 1996;11:151-6
4.1 - 5
5 (11 %)
41
>5
18 (50 %)
19
Substrate Provision
• Carbohydrates:
– maximum glucose oxidation rate:
5mg/kg/min.
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
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
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
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*
ICU Los*
Hospital Los*
27 ± 21
29 ± 22
39 ± 24
15 ± 12
18 ± 12
27 ± 16
Survival
Non-protein kcal/kg
% kcal as Lipid
Amino Acids (g/kg-d)
30/30
29 ± 2
25 ± 4
1.6 ± 0.2
25/27
22 ± 1
0
1.5 ± 0.1
* in days, LOS = length of stay
Data expressed means ± SD
Battistella et al. J Trauma 39: 164, 1995
0.01
0.02
0.03
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.
Nutritional Support
•
•
•
•
Energy Glucose Protein Lipid -
25 kcal/kg/day
Do not exceed 5mg/kg/min
1.5 gr/kg/day
Do not exceed 0.11 gr/kg/hr
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.
Questions…?