Download Nutrition in the surgical patient

Nutrition in the Critically Ill patient
Dr. Gwynne Jones
CCM Surgical Refreshment
December 2010
5/23/2017
Are Two Sphyncters Better Than
One?
• Why feed?
• All would agree that food is an
important part of a balanced diet.
5/23/2017
Nutrition:
Aims
• Preserve lean body mass - Protein
• Increase protein synthesis or reduce
catabolism
• Improve/maintain immune-function
• Shorten hospital stay
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Nutrition:
MEANS
• Normal food
• Enteral nutrition
• Parenteral nutrition
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MALNUTRITION:Caloric need during illness
• How many calories would you feed your postoperative patient?
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MALNUTRITION:Caloric need during illness
• ?
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MALNUTRITION:Caloric need during illness
• Around 25 calories/Kg/day.
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MALNUTRITION:Caloric need during illness
• How much protein would you feed your postoperative patient?
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MALNUTRITION:Caloric need during illness
• About 1.5 Gm amino acids/Kg/day.
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Nutrition: Definitions
• Malnutrition: a disproportion
between intake and expenditure of
energy and/or essential nutrients
• Starvation: first fat, then protein at
low speed
• Catabolic Disease: fat and protein
simultaneously
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NUTRITION: Maintenance of Lean Body Mass
• Maintenance of cell membrane function
• Cell replication
• Protein Synthesis (structural, messengers,
etc.)
• Muscle contraction (heart, diaphragm,
etc.)
• Energy generation
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Nutrition: Definitions
The Metabolic/Nutritional Syndrome of Critical Illness
•
•
•
•
•
Malnutrition/catabolism
Hyperglycemia/Insulin Resistance
Impaired Immune Function
Abnormal Neuro-endocrine Function
Neuro-muscular weakness
• Shock from any cause is an Energy Crisis
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Nutrition: Metabolic Profiles
Body Composition
• Fat free body water in normal state is + 73%.
• This may increase to 84% in the
hypermetabolic/hypercatabolic patient.
• This is associated with a loss of lean body mass
(fewer and smaller cells). These are the working
parts whose loss accounts for the progressive loss
of physiological function.
• Smaller cells reduce protein anabolic function.
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Nutrition: Metabolic Profiles
Body Composition
100
90
80
70
60
50
40
30
20
10
0
Normal
Critical Illness
Weight
%
FAT
Extracellular water
Body cell mass
1st Qtr
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3rd Qtr
Nutrition: Metabolic Profiles
Protein Catabolism
Protein
metabolism
Breakdown
Synthesis
Severity of trauma/sepsis
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Nutrition: Metabolic Profiles
Protein Catabolism
(N2) losses/ day
• Minor surgery:
3-5g
• Major surgery:
4-10g
• Multiple trauma/burns: 15-20g
• Head injury:
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20-25g
Nutrition: Metabolic Profiles
Protein Catabolism
(losses/day)
N2/day Protein/day
• Minor surgery:
3-5g 18.25-31.25 G
• Major surgery:
4-10G
25-62.5 G
• Multiple trauma/burns:
15-20G
48-125 G
• Head injury:
20-25G
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125-155G
Nutrition: Metabolic Profiles
Starvation
• Nitrogen balance Negative
Catabolic Disease
Very Negative
• Protein turnover
to
• Muscle catabolism
to
• Visceral catabolism
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• Urea
production
or
or
Nutrition: Metabolic Profiles
Starvation
•
•
•
•
•
•
Metabolic rate
Blood Sugar
Insulin level
Glucagon level
Ketone production
Gluconeogenesis
• Lipolysis
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Catabolic Disease
to
or
to
to
to
to
Triglygeride
recycling
Nutrition: Metabolic Profiles
Starvation
Catabolic Disease
Metabolic rate
to
Severely ill patients (septic, major trauma or postoperative) are hypermetabolic and hypercatabolic.
Oxygen consumption may be increased 50-100%.
This metabolic activity is needed to maintain high
cardiac output and ventilatory needs, liver acute
phase response and increased immunological
activity for healing.
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Nutrition: Metabolic Profiles
Starvation
• Blood Sugar
• Insulin level
or
Catabolic Disease
to
to
to
• Glucagon level
This is the stress glucose response. There is
insulin resistance both at receptor and postreceptor level.
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Hyperglycemia
is immuno-depressive.
Nutrition: Metabolic Profiles
Starvation
Catabolic Disease
• Ketone production
Although ketone utilisation is still possible, the
metabolism is altered such that ketones cannot
be synthesised. This reduces fuel efficiency,
especially in the brain, increasing energy needs
and gluconeogenesis
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Nutrition: Metabolic Profiles
Starvation
• Lipolysis
Catabolic Disease
Triglygeride
recycling
Lipids are well used in the stress state. Lipolysis
may be so activated that free fatty acid provision
exceeds requirements.
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Nutrition: Metabolic Profiles
Starvation
• Lipolysis
Catabolic Disease
Triglygeride
recycling
Fatty Acids are toxic. They are particularly toxic
for the Mitochondria.
Fatty Acids are re-esterified often producing
hyperlipidemia. This is especially so with high
lipid intakes.
Hyperlipidemia is immuno-depressive.
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MALNUTRITION: Assessment
Anthropometry
• Triceps and subscapular skinfold thicknesses provide
an index of body fat
• Midarm muscle circumference provides a measure of
muscle mass
• Unfortunately 20%- 30% of healthy controls seem
malnourished
• Markedly reduced values ( <5th percentile) do have a
poor outcome
In Our Society these are almost useless
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MALNUTRITION: Assessment
Clinical Assessment: Still Best
• Subjective Global Assessment (SGA)
encompasses:
• Nutrient intake (recent dietary intake, weight
loss, malabsorbtion)
• Effect of malnutrition on organ function and
body composition
• The patient’s disease and its influence on nutrient
requirements
– [ Detsky et al. JPEN 1987; 11: 8 ]
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MALNUTRITION: Assessment
Immune Competence
• Delayed Cutaneous Hypersensitivity
(DCH), anergy is a good predictor of
poor outcome but is not only a nutritional
marker
• In-vivo and in-vitro immune analyses are
becoming more valuable as are Cytokine
levels, but these again are not only
influenced by nutrition
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MALNUTRITION: Assessment
Muscle Function
• Grip strength
• Respiratory muscle strength
• Response of muscle to electrical
stimulation
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MALNUTRITION: Assessment
Serum Protein Concentrations
• Albumin: best independent predictor
(with age) of outcome. However not
entirely a marker of nutrition
– Prealbumin
– Tranferrin
– Haptoglobin
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Negative Acute
Phase Proteins
Nutritional goal in ICU
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Nutrition:Does it work?
•
•
•
•
•
•
Is outcome better with feeding?
TPN or ENTERAL nutrition?
Early feeding?
What quantities?
What ideal qualities?
Immuno-nutrition?
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Nutrition: Metabolic Profiles
100
Weight%
Decision Box
Increased
complications
50
†
Starvation
Hypermetabolism/
Hypercatabolism
4
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8 12
Weeks
†
14
16
MALNUTRITION:
Measurement of metabolism in MOF.
Bartlett et al. Surgery1982;92:771-779
100
80
Survival
%
60
40
20
0
positive
0-10K-ve
>10k-ve
Cumulative Caloric Balance
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MALNUTRITION:
Inflammatory bowel disease; Christie&Hill
Grip strength
100
%
Normal
Value
Gastroenterology
1990;99:730-736
Vital capacity
50
0 7 14
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Days
200
Nutrition: Metabolic Profiles
Elective abdominal surgery
depresses muscle protein B Peterson et al.
Br.J.Surg1990;
synthesis and increases fatigue
77:796-800
Fatigue
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5 Post-operative day
25
30
Nutrition: Metabolic Profiles
• Ebb
Phase:
acute
trauma/
shock
period
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Flow Phase:
hypermetabolism,
hypercatabolism
followed by healing
Nutrition: Metabolic Profiles
• IV carbohydrate or fat totally inhibits
gluconeogenesis in normal state.
• Provision of all measured caloric needs in
stressed patients ( severe sepsis, severe trauma
etc.) is able to reduce gluconeogenesis by only
50%.
• Thus, even optimal nutrition in the highly
stressed cannot stop protein/ lean body wasting,
only
reduce
the
rate
of
this
loss.
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Nutrition: Metabolic Profiles
• In the normal fasting state, 10% of energy needs
are provided by oxidation of amino acids.
• This protein oxidation increases to 15% after
eating.
• Oxidation of amino acids may increase to 25%
in the highly stressed patient.
• This obligates provision of a high protein intake
( + 1.5 G/Kg/day )
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MALNUTRITION:Peri-operative TPN
The VA TPN study group NEJM1991;325:525-532
395 mal-nourished patients requiring
non-urgent laparotomy or thoracotomy
TPN 7-10
days pre-op
x9
x3
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Non-infectious complications
Mild malnourished
Severe malnourished
Infectious complications
Mild malnourished
Severe malnourished
Control
Nutrition: TEN vs TPN
Moore et al. Annals of surg 1992;216:172-183
75 patients with severe trauma(ATI>15<40) randomised at
laparotomy to receive early feeding (within 72hrs.) with
iso-caloric, iso-nitrogenous solutions. Enteral fee via
needle catheter jejunostomy using Vivonex. TPN using
Freamine. TEN (29pts), TPN (30pts) well matched in age
and illness severity.
TPN
TEN
Infectious
complications
All infections
37%
17%
Major sepsis
20%
3%
Nutritional/
Albumin
metabolic
Nitrogen balance +0.1gm
-0.3gm
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NUTRITION:Aim of early enteral feeding
•
•
•
•
•
Anabolism/ Reduction of Catabolism
Avoidance of Hypermetabolism
Nurturing of gut micro-organisms
maintenance of gut mucosal health
Improving outcome?
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Nutrition:TEN VS TPN
Alexander et al. JPEN 1986;10:139
• Wesley Alexander has done innumerable
nutritional manipulations in poor, unfortunate
flame burned guinea pigs.
• Early gut feeding, especially of whole protein
reduces hypercatabolism, reduces muscle loss
and maintains gut integrity.
• His specially formatted EN solution improved
outcome in severely burned humans in
comparison to usual EN
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NUTRITION: The gut as immune organ
• Fasted animals have greater metabolic
response to stress than fed animals
• Human “volunteers” fed parenterally for
one week have a greater metabolic
response to endotoxin administration than
do enterally fed “volunteers”
• Metabolic effect lost if feeding not started
within 24 hours
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Nutrition:TEN VS TPN
Fong et al. Ann. Surg.1989;210:449-457
• TPN and bowel rest modify metabolic response to
endotoxin in humans.
• 12 healthy volunteers. Subjected to 7 days of either
parenteral or enteral feed of equivalent protein &
caloric content. Fasting overnight on day 7 then Am dose
of endotoxin.
• TPN group much sicker.
Stress
hormone
level
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TNF
NUTRITION:
Gut hypothesis of multi-organ failure
• Gut mucosal ischemia/permeability increase
• Gut micro-organisms or their toxins translocate
to mesenteric lymph glands or beyond
• Macrophage ingestion induces mediator release
• Clinical features of “sepsis’ and/or organ
dysfunction
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NUTRITION:
OXYGEN TRANSPORT
Capillary system of Gut Mucosa
Gut Mucosa
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Arteriolar Vasoconstriction produces
movement of oxygen
between arteriole and
venule. This leaves the villi
tips ischemic.
Prolonged shut-down
produces necrosis of the tips
of the villi. This is a
precedent to translocation.
NUTRITION: Gut bacteria
• Stomach: 102 organisms/ml.
• Small Intestine: intermediate numbers
increasing distally.
• Large Bowel: 109-1016 organisms/ml.
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NUTRITION: Colonisation
• Stomach: 102 organisms/ml.
• Small Intestine: intermediate numbers increasing distally.
• Large Bowel: 109-1016 organisms/ml.
• The progressive movement of gut organisms
proximally.
• This process is impeded by:
– Peristalsis
– Stomach acidity
– Normal gut ecology and food
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NUTRITION: Ileus.
• Paralytic Ileus is the transient
impairment of bowel motility after
abdominal surgery, other injury or severe
illness.
• Migrating Myoelectric Complex (MMC),
spikes occuring on the gut basal electrical
rhythm producing a propulsive
peristaltic wave.
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NUTRITION: Paralytic Ileus
.
• Paralytic Ileus:
– Most profound in large bowel with loss of
mass movement response and gastro-colic
reflex.
– The stomach is involved to a lesser degree.
– The small bowel is involved least.
Absorptive function is rarely reduced.
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NUTRITION: Paralytic Ileus
– Abnormal distension of a segment of bowel,
reflexly inhibits tone and motility of adjacent
bowel.
– This inhibitory reflex is centred on the spinal cord
and effected through sympathetic pathways.
– The longer the segment of distended bowel, the less
the intraluminal pressure needs to be to trigger the
reflex.
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NUTRITION: Paralytic Ileus
– Abnormal distension of a segment of bowel, reflexly inhibits
tone and motility of adjacent bowel.
– This inhibitory reflex is centred on the spinal cord and
effected through sympathetic pathways.
– The longer the segment of distended bowel, the less the
intraluminal pressure needs to be to trigger the reflex.
– Bowel dilatation breeds bowel dilatation
and indicates the need for
decompression.
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NUTRITION: Paralytic Ileus.
• Factors Aggravating Paralytic Ileus:
–
–
–
–
–
–
Drugs (esp opiates)
Diabetes
Electrolyte abnormalities
Shock
Respiratory failure
Trauma, sepsis, CNS disease, acidemia
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Are Two Sphyncters Better Than
One? Paralytic Ileus.
• Factors Aggravating Paralytic Ileus:
–Absence of food
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Are Two Sphyncters Better Than
One? Paralytic Ileus.
• Factors Aggravating Paralytic Ileus:
–Absence of food
–The propulsive peristaltic
activity and its underlying
myo-electrical activity need
sustained activity to maintain
their function.
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NUTRITION:Aim of early enteral feeding
Purported benefit of EN
Direct provision of
energy(glutamine,
SCFA)
Enterocyte trophic
hormone stimulation
eg Bombesin,
Increased biliary and
Urogastrone
pancreatic secretion
Increased mucosal
blood flow
Local autonomic
stimulation
Influence on gut permeability, translocation, metabolism
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When to start enteral nutrition?
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The Gut in Critical Illness
• The surface area of the intestinal mucosa is
300M2.
• It is adequate for digestion and absorption.
• There is a symbiotic relationship between the
host and the microbial population built up
over aeons.
• This allows both host and intestinal flora to
live in harmony.
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The Gut in Critical Illness
• There is a symbiotic relationship between the host and the
microbial population built up over eons. This relationship
prevents bacterial invasion and sepsis.
• Disturbance of either population is important.
• Always remember that there are more bacteria in
our gut then human cells in the body. We are the
parasites.
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NUTRITION: Gut bacteria
• Intestinal bacteria are saprophytic
• Starvation changes bacterial population
1. numbers 2. behavior (adherence/ toxin
production.)
• Some nutrients possess antibacterial
effects
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MALNUTRITION: Assessment
Clinical Assessment
• Effect of malnutrition on organ function and
body composition.
• You are due to operate on a patient urgently.
Would you prefer a patient who is malnourished
and has eaten until the day before surgery or a
patient who is well nourished but who has been
unable to eat for several days?
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MALNUTRITION:Caloric need during illness
• Streat et al. (J.Trauma1987;27:262-266)
• They measured body composition by in-vivo
electron analysis.
• Feeding more than 25KCal/Kg/day and 1.5G
Amino Acids/Kg/day only succeeded in
increasing fat deposition without increase in
protein anabolism.
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Enteral or Parenteral??
5/23/2017
NUTRITION: Arginine
• A conditionally essential amino acid.
• Levels fall rapidly in acute illness(50%plasma,
30%muscle). Level related strongly with
survival.
• Substrate for Nitric Oxide generation.
5/23/2017
NUTRITION:Arginine
• Supplementation of Arginine has shown:
improved nitrogen balance
improved wound healing and wound strength
• Secretogogue function:
growth hormone & Insulin like growth factor
Prolactin
Insulin & Glucagon
5/23/2017
NUTRITION:Arginine
• Substrate for Nitric Oxide
5/23/2017
• Arginine Supplementation is NOT recommended currently.
5/23/2017
NUTRITION:Glutamine
• Conditionally essential amino acid
• Rapidly falls in acute illness (esp. muscle)
• Muscle content important for protein
anabolism
• Important for normal function of rapidly
dividing cells (enterocytes, PMNs) and cells
requiring rapid bursts of activity (lymphocytes,
macrophages)
• 5/23/2017
Important for glutathione system
NUTRITION:Glutamine
Gln.
in
FOOD
GUT
Circulating
glutamine
pool
MUSCLE
LYMPHOCYTE
MACROPHAGE
PMN
KIDNEY
Gln.
Glutamate
LIVER
5/23/2017
LUNGS
ACID/BASE
NH4
NUTRITION:Glutamine
The role of Gln. In host defence
• It is the most abundant amino acid in the
body and in the intracellular free AA pool
• Its production by skeletal muscle is
dramatically upregulated in times of
stress and sepsis
• It is the principal carrier of nitrogen
between tissues and regulates protein
synthesis
5/23/2017
NUTRITION:Glutamine
The role of Gln. In host defence
• It is an essential precursor of nucleotide
synthesis
• It serves as a primary substrate for renal
ammoniagenesis and arginine synthesis
5/23/2017
NUTRITION:Glutamine
The role of Gln. In host defence
• Glutamine + Cysteine + Glycine = Glutathione.
• This is a major intra-cellular anti-oxidant.
5/23/2017
NUTRITION:Glutamine
The role of Gln. In host defence
• It is a primary oxidative fuel for rapidly
dividing cells (esp. enterocytes and immune
cells)
• The gut (enterocytes) uses Glutamine as a
primary fuel source.
• Little Glutamine reaches the plasma from
the gut in critically ill patients.
5/23/2017
NUTRITION:Glutamine
The role of Gln. In host defence
• TPN supplemented with Gln. Maintained
intestinal and respiratory tract IgA and mucosal
defence in mice
• This is achieved through maintenance of Th2
cytokines IL4, IL6 & IL10
5/23/2017
NUTRITION: Human outcome of immune enhancing enteral
feeding protocols.
Glutamine
• enteral nutrition dose ~ 0.3 gm/kg/day
• consider in burn/trauma patients
• ? other critically ill patients – lack of evidence
5/23/2017
NUTRITION:Omega 3 fatty acid
• Omega 6 FFA
• Arachidonic acid
• 2 series prostaglandins
PGI2,TXA2,PGE2
• 4 series leukotrienes-esp
LTB4
5/23/2017
• Omega 3 FFA
• Eicosapentanoic acid
• 3 series prostaglandins
PGI3, TXA3, PGE3
• 5 series leukotrienesesp LTB5
NUTRITION:Omega 3 fatty acid
• Enteral feeding with a diet supplemented
with eicosopentanoic acid, -linolenic
acid and anti-oxidants improved outcome
in patients with ARDS.
(Gadek JE et al. Crit..Care Med.1999;27:1409-1420)
5/23/2017
NUTRITION:Omega 3 fatty acid
Mortality100%
from
severe
sepsis/
septic
shock
0%
100%
Membrane content of Omega 3
PUFA
5/23/2017
NUTRITION: Human outcome of immune enhancing enteral feeding
protocols.
Fish Oils
– Fish Oils Enriched EN improved survival
in patients with ARDS/ALI
– ? decrease ventilator days and organ
failure
5/23/2017
NUTRITION:Nucleotides
• In critical illness, the body is unable to
make rapidly enough de novo or from the
scavenge pathway
• Deficiency in animals allows for allograft
acceptance
• Provision increases foreign graft rejection
• NB. Mother’s Milk
5/23/2017
NUTRITION:Vitamins & Minerals
•
•
•
•
•
Anti-Oxidants
Selenium
Zinc
Iron
B vitamins
5/23/2017
NUTRITION:Vitamins & Minerals
• Tight Sugar Control
5/23/2017
The Gut in Critical Illness
The common Mucosal Immune Hypothesis
• Peyer’s Patches are mostly in the small intestine.
• There is one layer of columnar epithelium, goblet
cells and microvillus (M) cells.
• M cells present antigen to underlying dendritic
cells and macrophages.
• These Ag are presented to naïve CD4+ T cells and
B cells for development of immune effector cells
and cytokines.
5/23/2017
The Gut in Critical Illness
• Defence mechanisms of the gut mucosa:
–
–
–
–
–
–
mucous coat.
Glycocalyx
Resident micro-flora (colonisation resistance).
Peristalsis.
Proteolytic GI sectetions.
Innate immune defences (lactoferrin, lysosyme, etc.).
–Specific IgA
5/23/2017
The Gut in Critical Illness
The common Mucosal Immune Hypothesis
Ingested
Antigen
Inhaled
Antigen
Genito-urinary Tract
Mammary Glands
Lamina
Propria
GALT
Peyer’s
Patches
5/23/2017
Blood
Stream
Nasal
Passages
MAdCAM
MLN
Specific
IgA
Thoracic Duct
CLN
NALT
When to start enteral nutrition?
Assumptions
5/23/2017
Nutritional goal in ICU
Assumptions
Timing of Nutritional Support
There are 8 RCTs (level 2 studies) of early [within
24-48 hours] enteral nutrition versus delayed
EN, PN or oral food intake.
Early EN was associated with a trend towards a
reduction in infectious complications
[RR 0.66. 95% CI 0.36-0.22. p=0.19]
(Criticalcarenutrition.com)
5/23/2017
The Impact of Permissive Underfeeding/Targeted Feeding on
Mortality and Morbidity in Adult Critically Ill Patients: A Multicentre Randomised Controlled Trial.
There are several studies showing low caloric intake to
be detrimental and higher caloric intake may be
associated with improved outcomes
Taylor; 82 head injured patients (CCM 1999) [RCT]
ACCEPT (CMAJ) [Cluster RCT]
Rubinson; 138 adult ICU pts. (CCM 2004) [Prospective
Cohort]
Singer; 53 adult ICU pts (Clin Nutr 2004) [RCT]
Villet; 48 adult ICU pts. (Clin Nutr. 2005) [Prospective
Observational
Faisy;
38 adult ICU pts. (Br J Nutr. 2008) [Prospective Observational
5/23/2017
Relationship Between Increased
Calories and 60 day Mortality
BMI Group
P-value
Odds
95%
Ratio Confidence
Limits
Overall
0.76
0.61
0.95
0.014
<20
0.52
0.29
0.95
0.033
20-<25
0.62
0.44
0.88
0.007
25-<30
1.05
0.75
1.49
0.768
30-<35
1.04
0.64
1.68
0.889
35-<40
0.36
0.16
0.80
0.012
>=40
0.63
0.32
1.24
0.180
Legend: Odds of 60-day Mortality per 1000 kcals received per day adjusting for nutrition days,
BMI, age, admission category, admission diagnosis and APACHE II score.
5/23/2017
RESULTS:
5/23/2017
WHO IS AT RISK?
References
5/23/2017