Metabolic and Nutritional Support of the Trauma Patient

Bradley J. Phillips, MD

Burn-Trauma-ICUAdults & 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

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

Metabolic response to injury

Ebb phase:24 - 48 hrsfluid retentionelevated counter Regulator hormonesglycogenolysis, 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 hormonesGlucagon

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 downCortisol,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

MetabolicMetabolic cartcart

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 attemptto improve the accuracy of the Harris-Benedict equation

These multipliers tend to overestimate EE when compared to indirect calorimetry

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 ProvisionProtein:

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 < 4 4.1 - 5 >5Patients 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

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

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 0.01ICU Los* 29 ± 22 18 ± 12 0.02Hospital Los* 39 ± 24 27 ± 16 0.03

Survival 30/30 25/27Non-protein kcal/kg 29 ± 2 22 ± 1% kcal as Lipid 25 ± 4 0Amino Acids (g/kg-d) 1.6 ± 0.2 1.5 ± 0.1

* in days, LOS = length of stayData expressed means ± SDBattistella et al. J Trauma 39: 164, 1995

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 - 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

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…?