Lauri O. Byerley, PhD, RD

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

 Case Study  Phases of Injury  Physiological and Metabolic Consequence of Each Phase  Nutrition Support for Each Phase  Summarize

 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 collision-pics/ head-injury-1.jpg

 Trauma  Surgery  Sepsis (infection)  Burn

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

ADH, Antiduretic hormone; NH 3, ammonia.

 Involves most metabolic pathways  Accelerated metabolism of LBM  Negative nitrogen balance  Muscle wasting  Involves most metabolic pathways  Accelerated metabolism of LBM  Negative nitrogen balance  Muscle wasting

 <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.  <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

 3-10 days  Increased body temperature  Increased BMR  Increased O 2 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 (↑)

 days  Protein synthesis begins  Positive nitrogen balance

 Hormones involved: ◦ Growth hormone ◦ IGF

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

 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

 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***

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

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

 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? collision-pics/ head-injury-1.jpg

 Objectives of optimal metabolic and nutritional support in injury, trauma, burns, sepsis: 1.Detect and correct preexisting malnutrition 2.Prevent progressive protein-calorie malnutrition 3.Optimize patient’s metabolic state by managing fluid and electrolytes

 Clinical judgment must play a major role in deciding when to begin/offer nutrition support

 Energy  Protein  Vitamins, Minerals, Trace Elements  Nonprotein Substrate ◦ Carbohydrate ◦ Fat

 Enough but not too much  Excess calories: ◦ Hyperglycemia  Diuresis – complicates fluid/electrolyte balance ◦ Hepatic steatosis (fatty liver) ◦ Excess CO 2 production  Exacerbate respiratory insufficiency  Prolong weaning from mechanical ventilation

 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 collision-pics/ head-injury-1.jpg

 First, fluid resuscitation and treatment  When hemodynamically stable, begin nutrition support (usually within 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

 Energy  Protein  Fat  Carbohydrate  Vitamins, Minerals, Trace Elements

 By mouth  Enteral Nutrition  Parenteral Nutrition tutorials.blogspot.com/2011/07/healthy- eating.html ary/ServiceLoad/Article/old_man_hospit al_tstock.jpg

 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

 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

 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

 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, and improve wound health  Use controversial – some studies show reduced mortality

 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

 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 g.com/image- files/antioxidants.jpg

 Incorporated into cell membranes  Influence ◦ membrane stability ◦ membrane fluidity ◦ Cell mobility and ◦ Cell signaling pathways

 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

 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. collision-pics/ 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

Phase Dur- ationRolePhysiologicalHormones Nutritional Needs Ebb<24 hrs Maintenance of blood volume ↓BMR ↓temp ↓O 2 consumed ↑heart rate ↑Acute phase proteins Catechol- amines Cortisol Aldosterone Replace fluids Flow Catabolic3-10 days Maintenance of energy ↑BMR ↑temp ↑O 2 consumed Negative N balance ↑glucagon ↑insulin ↑cortisol ↑catecholami nes Insulin resistance Appropriate calories to maintain weight Adequate protein to stabilize or reverse negative N balance Anabolic10-60 days Replacement of lost tissue Positive N balance Growth hormone IGF Calories, protein and nutrients for anabolism

 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?

 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  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

 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  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

 Interleukin-1, interleukin-6, and tumor necrosis factor (TNF)  Released by phagocytes in response to tissue damage, infection, inflammation, and some drugs and chemicals  Interleukin-1, interleukin-6, and tumor necrosis factor (TNF)  Released by phagocytes in response to tissue damage, infection, inflammation, and some drugs and chemicals