Importance of Nutrition in Patient Healing and Recovery
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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
http://www.car-accidents.com/2008-
collision-pics/3-23-08-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
<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 (↑)
10-60 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.
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, 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
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?
http://www.car-accidents.com/2008-
collision-pics/3-23-08-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
http://www.car-accidents.com/2008-
collision-pics/3-23-08-head-injury-1.jpg
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
Energy
Protein
Fat
Carbohydrate
Vitamins, Minerals, Trace Elements
By mouth
Enteral Nutrition
Parenteral Nutrition
http://healthycare-
tutorials.blogspot.com/2011/07/healthy-
eating.html
http://www.dataphone.se/~hpn/mage.gif
http://media.rbi.com.au/GU_Media_Libr
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
http://www.secretsofhealthyeatin
g.com/image-
files/antioxidants.jpg
Incorporated into cell membranes
Influence
◦
membrane stability
◦
membrane fluidity
◦
Cell mobility and
◦
Cell signaling pathways
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
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.
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
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
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
Gain insight into the critical role of nutrition in aiding patients in their recovery from injuries and enhancing their physical well-being post-injury. Explore the phases of injury, the physiological and metabolic impacts of each phase, and the corresponding nutritional support strategies. Delve into a case study of a young male who sustained severe injuries in a motor vehicle accident and required intensive care. Understand the significance of proper nutrition in trauma, surgery, sepsis, and burns. Additionally, learn about metabolic pathways, muscle wasting, and hormonal responses in the body during the recovery process.
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Presentation Transcript
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 http://www.car-accidents.com/2008- collision-pics/3-23-08-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; NH3, ammonia.
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.
Hormones involved: Catecholamines Cortisol Aldosterone
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 ( )
10-60 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.
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, 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
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? http://www.car-accidents.com/2008- collision-pics/3-23-08-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 CO2 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 http://www.car-accidents.com/2008- collision-pics/3-23-08-head-injury-1.jpg
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
Energy Protein Fat Carbohydrate Vitamins, Minerals, Trace Elements
By mouth http://healthycare- tutorials.blogspot.com/2011/07/healthy- eating.html Enteral Nutrition http://media.rbi.com.au/GU_Media_Libr ary/ServiceLoad/Article/old_man_hospit al_tstock.jpg Parenteral Nutrition http://www.dataphone.se/~hpn/mage.gif
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 http://www.secretsofhealthyeatin g.com/image- files/antioxidants.jpg
Incorporated into cell membranes Influence membrane stability membrane fluidity Cell mobility and Cell signaling pathways 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 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. 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
Dur ation <24 hrs Dur- - ation Nutritional Needs Replace fluids Nutritional Needs Phase Ebb Phase Role Role Physiological BMR temp O2 consumed heart rate Acute phase proteins Physiological Hormones Catechol- amines Cortisol Aldosterone Hormones Maintenance of blood volume Flow Catabolic 3-10 days Maintenance of energy BMR temp O2 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 Calories, protein and nutrients for anabolism Anabolic 10-60 days Replacement of lost tissue Positive N balance Growth hormone IGF
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?
Aldosteronecorticosteroid that causes renal sodium retention Antidiuretic hormone (ADH) stimulates renal tubular water absorption These conserve water and salt to support circulating blood volume
ACTHacts 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
