Nutritional Management Following Injury

Lauri O. Byerley, PhD, RD

Gain appreciation for the importance of nutrition in helping your patients heal and physically improve.

Goal

Case Study Phases of Injury Physiological and Metabolic Consequence of

Each Phase Nutrition Support for Each Phase Summarize

Outline

25 YOWM in a MVA 9 months ago Suffered multiple fractures, contusions and

closed head injury Stayed 5 weeks in intensive care unit

◦ After 1 week – responded to physical stimuli but not verbal

◦ After 3 weeks – opened eyes and started responding to sound but not verbal commands

Case Study

http://www.car-accidents.com/2008-collision-pics/3-23-08-head-injury-1.jpg

Define Injury or Stress Trauma Surgery Sepsis (infection) Burn

Hypermetabolic Response to Stress

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.

Initial shock or ebb phase◦ Brief (<24 hours)◦ Metabolism depressed

Flow phase◦ Catabolic

Tissue Breakdown◦ Anabolic

Lost tissue is reformed

Phases of Injury

Immediate Physiologic and Metabolic Changes after Injury or Burn

ADH, Antiduretic hormone; NH3, ammonia.

Metabolic Response to Stress Involves most metabolic pathways Accelerated metabolism of LBM Negative nitrogen balance Muscle wasting

Ebb Phase <24 hours Hypovolemia, shock, tissue hypoxia Decreased cardiac output Increased heart rate Vasoconstriction Decreased oxygen consumption Decreased BMR Lowered body temperature Increased acute phase proteins Insulin levels drop because glucagon is

elevated.

Hormones involved:◦ Catecholamines◦ Cortisol◦ Aldosterone

Ebb Phase continued

Catabolic Flow Phase 3-10 days Increased body temperature Increased BMR Increased O2 consumption Total body protein catabolism begins

(negative nitrogen balance) Marked increase in glucose production,

FFAs, circulating insulin/glucagon/cortisol Insulin resistance

Hormones involved:◦ Glucagon (↑)◦ Insulin (↑)◦ Cortisol (↑)◦ Catecholamines (↑)

Catabolic Flow Phase continued

Anabolic Flow Phase 10-60 days Protein synthesis begins Positive nitrogen balance

Hormones involved:◦ Growth hormone◦ IGF

Anabolic Flow Phase continued

Skeletal Muscle Proteolysis

From Simmons RL, Steed DL: Basic science review for surgeons, Philadelphia, 1992, WB Saunders.

Metabolic Changes in Starvation

From Simmons RL, Steed DL: Basic science review for surgeons, Philadelphia, 1992, WB Saunders.

Starvation vs. Stress

Metabolic response to stress ≠ metabolic response to starvation

Starvation = ◦ decreased energy expenditure◦ use of alternative fuels◦ decreased protein wasting◦ stored glycogen used in 24 hours

Late starvation = fatty acids, ketones, and glycerol provide energy for all tissues except brain, nervous system, and RBCs

Starvation vs. Stress—cont’d Stress or Injury (Hypermetabolic state) =

◦ Accelerated energy expenditure, ◦ Increased glucose production ◦ Increased glucose cycling in liver and muscle

Hyperglycemia can occur either◦ Insulin resistance or◦ Excess glucose production via

gluconeogenesis and Cori cycle

***Muscle breakdown accelerated***

Hypermetabolic Response to Stress—Pathophysiology

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.

Hypermetabolic Response to Stress—Medical and Nutritional Management

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Maion F. Winkler and Ainsley Malone, 2002.

Maintain body mass, particularly lean body mass Prevent starvation and specific nutrient deficiencies Improve wound healing Manage infections Restore visceral and somatic protein losses Avoid or minimize complications associated with

enteral and parenteral nutrition Provide the correct amount and mix of nutrients to

limit or modulate the stress response and complications

Fluid management

Goals of nutritional support

Extent of injury will determine nutritional support.◦ Laceration, broken arm → case study

25 YOWM in a MVA 9 months ago◦ What do for him during this phase?

Case Study – Ebb Phase

http://www.car-accidents.com/2008-collision-pics/3-23-08-head-injury-1.jpg

Nutrition Objectives Objectives of optimal metabolic and

nutritional support in injury, trauma, burns, sepsis:

1. Detect and correct preexisting malnutrition2. Prevent progressive protein-calorie malnutrition3. Optimize patient’s metabolic state by

managing fluid and electrolytes

NUTRITIONAL ASSESSMENT Clinical judgment must play a major role in

deciding when to begin/offer nutrition support

Determine Nutrient Requirements Energy Protein Vitamins, Minerals, Trace Elements Nonprotein Substrate

◦ Carbohydrate◦ Fat

Energy Enough but not too much Excess calories:

◦ Hyperglycemia Diuresis – complicates fluid/electrolyte balance

◦ Hepatic steatosis (fatty liver)◦ Excess CO2 production

Exacerbate respiratory insufficiency Prolong weaning from mechanical ventilation

What Weight Do You Use? Lean body mass is highly correlated with

actual weight in persons of all sizes Studies have shown that determination of

energy needs using adjusted body weight becomes increasingly inaccurate as BMI increases

25 YOWM in a MVA 9 months ago 5’ 11”, 180 lbs at time of accident Transferred to ward – 135 lbs Received tube feeding Bed ridden without exercise

Case Study – Catabolic Flow Phase

http://www.car-accidents.com/2008-collision-pics/3-23-08-head-injury-1.jpg

Objectives First, fluid resuscitation and treatment When hemodynamically stable, begin

nutrition support (usually within 24-48 hours)

Nutrition support may not result in +N balance – want to slow loss of protein

Undernutrition can lead to protein synthesis, weakness, multiple organ dysfunction syndrome (MODS), death

Determine Nutrient Requirements Energy Protein Fat Carbohydrate Vitamins, Minerals, Trace Elements

Routes of Delivery By mouth

Enteral Nutrition

Parenteral Nutrition

http://healthycare-tutorials.blogspot.com/2011/07/healthy-eating.html

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http://media.rbi.com.au/GU_Media_Library/ServiceLoad/Article/old_man_hospital_tstock.jpg

Specialized Nutrients in Critical Care Immunonutrition and immunomodulaton

◦ gaining wider use in care of critically ill and injured patients.

Thesis – specific nutrients can…◦ enhance depressed immune system or ◦ modulate over reactive immune system

ASPEN BOD. JPEN 26;91SA, 1992

Include:◦ supplemental branched chain amino acids,◦ glutamine, ◦ arginine, ◦ omega-3 fatty acids, ◦ RNA, ◦ others

Specialized Nutrients in Critical Care Continued

Immune-enhancing formulas may reduce infectious complications in critically ill pts but not alter mortality

Mortality may actually be increased in some subgroups (septic patients)

Use is still controversial Meta-analysis shows reduced ventilator

days, reduced infectious morbidity, reduced hospital stay

Specialized Nutrients in Critical Care Continued

Along with alanine – makes up 70% of amino acids released after injury

Major carrier of nitrogen from muscle Non-essential amino acid (body can make) Major fuel for rapidly dividing cells Primary fuel for enterocytes

◦ Glutamine→alanine→glucose Use of glutamine as a fuel

spares glucose TPN often enriched with glutamine

Glutamine

Non-essential amino acid (body can make) Requirements increase with stress Appears necessary for normal T-lymphocyte

function Stimulates release of hormones – growth

hormone, prolactin, and insulin Studies show may increase weight

gain, increase nitrogen retention, andimprove wound health

Use controversial – some studies show reduced mortality

Arginine

Part of DNA and RNA Part of coenzymes involved in ATP

metabolism Rapidly dividing cells, like epithelial cells

and T lymphocytes, may not make Nucleotides are needed during stress. Addition of nucleotides to immune-

enhancing diets shown to reduce infections, ventilator days, hospital stay

Nucleotides

Vitamin C and E; selenium, zinc, and copper Meta-analysis (11 trials)

◦ Use significantly reduced mortality◦ No effect on infectious complications

Current recommendation…provide combination of all of these

Antioxidant Vitamins and Trace Minerals

http://www.secretsofhealthyeating.com/image-files/antioxidants.jpg

Incorporated into cell membranes Influence

◦ membrane stability ◦ membrane fluidity◦ Cell mobility and ◦ Cell signaling pathways

Omega 3 fatty acids

http://www.omega-3-forum.com/fattyacids.jpg

Essential amino Acids Oxidation increases with injury/stress May reduce morbidity and mortality Study – trauma patients

◦ Improved nitrogen retention, transferrin levels, lymphocyte counts

Use is still controversial

Branch Chain Amino Acids

http://extremelongevity.net/wp-content/uploads/Branched_chain_aa.jpg

25 YOWM in a MVA 9 months ago Patient is bedridden. He is able to move all 4 limbs without any

coordination. Does not appear to respond to voices. Tube fed – weight gain common. Stable enough to go to skilled nursing center Mother refuses skilled nursing center and takes

him home. Weight increases. Becomes constipated.

Case Study – Anabolic Flow Phase

http://www.car-accidents.com/2008-collision-pics/3-23-08-head-injury-1.jpg

Goal - replacement of lost tissue What has been happening? Reduced calories Added fiber to tube feeding Pushed water before and after each feeding Gave prune juice twice a day Get bed weight

Nutritional Needs

Phase

Dur-atio

n RolePhysiologic

alHormone

sNutritional

NeedsEbb <24

hrs•Maintenance of blood volume

↓BMR↓temp↓O2 consumed↑heart rate↑Acute phase proteins

•Catechol-amines•Cortisol•Aldosterone

•Replace fluids

FlowCatabolic

3-10 days

•Maintenance of energy

↑BMR↑temp↑O2 consumedNegative N balance

↑glucagon↑insulin↑cortisol↑catecholaminesInsulin resistance

•Appropriate calories to maintain weight•Adequate protein to stabilize or reverse negative N balance

Anabolic 10-60 days

•Replacement of lost tissue

Positive N balance

•Growth hormone•IGF

•Calories, protein and nutrients for anabolism

Summary

So why is this important for physical therapist?

What did this patient lose? What is this called? Is more dietary protein better? What happened when the patient was fed

too much? Any lessons for athletes here?

Questions

Hormonal Stress Response

Aldosterone—corticosteroid that causes renal sodium retention

Antidiuretic hormone (ADH)—stimulates renal tubular water absorption

These conserve water and salt to support circulating blood volume

Hormonal Stress Response cont’d

ACTH—acts on adrenal cortex to release cortisol (mobilizes amino acids from skeletal muscles)

Catecholamines—epinephrine and norepinephrine from renal medulla to stimulate hepatic glycogenolysis, fat mobilization, gluconeogenesis

Cytokines Interleukin-1, interleukin-6, and tumor

necrosis factor (TNF) Released by phagocytes in response

to tissue damage, infection, inflammation, and some drugs and chemicals